Osteopathic Considerations in Systemic Dysfunction (2nd Ed)

Osteopathic Considerations
in Systemic Dysfunction
Revised Second Edition
Michael L. Kuchera, D.O., F. A. A.O

Professor and Chairman
William A. Kuchera, D.O., F.A. A. 0

Professor
Osteopathic Considerations
in Systemic Dysfunction
Michael Kuchera, D.O., F.A.A.O.

William Kuchera, D.O., F.A.A.O.
Greyden Press, LLC

_ Dayton, Ohio
� Original Works
Greyden Press, LLC Original Works Books Dayton, Ohio
Osteopathic Considerations in Systemic Dysfunction
Copyright © 1994 by Michael & William Kuchera. All rights reserved. Printed in the United States of America.
Except as permitted under the United States Copyright Act of1976, no part of this publication may be reproduced or distributed
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ISBN 1-57074-154-9
Printer/ Binder: Greyden Press, LLC

"Osteopathic physicians must be able to give a reason for the treatment
"
they give, not so much to the patient, but to themselves. 1
A.T. Still, M.D.
"The inevitable result of the rapid strides in the study of bacteriology,

and pathologic change in tissues and secretions, �nd the comparatively
slow progress which has been made in studying the patient, has been an
undue emphasis of the importance of the disease, and a minimizing of the
importance of the patient who has it. The dawning of a better day in
"
medicine, however, is now evident ... 2
F.M.Pottenger, M.D.
"(Neuroscience) studies are establishing the physiological bases for

determination in man of the visceral consequences of spinal syndromes
"
for which manipulative therapy is advocated. 3
Horace W. Magoun, Ph.D.
1. Truhlar RE Doctor A.T. Still in the Living. Cleveland, privately printed, 1950, P 112.
2. Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co, 7th ed, 1953, P 34.
3. Magoun HW: Neuroscience studies in Goldstein M (ed) The Research Status of Spinal Manipulative Therapy, Bethesda
MD, US Department of Health, Education and Welfare (NINCDS Monograph #15), 1975, p 210.
THIS PAGE INTENTIONALLY LEFT BLANK
FOREWORD
Osteopathy is relatively a young profession in the history of medicine. Slightly

over 100 years ago, A.T. Still introduced his philosophy of medical care to the
world. The first school of osteopathy was established in Kirksville, Missouri in
1892. It was in this same time period that the germ theory was proposed and
eventually the allopathic profession adopted the perspective that this was "the
answer to all disease processes." With the discovery of Salversan and
eventually penicillin, the allopathic profession launched into an all-out effort to
find medicines which would be the "magic bullets." The germ theory of disease
promoted the concept that health would be restored and secure if the offending
"germ" was found and medically removed.
Because of this majority perspective there are thousands of articles and texts
reporting experiences and trials in the use of medications for the treatment of
systemic diseases. On the other hand there is relatively little published about
augmenting homeostasis or treating host factors in systemic diseases. This text
was written to augment the latter category and stresses the structure and function
that are pertinent to this perspective. Without specific knowledge of anatomy
and physiology, the osteopathic approach would become too "time consuming"
and would not be financially feasible to offer a patient with systemic disease.
Osteopathic physicians are educated to use and understand all current

medications and surgical procedures for the purpose of promoting health,
fighting the disease and supporting the host's physiology. Palpatory and
manipulative skills can be used effectively as well as efficiently to aid in
diagnosis and treatment of patients with systemic disease or dysfunction.
This text has been divided into several sections in order to present an
osteopathic approach to dysfunction manifesting in a particular system or
pertinent to a common clinical presentation. These divisions have been
primarily grouped by their common autonomic and lymphatic elements but the
physician must not be limited to management of the patient within a given
system (or section of this text). Because each patient is a unit, dysfunction or
disease affecting one part can have far-reaching manifestations.
This text does not propose to replace the many reference texts of medicine and
does not include a complete differential diagnosis or a complete treatment plan
for the clinical situations that are discussed. Its purpose is to explore selected
structural and functional considerations which may produce symptoms or
iv
compromise homeostasis. It also demonstrates, by example, clinical application
of the osteopathic philosophy in selected situations. Lastly, it attempts to show
where osteopathic manipulative treatments can be prescribed as primary or
adjunctive modalities available to the D. O. as they assist patients in reaching
their maximum health potential.
Even if the patient does not have specific joint somatic dysfunction,
manipulative management can be designed to address the following goals:
o .. support the patient's body systems that will be stressed by the

pathophysiology of the disease
o .. support the patient's natural protective and homeostatic reactions to disease
o .. neutralize detrimental responses of the patient's body to the disease process
o .. provide a synergistic and physiologic approach to the patient's medical
and/or surgical management
o .. provide a rapid and long-lasting benefit toward improving the patient's level
of health and immediate comfort
Dysfunction of the soma and its related elements plays a significant role in the
production of a variety of patient complaints, signs, and/or symptoms and
frequently accompanies underlying visceral dysfunction. For these reasons,
palpation for somatic dysfunction is an important part of an osteopathic
approach to making a differential diagnosis and it provides essential data for
developing a rational total treatment program for the patient. Because
osteopathic manipulative treatment is designed to treat the patient's soma and/or
to support systemic protective and homeostatic mechanisms, a therapeutic trial
of manipulation which addresses the patient's somatic component is an
important part of a rational treatment protocol for each patient's visit.
By studying anatomy and physiology from the philosophical vantage point

needed to formulate "rational osteopathic treatment," the osteopathic student
discovers a unique and valuable perspective of health and disease.
Interpretation of somatic clues through understanding of the physiology
underlying symptom development allows the physician to surmise the
dysfunction or pathophysiology occurring in a given individual patient and
offers valuable direction and information for the physical examination and the
differential diagnosis. Rather than simply diagnosing and treating symptoms or
symptom complexes, the osteopathic physician seeks to augment the health that
is found within the individual.
v
The following relevant comments are found in Pottenger's Symptoms of
!
Visceral Disease :
"Variability of symptoms is the rule in clinical medicine, a fact which

can be readily appreciated by understanding the nerve and chemical
control of physiologic function and the factors which influence them,
both physical and psychic."
"It is not only necessary to understand that symptoms produced by a

given disease may differ in different individuals and in the same
individual at different times, but it is equally necessary to bear in mind
that while the stimulus which would be expected to produce a given
symptom is present, the symptom may not appear or its reverse may
appear if the stimulus to the nerve is excessive, or the neuron itself is
hyperexcitable or a certain ionic concentration exists in the body cells.
It is necessary, therefore, always to bear in mind that inflammation in
organs gives origin to stimuli which have a tendency to produce such and
such symptoms, although the symptoms themselves may not
materialize."
"Most of the important symptoms arising from diseases of internal

viscera are reflex in nature. In order to understand these symptoms, one
must study the innervation of the various viscera and the
interrelationship which exists between them, also the interrelationship
which exists between the viscera and the skeletal structures. "
This text encourages the reader to reexamine familiar medical facts, anatomic
relationships and physiologic functions from the osteopathic perspective. This
perspective can then be carried into the diagnostic and therapeutic decisions
which will repeatedly be required of the medical student and the osteopathic
physician for the rest of their professional lives.
1. Pottenger F M Symptoms of Visceral Disease. St Louis, CV Mosby Co,

7th ed, 1 953, 140.
vi
TABLE OF CONTENTS
��1r J)1{��C:1rI()� ••.•••••.•••••••••••••••••.•.•••••••••.•.••••••••••••••.•••••.•.••••..••• 1
Introduction . . .. ..
. . . . . . . . . . . . . . . . . . .. . . 1
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pathophysiology . .. . . . . . . .
. . . . . . .
. . . . . . . . . . . .2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Reflex Connections .. . . . . . . . . . . . 2
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sympathetics ... ...

. . . . . . . . . . . . . 2
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Parasympathetics . . . . .
. . . . . . . . . . . .
. . 4
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Venous And Lymphatic Systems . . . 6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Neural System . . ..
. . . . .
. . . . . . . . . . . . . . . 6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Somatic System . . . .
. . . . . . . . . . . . 8
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Treatment . . . . . .
. . . . . . . . . . . . .. .
. . . . . . ... .
. . . . . . .. .. 12
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
The Eye . .. . . . . . . . ... .

. . . . . . . . . . . . . . . . . . . . . . . 13 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
The Ear .. . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
The Nose ... . .

. . . . . . . . . . . . . 16
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
The Throat. .. .. . .
. . . . . . .
. . . . . . . ..
. . . 17
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
The ENT Unit . .. . . . .

. . . . . .. . . 17
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Summary 19
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Additional EENT Bibliography.......................................................... 19

References .................................................................................. 19
1rII� <:()�()� <:()� .......................•••............................................. 23
Introduction ................................................................................ 23
Pathophysiology ........................................................................... 24
Treatment ................................................................................... 25
Summary.................................................................................... 29
References .................................................................................. 30
WWER R.ESPIR.ATORY DISORDERS ...............................................•... 33
Normal Functional Respiration .......................................................... 33

Pathophysiology . . . ...
. . . . . . . . . . . . . . .
. . . . . . . . . .. 36 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Reflex Action During Infection . . . .. . . 36 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sympathetics . . . . . . . . ... 36
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Parasympathetics ................................................................... 38
Somatic System ..................................................................... 38
Lymphatics .......................................................................... 39
vii
Treatment ....................................................... . . . ......................... 40
Pneumonia ..... . ......... . . ......... . ........ . . . . ......... . ...... . ......... . . . ....... 40
Sample of Treatment Protocol For Pneumonia .. . ...................... 45
Prevention of Postoperative Pulmonary Complications ....................... 46
Chronic Obstructive Pulmonary Disease ............ . ........................... 48
Asthma ....................... .......................... . . ............ . . . . ............ 48
Summary .................................................................................... 51
References .................................................................................. 51
CARDIOVASCULAR DISORDERS ........................................................ 53
Introduction ...... . . . ....................................................................... 53

Pathophysiology ........................................................................... 53
Sympathetics ..................................... ................................... 53
Parasympathetics .................... . . .. . . . ........................................ 55
Lymphatics ............................. . . . ........... ............................... 56
Somatic system .................................... . .......... . ............. . . ...... 57
Referred Patterns ......................................... . ................ . .. . . ... . 58
Treatment Summary ................................................................ . ... . . 59
Myocardial Infarction . .................... ........................ . . ............... 59
Essential Hypertension ........................................ . .................... 61
Congestive Heart Failure ........................ . . .............. . . . ............... 66
Arrhythmias ......................................................................... 67
Clinically Relevant Abstracts--Bibliography .................................... . ...... 68
Autonomic Nervous System ........................................... ........... 68
Lymphatics .... . . . .......... . ........................................................ 70
Text References ...................... . ............... . . . . ..................... . ............ 73
Additional Cardiac References ..................... . . . . ............................. . . . . 76
UPPER GI DISORDERS ...................................................................... 79
Introduction ........... . ........... . ... . . ...................... . ............... . .. . . . . . . . . .. 79

Pathophysiology ........................................................... . ............... 79
Viscerosensory And Visceromotor .......................................... . .... 79
Sympathetics ................................................................ . ... . ... 83
Parasympathetics ................. . ................................................. 84
Lymphatics . . ......................................... . .............................. 85
Somatic System ............................. . . . . . ................... . . . . . ........... 86
The Philosophy of Treatment ............................ . . . .......... . .. . ............... 87
Osteopathic Treatment . . . . . ................................... . ............... . ........... 89
Lymphatics And Fascias ............................... . . . . ........................ 89
Sympathetics ............................................................... . ........ 90
Parasympathetics ................................................................... 92
Summary ...................................... . ....... . .. . . . ..... . . . . . .............. . ....... 93
References .......... ........................................................................ 93
viii
WWER BOWEL DISORDERS ............................................................. 95
Introduction ............................................................................ ... 95 .
Pathophysiology ..................................... .................. .................... 96

Sympathetics ........................................................................ 96
Parasympathetics ................................................................ ... 97
Lymphatics .......................................................................... 98
Viscerosensory And Visceromotor............................................. 100
Somatic ............................................................................ 100
Osteopathic Manipulative Treatment ................................................. 101
Sympathetic Dominant Complaints............................................ 104
Parasympathetic Dominant Complaints ............................. ......... 104 .
Other Complaints................................................................. 105

Summary 106
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References. ............................................................................... 106
IR.R.ITABLE BOWEL SYNDROME- ...................................................... 109
Introduction .............................................................................. 109

Physiology..... ........................................................................... 111
Intrinsic Nerve Control.......................................................... 111
Extrinsic Nerve Control ......................................................... 112
Sympathetic Innervation......................................................... 112
Parasympathetic Innervation .................................................... 112
Characteristics ........................................................................... 113
Treatment Considerations .............................................................. 116
Pharmacologic Treatment ....................................................... 116
Osteopathic Manipulative Treatment ................................................. 117
Affecting The Somatic Component............................................ 118
Affecting Sympathetics . ......................................................... 118
Affecting Parasympathetics ..................................................... 119
Affecting The Lymphatic System .............................................. 120
Summary.................................................................................. 121
References.. .......... ............................... .............................. 122
GENITO'URIN'ARY TRACT DISORDERS ............................................. 123
Introduction .............................................................................. 123

Kidneys, Ureters And Bladder......................................................... 124
Sympathetics ...................................................................... 125
Parasympathetics ................................................................. 126
Lymphatics ........................................................................ 127
Viscerosensory/Visceromotor Reflexes ...... ..... ..... ....................... 127
Somatic System................................................................... 127
ix
Genital/Reproductive System .......................................................... 129
Sympathetics And Parasympathetics ........................................... 129
Lymphatics ............... ...................................... .
. .. ... .. . . . . . . . . . . 130
Viscerosensory And Visceromotor............................................. 131
Somatic System................................................................... 132
Treatment Conslderations .... ... ........ .... . . .. . . . . .... ... ....
. . . . . . . . . . . . . . . . . . . . . . . . 133
Urinary Tract Infections......................................................... 134
Renal Disease ..................................................................... 135
Prostatitis .. ........................................................................ 136
Ureterolithiasis ................................................................. '" 137
Dysmenorrhea .............. ... .... . .... . .... ..... ... ................
. . . . . . . . . . . . . 139
Sexual Dysfunction............................................................... 142
Erectile Dysfunction .. .. .................... ..........................
. . . . 142
Premature Ejaculation .................................................... 143
Dyspareunia ................................................................ 143
Infertility ................................................................... 144
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
TIlE OBSTETRICAL PATIEN'T .......................................................... 149
Existing Stresses Aggravated By Pregnancy......... .... .. .... .. . .. .... . . . . . . . . . . . . . 149

Gravity ............................................................................. 149
A Basic Physiological Relationship .................. ........... ..... . .... . . . . . 149
The Unique Valveless Venous System ........................................ 150
Stresses Added Specifically By Pregnancy .......................................... 151
Mechanical ..... .................................................. .. ... ...
. . . . . . . . . 151
Physiological... ................................................................... 151
Lymphatic ................... ...................... ... . .......
. ... .. .... . . . . . . . . . . . 151
Venous ............................................................................. 152
Hormonal.... ...................................................................... 152
Relative Contraindications to OMT................................................... 152
Distinctive Osteopathic Thinking ..................................... ... . .. ... . . . . . . . 152
An Aid in Preventative Care...... .............. ..................... ........ . . . 153
A Diagnostic Aid........................................ ......................... 153
A Treatment Advantage ......................................................... 153
Distinctive Osteopathic Treatment .................................................... 153
The Structural Stage .................... .... .... ...... ... .................... . . . . 153
The Congestive Stage............................................................ 155
The Preparatory Stage ........................................................... 156
Labor and Delivery ....... ................. ............... ....................
. . . 157
The Recovery And Maintenance Stage........................................ 157
References ......... ... ....................... .... . ... . ....................... .....
. . . . . . . . 158
x
RHEUMATOWGIC DISORDERS ......................... .............................. 159
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
Pathophysiology ... ...................................................................... 159
Sympathetics ...................................................................... 160
Somatic System................................................................... 161
Lymphatics ........................................................................ 162
Parasympathetics ................................................................. 163
Other Factors ..................................................................... 163
Treatment.. ............................................................................... 163
Osteopathic Manipulative Techniques ......................................... 164
Other Management Concerns................................................... 166
Summary. ................................................................................. 167
��" ()If ��])( ••.••..••••••.•••••••••••••••••••••••••••••••••.•.......•.••••••...... 169
Manipulation In The Pediatric Patient................................................ 171

Osteopathic Considerations In Psychiatry (Bibliography) ......................... 181
Osteopathic Considerations In Immunology (Bibliography)....................... 182
Hypersympathetic Activity On Selected Tissues (Korr) ........................... 183
Autonomic Influence On Selected Tissues........................................... 187
Osteopathic Manipulative Treatment In Systemic Dysfunction................... 189
Basic Plan And Goals............................................................ 189
Chart: Sympathetic/Parasympathetic Innervation ............................ 192
Ventral Abdominal Techniques:
Indications and Contraindications....................................... 227
Chapman I s Charts ................................................................ 232
PRACTICAL �EX FOR OSTEOPATHIC

MANIPULATIVE TECHNIQUE IN SYSTEMIC DISEAS .000000000000000000 234
xi
INDEX OF FIGURES
Figure 1 All Parasympathethic Ganglia of Head and Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Figure 2 Sympathetic Innervation to Head and Neck . . . . . . . . . . . . . . . . . . .
.. .. .. .. 2 .. . ... . ....
Figure 3 Anterior Chapman Points to Head, Neck, Bronchi . . . . . . . . . . . . . . . . . 3 .. . .. . . . . . . ..
Figure 4 Ciliary Ganglion to Eye (parasympathetic) . . . . . . . . .. .. . ... 5

. . . . . .. . . . . .. . . . . ......
Figure 5 Parasympathetic Innervation to Head and Neck . . . . .. . . . 5

........ ..... . .... ... . ...
Figure 6 Sphenopalatine Ganglion to Nasal Mucosa and Lacrimal Gland . . . . . . . . . 5 . ... . .
Figure 7 Richardson's Eye Exercise Chart . . . . . . . .. . .

........................ 13 .. .............
Figure 8 Cervical Sympathetic Ganglia . ..

........................... . . . . . . . . . . . . 26 ..... . .. ...
Figure 9 Important Landmarks of Normal Thoracic Inlet . . . .. . . . . 27

............. ..... .....
Figure 10 Sphenopalatine Ganglion (parasympathetics to Lacrimal Gland

and Respiratory Mucosa of Sinuses . . . . . .. . . . . . . . . . . . . . . 29
........ ... . . ... . . .. .
Figure 11 Diaphragmatic Action (A Major Lymphatic Pump) .. . . .. . . . . . . . . . 33 .. . . .. . ... . .
Figure 12 Innervation of the Lung

and Viscerovisceral and Viscerosomatic Reflexes . . . . . . . . . . . . . . . . 34 ... . .. . . . .
Figure 13 Anterior Chapman Points of Cardiopulmonary System . . . .. . . . . . . . . . . . . 37 . . . . . .
Figure 14 Diaphragmatic Action (A Major Lymphatic Pump) . . . . . . . . . . . . . . . . . . . . . . 39 . . . . .
Figure 15 Common Lymphatic Drainage of the body . . . . . .

....... . . . . . 40
. ...... .... . ..... .. .
Figure 16 General Movement of Ribs and Sternum During Respiration . . . . . 44 .. ... . .....
Figure 17 Sympathetic Innervation of Heart . . . .. .. ... . . . .... ...

........... .. . . 54
.. ... .. . . .....
Figure 18 Diagram of Sympathetic Innervation of Body . . . . . .... .... . . .. 54

.... ... ... .......
Figure 19 Parasympathetic Innervation of the Body . . . . . . . ...

. ... . . . . .. 55
.... ...... ...... . . ..
Figure 20 Lymphatic Drainage of the Body . . . . .........

........................... 56 .. .. . . ...
Figure 21 Travell Pectoralis Major Trigger Point

Associated With Tachyarrhythmias . . . . . . ... .. . . . ..
. . .... .... 57
. . .. . .. . .. . .. ...
Figure 22 Etiologies for Chest Pain . ... ...... .... . ...

......... .. .. ... . . . . . . . 58
... . . . . ... .... . . .
Figure 23 Cardiac Pain Pattern . . .. .

...................... ...
. ... . .. . . . . . . . . . 58
... .... ..... . . .. . .
Figure 24 Beal' s Palpatory Study Somatic Dysfunction

in Patients With Cardiovascular Di sease . . . . . . . . . . . . . . . . . 59
.... .. .. . . . .. . . . ...
Figure 25 Chart of Stile's Work Regarding OMT in ICU Patients With MI . . 60 ...... . ..
Figure 26 A Classification for Hypertension .. .

............. . . .. .... . ...... 61 . ..... ...... . ....
Figure 27 Mechanisms of Hypertension

(potentiators of Increased Peripheral Resistance) .... . 61
.............. ... ....
Figure 28 OMT Intervention in Hypertension (Effects Stress Levels) . . . . . . . .. 62 ....... . ..
Figure 29 OMT Intervention in Hypertension (Effects Kidneys and Adrenals) . . . . 63 ....
Figure 30 OMT Intervention in Hypertension (Effects Peripheral Resistance) . . . . 63 . .. ..
Figure 31 Hypothesis for Stress and Sympathicotonia

in Pathogenesis of Essential Hypertension .................................. 64
Figure 32 Location for OMT to Chapman's Posterior Adrenal Points . . . . . . . . . 65 . .. .. . ...
Figure 33 True Visceral Pain .................................................................. 80

Figure 34 Viscerosensory Pain (Viscerosomatic Pain) . . . .... . . . .
... 80
................. .. . ...
Figure 35 Peritoneocutaneous Reflex of Morley

(Direct Visceral-Somatic Extension of Pain) . . ... ..... 81 .....................
Figure 36 Phrenic Nerve Pain Referral . .

........ . . .
..... ..... ... . . . 81
.................. .... ...
Figure 37 Mayo Clinic Pain Pattern lllustrations . .. . .... .

... . . . .. . . . ...... ..82 . ..... . ........
Figure 38 Sympathetic Innervation of GI Tract ..

. .. . .. . . ......... . . . . . . . 83 ................ . ..
xii
Figure 39 Sympathetic Innervation of Body ..... . .......................................... 83
.
Figure 40 Parasympathetic Innervation of the GI Tract. ..... ............................. 84

.
Figure 41 Lymphatic Drainage of Upper GI Tract .. ..................................... 86

..
Figure 42 Treatment Approaches to Upper GI Disorders ............ ................... 87 . .
Figure 43 Posterior Attachments of Mesenteries ............ ............................. 89

.. .
Figure 44 Anterior Chapman Reflexes From Upper GI Tract ............................ 90

Figure 45 Collateral Sympathetic Ganglia Locations .......... ............................ 91
.
Figure 46 Viscerosomatic Reflex of Colon to Iliotibial Bands .................... ....... 96 .
Figure 47 Anterior/Posterior Chapman's Reflexes from Colon Dysfunction ........... 96

Figure 48 Sympathetic Innervation of the Body ... .... .... . . .......... ............... 97
. . . . . .
Figure 49 Parasympathetic Innervation of Intestinal Tract ................................ 97

Figure 50 Posterior Attachments of Abdominal Mesenteries ............................. 98
Figure 51 Cross Section Pelvic Floor and Ischiorectal Fossa ............................. 99
Figure 52 Anterior Chapman's Reflexes
From Genitourinary System Dysfunction ................................. 125
Figure 53 Innervation for Micturition and Neurologic Bladder Disorders ............ 126
Figure 54 Inguinal Hernia and Effects of Intra-abdominal/Pelvic Pressure ........... 128
Figure 55 Referred Pain Patterns of Iliolumbar Ligament Syndrome.................. 128
Figure 56 Coronal Section Through Urogenital Triangle ............................... 130
.
Figure 57 Pain Pattern and Mechanisms of Psoas Syndrome ........................... 132

Figure 58 Prostatodynia and Prostatitis ..... .............................................. 137
.
Figure 59 Etiology, Symptoms and Signs of Ureteral Irritation ............. .......... 138 .
Figure 60 Genital Innervation for Sexual Function ....................................... 143

Figure 61 Diagram of Congestion In Pregnancy .. ........ .............................. 149
. .
Figure 62 Autonomic Nervous System In Rheumatology ............................... 160

Figure 63 Circulation and Lymphatic and Venous Drainage of a loint. ............... 162
Figure 64 Location of Collateral Sympathetic Ganglia .................................. 199
Figure 65 Cervical Sympathetic Ganglia .... .. ... ..... ............................... 202
. . . . . .
Figure 66 Diagnostic Areas Related to Regional Congestion ........................... 206

Figure 67 Compensated and Uncompensated Patterns of Zink ... ..................... 207 .
Figure 68 Static Landmarks For Diagnosis

of Fascial Diaphragm at the Thoracic Inlet ............................... 209
Figure 69 Fascial Thoracic Inlet Sidebent and Rotated to the Right ................... 211
Figure 70 Fascial Thoracic Inlet Sidebent and Rotated to the Left. .................... 212
xiii
INDEX OF TABLES
Table 1 Travell Triggers With EENT Symptoms 9

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Table 2 Differential Points Associated with Functional Ear Components . . . . . . . . . . . . . .11

Table 3 Chart of OMT for Patients With EENT Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .18
Table 4 Chart of OMT for Patients With Upper Respiratory Disorders . . . . . . . . . . . . . . . .31
Table 5 1918 Flu Epidemic 41
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Table 6 Prevention of Postoperative Pulmonary Complications (Henshaw) . . . . . . . . . . .47

Table 7 Chart of OMT for Patients With Lower Respiratory Disorders . . . . . . . . . . . . . . . .50
Table 8 Postulated Time Intervals for Onset of OMT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .66
Table 9 Chart of OMT for Patients With Cardiovascular Disorders . . . . . . . . . . . . . . . . . . . .67
Table 10 Chart of OMT for Patients With Upper GI Disorders . . . . . . . . . . . . . . . . . . . . . . . . . .94
Table 11 Prevention and Treatment of Postoperative Paralytic Ileus (Herrmann) . . . 103
Table 12 Chart of OMT for Patients With Lower GI Disorders........................ 107
Table 13 Slow Wave Ratios For Normal Patients And Patients With IBS . . . . . . . . . . . . 113
Table 14 Chart of OMT For Patients With Genitourinary Disorder . . . . . . . . . . . . . . . . . . . 133
Table 15 Chart of OMT for Patients With Dysmenorrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Table 16 Chart of OMT For Patients With Rheumatologic Disorders................. 167
Table 17 Vision And Interest Of Infant (Chart)
From Birth to 12 Months . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
Table 18 Autonomic Nervous Influence in Selected Areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
Table 19 Chart of OMT For Patients With Systemic Disorders . . . . . . . . . . . . . . . . . . . . . . . . 190
Table 20 Chart of Autonomic Innervations of the Body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
Table 21 Muscles Used In Treatment of Rib Somatic Dysfunctions . . . . . . . . . . . . . . . . . . . 198
Table 22 Common Symptoms and Signs of Congestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
Table 23 Other Symptoms and Signs of Fascial Dysfunction........................... 205
Table 24 Ventral Abdominal Fascial Release and Pump Treatments . . . . . . . . . . . . . . . . . . 227
Table 25 Anterior Chapman's Reflexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
Table 26 Posterior Chapman's Reflexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
xiv
"My object is to make the Osteopath a philosopher,
and place him on the rock of reason."
-- A T Still, M.D.
. .
OSTEOPATIIIC CONSIDERATIONS IN EENT DYSFUNCTION
"All allergic manifestations have a 3-fold etiology: heredity, the

allergen, and the structural problem, which is the most fundamental
because it lowers resistance and invites malfunction. While nothing can
be done about heredity, resistance may be built up to the all rgen or it
may be avoided. The basic approach is through structure. " E
I. INTRODUCTION
A wide variety of symptoms and signs referable to the eyes, ears, nose, and/or
throat (BENT) will be presented by the patients seen in a busy general practice.
EENT pain and/or dysfunction as either a presenting complaint or as a fmding
of the clinical history and/or physical examination needs careful and thoughtful
evaluation by the generalist. The osteopathic practitioner combines somatic
palpatory clues and the knowledge of the interrelationships between structure
and function with a thorough history and a directed physical examination of the
EENT.
Osteopathic manipulative treatment to the

somatic component and considerations
toward enhancing body homeostatic
mechanisms can play a significant role in
designing effective treatment for these
patients. Often a successful therapeutic
trial with OMT directed at localized
dysfunctional states will eliminate the need
. for systemic treatment or for a more
extensive and expensive work-up seeking a
non-existent systemic etiology.
Common presenting symptoms or

conditions in the EENT system are
presented in this section for inclusion in
differential diagnosis and treatment design.
The somatic component or dysfunctional
state occurring with each clinical example
is representative of dysfunction in that
region.
Because of the interrelationship between structure and function, the presence of

dysfunction does not eliminate the possibility of coexisting structural etiologies.
1
ll. PATHOPHYSIOWGY
REFLEX CONNECTIONS:
Because of a variety of reflex connections, impulses arising from EENT tissues

can produce symptoms or dysfunctional states in other structures. 2 Asthma,
cephalgia and vertigo are all symptoms which may result from nasal and sinus
affections. Stimulation of vagal afferents by the irritation of a plug of wax
lodged against the tympanic membrane is clinically associated with a recurrent
cough reflex3 or with dizziness. 4 Both of these symptoms disappear when the
wax-irritant is removed.
Impulses originating from outside the EENT may also initiate EENT symptoms
because of reflex connections: Cough and hoarseness may be produced by
stimulation of pulmonary and pleural tissue; 5 increased nasal and pharyngeal
secretions may be produced by stimuli originating in either the lung or the upper
gastrointestinal tract. 6 The oculocervical reflex which can be used beneficially
in muscle energy osteopathic manipulative techniques has been implicated in the
cervical vertigo symptomatology which occurs in cervical spondylosis, cervical
inertial injuries (whiplash), cervical somatic dysfunction and cervical disk
disease.
An understanding of the Deep

PelrouJ
anatomy, physiology and
pathophysiology of the head,
neck and upper thoracic re
gion is vital if the clinician is
intent on providing optimum
care for patients with EENT
dysfunction.
SYMPATHETICS:
EENT structures derive their OA

sympathetic innervation from
cell bodies located in spinal AA
levels Tl-4 with synapses
}
between the pre-and post Palatine Nerves Inferior
ganglionic fibers occurring Sympathetic
in the upper thoracic or cer

Ganglion
vical sympathetic ganglia. Thoracic

Inlel
The sympathetic nerves gen
;
(Cervico
Thoracic
erally follow the arterial Jun '
supply to peripheral tissues.
2
Visceral afferent nerves, stimulated by organ dysfunction, often follow the same
pathways as sympathetic innervation. Excessive input from a viscera of the
head or neck produces facilitation of the upper thoracic cord segments and
results in reflex stimulation of somatic tissues innervated by TI-4. The
facilitated cord segment also encourages excessive sympathetic outflow from
that segment to its associated viscera (T1-4, to the head and neck); it is also
believed to be the basis for establishment of Chapman myofascial tender points
related to visceral dysfunction.
Palpatory changes in the upper thoracic and cervical paraspinal tissues as well as
traditional Chapman's reflex locations therefore indicate increased functional
activity of the sympathetic nervous system in this region. On the other hand,
7
physical findings such as Homer's syndrome (constricted pupil, ptosis, and
facial anhidrosis on the involved side) often indicate significant structural
involvement or blockage of the sympathetic nervous system; this needs to be
considered in the differential diagnostic process.
Increased sympathetic activity to the Chapman's Reflexes:

eye, ear, nose, and/or throat as well
Upper Respiratory Tract
as the upper thoracic musculature
augment the normal physiologic
responses that those tissues are Ear
capable of providing. In general,
the most common physiologic Pharynx
response is vasoco nstriction leading Tonsils
Larynx
to diminished nutrient supply to the
tissues and reduced lymphatico
venous drainage. The body's ability
to mount an immune response and
to obtain effective concentrations of
medications are reduced in areas of
vasoconstriction and tissue
congestion.
With chronic irritation, nasal and pharyngeal secretions from prolonged

sympathetic stimulation of the respiratory epithelium becomes thick and sticky
due to the increased number of goblet cells and decreased vascular elements.
Sympathetic stimulation of the nasopharyngeal mucous membranes produces
vasoconstriction, inhibits secretion, and results in dryness in several acute
8
situations, including fever. Often, dryness and cracking of the mucosa result
in a breakdown of normal mucosal defense mechanisms and permits secondary
bacterial infections to occur.
3
Dilation of the pupil (mydriasis) occurs with increased sympathetic activity to
the eye; pupillary constriction results from a reduction or loss of sympathetic
activity. Long term upper thoracic and cervical dysfunction with
sympathicotonia have been implicated in the development of cloudiness of the
lens. 9 In exophthalmic goiter, prolonged sympathetic activity producing
contraction of the Mullerian orbital muscle combined with edema and lymphoid
inflltration, 10 results in protrusion of the eyeball. Other eye phenomena in this
same condition are due to hyperparasympathetic activity, such as the failure of
the upper lid to follow the cornea when the eyes are lowered or a widening of
the lid slits due to increased tone of the levator palpebrae muscle.
Sympathetic fibers innervate blood vessels which supply the thyroid and also
innervate the cells which produce thyroid secretion. Increased local sympathetic
activation, generalized adrenal activity or increased thyrotropic hormone from
the anterior pituitary (any of these) increases thyroid glandular secretion. 11
Common EENT signs and/or symptoms associated with increased sympathetic

activity include photophobia, unsteadiness (slight vertigo), tinnitus, and
thickened nasopharyngeal secretions. Hyperesthesia of the pharyngeal tissues
usually makes patients anxious, causing them to "rasp, cough and expectorate to
rid themselves of non-existing mucosities or some imaginary foreign body in the
throat." Sweating is augmented and the patient may experience increased
fatigue, palpitations, tachycardia, and insomnia. With mydriasis (a hyper
sympathetic event), narrow angle glaucoma may be made worse and intraocular
pressures elevated.
While there are an abundance of symptoms produced by hypersympathetic

activity, objective signs are difficult to measure with screening physical
diagnostic tests. Palpatory changes as described earlier are accurate indicators
and when present, warrant consideration in both the diagnostic and therapeutic
arenas.
PARASYMPATIIETICS:
Parasympathetic nerve fibers to the pupil are supplied by the third cranial nerve
( oculomotor nerve). They synapse in the ciliary ganglia and then pass to the
ciliary muscle where parasympathetic contraction of the pupil opposes
sympathetic dilation. Contraction, from parasympathetic activity affecting the
lens, shortens the eye's focal point. According to Pottenger, "When the
excitability of the motor cells in the oculomotor nerve is very high, it may result
in accommodation spasm. ,,12
4
Parasympathetic nerve fibers to the
lacrimal gland as well as to the
nasopharyngeal mucosa travel via
the seventh cranial nerve (facial).
They synapse in the sphenopalatine
ganglia. Parasympathetic hyper
activity is responsible for the
production of tears from the
lacrimal glands and profuse, clear,
thin secretions from the mucosa of
the nasopharynx and sinuses.
Great Petrosal N.
In the absence of histo
(Parasympathetic) Superior logical changes which
VII Salivatory may be produced by
Nucleus
prolonged sympathicoto
nia, irritation of the
nasopharyngeal mucosa
results in a "runny nose"
Foramen
and watery eyes. A
sphenopalatine syndrome
is described as redness
and n engorgement of the
mucous membranes,
photophobia, tearing and
pain behind the eyeball,
nose, neck, ear or
temple. ,,13
PhatyngeaJ Ne.,...
This syndrome is said to

worsen cases of asthma due
to lowered resistance of
nasal mucosa to foreign
protein and inadequate
conditioning of the air
entering the lungs.
Superior
SalivUDfy
Parasympathetic nerves to N_YlI 'r.·
the thyroid arise from the (�)
superior and inferior
laryngealnerves and a
branch from the main vagus
nerve (cranial nerve X).
5
At this point its physiologic role in thyroid function is unknown; it is believed
to be neither an activator nor an inhibitor of thyroid activity.
VENOUS AND LYMPHATIC SYSTEMS:
85 % of the venous drainage from the head is accomplished via the jugular veins
which pass through the right and left jugular foramina, formed in the
occipitomastoid sutures between the occipital and the temporal bones. Venous
congestion of the head leads to symptoms of cephalgia and anxiety.
The first sign of lymphatic congestion affecting EENT structures and

attributable to fascial somatic dysfunction will appear as fullness in the
supraclavicular tissues. The pre-auricular, post-auricular, tonsilar,
submaxillary, submental, and posterior cervical lymph nodes should also be
palpated for evidence of infection. Manipulative goals are directed toward
opening lymphatic pathways while avoiding direct manipulation over swollen
lymph nodes.
Lymphatic congestion leads to boggy, edematous tissues which are generally

uncomfortable and which change local biochemical conditions and hinder
homeostatic mechanisms. In nasopharyngeal dysfunction there will be
diminished transport of nutrients to the tissues and a reduction in the movement
of metabolic wastes from the mucosa. This hampers healing while increasing
the possibilities of nasopharyngeal adhesions from repeated or serious infection.
Where the sclera, cornea, iris and ligamentum pectinatum meet is defined as the
angle of the anterior chamber of the eye. "Upon the integrity of this angle
depends the proper circulation of lymph to nourish the anterior portion of the
eye"; 14 glaucomatous changes have frequently been linked to poor lymphatic
drainage of the eye.
In the inner ear, absorption of endolymph is believed to be important in the

prevention of both endolymphatic hydrops ("glaucoma of the ear" 15) and
fibrosis of the endolymphatic duct which occurs in Meniere'S disease.
Meniere's disease is accompanied by symptoms of tinnitus, diminished hearing,
and vertigo.
NEURAL SYSTEM:
A variety of EENT symptoms can be primarily explained by the effect of

somatic dysfunction on motor or sensory nerves in the cranial and/or cervical
regions. (Table 1, page 9)
A trauma history is important as EENT symptoms in a child or an adult often

have their onset as a consequence of a difficult delivery or a trauma such as the
6
inertial injury (whiplash) incurred in a motor vehicle accident. Dentaltrauma
should also be a routine part of the historicalquestioning because of its
propensity for creating cranialsomatic dysfunction.
While the two most common pathophysiologic causes of extraocular muscle

palsy are diabetes mellitus and aneurysm, extraocular muscle dysfunction is also
a frequent sign of cranialsomatic dysfunction and often responds well to
osteopathic manipulative treatment directed at the attachments of the
petrosphenoidalligament. Because this ligament is formed by the anterior
extensions of the fixed margins of the tentorum cerebelli to the body of the
sphenoidal bone, treatment is typically directed to its attachments, particularly
to the temporal and sphenoid bones.
Innervation to the extraocular muscles--cranialnerves ill, IV and VI--is

particularly vulnerable to dural stress as these nerves pass in close relationship
to the petrosphenoidal ligament. Post-traumatically, symptoms of cranial nerve
VI are the most common because this is the most vulnerable of the three nerves
as it passes under the petrosphenoidal ligament. 16 Cranialnerve VI innervates
the lateral rectus muscle so its dysfunction leads to medialstrabismus. The
effect of extraocular muscle dysfunction ranges from mild eye fatigue, headache
and blurred or double vision to amblyopia, mild nystagmus, or strabismus. Any
of these dysfunctions may respond favorably to OMT of the cranium. 17
Other cranialnerves may be affected and lead to EENT symptoms.

Dysfunction involving the olfactory nerve18 (cranialnerve I) may lead to an
altered sense of smell or to an impression of an odor that is not present. The
trigeminal nerve (CN V) carries sensory information from many structures
including the anterior and middle cranial fossae, the tentorum cerebelli, the
mastoid air cells, the nasal mucosa, the cornea, and the temporomandibular
joints. Dysfunction of the fifth cranialnerve may lead to headache19 perceived
in the anterior fossa, eyebrows, or sinuses; it is also considered in the
differentialdiagnosis and treatment of trigeminalneuralgia (tic douloureux 20
r
The buccal branch of cranialnerve V may be entrapped by trigger points2 in
the lateral pterygoid muscle and produce tingling in the cheek.
Dysfunction of cranial nerve VII is associated with complaint of a metallic taste

or altered salivation. Finding somatic dysfunction in the cranium which could
affect the facial nerve (CN VI is also quite helpful in the differential diagnosis
�
and treatment of Bell's palsy. 2 Vertigo, nystagmus and tinnitus are symptoms
which may arise from involvement of the vestibulocochlear nerve (CN VIII). 23
With dysfunction of cranial nerves IX and X, infants may have poor suckling24
or failure to thrive because of poor SWallowing. Dysarthria may result from
dysfunction of cranial nerve XII.
7
Palpation of the cranium for obvious strain patterns, occipital compression, and
temporal malalignment is extremely helpful in ruling out cranial dysfunctional
states which could lead to EENT symptoms. Treatment of any somatic
dysfunction found is helpful in addressing the physiologic portion of the
treatment protocol.
TIlE SOMATIC SYSTEM:
The myofascial system plays a significant role in EENT symptomatology. A

number of myofascial trigger points (fPs) have been well documented by
Travell and Simons that refer pain to, and/or cause dysfunction of, the eye, ear,
nose, Eustachian tube, and throat. Specific questions relating to the activation
of the pertinent muscles outlined in Table 1 (page 9) should therefore be posed.
All myofascial trigger points and particularly those in the head and neck region,
are aggravated by cold and emotional stress. In this area, emotional stress
symptoms25 such as bruxism and clenching of the teeth are particularly pertinent
as they produce TPs in the masseter and pterygoid muscles. Frowning or
squinting sets up TPs26 in the orbicularis oculi and occipitalis muscles. These
muscles are also activated by excessive gum chewing, worn teeth or dentures,
occlusal disharmony, TMJ, and prolonged dental procedures.
Symptoms referred by myofascial dysfunction to the eye are most prominently

seen with TPs in the sternal division of the sternocleidomastoid muscle. 27
Motor vehicle accidents, especially those from the rear28 when the head is
turned, frequently cause trigger points in the sternocleidomastoid, splenius
cervicis, and trapezius muscles. Postural disorders must be ruled out29 as a
perpetuating factor in those cases where the trigger points are difficult to
eradicate.
Because of ipsilateral visual disturbances including blurring, diminution of

perceived light and apparent ptosis from spasm of the orbicularis oculi in the
reference zone, the patient may report a need to tip the head backwards to look
up. TPs in the obicularis oculi muscle will also cause excess ipsilateral
lacrimation and conjunctival reddening due to vascular engorgement. 30 TPs in
the orbicularis oculi muscle may result in patient complaints of "jumpy print"
while reading. 31 Splenius cervicis TPs32 will produce ipsilateral blurring of
near vision without conjunctivitis or dizziness as well as pain in the eye and
orbit. Those in the occipitalis muscle refer pain behind the eye and in the
eyeball and eyelid while those in the trapezius might refer pain to the back of
the orbit.
The underlying cause of functional ear symptoms should be carefully and

systematically sorted out. The role of cranial nerve dysfunction and lymphatic
congestion has already been discussed with regard to tinnitus, vertigo, and/or
hearing disorders. Cranial somatic dysfunction is a frequent cause of functional
8
symptoms. External rotation of the temporal bone is associated with low
pitched roaring tinnitus; fixed internal rotation associated with high-pitched
tinnitus; and both potentially causing vertigo. 33
TABLE I: TRAVELL TRIGGERS WITH EEHT SYMPTOMS;
EYE SYMPTOMS AND / OR PAIN:
Sternal Division of Sternocleidomastoid Muscle

Splenius Cervicis Muscle
Occipitalis Muscle
Orbicularis Oculi Muscle
Trapezius Muscle
EAR PAIN, TINNITUS, AND/ OR DIMINISHED BEARING:
Deep Portion of Masseter Muscle

Clavicular Portion of Sternocleidomastoid Muscle
Medial Pterygoid Muscle
Occipitalis Muscle (Possible)
EUSTACHIAN TUBE DYSFUNCTION:
NOSE PAIN:
Orbicularis Oculi Muscle
MAXILLARY SINUS PAIN AND / OR SINUS SYMPTOMS:
Lateral Pterygoid Muscle

Masseter Muscle
Sternal Division of Sternocleidomastoid Muscle
THROAT PAIN AND / OR PAIN OR DIFFICULTY SWALLOWING:

Digastric Muscle
CRANIAL HERVE ENTRAPMENT:
VA (Buccal Nerve Branch) : Lateral Pterygoid Muscle

XI .. Sternocleidomastoid Muscle
9
Otalgia can be referred34 from teeth, tongue, tonsils, esophagus, TMJ and from
cervical/cranial somatic dysfunction through cranial nerves V, IX and X or C l-
2 . To these factors can be added Eustachian tube dysfunction and myofascial
trigger points.
Both secretory and acute otitis media often arise from Eustachian tube
dysfunction. The middle ear is normally ventilated 3-4 times per minute as the
Eustachian tube opens during swallowing, sneezing or yawning. Even mild
infection can cause mucosal swelling sufficient to block the Eustachian tube35
leading to pressure changes within the middle ear, retraction of the tympanic
membrane, serous otitis and hearing loss. Under these conditions oxygen is
absorbed through the blood vessels in the mucous membrane of the middle ear.
In the pathogenesis of secretory otitis media, a relative negative pressure
develops with Eustachian tube dysfunction leading to mild retraction of the
tympanic membrane. This can be demonstrated on physical examination by
abnormal light reflection on the tympanic membrane and by poor insufflation.
The negative middle ear pressure causes a transudate from the blood vessels of
the mucous membrane of the middle ear. This produces an amber to gray
colored appearance to the tympanic membrane, a fluid level and bubbles may be
seen on otologic examination. A conductive hearing deficit develops in patients
with secretory otitis and it may last for months.
Stein I s textbook, Internal Medicine, states that the most important predisposing
factor in developing acute otitis media is an acute nasopharyngeal infection,
usually viral, causing Eustachian tube dysfunction that allows microbial
proliferation and infection in the middle ear, especially when combined with
other inadequate host factors. 3 6 Cranial somatic dysfunction has also proven to
be a predisposing factor for recurrent pediatric otitis media. 37
Eustachian tube dysfunction may occur from tissue swelling, edema, and/or
adhesions forming after tonsillectomy or after repeated or serious infections. It
may also arise from trigger points in the medial pterygoid3 8 muscle or from
dysfunction of cranial nerve X. Additionally, it has been associated with cranial
somatic dysfunction39--especially internal rotation of the temporal bone or
torsion or sidebending-rotation of the sphenobasilar symphysis. Regardless of
the etiology, Eustachian tube dysfunction has been associated with a variety of
patient signs, symptoms, or disorders including diminished hearing, pain with
altitude changes, tinnitus, recurrent infections, secretory and acute otitis media,
asymmetrical elevation of the uvula upon phonation, and vertigo. Because any
of these symptoms may arise from Eustachian tube dysfunction, physical
examination of the posterior pharynx, palpation of the medial pterygoid muscle
and cranium, and visualization with insufflation of the tympanic membrane
should be performed.
10
TABLE 2: SELECTED DIFFERENTIAL POINTS IN DIAGNOSES
ASSOCIATED WITH FUNCTIONAL EAR COMPONENTS
DIAGNOSIS EAR TINNITUS DECREASED VERTIGO /
SENSATION HEARING DIZZINESS
Meniere's Disease Fullness 85-90% Unilateral 85-95% Unilateral Vertigo

10-15% Bilateral
Hypothyroidi£m (-) (-) Bilateral Dizzy I

I
I
( -) (-)
•
Hyperthyroidism Bilateral ll. ghtheadedness ·
.
Eustachian Fullness (+) Unilateral Conductive (? )

Dysfunction Unilaterally
Labyrinthitis (+/-) ( -) (+) Dizzy
Temporal Bone with OA or (+/-) Unilateral (+/-) Dizzy or

Somatic Dysfunction vagal involv. Vertigo
TP Deep Masseter Deep Pain Unilateral ( -) ( -)
TP Clavicular (+/-) ( -) Unilateral contributes to

Portion of Carsickness
Sternocleidomastoid Seasickness
TP Medial Pterygoid Stuffiness (-) ( -) (-)
TP Occipitalis Ache (-) Slightly (-)
Post-Concussion ( -) (+/-) Sensorineural Vertigo

Syndrome
Salicylate Toxicity ( -) Bilateral (- ) ( -)

Other ear symptoms attributable to myofascial trigger points (TPs) include those
in the deep portion of the masseter, the clavicular portion of the
sternocleidomastoid (SCM), the medial pterygoid, and according to Kellgren,
the occipitalis muscle. Variables in the presentation of these points and other
differentials are detailed in Table 2 on page 11.
The low roaring tinnitus experienced in TPs from the deep portion of the
masseter40 muscle will often vary when the jaw is opened wide. The stuffiness
in the ear caused by TPs in the medial pterygoid41 muscle is felt to be due to
Eustachian tube dysfunction which arises from inability of the tensor veli
palatini muscle to move the medial pterygoid and associated fascia aside to open
that structure. Not included in Table 2, are the TPs of the trapezius42 which
includes among its many other referral sites, the postauricular area.
Sinus sym toms can also arise from myofascial structures. TPs in the lateral
�
pterygoid muscle refer severe pain to the maxillary region as well as
autonomically stimulating excessive secretions from the maxillary sinuses. Pain
referred from this TP and from TPs in the superficial upper portion of the
masseter muscle give rise to complaints of "sinus attack" and often result in
incorrect and therefore ineffective treatment for sinusitis. Dysfunctional TPs in
the sternal division of the sternocleidomastoid44 cause coryza and maxillary
sinus congestion. Nose pain, per se, is rarely caused by TPs other than those in
the orbicularis oculi45 muscle.
Throat pain arises from myofascial triggers in either the medial pterygoid46 and
digastric47 muscles. Swallowing is painful with the former and difficult with
the latter.
ill. TREATMENT
After a thorough diagnostic evaluation, a tentative diagnosis is made.

Formation of a rational osteopathic treatment for this initial diagnosis must:
o .. consider the patient's body as a unit

o .. support structure and functional components
o .. support and enhance the homeostatic mechanisms involved
The most effective treatment plan is directed at the cause of the complaints and
not at the symptoms.
In general, this section will consider primarily the manipulative techniques

which fulfill the objectives mentioned in the previous paragraph. Treatment of
the upper thoracic and cervical regions effectively addresses the sympathetic
component. Lymphatic congestion is best accomplished by first opening the
pathways--especially the thoracic inlet and anterior and posterior cervical soft
12
tissues--and then enhancing the fluid movement with diaphragmatic techniques,
lymph pumps and effleurage. Treatment of the parasympathetic component,
when it is present, often involves use of manipulative techniques to the cranium
and/or occipitocervical junction. In certain circumstances, specific manipulative
techniques, exercises or dietary considerations may be applied to the general
treatment plan outlined above.
THE EYE: 3 •
A •
2
• •
• •
Effleurage over the eyelid and globe
•
is often beneficial with edema of the •
eyelid and scleral edema. Avoid 8 5 9

stroking over the lid when the •
•
patient is wearing contacts or if any
•
•
other ophthalmic foreign body is •
•
suspected. •
B
•
4
Some patients have an impaired

ability to focus their eyes and,
whether near- or far-sighted, may
benefit from a series of eye
BEH
exercises develope4 by H.A.
Richardson, D.O. 48 TRBAE
I HEZBFD
Using an enlarged chart like the one
FOSGACNHO
illustrated above, this is one of six
ROD B A E D F H P Z
eye exercises that Dr. Richardson
O MD V L R W C X P Z AO
had his patients perform.
-To be effective the patient must be motivated enough to perform the exercises
regularly. Pin a large AB- test chart on the wall with the figure 5 on a direct line with
-
the end of your nose. Stand three inches away and see that your nose is on a direct line
with the figure 5. Now look at No.1, then at No.2, then back to No.1. Do this five
times, stretching the muscles of the eyes each time. Then shift from No. 3 to No.4,
five times each way. Do not move the head. Then shift from No.8 to No.9 five times
each way. Then look up at A and down at B five times up and down. Then while you
remain the same distance from the chart, starting at A, shift the eyes from one dot to
the other all the way around the circle back to A. Do this five times to the right, then
five times to the left. Blink each time that you look at a dot; but do not move your
head when exercising. Now close the eyes tightly five times. Then look at No.5 and
close the eyes for a second; then open them and look at No.5 again. Open and close
them five times, looking at No.5 again. Open and close them five times, looking at
No.5 each time. This exercises both the internal and external rectus muscles at the
same time. Now close your eyes and cover them with the palms of the hands, being
sure to exclude all light and relax in this position for five minutes. If one eye is weaker
13
than the other, you should cover the stronger eye and do more exercising with the
weaker eye. Now take your seat at about ten feet from the • AB· test chart and read all
of the letters on the card, shifting the eyes rapidly from the bottom to the top of each
letter, blinking every time you shift the eyes.
After you have read all of the letters on the card at least once, you should
again cover the eyes with the palms of the hands and relax for a few minutes
being careful not to put any pressure on the eyeballs.•
49
T.J. Ruddy, D.O. , 50 an osteopathic ophthalmologist, also developed a series of

muscle energy techniques designed to balance extra-ocular muscle tone. These
techniques utilize traditional muscle energy principles with the physician
applying resistance against the ocular globe as the patient attempts to look in a
specific direction. This form of OMT, combined with cranial techniques to
improve the structure-function relationship of extraocular muscle innervation,
has been helpful in patients with functional diplopia, strabismus, cephalgia
secondary to eye strain, amblyopia, and other conditions in which somatic
dysfunction of the extraocular muscles plays a role.
Another technique applied directly to the globe has been utilized for patients
with mild chronic glaucoma. 51 The purpose of this technique is to improve
fluid drainage and constitutes part of a total treatment program. With the
patient' s eyes closed, the physician places a finger across the eyelid from lateral
to medial. With a finger of the other hand, a light percussion is performed over
finger that lies on the closed eyelid. In one study, intraocular tension averaged
3-5 mm Hg reduction 60 minutes after an OMT regimen. 52 In a double blind,
randomized study of intraocular pressure of normal and chronic, open angle
glaucoma patients, significant pressure changes were also seen 6 to 60 minutes
after osteopathic manipUlative treatment. 53 Acute closed-angle glaucoma, on
the other hand, is an ocular emergency which may produce blindness in 3-5
days unless treated medically.
Where structural problems such as entropion or extropion lead to functional

disorders such as poor drainage of tears through the nasolacrimal system or
chronic recurrent pathophysiology such as the inflammation seen in chronic
conjunctivitis, the best treatment is probably surgical repair of the structural
disorder. However, where functional problems lead to eye pain, blurred vision
or reddening, manipUlative or spray-and-stretch techniques should be applied to
specific trigger muscles. (See Table I, page 9.)
TIlE EAR:
In patients with significant cranial somatic dysfunction who are also

experiencing vertigo or tinnitus, a therapeutic trial of manipulation is warranted.
Goals include achieving a balance between the temporal bones, normalizing the
14
cranial rhythmic impulse, and removing areas of dural strain. In addition, each
of the muscles listed in Table 2 page 1 1 that meet the patient' s presentation
should be palpated and treated if a myofascial trigger is found.
Patients with structural adhesions affecting the Eustachian tube may complain of
deafness, otalgia with altitude changes, recurrent otitis media, vertigo and/or
tinnitis. They may benefit from lysis of these nasopharyngeal adhesions. A
techni�ue, referred to as "finger surgery" , was popularized by C.H. Muncie,
M.D. iI It is often effective in modifying the structure sufficiently to restore
normal Eustachian tube function.
Yawning and swallowing are essential to normal Eustachian tube function,

therefore dysfunction affecting cranial nerves IX, or V, or any of the myofascial
structures involved in these actions can compromise maximal Eustachian tube
function. Myofascial dysfunction in the medial pterygoid muscles and those
attached to the hyoid bone are particularly likely to disturb the opening of the
Eustachian tube. These dysfunctions respond well to OMT.
The frequency of pediatric otitis media is increased in relation to a number of

somatic factors (number of cranial strain patterns, 55 presence of plagiocephaly,
or Eustachian tube dysfunction56) , environmental factors (exposure to tobacco
smoking57 and woodheating, 58 or participation in day care) , and familial factors
(history of sibling or parental otitis media) . 59
The treatment of choice for acute otitis media would address the underlying
Eustachian tube dysfunction, provide antibiotics capable of managing both
0
Strept pneumonia and Hemophilus injluenza6 and support host elements. Such
a regimen permits the body ' s homeostatic elements the best opportunity to
interrupt the natural progress of the disease , spontaneous perforation of the
tympanic membrane with closure and return of hearing in 1-2 weeks. Because
secretory otitis media has a sterile effusion, antibiotics are not helpful unless it
is associated with a bacterial rhinitis, sinusitis, or nasopharyngitis.
Pseudoephedrine for vasoconstriction may be of some symptomatic relief, but
the osteopathic physician should go back and treat any underlying
nasopharyngeal structural or functional condition which may be causing the
Eustachian tube dysfunction. Antihistamines may only be appropriate when
allergic factors are associated with Eustachian tube dysfunction.
ManipUlative treatment in Meniere's disease has been specifically described as

"beneficial . ,,61 One study of OMT in Meniere' s patients revealed excellent
results or significant improvement in 79 % of cases. 62 OMT addressing dural
restrictions, and especially those associated with temporal bone dysfunction, 63 is
particularly helpful in our experience as are diagnosis and treatment of the
lymphatic and autonomic components.
15
THE NOSE AND SINUSES:
w. Hadley Hon Ill, D.O. in his article, "Current concepts in management of

sinus disease, " states, "OMT should be included in the treatment of sinusitis. "
He notes that OMT should address parasympathetic and sympathetic fibers as
homeostasis of their autonomic functions may prevent ostial occlusion. Sensory
fibers to the sinuses (originating in the trigeminal nerve) should also be
addressed.
Stimulation of the sphenopalatine ganglia65 results in a brief period in which

there is production of profuse, thin nasal secretions, a parasympathetic
response. This may prove helpful in the symptomatic relief of patients with
sinusitis or patients whose thick nasal secretions have been difficult to clear
from the nasal passageways. The pressure applied to the site needed to affect
the sphenopalatine ganglion will elicit "exquisite" tenderness if active lateral
pterygoid myofascial trigger points are present. 66 Often the referred maxillary
sinus pain and autonomically induced excessive secretions will resolve with the
inhibition that occurs with this technique. 67 Research utilizing rhinomanometry
has shown that following osteopathic manipulative treatment there is a reduction
in the amount of work required by the nose during breathing. 68
Manipulative techniques to free somatic dysfunction in the cranium69 (especially

the frontal-ethmoidal and facial bones) or to improve the pumping motion
through the vomer are beneficial for imprOVed nasal sinus function. They are
extremely helpful in patients with dysfunctional, allergic, or infectious
etiologies for rhinitis, acute sinusitis, or the pharyngitis resulting from post
nasal drainage. CV4 cranial technique is felt to act through fluid mobilization
and increased pump potency; regardless of mechanism, shortly after applying
this technique, most patients note significant clearing of the sinuses.
Treatment to normalize the body' s response to sensory input along branches of

the trigeminal is helpful in reducing reflex symptoms ranging from sinus
headache to sneezing. This may be accomplished with gentle rotatory
stimulation over the bony foramina of the supraorbital and infraorbital nerves.
(See the next section entitled "Osteopathic Considerations in the Common
Cold. ")
In patients with structural abnormalities such as nasal septal deformity or

chronic sinusitis, surgery becomes the osteopathic treatment of choice. 70 When
functional and otherwise transient changes in acute sinusitis are inadequately
treated, irreversible structural changes may result. Thus, in chronic sinusitis,
when the normal ciliated epithelium is replaced with stratified squamous cells
incapable of homeostatic clearance mechanisms, 71 antibiotic and manipulative
therapy is rendered ineffective. Hoyt notes, "Functional sinus surgery offers
16
new hope to the patient who has failed to respond to conservative osteopathic
medical treatment" 72 and can relieve associated somatic cephalgic
manifestations.
THE THROAT:
The techniques described previously for the Eustachian tube and sphenopalatine
ganglia are also indicated to treat dysfunctions of the pharynx. Soft tissue
techniques to the anterior cervical fascia and gentle manipulation to correct any
hyoid dysfunction are also extremely beneficial in reestablishing normal
function in this region and permits the patient significant symptomatic relief.
Addressing the anterior cervical fascias and hyoid bone is frequently helpful in
thyroid dysfunction, but because this is an endocrine gland and under the
control of the pituitary, evaluation and treatment of any cranial dysfunction73
should also be performed.
THE ENT UNIT:
Mandibular drainage technique is effective in encouraging drainage from the

nasopharyngeal area and opening the Eustachian tube. It is therefore helpful in
decongestion of a large part of the ENT unit.
The procedure is described by Angus Cathie, D.O. (after Galbreath) in his

discussion of the sinobronchial syndrome74 and is also mentioned by Harold 1.
Magoun, D.0. 15 The patient is treated in the supine position with a slight
elevation of the head which is rotated 900 to the non-involved side. The
operator stabilizes the frontoparietal region with one hand and places his/her
fingers of the other hand below the zygomatic arch and over the TMJ with the
heel near the symphysis menti. The patient is instructed to relax his/her jaw
while the operator applies a slow, firm pressure downward, forward, and
medial. This is released and repeated alternately to apply a "make/break
tension" to the pterygoid muscles. This decongests the rich pterygoid venous
plexus which drains the tissues noted above. Relaxation of the medial pterygoid
muscle also enables the tensor veli palatini muscle to functionally open the
Eustachian tube.
While usually utilized to facilitate diagnosis, treatment of ENT Chapman' s

points with generalized soft tissue techniques or specific rotatory stimulation can
be postulated to beneficially modify sympathetic outflow. It is noted that
symptomatic relief is afforded the upper respiratory tract when these reflex
points are treated as a system. For comfort and practicality, the posterior points
are treated first and the anterior points may be gently treated if they remain.
17
t CRI � t Endolymphatic Flow
Oculocervical - Muscle Energy
Cervicals C3-S (Phrenic Nerve)
Tl-12 and Ribs 1-12 (Somatic Nerves and Respiration)
Thoracolumbar Junction (Diaphragm Attachment)
Medial pterygoid muscle
Somatic Dysfunction Hyoid Soft Tissue for Eustachian Tube
facH. seg.
Sympathetics I
I
Parasympathetics I
Rib Raising TREATMENT PLAN FOR Sphenopalatine
Tl-4 EENT DYSFUNCTION Ganglion Technique,
Cervical Fascias Cranial OMT to Affect
(Cerv. Ganglia) Cranial N erves
Chapman's Reflexes (Cranial N-VII )
Eye:
Tl-2 I Lymphatics
1
Ciliospinal Center
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
Ruddy's Resistive Duction
Ocular - Muscle Energy
Stroking (Ocular)
SYMPATHETIC EFFECTS
t Tone:
t Vasoconstriction
t Thickens Secretions ( t Number of Goblet Cells)
.j. Drainage
Mydriasis � Worsening of Glaucoma
LYMPHATIC EFFECTS
Impaired Lymph Flow:
.j. Drainage
t Congestion
t Endolymphatic Pressure � Possible Fibrosis of
Endolymphatic Channel
L
with stasis
� �
Menie e's Disease
PARASYMPATHETIC EFFECTS
t Tone:
t Thinning of Secretions
Improved Drainage
18
IV. SUMM ARY
Reflex mechanisms are extremely active in integrated EENT functions. Somatic

dysfunction modifies normal reflex activities and may produce dysfunctional
states whose symptoms must be differentiated as to whether they are functional
(somatic dysfunction) or pathological. In disease situations, somatic
dysfunction reduces the efficacy of the body ' s homeostatic mechanism.
Successful manipulation of somatic dysfunction constitutes either a therapeutic
trial or an important support to homeostasis. Its incorporation into the treatment
program speeds healing and decreases morbidity while simultaneously providing
symptomatic relief for the patient.
ADDITIONAL EENT BmLIOGRAPHY:
Norfolk DF: Cranial nerve syndromes: relationship to musculoskeletal lesions

of the cervical spine. The Journal of Osteopathy 1962; 69(8) : 17-22.
Gayral L, Neuwirth E: Oto-neuro-ophalmologic manifestations of cervical
origin. New York State J Med 1954; 54: 1920- 1922 .
REFERENCES:
1. Magoun ill: Osteopathy in the Cranial Field. Kirksville, Journal Printing

Co, 3rd ed, 1976, P 276.
2. Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co,
7th ed, 1953. pp 239-40, 374-39 1.
3. Op cit p 381.
4. Travell JG, Simons DG Myofascial Pain and Dysfunction: The Trigger
Point Manual. Baltimore, Williams and Wilkins, 1983 , p 209.
7th ed, 1953, p 239.
6. Op cit pp 239-240, 378.
7. Stein JH (ed) Internal Medicine. Boston, Little, Brown & Co, 3rd ed,
1990, P 1 897.
7th ed, 1953, pp 377-8.
9. Cole WV: Experimental evidence, in Hoag JM (ed) Osteopathic Medicine.
New York, MCGraw-Hill, 1969, ch 8, p 1 19.
7th ed, 1953, pp 384-6.
1 1. Cole WV: Experimental evidence, in Hoag JM (ed) OsteQPathic Medicine.
New York, McGraw-Hill, 1969, ch 8, P 1 19.
7th ed, 1953, P 385.
13. Magoun HW: Neuroscience studies in Goldstein M (ed) The ReSearch
Status of Spinal Manipulative Therapy, Bethesda MD, US Department of
19
Health, Education and Welfare (NINCDS Monograph #15) , 1975, pp
2 13-6.
14. Wolf AH: Osteopathic manipulation in eye, ear, nose, and throat disease.
AAO Yearbook 1962: 133-40
15. Gibson WPR: The diagnosis and treatment of Meniere' s disease. The
Practitioner 1978; 22 1 : 71 8-722.
16. Magoun HI Osteopathy in the Cranial Field. Kirksville, Journal Printing
Company, 3rd ed, 1976, P 293.
17. Op cit pp 267,284, 293.
18. Op cit P 167.
19. Op cit pp 76, 1 85 , 290.
20. Op cit pp 294-300.
21. Travell JG, Simons DG Myofascial Pain and Dysfunction: A Trigger Point
Manual. Baltimore, Williams & Wilkins, 1983, p 266.
22. Magoun HI OsteQPathy in the Cranial Field. Kirksville, Journal Printing
Company, 3rd ed, 1976, P 269.
23. Op cit P 150.
24. Op cit p 234.
Manual. Baltimore, Williams & Wilkins, 1983 , pp 219, 249.
26. Op cit pp 285, 293.
27. Op cit P 203.
28. Op cit P 299.
29. Op cit pp 103- 1 14.
30. Op cit P 203.
31. Op cit pp 296, 298.
32. Op cit pp 285, 288.
Company, 3rd ed, 1976, pp 15 1 , 215.
34. Op cit P 286.
35 . Moore KL Clinically Oriented Anatomy. Baltimore, Williams & Wilkins,
2nd ed, 1985 , P 970.
36. Stein JH Internal Medicine. Boston, Little, Brown, & Co, 3rd ed, 1990, P
1262.
37. Degenhardt BD, Kuchera ML: The prevalence of cranial dysfunction in
children with a history of otitis media from kindergarten to third grade.
Mead-Johnson Fellowship Paper, 1993.
39. Magoun HI OsteQpathy in the Cranial Field. Kirksville, Journal Printing
Company, 3rd ed, 1976, pp 15 1 , 215.
40. Op cit p 22 1 .
41. Op cit p 249.
42. Op cit p 1 84.
43 . Op cit pp 263-4.
44. Op cit p 203.
45 . Op cit p 282.
46. Op cit p 252.
47. Op cit p 276.
20
48. Richardson RA Increasing The Strength Of The Eyes and the Eye Muscles
Without the Aid of Glasses . Kansas City, The Eyesight and Health
Association, 1925 .
49. Op cit pp 52-53.
50. Ruddy TJ: Osteopathic manipulation in eye, ear, nose, and throat disease.
AAO Yearbook 1962: pp 133-40.
5 1 . Ibid
52. Misischia PJ: The evaluation of intraocular tension following osteopathic
manipulation. JAOA July 198 1 , 80:750.
53. Feely RA, Castillo TA, Greiner JV. Osteopathic manipulative treatment
and intraocular pressure. JAOA Sept 82, 82:60.
54. Muncie CH Prevention and Cure of Deafness Through Muncie
Reconstructive Method. 1960.
55 . Degenhardt BD, Kuchera ML: The prevalence of cranial dysfunction in
56. Stein HI Internal Medicine. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
57. Hinton AE: Surgery for otitis media with effusion in children and its
relationship to parental smoking. J Laryngol Otol 103: 550, 1989.
Mead-Johnson Fellowship Paper, 1993 .
60. Stein HI Internal Medicine. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
6 1 . Cole WV: Disorders of the nervous system, in Hoag 1M (ed) Osteo.path ic
Medicine. New York, McGraw-Hill, 1969, ch 20, p 315.
62. Korr 1M (ed) The Neurobiologic Mechanisms in Manipulative Thenmy.
New York, Plenum Press, 1977, p 61 .
63. Magoun m Osteopathy in the Cranial Field. Kirksville, Journal Printing
Co, 3rd ed, 1976, p 28 1 .
64. Hoyt (III) WH: Current concepts in management of sinus disease. JAOA
October 1990; 90(10); pp 913-9 19.
65 . Op cit p 1 83.
Manual . Baltimore, Williams & Wilkins, 1983, p 265 .
67. Op cit p 263.
68. Kaluza, Sherbin M: "The physiologic response of the nose to osteopathic
manipUlative treatment: Preliminary report. " JAOA May 83, 82:654-60
69. Magoun m Osteopathy in the Cranial Field. Kirksville, Journal Printing
Co, 3rd ed, 1976, pp 289-29 1 .
70. Rebik JM, McIntire LD, Hoyt WH (III), McIntire KD : Ethmoid sinus
disease and nasal septal deformities as etiologies of chronic cephalgia:
Results of surgical management. JAOA (October 1990) : 897-907.
7 1 . Stein HI Internal Medicine. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
72. Hoyt (III) WH: Current concepts in management of sinus disease. JAOA
October 1990; 90(10); p 9 1 8.
21
73 . Magoun HI Osteopathy in the Cranial Field. Kirksville, Journal Printing
Co, 3rd ed, 1976, p 2 14.
74. Cathie A: Sino-bronchial syndrome. AAO Yearbook, 1974: 180-l .
Co, 3rd ed, 1976, P 215.
22
OSTEOPATHIC CONSIDERATIONS IN THE COMMON COLD
AND OTHER UPPER RESPIRATORY INFECTIONS
I. INTRODUCTION
Probably no disease causes so much aggravation to so many people as the

common cold. Its viral etiology makes treatment with antibiotics ineffective; in
fact, studies indicate that the use of antibiotics in a viral infection only prolongs
the symptomatic stage of the infection. Modern medical treatment consists of
symptomatic care with a polypharmacy that often includes antihistamines,
analgesics and decongestants administered by spray, tablets or capsules. This is
a less than optimum protocol.
The common cold affects the function of the upper respiratory tract--nasal
passages, sinuses, ears, pharynx and bronchial tubes. The nasal passages are a
very small part of the total human anatomy but they have a very important role
in the maintenance of health. Though they are only 4 inches in length from the
nares to the posterior pharynx, air from a single inhalation travels that distance
in 114 second, is warmed to 96.8 degrees, 75% humidified, and practically
filtered clean regardless of the condition of the air outside the body.
A special type of respiratory epithelium, composed of a combination of ciliated

columnar and goblet cells, provides the means of effectively filtering and
moisturizing the air. In a state of health, the epithelial ratio of goblet to ciliated
cells is maintained by a predominant influence from its parasympathetic
innervation. The resulting secretion is present in two layers and normally the
layer of mucus next to the cells is clear with a saliva-like consistency.
Inhaled air is warmed and humidified by the structural nature of three nasal
turbinates which line each nasal passage. These turbinates increase the surface
area to which inhaled air is exposed and dilation of their abundant thin-walled
blood vessels effectively warms the air, even in a very cold external
environment.
Because of their shape and location, the turbulence of the inhaled air is
increased so that foreign particles are thrown against the fluent but sticky
superficial layer of the mucous blanket. F�reign particles stick to this
superficial layer where lysozyme, an enzyme present in this mucus, kills virus
and bacteria on contact. Both layers of the entire mucous blanket are moved
slowly toward the back of the pharynx by the action of the ciliated cells as their
cilia move the deeper saliva-like layer of mucus.
Mucus that arrives at the posterior pharynx is usually swallowed. The mucous
blanket is completely replaced 3-4 times in every 24 hour period, amounting to
23
a normal total production of 1.5 pints of mucus per day. Any bacteria or virus
remaining alive after being swallowed will be killed by the gastric acid in the
stomach.
The constant movement of air through the nasal passages would dry out the
mucous membranes without homeostatic mech anisms. In order to protect the
mucosal blanket and the nasal epithelium from drying out, 80% of the normal
population have "nasal cycles." These are alternating patency cycles of the
nasal passages during which one naris assumes the dominant role of air passage
while the other one "rests". When working properly, this fluctuation is not
noticed because the total air resistance is unchanged. If one or both nares are
unable to dilate because of allergic congestion, infection, or some structural
problem such as nasal deviation or a fractured nose, the total resistance to the
air passing through the nasal passages is greatly increased. Patients with any of
these conditions interpret the usual resting stage of the nasal cycle as "nasal
congestion".
It is important to remember that the same stratified ciliated columnar epithelium

which lines the nasal passages also lines the sinuses and the bronchial tubes.
(Stratified squamous epithelium in the respiratory tract is found only in the
posterior pharynx.)
ll. PATHOPHYSIOWGY
Infection begins with decreased resistance of the host. A person can often recall
many etiological stressful situations which can reduce resistance of the body.
Initially there appears to be increased parasympathetic activity and the mucus
becomes more profuse and watery. The common cold viruses, such as the
rhinovirus, do not attack the epithelial cell walls but produce inflammation with
increased transudation of fluids rich in kinins (bradykinins, lysylbradykinin).
These set up the symptoms of inflammation and predispose to bacterial
infection. Perhaps the body is trying to functionally flush out or dilute the
pathogen or irritant. As the viral invasion becomes more advanced, visceral
afferent impulses to the spinal cord increase. Most visceral afferent nerves
share the fascial pathways traveled by the sympathetic nerves which innervate
that organ, so these impulses arrive at the same cord levels as that organ's
sympathetic innervation. Afferent impulses from the sinuses and other head
structures synapse in the dorsal horns of spinal cord segments Tl-4 and those
from the bronchial tree feed into the spinal cord at the T l-6 levels.
Reduction in the natural resistance of the body to protect and defend the air
passages allows secondary bacterial infection to occur and in the case of the
influenza virus, a direct attack upon the cell wall of the respiratory epithelium.
Influenza virus invades the epithelial cells to use the cells' own metabolic
processes in the production of more viruses. The fate of the infected cells
24
depends upon how severely the virus disturbs the cells' metabolism. There may
be local congestion, mucosal ulceration, sloughing, and exudate formation.
Exudate makes an excellent media for bacterial growth and bacteria in the
region take advantage of the denuded surfaces and "protein rich cellular broth."
Secondary infection by Haemophilus influenza and Staphlococcus pyogens
bacteria is common.
A steady stream of visceral afferent impulses from a dysfunctional upper

respiratory tract "facilitates" the upper four to six thoracic spinal cord segments
and permits viscerovisceral reflexes that result in excessive sympathetic output
to the respiratory epithelium of the head, neck and bronchial tubes. In the
common cold, palpatory evidence of tenderness and spasticity may be evident
from the cervical through the thoracolumbar junction, but especially from C l to
T 3.1
Presynaptic sympathetic fibers destined for the head and neck synapse in the
cervical sympathetic ganglia while those destined for the lungs and the bronchial
epithelium synapse in the TI-6 paraspinal chain ganglia. Postsynaptic
sympathetic fibers travel through the respiratory plexus to the bronchial
epithelium of the lungs or through the carotid plexus, the deep petrosal nerve,
the nerve of the pterygoid canal and then through the sphenopalatine ganglion
(without synapsing) to the respiratory epithelium of the head.
Hypersympathetic activity to the respiratory epithelium produces epithelial
hyperplasia. Epithelial hyperplasia is characterized by increased numbers of
goblet cells in relation to ciliated cells and encourages the production of
profuse, thick, sticky, tenacious, slow-moving mucosal discharge.
ill. TREATMENT
Medical treatment at an early stage usually includes a decongestant to

symptomatically reduce the air resistance through the nasal passages and make
breathing easier. This treatment is subjectively effective by constricting blood
vessels in the nasal mucosa; but in the long run, it actually encourages the
detrimental sympathetic effects listed in the previous paragraph. Sidney Harris
said, "A bad physician treats the symptoms, a good physician treats the disease,
and a rare physician treats the patient." The osteopathic curriculum strives to
produce the "good and rare physician." It is often necessary to treat the
symptoms, for various reasons, but know what will be gained and what may be
lost by doing so.
The principles of osteopathic manipulative treatment ( OMT) in helping the body

2
heal itself are outlined in OsteQPathic Medicine:
1. OMT stimulates blood supply
25
2. OMT increases venous and lymphatic drainage of the organ systems
possibly affected
3. OMT relieves muscle spasm, reducing restriction on breathing
4. OMT reduces reflex disturbances that may be impairing
a. Vasomotor regulation
b. The function of secondarily involved organs
c. Other defense responses
5. OMT improves circulation to and from the reticuloendothelial

system, to aid its responses to an invading agent"
Simple rib raising manipulation to CERVICAL SYMPATHETIC CHAIN
the upper six ribs reduces the

sensitivity of facilitated segments in
the thoracic area and results in
diminished sympathetic outflow to t>i!IT==r'- Superior CeMcaI
the mucosa of the nose, sinuses and Ganglion
bronchial tubes. Treatment of

related joint somatic dysfunction
reduces facilitation at the cord level
by removing its somatic influence.
Treatment of cervical myofascial
dysfunction opens fascial pathways Middle Cervical
Ganglion
for lymphatic drainage and
Inferior CervIcal
simultaneously influences posterior Ganglion
Chapman's points (suboccipital Ansa Subclavla
area) through somatovisceral reflex

action. Because of the fascial ties
and the proximity of the cervical A. EXTERNAL RESPIRATION
sympathetic ganglia to the vertebral
joints, treatment of somatic
A.. Ear
Lymphatic
System . "
. . .
Head and Neck
A
'NTERIOR POINTS: DIAGNOSTIC AIDS: •
-
Heart and Lungs

•
- - -Thoracic
B. Nasal Sinuses
UPPER RESPIRATORY TRACT (T1-4) •
•
P
�{=
•
u
t t
•
Abdomen -- -� ___ Abdominal m
•
P
D. Bronchus
•
•
Pelvis - - - - - - - Pelvic
s
•
5
·7 % 25%
Venous And Arterial
L7Phatic
L �:1 � .. J
5
%
Capillary
:
: ...
B. INTERNAL RESPIRATION
FUNCTION OF "A" DETERMINES FUNCTION OF "S"
26
dysfunction and fascial tension in the cervical area opens pathways for
lymphatic drainage and reduces visceral afferent influences that are active in
maintaining related facilitated cord segments. By reducing sympathetic
influence and allowing the more desirable parasympathetic effects to
predominate, the respiratory epithelium produces a thinner, more watery
secretion. Treatment of this area first will also reduce the outflow of
sympathetic impulses via facilitated upper cord segments.
Following treatment by rib raising, it is beneficial to turn the patient to his/her

side and provide a kneading type soft tissue treatment to the thoracolumbar
junction. This relaxes the patient and the lumbar attachments of the muscular
abdominal diaphragm, preparing the patient for a diaphragm redoming
treatment.
Increased interstitial fluid and mucosal swelling as a result of mucosal irritation,

inflammation, and infection produces an exigency for effective lymphatic
drainage to relieve congestion. Good lymphatic drainage requires unimpeded
lymphatic pathways from the site of infection back to the heart and effective
lymphatic pumping action from a well-domed abdominal diaphragm.
If not already accomplished, the following static landmarks should be examined

at the thoracic inlet. Fascial torsion of the inlet should be diagnosed and
effectively treated to remove any hindrance to this terminal drainage site for the
left and right lymphatic ducts.
Infradavicular Spaces
/ \ �
Left Right
Left Coracoclavicular Right Cor-acodavicular

Angle Angle
L R
Normal Static Landmarks of the Thoracic Inlet
Diagnose and treat any somatic dysfunction in the midcervical and O A areas.
This insures good phrenic nerve innervation to the diaphragm, relaxes the
fascial pathways for lymph flow through the cervical area and can influence the
parasympathetic response in respiration. The diaphragm is then redomed by any
27
one of a number of indirect or direct fascial manipulative techniques. (See pages
2 12-217 in the treatment section of this book.)
With lymphatic pathways freed and the diaphragm redomed, lymph flow is
initiated by using one of the many manipulative lymphatic pump procedures.
The pectoralis lift treatment applied for 2 minutes furnishes the pumping effect
of about 5 minutes of the usual intermittent chest pump treatment. This
technique is also applicable to patients with osteoporosis, metastatic di sease,
various types of postsurgical conditions and also OB patients with tender,
hypertrophied breasts. The pectoralis lift can often be safely taught to the
patient's family for their use on the patient at home. In addition to moving
fluids, the thoracic lymphatic pump has been shown to modify immune
function. 3,4
Attention is then directed to the face and sinus areas. The physician's fingers
are placed over the infraorbital, and later the supraorbital, foramina. The skin
and subcutaneous tissues are contacted and circular treatment is provided over
the nerve branches of the trigeminal nerve as they emerge from the maxillary
and frontal sinuses, respectively. These nerves provide the impulses which are
interpreted as pain from the respiratory epithelium of the sinuses. When the
sinuses are infected, the patient will be very sensitive to pressure over these
nerves as they exit from their foramina, a helpful clue to the diagnosis of
sinusitis. If these areas are not tender to the patient, "sinus treatment" is
probably not indicated. Though the treatment is initially uncomfortable in
patients with sinusitis, reasonable manipulative effort over these nerves helps to
relieve the subject's "sinus pain." Effleurage to the face often completes
lymphatic treatment.
S
Addition of a type of cranial treatment employs a frontonasal suture spread and
encourages the ethmoid bone of the skull to move freely and normally in the
ethmoid notch of the frontal bone. Good functional motion of the ethmoid and
frontal bones encourages a natural pumping action through the craniosacral
mechanism and improves sinus drainage. This cranial technique may be
incorporated by osteopathic students and physicians, even without having
complete training in the craniosacral concept.
In order to influence parasympathetic outflow to the sinus and nasal respiratory

epithelium it is efficacious to take a minute and treat the right and the left
sphenopalatine ganglia. This treatment has two main effects:
o .. Parasympathetic activity is a primary influence in the production of a

thinner, saliva-like secretion. Stimulation of this parasympathetic
ganglion provides an "internal irrigation" by thinning the thickened nasal
secretions and thus providing both symptomatic relief and improved
regional homeostasis.
28
o .. It encourages the autonomic system to establish a more normal cellular ratio
in the mucosal epithelium between the goblet and the ciliated columnar
epithelial cells. Parasympathetic impulses reduce the goblet cells and
increase the proportion of ciliated columnar cells.
The sphenopalatine ganglion is located in the sphenopalatine fossa of the skull

and hangs from the maxillary division of the trigeminal nerve. This is a
parasympathetic ganglion and it cannot be reached directly by the palpating
finger. It may be reached indirectly, through the open mouth of the patient, by
passing a cotted finger over the molars of the upper jaw, then lateral and
posterior to the maxillary ridge and then cephalad over the pterygoid plates (just
posterior to the maxillary ridge) to the extent permitted by the buccal mucosa in
6
the mouth. The patient is then asked to nod toward the palpating finger. Two
or three repetitions on each side of the mouth provides adequate treatment by
indirectly applying tension on the ganglion through the fascias of the pterygoid
muscles. Satisfactory treatment is signaled by tearing of the eye only on the
side of treatment, because the lacrimal gland shares the same parasympathetic
nerve supply.
Superior
SaJivatory
Nucleus VII
(Para&ymp) �....�
..
IV. SUMMARY
7
The osteopathic approach has been reported to decrease the symptoms and
duration of colds, to support the body's homeostatic mechanisms against
29
infection, and to prevent complications and recurrence. Osteopathic
manipulation provides increased comfort for the patient, balances and supports
physiologic protective and homeostatic mechanisms of the body, and provides
rewarding treatment for a patient with the common cold.
This section encourages the student of an osteopathic approach to understand,

incorporate, and record the following:
o .. The sympathetic and parasympathetic innervation to structures of the head

and the effects of each upon the respiratory epithelium and discharge of
the upper respiratory tract
o .. The lymphatic drainage pattern from the upper respiratory tract
o .. Manipulative techniques for treatment of the thoracic inlet, redoming the
diaphragm and initiating lymphatic flow
o .. Manipulative technique for applying effleurage of the face
o .. Sphenopalatine ganglion intraoral finger manipUlative technique
o .. The diagnosis and osteopathic treatment of cervical, rib, thoracic, and
thoracolumbar somatic dysfunction is indicated to remove the somatic
component of the facilitated spinal cord segments including occipital
(condylar) decompression, frontal/nasal spread, and CV4 techniques
REFERENCES:
1. Zirul E E: Infections caused by viruses, in Hoag JM Osteopathic Medicine.
New York, McGraw-Hill, 1969, ch 45, P 722.
2. Op cit P 720.
3. Measel JW, Jr: The effect of the lymphatic pump on the immune response:
I. Preliminary studies on the antibody response to pneumococcal
polysaccharide assayed by bacterial agglutination and passive
hemagglutination, J A O A Sept 1982; 82( 1):59-62.
4. Measel JW, Kafity A A: The effect of the lymphatic pump on the band T
cells in peripheral blood (abst). J AO A; 608.
5. Magoun H I: OsteQPathy in the Cranial Field. Kirksville, Journal Printing
Co, 3rd ed, 1976, pp 172, 290.
6. Op cit p 2 16.
7. Schmidt I C: Osteopathic manipUlative therapy as a primary factor in the
management of upper, middle, and pararespiratory infections. JAOA
Feb 1982; 8 1: 382-8.
30
Medial pterygoid muscle
Somatic Dysfunction Hyoid Soft Tissue for Eustachian Tube
facil. seg.
Sympathetics
Treatment Plan for:
I
I
Parasympathetics I
Rib Raising Sphenopalat'lone
Tl-4 The Common Cold, Ganglion Technique,
Cervical Fascias Rhinopharyngitis and Cranial OMT to Affect
(Cerv. Ganglia) Upper Respiratory Tract Inf. Cranial Nerves
Chapman's Reflexes (Cranial N-VII)
I Lymphatics
I
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
SYMPATHETIC EFFECTS
t Tone:
t Vasoconstriction
t Thickens Secretions (t Number of Goblet Cells)
J. Drainage
LYMPHATIC EFFECTS
J. Drainage
t Congestion
t Tone:
t Thinning of Secretions
Improved Drainage
31
NOTES:
32
OSTEOPATHIC CONSIDERATIONS IN
THE WWER RESPIRATORY DISORDERS
I. NORMAL FUNCTIONAL RE'iPIRATION:
Respiration is a dynamic
orchestration involving
coordinated reflex neural
activity, abdominal
diaphragmatic and various other
muscular contractions, motion of
fascial planes, and the
movement of over 146 joints of
the body. Efficiency of this
orchestration is necessary for
effective inhalation and
exhalation, respiration and for
the production of pressure
gradients between the thoracic
and abdominal cavities. The
cyclic pressure gradients act as a
pump for the lymphatic system
Diaphragm and encourage good flow of
Well Domed Diaphragm lymphatic fluids. It is also
Flattened
involved in aiding venous flow
�/- and a host of biochemical and
��-=->'+ physical reactions occurring in
the blood stream during
respiration.
Breathing and respiration are not the same. The purpose of "breathing" is to
move air from outside the body into the lungs, exchange oxygen in the air for
carbon dioxide in the blood stream, and then exhale the air. The purpose of
"respiration" is to provide for a similar exchange of these gases at the cellular
level. If this is to be accomplished with optimal clinical effect, breathing must
be coupled with good circulation in an interstitial tissue environment as free
from congestion as possible. The lung maintains its internal environment and
function via viscerovisceral and viscerosomatic reflexes.
Metabolic or respiratory acidosis or alkalosis results in a change of the blood's

pH and affects its hemoglobin-oxygen dissociation curves. This means that the
ability of hemoglobin to give up its oxygen to the cells will vary according to
2
the blood's pea and serum pH. Even small increases in oxygen to the tissues
33
is accompanied by a very great increase in protection of those tissues from
infection.
Niinikoski stated: "Any treatment that augments the local oxygen supply or
helps to avoid hypoperfusion tends to increase the rate of healing and decrease
susceptibility to infection. " Osteopathic manipulative treatment affects the
pulmonary environment through somatosomatic and somatovisceral reflexes. It
also affects the musculoskeletal mechanics involved in breathing, respiration and
lymph flow. These mechanisms have been researched by such scientists as
Bums, Hix, Olwen Gutensohn, Denslow, Korr, Krogh, Patterson, and Sato just
to name a few.
Decongestion of interstitial tissues and improvement of respiration through

mechanical and neuroreflex mechanisms are also encouraged by osteopathic
manipulation.
Through improve
ment of the body's
fascial pathways and
its own self-regula
tory mechanisms for
protection and
homeostasis, elec
trolyte balance, pH
adjustment, and the
delivery of oxygen to
the tissues occurs
more easily and op
timal tissue resistance
and repair capabilities
are encouraged.
In normal respiratory
activity, the solitary
nucleus of the respi
ratory center in the
medulla is informed
of the collapse of the
air sacs by way of
visceral afferent
nerve fibers.
34
These visceral afferents travel in the pathways of the vagus nerve. The reflex
response by the nucleus solitarius and the respiratory center in the medulla may
be modified by impulses received from the carotid body. The carotid body is
sensitive to CO2 concentrations in the blood.
A subsequent reflex arch from the nucleus solitarius to the mid-cervical area,
(C3,4,5) produces a contraction of the diaphragm via the phrenic nerve.
Somatic intercostal nerves, T l -12, are also called into action by this reflex
producing stabilization of the intercostal spaces but doing little to move the ribs
unless there is a call for very deep inhalation.
When the air sacs are filled, visceral afferent reflexes inhibit the nucleus
solitarius and the somatic reflex pathways cause the diaphragm and intercostal
muscles to relax.
o .. If the air sacs remain partially distended, the person's breathing may
become more shallow.
o .. If the serum carbon dioxide content is increased, as in respiratory acidosis,
viscerosomatic reflexes are initiated by the carotid body which result in
an increase in the rate of respiration.
o .. The result of these two actions is a patient with shallow, rapid respirations.
The tubular bronchial system is lined with special pseudostratified columnar,

ciliated epithelium which is supposed to protect and maintain the internal
environment of those passageways. It is important to remember that it is the
resultant balance between the sympathetic and parasympathetic nerve impulses
to the lung that determines the cellular make-up of the respiratory epithelium.
This means, especially, "the ratio of ciliated to goblet cells" in the lining of the
bronchial tubes. It is this ratio which determines the basic type of bronchial
secretions produced by the respiratory epithelium and thus determines the
functional and protective environment at the mucosal bronchial membrane
interface of respiration.
Parasympathetic influence via the vagus nerves is dominant in a normal

functioning lung. The cellular ratio of the bronchial epithelium is dependent
upon this parasympathetic dominance to produce a clear, saliva-like (but sticky)
mucous blanket. This type of mucous blanket is easily moved cephalad toward
the epiglottis by the action of the ciliated cells in the respiratory epithelium and
it keeps the bronchial passages moist and clean. Because of the dominant
parasympathetic:sympathetic influence in healthy lungs, there is normally a
slight increase in smooth muscle tone of the bronchial tubes.
35
ll. PATHOPHYSIOWGY - "REFLEX ACTION DURING INFECTION:"
Pulmonary disease, whether infectious or not, may be looked upon as the result
of the disruption or undesirable response of one or more of the protective
mechanisms. Any disruption of the mucosal blanket or irritation of the
epithelial lining of the bronchial tubes will obviously change the bronchial
environment. Constant dysfunction of the lung's normal reflex mechanisms is
associated with predictable pathophysiologic events. 1 Infection--viral or
bacterial--is one of the most common irritants of the respiratory mechanism,
although bronchial irritation produced by smoking is probably very common
and, unfortunately, is often unnoticed until cell changes have occurred.
Viral or bacterial infections produces local irritation of the bronchial epithelium.

An inflammatory response is set up which may spread into the parenchymal
tissue of the lung. Alveolar surfactant is reduced, exudate forms, and
eventually congestion and even edema of lung tissue ensues. Hours or days
later there is sloughing of some of the injured mucosa.
At this point, the patient has "tissue congestion" and possibly even some edema
which begins a compromise of the lung's cellular function in the process of
respiration. The stage is set for the "signs and symptoms" of an acute viral or
bacterial bronchial infection.
The respiratory mucosa of the trachea and bronchi is relatively insensitive to

pain, but the movement of mucus and cellular debris over raw areas in the
bronchial tubes activate a cough reflex. A cough can produce pressure changes
of up to 300 mmHg in the lung and can produce air velocity up to 500 mph.
While coughing is usually produced by a protective reflex, it may also be
damaging and dangerous to some patients and is a significant etiologic cause of
exhalation rib somatic dysfunction.
SYMPA THETIC RESPONSES:
Beginning with lung dysfunction and mucosal irritation, visceral afferent nerve
endings in the area of tissue injury are stimulated. This results in a visceral
afferent bombardment of the spinal cord from the TI-6 cord levels. When the
lungs are irritated, the six upper thoracic cord segments have been found,
experimentally, to have low reflex thresholds which discharge easily. This ease
of discharge is associated with the finding of sympathetic hyperactivity in the
related lung tissue. Viscerosomatic and somatovisceral reflexes occur in these
lowered threshold segments resulting in activation by emotional, somatic, or
visceral stimuli that are unrelated to the lung. This low threshold phenomenon
is termed facilitation.
36
Viscerosomatic reflexes are the viscera's contribution responsible for initiating
the facilitated cord segments in this example. Viscerosomatic reflexes will also
segmentally interact with nuclei of somatic nerves in the spinal cord to initiate
reflexes which provide the physician with palpable joint and musculoskeletal
indications of lung dysfunction. These increased secondary somatic impulses
produce palpable musculoskeletal indications of visceral disease in the TI-6 area
(especially T3-4 and somewhat preferentially on the left). Afferent impulses
from these somatic dysfunctions become the somatic contribution to the support
and prolongation of the facilitated cord segments. When the lung parenchyma
is involved, the inflammatory condition can produce direct irritation of the chest
wall and intercostal nerve with accompanying musculoskeletal dysfunction
adjacent to the lobe(s) involved. This produces pleuritic pain and is often
accompanied by a pleural friction rub which can be auscultated.
Primary visceral afferent activity is also felt to be responsible for the formation
of secondary myofascial tender points called Chapman's reflexes.
Cardiopulmonary System (T1-6)
Heart
':::::/�"" _-r-___ Upper Lung
N..�'-"-L
---2-- ower Lung
These points have distinct locations and can be used to help diagnose and then to
adjunctively treat the visceral dysfunction of the lungs and other visceral organs.
The anterior Chapman points for the upper lung and the lower lung are found in
the third and fourth intercostal space, respectively, next to the sternum.
The sympathetic nervous system is involved in all disease processes. Prolonged

sympathicotonia results in vasoconstriction with local hypoperfusion in the lung
and epithelial hyperplasia. It even directly influences pulmonary immune
function. Sodeman and Sodeman say: "The adaptive, protective reaction might
be far more damaging to the individual than the noxious agent or the beginning
dysfunction. "
37
Hypersympathetic effects in the lung are initially responsible for some dilation
of the bronchial tubes. This is not an undesirable effect at first; but persistence
of the protective sympathetic responses is also responsible for a relative
vasoconstriction of the arterioles in the area of tissue injury. Vasoconstriction
along with interstitial tissue congestion encourages hypoperfusion of the lung
tissues, the very tissues that need oxygen the most.
Another effect of hypersympathetic activity to the lung from the facilitated

segment is a process called epithelial hyperplasia. In this situation, goblet cells
in the bronchial epithelium increase. The ratio of goblet to ciliated cells
increases. Not only is more mucus produced by the respiratory mucous blanket
but the mucus becomes thick, profuse, tenacious and difficult to expectorate.
In this condition the patient not only has congested and edematous interstitial
tissues, but also has thick, sticky, profuse tenacious mucus in the bronchial
tubes. Edema of the distal air sacs may also be present in pneumonia, further
decreasing the capacity of the respiratory system by partially filling the air sacs
of the lung.
PARASYMPATHETIC RESPONSES:
It is known that the Hering-Breuer reflex mechanism cannot reflexly distinguish

between air sacs filled with air and air sacs filled with fluid; so the respiratory
center receives information from the vagus nerve to limit the excursion of the
diaphragm because the air sacs are filled. At the same time the respiratory
center receives information from the carotid body that more oxygen is needed
and the abdominal diaphragmatic rate should be increased. The result is often
shallow breathing at a rapid rate.
MUSCUWSKELETAL RESPONSE:
The mechanical and physical components of respiration are also stressed by the
pathophysiologic changes just described. The diaphragm is mechanically
stressed by relative immobility of ribs and spine (viscerosomatic reflexes) and
also by the tissue resistance caused by congestion in the lung. Increased work
load on the diaphragmatic muscle results in a strain of its attachments to the
lower six ribs and the thoracolumbar junction producing an increase in the
lumbar lordosis and a flattening of the dome of the diaphragm. The clinical
result is often a patient with a spastic, flattened diaphragm that displaces very
little volume during its contraction and relaxation.
2
Other palpatory clues to pulmonary dysfunction have been described. TI-6
paraspinal tissues, and especially T3-4 on the left, have increased tone and are
often tender from facilitation through viscerosomatic reflexes. Tl-12 may have
increased paraspinal tissue tone and tenderness when the lung parenchyma is
38
involved. These musculoskeletal effects often restrict chest cage excursion and
further diminish homeostasis. Another peak incidence of somatic dysfunction
noted in numerous studies of patients with pulmonary disease can be palpated at
3
C2.
Coughing incorporates rapid contraction of the intercostal muscles. Persistent

or unexpected coughing often results in exhalation somatic dysfunction of the
ribs which then complicates the homeostatic response to the underlying
pulmonary process involved. In severe chronic obstructive pulmonary disease,
fatigue of the scalenes may result in depression of the rust rib or exhalation
somatic dysfunction of rib 2, otherwise infrequent findings.
LYMPHATIC SYSTEM RESPONSES:
Normally contractions of the

abdominal diaphragm
EB
Diaphragm
Well Domed produce changes in volume
between the thoracic and
! �� abdominal cavities. When

the diaphragm is well
domed, the volume changes
Diaphragm
produce effective pressure
Flattened -
gradients between the
�3�+ thoracic and abdominal
cavities. In this way a pump
action for lymphatic flow is
produced. Flattening of the
diaphragm seriously
decreases volume
displacement and the
pressure gradient that the
diaphragm is able to produce
between the thorax and
abdominal cavities. In such
a situation there is a decrease
in the pressure between these
two areas at any given
"Breathing, the lymphatic pump."
moment. Decreased lymph
flow increases congestion of
tissues and can decrease
cardiac output.
Under normal conditions, lymphatic return to the heart in a 24-hour period is

equal to the entire serum volume of the body. There is no argument about the
importance of maintaining lymphatic flow from the lungs in disease or in health.
39
Extrapleural lymphatics drain to intercostal vessels, to axillary nodes, and then
into the left or right lymphatic duct; however, the drainage of the pleural sac
and lung tissues travels to pretracheal nodes and then into the right lymphatic
duct.
Basic medical and osteopathic

research have proven that chronic
lymphatic congestion with resultant
poor oxygenation of the cells is
associated with increased infection, Right
Lymphatic
increased mortality, increased
Duct
healing time, and increased fibrosis
and scarring if healing does occur.
Studies have also shown that tissue
congestion decreases the
effectiveness of medical therapy.
Respiratory therapy, pulmonary
toilet and osteopathic manipulative
treatment all have substantial effects
on the prognosis of a patient when
they are included in a program to
enhance homeostasis.
m. TREATMENT:
PNEUMONIA: Lymphatic Drainage4
Lower respiratory infections such as pneumonia typically produce symptoms of

high fever, hypoxia, tachypnea and toxic symptoms such as severe fatigue and
headache; often the patient will initially have a repetitive, non-productive, non
effective cough. These patients may have chest pain, especially with deep
inhalation.
It is also common to find patients with lower respiratory infections in which

these typical symptoms are not present. This is especially common in the
elderly patient. Their only complaints may be unexplained "toxic" fatigue,
heaviness in the chest and/or a severe headache. Acceptable supportive care
consists of bed rest to conserve energy, a light but nutritious diet with good
fluid intake, and heat to the chest or the back. Fluid and electrolytes must be
balanced and assured either by mouth or with intravenous drip.
Medical treatment consists of antibiotics, protection from non-productive cough,

loosening of secretions, oxygen as required and occasionally bronchodilators.
Early recognition of a lower respiratory tract infection is advantageous because
40
this allows early institution of an antibiotic that is believed to be specific or of a
broad enough spectrum before the cultures from deep expectorations and/or
from the blood have been reported. When the cultures are returned, the result
of the initial treatment is evaluated and the antibiotic changed if indicated.
Palpatory and auscultatory physical findings precede radiographic changes by
24-48 hours.
Sometimes the cough may be suppressed by the use of dextromethorphan,

codeine or other antitussive medications, especially if it is non-productive and
damaging to the patient; sometimes antihistamines are given in hopes of making
the patient more comfortable instead. Realize that these medications might
make the secretions less fluid and more difficult to expectorate from the
bronchial system. Treatment may be given to loosen the bronchial secretions
and aid the patient's natural defenses. Mucolytic expectorants and proper
hydration aid in the elimination of secretions and use of various mechanical
means such as postural clopping and intermittent positive-pressure breathing
procedures could be employed to reach this goal. Use of sympathomimetics to
dilate bronchial passages allows the patient to breathe easier but the benefits of
this type of medication must be weighed against the possibility of reducing
blood flow to the parenchymal tissues of the lung.
The development of medications and antibiotic treatment for pneumonias has

greatly reduced the patient's suffering from fever, hypoxia and systemic
toxemia; and it has reduced the mortality from pneumonias. The effectiveness
of these medications and the patient's comfort can be maximized by including
an intelligent plan for osteopathic manipulative treatments in the patient's
management program. These treatments need not be extensive to be effective;
in fact, too much manipulation early in the toxic stages of the infection will tire
the patient, reduce energy reserve and not enhance the treatment. 5 Suggested
protocol and plans for providing osteopathic manipulative treatment to patients
with pneumonia are presented on pages 45 and 50.
100,000 PEOPLE WITH VIRAL INFLUENZA IN THE 1918 EPIDEMIC
MEDICAL CARE OSTEOPATHIC MANIPULATION
OVERALL
MORTALITY 5% 0.25%
MORTALITY IF
PNEUMONIA 30-60% 10%
COMPLICATION
41
The effectiveness of osteopathic manipulative support for patients who were not
receiving effective medications was clinically tested during the flu epidemic of
1918. Antibiotics had not yet been discovered to help patients fight bacterial
complications. Even today, antibiotics are ineffective against viral infections.
6
In this study of 100,000 people with influenza, Smith reported that patients
who received osteopathic manipulation had a 0. 25% overall mortality and a
10% mortality rate if they developed pneumonia. The mortality rates for
patients who only received medical care and no osteopathic manipulation were
5% overall and 30-60% if they developed pneumonia.
Such a study would never be executed in today's scientific and effective medical
society; but this early survey indicates the power and effectiveness of
manipulative support of the body's own defenses. Combining medication with
manipulative treatment to support body homeostasis has been shown effective in
reducing the hospital stay length of stay by 10%.
1
Initial manipulative treatment in pneumonia has three main goals: Reduce

congestion, reduce sympathetic hyperactivity to the parenchyma of the lung, and
reduce mechanical impediments to thoracic cage respiratory motions. Effective
manipUlative treatment accomplishing these three goals would also encourage
removal of waste products for detoxification by the liver and removal by the
kidneys; reduce vascular constriction in the tissue areas of the pathology;
enhance more predictable antibiotic dose-to-tissue levels; improve respiration
and make the patient more comfortable. These goals are addressed easily and
efficiently applying basic manipUlative treatment techniques.
Clinically, some variation of rib raising manipulation is commonly performed

(see page 195) with special emphasis on the TI-6 area. The patient is usually
supine and the head of, the bed is elevated to provide ease in respiration for the
comfort of the patient. Rib raising can be administered to one side at a time or
both sides at once. The physician may also pass both hands under the patient's
spine and grasp the erector spinae mass (ESM) with the fingers on one side of
the ESM and the thenar and hypothenar eminences on the other side of the
ESM. The physician's hands are then closed to produce tolerable inhibitory
pressure on the erector spinae mass muscle. As this muscle group is grasped,
the typical rib raising posture of the patient occurs with elevation of the sternum
and ribs. While still grasping the muscle group; one hand or the other is
adjusted by right or left displacement of the patient's spine until pressure
between the two hands and the ESM of the patient seems to be as equal as
possible. Hold this until the ESM muscles relax; then slowly release the
pressures.
Rib raising not only relaxes the patient but is considered to effectively increase
the blood supply to the lung tissues by inhibitory sympathetic interference with
42
both vasomotor and bronchomotor control. 8 Prolonged hypersympathetic
influence to the bronchial epithelium increases the ratio of goblet cells and
encourages thick, sticky mucus. Effective rib raising should therefore reduce
the results of excessively prolonged sympathetic influence on the respiratory
mucosa, decrease the goblet cells in the mucosa and encourage a thin, saliva
like bronchial secretion. In addition to improving the arterial supply, rib raising
enhances venous and lymphatic drainage from the bronchial and peribronchial
tissues. 9 Rib raising techniques applied for about 30-90 seconds usually relax
the paraspinal musculature and effectively treats sympathetic imbalance.
Manipulation is then directed toward improvement of lymphatic flow. The

thoracic inlet is diagnosed for its fascial preference and is treated with indirect
fascial manipulation or muscle energy direct techniques to produce freedom of
fascial pathways in this terminal area of lymphatic drainage. Thoracic inlet
somatic dy�function can also be treated by thrust manipulation but the tissues of
a toxic patient do not tolerate thrust activation as well. The thoracolumbar area
is then relaxed with inhibition of the muscles in the erector spinae mass or by
kneading the soft tissues, to prepare the musculature for redoming of the
diaphragm. The abdominal diaphragm is then tested to determine whether both
sides of this muscle are working effectively. The diaphragm is redomed if
indicated using indirect or direct fascial methods with patient respiratory
cooperation, breathing in or out and holding that phase of respiration as the
physician directs the tissue release. A well-domed diaphragm produces greater
pressure gradients between the chest and abdomen during contraction and
relaxation; this indirectly results in greater efficiency in the movement of
interstitial fluids by producing a more effective pumping action upon the fluids
in the closed lymphatic system.
Mechanically the thoracic cage must be able to expand in all three planes for
optimal breathing. Somatic dysfunction of any of the 146 joints involved in this
process may be considered to limit maximal chest cage function and multiple
sites of somatic dysfunction may provoke signs and symptoms.
The usual form of rhythmic compression and release of the rib cage to
encourage movement of lymphatic fluids and even the pedal pump of Dalrymple
may not be tolerated by an overly fatigued and toxic patient.
Lymphatic flow can be safely accomplished by grasping the pectoralis muscle

near its tendinous attachment, pulling cephalad and slightly medially to tissue
tolerance and then holding for a period of seconds or a minute or so. In effect,
this procedure pulls superiorly on the attachments of the pectoralis major muscle
to the upper seven ribs. With each inhalation by the patient this technique
increases the volume of inhaled air. An additional 400 cc of air can be inhaled
with each breath for each additional centimeter of chest cage diameter.
43
A=Ordinary Exhalation
B=Quiet Inhalation
C=Deep Inhalation
Exhalation rib
somatic dysfunction
particularly limits
chest expansion,
while causing pain
and splinted
breathing.
Exhalation rib
dysfunction is most
frequently caused by
coughing and
therefore plays a
major complicating
role in many primary
Lateral view of sternum with first and seventh ribs attached.
The diagram iUustrates motion of these structures during respiration. respiratory problems.
Rib raising techniques may mobilize this dysfunction, but often specific OMT to
the involved rib(s) is necessary to restore the homeostatic benefits obtained from
effective breathing. Examination and treatment should not be limited to rib
dysfunction however; OMT to restore normal motion to the thoracic vertebrae,
sternum, and even the shoulder girdle have all been shown to improve the depth
of breathing and to reduce the work associated with that breath. These may be
the only treatments performed at the initial visit unless the patient also has
somatic dysfunction at the base of the occiput and/or in the upper cervical
reglOn.
Headache is not uncommon in patients with respiratory dysfunction and is often

an obvious clue to the frequently found somatic dysfunction in this region. The
vagus has connections with the first and second cervical nerves and this may be
the functional connection between the lung problem and the symptom of
headache. Manipulation of any cervical somatic dysfunction, especially of the
OA or AA should make the patient more comfortable and also normalize
parasympathetic influence to the lungs through the vagus nerve.
Treatment for the hypersympathetic activity that is found in every disease

process is often treated first. Hypersympathetic activity to an organ is enhanced
by a facilitation of the cord segments related to the sympathetic innervation for
the affected organ. The cord segments become facilitated by direct visceral
afferent bombardment from excessive afferent impulses originating in the
irritated lung tissues. Manipulation at any other area of the spine would send
impulses past these cord segments of low threshold and very likely produce an
outburst of sympathetic impulses to the lung from those segments. Therefore in
many instances, it is physiologically desirable to calm down the sensitivity of
the facilitated segments before manipulating other areas.
44
On subsequent manipulative treatments the continued function of these areas is
easily determined and treated as necessary. Other areas and types of treatment
can then be given as indicated by the patient's symptoms and by examination of
the patient. Administering soft tissue treatment to the paraspinal areas while
communicating with the patient not only provides information needed by the
physician and the patient but also provides a tonic effect, improves comfort and
provides palpatory information to visceral areas needing support and alpatory
evidence of the vitality of the patient. Liver pump and splenic pump R0
manipulation, carefully applied, are believed to encourage detoxification and
have been shown to increase circulation of WBCs, respectively. Manipulation
also tends to prevent the complication of constipation commonly produced by
inactivity and systemic toxicity.
Osteopathic manipulation in the treatment program of a patient with lower

respiratory infection improves the patient's comfort and supports that patient's
own self-healing and protective mechanisms. Osteopathic manipulation is
provided for the patient's needs and by understanding the stresses that a patient
should encounter with a certain disease; there is not a specific list of techniques
used for a patient with a systemic disease. Osteopathic manipulation to support
the patient works synergistically with the medical program directed toward the
infectious agent and/or the disease.
Staging a patient according to the severity of symptoms has been shown to be

useful when planning an osteopathic manipulative treatment program which will
be beneficial for a patient with pneumonia. The following is a suggested
osteopathic manipulative treatment protocol for hospitalized patients with
pneumonia: 11
SAMPLE OF TREATMENT PROTOCOL FOR PNEUMONIA:
Manipulative treatment in the hospitalized patient with pneumonia is suggested

at least daily and ideally, three times a day. Charts and suggestions are only
guides and it is the physician's examination of each patient that makes the final
determination of the systems that should be supported and the areas that require
manipulative treatment.
STAGE I: Moderate distress, febrile, non-productive cough, usually mildly to

moderately dehydrated, exhibiting some degree of electrolyte imbalance.
A. Rib raising to point of tissue release in the paravertebral area on

each side. Begin with the area of greatest involvement. In lobar
pneumonia this would correspond with the ribs in direct
contiguity with the lobar region of involvement. With bronchial
pneumonia the entire rib cage region from T l through 12 is often
involved.
45
B. Bilateral soft tissue myofascial release of the thoracic inlet fascias
and similar treatment to the upper thoracic subscapular muscular
and fascial tensions.
C. Bilateral inhibition of paravertebral muscles in the occipitoatlantal
area and down at least to C5.
D. Bilateral occipital pressures towards cranial extension (CV4) if
able to provide this treatment properly, is useful especially if
temperatures are 101-1030
STAGE IT: Diminished distress, lysis of fever, early productive cough,

restoration of fluids and electrolyte balance.
A. Bilateral soft tissue myofascial release of subscapular muscles and

fascia, rib raising by inhibition of paravertebral muscles to point
of tissue effect. Address treatment especially to tissues which are
most significantly effected as determined by palpation.
B. Bilateral soft tissue myofascial release treatment to anterior
cervical fascias.
C. Bilateral soft tissue myofascial release treatment of the intercostal
muscles and fascias.
D. Specific mobilization of C7 to T4.
E. Gentle inhibition of the superior cervical segment. Extend this
treatment down to C5.
STAGE m: Convalescent, afebrile, productive cough, restoration of fluid and

electrolytes balance has been accomplished.
A. Rib raising each thoracic paravertebral area until tissue effect is

palpable.
B. Lymphatic pump either by bilateral pedal pressure or thoracic
pump.
C. Specific mobilization of segmental vertebral somatic dysfunction
as indicated.
PREVENTION OF POSTOPERATIVE PULMONARY

COMPLICATIONS:
The two most common postoperative complications are ileus and pulmonary
dysfunction. Upper gastrointestinal (GI) surgery is more likely to result in
postoperative pulmonary complications than lower GI surgery, probably due to
the proximity of the surgery to the diaphragm. Somatic dysfunction (C3-5:
phrenic nerve) can compromise respiratory homeostasis. Henshaw12
demonstrates the importance of treating this area pre-operatively to prevent
respiratory complications following GI surgery.
46
INCIDENCE OF POST-OPERATIVE
PULMONARY COMPLICATIONS
69%
38%
2X
8 %
3X
27
. :Itr %
LOWER ABDOMINAL LOWER ABDOMINAL UPPER ABDOMINAL UPPER ABDOMINAL

SURGERY SOMATIC DYSFUNCTION SURGERY SOMATIC DYSFUNCTION
General Population C3- C5 General PopUlation C3- C5
SURGICAL POPULATION WITH PRE-OP
C 3-5 SOMATIC DYSFUNCTION
109 CASES
I
OMU Prior to
Surgery
85.3%
\ No OMU Prior
To Surgery
/
53
. %
16 X
Post - Op
Pulmonary
Complications
)
(
3Cases
75
Post - Op
Pulmonary
Complications
Henshaw. The D.O .• Sept. 63. pp 132-3
47
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD):
Both functional and structural changes take place in chronic obstructive

pulmonary disease that eventually affect the entire body unit. Hyperinflation
with alveolar wall destruction leads to a reduction in the total alveolar area of
the lungs and a concomitant loss of pulmonary capillaries. Hypoxia results and
pulmonary vascular resistance is increased as is cardiac output. Pulmonary
hypertension and right-sided heart failure may develop. Structurally, the patient
usually develops a barrel chest and often the accessory muscles of respiration
become over used. Hypertrophied scalenes may cause neurovascular
compromise affecting the upper extremity.
The general guidelines discussed in the previous section on pneumonia are also
applicable for supporting homeostasis in patients with chronic obstructive lung
disease. Manipulative treatment to aid in chest cage motion, thoracic drainage,
and diaphragmatic function are "extremely important" 13. Somatic dysfunction
in the upper thoracic and cervical areas is also treated to reduce segmental
facilitation and to normalize autonomic activity important in both vasomotor and
bronchomotor tone. With better blood flow to the involved tissues, COPD
patients with properly managed somatic factors are clinically expected to require
smaller and less frequent doses of medication.14 Use of osteopathic
manipulative treatment in COPD patients has been documented15 to
significantly benefit pC02, 02 saturation, total lun capacity, and residual
l
volume. In a study of chronic bronchitis patients, 1 92 % of the patients in the
OMT group:
- were able to walk greater distances

- had fewer colds and upper respiratory tract infections
- had less dyspnea
. . . than prior to their manipulative management.
ASTIIMA:
Bronchial asthma is characterized by bronchospasm with trapping of both air

and secretions leading to signs and symptoms of dyspnea, hypoxia, bronchial
expiratory rales, and paroxysmal cough. The secretions are often excessively
viscous and sputum is white, frothy, tenacious, mucoid, and shows microscopic
eosinophils and Charcot-Leyden crystals. Both bronchospasm and increased
bronchial secretions may be caused by overactivity of the bronchial branches of
the vagus nerve.17 Individuals that have hay fever or asthma therefore are
generally vagotonic and also "are particularly prone to parasympathetic reflexes
in the gastrointestinal tract. .,18 Often patients with asthma also have high
narrow palates corresponding to the extension cranial mechanics frequently
48
associated with this respiratory problem.19 Sudden stress factors -- emotional,
physical, or environmental -- will often trigger an asthmatic attack.
In addition to identification of inciting factors with management aimed at

avoidance or hyposensitization, various medications for prevention or
symptomatic relief are utilized. In this section, however, only OMT will be
discussed in detail. The "efficacy (of OMT) in asthma is particularly
remarkable. ,,20 Stiles reports a 14% reduction in hospital length of stay (pre
DRG) when OMT was added to the medical management of asthmatic
patients.21 The text, Osteopathic Medicine, proposes the following:22
"Rather than being merely adjunctive, osteopathic management of

asthma is directed primarily toward the basic disturbance. Asthma is an
outstanding example of a functional derangement. It dramatically
illustrates how unbalanced homeostatic control can alter normal
bronchial muscle tone, secretion, and vasomotor function to cause a
seriously disabling state and ultimately, irreversible organic damage.
The functional basis strongly suggests that somatovisceral reflexes may
well be contributory or localizing causes. Such reflexes can convert
subjective discomfort into a full-blown attack. "
The goals for the use of osteopathic manipulative treatment during an attack
may be dramatically different than the goals proposed for the use of OMT
between attacks. During an attack, some clinicians may attempt to initially
stimulate the sympathetics for the bronchodilator response that results and,
carefully considering the significant spasm of the thoracic musculature induced
by viscerosomatic reflexes, may assist breathing and respiration with a seated
thoracic pump technique. The soft tissues should not be overtreated however.
Pottenger notes23 that either inhibition of the vagus or stimulation of the
sympathetics are physiologically correct in addressing the patient with asthma.
Other clinicians start with CV4 technique, correct the sphenobasilar extension
mechanics, and manipulatate to normalize the vagus.24
Empirically, somatic dysfunction of the third or fourth rib is often demonstrated

and, as with most viscerosomatic induced dysfunctions, responds poorly to high
velocity, low amplitude techniques; other activating forces such as muscle
energy or indirect methods can be quite effective. Treatment of the
sphenopalatine ganglion may also be helpful.25 OMT is believed to raise the
threshold to irritating stimuli and to superimposed psychogenic disturbances.26
Between attacks, maximal thoracic, sternal, and costal motion is sought.

Research by Perrin T. Wilson and by R.S. Koch demonstrated that OMT
between acute asthmatic episodes is able to decrease the frequency and severity
of attacks as well as the need for medications.27
49
BASIC PLAN FOR OSTEOPATHIC MANIPULATION OF PATIENTS WITH WWER
PULMONARY DYSFUNCTION:
cervicals C3-S (Phrenic Nerve)

sternum
somatic Dysfunction
facil. seg.
Sympathetics I
I
Parasympathetics
I
Rib Raising
Tl-6
Chapman's Reflexes
Treatment Plan For
Pulmonary Dysfunction
OA, AA
Cranial
]-
Vagus
Nerve
I Lymphatics
I
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
SYMPATHETIC EFFECTS
t Tone:
1. t Thickening of secretions
2. t Vasoconstriction to Lung Tissue
3. t Bronchiole Dilation
LYMPHATIC EFFECTS

1. t Tissue Congestion
t Tone:
1. Thinning of secretions
2 . Profuse secretions
3. Relative Bronchiole constriction
50
IV. SUMMARY :
The ability to advantageously integrate and administer the combination of

proper medical care and distinctive osteopathic manipulation to support the
patient's respiratory system and compensatory mechanisms, depends upon a
combination of these factors:
o .. the osteopathic physician's understanding of normal and altered reflex

patterns
o .. the pathophysiologic properties of the disease
o .. the ability of the physician to evaluate the patient's individual reaction to
the disease process
o .. the physician's knowledge and skills to provide effective and efficient
manipulative techniques which will reduce hypersympathetic tone,
remove biomechanical impediments to optimum chest cage motion,
improve diaphragmatic function, move lymphatic fluids, and ensure
more appropriate parasympathetic responses so that they can be provided
for the patient when indicated.
A physician must treat the patient according to the present and future needs of
that patient indicated by a physical examination, the estimation of impending
stresses, the pathophysiological nature of the di sease and according to that
physician's training, belief, and knowledge regarding body homeostasis and the
direct interrelationship of structure and function.
REFERENCES:
1. Killough, JH: Protective Mechanisms of the Lungs; Pulmonary Disease;

Pleural Disease, in Sodeman and Sodeman's (ed) Pathologic Physiology.
Philadelphia, W.B. Saunders Company, 1979, ch 16, p 455
2. Beal MC, Morlock JW: Somatic dysfunction associated with pulmonary
disease. JAOA Oct 1984; 84(2): 179-183.
3. Ibid
4. Killough, JH: Protective Mechanisms of the Lungs; Pulmonary Disease;
Pleural Disease, in Sodeman and Sodeman's (ed) Pathologic Physiology.
Philadelphia, W.B. Saunders Company, 1979, ch 16, p 452
5. D'Alonzo AF, Evans DJ: Disorders of the respiratory system, in Hoag JM
(ed) OsteQPathic Medicine. New York, McGraw-Hill, 1969, ch 29, p
465.
6. Death statistics reveal comparative values of osteopath and drug treatments.
OsteQPathic Physician December 1918; 34: 1-2.
and Osteopathy's epidemic record. Osteopathic Physician July 1919; 33: 1.
7. Fitzgerald M, (Stiles E): Osteopathic hospitals' solution to DRGs may be
OMT. The DO Nov 1984: 97-101.
51
8. D'Alonzo AF, Evans DJ: Disorders of the respiratory system, in Hoag JM
(ed) Osteo.pathic Medicine. New York, McGraw-Hill, 1969, ch 29, p
476.
9. Ibid
10. Purse FM: Infectious diseases in children, in Hoag 1M (ed) Osteopathic
Medicine. New York, McGraw-Hill, 1969, ch 49, pp 747, 751.
11. Chila, T: (Adapted from a clinical research project in pneumonia), OU
COM Department of General Practice.
12. Henshaw The D.O. Sept 1963; 132-133.
13. D'Alonzo AF, Evans DJ: Disorders of the respiratory system, in Hoag 1M
(ed) Osteopathic Medicine. New York, McGraw-Hill, 1969, ch 29, pp
464-465.
14. Stiles E: Manipulative management of chronic lung disease. OsteQpathic
Annals Aug 1981; 9(8): 300-304.
15. Howell RK, Allen TW, Kappler RE: The influence of osteopathic
manipulative therapy in the management of patients with chronic
obstructive lung disease. JAOA Apr 1975; 74: 757-760.
16. Magoun HW: Neuroscience studies, in Goldstein M (ed) The ReSearch
Status of Spinal Manipulative Therapy, Bethesda MD, US Department of
Health, Education and Welfare (NINCDS Monograph #15), 1975, pp
295, 301.
7th ed, 1953, P 124.
18. Op cit P 270.
Co, 3rd ed, 1976, P 268.
20. Umanzio CB: The allergic response, in Hoag JM Osteopathic Medicine.
,
New York, McGraw-Hill, 1969, ch 43, p 693.

OMT. The DO Nov 1984: 97-101.
22. Umanzio CB: The allergic response, in Hoag JM (ed) Osteopathic
7th ed, 1953, p 125.
Co, 3rd ed, 1976, P 268.
25. Op cit p 268.
26. Umanzio CB: The allergic response, in Hoag JM (ed) Osteopathic
27. Northup GW (ed) OsteQpathic Research: Growth and Develo,pment. AOA,
1987, pp 82-83.
52
OSTEOPATIIIC CONSIDERATIONS
IN CARDIOVASCULAR DISORDERS
I. INTRODUCTION
"The rule of the artery is supreme. "

-- A. T. Still
The autonomic and lymphatic systems and their effects upon the function of the
cardiovascular system have probably been studied more extensively than any
other system. This is reflective of the significant impact that these elements
have in cardiovascular function and the support of cardiovascular homeostasis in
patients with severe compromise. Osteopathic manipulative treatment (OMT)
has been shown by Stiles to significantly decrease both the mortality and the
morbidity of patients with cardiovascular diseases and dysfunctions. 1 Rogers
reports that OMT has been demonstrated to be of significant value in some
patients with coronary insufficiency.2
This section briefly outlines considerations relevant in hypertension and

atherosclerosis, cardiac arrhythmias, congestive heart failure, and myocardial
infarction. Modalities such as diet, medication, exercise, stress reduction and
cessation of smoking have great relevance to the complete osteopathic treatment
program and these should be integrated into a total treatment program for the
patient; however, in this chapter only the manipulative elements will be
considered in depth.
ll. PATHOPHYSIOLOGY
SYMPATHETICS:
The sympathetic innervation of the heart has its origins in cord segments Tl-6
with synapses occurring between pre-and post-ganglionic fibers in the upper
thoracic and/or cervical chain ganglia. While not totally ipsilateral, there are
definite right- and left-sided distributions of sympathetic fibers to the heart.
The fibers originating on the right tend to pass to the right deep cardiac plexus
to innervate the right heart and the sinoatrial (SA) node. Hypersympathetic
activity to these right-sided fibers predisposes to supraventricular
tachyarrhythmias.
53
The fibers originating on the left
R Left tend to innervate the left deep
Cervical cardiac plexus and the
Ganglia
atrioventricular (AV) nodes.
,---+=- Hypersympathetic activity of these
Superior
fibers predisposes to ectopic foci
and ventricular fibrillation. 3
Sympathetic stimulation of selected
fibers may increase the force of the
heart beat, shorten the time of
systole, increase ventricular output
and increase the rate of contraction
of the heart muscle without
increasing blood pressure or raise
the blood pressure without a general
change in vasomotor tone of the
body. Asymmetries in sympathetic
tone may play a role in the genesis
of serious arrhythmias. 4
Sympathetic Innervation of the Heart
SYMPATHETIC HEAD
NERVES
Increased sympathetic tone increases
morbidity following myocardial
infarction, it inhibits the
development of collateral SUPRASTERNAL
circulation, and it can adversely NOTCH
ANGLE OF
affect the degree of recovery from LOUIS
myocardial injury. 5 Increased
sympathetic tone to the coronary ARMS
vessels has been linked with
coronary vasospasm.
Sympathetic nerve fibers are distributed

to all blood vessels and generally cause
constriction of the circular smooth a. UPPER GI TRACT
muscles found in the vascular system.

Sympathetic tone normally maintains
LEGS \
b. SMAllINTESTlNES
'GHT HALF COLON
J,
the majority of blood vessels constricted
C.
to one-half their maximum diameter and -UMBIUCUS
therefore reduction of sympathetic tone

LEFT HALF COLON
produces a relative vasodilation. An
overview of the sympathetic supply to
vessels of various regions is seen in the
adjacent diagram.
Sympathetic Innervation to Blood Vessels
54
Physiologically, these vasomotor nerves are generally unopposed and their
activation typically produces vasoconstriction with reduced blood flow to the
body tissues. Vasoconstriction can produce a shunt of blood from one area to
another; and it usually increases total peripheral resistance and increases cardiac
work-load. Veins are also constricted in response to sympathetic stimuli but the
venous response is weaker than that in the arteries and arterioles. Sympathetic
hyperactivity to the vascular supply of the kidney has been implicated as a
possible cause of essential hypertension.
PARASYMPATHETICS:
Parasympathetic innervation to areas of the heart is also predominantly

ipsilateral. The right vagus primarily innervates the heart through the sinoatrial
(SA) node and its hyperactivity predisposes the heart to sinus bradyarrhythmias.
The left vagus primarily innervates the heart through the atrioventricular (AV)
node where hyperactivity predisposes to AV blocks. The heart may be reflexly
slowed by stimulating the visceral afferents of selected organs. This seems to
occur because of their common vagal innervation. Irritation of the pulmonary
branches of the vagus produce the strongest inhibitory reflex influence on the
heart. Irritation of the larynx, pressure on the carotid body or the pressure on
the globe of the eye (oculocardiac reflex) will also reflexly slow the heart from
stimulation of visceral afferents that activate vagal efferents. Normally, the
oculocardiac reflex will provoke a slowing of 5-13 beats per minute; however,
g
it will not slow the heart at all in sympathecotonic atients while slowing the
heart 10-12 beats per minute in vagotonic patients.
Left
Somatic dysfunction of the Vagus
occipitomastoid suture, OA,
AA and/or C2 areas (where
there are significant vagal
connections) presumably
produces effects through this
afferent activation of vagal
reflexes.
Parasympathetics are also

involved in regulation of
peripheral arteriolar
vasculature, but only in a
few select situations. In
these areas the
parasympathetic response in
the local arterial vessels is
vasodilation: Parasympathetic (Vagal) Innervation of Heart
55
o .. submaxillary gland vessels via fibers in the small petrosal nerve (from
cranial nerve VII)
o .. parotid gland vessels via fibers in the small petrosal nerve (from cranial
nerve IX)
o .. vessels in the blush region of the face
o .. vessels in the tongue via the lingual nerve
o .. vessels of the penis via the nervus erigens
LYMPHATICS:
Lymphatic drainage from the heart and lungs is carried back to the heart
primarily by the right lymphatic duct.7 Impaired lymphatic drainage from the
heart is known to severely compromise homeostasis and has been implicated in
reduced collateral circulation and increased morbidity and mortality from
ischemia and infection. 8
Congestion of cardiac tissues may result in

arrhythmias or changes in the EKG pattern
(sick sinus syndrome).9 Peripherally
compromised lymphatic drainage has been
linked to the pathogenesis of atherosclerosis
and to the development of hypertension.
10
It plays a significant role in pulmonary
edema, ascites, hepatomegaly, and the
peripheral edema seen in congestive heart
failure. Electrolyte imbalance which can
result from the development of peripheral
edema plays a significant role in the @'{)
morbidity seen in patients with congestive
heart failure.
The diameter of the thoracic duct and other large lymphatic channels is also
under sympathetic control. This fact should be considered in any treatment
protocol designed to improve lymphatic drainage. Hypersympathetic activity
can reduce lymphatic flow capacity.
56
SOMATIC SYSTEM:
Severe scoliosis with a thoracic curve greater than 750, seriously compromises
cardiac function. Other postural changes are more common and have their
effects through somatovisceral reflex changes or segmental facilitation.
In our experience, patients with

flattened thoracic kyphoses or with
postural cross-overs in the upper
thoracic spine tend to have periods
of tachyarrhythmias when stressed.
This is also the case in patients with
a well-documented Travell
triggerpoint located in the right
pectoralis muscle.11 This
triggerpoint, in which posture may
play an etiologic or perpetuating
role, causes supraventricular
tachyarrhythmias. When this is the
etiology, the cardiac arrhythmia
disappears when the triggerpoint is
effectively treated.
Pectoralis "Arrhythmia" Trigger Point
Compensatory musculoskeletal problems may reflexly affect cardiac function.

Treatment of the underlying postural stressor will usually be necessary before
manipUlative treatment of the compensatory somatic dysfunctions will result in
lasting change.
Gait should also be analyzed and especially treated in patients with

compromised functional activity from diminished cardiac output. Abnormal
gait may increase cardiac work by up to 300%12 and this may surpass the
patient's energy reserves. Correction of an abnormal gait may allow a severely
compromised patient to achieve a degree of independence in their activities of
daily living.
Somatic factors also play a significant role in the differential diagnosis of

perceived cardiac complaints. Anterior chest wall syndrome is often a generic
term for any one of a variety of somatic elements which cause substernal and/or
chest pains. Anterior chest wall syndrome is frequently misconstrued as
57
representing cardiac dysfunction. A partial list of specific entities falling into
this category might include cervical, thoracic, sternal, or rib somatic
dysfunction, costochondritis (Tietze's syndrome), intercostal neuritis,
myofascial triggerpoints in pectoralis major, pectoralis minor, or sternalis
muscles, or unrecognized rib fracture. It must be emphatically stated that
somatic factors can co-exist with cardiac di sease and that spinal segmental
facilitation may augment the severity of one and/or the other. Correction of a
diagnosed somatic problem, while it may relieve some of the cardiac
symptomatology, cannot rule out the need for further cardiovascular diagnostics
and/or therapeutics in a given patient.
REFERRED PATTERNS: can be referred from numerous sites
CHEST PAIN: Emergencies CHEST PAIN: l.es& Emergent
Somatic Dysfunction of Ribs and Thoracic Vertebrae

(thIs Is often overlooked etiology of chest pain)
Pain patterns in somatic tissues from

cardiac and coronary dysfunctions
have also been well documented.
Referred pain via the cardiac
viscerosensory reflex from the
coronary arteries (angina) is
classically described as radiating to
the upper half of the left chest, with
referral out and down the inner
surface of the arm and hand to the
t
ends of the little and ring fingers. It
may also refer up the neck and into
the jaw.
Referred Pain
Myocardial Infarction
58
This classic pain distribution into dermatomes C8-T3 is particularly true when
the ventricle is involved; when the atria are involved, the pain is found lower
in the chest wall, in areas of the T4-6 dermatomes.
lOCA TlON AND INCIDENCE OF THORACIC SOAIATlC Referral via the cardiac
DYSFUNCTlON IN N CARDIAC
PATlENTS visceromotor reflex leads to
100 92
muscular contraction and spasm in
the up�r intercostal muscles.
90 83 Larson, 13 Beal14" and Nicholas , 15
80 as well as numerous other
i
•
70 osteopathic physicians, have
separately reported the consistency
l 60
li 53
of palpatory changes primarily on
ci the left side at the levels of T2, 3,4
e 50
� as being associated with cardiac
c:
•
" 40 disorders. Palpatory findings of
�
I!'
30 29 somatic dysfunction at T l -5 on the

22 18 left demonstrate 73 %16 to 79 % 17
20 accuracy compared to angiography
10 8 6 in determining the presence or
0 0 il 1 • 10 absence of coronary artery disease.
T 8T7T6 TsT4T3 T2 T1 T1 T2T3T4TS Chapman I s reflexes from the heart
© Thoracic Spine ® Thoracic Spine are also consistent with these
� Location � levels. IS The posterior and inferior
walls of the heart are heavily
Adapted from data by Myron Beal. DO. FAAO
"Palpatory Testing for Somatic Dysfunction in innervated by cholinergic fibers.
Patients with Cardiovascular Disease"
.IAQA 82 (11) pp. 822-831
While anterior wall myocardial infarctions predictably demonstrate
viscerosomatic changes in the T l-4 paraspinal musculoskeletal on the left,19
posterior or inferior wall myocardial infarctions are accompanied by increased
acetylcholine and bradyarrhythmias. Thoracic palpatory findings at T2 are less
predictable in posterior and inferior wall infarctions. In myocardial infarction
(especially with involvement of the posterior or inferior wall), these palpatory
changes at C220 may need some explanation. According to some clinicians, an
autonomic rationale can be postulated as an explanation because of the vagal
connections to the C2 area.
The recurrent finding of somatic dysfunction or pain in the neck,

cervicothoracic junction, upper thoracic area, chest, shoulder or arm should
alert the physician to the possibility of a significant cardiac etiology. Likewise,
while a myofascial triggerpoint in the pectoralis major may lead to functional
cardiac changes, cardiac pathology may reflexly produce triggerpoints in the
pectoralis myofascial tissues. 21
59
m. TREATMENT SUMMARY - SELECTED EXAMPLES
MYOCARDIAL INFARCTION:
The majority of patients seen within 30 minutes of acute myocardial infarction

demonstrate signs of autonomic disturbance. 22 This is evidenced as
sympathicotonia in the upper six thoracics (particularly T2-3 on the left) in
patients with anterior infarction and as vagal hyperactivity (C2 and cranial base)
in patients with inferior wall infarction. All MI patients would theoretically
benefit from reducing the sympathetically associated cardiocardiac reflexes (C8-
T5) so as to prevent ventricular arrhythmias; concern also exists for those with
excessive parasympathetic activity which can lead to hypotension and
subsequent diminished coronary blood flow to ischemic areas of the
myocardium. 23
50 Patients with Myocardial Infarction
For patients in the intensive care
Adapted from warII by Ed Stiles. 00
unit following myocardial infarc
90
tion, patients with angina, or
patients with other serious cardiac .... eJ�
80
insults, treatment is therefore 0---0 No OMT
directed at calming the sympathetic 70 • • WithOMT

hyperactivity especially in the upper 60
thoracic spine to reduce inappropri
ate cardiocardiac reflexes, lower the 50
incidence of ectopic foci and
40
ventricular fibrillation, and to
remove at least one factor which 30
L····_· ........+.. .... . .. ..... ".+ ... . -�""'" 26%
discourages development of collat ...... _. . _._. . . . . -............-.
20
eral circulation. This is usually the L-·-i··········································· 1--·····...···:�..... 16%
first manipulative goal in the 10
treatment sequence because ascend
ing input from other manipulative
techniques might otherwise be
focused through facilitated segments
into the injured myocardial region.
When integrated with effective medical management for this and other acute
goals, specific osteopathic manipulative treatment should probably be limited to
indirect techniques to avoid undue transient elevation of sympathetic activity to
the heart from the treatment itself. OMT may also be applied in the form of
generalized paraspinal inhibition to decrease total peripheral resistance24 and
cardiac workload.
60
Any thoracic inlet dysfunction is treated with indirect technique and if chest
compressions have been applied during an emergency cardiac resuscitation, both
the ribs and the sternum may benefit from indirect correction of the
dysfunctions that are most certainly present. An excellent case can be made to
also include treatment of hyoid dysfunction because of the fascial continuity to
the mediastinum. Pectoral traction would probably be the treatment of choice to
enhance lymphaticovenous return. The diaphragm may also be redomed using
indirect techniques. Diagnosis and treatment of C2 superiorly including the
base of the skull are performed in an attempt to address parasympathetic activity
to the heart. CV4 is a technique that is helpful in fluid homeostasis as well as
in lowering the patient's stress levels. Osteopathic manipulative treatment along
the lines outlined in this section have been demonstrated to significantly lower
the incidence of arrhythmias and mortality in post-MI patients25 and to lower
total peripheral resistance. 26
Regardless of the techniques selected, a number of physiologic goals are

considered to be addressed effectively by OMT. Thus OMT has been advocated
for coronary heart disease by osteopathic manipulative specialists27,28,29 and
osteopathic cardioiogists30 alike.
ESSENTIAL HYPERTENSION:
Hypertension is a common problem HYPERTENSION IN ADULTS IN U.S.A.

affecting more than 15 % of the US
adult population. Of these cases,
approximately 85 % are considered
to have primary or essential
hypertension.
20% Hypertensive
2:1 Black:White
-
Most authors postulate essential

hypertension to have a multifactorial
etiology with a possible genetic
predisposition aggravated by
environmental and habitual factors
as well as neurogenic, humoral, and Secondary 15%
vascular factors.
61
Functional elements are frequently implicated in the process:
o . . most patients with essential hypertension demonstrate vascular and cardiac

hyper-reactivity to sympathetic stimuli; 31
o .. prolonged sympathetic stimuli to the kidneys creates a functional retention
of water and salt and elevated arterial pressure;
o . . venoconstriction is seen in the early labile phase of essential hypertension
with an increased cardiac output accompanied by inappropriately normal
peripheral resistance. 32
r- EMOTIONAL STATE Eventually peripheral
( resistance increases
�7 D\1 ((""'£\05"
CEREBRAL
CORTEX and cardiac output
HYPOTHALAMUS
RESET BAROCEPTORS returns to normal.
E
With prolonged
hypertension, the
homeostatic mecha
PERIPHERAL ....- ---,
..L..-
nism incorporated in
__
ANS
RESISTANCE '-------'
I
the carotid sinus
VA5C
SWEWNG
� RENAL
ISCHEMIA
baroreceptors resets
and tends to maintain
the increased arterial
\ pressure. 33 The ad
�\
I INCREASED
SODIUM
RETENTION t ANGIOTENSIN
CONTRACTILITY
TUBULAR
NA LOAD
jacent figure summa
rizes the physiologic
(
RENIN J
ALTER factors involved in
ELECTROLYTES ""'- blood pressure
t
ALDOSTERONE
regulation.
"'-I ADRENAL I
NEUROGENIC HYPERTENSION
62
.)t S�PA77{��E �
I�DR ENA q "0-11 TIO-I1
I KIDNI t
Peripheral sisIance
t
ReIeue �i_
C.O. and
�
Peri."..,,,
�
Glomerular Rltratlon �
ResisIaIIce
1
�
AOHt
1tBLOOD PRESSURE 14
c:e.T..o.� _l...
.J'ElecIolyt.t ..
Retained Auids
Barorecepto rs
CN IX
CN X
'-----I� Hypertensio n
Based on physiologic mechanisms in these areas, OMT to support homeostasis

should be effective in patients with hypertension. Regular osteopathic
manipulative treatment is therefore felt to break the cycle of increasingly
frequent episodes of sympathicotonia and delay the stage of fIxed hypertension.
According to Osteopathic Medicine, "Effective management of primary
hypertension will postpone for years the time when compensatory mechanisms
become exhausted and the effects of nephrosclerosis are manifested. ,,34 Due to
the widespread distribution of the sympathetic nervous system, treatment is
usually directed to the entire spinal column.
63
Stress reduction is extremely helpful in reducing cardiovascular manifestations
especially in patients with evidence of the presence of facilitated spinal cord
segments.
Adapted from Kaplan NM

Hypertensipn 1979; 1 :546.
Increased
Renin
Release
Constriction Increased Inaeased

of Renal Filtration Sodium
Efferent Arterioles Resorption
Factor
Thickening of Relative
Transiently Resistant Auid Volume
Excess
Inaeased Vessels
Systemic
Blood Pressure
Inaeased Peripheral Deaeased

Resistance Renin
Release
Nephrosclerosis
This diagram illustrates a hypothesis for the role of stress and the sympathetic
nervous system in the pathogenesis of essential hypertension. It is adapted from
Kaplan NM Hypertension 1979; 1: 546. 35
64
Patients with any cardiovascular dysfunction should also be given the benefit of
treatment to address kidney and adrenal function because of these organs'
intimate coordination in the maintenance of body homeostasis.
One study of hypertensive patients

in which Chapman's posterior
points to the adrenals were treated
resulted in a blood pressure drop of
15 mm Hg systolic and 8 mm Hg
diastolic pressure36 and serum
aldosterone levels in hypertensive
patients have been demonstrated to
decrease 36 hours post-OMT. 37 In
another study of 100 hypertensive
patients treated with OMT only,
there was an average drop of 33 mm Rotatory stimulation of the posterior Chapman's
Hg systolic (from 199 to 166 mm points (T11-12) depicted above have been
Hg) and 9 mm Hg diastolic (from shown to effectively lower blood pressure and
38
123 to 114 mm Hg). 38 decrease serum aldosterone levels.
Rotatory stimulation of the posterior adrenal Chapman's points depicted in the

diagram above has been shown to effectively lower blood pressure and decrease
serum aldosterone levels. 39
Reduction of both systolic and diastolic blood pressure is the "rule" following
OMT. 40 "Whatever technique is used, it should be slow-moving and gentle to
augment rest and relaxation, promote autonomic balance and release fascial
contractures. ,,41 The following chart postulates mechanisms for the treatment
used in hypertensive patients based on the clinical results seen and the anatomic
area being treated:
65
POSTULATED MECHANISMS FOR
OSTEOPATHIC MANIPULATION
TREATMENT MECHANISMS ONSET FULL EFFECT
OA
OCCIPITOMASTOID NEURAL 30 SEC 30 SEC
TECHNIQUE
RIBS STRESS-
GENERAL OMT RELAXATION; 30 SEC 16 HRS.
BIOFEEDBACK ANS
THORACOLUMBAR
JUNCTION RENIN-
CHAPMAN'S ANGIOTENSIN; 2 MIN ?
REFLEXES ANS
FASCIAS BODY FLUID

CV4 SHIFTS 10 MIN 1-2 DAYS
CONGESTIVE HEART FAILURE:
Physicians should place special emphasis on lymphatic goals when treating

patients with congestive heart failure (CHF) in addition to the general approach
to the autonomics discussed throughout this chapter. In CHF 3 to 40 times the
3
resting amount of lymphatic return challenges the system. 42,4 Dilation of the
thoracic duct to several times its normal size may occur causing leakage out of
the duct and subsequent ascites. Inability to accept further lymphatic fluid
results in peripheral edema.
Increased venous and lymphatic return can be translated into increased cardiac
output and homeostatic resistance to extension of injury following myocardial
infarction. Optimal respiratory function is vital for the maintenance of
treatment effects directed at lymphatic and venous return. For this reason
additional time is felt to be well spent on treating diaphragmatic and thoracic
cage somatic dysfunction. Lymphatic pumps and effleurage aid in fluid
homeostasis and help to restore protein and electrolyte levels in these patients.
OMT should not overload the circulatory system but may decrease the
inefficiency of a dilated thoracic duct and restore lymphatic rates to resting
physiologic levels purported to be maximal at approximately 1 ml per minute.
66
ARRHYTHMIAS:
"The comprehensive approach of osteopathic medicine seems

peculiarly suited to cardiac arrhythmias. Chemotherapy can be
lifesaving, but perhaps some of those life-threatening emergencies
could be avoided if the physician would seek out and treat early
sites of dysfunction however remote from the hean proper, or
would view the onset of arrhythmia in the light of homeostatic
and structural mechanisms. M
Rational osteopathic management including OMT is described in the text,

OsteQpathic Medicine, for sinus tachycardia, sinus bradycardia, sinoatrial block,
atrioventricular block, extrasystole, paroxysmal atrial tachycardia, paroxysmal
ventricular tachycardia, atrial flutter, atrial fibrillation, and conduction
deficits. 45 Homeostatic support includes OMT directed towards reduction of
segmental facilitation in the upper thoracics and use of techniques to modify
�
vagal tonicity (such as pressure over the eyes, massa ng the carotid sinus,
strong forward bending of the head [Erben's reflex], Valsalva maneuver, or
treatment of occipital-OA-AA-C2 dysfunction). Structural support also includes
appropriate attention to postural factors and correction of trigger points,
especially those in the pectoralis (described on page 57) or sternalis muscles.
OSTEOPATHIC MANIPULATION OF A PATIENT WITH CARDIAC

DYSFUNCTION
Somatic Dysfunction
facil. seg.
Sympathetics : paraSympathetics l
Cervical Ganglion Treatment Plan OA, AA va gus
Rib Raising For Cranial J Nerve
Tl-6 Cardiac Dysfunction
Chapman's Reflexes
T lO-L2
Adrenal
Kidney I Lymphatics
Thoracic Inlets
I
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
67
SYMPATHETIC EFFECTS
t Tone· •
:-G
Increased
1. t Heart Rate and t Vasoconstriction Cardiac
2. t Cardiac Irritability � Arrhythmias Work
3. Coronary Artery Vasospasm
,J. Tone:
1. ,J. Venous Capacity

2. ,J. Ability to Develop Collateral Circulation
LYMPHATIC EFFECTS
Impaired Flow:
1. t Central Venous Pressure

2. t Tissue Congestion � Decreased 02 and Nutrients
to the Myocardium
3. t In Size of Infarction from M I
4. t Risk of Subacute Bacterial Endocarditis
t Tone:
1. Bradyarrhythmias via SA Node (Right Vagus)

2. Heart Block via the AV Node (Left Vagus)
3. Hypotension and Diminished Coronary Blood Flow
in Inferior M I
IV. CLINICALLY RELEVANT ABSTRACTS - BffiLIOGRAPHY
The following section briefly abstracts a few points supportive of the postulated
role that structure-function interrelationships and/or homeostatic factors play in
an osteopathic approach to treatment of the cardiovascular system. The reader
is encouraged to review the complete article for specifics or qualifications and to
integrate their findings into the brief descriptions of osteopathic care offered in
this chapter.
AUTONOMIC NERVOUS SYSTEM:
1. "The observation that in the majority of patients seen within 30 minutes after
the onset of acute myocardial infarction there were signs of 'autonomic
disturbance,' namely signs of sympathetic hyperactivity mostly in patients with
anterior infarction and signs of vagal hyperactivity mostly in patients with
inferior infarction, not only represented a major contribution but also provided a
necessary link between experimental studies and clinical reality. "47
68
2. Active visceral afferent impulses from the heart produce reflex effects which
are mediated at spinal levels through a cardio-cardiac reflex (viscerovisceral)
and are involved in extending the degree of myocardial injury in myocardial
infarction. Occlusion of the left circumflex coronary artery in dogs lead to
tachycardia. It was also observed that if denervation of the sympathetics was
§
performed first and then a coronary artery was occluded, those do s had smaller
areas of myocardial infarction than dogs that were not denervated. 8
3. "There is a link between the magnitude of sympathetic activity in humans

with myocardial infarction and the heart muscle metabolism, and accompanying
hemodynamics and clinical disorders. The nature of the adrenergic response
remains mysterious. In particular, it is not known why this response
(sympathicotonia) is large in one individual and only moderate in another. ,,49
4. Stimulation of sympathetic nerves lowers the cardiac muscle's threshold for

ventricular fibrillation in animals and has been seen to increase coronary
vascular resistance in patients with ischemic heart disease. 50
5. Sudden death is the result of ventricular fibrillation. This condition can be

reversed if realized and if equipment is available for treatment. Transient risk
factors induce electrical instability and in the electrically unstable heart there is
increased susceptibility to ventricular fibrillation. These transient risk factors
are generally derived from activities higher up in the nervous system:
o . . sympathetic pathways from the hypothalamus are implicated in the genesis

of ventricular arrhythmias
o . . the left stellate ganglion is dominant in the enhancement of sympathetic
efferent activity which predisposes to ventricular fibrillation
o .. stimulation of the left stellate ganglion is associated with increases in the
inotropic effect to the heart while right-sided stellate stimulation
increases both chronotropic and inotropic effects
o . . influence of circulating adrenal catecholamines on cardiac excitability is
considerably less than the influence of the neural input to the heart from
the stellate ganglion
In summary, increased sympathetic activity predisposes the heart to ventricular

fibrillation. Protection can be achieved with surgical denervation,
pharmacologic denervation, or procedures which reflexly reduce sympathetic
tone. 51
6. The most striking and convincing evidence that sympathetic neural inputs are
active in provoking malignant ventricular arrhythmias is demonstrated by the
series of disorders of ventricular repolarization known collectively as the long
Q-T syndrome. A variety of sensory inputs, ranging from emotionally stressful
69
events to noise and exertion, may trigger ventricular tachycardia or ventricular
fibrillation. An imbalance between the right and left stellate ganglionic
sympathetic impulses to the heart has been postulated as being the mechanism
responsible for this. 52
7. A cardio-cardiac reflex takes place within a few seconds of ischemia and

plays an important role in the genesis of early ventricular arrhythmias.
y
Interru tion of visceral afferents from C8-T5 reduces the arrhythmias to a major
extent. 3
8. On initial examination, patients with sinus tachycardia were found to have

sympathetic overactivity.
Transient hypertension in the absence of sinus tachycardia was also regarded as

evidence of sympathetic activity. Patients with sinus bradycardia or AV block
were considered to have parasympathetic overactivity. Sympathetic and
parasympathetic overactivity may coexist in cardiac patient.
The anatomical distribution of vagal receptors may explain the greater frequency
of parasympathetic overactivity in patients with posterior infarction . . . reflex
vagal overactivity may produce AV block. 54
9. Experiments revealed that when sympathetic nerves to the kidneys are

stimulated continuously for several weeks, fluid retention from reduced renal
function occurs and results in chronically elevated arterial pressure as long as
the sympathetic stimulation continues. It is therefore logically theorized that
sympathetic stimulation of the kidney produces chronic elevation of arterial
pressure.
Essential hypertension is probably produced by functional retention of water and

salt by the kidneys. 55
LYMPHATICS:
1. Respiratory activity is the principal mechanism underlying the flow of lymph

from the thoracic duct into the venous system. It appears that the capacity for
transfer of lymph is delicately adjusted to the normal rate of lymph production.
Patients with systemic or portal venous circulatory congestion convert the
plasma into lymph at an abnormally high rate. Available evidence indicates that
this excessive volume of lymph, amounting at times to 3-4 times the blood
volume in a 24 hour period, eventually exceeds the flow capacity of the thoracic
duct/venous junction. The flow capacity of this junction appears to underlay
distension of the duct and the formation of ascites. ,,56
70
2. "Kellner in 1955 reported an interesting study of the relationship of lymph
and its possible role in the pathogenesis of atherosclerosis."
"It seems likely that under normal circumstances there is a constant flow of
fluid containing various serum lipids and protein across the endothelium into the
walls of the blood vessels; this material normally passes through the wall and is
completely removed by way of vasovasorum and lymphatics. In certain
conditions, however, where there are increased amounts of lipid in the blood or
where there are excessive quantities of certain types of lipids, the removal of
these particles from the wall of the vessel is incomplete and some remain to
initiate the process of atherosclerosis."
"In hypertension, increased hydrostatic pressure appears to cause an increase in

the quantity of serolipoprotein that diffuses across the vessel wall, thereby
increasing the possibility for incomplete removal and hence for the deposition of
lipids."
"In this theoretical formulation of the pathogenesis of atherosclerosis, the artery

wall is regarded as an organ which is constantly bathed by a serum transudate
containing, among other things, various serolipoproteins, most of which pass on
through, some of which doubtless are metabolized locally and a few of which
remain behind to cause mischief. ,, 57
3. If by anatomic fault or abnormal physiologic mechanisms, lymphaticovenous

communications fail to function, the rate of edema of the limbs or organs in
congestive heart failure may be increased or resolution (including response to
therapy) may be impeded.
"Data so far suggests that lymphaticovenous communications or, more broadly,

adequate lymph flow plays a part in minimizing pathologic manifestations of
disordered lymph flow from a particular organ or limb."58
4. There exists at present a "state of insufficient training of most physicians in

lymphology. ,,59
60
5. In a study of 28 dogs and 10 humans: "Insufficiency of the cardiac lymph
circulation has not only a theoretical but also clinical importance in the
pathogenesis of arrhythmias."
In cardiac lymphostasis the following was observed:
o .. dilated lymph vessels, interstitial edema, edematous swelling of the

myofibrils and changes in atrial action potentials
o .. shortened effective refractory period of atrium and ventricle (irritability)
o .. diminished SA node automatism
71
o .. slowed AV conduction (prolonged P-Q -- > AV blocks)
o .. EKG changes similar to sick sinus syndrome
6. The protective role of the pulmonary lymphatic system is dramatically

evident when there is an abrupt development of pulmonary edema in a
previously asymptomatic patient with advanced mitral stenosis. These people
develop congestive heart failure and often demonstrate a functional expansion of
the pulmonary lymphatics over a period of time. The expansion with increased
lymph flow may be a compensatory mechanism to remove the overt pulmonary
edema.61
7. Experimental evidence by a team of cardiologists at Michael Reese Hospital

(Chicago) notes: Fibrous and elastic tissue increases significantly in the
ventricular endocardium when a dog's cardiac lymph flow is chronically
impaired. Impairment of cardiac lymph flow may similarly cause
endo myocardial fibrosis and endocardial fibroelastosis in humans.
Ventricular subendocardial hemorrhages frequently occurred soon after lymph

flow obstruction in the heart of dogs. Areas of hemorrhage might lead to
fibrosis when cardiac lymph drainage was chronically inadequate. Autologous
blood injected into the left ventricle of lymph-impeded animals led to marked
fibrosis and changes resembling the pathology seen after acute myocardial
infarction. This was compared to few abnormalities found in controls with
normal cardiac lymph flow.
Dogs with impaired cardiac lymph drainage were injected with bacteria and
most developed endocarditis of the mitral valve. This was compared to no
occurrences in controls with normal lymph flow. Researchers were lead to
conclude that chronic interference with lymph flow predisposes to infection and
inflammation. If impaired drainage from the heart is one of the factors that
predispose a human to bacterial endocarditis, then "it is conceivable that this is
one of the means by which rheumatic fever predisposes to subsequent bacterial
infection."
It is unquestionable, the lymphatic system was important in the reparative

processes seen in dogs after the injection of autologous blood into the
myocardium and lymph flow may prove to be equally significant in healing after
acute myocardial infarction. Animals with intact lymphatic drainage of the
heart undergoing the same injection showed much smaller or absent areas of
infarction and had a lower mortality and morbidity than animals with impaired
lymphatic drainage.
Dr. Dumont of NY University studied the effect of cannulizing and venting nine
patients who were in the final stages of heart disease and had huge distended
thoracic ducts from lymph under pressure. Within 24 hours, central venous
72
pressures fell toward normal and distended neck veins, peripheral edema, ascites
and liver tenderness all diminished or disappeared. Liver edges no longer
projected out under the costal margin. 62
REFERENCES:
1. Fitzgerald M, (Stiles, E): Osteopathic hospitals' solution to DRGs may be

OMT. The DO Nov 1984: 97-101.
2. Rogers JT, Rogers Je: The role of osteopathic manipulative therapy in the
treatment of coronary heart disease. JAOA Sept 1976; 76: 71-81.
3. Corr PB, Gillis RA: Autonomic neural influences on the dysrhythmias
resulting from myocardial infarction. Circ ReSearch July 1978; 43(1):
1-9.
and Lown B, Verrier RL, Rabinowitz SH: Neural and psychologic
mechanisms and the problem of sudden cardiac death. Am J Cardio
May 26, 1977; 39: 890-902.
4. Ibid (Lown et al. )
5. J Autonomic Nervous System, 1981.
7th ed, 1953, p 111.
7. Sodeman WA, Sodeman TM Pathologic Physiology: Mechanisms of
Disease. Philadelphia, WB Saunders, Sixth Edition, 1979.
8. Miller AJ: The lymphatic system and cardiac disease, in Mayerson HS
(ed) Lymph and the Lymphatic System, CC Thomas 1968, pp 213-229.
and Lymphatics' role stressed in cardiovascular disease. Med World News
Jan 21, 1966; pp 100-101.
9. Foldi Progress in Lymphology, pp 84-85.
10. Mayerson HS: One aspect of the role of the lymphatic system in
cardiovascular function, in National Conference on Cardiovascular
Diseases The Heart and Circulation. Washington, 1965, Vol 1, pp 90-
91.
Manual. Baltimore, Williams & Wilkins, 1983, ch 42.
12. Saunders JB: The major determinants in normal and pathological gait.
The Journal of Bone and Joint Surgery Jul 1953; 35-A(3): 543-558.
13. Larson NJ: Summary of site and occurence of paraspinal soft tissue
changes of patients in the intensive care unit. JAOA May 1976; 75:
840-842.
14. BealMC: Viscerosomatic reflexes: A review. JAOA Dec 1985: 786-801.
15. Nicholas AS , DeBias DA, Ehrenfeuchter W, England KM, England RW,
Greene CH, Heilig D, Kirschbaum: A somatic component to
myocardial infarction. Brit Med J July 6, 1985; 291: 13-17.
16. Cox JM, Gorbis S , Dick LM: Palpable musculoskeletal findings in
coronary artery disease: Results of a double-blind study. JAOA Jul
1983; 82(11): 832-36.
17. Beal MC , Kleiber GE: Somatic dysfunction as a predictor of coronary
artery di sease. lA.QA May 85; 85(5): 302-307.
73
18. Byrnes TR, Kuchera ML, Guffey JM, Steele KM, Beatty DR, Haman JL,
Lockwood MD: Correlation of palpatory findings with visceral
diagnoses. JAOA 92(9):1177, Sept 1992.
19. Rosero H et al: Correlation of palpatory observations with anatomic locus
of acute myocardial infarction. JAOA Feb 1987; 87: 119.
20. Bea1 Me: Palpatory testing for somatic dysfunction in patients with
cardiovascular disease. JAOA Jul 1983; 82(11): 822-831.
21. Travell JG, Simons DG Myofascial Pain and Dysfunction: The Trigger
Point Manual, Williams & Wilkins, 1983, pp 585-586.
22. Schwartz PJ, Stone HL: The role of the autonomic nervous system in
sudden coronary death. Annals NY Academy of Sciences 1982;
382:162-180.
23. Ibid
24. Burchett G, Dickey J, Kuchera M: Somatovisceral effects of osteopathic
manipulative treatment on cardiovascular function in patients (abst).
JAOA 1984; 84(1): 74.
OMT. The DO Nov 1984: 97-101.
26. Burchett G, Dickey J, and Kuchera M: Somatovisceral effects of
osteopathic manipulative treatment on cardiovascular function in patients
(abst). JAOA 1984; 84(1): 74.
27. Patriquin DA: Manipulation for the patient with myocardial infarction.
Osteopathic Symposium February, 1975; pp 16-17.
28. Stookey JR: OMT for angina. Osteopathic Symposium March 1975; pp
16-18.
29. Frymann V: Osteopathic manipulation held to aid heart function. Clinical
Trends in Osteopathic Medicine March-April 1976; pp 1, 5.
30. Rogers JT, Rogers JC: The role of osteopathic manipulative therapy in the
treatment of coronary heart disease. JAOA Sept 1976, 76:71-81.
31. Merck Manual, Rahway NJ, MSD Research Lab, 15th ed, 1987,
P 390.
32. Op cit p 393.
33. Op cit P 390.
34. Daiber WF: Disorders of the kidneys in Hoag JM (ed) Osteopathic
Medicine. New York, McGraw-Hill, 1969, ch 39, pp 644-5.
35. Kaplan NM: Arterial hypertension, in Stein JH (ed) Internal Medicine.
Boston, Little, Brown and Co, 3rd ed, 1990, P 240.
36. Mannino JR: The application of neurologic reflexes to the treatment of
hypertension. JAOA; 79(10): 607-608.
hypertension. JAOA Dec 1979; 79: 225-231.
38. Northup TL: Manipulative management of hypertension. JAOA Aug
1961; 60: 973-978.
hypertension. JAOA Dec 1979; 79: 225-231.
40. Daiber WF: Disorders of the kidneys in Hoag JM (ed) Osteopathic
Co, 3rd ed, 1976, P 280.
74
42. Dumont AE, Clauss RH, Reed GI: Lymph drainage in patients with
congestive heart failure, comparison with findings in hepatic cirrhosis.
NEJM 1963; 269: 949-952.
43. Lymphatics' role stressed in cardiovascular di sease . Med World News
Ianuary 21, 1966: 100-101.
44. Baldwin W, Ir: Cardiac arrhythmias, in Hoag 1M (ed) Osteopathic
45. Op cit pp 480-486.
7th ed, 1953, P 111.
47. Schwartz PI, Stone HL: The role of the autonomic nervous system in
sudden coronary death. Annals NY Acad Sci 1982; 82: 162-180.
48. I Autonomic Nervous System, 1981.
49. Circ ReSearch 1981; 48: 6.
50. NEJM August 21, 1980.
51. Lown B, Verrier RL, Rabinowitz SH: Neural and psychologic mechanisms
and the problem of sudden cardiac death. Am I Cardio 1977; 39: 890-
902.
52. DeSilva RA: Central nervous system risk factors for sudden cardiac death.
Annals NY Acad Sci 1982; 382: 143-161.
53. Schwartz PI, Stone HL: The role of the autonomic nervous system in
sudden coronary death. Annals NY Acad Sci 1982; 382: 162-180.
54. Autonomic disturbance at the onset of acute myocardial infarction. Neural
Mechanisms in Cardiac Arrhythmias, 1978.
55. Guyton Textbook of Physiology.
56. Am I of the Med Sci 1975; 269: 3.
57. Mayerson HS: One aspect of the role of the lymphatic system in
cardiovascular function, in National Conference on Cardiovascular
Diseases The Heart and Circulation. Washington, 1965, vol 1, pp 90-
91.
58. Threefoot S: Lymphaticovenous communications, in Lymph and the
Lymphatic System. CC Thomas, 1968, ch 2.
59. Foldi Progress 10 Lymphology.
60. Op cit pp 84-85.
61. Mayerson HS Proceedings of the Conference on Lymph and the Lymphatic
System. CC Thomas, 1968.
62. Miller AI: The lymphatic system and cardiac disease, in Lymph and the
Lymphatic System, CC Thomas, 1968, pp 217-229.
and Lymphatics' role stressed in cardiovascular disease. Med World News
Ian 21, 1966: 100-101.
75
ADDITIONAL CARDIAC BmLIOGRAPHY:
INFLUENCES PRESENTLY UNCLASSIFIED
Beal MC: Viscerosomatic reflexes: A review. JAOA Dec 1985; 85: 786-801.
Blood HA: Manipulative management of hypertension. AAO Yearbook 1964;
189-195.
Burchett GB: Somatic manifestations of ischemic heart di sease. Osteopathic
Annals Sep 1976; 45-50.
Clymer DO: Effects of osteopathic manipulation on several different
physiologic functions: Part III. JAOA Oct 1972; 72: 201-207.
Cox JM: Palpable musculoskeletal findings in coronary artery disease: Results
of a double blind study. JAOA July 1983; 82: 832-836.
Fichera AP, Celander DR: Effect of osteopathic manipulative therapy on
autonomic tone as evidenced by blood pressure changes and activity of
the fibrinolytic system. JAOA Jun 1969; 68: 72-74.
Frymann V: In cardiac patients: Osteopathic manipulation held to aid heart
function. Clinical Trends Osteopathic Medicine Mar-Apr 1976; 2: 1, 5.
Johnson FE: Some observations on the use of osteopathic therapy in the care of
patients with cardiac disease. JAOA May 1972; 71: 799-804.
Kellner A: Lipid and protein content of tissue fluid in normal and hyper-lipimic
rabbits, in Symposium on Atherosclerosis. Washington DC, National
Academy of Sciences National Research Council Publication, 1955, pp
42-49
Lymphatics role stressed in cardiovascular disease. Medical World News Jan
21, 1966: 100-101.
Malliani A: Evidence for a spinal sympathetic regulation of cardiovascular
functions. Experentia 1970; 26): 965-966.
Mayerson HS: One aspect of role of lymphatic system in cardiovascular
function in The Heart and Circulation: Vol 1. (RC 681-AIN 3) , pp 90-
91.
Miller A: Effects of soft tissue manipulative therapy and factors regulating
blood pressure. JAOA May 1967; 66: 990-991.
Miller AI: The lymphatic system and cardiac disease (Chap. X) , in Mayerson
HS (ed) Proceedin�s of the Conference on Lymph and the Lymphatic
System . CC Thomas, 1968.
Nicholas AS, et al: A Somatic component to myocardial infarction. British
Medical Journal Ju1 6, 1985; 291: 13-17.
Patriquin DA: Manipulation for the patient with myocardial infarction.
Osteopathic Symposium Feb 1975; 16.
Reder RF: The role of the sympathetic nervous system in sudden cardiac death.
Dru� Therapy (Hospital) Ju1 1978; 43-55.
76
Richmond WO: Influence of somatic manipulation in coronary artery disease
evaluated by a controlled method. JAOA Jan 1942; 41: 217-225.
Rogers JL: The role of osteopathic manipulative therapy in the treatment of
coronary heart disease. JAOA Sep 1976; 76: 21-31.
Stiles E: Congestive heart failure. Osteopathic Medicine Aug 1976; 76-78.
Stiles EO: Osteopathic approach to the hypertensive patient. Osteopathic
Medicine Apr 1977; 44-45.
Stookey JR: OMT for angina. OsteQPathic Symposium Mar 1975; 16-18.
Thomas PE: The role of the autonomic nervous system in arteriosclerosis.
Osteopathic Annals Jan 1974; 12: 17-20.
Tilley M: The somatic component in heart disease. OsteQpathic Annals May
1974; 30-43.
TIlE TIlORACOLUMBAR REGION AND CHAPMAN'S REFLEX

INFLUENCES
Mannino JR: The application of neurologic reflexes to the treatment of

hypertension. JAOA Dec 1979; 79(4): 225-231.
Comments on hypertension study. JAOA; 79(10): 607-608.
Value of manipulation unresolved by hypertensive study. JAOA; 79(11): 667-
668.
TIlE CERVICAL REGION INFLUENCES
Johnson W: Palpatory findings in the cervicothoracic region: Variations in

normotensive and hypertensive subjects, A preliminary report. JAOA
Jan 1980; 79(5): 300-308.
CRANIAL CONCEPT INFLUENCES
Magouil HI OsteQpathy in the Cranial Field. Kirksville MO, Journal Printing

Co, 3rd ed, 1966, pp 114-115, 176, 179, 280.
Northup TL: Osteopathic cranial technique and its influence on hypertension.
AAO Yearbook 1948: 70-77.
BEHAVIOR MODIFICATION INFLUENCE
Combined pharmacological and psychosocial therapies for hypertension

discussed. Behavioral Medicine Sept 1980; 7(9): 3.
Relaxing hypertension in the long run. Emergency Medicine Jan 15, 1981;
177.
Wadden T, De La Torre C: Relaxation therapy as an adjunct treatment for
essential hypertension. Journal of Family Practice 1980; 11(6): 901-
903.
77
DIETARY CONSIDERATIONS
Hunt JC: The influence of diet on hypertension management. Dialogues in

Hypertension 1980; IV: 37-47.
Silverberg DS: Treating hypertension with diet. Consultant Jul 1980; 115-120.
RISK CONSIDERATIONS
Finnerty FA: Hypertension: Current management, Part I, Selecting and

evaluating the patient. Consultant Jan 1978; 163-168.
Thind G: Factors influencing hypertension prognosis and treatment. Practical
Cardiology Apr 1980; 6(4): 31-39.
Klatsky AL: Alcohol and hypertension: Does drinking increase the risk?
Primary Cardiology May 1978; 31-35, 64-65.
NOTES:
78
OSTEOPATHIC CONSIDERATIONS IN UPPER GI DISORDERS
"Manipulative therapy can play a major role in the management

of the ulcer problem, both specifically and supportively, and it
should be a routine and continuing feature of the emergency,
maintenance, and follow-up care of the patient. ,,1
I. INTRODUCTION
Along with backache and the common cold, gastrointestinal (OI) dysfunction is
a very common cause for absence from work. Regardless of the etiology for
the gastrointestinal upset, there will always be general and local as well as
metabolic and cellular dysfunctions. Oood therapeutic results from
manipulation have been clinically reported by osteopathic physicians and
supported for almost 100 years by patients who have received this distinctive
manipulative treatment as a part of their total medical management.
Osteopathic manipulative treatment of patients with musculoskeletal dysfunction

is understood by most individuals. The present understanding of
pathophysiologic mechanisms and recent research in reflex neurophysiology has
identified where and how osteopathic manipUlation is also clinically effective in
systemic dysfunction and disease. The "cause/effect approach" which these
studies suggest should encourage the incorporation of directed manipulative care
in treatment programs for patients with systemic disease and should stimulate
more clinical research for documentation of the specific effects of manipulation
in patients with gastrointestinal disease. Osteopathic manipulation is not given
instead of medication nor are its effects upon the body's homeostatic
mechanisms duplicated by the medications. Osteopathic manipulation directed
toward improving the physiologic function of the patient and the use of
pharmaceuticals directed mainly toward the disease work synergistically to
encourage the patient's optimal ability to recover and to stay well.
ll. PATHOPHYSIOWGY
VISCEROSENSORY AND VISCEROMOTOR PATTERNS:
Pain patterns from viscerosomatic dysfunction are extremely important when

performing a differential diagnosis on a patient with gastrointestinal (01)
complaints or when making clinical judgment of the severity of the underlying
problem. Proper clinical analysis of these patterns requires a thorough
understanding of both 01 anatomy and neuroanatomy. Knowledge of the
segmental innervation of 01 organs and the location of the appropriately
79
associated collateral sympathetic ganglion (see page 107) is vital for localizing
the source of pain.
Pacinian corpuscles and free nerve SomestheUc

endings are located in the wall of Cortex
any given viscera. These receptors

are activated by spasm or stretch; t Thalamus
pain sensation is carried by visceral

afferent fibers which travel a course
similar to the corresponding
splanchnic nerves.
True visceral pain carried by

visceral afferent fibers often spills
over into related right or left
somatic segments in the back
(depending upon which side the
affected organ is on) and to the
midline of the trunk (in organs Viscera
derived from midline embryological 1. True visceral pain: This is early pain from
irritation, stretching, contraction or exag
structures) .
gerated physiologic motor activity and dys
function. It is midline pain, poorly localized
and described as a vague, deep, diffuse
burning ache.
All pain receptors which transmit

impulses through visceral afferent
fibers and the cerebrospinal tract are
found within 2 cm of the gut and
are stimulated by edema, pressure,
torsion, traction, infiltration,
bacterial toxins, enzymes, or
friction. More specifically, they are
found in the anterior and lateral
parietal peritoneum, the lesser
2. Viscerosensory pain often called visceroso omentum, the mesentery, and the
matic pain: This involves facilitated cord mesocolon.
segments which permit visceral hypersympa
thicotonia as well as paraspinal somatic
changes, j oint somatic dysfunction, and der
matome hyperalgesia in somatic areas relat
ed to the viscera's sympathethic innervation.
80
There are no receptors for pain in
the visceral peritoneum; therefore
the greater omentum and the spleen
and its capsule are pain-insensitive
structures. These structures produce
awareness of pain only if they affect
some adjacent, pain-sensitive
structure. Visceral pain may
become severe enough to spill over
to areas of corresponding somatic
segmental cerebrospinal distribu
tion. Early in most disease
processes, smooth muscle spasm or
stretch will elicit visceral pain
@ which is poorly localized and often
3. Percutaneous Reflex of Morley: This described as gnawing, burning, or
is direct transfer of inflammatory irritation cramping. Sweating, nausea,
from the viscera to the parietal peritoneum
vomiting, pallor, and a relentless
and abdominal wall without reflex through
the visceral afferent nerve on a somatic attempt to squirm away from the
afferent near the mesentary. It produces pain is particularly characteristic of
abdominal wall rigidity, pain, and rebound patients who are experiencing
tenderness.
visceral pain. None of these
common symptoms of visceral pain
accompany somatic pain.
Somatic pain arises when the underlying visceral process progresses past the
visceral serosa and stimulates adjacent somatic sensory nerves. Somatic pain is
well-localized, asymmetric, and aggravated by jarring motions. Somatic pain
may be added to the visceral pain pattern or it may overwhelm and mask it.
Phrenic pain (C3-5 referral area)

occurs when either the hemi
diaphragm or Glisson's capsule of
the liver is stimulated. Its somatic
zone of referred pain is the
ipsilateral shoulder cap. In 5 % of
patients, the fibers of the right
phrenic nerve also reach the lesser
omentum. In those people,
stimulation of the lesser omentum
would also produce phrenic type
referred pain referral to the soma.
81
As a consequence of the spinal cord region becoming facilitated from increased
and prolonged visceral afferent input, palpatory tissue changes and tenderness to
palpation becomes evident in the segmental T5-9 paraspinal tissues, collateral
ganglia and Chapman's reflex sites (page 232). Posteriorly, the small rotatores
paraspinal muscles seem to be more frequently affected and their motion
characteristics and the location of their dysfunction is a key to the source of the
visceral dysfunction, They tend to exhibit the non-neutral type motion with a
preference for backward bending and rotation and sidebending to the same side
as the organ involved. While not contraindicated, high velocity, low amplitude
(HVLA) OMT, is often found to be ineffective and is met with a rubbery
resistance when applied to viscerosomatic dysfunction of this sort. This
response should alert the clinician to look for an underlying visceral cause. If
secondary somatic dysfunction is successfully treated with OMT, it often recurs;
therefore, recurrent thoracic or rib somatic dysfunction without an apparent
primary biomechanical cause should provoke a thorough examination for
associated visceral organ dysfunction.
Common pain patterns for perforated and non-perforated upper abdominal

problems were compiled by a group of physicians from the Mayo Clinic. 2 The
following figures are illustrations adapted from that atlas.
TYPICAL PAIN PATTERN TYPICAL PAIN PATTERN
PEPTIC ULCER CHOLELITHIASIS WITH COLIC
82
SYMPATHETICS:
The autonomic nervous system (ANS) innervates the viscera and most
physiologists consider it soley an efferent system. Visceral afferent fibers report
visceral dysfunction and they usually travel afferently along adjacent pathways
as the corresponding efferent thoracic and lumbar sympathetic splanchnic
nerves.
1j .....
-- CI-2 Level
8+---C6 Level
InnervaUon
of the
Legs
L4 L.eveI -"7"'f..
- . ..
Somatic clues secondary to visceral dysfunction are mediated by visceral

afferents to the cord and related somatic efferent fibers to the soma. These
reflexes are called viscerosomatic reflexes.
These reflexes are responsible for much of the typical objective somatic pain
patterns seen from visceral problems. They are also responsible for palpable
Chapman s reflexes, and the characteristic paraspinal tissue texture changes
I
related to facilitated cord segments T5-9 and T l O- l l . Visceral afferent activity

is responsible for the early tissue changes palpable over the midline collateral
sympathetic ganglia.
The sympathetic portion of the ANS has the unique ability to produce rapid and
widespread organ and somatic changes required to meet stressful situations.
Activation of one sympathetic fiber produces anywhere from four to forty post
ganglionic fiber activations. This is not always beneficial in dysfunction,
illness, or disease where the patient has no need for the "fight or flight"
function of the sympathetic system. Sodeman and Sodeman in Pathologic
Physiology: Mechanisms of Disease state, "The adaptive protective reaction
might be far more damaging to the individual than the noxious agent of the
83
beginning dysfunction. ,,3 This is the situation occurring with prolonged
sympathetic hyperactivity in GI dysfunction or disease.
Increased sympathetic tone decreases mucosal defenses against digestive acids

and enzymes by producing vasoconstriction and alteration of the bicarbonate and
mucous buffers. More patients develop inflammation or ulceration in the upper
GI system from reduced mucosal defenses (from sympathicotonia) than from
hyperacidity. Sympathetic activity also plays an important role in sphincter tone
within the GI system. The normalization of facilitated segments and the
associated sympathetic outflow from the T5-Tll region reduces gastrointestinal
vasoconstriction and allows an increase in mucous secretion from Brunner's
glands permitting homeostatic mechanisms to operate to protect mucous
membranes.4
In diseased patients, prolonged hypersympathetic activity can initiate processes

that are detrimental to survival. Gilsdorf and his group in 1965 reported in
lAMA that cats with nonlethal pancreatitis would develop hemorrhagic
necrotizing pancreatitis leading to the death of the animal when subjected to
increased sympathetic stimulation; Block and others, writing in Surgical
Gynecology and Obstetrics in 1954, indicated that ischemia changed nonlethal
pancreatitis to lethal pancreatitis. From studying the world literature, Dr. Korr
emphatically states, "In every disease process there is hypersympathetic activity;
sustained sympathetic activity is a common factor in disease. "
PARASYMPATHETICS:
Right Left The parasympathetic portion of the

vagus� � Vagus ANS tends to dominate innervation
� ,Y. of the viscera during "normal, " long
term, restful activity. In the upper
GI tract, parasympathetic
innervation is supplied by the vagus
nerve (eN X) which exits the skull
through the jugular foramen, which
is formed by the joining of the
jugular notch of the temporal and
the jugular notch of the occipital
bones. The left vagus supplies the
greater curvature of the stomach and
extends to the duodenum; the right
vagus supplies the lesser curvature
Parasympathetic
Innervation VI8 of the stomach, the small intestines,
the Vagus Nerves the right colon and the organs and
and
the Splanchnic Nerve glands up to the midtransverse
colon.
84
Parasympathetic stimulation will increase the secretion rate of almost all
gastrointestinal glands. 5
The most inferior ganglion of the vagus nerve, the ganglion nodosum, extends
into the cervical area and lies in fascias which are just anterior to the OA and
AA joints. The vagus also has connections with the first two cervical somatic
nerves which provide neurologic pathways for fibers carrying pain fibers from
the posterior portion of the head (Le. the occipital nerves). This connection
may explain the occipital headaches which are often a part of the "subjective"
symptomatology of a patient with upper GI or pulmonary disease, especially in
upper GI viral dysfunctions or viral pneumonia.
This connection may also explain the nausea and vomiting that accompanies
certain headaches and the palpatory clues found at the OA and C2 areas are
related to dysfunction in viscera innervated by the vagus nerve. The
parasympathetic system will also often produce symptoms of disease.
Parasympathetic reflexes give the physician an explanation for many of the
symptoms which are designated as nervous type or "functional disorders. "
These include hyperchlorhydria, nausea, hypermotility of the intestines, spastic
colon, irritable bowel, bradycardia, asthma, hay fever, epiphoria, cough,
hoarseness and excessive nasal discharge. The parasympathetic nervous system
may also produce changes in tissues of its innervation, making that organ more
susceptible to infection or chronic trophic change. It appears that all organs
innervated by the vagus nerve are intimately bound together and capable of
readily transmitting reflexes to and receiving reflexes from each other. This
may be why the larynx is so often involved when there is a problem with some
other part of the GI tract also innervated by cranial nerve X.6
LYMPHATICS:
The lymphatic system is absolutely necessary for good health and is even more
important and frequently overworked during body dysfunction and disease.
Extensive experimental studies in cats and dogs indicate that the lymphatic
system must be able to increase its normal flow capacity by 4-5 times with some
body stresses and in some chronic pathological syndromes such as congestive
heart failure, up to 40 times its resting capacity. Because of these demands on
its peak function, even a slight mechanical impedance of its lymphatic pathways
or hindrance to the function of the diaphragm (which acts as its extrinsic pump)
might greatly reduce the body's ability to recover from a disease process.
Lymph from the GI tract as well as all other organs and systems below the
diaphragm drain from small lymphatic channels into the cisterna chyli. This is
an irregular fibromuscular sac about the size of a cigarette, wedged between the
aorta and the right crus of the diaphragm and just in front of the bodies of the
85
fIrst two lumbar vertebrae. It also marks the start of the left lymphatic duct,
called the thoracic duct.
The thoracic duct is about 18 inches

long and extends from the cisterna
chyli up through the fascias of the
left thoracic inlet, into the neck for
a distance of about 1 112 inches
above the clavicle, arches over the
pleura and apex of the left lung, and
then passes back through the
thoracic inlet to fInally empty into
the junction of the left internal
jugular and left subclavian veins.
The vital flow of lymph may be
hindered by a poorly effIcient,
flattened diaphragm or by torsion of
the fascias around the lymphatic
channels located in the mesenteries
or at the thoracic inlet. The fIrst Upper Gastrointestinal Tract
sign of terminal lymphatic drainage
dysfunction in the abdomen may be
a palpable fullness in the sub
xiphoid soft tissues.
Studies show that the incidence of pancreatitis is increased in gallbladder disease

if their common lymphatic drainage route is compromised. Lymphatic drainage
from the liver is increased greatly by minor pressure changes and so lymphatic
drainage is greatly influenced by the depth of respirations and manipulative
treatments (such as the liver pump) which create intermittent pressure charges.
SOMATIC SYSTEM:
Locating and correlating palpable changes in the musculoskeletal system are

very helpful when considering a diagnosis of visceral di sease. Reflex muscle
spasm is often present in addition to segmental paraspinal somatic dysfunction,
Chapman's reflexes and collateral ganglion tenderness. Guarding, rigidity and
myofascial trigger points are all expressions of this phenomenon and all should
be considered when performing a physical examination. Unless these areas are
treated, pain patterns may be perpetuated. Travell reports, "Pain, which
previously had responded to medical therapy for a duodenal ulcer, became
unresponsive and persisted until trigger points in the abdominal musculature
were found and inactivated."7 Peptic ulcer disease has been found to be
associated with abdominal myofascial trigger points which in turn continued to
produce a somatic pain referral pattern similar to that originally produced by the
86
visceral disturbance; in these patients, even after the ulcer healed, both the
patient and physician are often misled to believe that a visceral problem
remained. This is believed to be the case in postcholecystectomy syndrome
where OMT commonly alleviates symptoms of gallbladder dysfunction and the
typical gallbladder-type referred pain which remain even after surgical removal
of the gallbladder.
ill. THE PHILOSOPHY OF TREATMENT
The exact diagnosis is important when formulating specific medical and

manipulative treatment and when predicting the prognosis for a patient with
some type of disease process; however, from a functional standpoint, specific
evaluation of the body's attempted homeostatic reactions to its dysfunction is
often more useful than the specific visceral diagnosis when deciding where, how
and what manipulative treatment to give. If the physician understands the
general pathophysiology and responses of the upper GI tract to a disease process
and can determine the responses of the patient to the dysfunction, manipulation
can be beneficially administered even during the diagnostic work-up stages, to
relax the patient and to support body homeostasis.
UPPER GASTROINTESTINAL DISEASE
History
Symptoms
Campylobacter
Pylori
Prostaglandins
87
Therefore, the goal is not to diagnose and treat "joint dysfunction. " The goal of
treating patients in this manner involves administering rib raising and paraspinal
inhibition for autonomic imbalance and reflex dysfunctions, improving
circulatory and trophic factors, modifying fascial patterns which hinder ,
lymphatic pathways and the pumps, and treating the base of the skull and upper
cervical area to affect parasympathetic function. If specific joint somatic
dysfunction is palpable it should be diagnosed and treated appropriately, because
it represents a somatic contribution to the maintenance of the facilitated
segments of the cord and thus hinders the viscera by its promotion of
sympathetic hyperactivity, termed sympathicotonia.
It is not unusual to see patients suffering from pain and cramping discomfort
due to GI dysfunction of many types, waiting uncomfortably for 1-3 days while
the "specific diagnosis" is being obtained through multiple test procedures.
Manipulative treatment for those patients could be started early. This would not
interfere with the diagnosis in any way, once the search for an organic etiology
was planned and in progress; in fact, the responses of the musculoskeletal
system may help guide a more economical or complete approach to the
diagnosis. It would make the patient more comfortable by beginning
normalization of altered physiologic processes at a connective tissue or cellular
level. Manipulative treatment would most likely reduce the amount of pain
medication required for patient comfort and would help prepare the patient's
body for better acceptance, distribution and utilization of any specific
medications prescribed once the pathologic diagnosis is secured. If the process
was functional, then often the "negative" work-up for organic structural causes
will be accompanied by a patient who no longer has complaints.
Osteopathic manipulation for a patient with systemic di sease is primarily

directed toward balancing autonomic activity and improving lymphatic flow.
This type of treatment should relieve, improve and enhance the patient's own
abilities:
o to improve visceral response to stress

o to relieve congestion
o to improve circulation
o to enhance the removal of waste products from the tissues
o to improve cardiac output
o to improve oxygenation and nutrition at a cellular level
o to enhance resistance to infection
o to enhance more predictable tissue levels and patient response to specific
medications
o to enhance relaxation and comfort of the patient during diagnostic
procedures and any specific treatment program
88
IV. OSTEOPATHIC TREATMENT FOR PATIENT WITH UPPER GI
DYSFUNCTION
LYMPHATICS AND FASCIAS:
The visceral organs are suspended from the dorsal surface of the abdominal
cavity by mesenteries. Through these connective tissue pathways pass the
arterial blood supply, the venous and lymphatic drainage vessels, and the
sympathetic, parasympathetic and visceral afferent nerves of the viscera.
The most important mesentery to

the osteopathic physician who is
treating upper GI dysfunction is the
mesentery for attachment of the
small intestines. This mesentery
can be located in the patient by
constructing an imaginary line from
1 inch to the left and 1 inch above
the umbilicus to a point in the lower
right quadrant of the abdomen just
anterior to the right sacroiliac joint.
Thirty feet of intestines are attached
to this six-inch mesenteric base.
Location of Mesenteric Attachments
A manipulative technique to reduce congestion and improve circulation to the

small intestines is called a "mesenteric lift" and is helpful in freeing lymphatic
pathways from the small intestines. The small intestines usually lie in the
suprapubic and lower left abdominal quadrants. This ventral abdominal
technique for the small intestines is performed by carefully lifting them upward
and to the right side of the abdomen while using the patient's respiratory force
for activation (see page 227). The patient's respiratory force is activated by
having the patient breathe in and hold the breath until air hunger occurs. The
physician should be sensitive to the tissue response under the palpating fingers
and keep the patient comfortable while providing a gentle encouragement to the
tissues being treated. About the time the patient needs to take a breath, the
physician will feel a mesenteric release (although occasionally 2-3 breath cycles
will be required before a release is palpated). Visceral manipulation using
release techniques for each upper GI organ has been described in detail by Jean
Pierre Barra!, D.D.,s and may be employed to help maximize visceral function.
The·fascial pattern of the thoracic inlet and the inferior thoracic outlet must also
be evaluated. These fascial areas are treated as indicated and the diaphragm
must be well domed. "Domed" means that both leaves of the relaxed
89
diaphragm are optimally concave inferiorly (convex superiorly) and that they
work symmetrically during respiration. Treatment of a dysfunction of the
thoracoabdominal diaphragm might include soft tissue to the paraspinal muscles
and quadratus lumborum as well as direct or indirect fascial treatment directed
at the diaphragmatic attachments--the thoracolumbar junction, the lower six
ribs, and/or the sternum.
R L
SYMPATHETICS:
Any stress or dys

function of the upper
GJ tract causes a bar
rage of visceral affer
ent impulses to bom
bard the cord. Vis
ceral afferents from
the upper GJ tract
and small intestines
travel first through
the celiac or superior CHAPMAN'S
mesenteric collateral REFLEXES
ganglia. They then
travel through the
chain ganglia to cord
levels T5 to TIL 9 1/2
Since these impulses tend to travel the same pathways as corresponding

sympathetic efferents, any resultant facilitated segments are more likely to be at
the levels of sympathetic innervation to the organ in trouble. Studies confirm
that somatic palpatory clues to upper GJ and small intestinal dysfunction occur
in the paraspinal somatic tissues from T5 to TIL
Chapman s system of anterior and posterior myofascial tender points related to

I
specific visceral dysfunction are particularly helpful in diagnosis of GJ dysfunc

tion.10 They are considered to be produced by viscerosomatic reflexes which
generally fit a sympathetic reflex pattern.
Charts for the entire Chapman system of anterior and posterior myofascial
points can be obtainedll and are reproduced in diagrams on pages 232 and 233.
The anterior points are most useful as indicators of dysfunction because they are
easily located and are more sensitive to light palpation. They correlate well
with final hospital diagnoses.12 The posterior points are less tender; therefore,
they are less often used as diagnostic clues. Some physicians use the posterior
90
points for localized soft tissue treatment in an attempt to influence a specific
organ s autonomic balance.
I
The above knowledge helps a physician diagnose and plan manipulative

treatment for upper GI disease and dysfunction. Treatment to normalize
sympathetic hyperactivity is clinically effective and may be administered in
several different areas including the sementally associated vertebrae (facilitated
segments), the ribs (sympathetic chain ganglia), the specific collateral ganglion,
and the Chapman s reflex tender points.
I
Any treatment to the sympathetic ganglia will initially stimulate sympathetic

activity to the organs of sympathetic innervation, but this effect is localized near
the segments treated and is short-lived. The lasting effect is believed to be
produced through stimulation of the long very slow sympathetic fibers, which
cause inhibition of sympathetic outflow in the areas treated. This reaction is
centrally mediated and is longer acting. It serves to improve blood flow and
maximize homeostasis including mucosal barriers to areas of the GI system
sharing the same segmental distribution.
o .. RIB RAISING: The most common manipulative method to modify

sympathetic activity utilizes rib raising techniques (page 195) to the
appropriate rib areas, i.e. T5-Tll for the upper GI tract and small
intestines. Since the chain ganglia of the sympathetics lie in the fascias
over the heads of the ribs, rib raising produces the reflexes which
clinically normalize sympathetic activity. This technique can be
administered with the patient in the supine, lateral recumbent or sitting
position. Treatment only needs to be long enough for the physician to
sense palpable tissue change. This may take a few seconds to a few
minutes.
It is known that spinal impulses passing through a facilitated area of the

spinal cord will produce bursts of sympathetic activity to the viscera
innervated by those segments. For this reason, treatment of segmental
spinal somatic dysfunctions related to areas of suspected facilitated cord
segments often precedes manipulative techniques to other tissues in other
areas.
o .. VENTRAL ABDOMINAL INHIBITION: Treatment by ventral abdominal

inhibition to the appropriate collateral sympathetic ganglia (page 2(0)
until tissue change is palpable is also considered to reduce sympathetic
hyperactivity of their respective spinal levels. It is known that the
collateral ganglia are able to provide some regional control of the viscera
without relay to the central nervous system and are not "just switching
stations" for autonomic activity.
91
These ganglia are located in the midline of
the abdomen--anterior to the abdominal
aorta and between the xiphoid process and
the umbilicus. The celiac ganglion is
Mesenteric associated with T5-9; the superior
mesenteric ganglion with TlO-U; and the
inferior mesenteric ganglion with TI2-L2.
The first two named ganglia are often
involved in upper GI disorders while the
Location of Collateral inferior mesenteric ganglioh is involved in
Sympathetic Ganglia lower GI and pelvic problems.
0 CHAPMAN'S MYOFASCIAL POINTS: (See pages 232 and 233)

. .
Sympathetic hyperactivity can also be treated by manipulation of

posterior Chapman's reflex points. The anterior Chapman's points are
easily accessible and more tender to manipulation so are used for
diagnosis. Memorize the common anterior Chapman's points related to
the gastrointestinal system. When performing a physical examination,
these clues to visceral dysfunction can be checked in just a few seconds.
These ganglioform reflex points are believed to be produced in the deep
myofascial tissues by viscersomatic reflexes resulting in increased
hypersympathetic. If one or more are tender to palpation, ask specific
questions related organ's dysfunction and correlate this with findings
from palpation of the collateral sympathetic ganglia and related
paraspinal tissues. To treat the posterior points related to the upper GI
tract and small intestines, circular soft tissue pressure of moderate
intensity is administered between the proper intertransverse processes
until the points disappear. Posterior Chapman's points related to the
upper GI system in the intertransverse spaces will usually correlate with
tender anterior Chapman's points located in the respective ipsilateral
intercostal spaces.
PARASYMPATHETIC SYSTEM:
Beneficial treatment to improve parasympathetic innervation to the upper GI

tract is directed primarily toward removing joint somatic dysfunction of the
cervical spine (especially in the area of the OA and AA joints), treating the soft
tissues of the suboccipital area and utilizing condylar decompression techniques
to relieve fascial tensions around the ganglion nodosum and the vagal trunks. If
the physician is trained in cranial treatment techniques, treating somatic
dysfunctions of the occipitomastoid suture area will release tensions felt to affect
the vagal nerve as it exits the skull through the jugular foramen. This treatment
is also effective in helping to relieve tensions associated with suboccipital and
occipital headaches which often accompany GI disturbances.
92
VI. SUMMARY
It has been shown that removal of musculoskeletal dysfunction may alter

associated, secondary visceral dysfunction; however, if the musculoskeletal
etiology remains too long, the reflex pathway seems to be "learned by the
cord, " so that the dysfunction of the viscera may be reestablished even after the
somatic dysfunction is removed. Patterson hypothesizes that this may be a basis
for a patient's predisposition to chronic disease and may indicate evidence
supporting early osteopathic manipulation as a means of preventing diseases as
well as a means of supporting a body that has disease.
Osteopathic manipulation provides an additional and synergistic approach to the

usual medical treatment of GI disease and dysfunction. No matter how effective
medicines become, drug specificity and sophistication does not excuse an
osteopathic physician from the responsibility of supporting the patient's own
defenses. Intelligent, physician-directed manipulation provides this support for
the patient by enhancing the self-regulatory mechanisms of the body unit using
OMT to improve the body's structure and function.
REFERENCES:
1. Strong WB: Disorders of the digestive system, in Hoag 1M (ed)

Osteopathic Medicine. New York, McGraw-Hill, 1969, ch 38, p 573.
2. Smith LA et al An Atlas of Pain Patterns: Sites and Behavior of Pain in
Certain Common Diseases of the Upper Abdomen. Springfield IL, CC
Thomas, 1961.
3. Sodeman WA, Sodeman TM Pathologic Physiology: Mechanisms of
Disease. Philadelphia, WB Saunders, 6th ed, 1979.
4. Strong WB: Disorders of the digestive system, in Hoag 1M (ed)
1953, 7th ed, 262.
6. Op cit pp 211-215.
7. Travell IG, Simons DG Myofascial Pain and Dysfunction: A Trigger Point
8. Barral IP, Mercier P Visceral Manipulation. Seattle WA, Eastland Press,
1988.
9. Beal MC: Viscerosomatic reflexes: A review. lAOA Dec 198;85:786-
80 1.
10. Owens C An Endocrine Interpretation of Chapman's Reflexes. Carmel
CA, 1963.
11. Contact the Department of Osteopathic Theory and Methods at the
Kirksville College of Osteopathic Medicine, 800 West Jefferson Street,
Kirksville, Mo. 63501
12. Byrnes TR, Kuchera ML, Guffey 1M, Steele KM , Beatty DR, Haman JL,
Lockwood MD: Correlation of palpatory findings with visceral
diagnoses. JAOA 92(9): 1177, Sept 1992.
93
OSTEOPATHIC MANIPULATION OF A PATIENT WITH
UPPER GASTROINTESTINAL DYSFUNCTION

Somatic Dysfunction
facil. seg.
Sympathetics I
I
Parasympathetics I
Treatment Plan for AA,
I
Rib Raising OA, C2 - Vagus
TS-9 Upper Gastrointestinal Cranial Nerve
TIO-ll Dysfunction
Chapman's Reflexes
Collateral
Ganglia I Lymphatics
I
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
Mesenteric OMT (Ventral Abdominal Techniques)
SYMPATHETIC (PATHO)PHYSIOWGY
t Tone:
1. t Vascular Tone � l 0 2 and Nutrients to tissues
� t Mucosal Sensitivity to H+ concentration and Alters
the Mucosal Barrier
2. Relaxation of Gallbladder and Ducts
3. l Peristalsis � Constipation
LYMPHATIC (PATHO)PHYSIOWGY

1. t Tissue Congestion and Impaired Nutrient Absorption from
the Bowel
2. t Risk of Pancreatic Complications in Gallbladder
Disease/Dysfunction
PARASYMPATHETIC (PATHO)PHYSIOWGY
t Tone:
1. t Acid Secretion
2. Contraction of Gallbladder and Ducts
3. Peristalsis � Diarrhea
94
OSTEOPATHIC CONSIDERATIONS IN WWER BOWEL DISORDERS
I. INTRODUCTION
Beginning cellular and organ dysfunctions associated with disturbed metabolism,

congested tissues, cloudy swelling, lactic acid accumulation and tissue acidosis
are reversible with early treatment. Visceral irritation and disease increase
visceral afferent nerve activity and are often associated with hypersympathetic
bombardment of the associated organs. Sympathetic nerve impulses may
protect the body from external dangers but when they remain hyperactive, due
to cord facilitation, they become a roadblock to rapid healing and restoration of
health and can even produce potentially lethal conditions. Hypersympathetic
activity is present in post-surgical patients and all patients with systemic
diseases.
The rate of healing of body tissues is dependent upon the ability of the body to
remove waste products from the tissues and to deliver oxygen and other
nutrients to the area of tissue dysfunction, injury, or the site of a surgical
intervention. This "is built in" to the body as self-regulating mechanisms which
in turn require good arterial, venous and lymphatic circulation, as well as a
good nerve supply. These prerequisites of the self-regulating mechanisms
depend upon good circulation and accurate reports from visceral afferent nerves.
Hypoperfusion results in low tissue resistance to infection and when infected,

these tissues remain infected longer than tissues with good perfusion and
nutrition. Studies by Niinikoski (1980) reveal that white blood cells selectively
kill bacteria by using superoxide and that "any treatment that augments the local
oxygen supply to the tissues and helps to avoid hypoperfusion increases the rate
of healing and decreases the susceptibility to infection." Han and McKay
concluded from experimentation involving animal inoculations of staphylococcal
bacteria that "even small increases in oxygen to a tissue resulted in a relative
large increase in its resistance to infection and greatly increased its ability to
recover from the infection."
Osteopathic manipulative treatment in bowel disease and bowel dysfunction is

often directed toward and related to improving blood and lymphatic flow and
balancing the autonomic impulses to and from the bowel. Effective osteopathic
treatment improves the circulation and oxygenation of the tissues. When
performing or ordering manipUlative treatment for lower GI diseases, certain
functional anatomical and neurologic peculiarities of the colon must be kept in
mind.
95
ll. PATHOPHYSIOWGY
SYMPATHETICS:
Sympathetic hyperactivity reflecting

a disease process is usually
associated with facilitated segments
TIO-TIl when the right half of the
colon is involved and facilitation of
T12-L2 when the left half of the
colon is involved. Disorders of the
colon usually produce
viscerosomatic reflexes which
increase thoracolumbar paraspinal
muscle tension and produce pain in
TlO-11 or T12-L2 areas of the
spine.
Sympathetic hyperactivity is also

believed to be indicated by
CHAPMAN REFLEXES
viscerosomatic myofascial tender
points called Chapman's points. 1
This myofascial system of diagnosis
and treatment is attributed to Frank
Chapman, D.O. The anterior
Chapman's points are helpful clues
to colon dysfunction and are found
Posterior Points as tender, palpable fascial
ganglioform nodulations on the
Cecum
II-+-Sigmoid lateral side of the thighs in the
anterior half of the iliotibial bands
Ascending Colon Descending Colon from the greater trochanters to the
lateral epicondyles of the femur.
Hepatic Flexure ,,.-r- Splenic Flexure
These areas become tender to light
pressure with most colon
dysfunction; however, it has been
Anterior Points clinically observed that some colon
cancers may not produce
Chapman's reflexes though it is not known exactly why this is true. It is
theorized that tissue inflammation and/or irritation is required to initiate these
reflexes through the visceral afferent and sympathetic systems.
96
With diseases of the colon, the Sympathetic Innervation of
inferior collateral sympathetic The lower Bowel
·0----- C1-2
ganglion, located in the midline of �
the abdomen and just above the
umbilicus, is often palpable and
�"---T
-- 2
tender. This palpatory change is
also believed to indicate sympathetic �---T4
hyperactivity to the colon as a result
of visceral afferent bombardment
with its influence upon facilitation
of related cord segments. \J---T9
Celiac
The collateral ganglia in the midline Sup. Mesenteric
of the abdomen have self-contained Inf. Mesenteric

mechanisms which can attempt
.--4--- L3-4
control and reaction to regional
visceral dysfunction; therefore, they
are capable of controlling function
locally without reporting to the
spinal cord. �istal HaH of
1_ T�ans�erse Colon,
Sigmoid Colon and
Rectum
-
Right Left
vagusy
�
Sympathetic hyperactivity of the

lower GI system is associated with
findings and symptoms of ileus,
constipation, abdominal distention
and flatulence.
PARASYMPATHETICS:
Manipulative techniques to
normalize parasympathetic activity
to the colon may be especially
useful in the care of patients with
colitis, Crohn's disease, irritable
bowel syndrome, or idiopathic
diarrhea. The vagus nerve provides
Parasympathethic
Inl'l8fVation of parasympathetic innervation to the
The Vagus Nerves right side of the colon.
And
Pelvic Splanchnic Nerve
97
The left vagal innervation extends only to the greater curvature of the stomach
and the pyloric area of the GI tract. The right vagus nerve also innervates the
upper GI tract, including the lesser curvature of the stomach, the liver and gall
bladder and then continues on to innervate all of the small intestines and the
right half of the colon. The pelvic splanchnic nerves with their origin from
cord segments S2,3,4, supply the parasympathetic innervation of the left half of
the colon and the pelvis.
This split in parasympathetic innervation must be kept in mind when looking for
somatic dysfunction which could have an affect on the right or the left half of
the colon.
Parasympathetic hyperactivity in the lower GI system increases bowel motility

and glandular secretions and is associated with diarrhea. Hypoactivity of the
parasympathetic system results in the opposite manifestations of bowel function,
namely decreased bowel motility and glandular secretion as well as constipation.
When there is hyperactivity of both the parasympathetic and. the sympathetic
systems to the bowel the functional disorder tends to manifest as an irritable
bowel syndrome. (See Irritable Bowel Syndrome, page 109.)
LYMPHATICS:
With dysfunction of the tissues of the colon there are cellular and tissue
metabolic changes which lead to increased interstitial fluids and tissue
congestion. The result is accumulation of waste products, reduced oxygenation
and decreased nutrition to the cells. These changes increase the colon's
susceptibility to inflammation and infection and increases its healing time when
stressed. Congestion also increases the likelihood of fibrosis with increased
scarring in the healing process. Fibrosis can worsen the prognosis in patients
with colitis or Crohn's disease.
One Inch over
Six
Inches
long
Location of Mesenteric Attachments
98
Vessels and nerves to and from the intestines must travel in mesenteries.
Though these mesenteries are broad, the very thin walls of the lymphatic and
venous channels are vulnerable to pressure from surrounding edematous tissues.
Canine studies indicate that tissue congestion interferes with the effective
medical treatment of disease processes. 2
In these studies there was uneven distribution and accumulation of the active
drug in the dogs' tissues and the drug's by-products accumulated in the
congested tissues; often the tissues which needed the active component the most
were the tissues that got the least concentration.
According to Sam Threefoot, M.D., director of the New Orleans Research

Institute, "When lymphatic flood channels fail to function because of anatomical
fault or abnormal physiologic mechanisms, therapy is impeded. ,,3
Because the interstitial fluids from a congested colon drain through the thoracic
duct, any restriction of the lymphatic pathways to the duct, the fascias through
which the duct passes, or the fascias at the thoracic inlet would be associated
with increased tissue congestion. Thoracic diaphragm function should be
ascertained because of its importance in moving both venous and lymphatic
fluids. The ability of the pelvic diaphragm to passively and synchronously
move with the abdominal diaphragm should also be considered when treating
conditions associated with abdominopelvic congestion.
It is possible that patients with disease processes or prior surgery involving the
lower sigmoid, rectum, and anal areas will have asymmetry or spasm of the
pelvic diaphragm. The pelvic diaphragm is a funnel-shaped muscle attaching to
the lateral walls of the true pelvis and angling inferiorly and medially to attach
to the urogenital diaphragm and the midline structures of the urogenital and anal
triangles. There are right and left leaves of the pelvic diaphragm.
1. Pelvic Diaphragm
2. Ischiorectal Fossa
3. Obturator Internus Muscle
4. Ischial Tuberosity
5. Iliacus (Bone)
6. Acetabulum
7. Alcock's Canal (Pudendal Canal)
8. External Anal Sphincter
9. Rectum
10. Tendinous Arch of Obturator
Internus Fascia
11. Anal Canal
99
The spaces below the pelvic diaphragm and between the diaphragm and the
structures on the lateral walls of the true pelvis are ftlled with fat and are called
the ischiorectal fossae. The pelvic diaphragm is innervated by the pudendal
nerve originating from sacral roots S2,3,4. As mentioned earlier, these same
cord segments provide the origin for the pelvic splanchnic nerves which supply
the parasympathetic innervation to the left half of the colon, pelvis, and
perineum. The pelvic diaphragm works most effectively when it is relaxed and
can work passively and synchronously with the abdominal diaphragm.
Tension of the pelvic diaphragm is diagnosed by gently but fmnly inserting the
extended fingers of one hand into the lateral margin of one ischiorectal fossa,
along the lateral side of the rectal triangle of the perineum. The same
examination is carried out on the other side and the tensions of the muscle on
the two sides are compared. An indication of the pelvic diaphragm tension
could also be obtained during the performance of the usual rectal or vaginal
examination. OMT to this region is described on page 2 16.
VISCEROSENSORY AND VISCEROMOTOR PATTERNS
The general principles listed in the previous chapter (Osteopathic Considerations

in Upper GI Disorders) are also pertinent for the lower bowel.
SOMATIC
It is well documented that severe insult, such as a vertebral fracture, to

thoracolumbar segmental levels will cause a somatovisceral reflex resulting in
4
paralytic ileus. Travell and Simons report several other visceral symptoms
resulting from abdominal myofascial trigger points including diarrhea,
vomiting, belching, food intolerance, and colic in the infant or excessive
burping in an adult.
The somatic component of the viscerosomatic reflex that takes place because of
the handling of the bowel during some surgeries is capable of initiating a
secondary somatovisceral reflex which results in and maintains a paralytic post
operative ileus. (See study of effects of osteopathic manipulation in prevention
and treatment of post-op ileus pages 103.) Treatment of the somatic component
alleviates the symptoms of the resulting visceral dysfunction.
100
m. OSTEOPATHIC MANIPULATIVE TREATMENT OF COWN
DYSFUNCTION
SUGGESTED PROTOCOL FOR PROVIDING OSTEOPATHIC

MANIPULATIVE TREATMENT TO POST-OPERATIVE
PATIENTS:
ADMINISTRATION IN GENERAL:
This protocol is especially useful in treatment of patients who have had

abdominopelvic surgery. Optimum treatment frequency is three times a day
until bowel sounds are heard regularly. Osteopathic manipulative technique and
dosage must be modified depending upon the surgical site, placement of
drainage tubes and location of incision and dressings.
STAGE I:
In the immediate post-operative period there are unequilibrated

hemodynamics and electrolyte imbalance. Bowel sounds are very
poor or absent on auscultation. There is shallow breathing from
neuromuscular splinting. Palpation reveals significant reflex
hypertonicity of paraspinal muscles from surgical interruption of
associated dermatome and myotome segments while
viscerosomatic reflexes from the surgical and manual irritation of
the viscera also contribute to the paraspinal hypertonicity.
TREATMENT:
A. Gentle inhibition of hypertonic paravertebral muscles to

·point of tissue relaxation (2-5 minutes total time)
B. Gentle inhibition of hypertonic paravertebral muscles in
thoracic region. This is most effectively directed toward
spinal segments which are associated with the surgical site
via supplying sympathetic innervation to the involved
viscera.
C. Indirect method fascial release manipulation of the
diaphragm, thoracic inlet and mid-cervical spine
STAGE II:
In this stage, there is less reflex neuromuscular splinting.

Hemodynamics and electrolytes are near normal. Bowel sounds
are present. The patient may be taking oral fluids. The
breathing pattern has improved.
101
TREATMENT:
A.Apply inhibition to paravertebral muscles, especially at the

paravertebral segments related to the sympathetic
innervation of viscera involved in the area of surgery.
Treat the segments until there is tissue change under the
treating fingers
B. Rib raising each side (1-3 minutes)
C. Indirect method fascial release to thoracic and sternal region
myofascial tissues
D. Indirect method fascial release to tissues near surgical site
E. Inhibition of cervical paravertebral areas as indicated by
palpatory evaluation of the patient
STAGE III.
In this stage the patient is ambulating fairly well. Oral intake is

improving. There is minimal reflex neuromuscular splinting.
TREATMENT:
A. Inhibition of paravertebral muscles at paravertebral segments

associated with surgery (1-3 minutes)
B. Specific mobilization of segmental vertebral units or regions
as indicated
C. Pectoral traction with modified classic lymphatic pump or
pedal pump as possible and determined by evaluation of
the patient (2 minutes as tolerated)
FOR OPTIMAL TREATMENT:
Add bilateral condylar decompression and CV4 treatment. This

is a significant benefit to patients at all post-operative stages.
Providing the CV4 treatment in these patients is limited only by
the physician's ability to use it properly.
Abdominal mesenteric lift techniques help to decongest the colon and may be
used when no abscess, abdominal aneurysm or acute infection is present in the
area of treatment. Lymph flow is encouraged by appropriate lymphatic pumps
(intermittent chest pressure, pectoralis lift or by utilizing a rocking motion of
the abdominal contents through production of intermittent cephalad pressure
through the lower extremities). See page 227 for ventral abdominal techniques
and page 218 for lymphatic pumps. Visceral manipulations for each lower GI
structure and pelvic organ have also been described in detail by Barral5 and may
be employeed to maximize visceral function.
102
ILEUS PREVENTION TREATMENT:
ILEUS RATE 0.3 %
317 CASES 1----- OUT ------II��

SURGERY
1/317
ILEUS RATE 7.S %
92 CASES 1---- NO OUT--__

��
SURGERY
OMT X 2 MINUTES
BOWEL SOUNDS
TREATMENT
AVERAGE OF 5.7 HOURS
AVERAGE OF 3 DAYS
GAS PASSED
AVERAGE OF 8 HOURS
Herrmann. The 0 0 ,Oct. 65, pp 163-4
The above ileus prevention study6 demonstrates the general importance and
efficacy of osteopathic manipulative treatment in interrupting inappropriate
viscerosomatic-somatovisceral cycles.
103
SUPPORTIVE MANIPULATION FOR PATIENTS WITH SPECIFIC
FUNCTIONAL PROBLEMS AND COMPLAINTS:
PATIENTS WITH SYMPATHETIC DOMINANT COMPLAINTS:

constipation, abdominal pain, flatulence, and distention.
In these patients the physician should palpate the iliotibial bands looking for
diagnostic anterior Chapman points which might be related to colon irritation.
The lumbothoracic and the lumbosacral areas are then relaxed with kneading
and stretching soft tissue treatment. This addresses the important sympathetic
levels while simultaneously relaxing the posterior attachments of the abdominal
diaphragm. It also accomplishes treatment of the posterior Chapman points.
The posterior Chapman points for the colon are located in a triangular area on
each side of the lumbar spine. This area can be outlined (see page 96) by
drawing an imaginary line from the crest of each ilium to the spine, then
passing up the spine to the superior level of L2, and then connecting that point
with the crest of the ilium again. Chapman found that light circular pressure or
kneading to the triangular posterior Chapman area in the lumbar paraspinal
tissues or light circular pressure and soft tissue to the iliotiqial bands greatly
reduces detrimental sympathetic outflow to the colon.
Hypersympathetic activity to the right colon is effectively reduced by rib raising

in the TlO-12 area and by paraspinal soft tissue techniques administered to the
T12-L2 area of the spine. With the patient in the supine position, the midline of
the abdomen between the xiphoid process and the umbilicus is palpated for
tenderness, especially just above the umbilicus over the inferior mesenteric
ganglion. If it is palpable and tender, carefully controlled inhibitory pressure is
applied until a palpable relaxation of the tissues occurs in that area. It is
clinically observed that manipulative treatments directed toward reducing
sympathetic outflow reduce the pain experienced by patients with colon
dysfunction. Manipulative treatment in the form of paraspinal inhibition to the
thoracolumbar area also initiates bowel activity in patients with ileus and rapidly
diminishes abdominal bloating.
PATIENTS WITH PARASYMPATHETIC DOMINANT

COMPLAINTS: headache, nausea, vomiting, diarrhea, cramps or pain
from the GI tract.
When associated with right-sided colon dysfunction, examination and

manipulation are usually directed to the OA, AA, and occipitomastoid suture
areas. More tissue dysfunction would be expected in the right suboccipital area
104
because the right vagus nerve innervates the right colon. The right and left
ganglia nodosum of the vagus lie in the fascial tissues just anterior to the OA
and AA joints. These ganglia lie in and just below the jugular foramina of the
skull. These areas should be examined for fascial tension or specific joint
somatic dysfunction; the motion pattern and mobility of the cranium should also
be determined. Condylar decompression and cranial techniques to ensure
symmetry of motion in the occipitotemporal region (if the physician is trained in
cranial manipulation) is effective treatment in a patient expressing symptoms
related to the parasympathetic system. While in the area, the physician may as
well palpate for somatic dysfunction of C3-5, because this area influences the
phrenic nerve and function of the abdominal diaphragm.
When associated with left-sided colon dysfunction or pain, diagnose and

manipulate somatic dysfunction of the sacrum, innominates, and lumbosacral
regions. It is particularly important to check for unilateral sacral shear somatic
dysfunction and the ability of the sacrum to passively rock about its involuntary
superior transverse axis (the respiratory axis) between the innominates.
PATIENTS WITH OTHER RELATED COMPLAINTS: In all diseases

of the colon, fatigue, constipation, diarrhea, pain and cramps may be
related to lymphatic congestion of the colon.
The first step toward increasing lymphatic drainage from the colon is to check
for fascial torsions and joint somatic dysfunction at the thoracic inlet. This
includes examination of ribs 1 and 2, the first four thoracic vertebrae and the
manubrium of the sternum. Any joint or fascial somatic dysfunction related to
these tissues should be treated.
The patient may then be turned to the lateral recumbent position and given soft
tissue treatment to relax the tissues of the lumbosacral junction. L l,2,3, is the
area of the spinal attachment of the diaphragm and must be relaxed before the
diaphragm can be redomed. The abdominal diaphragm also attaches to the
lower 6 ribs and the xiphoid process. The diaphragm may be redomed with
direct or indirect fascial techniques. It must be functioning properly in order to
provide the effective pressure gradients needed to "pump" lymph from the
abdomen to the thorax.
The pelvic diaphragm should be palpated and if treatment is indicated it can be

accomplished by using an ischiorectal fossa technique (see page 216),
Relaxation of the pelvic diaphragm through ischiorectal fossa techniques (or
through transvaginal and anal digital inhibition treatment) helps to relieve
congestion and pain originating in the pelvis and also relieves perineural edema
105
of the pelvic parasympathetic nerves or the somatic pudendal nerve (both having
their origin from nerve roots S2,3,4).
IV. SUMMARY
Osteopathic manipulation is physiologic treatment of a patient that may be

directed toward systemic dysfunction and/or the body's response to a disease
process. It is the condition of the body itself which determines whether, how
efficiently and how completely a person will recover from a surgery, a systemic
disease or an infective process. The development and the use of more powerful
and specific drugs as a means of improving a patient's recovery will have
varying effects depending upon the physician's ability (or inability) to improve
or restore that patient's own physiologic mechanisms and resistance.
Remember, for antibiotics to be effective, host resistance must be active no
matter how good or how specific the medical treatments become. Osteopathic
manipulative treatment enhances the homeostasis mechanisms of the patient who
has the illness or dysfunction.
REFERENCES:
1. Owens C An Endocrine InterPretation of Chapman's Reflexes. Carmel CA,

1963.
2. Miller AI: The lymphatic system and cardiac disease, in Lymph and the
Lymphatic System, CC Thomas, 1968, pp 213-229.
3. Threefoot S: Lymphaticovenous communications, in Mayerson HS (ed)
Lymph and the Lymphatic System. Springfield IL, CC Thomas, 1968,
ch 2, pp 17-52.
Manual, Baltimore, Williams & Wilkins, 1983, p 672.
5. Barral JP, Mercier P Visceral Manipulation. Seattle WA, Eastland Press,
1988.
6. Herrmann E, The D.O., Oct. 1965, pp 163-4.
106
SYMPATHETIC INNERVATION OF THE GI TRACT AND PLAN FOR USE OF
OSTEOPATHIC MANIPULATIVE TREATMENT
Anatomical Nam.. Anatomical No. Group Functlonal lnnervaUon Collateral Sympathetic Ganglon
Greater
Splanchnic Nerve TS-9
Lesser
1 T S -9 -- Stomach, Uver
(10) Pancreas, Duodenum
- Celiac Ganglion
Splanchnic Nerve T10-1 1 1 T10-11 - Small Intestines -- Superior Mesenteric Ganglion

(12) and Right Colon
Least Splanchnic
Nerve T12
T12-L2 - Left Colon and -- Inferior Mesenteric Ganglion

Pelvic Organs
Lumbar Splanch nic
Nerve Ll-2
Somatic Dysfunction
facilitated cord
segment
I
Sympathetics
I
Parasympathetics
I
Rib Raising OA,M
Vagus Nerves
T5-10 Treatment Plan Cranial
Tl0-12 GI Disease or Dysfunction
L1-2 (inhibition) Sacroiliac
Pelvic Splanchnic
Chapman's Reflexes Sacral
Nerves
Collateral Ganglia Pelvic Bone
I Lymphatics
I (innominate)
Thoracic Inlets
Abdominal Diaphragm
Mesenteries
Pelvic Diaphragm
Initiate Flow
107
NOTES:
108
OSTEOPATIIIC CONSIDERATIONS
IN IRRITABLE BOWEL SYNDROME
"The high incidence of co-existing musculoskeletal defects as

contributing factors makes this (irritable bowel) syndrome
particularly interesting to the osteopathic physician. ,,1
I. INTRODUCTION
The gastrointestinal tract is in a constant state of physiologic and biochemical

activity, yet man is usually unaware of its function until it "rebels" causing gas,
pain, or a change in frequency or type of bowel movements. It has been
reported physicians will fail to discover an objective diagnosis or organic cause
for 50% of people presenting with intestinal complaints.
For almost 100 years, osteopathic physicians have clinically used viscerosomatic
reflexes to help them in their diagnosis and treatment of visceral and systemic
disorders and disease. Through the work of Denslow, Hix, Korr, Patterson and
Sato, these reflexes have been scientifically established. In spite of this
evidence, these functional reflexes are seldom considered in present day medical
texts and journals. They are also seldom referred to as an explanation for the
pathogenesis of gastrointestinal disease processes, its symptoms or functional
disorders.
In medical circles, "functional" often means that the symptoms can't be

explained by present structural or biochemical knowledge; some physicians
equate "functional" with psychological. One definition was found which
conceded that there is a physiologic basis for the symptoms experienced by
patients with functional disease.
Irritable bowel syndrome (lBS) is one of these functional diseases and has quite
a common occurrence. It is a complex that is chronic, recurrent, intermittent,
non-contagious and apparently non-pathological. Its importance to physicians is
related to the fact that these patients present with symptoms which could be a
part of any number of serious diseases. Major symptoms include complaints of
abdominal pain usually related to meals and abnormal or irregular bowel habits,
diarrhea and/or constipation. Secon(Iary complaints may be distention of the
abdomen, bloating, flatulence, and a sense of incomplete emptying of the
bowel.
Once these symptoms are established in a person with IBS they rarely disappear;
neither do they progress. If the symptoms of a person with IBS change
radically, the physician must consider that a pathologic organic di sease may be
developing. These patients often have a high degree of stress in their lives.
10 9
They typically are rigid thinkers, orderly, and conscientious. They are usually
preoccupied with planning and details. It has been reported that 70-80% of the
patients with IBS have neurotic personalities but these traits are usually mild.
Some studies have reported that psychiatric illness of the patient often precedes
the diagnosis of irritable bowel syndrome. Actually many general practice
physicians feel this psychiatric factor has been over-emphasized. Depression is
common but it is often hidden by somatic complaints.
IBS should not be a wastebasket diagnosis given to a patient when symptoms do

not fit other GI diseases. The typical patient with IBS is less than forty years of
age but not over fifty, with recurrent abdominal pains and a history of an altered
bowel habit. Since this history also fits so many organic pathologic diseases,
the diagnosis of IBS is dependent upon the exclusion of pathologic problems.
These organic disease possibilities include: Crohn's disease, ulcerative colitis,
cancer of the colon, gastric/duodenal ulcer, cholelithiasis and amebiasis.
Unlike the diseases mentioned above, patients with the functional irritable bowel
syndrome:
o .. Do not lose weight.

o .. Do not have fever.
o .. Do not have rectal ulcerations.
o .. Do not have rectal bleeding.
o .. Do not have anemia.
o .. Are not more likely to develop cancer of the colon than people who do not
have IBS.
Early work-up of the patient relieves the anxiety of both the physician and the
patient. It certainly prevents the physician from later performing piece-meal
and repeated investigations because of an ambiguous understanding of the
patient's symptoms and the chronic and frustrating nature of this "disease".
Minimal basic work-up might include any or all of the following:
o .. CBC and Sed Rate--evidence of anemia or infection,

o .. Three stool specimens for occult blood, ova and parasites (including
Giardia),
o .. Sigmoidoscopy and a warm slide prep for amoeba; biopsy if needed.
o .. A double contrast barium study looking for ulcerations, polyps, tumors or
spasm.
If the patient also complains of dyspepsia, a gallbladder study should be

ordered. If there is a complaint of diarrhea as well, a small bowel study should
be ordered.
110
ll. PHYSIOWGY OF TIlE INTESTINAL TRACT
The intestines have both an extrinsic and an intrinsic control system.

Intrinsically, the smooth muscle membranes of the bowel possess spontaneous
electrophysiologic mechanisms capable of actively generating electrochemical
gradients. These gradients can be stored and then discharged as electrical
currents. The resultant cyclic activity of the smooth muscle of the gut is called
"slow wave activity." Since spike potentials are produced in the same area of
each slow wave and each results in a contraction, it is the slow wave frequency
that determines the type of motor activity found in the intestines. There are two
major slow wave frequencies: 6 and 3 cycle per minute. The normal smooth
muscle membrane of the bowel in a person without bowel dysfunction or
disease, has a balance of 90% of the 6 cpm and 10% of the 3 cpm slow waves.
(See table page 113)
Functionally, these are the contractions normally found in the bowel:
o . . "propulsive contractions"--moves material through the gut.

o .
. "retropulsive contractions "--movescontents back toward the stomach.
The retropulsive contractions are more common in the ascending and
transverse colon in order to slow the forward flow of the feces and to
allow time for storage and additional time for absorption of fluids.
o .. "non-propulsive contractions"--just mix the contents of the bowel and
move the material from one haustra to the next.
0 .. "mass movement" -normally occur once or twice a day. This contraction
-
squeezes off the main fecal mass stored in the cecum and ascending
colon and moves it rapidly (in just a few minutes) over to the sigmoid
colon.
o .. "gastrocolic reflex"--is a mass movement that occurs shortly after a meal.
Unless it is frequent and excessive, it is considered a normal event. It is
usually initiated by the hormone called gastrin.
The nervous control of the intestinal tract may be generally divided into two
divisions, the intrinsic and the extrinsic portions. The function of the plexi,
their nerve pathways and the overall benefit to the function of the entire body
determines whether a given stress for a patient becomes conscious or remains
subconscious; whether the reaction will be long-lasting or fleeting; or whether
the response will set the stage for visceral pathology or not.
TIlE INTRINSIC NERVE CONTROL SYSTEM OF TIlE INTESTINES:
The intrinsic control system consists of the autonomic plexi within the wall of
the intestines at which synapses between visceral afferents, the parasympathetic,
and sympathetic nerve endings take place. At any one place along the intestine,
the area's plexus modifies autonomic activity according to the local needs of
111
that region of intestine. Smooth muscle in a section of the intestine can
therefore respond to its local environment and can digest and move food along
even if the extrinsic nerve supply has been surgically severed. Because this type
of control is entirely unrelated to the external environment, it is termed
vegetative and primitive. It is unrelated to the needs of the rest of the body as a
whole.
TIlE EXTRINSIC NERVE CONTROL SYSTEM OF TIlE INTESTINES:
The Gl tract coordinates its activity with other body systems and the external
environment by way of the extrinsic autonomic nervous system. This extrinsic
control of the intestine with its parasympathetic and sympathetic connections
between the gut, the spinal cord, and the brain provides continuity and
coordination between the internal control system and the rest of the body
systems and the environment.
Because of its extrinsic connections, the Gl tract can respond and its functions
canbe altered whenever the body is stressed psychologically, physically,
chemically or traumatically.
TIlE SYMPATIlETIC INNERVATION OF TIlE INTESTINES:
Sympathetic innervation to the Gl tract has its origin in cord segments T5-L2
and innervates the intestines by way of the collateral sympathetic ganglia in the
abdomen. The collateral ganglia are labeled celiac, superior mesenteric, and
inferior mesenteric.
TIlE PARASYMPATHETIC INNERVATION OF TIlE INTESTINES:
Parasympathetic innervation is supplied by the vagus (cranial nerve X) to the

upper Gl, small intestines and right half of the colon; the pelvic splanchnic
nerves (S2,3,4) supply parasympathetic innervation to the left half of the colon
and the pelvis.
Research models indicate that dysfunction of the musculoskeletal system can

produce visceral dysfunction in related viscera. This occurs via a
somatovisceral reflex. If the musculoskeletal somatic dysfunction was removed
"soon enough," the secondary visceral dysfunction disappeared.
If, however, the somatic dysfunction was left "too long," the visceral
dysfunctions initially improved slightly but then become fully established again,
even though the joint somatic dysfunction did not return. Apparently the reflex
pattern was "burned into the nervous system" (learned). It has therefore been
theorized that a directed program to keep people free from musculoskeletal
112
somatic dysfunction could become a program for prevention of later internal
disease. Further research is warranted in this area.
ffi. CHARACTERISTICS OF A PATIENT WITH IRRITABLE BOWEL

SYNDROME:
The slow wave ratio in the intestine changes: In irritable bowel disease the
patient's intestines have a different ratio of the 2 slow wave types: The 6 cpm
waves are reduced from 90 to 60 % and the 3 cpm waves are increased from 10
to 40%.
NORMAL BOWEL IBS

SLOW WAVES PATIENT PATIENT
6 cpm 90% 60%
3 cpm 10 % 40 %
This new ratio hinders the forward flow of fecal contents and therefore produces
a "functional obstruction." The change in the ratio of slow waves is present
whether or not the patient is having symptoms. It is interesting to note that the
increase in 3 cpm slow waves found in IBS patients is not found in patients with
"pathologic diseases" such as ulcerative colitis or pancreatitis.
Patients with irritable bowel have the following functional characteristics:
Delayed and prolonged reactions to stimuli: In the fasting state, the spike
potentials of a normal patient and the patient with irritable bowel syndrome are
about the same. After a meal the normal patient has a rapid increase in spike
potentials reaching a peak at about 40 minutes and shortly after returning to a
normal resting level. This is considered a normal gastrocolic reflex. In the
patient with irritable bowel syndrome, there is a delay and then a steady rise of
the spike potentials. They only reach about 60% of their peak levels at 40
minutes and do not reach their peak until 90 minutes. The IDS patient's
response is delayed and prolonged to normal changes in the internal
environment. This is not in the best interest of the patient's total health.
Decreased nerve threshold levels encouraging excessive reaction to stimuli

that would otherwise be considered to be nonnal: In a study demonstrating
this phenomenon, a balloon was placed in the rectosigmoid region of normal
patients and also in patients with IDS. Just placement of the balloon into that
region of the intestine caused immediate and delayed contractions in the patient
113
with irritable bowel syndrome. Then, with 60 cc of air in the balloon, 55 % of
the patients with ms complained of pain while only 6% of the "normal
patients" had pain. Even with only 20 cc of air in the balloon, 50% of the
patients with IBS still had pain.
Apparently, excessive contractility of the bowel over a long period of time

reduces the bowel's threshold to distension. As a result, even the usual amounts
of intestinal gas cause the patient to have pain. The gut will remain overactive
long after the stimulus is removed.
Intense emotional reactions: One of the most important factors determining

"intensity of reaction" in patients with IBS, is the emotional level at which they
live their lives. Anxiety should trigger sympathetic over activity and therefore
2
reduced bowel function and activity should be expected. Gillhorn at the
University of Minnesota suggested that "the hypothalamus can tune against
3
itself." By this he meant that once the initial panic has subsided, the
sympathetic effect is overruled by excessive induction of parasympathetic
stimuli. A hypothalamic tuning can be either parasympathetic or sympathetic in
response and may extend to related viscera such as the small intestine or the
urinary tract.
Abnormal contraction patterns of the intestines: IBS patients may have

"narrowing" of the intestines which produces diarrhea. This pattern is often
found in the terminal small bowel and abnormal contractions in the cecum and
ascending colon. They may have "segmentation" which is another abnormal
pattern of contractions associated with the pain and flatulence of spastic
constipation. This latter type of contraction causes "functional obstruction." If
narrowing and segmentation occur together, the result is abdominal pain with
constipation and stool with excessive mucus--but no blood.
Excessive gas: Man normally produces 6-8 liters of gas in the intestine every
day, so gas is not abnormal in the intestinal tract.
The gas may be obtained from our external environment through swallowing
air. This accounts mainly for the presence of nitrogen and oxygen. The gas
produced in the normal bowel itself is the source of its carbon dioxide and
hydrogen gas, but 30% of patients also produce methane gas. This gas is
apparently produced through the action of some intestinal bacteria that still
remain unidentified. If it were possible to develop a practical way to identify
the people who produce methane gas, they could be watched closely; because
85 % of these patients will develop cancer of the colon. People who develop
cancer of the colon also produce methane gas in their colons.
All of the gases mentioned up to this point are odorless. Offensive odors from
intestinal gas indicates the presence of trace gases which contain sulfa or various
114
amine compounds and are more likely to be present when there is some bowel
dysfunction.
Gas in the bowel can be absorbed if the partial pressures between the intestine
and the gas in the capillary is appropriate, if the blood flow around the lumen is
sufficient, and if the peristaltic activity is normal. Intestinal gas can be
absorbed, passed rectally, belched, or, in certain cases, excreted by the lungs.
A medical researcher has observed and reported that patients with excessive
flatulence often have increased low back lordosis. He might be describing the
somatic effects of viscerosomatic reflexes activated through visceral afferent
nerves from the colon and small intestine to the somatic nerves in the
thoracolumbar area. The lordosis of the low back area might also be affecting
the function of the intestine via a somatovisceral reflex.
Pain in the abdomen: Abdominal pain is a common complaint and results

from a complex interplay of emotions, sensory factors and motor activity as
well as neurologic and hormonal influences. 65 % of the patients complain of
pain below the umbilicus, 10% above the umbilicus: 25 % complain of pain
above and below the umbilicus at the same time.
The pain lasts for minutes in 30%, hours in 50% and days in 20%. Though
pain located in the upper right quadrant does not occur very often, it must be
carefully distinguished from pain caused by gallbladder disease or cholelithiasis.
If a gallbladder is removed unnecessarily in a patient with ms, the so-called
"gallbladder pain" will increase because there is an increase, and constant
release, of cholecystokinin (CCK) into the intestine after cholecystectomy. This
enzyme increases bowel spasms.
Abdominal pain is due to various mechanisms:
I Distention pain
Distention pain is not produced by stretching in the bowel wall, but by an

attempt to stretch the mesenteries and serosal covering of the bowel beyond its
normal length. Mesenteric and serosal tissues do not stretch. Distention is
therefore limited by the serosal and mesenteric circumference allowed by the
intestine. Lymphatic edema or venous congestion of the mesenteric tissue of the
gut wall would reduce the amount of gas tolerated before pain from mesenteric
pull would occur.
115
Contraction pain
Contraction pain is produced by contraction of the intestine on a fixed and

incompressible mass of stool.
Compression pain
Compression pain is due to bowel contraction on an empty lumen and is

apparently produced by pressure on sensitive mucosal and submucosal
structures.
Both contraction pain and compression pain can be helped with the use of bulk
and by reducing parasympathetic influence through some physical or medical
means such as an anticholinergic agent.
IV. TREATMENT CONSIDERATIONS
Treatment of irritable bowel syndrome is important and often consists of some

combination of OMT, dietary counselling, and medical prescription. The basic
aim of all treatment is to remove the cause when a cause is present. When a
cause is not evident, the treatment is symptomatic.
PHARMACOWGIC TREATMENT:
o .. Antispasmodics taken before meals reduce the degree of gastrocolic reflex

reaction in some people and also reduce the intralumenal pressure of the
intestine.
o .. Tranquilizers or a tricyclic, like Elavil, may be helpful to control
depression. Tranquilizers probably work best in right-sided abdominal
pains because nervous, anxious patients usually have increased ileal
intestinal flow. Many people think it is the atropine effect of these drugs
that provide the beneficial effects on the GI tract.
o .. Antacids and/or H2 inhibitors may be used to reduce the hydrogen radicals
available for reaction with the bicarbonates found in the secretions of the .
gallbladder, pancreas and bowel. This reduces their reaction with
bicarbonates to form water and carbon dioxide gas, further increasing
intestinal gas and intestinal distention. Recall that antacids can
themselves influence the bowel toward constipation or diarrhea
depending on their formulation.
116
DIETARY TREATMENT:
o . . Non-absorbable bulk: Bulk in the diet in adequate amounts will provide

50% reduction in the bowel symptoms. Patients will complain of less
abdominal pain because of reduced intralumenal pressure and they will
have reduced mucorrhea.
o . . Wheat bran, 2 ThIs per day, divided and taken with meals, may be
successful; or a polycarbophil tablet with meals may provide a gelatinous
stool.
o . . Bulk should be started slowly and increased slowly because sudden
increased bulk in the diet will itself upset the intestinal tract.
o . . Reduce the lactose intake. Lactose is the sugar found in milk. Lactase is a
natural enzyme which permits normal breakdown of lactose. Lactase
levels can be low in people anywhere in the world and is not an
uncommon finding. The patient can be tested by removing milk from
the diet for a 2-week period to see if the symptoms of bowel dysfunction
are reduced. Lactase can also be added to milk and milk products to aid
digestion.
o . . Restrict fat from the diet because fat stimulates bowel spasm and it also
reacts with the bicarbonate radical in the small bowel to produce carbon
dioxide gas.
OSTEOPATIlJC MANIPULATIVE TREATMENT:
Irritable bowel syndrome is considered a "functional condition" without a

known cause, but characterized by certain identifiable "functional and
physiologic reactions. " IBS patients react excessively to internal stimuli and are
influenced heavily by external stimuli through the extrinsic autonomic control
connections.
For these reasons, osteopathic manipulation is effective by improving function

structure relationships. Medicine, dietary modifications and osteopathic
manipulative treatment in the management of this functional disease provide
increased patient comfort and clinical improvement far beyond that expected by
each type of treatment used alone. The physician' s goals should be to normalize
autonomic activity to the intestine, promote good lymphatic flow, and normalize
joint somatic dysfunction--especially in the areas of sympathetic innervation to
the GJ tract. (See page 107) Treatment directed toward the support of the
body's own self-regulatory mechanisms in a patient with a functional disease, is
a practical conclusion based on an understanding of anatomy and physiology.
Successful treatment of the patient with ms often depends upon how much
effort the physician exerts toward understanding the mechanisms of the disease
117
process or the dysfunction. Osteopathic considerations in systemic dysfunction
therefore should begin with a thorough understanding of the pathophysiology of
IDS.
Support provided by specific osteopathic manipulative techniques is designed to:
o .. balance the extrinsic autonomic nervous system, both sympathetic and

parasympathetic.
o .. relieve lymphatic and venous congestion in the intestinal tract.
o .. remove chronic joint somatic dysfunctions which play a role in perpetuating
detrimental facilitated cord segments.
MANIPULATION AFFECTING THE SOMATIC COMPONENT:
It has been reported that somatic dysfunction can be associated with, or

potentiated by, visceral dysfunction; and a vicious cycle of viscerosomatic and
somatovisceral reflexes can be postulated. Palpable somatic paraspinal findings
produced by viscerosomatic reflex pathways can be used as clues to the location
of internal visceral dysfunction. General stress, structural problems, abnormal
posture, and trauma can each produce spinal joint somatic dysfunction. Somatic
dysfunction of joints is also associated with the facilitated segment and
sympathicotonia.
MANIPULATION AFFECTING SYMPATHETICS:
Though sympathetic activity may help in "fight or flight" situations, its

perpetuation is detrimental to the healing process. With the understanding that
hypersympathetic activity is present in all dysfunctions and diseases,
hypersympathetic activity can be treated by osteopathic manipulation at a
number of sites and in the following ways:
Rib raising and segmental osteopathic manipulative treatment:
In IBS, supine paraspinal "rib raising" inhibition (see page 195) and soft tissue
to the thoracolumbar area (T1O-L2) is especially beneficial.
Treatment of the collateral sympathetic ganglia:
Use inhibitory ventral abdominal techniques. In a patient with IDS, the midline
area between the xiphoid process and the umbilicus is tense to palpation and it is
tender to the patient even when palpated lightly. Just a few seconds of steady
118
"humane" pressure over the ganglia reduces the palpable tension and relieves
the patient's subjective discomfort.
I Treatment of Chapman's reflexes:

Chapman's reflexes are believed to be produced by viscerosomatic, visceral
afferent induced reflexes referred from visceral dysfunction to the soma. They
can be very specifically mapped out on the body and charts are available. (Refer
to pages 232 and 233.)
Most physicians use the anterior points to identify the organ which may have
dysfunction. Anterior points for the small intestine refer to the anterior
intercostal spaces 8, 9, and 10 on each side. Chapman's reflexes from the colon
are found in the iliotibial bands, a 2-inch strip on the lateral side of each thigh.
These can be treated with soft tissue kneading, a mechanical percussion
hammer, or other types of vibration to produce an effective somatovisceral
influence on the sympathetic innervation to the colon.
MANIPULATION AFFECTING PARASYMPATHETICS:
The effects of manipulation directed toward normalization of parasympathetic

activity have relatively little experimental verification. Clinical effects,
however, are observed. The pelvic splanchnic nerve provides parasympathetic
innervation to the left half of the colon and pelvic organs while the vagus
provides innervation to the rest of the GI tract.
Treatment of somatic dysfunction of the sacroiliac joints:
The pelvic splanchnics have an S2,3,4 origin while the sacroiliac joint
incorporates sacral segments 1, 2, and 3. Because of this anatomic proximity,
IDS symptomatology is considered to be affected by somatic dysfunctions of the
sacrum--torsion, rotations, shears--or by sacroiliac somatic dysfunction-
anterior, posterior and superior innominate shear. Therefore, somatic
dysfunctions of these areas are specifically manipulated to normalize the
parasympathetic activity to the left colon.
Anterior pressure and rocking over the sacrum of a patient, prone on the table,
has been found to clinically modify parasympathetic tone, even in the absence
of specific sacral somatic dysfunction.
119
Treatment of the OA, AA, C2 and use of condylar decompression:
The right vagus nerve supplies parasympathetic innervation to the right half of
the colon and small intestines and may be affected by somatic dysfunction at the
OA, AA, C2 and the lambdoidal suture of the cranium, especially in the area of
the jugular foramen and the occipitomastoid suture. Osteopathic manipulation
of somatic dysfunction palpable in these areas is effective in normalizing
parasympathetic activity to the proximal GI tract and the right half of the colon.
MANIPULATION AFFECTING THE LYMPHATIC SYSTEM:
With organ and tissue dysfunction there will be lymphatic and venous
congestion. This interferes with blood, nerve, nutrition and oxygenation of
tissues and results in the increase of toxic waste products in and around the
cells. Congestion also hinders the plexi for intrinsic autonomic control and
reduces the intestine's ability to inform the CNS of the exact nature of local
conditions. This information is necessary so that the local responses will be
appropriate to the needs of the entire body and to its external environment.
Techniques often used to affect the lymphaticovenous system include:
Soft tissue treatment to the thoracolumbar junction:
This prepares the fascias and other soft tissues for abdominal diaphragmatic
redoming.
Treatment to the thoracic inlet and redoming of the abdominal diaphragm:
Basic for opening the pathway for lymphatic drainage and for support of the
extrinsic lymphatic pump.
I Ventral abdominal techniques:

These are directed toward the mesenteries to help relieve the congestive effects
of visceroptosis, to free the fascial planes of the mesenteries, to reduce
abdominal pain, to provide better circulation to the intestines, to improve
lymphatic flow, and to insure more appropriate autonomic responses.
12 0
VI. SUMMARY
Osteopathic physicians have the ability to use proven pharmacologic and dietary
treatment wisely and to provide manipulative support to the patient's own body
mechanisms. The body also has inherent mechanisms to combat dysfunction or
disease. They recognize that these mechanisms may not always be working at
their optimal level of efficiency as evidenced by the wide variety and range of
responses observed in a group of patients exposed to a similar stress. It is easy
to comprehend that inherent compensatory mechanisms often require assistance
to permit them to function at their optimal levels and capacities.
The result of osteopathic manipulative treatment is palpable in the tissues.

Functional changes are clinically observable and subjective improvements are
voiced by the patients. Good results are not limited to the office visit or the
immediate post-treatment period, but continue on; apparently it is possible to
tune the intrinsic mechanisms to a new level of performance.
Manipulation, as a part of the management of a patient with irritable bowel

syndrome, allows the physician to better control that patient's responses to life
stress and helps to give the patient physiologic relief from his symptoms.
Osteopathic manipulation benefits the patient by providing relaxation,
normalizing extrinsic and intrinsic autonomic control mechanisms and relieving
congestion.
Osteopathic manipulation is directed toward the patient, for the patient who has
dysfunction or disease. It allows a personal manipulative prescription for the
specific needs of that particular patient.
RECOMMENDED READING FOR OSTEOPATHIC CONSIDERATIONS

IN PATIENTS WITH IRRITABLE BOWEL SYNDROME:
Sleisenger MH, Fordtran JS Gastrointestinal Diseases. Saunders Co, 3rd ed,

1983.
Seroka T, Jacobson E Gastrointestinal Physiology. Williams and Wilkins,
1983.
Battle WM, Kohen S, Snape W: Inhibition of postprandial colonic immobility
after ingestion of an amino acid mixture. Digestive Diseases and
Sciences Sep 1980; 25(9): 647-652.
Ritchie JA, Truelove SE: Comparisons of various treatment for irritable
syndrome. British Medical Journal Nov 15, 1980; 281: 1317-1319.
Sullivan M, Kohen S, Snape W: Colonic myoelectric activity in irritable bowel
syndrome. Effects of Eating and Anticholinergics: 878-883.
Kailbinger H, Weilkrauch TR: Drugs increasing gastrointestinal pharmacology.
Karger, Basel 1982; 25: 61-72.
12 1
Patriquin D: Eponym syndrome blindness: Is there a cure? JAOA Mar 1984;
83(7): 516/95-521-100.
Lazarus B: Overview of irritable bowel syndrome. JAOA 6/11-20/11.
Masterson E: Irritable bowel syndrome: An osteopathic approach. Osteopathic
Annals Jan 1984; 12(1):-12121-18/31.
Denslow JS: Functional colitis: Etiology. AAO Yearbook Vol 1, 1965, pp
192-197.
McBain: Treatment of functional colon. AAO Yearbook Vol 1, 1965, pp 190-
191.
Round Table: Upper gastrointestinal diseases. Clinical Challenges 1984; 1(3):
2-83.
Burnstock G, O'Brien R, Vrbova G: Somatic and Autonomic Nerve-Muscle
Interactions. Amsterdam, Elsevier, 1983, pp 383-351.
REFERENCES:
1. Strong WB : Disorders of the digestive system, in Hoag JM (ed)

2. Almy TP et al: Alternatives In Colon Function. Gastroenterology 1949;
12: 425-436.
3. Gilhorn in Autonomic Imbalance In The Hypothalamus. U of Minnesota
Press, 1957.
12 2
OSTEOPATHIC CONSIDERATIONS
IN GENITOURINARY TRACT DISORDERS
" The more the osteopathic urologist makes use of manipulative
therapy, the sooner (s)he becomes aware that special

manipulative measures can improve and someti'!les effect
recovery from various genitourinary disorders. "
I. INTRODUCTION
Poor posture and compromised body mechanics have long been implicated in a
wide range of functional disorders including those affecting the genitourinary
system. Goldthwait in the text, Essentials of Body Mechanics in Health and
Disease, discusses the role of bad body mechanics, chronic passive congestion,
the failure of the diaphragmatic pump and pressure on sympathetic ganglia as
factors promoting irregularities in organ function. "These disturbances, if
continued long enough, may lead to diseases in later life. Faulty body
mechanics in early life, then, becomes a vital factor in the production of the
vicious cycle of chronic disease and presents the chief point of attack in its
prevention. ,,2
Specifically, Goldthwait suggests that one of the first goals of treatment might
be to restore good body mechanics:
" A loose kidney is found almost always with a faulty posture. The
drooped thorax obliterates the forward thrust of the ribs and relaxes the
diaphragm, thus pushing the liver downward on the kidney to the right.
Because of this pressure, the protecting fat is rapidly lost and ptosis of
the kidney follows. Chronic passive congestion, kinked ureters,
hydronephrosis, orthostatic albuminuria, urinary stasis, stones and
infection are possible outcomes, since function of the kidneys is
dependent on full blood and nerve supply and on free drainage--all of
which ptosis may disturb. The normal position of the kidneys can be
8
restored, and the protecting fat re laced, by relieving the downward
pressure of bad body mechanics. II
Osteopathic considerations therefore include not only a complete history and

examination of genitourinary (GU) structures and/or functions, but also extend
to the posture of the patient and to related somatic dysfunction (neural,
lymphatic, and circulatory elements) involved in homeostasis of these organs.
The importance of the thoracic and pelvic diaphragms and the fascias
surrounding the GU organs is crucial to a treatment protocol stressing
homeostatic support of the patient with GU dysfunction.
123
This section delineates general somatic, autonomic, circulatory, and fascial
considerations as they pertain to the pathophysiology occurring in patients with
genitourinary disorders.
ll. KIDNEYS, URETERS AND BLADDER (KUB)
The kidneys control both volume and composition of body fluids by regulating
the excretion of water and solutes. Urine, formed in the kidneys, contains
metabolic waste products, foreign substances (including pharmacologic by
products) and other water-soluble constituents of the body in quantities
depending upon homeostatic needs and the functional ability of the kidney at
any given time. The kidneys are also involved in blood pressure control and red
blood cell production.
The kidneys are retroperitoneal structures encased in fatty tissue. A tough

areolar fascia surrounds the kidney, splits into two layers which are not
continuous inferiorly, allowing the kidneys to move downward with the
diaphragm during inhalation. This factor is utilized in the routine physical
examination by having the patient take a deep inhalation so the kidney will
move downward and allow itself to be more easily palpated. A "floating
kidney" may be detected in this manner and kidney enlargement may reflect
hydronephrosis, cancer, or polycystic kidney disease. Because of the continuity
of fascias, diaphragmatic descent is the chief factor in venous as well as
lymphatic return from the GU viscera. Diaphragmatic motion can be reduced
by somatic dysfunction of the thoracolumbar junction or lower ribs,
hyperlordosis, somatic dysfunction affecting the phrenic nerve (C3-5) and/or
spasm of the quadratus lumborum or psoas muscles.
The psoas muscle courses obliquely causing lateral displacement of the lower
poles of each kidney. Any limitation of motion in the upper lumbar vertebrae
(as can occur with psoas spasm) will result in fascial restriction of the motion of
the kidneys. The ureters adhere directly to the peritoneum and descend on the
psoas fascia, cross the genitofemoral nerve, and continue into the pelvis to the
bladder. Psoas contracture or spasm may also cause the fascias to adversely
affect ureteral function.
The bladder and urethra carry with them the same innervation as the systems
from which they were embryologically derived. The sphincter, trigone and
ureteral orifices are activated by the sympathetics (whose cell bodies originate
from cord segments T12-L2) and are inhibited by the parasympathetics
(originating from S2-4). The bladder wall is activated by the parasympathetics
and inhibited by the sympathetics.
124
SYMPATIlETICS:
Sympathetic innervation to the kidneys and ureters begins in sympathetic cell

bodies in the spinal cord at the level of TIO-Ll. The preganglionic fibers for
kidney and upper ureter synapse primarily in the superior mesenteric collateral
ganglion; while those for the lower ureter synapse primarily in the inferior
mesenteric ganglion. The sympathetic preganglionic fibers to the bladder arise
from cell bodies in the T12-L2 level of the cord and synapse in the inferior
mesenteric collateral ganglion. Sympathetic stimulation causes vasoconstriction
of afferent arterioles, decreases the glomerular filtration rate (GFR), and results
in decreased urine volume.4 This response is exaggerated with emotional
stress.5 Increased sympathetic tone decreases ureteral peristaltic waves and may
cause ureterospasm. Ureteral stimulation, as might occur with a ureteral stone,
selects the kidney as a target organ for sympathetic discharge triggered by
rostral reflex centers. 6 Functional urinary obstruction can occur with
visceromotor reflex alterations arising from somatic dysfunction.7 8 9 It also
, ,
relaxes the bladder wall, which may result in reflux and incomplete emptying of
the bladder. Guyton suggests a role for chronic sympathicotonia to the kidneys
in the etiology of essential hypertension. His physiology text suggests that
essential hypertension is probably invoked by a ''functional retention" of water
and salt by the kidneys:
". . . experiments show when sympathetic nerves to kidneys are stimulated

continuously for several weeks, renal retention of fluid occurs and causes
chronically elevated arterial pressure as long as the sympathetic stimulation
continues. Therefore, it is possible for nervous stimulation of the kidneys to
cause chronic elevation of arterial pressure. ,,10
CHAPMAN'S POINTS RELATED TO THE

GENITO-URINARY SYSTEM (T10-l2;
Superior Mesenteric Ganglion,
Inferior Mesenteric Ganglion)
Anterior Chapman's
Key to palpating pertin ent points:
viscerosomatic
reflexes11 for the A. Adrenals
bladder are located B. Kidneys
C. Bladder
periumbilically with D. Prostate or Broad
those referable to the Ugament
E. Gonads
kidney located on the F. Uterus
ipsilateral side, one
inch lateral and one
inch superior to the
umbilicus.
125
Posterior Chapman's points are located in the intertransverse space (midway
between spines and transverse process tips of Ll-2 and T12-Ll respectively.
PARASYMPATHETICS:
The parasympathetics which supply the kidney arise from the vagus nerve. The
proximal portion of the ureters are supplied by the vagus and the distal portion
by the pelvic splanchnic nerves (S2-4). The bladder's parasympathetic nerves
come only from the pelvic splanchnic nerves. It is not known how the
parasympathetic nerves affect the kidney but in the ureters they maintain normal
peristaltic waves.
As the bladder fills, visceral afferents in the bladder wall transmit impulses to
Ll-2 to sense "fullness"; at the same time, visceral afferents to S2-4 initiate a
parasympathetic reflex to increase the bladder wall tone and, eventually, a
simultaneous relaxation of the internal urethral sphincter. Then, with the
voluntary relaxation of the external urethral sphincter via impulses from S2-4
�
(the pudendal nerve) and the simultaneous mpathetic relaxation to the external
urinary sphincter, micturation takes place. 1 While the external urethral
sphincter is primarily under voluntary control, sympathetic relaxation must also
simultaneously occur during voiding.
.------,I -- Inhibits Urination

URINARY area near leg region of cortex
Cerebrum and
INNERVATION Thalamus
-- Initiates Urination
by constant contracting
abdominal muscles
Cortical or Corticospinal Lesion

- Infant Urination'"' Reflex
(��ffo/.:i!p�la4��:.)
Inferior Mesenteric
"Can't feel fullness but
Ganglion
ina-eased pressure causes
need to urinate."
Transection Above Sacrum
(�? A9t§Nm:,i9�1��t)
"Can feel fullness but
emptying is a reflex."
Cauda Equina or
Pelvic Splanchnic Lesion
(' ·
;ffl'P.§�qhi# E!lildden)
Pudendal Nerve
126
LYMPHATICS:
Renal lymphatics draining the capsule and parenchyma flow into the preaortic
nodes before travelling up the thoracic duct to the subclavian vein. The
synchronous motion of thoracic and pelvic diaphragms is vital to lymphatic
drainage from the urinary system. The purpose of the lymphatics is to drain the
capsule and parenchyma, acting as a "safety valve system that aids in the
clearance of waste products of the kidney as well as fluid, electrolytes, and
infectious or antibiotic products. " It has been shown that during acute ureteral
obstruction, renal hilar lymph flow increases up to 300%.13 With renal vein or
ureteral obstruction, capsular lymphatics are known to dilate to prevent renal
damage while Babics and Renyl-Vamos ascribe the survival and continued
performance of the hydronephrotic kidney to the fact that "urine passes from the
renal pelvis into the interstitial space of the kidney where it is continuously
absorbed into the lymphatics. "
The countercurrent exchange concept of urine formation visualizes the vasa

recta as important in carrying off salt and water. An osmotic gradient must be
maintained between the interstitium and the plasma for these vessels to function
properly. This gradient is maintained only through adequate lymphatic
drainage. Interference with lymphatic drainage has been shown to cause a rise
in the oncotic pressure of the interstitium and an inability of the kidney to
concentrate urine.
VISCEROSENSORYIVISCEROMOTOR REFLEXES:
The renal visceromotor reflex will cause increased tonus to the thoracolumbar
junction and a positive Lloyd I s punch test. The renal viscerosensory reflex is
usually described as an ache rather than as a pain. It may refer only to the
thoracolumbar area, the flank, or both. The ureteral viscerosensory reflex
(ureterocolic) usually extends from the lumbar region and the iliac fossa over
the front of the abdomen and into the scrotum or labia. The ureteromotor reflex
also causes the abdominal, erector spinae and the cremasteric muscles to become
tense. As a stone passes through the ureters, palpatory changes from
visceromotor reflexes will progress from TlO into the lumbar region.
SOMATIC SYSTEM:
External sphincter tone relies on reasonable innervation from the pudendal nerve
(S2-4). When there is a sudden increase in intra-abdominal pressure, the pelvic
diaphragm with the external sphincters will contract in response to a protective
reflex arc. If the contraction of the sphincter is inadequate, urinary
incontinence may occur when that person coughs, sneezes or lifts a heavy
object. This problem is more frequent in female patients.
127
Inguinal Hernia
When the pelvic diaphragm has
increased tone or is spastic and can
not work synchronously with the
thoracic diaphragm, there will often
be a resultant elevation of intra
abdominal/intrapelvic pressure.
This can aggravate the symptoms in
patients with inguinal or esophageal
hernias. Pelvic floor tension
myalgia can also lead to a variety of Treatment pmtocgl
urinary symptoms ranging from 1. Reduce Hernia

testicular ache to frequency and 2. Remove Stre&&e& on Pelvic Roof
3. Dim in ish Intra-abdominal Pressure
urgency. 14 4. Elective Sur gical Repair
Postural disorders, particularly short leg syndrome, and psoas spasm frequently
cause backache and when accompanied by functionally induced urinary changes
are often misconstrued as urinary tract infection. 15
Postural disorders have

Referred Pain From
The Iliolumbar ligament Is one of further been implicated as a
the earliest aIluctur.. aIlalned In Iliolumbar Ugament
postural decompensation and
cause of pelvic diaphragm
should be palpated In all patients tension myalgia, whose
In which thla la auapected. Pain
may be localized to the aIles of symptoms are frequently
attachment or may refer Into the misdiagnosed as
prostatitis. 16
lateral thigh and/or groin. X rays
may show ligament calcification or
bony exoatoala In cases of chronic
postural atraln. Treatment of acute
aymptomatology may Include Iliolumbar ligament strain is
counteratraln, NSAIDa and oc also a frequent consequence
caaIonally local injection. However,
the underlying postural cause of postural disorders and is
should be identified and treated.
Appropriate orthotic adjuncta-heel
acutely activated by lifting.
11ft In patient with ahort leg ayn Because of the mechanism of
drome or a LevJtor®ln patient onset and of the referred
with hyperIordoaia or spondylolls
theal.-Ia often necessary to
pain pattern into the groin
prevent reoccurances. region, iliolumbar ligament
Pain pattern modified from
strain is often perceived by
George S. Hackett MD, FACS the patient to be caused by
an inguinal hernia.
128
Somatic dysfunction of the pubic symphysis with tension in the urogenital
diaphragm or the puboprostatic or pubovesicular ligaments may cause dysuria,
urgency or frequency of urination. This may be experienced by postpartum
women or patients who have had either cystoscopy or perineal surgery wherein
the somatic dysfunction can be obtained while they are being incorrectly helped
out of the stirrups following the procedure. In children, this somatic
dysfunction has been associated with nocturnal enuresis.
17
Trigger points in the lower abdomen may cause urinary frequency and
urgency, sphincter spasm, and residual urine, or pain in the urinary bladder. In
one reported case, treatment of a trigger point in an old appendectomy scar
relieved the symptoms of frequency and urgency and increased the patient's
18
bladder capacity by 45 %.
m. THE GENITAL/REPRODUCTIVE SYSTEM
The Mullerian and Wolffian ducts are of epiblastic origin so the muscles that
surround these ducts in the pelvis are innervated by the dermal systems
distribution of sympathetic nerves. The Mullerian ducts become the fallopian
tubes and form the uterus and vagina. The Wolffian duct gives origin to the vas
deferens and ejaculatory duct.
SYMPATHETICS AND PARASYMPATHETICS:
The fallopian tubes, uterus, vagina, vas deferens and seminal vesicles (with the
exception of the cervix) are activated by sympathetics having cell body origins
from TIl to Tl2 in the spinal cord. Because of their embryologic origin, the
sympathetic nerves are the only innervation to most of these structures;
however, the cervix, vagina, clitoris and walls of the urethra are supplied with a
few parasympathetic fibers from S2-4. The majority of the synapses between
pre- and post-ganglionic sympathetic fibers occur in the inferior mesenteric
ganglion. A separate nerve supply for the cervix is created by the pelvic
splanchnic nerves (parasympathetic) and activates the cervix while producing
some inhibitory influence on the body of the uterus.
The prostate, as well as the Cowper and Bartholin glands, have secretory
sympathetic fibers originating from TI2-L2. Stimulation of the hypogastric
plexus of nerves, which carries the sympathetic fibers from TI2-L2, produces
true glandular secretion from the prostate gland structure while stimulation of
the pudendal nerve forces the secretions out the urethra by contracting
musculature.
Anterior Chapman's points to the prostate or broad ligament are located in the
myofascial tissues along the posterior margin of the iliotibial band. Tenderness
129
to moderate pressure over this area or tenderness and a palpatory sense of
resistance to palpation over the inferior mesenteric collateral ganglion or the
T12-L2 paraspinal tissues should increase the level of suspicion of dysfunction
arising from one of these structures.
Stimulation of parasympathetic fibers from S2-4 will relax the smooth

musculature of the corpora cavernosa in the penis and results in an erection as
the muscle fills with blood. The penis also has sympathetic fibers from Ll-2
which innervate the smooth musculature involved in orgasm and ejaCUlation.
Impotence may be associated with reduction of parasympathetic tone resulting in
the impairment of erectile capabilities; or it may be associated with reduction of
sympathetic activity (as occurs in diabetics), resulting in dysfunctional
ejaculation disorders. Hypersympathetic tone producing premature ejaculation
could easily come from facilitation of segments at the thoracolumbar level,
especially Ll-2.
The testes and ovaries (gonadal tissues) produce hormonal secretions which have
a marked influence on the growth and energies of the individual. These
secretions are under the control of the sympathetic fibers, originating in the
TIO-ll spinal cord area. They synapse in the superior mesenteric collateral
ganglion. These nerves produce their effect primarily through their action on
the gonadal vascular supply. Anterior Chapman I s points associated with the
gonadal tissues are located on the superior surface of the pubic bones.
Parasympathetic supply is from S2-4 but its effects are unknown except for the
fact that it does not affect secretory activity of the gonads.
LYMPHATICS:
Pelvic organs are dependent

upon the synchronous Peritoneum --. ,
Superior
motion of the active thoracic Pubic Ramus
/
diaphragm with the passive
pelvic diaphragm during Obturator
Ve&&eIa & N.
respiration. The prostate
actually fills an anatomical IR....... ObIOIrUat,____
.........
urogenital defect in the
pelvic diaphragm and is
continuously massaged by
the passive motion imparted
by respiratory activity when l&chiorectaJ Fossa OIAPHRAGM
the pelvic floor is free to

move.
This anatomical and functional symbiosis is considered necessary for the

establishment of effective lymphatic flow.
130
Pelvic congestion also plays a major role in the symptomatology noted in
patients with dysmenorrhea, ovarian cysts, or with premenstrual syndrome.
Increased vaginal leukorrhea has been associated with the venous and lymphatic
stasis of pelvic congestion. 19 In premenstrual syndrome (PMS) congestion and
fluid retention are responsible for generalized edema, backache, headache,
mastalgia, pelvic pain, nervousness, irritability, emotional instability,
depression and weight gain. The syndrome has a postulated hormonal basis, but
hormonal manipulation has been less helpful in the treatment than would be
expected from this theoretical etiology. The adjunctive use of diuretics at the
first indication of PMS and the use of NSAIDs has also been beneficial in some
cases through their effects in modifying congestion, inflammation and
prostaglandin activity.
VISCEROSENSORY AND VISCEROMOTOR:
Viscerosensory reflexes from the gonads are of considerable clinical

importance. They produce pain in the groin which at times seems to radiate
down the thigh. The etiology of pain referred from the iliolumbar ligaments
should be carefully considered in the differential diagnosis of genitourinary tract
disorders. Visceromotor reflexes from the genitourinary tract cause rigidity in
the lowest portion of the abdominal musculature and in the TIO-li paraspinal
musculature.
Motor reflexes from the uterus are not very pronounced, however the sensory
reflex is definite and well recognized; pain is a common sign in both uterine and
tubal disorders. Pain arising from the fallopian tubes may be felt in the flank,
iliac fossa, and down the anterior thigh to the knee. Uterine pain is felt in the
thoracolumbar junction, the abdomen, and occasionally in the sacral region.
20
Segmental referred pain and spinal palpatory changes from the female
reproductive tract has been most frequently described as being located at TIO
for the ovaries, T l l-12 for fallopian tubes, TIO-LI for the uterus, and S2-4 for
the cervix.
The prostate displays viscerosensory reflexes, traveling via its sympathetic and
parasympathetic routes, as pain in both the thoracolumbar and sacral regions.
Pain may also be felt in the glans penis with accompanying urinary frequency
and rectal discomfort because of the common connection of these tissues with
the pelvic nerve.
"The penis is more often the subject of reflex sensation than the cause of it. ,,21
Because it is bound to urogenital and rectal structures by filaments of the pelvic
nerve, it is subject to reflex sensory disturbances originating from dysfunction
of renal, ureteral, bladder, urethral, testicular or prostatic tissues. Infection or
131
inflammation of these structures will facilitate the Ll-2 segments causing almost
continuous sexual desire.
The mechanisms of many

"aphrodisiacs" can be traced to their
ability to irritate or inflame the
bladder to set up this type of
facilitation. The location of the
l
inner thigh "erogenous zones" also
correlates with areas which when
stimulated would enhance neural
input into the cord at these levels.
SOMATIC:
Dysfunction of the psoas muscle has

been implicated in gynecologic dys
function because of its anatomic
proximity to affect various physio
logic mechanisms important to this
system - vascular, neurologic, and
lymphatic. Chronic psoas spasm
has been reported to cause anovula
tion22 and is also reflective of the so
called genitoiliopsoatic syndrome
wherein chronic ovarian
inflammation causes reflex psoas
spasm.23
Postural disorders, myofascial trigger points and pelvic somatic dysfunction also
contribute to pain patterns and symptoms commonly associated with
genitoreproductive tract disorders. Short leg syndrome is not only implicated in
low back and lower abdominal pain but also in pelvic pain.24 Symptoms of
�
dysmenorrhea are fr uently intensified by trigger points in the lower rectus
abdominus muscles. Somatic dysfunction of the sacroiliac joint or muscle
spasm in that area may refer pain suggestive of uterine cervical disorders.26
OTHER:
Psychoemotional factors play a very significant role in genitoreproductive

functions. Reduction of stress has been a valuable therapeutic element in caring
for patients with functional infertility, frigidity and impotence.
132
IV. TREATMENT CONSIDERATIONS
The specific techniques provided are much less important than accomplishing
goals which support patient homeostasis and maximize structure/function
relationships.
PLAN FOR OSTEOPATHIC MANIPULATION OF PATIENT WITH

UROWGICAL DYSFUNCTION:
C3-S (Phrenic Nerve)

Sacroiliacs (Pudendal Nerve, S2,3,4)
Somatic Dysfunction
facil. seg.
Sympathetics I
I
Parasympathetics I
Rib Raising OA, AA Vagus
J
TlO-L2
Chapman's Reflexes
Inferior Mesenteric
Treatment Plan
Urologic Dysfunction
Cranial
S2-4
Sacrum
] Nerves
Pelvic
Splanch.
Ganglion SI Jnts Nerves
Adrenal
Kidney l Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
SYMPATHETIC (pATHO)PHYSIOWGY:
t Tone:
1. t Afferent Arteriole Constriction to Kidney

2. Ureterospasm and , Peristalsis of Ureters
3. Relaxation of Bladder Wall Leading to Reflux
4. t Tone to External Urinary Sphincter
Effects:
, GFR ... 'Urinary Output

Elevates Blood Pressure
Ureterospasm ... 'Urine Flow through the Ureters
Encourages Incomplete Emptying of Bladder
Encourages Ureteral/Prostatic Reflux from Bladder
Complaints of Premature or Retrograde Ejaculation
133
LYMPHATIC (PATHO)PHYSIOWGY:
Impaired Lymphatic Flow Effects:
1. t Oncotic Interstitial Pressure -

Disrupted Countercurrent Exchange -
, Ability to Concentrate Urine Properly
2. t Risk of Kidney Damage Because of Ureteral
Obstruction
PARASYMPATHETIC (PATHO)PHYSIOWGY:
t Tone:
1. t Peristalsis of Ureters
2. t Bladder Wall Tone
3. Relaxes Internal Urinary Sphincter
, Tone:
1. Incomplete Emptying of Bladder

2. Impotence
3. Tightens Internal Urinary Sphincter
URINARY TRACT INFECTIONS (UTn:
Urinary tract infections (UTI) are among the most frequent bacterial infections
encountered and the most common disease process occurring in the GU system.
UTIs are ten times more frequent in women than men. If there is a kidney
infection and/or posterior peritoneal irritation, the Lloyd's punch test will
usually be positive. Chapman's reflexes, collateral ganglion involvement, and
the pattern of segmental somatic dysfunction help establish a correct differential
diagnosis and correlate with the extent of the inflammation. Except for some
simple UTIs, investigation is necessary to detect obstructive uropathies, urinary
calculi, or other predisposing or perpetuating factors; further investigation is
also statistically warranted in male patients with UTI. It should be noted that
chronic bacterial prostatitis is the most common cause of relapsing bladder
infection (cystitis) in males.
Osteopathic considerations include ruling out pubic symphyseal and pelvic floor
somatic dysfunctions which may produce symptoms of dysuria and frequency.
Treatment of pelvic floor somatic dysfunction is helpful in reducing specific
mechanical contributions to symptoms as well as aiding in the relief of the
prostatic congestion that these somatic dysfunctions can produce.
134
Incomplete emptying, reflux and loss of normal ureteral peristalsis are risk
factors for ascending infection and should be addressed by treatment to both the
thoracolumbar junction (T1O-L2) and the sacroiliac joint (SI-3). Treating a
patient to reduce sympathetic hyperactivity is felt to help the body deal with
local and systemic infections by removing a factor hindering tissue defense and
promoting mechanisms which lead to reduced tissue congestion and adequate
tissue antibiotic levels.
Modification of urinary pH is often an effective treatment of urinary tract

infections and can be accomplished with medication or to a lesser degree, with
cranberry juice. Intake of fluids in general is important.
RENAL DISEASE:
All appropriate measures to prevent or limit renal structural changes in

infectious or obstructive uropathies should be taken and this goal is maximized
with early recognition of GU dysfunctional states. With regard to acute
glomerulonephritis, OsteQPathic Medicine notes27 that somatic dysfunction "at
TIl, T12, and LI should be considered as an etiologic component in view of
the proven pathologic changes apparently associated with such (somatic
dysfunction). In this regard manipulative treatment might well be a preventive
aid." A similar statement is made with regard to acute pyelonephritis, "Patients
having (TIl, T12, and LI somatic dysfunction) are much more vulnerable to
acute pyelonephritis and they are much less likely to respond to treatment, if
spinal manipulation is not part of the program of management."28 Even when
significant structural change has occurred, as in chronic glomerulonephritis,
OMT to these areas to limit dysfunctional reflex activity while "not curative ...
will improve renal circulation and is considered decongestive."29
Renal failure with resultant azotemia and uremia is "one example in which
applied osteopathic manipulative therapy has in the past produced dramatic
results. "30 OMT to the TIO-L2 region in an attempt to maximize renal
circulation in patients with renal failure "permit a much faster convalescence. "31
Sterritt reports a case study in which OMT to the thoracolumbar area is credited
with improving urinary output and substantially decreasing a critically elevated
BUN.3Z
The general concept of the osteopathic manipUlative approach is that by

eliminating the somatic dysfunction component with its related effect on neural,
lymphatic and vascular elements the diseased kidney will function maximally
within its existing structural limitations. Beyond this, any failed or incomplete
homeostatic mechanisms are replaced by artificial mechanisms - medication,
correction of electrolyte imbalance and acidosis, and potentially dialysis. To
this end, manipulative treatment to assist the homeostatic responses of patients
with renal disorders is not disease-specific but rather host-specific.
135
PROSTATITIS:
Prostatitis is not one disease. Common prostatitis syndromes include acute

bacterial prostatitis, chronic bacterial prostatitis, nonbacterial prostatitis, and
prostatodynia. 33 Treatment varies depending on the type of syndrome present.
Acute bacterial prostatitis is characterized by fever, chills, myalgia and/or

arthralgias, dribbling and/or slowed urinary stream, perineal and low back pain.
It may be accompanied by gross hematuria. The gland will be tender, warm
and swollen to palpation. Digital massage in an acutely infected gland should
be avoided because of the risk of bacteremia. Because cystitis usually
accompanies bacterial prostatitis, culture of voided bladder urine usually allows
identification of the pathogen. The chemical structure of trimethoprim permits
it to penetrate the prostatic wall achieving high levels in the prostatic secretions.
This makes trimethoprim or the combination of trimethoprim with
sulfamethoxazole the drugs of choice at the present time. OMT addressing the
ischiorectal fossa, T12-L2 and S2-4 regions is the manipulative treatment of
choice in maximizing prostatic levels of antibiotics and in assisting the body's
natural defenses. Inadequate prostatic treatment in these patients can lead to
chronic relapsing urinary tract infections from ascending infection.
Many patients with chronic bacterial prostatitis have no prior history of an acute
prostatitis. Chills and fevers are unusual; dysuria, urgency, frequency and
nocturia are common. There are no characteristic palpable prostatic findings in
this disorder. Because adequate drug concentrations rarely are achieved in the
prostatic secretions of these patients, the pathogen obtains sanctuary there; thus,
the hallmark in diagnosis of chronic prostatitis is recurring urinary tract
infections, always produced by the same pathogen. Infected prostatic calculi
may or may not be associated with chronic bacterial prostatitis. Medical and
manipulative management is the same as in acute bacterial prostatitis but the
prognosis for complete "cure" is much poorer; surgical intervention is probably
indicated for those with prostatic calculi.
Chronic non-bacterial prostatitis is more common than bacterial prostatitis;

however, these patients rarely have histories of UTI and cultures fail to grow a
pathogenic organism. Cells found in the prostatic secretions suggest an
inflammatory component. Because the cause of non-bacterial prostatitis is
"unknown," treatment is empirical, traditionally involving hot sitz baths and
periodic prostatic massage. While these may prove helpful, the osteopathic
approach adds manipUlative treatment to correct any somatic dysfunction found
in both the T12-L2 and S2-4 regions and to improve the function of the pelvic
floor; the latter producing a physiologic "massage" of the prostate, occurring
each time the patient takes a breath.
136
URETHRAL HYPERTONIA MAY LEAD TO OR BE CAUSED BY
CHRONIC NONSPECIFIC PROSTATITIS (Adapted from Barbalia83�
*
1. "PROSTATODYNIA"
3. NON-SPECIFIC (painful Male
LOCAL FACTORS .---- PROSTATITIS Urethral Syndrome)
t t
I
(Intraprostatic Reflex)
I (Clinical Form)
INCREASED SYMPATHETIC -� URETHRAL

STIMULATION HYPERTONIA
t (Subclinical Form)
I
.&.
DISTANT FACTORS 2. CHRONIC

(Stress, Psychogenic PROSTATITIS
Causes Etc.) (No symptoms)
• Since prostatodynia literally means painful prostate, a better term to use might be ·painful
male urethral syndrome.· In this syndrome, the increased urethral tone causes a painful urethra
and not pain in the prostate (which in the over-whelming majority of these cases is nontender on
palpation. )
Prostatodynia presents with variable pelvic pain, intermittent urgency,

frequency, nocturia and dysuria as well as hesitancy and weakening of the
urinary stream. Bacterial pathogens and inflammatory cells are not seen in the
�
urine or prostatic e ressate. Heightened sympathetic tone34 and pelvic
diaphragm tension3 are reported to play a role in this symptom profile. The
sympathetic dyssynergia causes spasm during voiding and seems to play a
�
particularly s nificant role in patients with certain types of neurogenic
obstruction. 3
Recommended treatment would address the pelvic floo�7 and sympathetic

mechanisms38 involved as well as any postural, psychic, emotional or cultural
stressors39 which aggravate these mechanisms.
URETEROLITHIASIS (CALCULI):
Approximately 1 11 000 adults annually will acutely suffer through the passage of
at least one calculus through the ureter, bladder, and urethra. While many
137
calculi are "silent ", they typically produce excruciating pain in the
thoracolumbar region radiating into common pain patterns in the back, lower
abdomen, flank, and/or thigh.
Back pain or renal colic may

URETERAL IRRITATION
occur with calculi in the @>
calyces, renal pelvis, or SYMPTOMS I SIGNS
upper ureter; while stones in Rank Pain
the bladder may cause Paraspinal Spasm
suprapubic pain. Somatic Dysfunction
Chapman's Points (Ureter)
Nausea, vomiting, CAUSES:

abdominal distension, or the 1. Ureterospasm
development of ileus are 2. Calculus
secondary gastrointestinal 3. Psoas Spasm
symptoms which may com
plicate or mask the correct
diagnosis. Fever, chills,
TREATMENT PROTOCOL
Inhibit Paraspinals T1 O-L2

urinary frequency and Treat Chapman Points
hematuria are common signs Treat Psoas Spasm
and symptoms. Occasionally (Check Lt. L2 for NN)
the ipsilateral kidney will

Treat Somatic Dysfunction
of Thoracolumbar Junction
reflexly and transiently other
become nonfunctional.
In cases with unilateral ureteral stones, the ipsilateral kidney becomes

hypersensitive to emotional stress. Patients with unilateral renal disease
demonstrate ipsilateral diminished renal blood flow and reduced GFR for 30-50
minutes. 40
Predictable and predictive palpatory findings can be noted as the stone passes
through the GU system. Because the pain is made worse and the passage of a
calculus is slowed by ureterospasm, treatment considerations should include
reduction of hypersympathicotonia through the use of thoracolumbar paraspinal
inhibition and/or gentle rib raising techniques.
In the choice of pain medication, morphine should be avoided since this narcotic
is more likely than demerol to produce an increase in smooth muscle spasm.
Demerol does not cause significant ureteral smooth muscle contraction and is
therefore a better pharmacologic choice for analgesia in this situation. The
patient may appreciate paraspinal inhibition manipulation at the spinal level of
reflex spasm until the demerol injection takes effect.
1 38
In cases of excruciating pain, most other OMT would be delayed until at least
partial pain management has been achieved. When less pain is being
experienced, the patient may benefit from counterstrain treatment of palpable
�
anterior myofascial tender points including common seen genitourinary
Chapman's reflex points and Jones' iliopsoas points. 1 Physiologic ureteral
peristalsis should be assisted in all patients by diagnosing and treating the
sacroiliacs as indicated. Also, the importance of adequate lymphatic drainage as
a "safety valve" preventing complications and tissue damage has already been
pointed out in the section on pathophysiology.
If the stone cannot be successfully passed, sonic disruption, cystoscopic basket

extraction, or surgical removal may be necessary to reestablish normal function
and prevent renal damage.
It is important to try to determine the pathogenesis of the stone so that proper

prophylaxis can be planned to prevent recurrence. Fluids, dietary counselling,
and modification of urinary pH along with a manipUlative program designed to
maintain or augment homeostatic GU mechanisms, can then be intelligently
prescribed.
DYSMENORRHEA:
Primary dysmenorrhea should be differentiated from the many causes of

secondary dysmenorrhea. The etiology of primary dysmenorrhea is unknown,
but it occurs only with ovulatory cycles. This complaint of painful menstruation
is quite common among young women. Both primary and secondary
dysmenorrhea are aggravated by stress. An autonomic postural role has been
implicated and the incidence of dysmenorrhea in college women is significant �
greater in those with increased lumbar curvatures than in control populations.
An acutely anteverted cervix, in which the fundus is tipped anteriorly relative to
the uterus, is one structural factor which is occasionally associated with
dysmenorrhea. The cramp-like pain of dysmenorrhea is usually located in the
lower abdomen but may include the back and thighs.
Treatment of any associated myofascial trigger points in the lower rectus

43
abdominus will reduce symptoms of dysmenorrhea. Dysmenorrhea may be
associated with urinary frequency, pelvic soreness, abdominal distension,
nausea, diarrhea, headache, depression, or irritability. Again, stress aggravates
both primary and secondary dysmenorrhea as well as segmental facilitation and
myofascial trigger points.
"Dysmenorrhea is one of the disorders in which osteopathic manipulative

44
treatment (see chart on page 141) offers a great potential benefit." The
symptoms of primary dysmenorrhea are felt to arise from an imbalance in both
139
the sympathetic and the parasympathetic systems as well as from somatic
dysfunction causing a significant amount of venous and lymphatic congestion.
Treatment to normalize both the sympathetics arising from T12-L2 (controlling
uterine contraction and vasoconstriction) and the parasympathetics arising from
S2-4 (controlling uterine inhibition and vasodilation) is a major goal; yet, this
does not necessarily mean inhibiting one system and stimulating the other.
Techniques to increase venous and lymphatic drainage of the pelvic organs often
provides significant relief and is the other major goal of treatment.
One very effective manipulative technique used in accomplishing the goals

outlined above involves a firm, continuous pressure over the sacral base with
the patient in the prone position. This technique has an effect on the
parasympathetics but is even more effective in fluid mobilization. The
technique takes the sacral base anteriorly or into the "extension phase" of the
craniosacral mechanism and is therefore equivalent to performing a CV4 cranial
technique which is primarily used to help relieve tissue congestion in the body.
Another technique that is effective in the acute phase is accomplished by gently
rocking the prone patient' s sacrum with its natural rhythm of 10- 14 times a
minute. This is postulated to improve the patient's parasympathetic outflow to
the involved organs. Aspirin or NSAIDs may also be beneficial because they
antagonize the spasmogenic action of prostaglandins and provide mild analgesia.
The monthly appearance of some cases of dysmenorrhea would benefit from

monthly OMT to reduce the severity of symptoms. This is particularly true
when they significantly impact the patient's abilities to participate in work,
school, or home activities-of-daily-living. Functional dysmenorrhea may
respond to an osteopathic manipulative approach which treats the functional
cause. Osteopathic diagnosis and manipulative treatment may be clinically
successful in relieving dysmenorrhea, particularly in the following situations:
o . . Using OMT and progressive heel lift treatment for correction of a short leg
syndrome having a thoracolumbar cross-over and sacroiliac strain.
o . . Manipulation of craniosacral somatic dysfunction in a patient whose history
reveals that the dysmenorrhea began after starting orthodontic treatment.
o . . Manipulation to remove a sacral shear in a teenage patient who reports that
the dysmenorrhea began after a "pratfall" . (Questioning the patient
about specific activities such as roller skating, ice skating, and
gymnastics can be very helpful in triggering the memory of significant
trauma of this sort.)
The knee-chest position is used as an "exercise" which is frequently helpful in

patients with dysmenorrhea. Requiring only 5-10 minutes to perform, this
procedure is not a muscle strengthening exercise, but rather a body position to
encourage optimal venous and lymphatic drainage from the pelvis and permit
the uterus to lift out of the pelvis.
140
A PLAN FOR OSTEOPATHIC MANIPULATION OF A PATIENT WITH DYSMENORRHEA
Somatic Dysfunction
facil. seg.
Sympathetics I Parasympathetics I
I
Rib Raising
TlO-ll (Ovary) Treatment Plan For
S2-4
Sacrum
} Pelvic
Splanchnic
T12-L2 (Uterus) Patient with Dysmenorrhea SI Jnts Nerves
Superior and Inferior
Mesenteric
Ganglia
I Lymphatics
I
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
Knee Chest Position
SYMPATHETIC (PATHO)PHYSIOLOGY (TIO-ll) and (T12-L2)
t Tone:
1. t Vasoconstriction � Poor Nutrition and 02 Exchange

2. t uterine contractions
3. � Threshold for Pain (from uterine body)
LYMPHATIC (PATHO)PHYSIOLOGY
Impaired Lymphatic Flow:
1. � Lymph Flow
2. t Tissue Congestion � Bloating and Discomfort
PARASYMPATHETIC (PATHO)PHYSIOLOGY (S2,3,4)
t Tone:
1. t Relaxation of uterine Muscle

2. t Vasodilation
3. � Threshold for Pain (from the cervix)
141
KNEE-CHEST
POSITION
Dorland WA, TheAmerican IllustratedMedicalDictionary

Twenty-second edition, WB Saunders, 1 951
With the ,patient resting her head and neck and chest down on her arms and with
her pelvis raised to a position just above her knees (the knee-chest position) , the
abdominal contents will move with the pull of gravity out of the pelvis and
allow decongestion of the uterus . The patient may need to open the labia
momentarily to permit air into the vagina before the uterus moves. The patient
should do this exercise before retiring at night to obtain a maximal decongestive
effect.
SEXUAL DYSFUNCTION:
Proper sexual functioning involves a complex interaction of somatic ,

parasympathetic , and sympathetic reflexes and the body unit tenet of the
osteopathic profession incorporating mental, emotional, and spiritual factors
which must be considered in this bodily function. Physiologic mechanisms
approximately parallel one another in men and women. Sexual dysfunction can
easily occur with imbalance in the autonomic nervous system , with negative
cortical influence , as well as with damage to neural , vascular or hormonal
mechanisms . OMT has been postulated to play a significant role in correcting
functional components of sexual dysfunction in several states including the
following :
o . . ERECTILE DYSFUNCTION (IMPOTENCE): At least half of the adult

male population has experienced the inability to complete sexual
intercourse in 25 % or more of opportunities because of erectile
dysfunction. Psychic factors are usually the cause ; however , other
functional disorders may play a significant role in this problem .
Erection is dependent upon somatic input through the pudendal nerve
(S2-4) and parasympathetic reflexes (S2-4) and therefore manipulative
treatment to remove any sacroiliac somatic dysfunction may be helpful
when organic reasons have been ruled out.
142
In the female, the physiologic equivalent would be dysfunction of
arousal and lubrication. These conditions may also play a role in
development of frigidity and/or dyspareunia.
Genital Innervation
Sexual Function
[ErecliQn)- Pudendal N. .
52.3.4 (Somatic)
co . . . . .. . .
Pelvic Splanchnic N.
52.3.4 (Parasympathetic)
(9
. . tQWMt
. .... .. ) - Lumbar Splanchnic N.
Emotion L1 .2 (Sympathetic)
Vision (E' cura" """""""
.·"J'ft"""" oonJ- ,,:s Lumbar Splanchnic N.
Fear via Hypogastric N. (symp.)
Thought to Vas. and Seminal
V_aI Vesides
Somatic
8
_
4
� ___ _ Vas Deferens
'__
_ ___ Seminal Vesides
'_____ Prostate
�____ External Sphincter
Corpus Cavernosum
Corpora spongiosum
.,.;::'--
__ � Bulbocavernosum
Dorsal Nerve of Penis
Pudendal Nerve
f,0
\.J
�------�
Key
P • Prostatic Plexu.
(Somatic) 1M • Inferior Me.enterlc
Ganglion
0 • • PREMATURE FJACULATION: Ejaculation is primarily a

sympathetically-mediated event activated through L l -2 and aided by
somatic influence from S2-4. Osteopathic manipulation to somatic
dysfunctions in the Ll-2 area of the spine and efforts to reduce visceral
afferent information to L l -2 (Le. treatment for left colon or pelvic
disorders) may help a patient who is having this type of ejaculation
dysfunction. OMT to these areas reduces facilitation to the Ll-2
sympathetic centers in the spinal cord. Educating the patient to interrupt
sensory input from the penis and/or L l -2 dermatomes prior to orgasm
and ejaculation is also helpful.
0 • . DYSPAREUNIA: This condition may arise from spasm of the vagina,

inadequate lubrication, pelvic floor spasm, or lesions and abnormalities
of the female genital tract. The success of osteopathic treatment in
patients with this problem is related to the correction of somatic
143
dysfunction which affects the attachments of the pelvic diaphragm and
normalize parasympathetic reflex activity permitting formation of
adequate vaginal lubrication. In the atrophic vagina, estrogen creams
may be helpful.
0 •• INFERTILITY: Approximately 10% of married couples in the United

States have infertility. Because fertility requires function and
coordination of the physiologic mechanisms of two individuals, there is a
great potential for a dysfunctional cause of infertility. Female structural
tubal disorders are only accountable for 30% of the cases. Male gonadal
deficiency accounts for 40% , female hormonal deficiency 20 % , and
"hostile" cervical environment 10 % .
Because of cost, mental duress, and time involved in the investigation of

infertility, the osteopathic general practice approach incorporates a
therapeutic trial of OMT, education, reassurance and correction of any
structural, infectious, or emotional stresses which might interfere with
correct functioning. Structurally, emphasis is placed on normalizing
thoracolumbar and pelvic somatic dysfunction and reducing postural
disorders which might be involved in perpetuating segmental facilitation.
Craniosacral evaluation and treatment to assure that there is no
functional pituitary-ovarian axis problem are also considered beneficial.
Couples in which irregular menstrual cycles were a complicating factor

often report they had increased opportunity for better and less stressful
timing of the critical period of ovulation and conception after OMT
promoted regularized periods. Preliminary studies have suggested an
elevation in previously low spermatic counts following systemic OMT. 45
Certainly there is a general reduction in stress which, when coupled with
the removal of somatic and visceral components of "the neurologic lens"
(segmental facilitation) , offers improved physiologic function. This
approach has often rewarded the couple with clinical success, a long
awaited pregnancy. 46
An infertility workup becomes necessary only when there is failure of a

clinical therapeutic trial of osteopathic management over a reasonable
length of time. This program must be individually designed to treat
infections and rule out other organic disease, maximize the patients' own
reproductive function and create a favorable environment for
implantation and fetal growth.
ADDmONAL GENITOURINARY BmLIOGRAPHY:
Goldthwait, Brown, Swain, Kulans Essentials of Body Mechanics in Health and

Disease. 5th ed, 1952.
144
Winter CC Practical Urology. Mosby Co, 1969.
Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co, 7th ed,
1 953.
Szwed II et al: The effect of IV mannitol on renal hemodynamics and renal
lymph recovery during acute ureteral obstruction , in Foldi (ed) Progress
in Lymphology. 1967, pp 123-26.
REFERENCE:
1 . Sterrett HW , Ir: Disorders of the urinary system, in Hoag 1M (ed)
Osteru>athic Medicine. New York, McGraw-Hill, 1 969, ch 40, P 657.
2. Goldthwait, Brown, Swain, Kuhns Essentials of Body Mechanics in Health
and Disease. 5th ed, 1952.
3. Ibid
4. Hix EL: Viscerovisceral and somatovisceral reflex communications, in Korr
1M (ed) , The Physiological Basis of Osteopathic Medicine, New York,
Insight Publ Company Inc, 1975 , pp 87-8.
5. Ibid
6. Op cit P 89.
7. Daiber WF : Disorders of the kidneys, in Hoag JM (ed) Osteopathic
Medicine. New York, McGraw-Hill, 1 969, ch 39, P 640.
8 . Awad S A , Downie JW : Sympathetic dyssynergia i n the region o f the
external sphincter: A possible source of lower urinary tract obstruction.
Journal of Urology 1977; 1 1 8:636-640.
9 . Barbalias GA, Meares EM, Sant GR: Prostatodynia: Clinical and
urodynamic characteristics. Iournal of Urology 1 983; 130: 5 14-5 17.
10. Guyton Textbook of Physiology.
1 1 . Owens C An Endocrine Interpretation of Chapman ' s Reflexes. Carmel CA,
1 963.
12. Awad SA, Downie JW: Sympathetic dyssynergia in the region of the
Journal of Urology 1977; 1 1 8:636-640.
13. Saunders JB: The major determinants in normal and pathological gait.
Journal of Bone and Joint Surgery luI 1 953; 35-A(3): 543-558 .
1 4 . Segura JW, Opitz IL, and Greene LF: Prostatosis, prostatitis or pelvic
floor tension myalgia? Journal of Urology 1 979: 122: 168-1 69.
15. Sterrett HW , Ir: Disorders of the urinary system, in Hoag JM (ed)
Osteopathic Medicine. New York, McGraw-Hill, 1969, ch 40, P 664.
16. Sinaki M, Merritt IL, Sillwell GK: Tension myalgia of the pelvic floor.
Mayo Clin Proc 1977; 52:717-722.
i
17. Travell JG, Simons DG Myofascial Pain and D sfunction: A Trigger Point
Manual, Baltimore, Williams & Wilkins, 19 3 , P 67 1 .
1 8 . Ibid
19. Burrows EA: Disorders of the female reproductive system, in Hoag 1M
Osteru>athic Medicine. New York, McGraw-Hill, 1969, ch 42, P 68 1 .
20. Op cit P 677.
145
2 1 . Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co,
1953, 7th ed, P 401 .
22. Dobrik I : Disorders of the iliopsoas muscle and its role i n gynecologic
diseases. J Manual Med 1989; 4(4) : 130- 133.
23 . Ibid
24. Ibid
Manual. Baltimore, Williams & Wilkins, 1983 , p 665 .
26. Burrows EA: Disorders of the female reproductive system, in Hoag 1M
27. Daiber WF: Disorders of the kidneys, in Hoag JM (ed) OsteQPathic
28. Op cit P 639.
29. Ibid
30. Sterrett HW, Jr: Disorders of the urinary system, in Hoag JM (ed)
3 1 . Op cit P 661 .
32. Op cit pp 663-664.
33. Drach GW, Fair WR, Meares EM and Stamey TA: Classification of
benign diseases associated with prostatic pain: Prostatitis or
prostatodynia? Journal of Urology 1978; 120:266.
34. Barbalias GA, Meares EM, and Sant GR: Prostatodynia: Clinical and
urodynamic characteristics. Journal of Urology 1983 ; 1 30:5 14-5 17.
35. Sinaki M, Merritt JL, Sillwell GK: Tension myalgia of the pelvic floor.
Mayo Clin Proc 1977; 52:717-722.
36. Awad SA, Downie JW: Sympathetic dyssynergia in the region of the
Journal of Urology, 1977; 1 1 8:636-640.
37. Segura JW, Opitz JL, Greene LF: Prostatosis, prostatitis of pelvic floor
tension myalgia? Journal of Urology 1979; 122: 168-1 69.
38. Awad SA, Downie JW: Sympathetic dyssenergia in the region of the
Journal of Urology 1977; 1 1 8: 636-640.
39. Nilsson IK, Colleen S, Mardh PA: Relationship between psychological and
laboratory findings in patients with symptoms of non-acute prostatitis, in
Danielsson D, Juhlin L, and Mardh PA (eds) Genital Infections and
Their Complications . Stockholm, Almquist and Wiksell Inti, 1975, pp
133- 144.
40. Hix EL: Viscerovisceral and somatovisceral reflex communication, in
Korr 1M (ed), The Physiologic Basis of Osteopathic Manipulation. New
York, Insight Publishing Co, Inc, 1975, p. 9 1 .
4 1 . Jones L Strain and Counterstrain. AAO, Colorado Springs, 198 1 .
42. Jenness M: The role of thermography and postural measurement in
structural diagnosis, in Goldstein M, The Research Status of Spinal
Manipulative Therapy. Bethesda MD, US Department of Health
Education and Welfare (NINCDS Monograph #15) 1975, P 258.
Manual. Baltimore, Williams & Wilkins, 1983, p 665 .
146
44. Burrows EA: Disorders of the female reproductive system, in Hoag JM
(ed) Osteo.pathic Medicine. New York, McGraw-Hill, 1969, ch 42, p
682.
45. Sterrett HW, Jr: Disorders of the male genitourinary system, in Hoag JM
(ed) Osteo.pathic Medicine. New York, McGraw-Hill, 1969, ch 4 1 , p
673 .
and G Slattery, DO, PhD -- unpublished case history, KCOM.
46. Ibid (Sterrett)
and Burrows EA: Disorders of the female reproductive system, in Hoag
1M (ed) Osteopathic Medicine. New York, McGraw-Hill , 1 969, ch 42,
p 678.
147
NOTES:
148
OSTEOPATIIIC CONSIDERATIONS IN THE OBSTETRICAL PATIENT
"It is physiologically imperative that we provide for optimal growth and

development of the fetus while preserving the maternal homeostasis." Although
expressed by Dr. Roy Pitkin, an obstetrician from The Iowa University School
of Medicine who is noted for his knowledge of nutrition in the OB patient, this
also sums up the osteopathic perspective applied in obstetrics. Total care for the
obstetrical patient is a physician's desire regardless of his medical degree;
however, a physician's ability to provide total care to the patient is, in fact, a
variable.
I. EXISTING STRESSES AGGRAVATED BY PREGNANCY
GRAVITY:
o .. Gravity mainly affects the A-P postural curves aggravating lumbar and
cervical lordoses and thoracic kyphosis..
o .. Gravity, activity, habits and stresses of motion produce fascial torsions.
o .. The normal aging process amplifies the effects of gravity and/or fascial
torsions.
A BASIC PHYSIOWGICAL RELATIONSHIP: More blood gets to the

tissues than can be returned by the venous system.
Blood gets to the cells via the

arteries and into the interstitial
( ·CONGESTION· )
Malaise
spaces through the capillaries. The � Confusion
interstitial tissue fluids get back to Headache
Irritability
the heart via the venous system with
Backache Dizziness
necessary and vital assistance from
,
Ax;::smic NauseaIVomiting
the lymphatic system (which has no

intrinsic pump).
Pelvis:
Hemorrhoids
Abdomen:
o .. More blood gets to the tissues Vulvar
Constipation
Varicosities
than can be removed by the 1 Maternal Uver Congestion
Panaeatic
venous system; therefore the , Nutrition
Intrauterine Congestion
lymphatic system is essential Growth Retardation Vasomotor
if tissue congestion is to be Small for Instability

Gestation Age
prevented--in fact, it is Legs: Legs:
essential for life itself. Varicosities Cramps. Edema
Anything which increases circulation to the cells will result in increased

interstitial tissue fluids and result in increased demands upon the
149
lymphatic system to move these fluids in order to prevent tissue
congestion or edema.
o .. The abdominal diaphragm functions as an "extrinsic" pump for the

lymphatic system. When working well, it produces effective pressure
gradients between the chest and the abdominal cavities. The pressure
gradients, along with the valves in the larger lymphatic vessels, produce
a most effective force for the one-way flow of lymph back to the venous
system and the heart. Sympathetic impulses are capable of constricting
larger lymphatic vessels; therefore, hypersympathetic tone is a factor
which decreases lymph flow and promotes tissue congestion.
THE UNIQUE VALVELESS VENOUS SYSTEM: The eNS, spinal cord

and the bony vertebral column contain a "valveless venous system. "
Physiological factors working upon the valveless venous system of the spine
have the ability to produce patterns of flow which result in venous congestion in
the tissues they are supposed to drain, decrease organ function and generally
increase a person I s level of stress.
o .. Because there are no valves in these venous plexuses, blood is free to move
in either direction depending upon the path of least resistance.
o .. About 80 % of the blood from the brain and its meninges exits the jugular
foramina of the skull by way of the jugular veins. Blood from the spinal
cord, its membranes, and the bony vertebral column (the spine) usually
passes through communicating veins, to enter the veins of the azygos and
hemiazygos system. The communicating veins are also valveless and not
consistently present at each lumbar and thoracic level. The venous blood
from these areas usually drains into the heart via the superior vena cava.
A secondary pathway for drainage of the profuse venous plexuses of the

spinal cord and vertebral system is provided through anastomoses of
these plexuses with the vertebral and the internal jugular veins at the
base of the skull.
o .. Venous blood in this closed system is "pushed" by the arterial blood volume
propelled by the contractions of the heart and pulled by pressure
gradients largely arising from respiratory efforts. The amount and
proportion of venous blood which travels through the valveless
communicating veins or through the anastomoses with the vertebral and
internal jugular veins is affected by any change in the resting pressure in
the thorax or abdomen; flow through this secondary route is also
increased by any decrease in the gradient of pressure between the
abdominal and thoracic cavities. These physical factors can produce
150
flow dynamics which lead to relative congestion in the eNS, the spinal
membranes and/or the bony vertebral spine.
ll. STRESSES ADDED SPECIFICALLY BY PREGNANCY
Stresses of a normal pregnancy produce a relatively rapid aging process which is

usually reversible. These stresses are produced through mechanical,
physiological, venous/lymphatic and hormonal changes.
MECHANICAL: The musculoskeletal system and the body's center of

gravity is changed.
Organ hypertrophy and mechanical stress produce structural change and a shift
in the body's center of gravity. The changes brought about by mechanical stress
are accelerated by the effect of circulating hormones of pregnancy which tend to
weaken muscle and supporting ligaments.
It has been shown that dysfunction in the musculoskeletal system can increase
the energy requirements of an individual up to 300%.
PHYSIOWGICAL: Interstitial fluids are increased.
Additional production of interstitial fluids is brought about by the increased

circulation necessary to meet the additional metabolic demands of the growing
fetus and placenta and to support the hypertrophy of the uterus and other
organs. Increased levels of estrogen and adrenal hormones also promote fluid
retention in the body's tissues.
LYMPHATIC: There is decreased efficiency in the removal of excessive

interstitial fluids.
Fascial torsions hinder the flow of lymph through lymphatic vessels travelling
through the connective tissues; organ hypertrophy and downward drag of the
abdominal wall produce volume changes in the abdomen and thorax; structural
stresses (increased lumbar lordotic curves, thoracic kyphotic curves, tension on
the diaphragm, and anterior sacral base) and the downward drag of the
abdominal and thoracic wall may act singly or in concert to promote poor
diaphragmatic excursion. All of these factors decrease the diaphragm's ability
to produce the most effective pressure gradients necessary to promote good
lymphatic flow and to reduce tissue congestion. It is clinically observed that
generalized symptoms of lymphatic and venous congestion present as clinical
·problems, especially in the last trimester of a patient's prenatal care.
15 1
VENOUS: There is a tendency for venous congestion of the central nervous
system (CNS).
There is a drastic change in the volume of organs which occupy the abdomen as
well as changes in the relative volume and pressure gradients between the
abdominal and thoracic cavities. These changes tend to increase the cavity
pressures and encourage a relative reversal of venous blood flow in the valveless
communicating, vertebral and spinal membrane vessels and lead to relative
congestion of the central nervous system (eNS). Symptoms of venous
congestion are more evident in the early part of the first trimester, the last
trimester, and in the postpartum period.
HORMONAL: Increases in hormone production encourage tissue

congestion.
Increased levels of certain hormones during pregnancy promote biological

weakening of muscles and ligaments and encourage fluid retention. These
changes then permit a focusing of mechanical stress onto certain
biomechanically sensitive areas of the body, reducing effectiveness of the
diaphragm's lymphatic pump action, and directly increasing interstitial fluids
while at the same time promoting changes which result in obstruction of
lymphatic pathways back to the heart.
RELATIVE CONTRAINDICATIONS TO OMT:
While OMT can be helpful in pre-eclampsia, the seizure threshold is low in

toxemia of pregnancy and OMT is seldom a part of a treatment protocol. OMT
is also usually avoided during premature rupture of membranes, premature
labor, abruptio placentae, and ectopic pregnancies.
m. DISTINCTIVE OSTEOPATHIC THINKING:
Distinctive osteopathic thinking to improve the compensation and comfort of the

OB patient is based upon three premises:
o . . There are mechanical, physiological and biological stresses inherent even in

the patient who is destined to have a normal pregnancy.
o .. The body has self-regulatory mechanisms which will provide optimal
compensation for the stresses of pregnancy if they are free to work
efficiently.
o . . Distinctive osteopathic care is based upon the belief and the clinical
observations that within the body unit, structure and function are
reciprocally interrelated and interwoven with optimum homeostasis.
152
AN AID IN PREVENTIVE CARE: Postural analysis and palpatory
examination early in pregnancy can identify areas of somatic dysfunction which,
if uncorrected, act to focus the stresses of pregnancy on vulnerable sites within
the body unit.
A DIAGNOSTIC AID: Both visceral and structural dysfunction are indicated

by palpable changes in the somatic structures.
A TREATMENT ADVANTAGE: Proper osteopathic manipulative treatment to

the areas of structural dysfunction is associated with improvement of visceral
and somatic function.
IV. DISTINCTIVE OSTEOPATHIC TREATMENT:
Any licensed physician who accepts the care of obstetrical patients should have
been trained to take care of her medical and delivery needs. In addition to this,
an osteopathic physician is trained to appreciate and treat the musculoskeletal
and physiological stresses which occur in pregnancy. Manipulative treatment
normalizes somatic dysfunction which produces andlor focuses mechanical
stress. It also improves the efficiency of mechanical and physiologic
components of the patient's compensatory and homeostatic processes. The
energy that is subsequently saved through improved body efficiency and
removal of somatic dysfunction will be available for fetal growth and for the
betterment of maternal physical and mental health.
"THE STRUCTURAL STAGE:" Frrst visit to 28th week of gestation -

Monthly visits:
0-12 WEEKS:
The patient usually makes her first visit during the 9th-12th week of pregnancy
and although she has experienced some of the early signs and symptoms of
pregnancy, her structure is little affected at this stage. During these first three
months, the patient normally gains about 2.5 to 4.5 pounds.
At the patient's first visit the physician obtains a complete history including the
history of past pregnancies, deliveries, family history of significant diseases,
and asks about habits--smoking, coffee, alcohol or the use of drugs. If drugs
have been used it is important to know if the patient has stopped them--and if
so, how long ago. The physician should find out about the patient's eating
habits.
At the first visit the physician establishes rapport with the patient and the patient
establishes a lasting impression of her physician. This is important, but is not
153
unique to osteopathic care. The remainder of this chapter will try to highlight
the osteopathic differences in management.
The osteopathic physician is very interested in any history of past accidents to

the head or the rest of the musculoskeletal system. This includes car accidents,
blows to the head, falls down the stairs, or falls on the buttocks. This may be
just routine information in most medical histories but, to the osteopathic
physician, a positive response to any of these questions must be investigated.
These stresses may have resulted in persistent somatic dysfunction which could
affect the patient's ability to effectively compensate for the stress of pregnancy.
The patient is asked if she has any present musculoskeletal complaints. During
the routine physical, palpatory evidence of these and other somatic dysfunctions
and structural abnormalities such as a short leg, a sacral shear, or scoliosis is
sought.
o .. In the standing position quickly observe and record the levelness of the
various regional horizontal planes--occipital, shoulder, iliac crests, PSIS,
and trochanteric. The spine is observed and palpated for rotoscoliosis as
the patient bends forward at the waist.
o .. In the sitting position the preference for fascial motion at the thoracic inlet
can be quickly assessed to see whether it is symmetrical or whether it
conforms (or not) to the common compensatory pattern as described by
the late Dr. Gordon Zink. A problem with the fascial inlet patterns must
be differentiated from the somewhat similar findings of an elevated 1st
rib somatic dysfunction. The ribs and the thoracic and lumbar spine can
also be evaluated for segmental somatic dysfunction in the sitting
position.
At this time the physician may manipulate any somatic dysfunction that
has been identified. (The sitting or standing pillow technique--utilizing a
pillow to localize the thrust--is very helpful in treating the pregnant
patient, even during the third trimester.
o .. With the patient in the supine position, the rest of the regional fascial
patterning (OA, thoracolumbar and lumbosacral) can be evaluated and
the pelvis can be palpated for somatic dysfunction (SD) of the
innominates or pubic bones. The physician usually proceeds to treat the
SD found in these areas, using any osteopathic manipulative technique
tolerated by the patient. Most techniques which would be performed in
a patient who is not pregnant can be used in the pregnant patient at this
stage of her pregnancy.
o .. In the prone position (an easy position to assume during this early part of
pregnancy) the sacrum can be evaluated and treated as indicated. A
sacral shear (a non-physiological somatic dysfunction) must be removed
or the patient will be assured of having backaches during pregnancy and
154
manipulative treatments for other somatic dysfunction will not have a
lasting effect.
o .. Finally, have the patient assume the supine position again and check the
cervical spine and the craniosacral mechanism by palpation and motion
testing. Any somatic dysfunction in these regions should be treated at
this time.
From the history, physical examination, and her subjective and tissue response
to treatment, the physician can determine the osteopathic manipulative care
necessary, the probable dosage indicated, and what the manipulative treatments
should be able to accomplish before delivery.
12-28 WEEKS:
During the second half of the structural stage, the physician still sees the patient
at monthly intervals, although if indicated, more frequent appointments are
provided. A little extra time now will save a lot of time and worry later on in
the pregnancy. At each visit, part of the care is directed toward manipulation of
SD (which may be a part of her complaints) and/or part toward manipulative
support of body structures and processes which the osteopathic physician knows
will be under stress. This treatment is easily carried out as the patient talks to
the physician and the physician talks to her. "The time to talk to each other" is
extremely important to the patient/doctor relationship and to mutual trust.
It is known that during the structural stage (the second trimester), there will be
obvious changes in her body structure--increased fat storage, growth of the
uterus, hypertrophy of the breast and other tissues, blood volume expansion,
and a shift in the patient's center of gravity. The pelvis will rock forward,
lumbar lordosis will increase, and a compensatory thoracic kyphosis will
develop along with a cervical/suboccipital strain. Near the end of this first
stage (second trimester), clinical evidence of tissue congestion may begin to
appear.
Muscles and ligaments become more vulnerable to the mechanical stresses as

biological effects of increased levels of hormones weaken their strength. These
structural effects of stress are often subjective and are usually very obvious to
the osteopathic physician.
"TIlE CONGESTIVE STAGE:" Visits Every 3 Weeks:
28-36TH WEEK:
This part of the pregnancy is called the "congestive phase." Congestion occurs
when more fluid accumulates in the tissues than can be effectively removed by
the venous and lymphatic systems. This congestion is partly mechanical, partly
155
hormonal, and partly biological. Circulating hormones, in increased amounts,
have the tendency to encourage the body to hold water in the tissues. The
patient's symptoms vary depending upon which tissues become congested.
Tissue congestion is also associated with decreased oxygenation and nutrition of
the cells and is related to increased accumulation of metabolites in the soft
tissues.
During this stage of pregnancy, the expanding uterus is well above the
umbilicus and is pushing toward the xiphoid process. It causes a mechanical,
" ball-valve," effect between the veins of the legs and their abdominal
connection with the inferior vena cava, and is mechanically responsible for
some of the leg edema of late pregnancy. It also makes it difficult for some,
women to lie supine without becoming hypotensive. The uterus also pushes up
under the diaphragm and the lower ribs. This limits the chest volume that can
be obtained during respiration and directly affects the thoracic:abdominal
pressure gradients which can be obtained.
The diaphragm must also work harder against the increased mass of abdominal
and pelvic contents and this results in its increased tone. The diaphragm at this
stage of the pregnancy is unable to produce optimal volume displacements
between the thorax and the abdomen during contraction and relaxation and is
associated with inefficiency in pumping the lymph back to the heart. A greater
volume displacement is achieved through correction of thoracoabdominal and
pelvic floor dysfunction.
Although the physician must continue to be alert for mechanical decompensation

and treat to maintain good structure during this second stage as indicated, it is
most important to check the common compensatory pattern (CCP) in order to
maintain freedom of the fascial pathways and thus improve lymphatic drainage.
(See page 207) Osteopathic manipulative treatment is directed toward
maintaining symmetry of the thoracic inlet, relaxing the thoracolumbar junction
(attachment of the abdominal diaphragm), and keeping the diaphragm well
domed. After OMT, the abdomen feels softer and more mobile and
diaphragmatic excursion is fuller. This type of treatment improves the
efficiency of the thoracoabdominal pump and therefore improves lymphatic
flow. Lymphatic flow can be " encouraged" by the use of the pectoralis lift
technique (see page 230). The usual manipulative " chest pumps" may be
uncomfortable because of hypertrophy and increased sensitivity of the breasts.
"TIlE PREPARATORY STAGE:" 36 WEEKS TO DELIVERY - Weekly

visits:
This is the final stage of pre-delivery care. If the patient ever expresses a
feeling of " really being pregnant," this is the time. During this third stage of
prenatal care, it is necessary to continue to maintain good structural balance and
156
to support lymphatic flow, but it is imparative to emphasize two additional areas
of care for the obstetrical patient:
o .. Begin to build the psychological support that the patient will need for
delivery. Emphasize the positive points in her prenatal experience and
help her to plan for the delivery.
o .. Carefully check the craniosacral mechanism to be sure it has a normal
configuration, rate, and amplitude so that it will aid normal hormonal
and neural function during labor and delivery.
If the osteopathic physician has been able to accomplish the goals

presented to this point, the labor and delivery will usually go smoothly.
If complications should occur, the patient is in better condition to
compensate and reach a new homeostatic level.
"LABOR AND DELIVERY:"
OMT is infrequently used during the delivery itself; however, sacral pressure is
frequently comforting during labor and can be taught to the husband to be
performed periodically or at his wife's request. The physician may elect to use
CV4 technique in postdate gravida women to induce uterine contraction1 or to
overcome uterine inertia during labor.
" THE RECOVERY AND MAINTENANCE STAGE:" Delivery to 6 weeks

postpartum 2 visits:
-
o .. On the second day postpartum, the patient should be taken to the treatment
room where a screening structural examination and indicated
manipulative treatment is performed. The physician can use soft tissue,
muscle energy, indirect, Jones counterstrain, cranial methods and even
thrust manipUlation, as needed.
The effects of circulating maternal hormones are still evident in the

articular and ligamentous structures making treatment methods easier.
Successful manipulation places the j oints in good functional position as
the hormonal effect wears off and the ligaments begin to return to their
normal tension and strength.
During this stage of treatment the physician is still interested in treating

the patient to improve lymphatic flow. Breast engorgement which
occurs on the second day in the multipara and on the third day in the
primipara is probably hormonal in etiology, but clinical experience
indicates that patients with good lymphatic flow tend to have decreased
complaints of breast congestion and a reduced incidence of the
" postpartum blues."
157
Careful check of the sacrum during this early postpartum treatment
session is essential. The mechanical progression of the infant through
the birth canal and the lithotomy position of the patient during delivery
encourages anterior sacral base somatic dysfunction and the extension
phase of the craniosacral mechanism. It has been observed that
significant anterior sacral base somatic dysfunction is associated with
patient complaints of fatigue, depression, and low energy. The
mechanical etiology of these symptoms can be avoided if the physician
finds and treats this somatic dysfunction early and effectively.
o .. The usual final HOB" visit is at 6 weeks postpartum. The patient's progress
up to this point is evaluated and a gyn/pap smear is repeated. If the
obstetrical patient is treated as outlined, it is not common to find any
specific somatic dysfunction to treat and the patient presents herself as
being well and happy. This is the time to make sure she has a
contraceptive program if desired, realizes the importance of self-breast
exam and yearly gyn/pap smears, understands the importance of (and has
an appointment for) a follow-up visit regarding any chronic problems
that require further care. Osteopathic manipulative care is a part of the
total care of the obstetrical patient. Its inclusion makes the prenatal time
and delivery more comfortable for the patient, enforces a quicker and
more complete recovery from delivery, and enhances this wonderful
miraculous event of life.
REFERENCES:
1. Gitlin RS, Wolf DL: Uterine contractions following osteopathic cranial manipUlation -- A
pilot study. JAOA 92(9): 1183, Sept 1992.
2. Zink JG, Lawson WG: Pressure gradients in the osteopathic manipulative management of
the obstetrical patient. Osteopathic Annals May 1979; 7(5): 208-214.
3. Zink JG, Lawson WG: An osteopathic structural examination and functional interpretation
of the soma. Osteopathic Annals Dec 1979; 7(12): 433-440.
4. Kuchera WA: Osteopathic considerations in the obstetrical patient. FAAO Thesis 1989.
5. Saunders JB et al: The major determinants in normal and pathological gait. Journal of
Bone and Joint Surgery Jul 1953; 35-A(3): 543-558.
6. Pitkin RM: Assessment of nutritional status of mother, fetus, and newborn. The American
Journal of Clinical Nutrition Apr 1981; 34: 658-668.
7. Heckman JD: Managing musculoskeletal problems in pregnant patients, part I. The Journal
Of Musculoskeletal Medicine June 1984: 14-24.
8. Dilts PV, Jr, Gerbie, Sciarra: Exercise and physical activity during pregnancy, in Shrock P
(ed) Gynecology And Obstetrics. Philadelphia, Harper And Row, vol 2, rev ed, 1985,
ch 8.
158
OSTEOPATHIC CONSIDERATIONS
IN RHEUMATOWGIC DISORDERS
I. INTRODUCTION
Osteopathic manipulative treatment (OMT) is an extremely valuable component

in the care of a patient with a rheumatologic condition. While the adjective,
"rheumatologic", denotes a joint musculoskeletal disorder, many rheumatologic
disorders such as rheumatoid arthritis (RA) are chronic systemic disease s. By
indirectly reducing the side effects of medications, directly enhancing
homeostatic mechanisms, and maximizing function within the patient's existing
structure, osteopathic palpatory diagnosis and manipulative treatment play
special roles in the management of chronic illnesses. This section will focus
primarily on the rationale for OMT in a patient with rheumatoid arthritis, but
the rationale can be extended to other rheumatologic conditions.
n. PATHOPHYSIOWGY
Articular cartilage is avascular,

therefore its nutrition needs to be
considered in any discussion of the TYPICAL JOINT
pathogenesis of rheumatologic L
disease. Synovial fluid provides the
joint access to nutrients as well as
A
t
serving as a site for the disposal of
metabolic wastes and immune
complexes. In addition, the efficacy
of any prescribed anti-inflammatory
medications is dependent on their
concentration in the synovial fluids.
The transference of nutrients and
medications into the synovial fluid
and of immune complexes and other
wastes out is dependent on
diffusion. For this reason, factors
A Arterial Supply
affecting diffusion such as blood
-
V .. Venous Drainage
flow, concentration of nutrients and L - Lymphatic Drainage
waste products in the region, and

synovial membrane permeability are
extremely relevant.
159
On the basis of histologic studies, cartilage is best preserved in those parts of
the joint where the articular surface is subjected to intermittent compressive
contact. This type of contact improves local nutrition of the cartilage and
mobilizes immune complexes from the area. Accumulation of immune
complexes is associated with increased joint destruction.
SYMPAmETICS:
In joints with rheumatoid arthritis, oxygen consumption is increased up to

twenty times the amount used by a normal synovial membrane. Increased
sympathetic activity further compromises blood flow to the involved joint(s) and
reduces the delivery of nutrients (including oxygen) and medication to the area
where it is needed the most. Tissue hypoxia may result in the release of
polymorphonuclear leukocytes which promote multilamination of the basement
membrane. This thickening further diminishes diffusion into and out of the
synovial fluid of the joint.
AUTONOMIC NERVOUS SYSTEM: ROLE IN RHEUMATOLOGY
To Hypothalamus
Substantia
Gelatinosa z...L...I-:d'
11A..�1I-+-J-j"nelrent Pain
(& Shunting)
T2-T8 Upper Extremities
Tl1-L2 Lower Extremities
Reduced Blood Row Reduced Drainage
1. Nutrition 1. Fluids
2. t 02 Anoxia 2 .• Proteins
3. t Ax Levels 3.• Immune Complexes
Because structure and function are interrelated and because rheumatoid arthritis
alters joint structure, it should not be surprising that arthritis leads to the
development of somatic dysfunction. Continuous afferent input to the cord
from a dysfunctional joint incites facilitation in those cord segments. The flare
up of a patient's arthritic joint with resultant segmental spinal cord facilitation is
160
often accompanied by dysfunction of the viscera that share sympathetic
innervation from those cord segments. This relationship can also be reversed,
i. e. certain visceral diseases are associated with arthritic complications. The
relationship of arthritis in the spine and lower extremity in patients with colitis
is a common example of this relationship. The somatic innervation and somatic
afferent referral to the spinal cord from the lower extremities are located from
TII-L2 while the sympathetic innervation to the colon is also found from TIO
L2. Likewise, increased afferent input from upper extremity joints to the T2-T8
sections of the spinal cord may reflexly increase the sympathetic activity to the
upper gastrointestinal tract (f5-9) leading to reduced tolerance of the non
steroidal anti-inflammatory drugs (NSAIDs) used in the treatment of arthritis.
The sympathetic nervous system is capable of augmenting the symptomatology

and pathogenesis of rheumatoid arthritis. Increased sympathetic activity
sensitizes the patient's perception of pain both peripherally and centrally and
plays a role in the muscle spasm and contracture that limits range of motion and
intensifies deformity. Noxious somatic input reflexly sets up pathophysiologic
change which bring about symptoms and signs which, carried to extreme, may
result in a diagnosis of reflex sympathetic dystrophy (RSD). The sympathetic
hyperactivity in this condition is also involved in initiating the bony erosion seen
in joints of patients with rheumatoid arthritis. It has been reported that there is
hypersympathetic activity in patients with RA, RSD and osteoporosis and that
bilateral sympathectomy often helps limit bony erosion significantly in these
patients.
Kelley's Textbook of Rheumatology states that even in the most aggressive

cases of RA, only minimal reversible change occurs until after the lesion
becomes chronic. "Chronicity" seems to take eight or more weeks. This
information suggests a timeframe during which treatment directed toward the
sympathetic nervous system may result in prevention by addressing reversible
functional changes before they become structural.
SOMATIC SYSTEM:
Somatic dysfunction plays a role in the pathogenesis of arthritic change. Poor

posture, increased weight, and/or misalignment of the spine or lower extremities
each increase the mechanical stress placed upon a patient's joints. Short leg
syndrome is especially stressful to lower extremity joints and it has been
associated with increased incidence of hip osteoarthritis on the long leg side. It
has also been implicated in temporomandibular joint dysfunction with
subsequent arthritic change. Lack of joint motion as will occur with somatic
dysfunction, encourages degeneration and fibrosis. It has been shown that
passive range of motion can aid in cartilage regeneration. Like somatic
dysfunction, arthritic change is usually manifested first in the minor motions of
a joint.
161
Arthritic patients and many of the patients that have been improperly labeled as
having "arthritis" have a great deal of myofascial somatic dysfunction. Travell
and Simons report that clinically there is a high incidence of myofascial
triggerpoints and tenderpoints in patients with joint problems. They have
demonstrated that pain and tenderness in the joints of these "arthritic" patients
often improve or disappear if the adjacent triggerpoints are treated. Treatment
of myofascial somatic dysfunction, including triggerpoint treatment, frequently
restores significant range-of-motion (ROM) to these joints. According to
Travell this even seems to benefit joints that have appeared to have been
ankylosed for years. Signs and symptoms including inflammation, effusion,
soft tissue swelling and synovial crepitus frequently disappear.
There is a strong association between the somatic and the psychoemotional

levels of patients who have myofascial triggerpoints. Surveys suggest that as
many as 10% of these patients seek psychiatric care or think that they should.
Many psychic effects commonly seen in rheumatologic patients (including
depression and self-centeredness) have been reported to subside with treatment
of myofascial somatic dysfunction.
LYMPHATICS:
The effects of the sympathetic

nervous system upon local
circulation and the diffusion,
+-_ Thoracic nutrition and removal of waste
---,..,.
--r('" (Fascial Diaphragm) products (including immune
complexes) from a rheumatic joint
have already been presented. (See
page 160.) The lymphatics,
however, are vital to the circulatory
--7-- Abdominal
Diaphragm link and are particularly important
in moving the immune complexes
1l--· Lymlpha1tic Vessel
out of the area before they can cause
damage to the joint. Manipulative
Reduced Drainage treatment to enhance lymphatic
1.+ Auids homeostasis moves waste products
2. + Protein out of the joint area thereby
3. t Immune Complexes reducing diffusion gradients. This
treatment begins with opening
drainage pathways and is an integral
part of rational osteopathic care.
Tendon sheaths are rich in lymphatic vessels and therefore lymphatic treatment
should be utilized in tenosynovitis. Failure to reduce or relieve lymphatic
162
congestion and the protein contained in the edematous fluid promotes fibrosis
and thickening of the tissues. This, in tum, reduces ROM, encourages the
formation of contractures around joints and subsequently further compromises
lymphatic drainage.
It is known that immune reactions involving local synovial cells produce by
products which are associated with joint destruction proportional to their
concentrations in the synovial fluid. In some severe cases,
lymphoplasmaphoresis has been effectively used to promote diffusion gradients
which are able to pull immune complexes out of the synovium. Expensive and
dangerous surgical thoracic duct drainage has been found to be beneficial in
some patients with systemic lupus erythematosus (SLE), myasthenia gravis,
glomerulitis and rheumatoid arthritis.
PARASYMPATHETICS:
The parasympathetics play essentially no direct role in the musculoskeletal

symptomatology of the arthritic patient; but because the body is a unit and
rheumatologic disorders have chronic, systemic effects, consideration for
improving the function of the parasympathetic nervous system in rheumatic
patients is important because of its support of the visceral functions of the body.
OTHER FACTORS:
Patients with chronic arthritis become toxic, either from disease, their chronic
use of medications, and/or from impaired excretion/metabolism. The physician
managing patients with rheumatologic conditions must remain alert for side
effects of medications or organ dysfunctions resulting from this toxicity. Total
management of any chronic disease involves eliminating all foci of infection and
visceral disease, supporting the patient's organs of detoxification and
elimination, and supporting the known mechanisms of body homeostasis.
ID. TREATMENT OF PATIENTS WITH RHEUMATOWGIC

DISORDERS
In order to address the rheumatologic patient's physical and psychologic needs,

a rational treatment protocol must demonstrate the physician's understanding of
the pathophysiology outlined above. General treatment goals include the
following:
o .. educate the patient regarding their disease process and the patient's
own responsibilities in carrying out programs designed to
maintain maximal function
o .. provide psychologic support
o .. alleviate pain and the pain-spasm-pain cycle
163
o .. decrease inflammation
o .. improve joint nutrition
o .. enhance removal of synovial waste products
o .. maintain and/or increase joint function
o .. decrease mechanical strain on affected joints
o .. correct existing deformity and prevent further deformity
OSTEOPATHIC MANIPULATIVE TECHNIQUES:
Recognizing the multisystem involvement of many of the rheumatologic

disorders, assessment and treatment design in each of the involved systems are
warranted. Soft tissue techniques address periarticular tissues and osteopathic
manipulative treatments (OMT) reduce hypersympathetic activity and improve
blood flow to the region. OMT directed toward removal of segmental
facilitation also helps alleviate pain and pain perception. Tender and inflamed
joints often respond best to indirect stacking or fascial unwinding manipulations,
especially when prior structural changes may have roughened and modified joint
surfaces. High velocity, low amplitude techniques (HVLA) are contraindicated
in the cervical region of patients with severe rheumatoid arthritis because the
high incidence of weakened cruciate ligaments is associated with potential
pathologic subluxations.
In patients with inflammatory rheumatic disease, OMT may cause a transitory

increase in joint pain; if this pain lasts more than 1-2 hours then either the
choice of activation for the manipulative technique was incorrect or the dosage
may have been excessive for that patient. A more general aching in the soft
tissues may occur even with the most gentle activating forces (indirect). If this
general ache lasts more than 24 hours it usually indicates that the physician
attempted to produce more changes than the patient's body was capable of
handling in a single visit and at that point in time. When this occurs, the OMT
dosage and type should be evaluated and adjusted on the next visit.
After opening lymphatic drainage pathways and maximizing the patient's own
respiratory pump, gentle joint pump techniques have been shown to be
especially beneficial in granting pain relief. Posterior axillary fold technique
(page 230) for patients with upper extremity congestion is particularly helpful.
The value of intermittent non-weight-bearing compression of joint surfaces has
been found to improve local nutrition and create beneficial histologic change in
rheumatologic joints. The mechanisms active in this finding may explain the
clinical results seen following this type of osteopathic manipulative treatment.
It is not uncommon for morning stiffness, a hallmark sign in rheumatoid
arthritis, to completely disappear after manipulative treatment is instituted and
reasonably provided as part of the maintenance management program. Proper
respiration and exercises directed toward maximizing respiratory abilities are
also helpful in maintaining the lymphatic goals of treatment.
164
A variety of techniques including compression, Fluori-MethaneR spray and
stretch, counterstrain positioning and injection have been shown to be beneficial
in removing myofascial triggerpoints. It should be noted that the most common
underlying or perpetuating factor associated with myofascial dysfunction is a
postural disorder. For this reason and because postural problems directly and
biomechanically stress the joints, postural analysis and treatment is often
necessary before any other conservative treatment program for rheumatologic
di sease becomes effective. Postural correction may necessitate a shoe lift,
LevitorR orthotic device, or an orthotic shoe. Conservative treatment also
includes patient education, osteopathic manipulative treatments, NSAIDs and/or
other medications, exercise, and modifications of activities-of-daily-living
(ADL).
Manipulative treatment of somatic dysfunction in the cranial region is frequently

employed because of its possible role in affecting the pituitary gland I s influence
on the adrenal function, the essential steroidal hormones secreted by the adrenal
cortex, and the pure sympathetic activity effect on the adrenal medulla. It is
postulated that manipulation of somatic dysfunctions in the lower thoracic area
also helps normalize hormonal levels through direct influence on adrenal
function.
A physician who understands viscerosomatic reflexes and closely monitors the

musculoskeletal system with palpatory examination has a substantial non
invasive advantage in the discovery of clues to visceral dysfunction. In the
arthritic patient, musculoskeletal clues may be initiated by immune-complex
deposition, toxicity from the medications used to treat chronic disease, or from
mechanical change. If discovered at a dysfunctional level, steps can often be
taken to prevent structural change. This connection is readily demonstrated
when monitoring Chapman I s reflex points, the celiac ganglion and the mid
thoracic paraspinal tissues in a patient taking NSAIDs. Early dysfunctional
gastrointestinal signs warrant immediate intervention because structural changes
in the form of gastritis and/or ulceration are common side effects of medical
treatment for arthritis. Sometimes side effects warrant withdrawing certain
medications from an otherwise successful medical treatment program. The
finding of a previously absent musculoskeletal somatic dysfunction suspected of
being viscerosomatic in nature, should prompt the physician to ask about new
stressors as well as to review current medications. Often correcting the somatic
dysfunction and then re-educating the patient to take their NSAIDs with food or
discussing methods of stress management are adequate to reverse these early
changes.
Treatment should be directed toward removal of factors contributing to spinal

cord segmental facilitation and also toward maximizing function in target organs
or in those organs important in the excretion of the toxins (liver, kidney, and
165
bowel). It is known that the liver plays an important role in the clearance of
soluble immune-complexes from the circulation and may play an important role
in preventing immune-complexes from being deposited in vessel walls elsewhere
in the body. Liver pump and CV4 techniques are frequently utilized to aid the
body in general detoxification.
OTHER MANAGEMENT CONCERNS:
Some exercises are designed to maintain flexibility and others are designed to
strengthen muscles where ligamentous support structures are inadequate.
Walking programs as well as "aqua-cize" (water exercise) have both been shown
to be beneficial to patients with rheumatoid arthritis.
The role of a specific dietary recommendation is nebulous at this time although

some general recommendations are pertinent. Certainly weight control in obese
patients is important in order to reduce biomechanical strain on joint structures.
Patients with osteoarthritis are often over-weight while patients with rheumatoid
arthritis are often under-nourished and warrant proper dietary education for
general health reasons. While most texts state that diet is ineffective in
managing arthritics, some patients are convinced that they experience arthritic
flares with intake of certain foods such as sugar, citrus fruit, milk, fermented
beverages, sodium benzoate, white flour, coffee and tea. Some physicians
claim that there is a link between "food allergies" and arthritis. Some studies
suggest that linoleic acid may be beneficial. Physicians can legitimately
recommend a healthy diet as being appropriate for the patient regardless of any
coexisting rheumatologic condition.
In patients with osteoporosis, bone mass is first lost in the anterior portion of
the thoracic vertebrae making this area particularly susceptible to compression
fractures. A loss of 30% of the bone mass is required before osteoporosis will
be evident on x-rays. It is prudent to avoid high velocity, low amplitude
treatments (HVLA) whenever osteoporosis is suspected. It is also best to
substitute another technique that will accomplish the desired goal for any
technique which places significant forward bending into the thoracic spine.
Patients with osteoarthritic changes may develop bony encroachment of the

neural foramena in the cervical or lumbar regions. Backward bending or
sidebending to the symptomatic side may increase the encroachment. Treatment
goals include reducing excessive lordotic cervical and lumbar postural curves,
promoting venous and lymphatic drainage in the area of the intervertebral area,
and avoiding positioning which might aggravate the neural symptomatology.
Structural intervention is often necessary in patients with rheumatoid arthritis.

In patients with significant joint effusion, drainage may prevent stretch of
existing support structures and provide symptomatic relief for that patient.
166
Surgical intervention for structural joint deformities is often helpful in
maintaining the patient's functional capabilities. The expertise of the
rheumatologist and!or orthopedist and a team approach to the patient's needs
can be extremely beneficial.
In patients with primary fibromyalgia syndrome who were already medicated

with appropriate doses of Flexeril or amytryptaline, counterstrain OMT to
tender points and systemic OMT to support homeostasis both improved
subjective quality of life while reducing pain levels, but only the systemic OMT
protocol was capable of reducing the number of tender points. After systemic
OMT, 25 % of patients in a KCOM study no longer fit the criteria for primary
fibromyalgia established by the American College of Rheumatology. *
IV. SUMMARY: SUGGFSTIONS FOR TREATMENT DFSIGN
PATHOPHYSIOLOGY OSTEOPATHIC CONSIDERATION
1. Passive ROM
Somatic 2. Correct Posture and
Arthritis <--> Dysfunction Alignment
3. Fascial Indirect OMT
4. Joint Pumps
Toxic 1. Lymphatic Drainage

2. Liver and GB Pumps
3. CV4
Poor Cartilage Nutrition 1. Soft Tissue

Periarticular Treatment
2. Indirect Stacking OMT
3. Joint Pumps
ANS Involvement 1. Treat Facilitated

Segments
2. Decrease SIV and VIS
Input
3. Rib Raising
4. Surg. or Rx Sympathetic
Blockade if Severe
Inflammation 1. Anti-Inflammatory Rx
2. Anti-Rheumatic Rx in
Severe Cases
3. Jnt. Pump and Lymphatic
Protocols
4. Use non-traumatic OMT
167
RHEUMATOWGIC BffiLIOGRAPHY:
*Lo KS, Kuchera ML, Preston SC, Jackson RW: Osteopathic manipulative
treatment in fibromyalgia syndrome. JAOA 92(9): 1 177, Sept 1992.
(JAOA article in review)
Stiles E: Osteopathic approach to rheumatoid arthritis. OsteQPathic Medicine
Aug 1977: 75-83.
Simkin P A: Synovial permeability in rheumatoid arthritis. Arthritis and
Rheumatism 1979; 22 (7): 689-96.
Rothschild and Masi: Pathogenesis of rheumatoid arthritis: A vascular
hypothesis. Seminars in Arthritis and Rheumatism 1982; 12 ( 1): 1 1-3 1.
Palmoski and Brandt: Aspirin aggravates the degeneration of canine joint
cartilage caused by immobilization. Arthritis and Rheumatism 1982; 25
( 1 1).
Wallace DJ et al: Plasmaphoresis and lymphoplasmophoresis in the
management of rheumatoid arthritis. Arthritis and Rheumatism 1979; 22
(7): 703-10.
Cercere F et a1: Evidence for the local production and utilization of immune
reactants in rheumatoid arthritis. Arthritis and Rheumatism 1982; 25
( 1 1): 1307-15.
Williams RC: Immunopathology of rheumatoid arthritis. Hospital Practice Feb
1978: 53-60.
Conditions of vessel wall deposition of immune complexes in immunologically
induced vascular diseases, in Deicher and Shulz (ed) Arthritis--Models
and Mechanism. Springer-Verlag, 198 1.
Cochrane W et al: Absorptive functions of the synovial membrane. Ann
Rheum Dis 1965; 24 (2): 2-15.
Levick JF: Contributions of the lymphatic and microvascular systems to fluid
absorption from the synovial cavity of the rabbit knee. J Physio 1980;
306: 445-461.
Weissmann G: Mediators of tissue damage in rheumatoid arthritis: Phagocytes
as secretory organs of rheumatoid inflammation. Triangle 1979; 18
(2/3): 45-52.
Enneking and Horowitz: The intra-articular effects of immobilization on human
knee. Journal of Bone and Joint Surgery 1972; 54A: 973-85
Chrisman OD et al: The protective effect of aspirin against degeneration of
human articular cartilage. Clinical Orthopaedics and Related Research
1972; 84: 193-196.
Mills and Sturrock: Clinical associations between arthritis and liver disease.
Annals of the Rheumatic Diseases 1982; 4 1: 295-307.
168
INDEX OF APPENDIX
Manipulation in the Pediatric Patient ••••••••••••••••••••••••••••••••••••••• 171
The Musculoskeletal System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
The Immune System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172
The Nervous System . . . . . . . . . . . . ... . . . . ... ...

. . . . .... ....
. . . . . .. . . . . .
. . . . . . 172
Overview of The Pediatric Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
Treatment Of The Pediatric Patient . . . . . . . . . . . . . . . . . . . . . .... . . . .. . . . . . . . . 176
References . .................................................................. 178
Vision And Interest Of Infant From Birth to 12 Months ............. 179
Osteopathic Considerations in Psychiatry ••••••..••••..•...••••••••••••••••• 181
Osteopathic Considerations in Immunology •••...••••...•.••••••••••••••••• 182
Hypersympathetic Activity on Selected Tissues (Korr) ••••••••••••••••••• 183
Autonomic Influence on Selected Tissues ••••••••••••••••••••••••••••••••••• 187
Osteopathic Manipulative Treatment In Systemic Dysfunction •••••••• 189
Ventral Techniques Indications and Contraindications . . . . . . . . . . . . . . . . 227
Anterior Chapman I s Reflexes (Chart) . . . . .. . . . . . . . . . . . .. . . . . . .

. . . . . . . . . . 232
Posterior Chapman I s Reflexes (Chart) . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . 233
Index For OMT In Systemic Disease •••••••••••••••••••••••••••••••••• 234
169
NOTES:
170
OSTEOPATlIIC CONSIDERATIONS IN TIlE PEDIATRIC PATIENT
The modem general practice of pediatrics contains a large amount of preventive

medicine. It offers the physician the opportunity to examine and begin a
program for a patient that is healthy; usually the mother brings her well baby to
you so that you can recommend and instruct her on measures (including
nutrition, immunizations, and structural screening) that will optimize the health
of this newborn infant (birth to age 2 years) or child (2 years old to puberty) .
Diagnosis and manipulative treatment programs for infants or children are
different from those for adults; in a large part this diversity is due to certain
anatomical and functional characteristics peculiar to the pediatric patient.
I. TIlE MUSCUWSKELETAL SYSTEM:
Though it is often said that the spine of the newborn is regionally flexed like a
large C-curve, the lumbosacral angle actually begins to form as early as the
fourth month of gestation age. The cervical curve has already begun to appear
at birth and will increase with the efforts of the infant to raise the head and hold
it erect. Activities like raising from the floor and crawling exercises develop
the erector spinae muscles and begin to coordinate patterns of interaction
between the nervous and musculoskeletal systems. The lumbar curve, however,
does not appear until upright weight bearing is assumed. Its normal backward
bending curvature gives spring to the spine and support of the pelvis, which
then becomes the anchor for the hip extensors and rotators. Postural curves
develop with weight bearing during childhood and postural abnormalities such
as scoliosis can progress rapidly during growth spurts. Proper screening of
posture should detect all scoliosis greater than 10 degrees; 1 scolioses measuring
more than 20 degrees should have the benefit of a specialist' s consultation.
Secondary scoliosis can result from postural compensation for short leg
syndrome, congenital spinal asymmetries, or even cranial somatic dysfunction
which unlevels the eyes.
The musculoskeletal system of the infant and child is still developing. Most of
the bones are cartilaginous to begin with and articulations between them are
very elastic and resilient. Fryette's motion characteristics do not apply to the
infant. Spinal motion patterns are nonspecific and restricted motion is usually
due to local muscle contraction or fascial pull and not bony joint somatic
dysfunction. The pediatric patient is surprisingly easy to treat. Although the
child thinks that the physician is playing a game with them, treatment is not just
haphazard but designed to move restricted joints and tissues through their ranges
of motion. Dysfunctions "work themselves out; " it is seldom necessary to use
thrusting type manipulation. Productive treatment time is very short with actual
completion accomplished in about 2-3 minutes. Soreness as a reaction to
treatment is rare.
171
ll. TIlE IMMUNE SYSTEM:
Since the immune system is just developing, its lymphatic tissues take every
opportunity to respond to an antigen; lymphadenopathy is often pronounced
even with minor infections. Infectious diseases are common in children. In
adults, viral adenopathy usually only involves the posterior cervical nodes. In
children, viral lymphadenopathy can either involve anterior or posterior cervical
lymphatic chains and usually results in an immune response that includes
formation of large, thickened, tender, congested lymph nodes and overlaying
skin that is moist, slick and hot. Anterior lymphadenopathy is often produced
by bacterial infection and these nodes are usually shotty, coarse, grainy and are
acutely tender to palpation.
It is clinically observed that infants and children respond rapidly to osteopathic

manipulative treatment. Sometimes their temperature will increase a degree or
two for a very short time after the treatment, then the fever will lyse and the
temperature will drop to near normal. Parents should be told that this will
happen. Children and infants get sick quickly but they also respond quickly to
proper treatment and support of homeostatic mechanisms.
ill. THE NERVOUS SYSTEM:
In the newborn, cranial somatic dysfunction from in utero forces or birth trauma
may result and should be evaluated during the initial physical examination. Any
obvious plagiocephaly or palpable cranial somatic dysfunction should be treated
as soon as possible because both have been associated with pediatric otitis
2 3
media, attention deficit and learning disorders, as well as colic, strabismus,
suckling disorders, and a host of other symptoms associated with cranial nerve
dysfunction. Dysfunction or injury to the nervous system is the most common
serious consequence of a difficult birth and cranial OMT is ideally employed as
early as possible to assist in structural-functional relationships. The pediatric
history should always consider a narrative of the birth and perinatal period.
Neural connections are still developing so infants and children often react
erratically, rapidly and very unpredictably to disease processes. With an
infection, a newborn often reacts with decreased temperature and, often,
bradycardia. In some newborns, the only symptoms of a severe infection may
be eating poorly, regurgitating, becoming less active or more irritable or shaky.
On the other hand, children (age two to puberty) may get very high
temperatures with mild infections, or near normal temperatures with serious
infections. Infants and children are also developing emotionally and socially.
See page 179 for a graphic representation depicting some of this growth.
172
IV. OVERVIEW OF TIlE PEDIATRIC EXAMINATION:
At first, infants and young children may be frightened, because the physician is
both a stranger and looks so big, tall, and threatening. Kneeling or sitting on a
stool may help reduce their fears by making the physician more "their" size. It
helps to appear happy and to always be kind and honest with these little
patients. Some physicians do not wear a white coat because in the mind of the
child, this may trigger some previous unfortunate, uncomfortable or frightening
incident.
The first prerequisite to successful clinical encounters with children is to gain

their confidence. It is essential that the physician knows the child's name and
repeats it during questioning and conversation. The mother can promote
security and safety by sitting close or holding the child on her lap during the
examination; at other times, there are occasions when it is best to have the
parent in the room, i.e. an overbearing parent or for an older child with a
personal need for non-judgmental advice or direction. After greeting the
mother and the patient, the very young child is best "ignored" while the history
is taken by questioning the mother, with only apparent casual glances given to
the child. He often doesn't understand the questions and, even if old enough to
talk, the answers cannot be entirely believed, especially if not supported by
physical and laboratory data. An adult often complains of pain and disability
while a child notices inconveniences to playtime activity. The physician must
deal more with objective signs as well as with the parent's anxieties about the
child's problem. It helps to occasionally touch the infant on the foot, or briefly
use some small talk during history taking. Avoid looking directly into the
young child's eyes because this will usually produce a definite and immediate
withdrawal response and often sets the tone for the rest of the pediatric
patient/physician encounter.
During the early part of this visit, the physician often tries not to reveal a
primary interest in the young child; in fact, it is best for the physician to obtain
as much information as possible while taking the history from the parent and
from casually observing the child's stance, activity level, and responses before
beginning to directly examine the patient. Usually by the time the history is
taken from the parent or primary care-giver and even though the physician has
seemed to be uninterested in the infant or child, with observation and casual
palpation metatarsal varus and tibial torsion have been evaluated. Sometime
during this early encounter it is possible to see that the child is able to move the
leg quickly and do so without pain.
While talking with the mother it is often possible to casually put a warm
stethoscope on the chest of the infant or child and pretend not to know the
stethoscope is there. He will look at the stethoscope, then at the physician (who
is looking at and talking to the mother), then at the stethoscope again; he really
173
is confused as to whether the physician is really doing anything to him or not.
Before the child figures out that the physician is gathering information about the
heart and lungs, the data has been obtained and no crying interferes with this
important evaluation.
Be sure that the head of the stethoscope is warmed. A rubber-rimmed

stethoscope bell will be less cold to the infant. Even a warm stethoscope or a
stethoscope with a rubber ring around it apparently can feel cool and startle a
child enough to make them cry. This suggested technique may improve chances
of obtaining good auscultatory data from an infant and will usually keep him
from crying: The physician's fingers are placed on the chest in about the
position at which the stethoscope is to be placed; the infant or child does not
seem to mind the touch of the hand, so the hand is placed on the chest with the
fingers in the areas where the heart and/or lungs are to be auscultated. Then,
one finger at a time is lifted and immediately replaced by the head of the
stethoscope on the chest The infant is usually unable to tell when the finger is
lifted and replaced by the stethoscope, so remains relaxed and doesn't cry. A
quiet infant or child improves the accuracy of auscultation.
Until a friendship has developed with you as the physician, never stare the
young child or infant eye to eye. It is very threatening to them and they will try
to get away as soon as the physician's eyes focus on theirs. It is necessary for
the physician to gain their confidence before they permit eye contact. How this
is accomplished depends upon the child's age and that undefinable "something"
that is present between the physician and each of the young patients. After the
child has become more accustomed to the physician, the cervical lymph glands
can be evaluated by palpation. This can be performed effectively in a short
period of time. Mobility of the hyoid and the anterior cervical fascias can be
assessed at the same time. The abdomen is gently squeezed several times,
looking for evidence of tenderness or masses. The ophthalmoscope is set at plus
8 diopters and at a distance of about 1 112 or 2 feet from the eye the light is
flashed ("peek-a-boo") in the child's eyes looking for a red reflex.
The ears are then examined. It is safer and more information is quickly
gathered using the biggest ear speculum in the diagnostic kit, even for the
newborn infant. Remember to pull the ear down and back to open the external
canal in an infant or young child. A single position of the speculum should
visualize the entire tympanic membrane. Saying "peek-a-boo" makes the infant
or young child think it's a game and he may hold very still. Examine the nose
using the same large ear speculum. The diagnostic handle (light) must be held
in such a way that the physician has good control during the examination so that
any sudden, unexpected motion of the child is followed instantly by the
otoscopic or auroscopic speculum to avoid scratch or contact damage of the
canal, drum, or mucosa. Though it is not a scientific word, "yuck" often makes
174
the young child laugh and present the other ear, nostril, or mouth to see if he
can get the same response from the physician.
Some otoscopic diagnostic heads have a place to hold a tongue blade, but often
these don 't direct the light to the right place. Frequently in the infant, the light
shines between their eyes instead of in the mouth. A special diagnostic head
used only for holding the tongue blade and directing the light directly along the
blade and into the mouth, is very helpful. If this special holder is not a part of
your equipment, a bright penlight, held and operated on the tongue blade may
be used. It allows the physician to control the light source and the tongue blade
with one hand and have the other hand free to control the patient' s head. If
possible, have the child open the mouth wide and "pant like a puppy dog. " The
tongue will automatically pull down, the soft palate will rise and it becomes
fairly easy to obtain a good view of the throat even without using the tongue
blade. Tongue blades tend to frighten children.
Again, it is helpful to make infants and young children think you are playing
with them. Sometimes the physician can hold the light up above the patient' s
head. When the child looks up at the light the mouth tends to open. Bring the
tongue blade down and touch the mouth saying, "oops " . When the child smiles
or laughs, carefully but quickly slip the tongue blade over the tongue and look
into the throat. A single gag , with you ready to quickly observe the view of the
entire pharynx, often all the way to the epiglottis, is all that is usually required.
Children seem to understand the words, "all done, " even at an early age; they
often won 't even cry. At that point tum away telling the child how good he/she
was.
If the pediatric patient can stand, have him do so and assess his posture. Then
have him bend over to touch his toes and look for a rib hump due to
rotoscoliosis. If present, have the patient swing his trunk off to the right and
left while still forward bent. The functional component of the rotoscoliotic
curve will reduce.
Infants and children don't usually like to lie down in a physician ' s office. If
you need to lay the infant down for some part of the examination such as
Ortalani ' s test for a congenital hip disorder, do that procedure last, if at all
possible. Often , once you lay the infant or child down , any friendship that has
been established is lost.
This section does not describe an entire examination but offers an approach
which considers the mind and spirit of the young child while beginning to
examine the body. These suggestions tend to work most, but not all, of the
time. Occasionally, there is a child who just won ' t cooperate. In this case,
after taking the history and making a reasonable attempt to become friends, the
exam must proceed in a calm, firm but gentle fashion using the humane
175
restraints of the mother and/or nurse, and a calm reassuring voice of the
physician.
v. TREATMENT OF mE PEDIATRIC PATIENT:
Like osteopathic treatment of any patient, osteopathic manipulative treatment of

a pediatric patient is based upon the application of principles and not upon
formulae or techniques. Treating infants and children is often easy because they
rarely have fibrosis and or chronic fixations; don't overtreat. Keep it simple
and make it fun. Manipulative treatment is administered to the pediatric patient
according to whether they are "pre-school" or "school age". Pre-school
children only require articular mobilization and soft tissue. School-age children
may require modified adult procedures.
Don't treat directly over infected lymphatic nodes; instead, treat around them
and support the body systems that help the infant fight infection and recover
from it effects. This means rib raising to reduce sympathetic hyperactivity
while moving fluids and fascial techniques to dome the diaphragm and start the
lymphatic pumps. Newborns and infants can be treated by placing them on the
physician's thigh or by placing them in a lateral recumbent position of the table
(your knee on the table in front of them) and administering soft tissue to the
paraspinal tissues. The physician can also pick the child up and treat while
walking around. The newborn can also be held against the chest and treated. A
physician who has children can becomed experienced by treating his/her own
children.
Insuring that the child gets solid foods during the time of high fever and
anorexia is not as important as being sure that the child gets plenty of fluids.
Children normally have a larger percentage of fluids in their bodies; many times
a child or infant must be admitted to a hospital because of dehydration and not
because of the disease process. So increase fluids, decongest peripheral tissues
and return sequestered interstitial fluid back into the circulation by using
lymphatic and fascial techniques."
Lymphatic pumps can be made fun for the child--"play with them". When the
infant gets a little fussy or tries to get away from a rhythmic chest pump,
suddenly stop and say, "Do you want more?" While they are trying to figure
out why they should want more, start it again; when he fusses again, you say
the same thing. Usually by the time he figures out that it's not really a game,
the treatment is over; "all done." Another approach to "treatment" is to grasp
feet and legs, lift their buttocks and their lower 2/3 of the body off the table,
then jiggle the lower extremities gently. Flex one leg and then the other onto
the chest, pushing each one gently and then extend the legs again. The child
may be turned over by using the legs and then the physician may "play
wheelbarrow" with them. This apparent play clinically promotes a type of
176
lymph pump, fluid drainage, and movement of the body tissues. The mother
can continue this "play-type" mobilization at home.
Remember, high velocity activation of osteopathic manipulative techniques is

usually not required in infants and young children and because epiphyseal plates
are still open, may not be the best choice of technique in this age group. Soft
tissue treatment and articulatory methods of treatment are very effective and
make it fun for the child. Again, do not over-treat. There is the "tick-tock
method" of treatment, in which the physician holds the chest of the child under
the arms and rocks him back and forth, from right to left, mobilizing the spine
and other tissues. The fascias of the thoracic inlet and the diaphragmatic area
should be treated. If the infant is getting an exanthema or prodromal of an
infectious disease, treatment clinically results in less rash, less fever and a
decrease in the severity of the disease. Pediatric patients benefit from
osteopathic diagnosis and manipulative treatment and both should be integrated
into pediatric care.
Inform the parents that commonly after manipulative treatment, the temperature
will briefly go up in a pediatric patient before coming down. Also educate them
that fever is not necessarily bad. Increased temperature is one of the body's
ways of mobilizing defenses against an infection. Viruses multiply best at
temperatures slightly below normal. Fever hinders viral replication and is a
way of increasing circulation and getting the immune substances to the infected
areas, helping the infant's own homeostatic mechanisms. It increases
metabolism and circulation and creates an environment poorly tolerated by
microorganisms.
Fever that is too high may cause convulsions and the threshold for convulsions
from fever varies from child to child; therefore, its level must be controlled. If
there is a febrile seizure history, then the physician must be more cautious in
instructing the parents in maintaining temperature control in the infant or child.
Aspirin may be associated with development of Reyes' Syndrome and therefore
it is not as good an antipyretic choice as acetaminophen. As a rule of thumb, a
0 0
fever under 10 1 F doesn't need to be treated. Above I02 F a dose of
acetaminophen ( 1 grain per age of life) could be given.
A physician knows that his/her management of a child has been successful if a

mother brings in one of her children and says, "Johnny cried because he wanted
to come in and see his doctor too." If you desire to read more on examination
of the child, read "How to examine a baby or a small child and how to keep
your cool" written by retired pediatrician, Robert Mercer, M.D.4 You can feel
the joy he had in being able to care for infants and children. Dr. Mercer says,
"The real reward of a successful examination is when the small person climbs
up on your lap for further friendly play; then you know for sure that you have
done a good job and established a new friendship in the process." When the
177
child likes "the doctor," a satisfying patient encounter becomes even more
enjoyable.
REFERENCES:
1. Kuchera WA, Kuchera ML: OsteQPathic Principles in Practice. 2nd

edition. KCOM Press, Kirksville MO, 1992, P 352.
Mead-Johnson Fellowship Paper, 1993
3. Frymann V: Relation of disturbances of craniosacral mechanism to
symptomatology of the newborn: Study of 1,250 infants. JAOA
65: 1059-1075, 1966
4. Mercer RD: How to examine a baby or a small child and keep your cool.
Cleveland Clinic Ouarterly Fall 1983; 50: 255-261.
178
PEDIATRIC GROWTH (Adapted from Wessel) 1
Hungry for companionship, staring is a baby's way of reaching out to others. Reaching for
the closeness necessary for healthy development. The infant progresses from the ability to
barely see to complex talents including coordination to seek, to remember,
and to imitate.
prefers complicated forms

to black and white reaches for toes and toys
watches surroundings more close by, then those
bright ob smiles in important; stops hanging, then those in
jects on response sucking to look at center of room. Laughs,
ceiling in
I
to smile
l
father, a curtain coos, grunts when sees
front or sunbeam on floor
I favorite toy
I 1 1
I I I I
1 Mo 2 Mo 3 Mo 4 Mo 5 Mo 6 Mo
I I
I knows mother I smiles and I dramatic development

by sight and coos to attract enjoy-ment for new
may smile mother's atten- places, as long as
tion. When she mother is along side;
disappears gets trips are exciting
solemn and may and taken in stride;
cry but when back
home again, relaxes,
begins to imitate facial smiles, coos in delight
expressions and to be safe at home
voice inflections again.
sees and visual games: peek-a-boo, complex

grabs hold and watch Mommy pick it
of his feet
7 Mo 8 Mo 9 Mo 10 Mo 11 Mo 12 Mo
I I
y
looks carefully can interlock fingers, pull them
at hands, navel, apart and repeat. Acts like is
toes as if they discovering hands for the first
were new time
begins to imitate his favorite adult's

mannerisms. Interested in tiny details
in wallpaper, pictures or blocks;
studies mother's jewelry, clothing, etc.
1. Wessel, MA; From A Baby's Point Of View: Associate Professor Of Pediatrics At Yale University.
179
Still-Hildreth Osteopathic Sanatorium
Macon, Missouri
Dedicated to the Treatment and Care of Nervous

and Mental Patients
1914 1939
180
OSTEOPATHIC CONSIDERATIONS IN PSYCHIATRY
BmLIOGRAPHY
Bradford, Spencer, G.; Role Of Osteopathic Manipulative Therapy In Emotional Disorders: A

Physiologic Hypothesis; JAOA; Vol. 64; No. 7; Jan 1965: 64-73
Dunn, Floyd E. ; Osteopathic Concepts In Psychiatry; JAOA; Vol. 49; No. 7; Mar 1950:
354-357
Espeland, Darryl, and Peters, Christian; OMT And Substance Abuse Rehabilitation;
Osteopathic Annals; Vol. 13; Feb 1985: 26-30
Sadder, Arthur M.; Restricted Blood Flow In Brain Found In Some Schizophrenics; Medical
Tribune; Jan 11, 1984
Woods, John M. ; Woods, Rachel H.; A Physical Finding Related To Psychiatric Disorders;
JAOA; Vol. 60; Aug 1961: 988-993
18 1
OSTEOPATHIC CONSIDERATIONS IN IMMUNOWGY
BmLIOGRAPHY:
Amalfitano, D.M.; The Osteopathic Thoracic-Lymphatic Pump: A Review of

the Historical Literature; Journal of Osteo.pathic Medicine; Apr-May,
1987: 20-24
Gunderson TG, Gordon RM: A study of the influence of spinal lesions on the
course of infections. IAOA 1932; 31: 390.
Measel, I.W.; The Effect of Lymphatic Pump in the Immune Response: 1.

Preliminary Studies in the Antibody Response to Pneumococcal
Polysaccharide Assayed by Bacterial Agglutination and Passive
Hemagglutination; IAOA; 82 (1): 28-31
Measel, I.W.; Introduction: Thoughts in Osteopathic Practice and Infectious

Diseases; Osteopathic Annals; 10 (3); Mar 1982: 7-11
Measel, I.W., et. al,; The Effect of the Lymphatic Pump in the B and T Cells
in Peripheral Blood; Osteopathic Annals; IAOA; 86 (9); Sep 1896: 608
Paul, R., et. al.; Interferon Levels in Human Subjects Throughout a 24-hour
Period Following Thoracic Lymphatic Pump Manipulation; IAOA; 86
(2); Feb 1986: 92-95
Purse FM: Clinical evaluation of osteopathic manipulative therapy in measles.

IAOA 1961; 61: 274.
Thorpe, R.; Osteopathic Manipulative Therapy for Infection; Osteopathic

Annals; 8 (9); Sep 1980: 30-34
The proceedings of an International Conference on this subject will soon be

available from the American Academy of Osteopathy. Conference co
chairpersons were Frank Willard, PhD and Michael Patterson, PhD.
182
HYPERSYMPATHETIC ACTIVITY ON SELECTED TISSUES
EXTRACTED FROM COLLECTED PAPERS OF I.M. KORR, PHD
1977-1989
Sympathetic hyperactivity does not introduce

any new qualities, only modifies the inherent
functional properties of the target tissues.
SKELETAL MUSCLE:
o .. Augments contraction similar to inotropic effect on cardiac muscle, "Orbeli

effect"
o .. Facilitates neuromuscular transmission
o .. Increases contracture formation after spinal cord trauma
PERIPHERAL SENSORY MECHANISM:
o .. Facilitation: increases rate of discharge and lowers threshold to fire (may

reach zero so that fires without direct stimulation of receptor)
o .. Exaggeration of response: reports a greater intensity of stimulation than is
actually occurring; increases or exaggerates the perception of pain
o .. The sensory mechanisms that have been demonstrated to respond in this
manner include:
--muscle spindle --tactile receptors

--taste receptors --olfactory apparatus
--Pacinian corpuscles --retina and cochlea
--carotid sinus chemoreceptors
CENTRAL NERVOUS SYSTEM:
o .. Strong influential connection between hypersympathetic activity in superior

cervical ganglion and subcortical activity, especially on the ipsilateral
side
o .. Primary influence is on the mechanisms responsible for generation of the
background electrical activity, the rhythm assimilation reaction and the
secondary components of the induced reaction to light
o .. Facilitating effects have been observed in the reticular formation, general
brain, cerebellum and spinal cord
183
COLLATERAL CIRCULATION:
o .. There is a decrease in development of collateral circulation; sympathectomy

increases the development of collateral circulation in areas of occlusion
o .. There is decreased mortality and morbidity in experimentally induced
myocardial infarction when sympathetics are cut
ADIPOSE TISSUE:
o .. Sympathetics are requisite for lipolysis independently from blood flow

(alpha for vasculature and beta for adipose tissue)
o .. Increases in glycogenolysis requires increased oxygen
ENDOCRINE SYSTEM:
o .. Sympathetic significantly influences the pineal gland and thereby influences

other endocrine systems; this is especially related to sexual development
and reproduction. Superior cervical ganglion influence on the pineal
gland through synthesis of melatonin
BONE GROWTH:
o .. Reduces the growth of longitudinal bone
RETICUWENDOTHELIAL SYSTEM:
o .. Increases circulating reticulocytes and normoblasts
SOME SPECIFIC CLINICAL REACTIONS TO SYMPATHICOTONIA:
ARTERIOSCLEROSIS:
Sustained stimulation of sympathetics produce histologic features of

arteriosclerosis and increases tendency towards thrombosis.
HYPERTENSION:
High activity of the peripheral sympathetic nervous system is felt to be

an important contributing factor in some forms of arterial hypertension.
184
HEART:
Increased sympathetic activity increases oxygen demands which

contribute to the extent and degree of cardiac ischemia and angina.
Sympathicotonia increases the extent of myocardial damage following

an MI.
(Experiments with cats) Post-MI there is a higher discharge of

sympathetic activity at T3 ramus communicans, termed a cardio-cardiac
reflex, which plays and important role in increased rate of dysrhythmia
and ventricular fibrillation. Sympathicotonia also lowers threshold to the
development of ectopic foci in the heart. Adrenergic blockade protects
the heart from these effects especially in the few hours post-MI and
lowers the mortality rates.
Increased sympathetic impulses to the kidney is implicated in the

retention of Na + and water in CHF patients.
PEDIATRICS:
Increased sympathetic activity has been implicated in the long Q-T

interval associated with Sudden Infant Death Syndrome.
URETERAL CALCULI:
Ureteral calculi produce ipsilateral facilitation of sympathetic activity.

Increased sympathetic activity is also implicated in poor ureteral
transport of fluids, a factor in calculi formation. If calculi are present in
the ureter, sympathetic hyperactivity decreases the peristalsis of the
ureters which hinders removal of the calculus from the ureter.
Superimposed emotions associated with increased sympathetic responses

may are found to reduce glomerular filtration rate (GFR).
THE SKELETAL SYSTEM:
Hypersympathetic activity retards bone growth. Sympatholytic treatment

restores bone growth to a normal rate.
There is reduced rheumatoid and osteoarthritic disease in the extremities

following sympathectomy.
185
TIlE EXTREMITIES:
Prolonged sympathetic activity in response to significant or relatively

insignificant trauma results in "reflex sympathetic dystrophy", a
syndrome including heightened pain, trophic changes, osteoporosis,
connective tissue disease, and an extremity that is cool, sweaty,
cyanotic, chronically edematous, and has thickened nails. Often these
changes are responsive to sympathectomy.
LIVER:
Sympathetic bombardment releases fatty acids from the periphery and

deposits them in the liver.
PANCREAS:
Sympathetic stimulation can convert a mild, nonlethal type of bile

induced pancreatitis into the necrotizing, hemorrhagic lethal form. This
is probably secondary to vasoconstriction and slight ischemia of the
pancreas.
OTIlER AREAS OF HYPERSYMPATIlETIC EFFECT:
Glaucoma, colitis, megacolon, peripheral vascular disease, postoperative

paralytic ileus, Dupuytren's contracture, irritable bowel syndrome (IBS),
pelvic congestion in women, etc.
186
AUTONOMIC NERVOUS SYSTEM INFLUENCE IN SELECTED AREAS
STRUCTURE SYMPATHETIC PARASYMPATHETIC
Pupil . . . • • • . . . . . . . . . . . . . • . Dilation • • . • . . . . . . . . . . Constriction
Ciliary Muscle . . . . . . . . . . . .
--------
• • . . . . . . . . . . . . Contraction
Lacrimal Gland . . . . . . • . • • • •
--------
. . . . • • . • • . . . . . Secretory
Mucous Glands (N-Th) . . . . . • Inhibition • . . . . . . • . • • . Secretory
Parotid Gland............. lnhibition . . . • . . . • . • . . Secretory
Submaxillary Gland . . . . . . • • lnhibition . . . . • . . . • . . . Secretory
Sublingual Gland . • . • . • . • . • lnhibition . . • . • . . . . . . . Secretory
Blood Vessels (Skin) ......Vasoconstriction ......- - -- - - - -
Pilomotor Muscles......... Contraction...........- -- -----
Sweat Glands • . . . . . . . . . . • . . Secretory . . . . . . . . • . . . •

--------
Common Carotid Artery • • . . • Vasoconstriction . . . • . .

--------
Mucous Glands (phx-Iarx) . • Vasoconstriction...... Secretory
Thyroid Gland . . . . . . . . . . . • . Vasoconstriction . . • • • .

--------
Heart.....................Excitation............ lnhibition
Bronchial Muscle • • . . . . . . . . Relaxation • • . . • . . • . . . . Contraction
Bronchial Glands • • . . . . . • • • lnhibition . . . . . . • . • • . . Secretory
Upper Body Vasculature . . • . Vasoconstriction . • • . . .

--------
Stomach . . • • • • . . . . • • • . . . . . • lnhibition . . • . . . . . . . . • Motor and Secretion
Liver • • . . . . . . . • • • . . . • . . . • • Glycogenolysis • . . . . . . . Glycogen Synthesis
Spleen . . . • • . . • • . . . . . . . . . . . Vasoconstriction . • • • • .
--------
Gallbladder and Ducts . . . • . Relaxation . . . . . . . . . • • • Contraction
Pancreas • • . • • . . • . • • • • • . . . • lnhibition . . . • . . . • . . . • Secretory
187
AUTONOMIC NERVOUS SYSTEM INFLUENCE IN SELECTED AREAS (cont)
STRUCTURE SYMPATHETIC PARASYMPATHETIC
Kidney • • • . . . . . . . • . . . . . . . . . Vasoconstriction...... --------
Adrenal Medulla . . . . . . . . . . • Adrenaline secretion.. --------
Intestinal Tract.......... Contraction . • . . . . . • • • • Relaxation
Rectal Sphincter • • • • . • . • • • Contraction . • . • • • . • . • . Relaxation
vesicle Sphincter ......... contraction . . . . • • • • . . . Relaxation
Vesicle Body .............. Relaxation . . . . . . . . . • . . Constriction
uterine Fundus ............ constriction . . . . . . . • • • Relaxation
uterine Cervix ............ Relaxation . . . . . . • . . . . . Constriction
Male Reproductive Organs.. Ejaculation . . . . . . . . . • . Erection
Ovary and Testes • • . • • • . • • • Vasoconstriction • . . . • . (unknown)
REFERRED PAIN: Generally, visceral afferent nerves from the viscera follow the same pathway as
traveled by the sympathetic innervation of the organ. Impulses from visceral nerve endings arrive
among the posterior hom cells as do impulses of somatic origin. Visceral referred pain will be noted
in the somatic segment(s) which share the same dorsal hom lamina V of neurons. There may be
superficial skin changes, reflex muscle spasm and vasomotor changes.
o .. Visceral referred pain may be gripping, cramping, aching, crushing, squeezing, tearing, stabbing
or burning.
o .. It is usually poorly localized.
o .. Referred pain may have rhythmic occurrence to it.
From hollow viscus: greatest intensity in 20-30 sec, lasts 2 minutes, quickly subsides, and
reoccurs again in minutes. From vascular areas: throbbing pain from inflammation and
chemical mediators; it increases in severity and lasts an extended period of time.
o .. Usually associated with other symptoms of visceral disease.

o .. People with viscerogenic pain get no relief from rest; they find more comfort if moving, trying
to find a position of comfort.
o .. See pages 79-82 for diagrammatic depiction of pain progression.
188
OSTEOPATHIC MANIPULATIVE TECHNIQUES
USE OF OSTEOPATHIC MANIPULATIVE TREATMENT

IN SYSTEMIC DYSFUNCTION
Dysfunction and disease change the local and regional intercellular

environments. An increase in interstitial tissue fluids is one of the results of this
tissue dysfunction. Resulting congestion disturbs local and regional biochemical
homeostasis. Disease and dysfunction also provoke receptors of visceral
afferent and/or somatic sensory nerves which then flood their spinal cord areas
with neural impulses. Afferent (sensory) impulses usually follow the same
fascial pathways as the sympathetic nerves innervating the affected organ or
organs. Occasionally, as from the alveoli of the lungs or from the cervix of the
uterus, visceral afferents follow the pathways of the organ I s parasympathetic
supply. In either case, constant bombardment by visceral afferent impulses
facilitates the spinal cord segments at their destination. This means a reduction
in the threshold of the synapses in the neuronal pool of the dorsal hom in those
regions of the spinal cord. Because there is "cross-talk" between these pools,
palpable somatic changes result from visceral dysfunction and visceral
dysfunction can also result from somatic dysfunction. Once facilitated cord
segments are established, stress of any kind (physical, mental or emotional) will
initiate an outburst of sympathetic impulses to their associated viscera even if
that stress has no direct relationship to the low threshold segments.
Successful osteopathic manipulative treatment for patients with systemic

dysfunction or di sease has these common goals:
o .. Reduce the two main factors responsible for initiating or sustaining

facilitated spinal cord segments, whether they be associated with somatic
and/or visceral dysfunction.
o .. Support homeostatic mechanisms by reducing somatic and visceral factors
that contribute to the maintenance of spinal cord facilitation. Reduction
of cord facilitation enables the body to make more appropriate reflex
responses to proprioceptive input.
o .. Support biomechanical mechanisms responsible for moving lymphatic fluids
from the interstitial spaces back to the circulation and for removing
metabolic by-products and medications from the intercellular
environment. This aids fluid homeostasis throughout the body.
o .. Support the parasympathetic nervous system by treatment of fascial
restrictions and somatic dysfunction in the regions of the sphenopalatine
ganglion, the cranium, the OA or the sacrum. These treatments promote
balance within the autonomic system and prepares the body to return
toward a homeostatic level which is more physiologic for that patient.
189
o . . SUpport the body processes and mechanisms which allow the body to
metabolize and use the food that is taken into the body.
o . . Support the mental, spiritual and emotional needs of the patient.
It should be readily apparent why initial osteopathic manipulative treatment is

often directed toward reducing facilitation and promoting a more appropriate
sympathetic response. The treatment program will usually progress toward
support of the body's lymphatic system; and finally, toward effecting
parasympathetic balance. Osteopathic manipulative management is specific for
each patient, providing treatment indicated by the history of that patient, the
known natural history of the disease process, and the palpatory findings on
examination of the patient. There are a variety of manipulative techniques that
can be used to affect somatic dysfunction, the autonomic nervous system, and
the lymphatics. It must be re-emphasized that the manipulative portion of a
management program is unique for each patient and is planned according to
each patient's individual needs.
A basic plan for the efficient use of the patient's neuromusculoskeletal

system during the formulation of a differential diagnosis and treatment plan
is very helpful. The following figure is a model for such a plan. It has been
found to be clinically useful in effectively and efficiently formulating and
executing supportive osteopathic manipulative treatment for a patient with
systemic disease.
Mid Cervicals
Tl - L2
Ribs
OA
Somatic Dysfunction Sacrum
facil. seg.
Sympathetics Parasympathetics I
Chain Ganglia Treat.ant plan J - Cranial Nerves
III, VII, IX, X
Collateral Ganglia Di.aa.e or Cranium,
Chapman's Reflexes Dy.function OA, AA, C2
I Lymphatics
L-________________�
I1 Pelvic
Splanchnic N.
Sacroiliac
Thoracic Inlets
Abdominal Diaphragm
Mesenteries
Pelvic Diaphragm
Lymphatic Pumps
190
SYMPATHETIC AND
PARASYMPATHETIC
INNERVATION
SYMPATHETIC HEAD � ---- PARASYMPATHETIC
NERVES CRANIAL NERVES
(T1-12) III. VII. IX
PARASYMPATHETIC
CRANIAL NERVE
X
SUPRASTERNAL
NOTCH
ANGLE OF
LOUIS
ARMS
�"""-__ a. UPPER GI TRACT
LEGS \
b. SMALL INTESTINES
�
RIGHT HALF COLON
_U"BIUCUS
LEFT HALF COLON
PELVIC SPLANCHNIC
NERVE (S 2.3.4)
(PARASYMPATHETIC)
191
COMPOSITE AUTONOMIC INNERVATION CHART
PARASYMPATHETIC SYMPATHETIC INNERVATIONS

INNERVATIONS
VISCERA THORACO REGIONAL CORD SPLANCHNIC COLLATERAL
CRANIOSACRAL LUMBAR AREAS LEVEL NERVES GANGLIA
HEAD AND NECK Tl-4 (CERV. GANGLIA)

CRANIAL III - PUPILS Tl-4
CRANIAL VII - LACRIMAL AND HEART Tl-6 (CERV. GANGLIA)
SALIVARY GLANDS- II Tl-4
CRANIAL VII - SINUSES Tl-4
CRANIAL IX, X - CAROTID BODY LUNGS Tl-6
AND SINUS Tl-4
CRANIAL X VAGUS - THYROID Tl-4

- TRACHEA/BRONCHI Tl-6 ENTIRE GI TRACT: TS-L2
� ? - MAMMARY GLANDS Tl-6
1.0
tv CRANIAL X VAGUS - ESOPHAGUS
..
LOWER 2/3
..
- AORTA UPPER GI TRACT TS-9 GREATER CELIAC
..
- HEART Tl-6 SPLANCHNIC GANGLION
- LUNGS AND SM INT./RHT COLON T10-ll LESSER SUP. MESENTERIC

VISCERAL PLEURA- Tl-6 SPLANCHNIC GANGLION
- STOMACH TS-9L
- DUODENUM TS-9 APPENDIX T12 LEAST AND
..
- LIVER LEFT COLON/PELVIS T12-L2 LUMBAR INF. MESENTERIC
GALL BLADDER TSR SPLANCHNIC GANGLION
AND DUCTS T6R
..
- SPLEEN T7L
-I
- PANCREAS - T7R
..
- RIGHT COLON - T10-ll
? - OVARY AND TESTES -II T10-ll
CRANIAL X VAGUS 11- SMALL INTESTINES -II T10-ll ADRENAL T10-ll
..
- KIDNEY T10-ll KIDNEY T10-ll
ENTIRE COLON --I T10-L2
..
- APPENDIX T12
continued on next page

continuation of autonomic innervation chart:
COMPOSITE AUTONOMIC INNERVATION CHART
PARASYMPATHETIC SYMPATHETIC INNERVATIONS

INNERVATIONS
VISCERA THORACO- REGIONAL CORD SPLANCHNIC COLLATERAL
CRANIOSACRAL LUMBAR AREAS LEVEL NERVES GANGLIA
�
PELV. SPLANCHNICS - LEFT COLON - T12-L2 UPPER URETER TlO-ll
\L') (NONE) ADRENAL - T10-11 LOWER URETER T12-L1
w
VAGUS - UPPER URETER - T10-11
PELV. SPLANCHNICS - LOWER URETER - T12-L1 BLADDER T12-L2
"
- BLADDER (BODY) - T12-L2
BLADDER TRIGONE T12-L2
"
- AND SPHINCTER -
- UTERINE BODY - T12-L2
I
"
"
- PROSTATE - T12-L2
"
- GENITAL CAVERNOUS
TISSUES I
(NONE) - ARMS - T2-8
(NONE) - LEGS - Tll-L2
-
--- �--� -
* PELVIC SPLANCHNIC = S 2, 3, 4 (PARASYMPATHETIC) (c)

1991
In order to use this plan, it is necessary to be familiar with sympathetic and
parasympathetic innervations for groups of organs. This is often where the plan
fails, because a physician may have trouble remembering the autonomic
innervations to organs. For this reason, sympathetic innervations of various
viscera were reviewed in many anatomical and neurological texts where there
seemed to be a wide and variable range of sympathetic innervation to any one
organ. Common visceral innervations were then grouped so that they could be
easily memorized while still maintaining their clinical relevance. The result was
the composite chart of autonomic innervation on pages 192 and 193. This chart
retains credible correlation with all of the different ranges of sympathetic
innervation presented by various authors, but is also much easier to memorize.
Recognize that intense visceral afferent activity from certain clinical situations
may result in a spread of the facilitated cord segments up or down in the
thoracolumbar spinal cord area and result in an increased range of palpable
somatic paraspinal involvement initiated by that organ system dysfunction. It
may even result in the expression of symptoms from other systems or organs
that happen to be innervated by sympathetic fibers from adjacent cord segments.
ll. TREATMENT SYMPATHETIC NERVOUS SYSTEM

DYSFUNCTION:
A. TREATMENT GOALS AND GENERAL MANIPULATIVE

TREATMENT PLAN:
Organs which are primarily or secondarily involved in dysfunction exhibit

characteristic changes or symptomatology of sympathicotonia. Diagnosis and
treatment can be directed to several anatomic-physiologic locations: The
thoracolumbar paraspinal chain ganglia, the collateral sympathetic (preaortic and
cervical) ganglia, through the facilitated spinal cord segments, or through
specific reflex systems such as Chapman' s and Travell' s myofascial points. The
spinal cord segments can be maintained in their facilitated state by being
bombarded by visceral or somatic afferent fibers from visceral and/or somatic
dysfunctions.
Set Goals: Because the sympathetic chain ganglia are anatomically located
anterior to the rib heads, any dysfunction that directly or indirectly and
"chronically" restricts fascia in this region may initiate and/or maintain
excessive sympathetic outflow to their reference organs. It naturally follows
that normal rib motion as well as reduced afferent input from paraspinal muscles
or the viscera, will help to reduce segmental cord facilitation.
194
Abdominal collateral sympathetic ganglia are able to control local and perhaps
some regional autonomic responses without reporting to the CNS. These
ganglia are also in the pathway of the visceral afferents that relay impulses of
GI or pelvic dysfunction to the CNS.
Animal studies have revealed evidence that early manipulation of somatic

dysfunction might act as a form of preventive medicine. Summarizing some of
his animal studies, Patterson1 purports:
o . . Persistent musculoskeletal dysfunction affecting a certain spinal cord

segment can affect the function of an internal organ related to that same
spinal cord segment.
o .. Removal of the musculoskeletal irritation produced by dysfunction allows
the related internal organ to return to its normal function.
o .. If the dysfunction of the musculoskeletal system remains long enough, it
apparently "bums a memory pattern" within the central nervous system
so that when the initial irritating musculoskeletal influence is removed,
the original dysfunction not only continues but grows in severity.
B. RIB RAISING TECHNIQUES:
Ribs should also move well to permit painless, effortless breathing. The
diaphragm is the extrinsic pump of the lymphatic system. Good diaphragmatic
action is supported by treatment of specific rib somatic dysfunction and by rib
raising techniques that increase the depth of respiration. Treatment of somatic
dysfunction and the mechanical principles applied in "rib raising" techniques
provoke maximum excursion of the rib cage, encourage maximum inhalation
and the generation of more effective negative intrathoracic pressure. This
increases lymphatic flow and also relaxes the patient. These techniques also
help to re-establish range-of-motion and thereby reduce excessive afferent input
to facilitated cord segments.
Rib raising is actually the primary manipulative method by which the

osteopathic physician affects the hypersympathetic activity initiated by
dysfunction or disease. Effective rib raising techniques lift and rotate the rib
heads; they, in turn, pull on the fascias that are common to a rib head and its
sympathetic chain ganglion. This initially "stimulates" reflex sympathetic
responses in the related organs, an event which the physician usually wishes to
reduce and prevent, especially as a long term circumstance. Reflex
neurophysiologists explain that the sympathetic activation produced by rib
raising is due to stimulation of fast and very fast efferent sympathetic fibers but
that this response is fairly localized and short lived. They also report that rib
raising techniques will additionally stimulate slow and very slow efferent
sympathetic fibers in the same ganglia and these fibers reflex as high as the
195
medullary centers. These latter reflexes are reported to be inhibitory to the
sympathetic system and also are long acting.
It is important to reduce the sensitivity of the spinal areas demonstrating

increased facilitation first, so that proprioceptor impulses produced by treatment
of other areas will not produce firing of these segments with lowered thresholds.
An optimal treatment protocol strives to maximize the body's own homeostatic
ability to maintain rib motion -- thus, dysfunction of the thoracics, sternum,
diaphragm (including lumbar attachments and cervicophrenic innervation), and
cranial elements might be considered and be appropriately treated. If a
physician applies the basic principles of rib raising treatment, a variety of
techniques can be formulated for utilization in the management of patients who
are in a variety of positions and who have a variety of medical conditions.
RIB RAISING FOR ACUTELY DEBILITATED PATIENTS: PATIENT

SUPINE
o .. Purpose(s):
o . . To decrease sympathetic facilitation

o . . To increase respiratory efficiency and depth
o .. To increase lymphatic return
o .. To reduce general stress and discomfort
o . . The operator sits beside patient and inserts both hands under the patient
contacting the angles of the ribs with the fingers of both hands.
o . . The operator must lift up (toward ceiling) sufficiently to move the rib and
its rib head (sternum should also rise) and pull slightly lateral to the
point of tissue resistance--ease of performing the lift is gained by using
the dorsal surface of the MCP joints as a fulcrum against the bed or
table.
o . . Additional lymphatic and/or respiratory benefits may possibly be gained by
using the hands and/or finger pads to pressure the ribs towards inhalation
(pump handle inhalation encouragement requires a caudal direction from
the finger pads at the posterior aspect of the rib to bring the anterior
portion superiorly; bucket handle rib motion requires a cephalad pull
from the posterior contact). The sympathetic effect of rib raising as
described is probably effective without any of this specially directed
activity.
o .. When the tissues relax, the operator should slowly reposition his or her
hands onto the next group of adjacent untreated rib angles and repeat the
procedure. The other side of the rib cage is treated in the same manner
until the entire rib cage has been treated.
196
RIB RAISING TECHNIQUE FOR LESS DEBILITATED PATIENTS:
PATIENT SUPINE
0 . . Purpose(s): Same as above.

o . . The operator stands at the head of the patient.
o . . The patient is supine and reaches up with both arms over head to encourage
raising of the ribs and in some manner, affixes hands around the
posterior aspect of the operator's waist or to a belt (or other material).
o .. The operator contacts the patient's rib angles by sliding the hands under
each side of the chest cage (approaching the rib angles from the sides of
the rib cage).
o .. The operator must lift up (toward ceiling) and lean backward sufficiently to
move the ribs and their rib heads.
o .. As the operator lifts and leans backwards and downward, the pull through
the patient's arms stretches the pectoral and latissimus dorsi muscles,
encouraging the ribs into inhalation
o .. This lift from the head of the bed or table is repeated until the ribs move
easily.
RIB RAISING FOR A SEATED PATIENT:
This is an especially helpful technique for patients that are uncomfortable or

unable to lie down.
o . . Patient is seated with arms crossed, the shoulders are flexed and the head
rested on the arms
o . . Operator stands at side of patient and supports the crossed arms with one
upper extremity; the other hand is placed across the patient's thoracic
spine contacting bilaterally as much of the rib as possible
o . . The patient is instructed to relax their back and allow their weight to fall
forward onto the operator's supporting arm
o . . The operator lifts and allows the patient to transfer their weight farther
forward onto the supporting arm; the other hand is used to create a
fulcrum in the thoracic spine for backward bending
o . . The process above is applied to the entire rib cage as is comfortable to the
patient
197
MUSCLES USED IN MUSCLE ENERGY RIB TECHNIQUES USED TO
ELEVATE OR DEPRESS RIB SOMATIC DYSFUNCTIONS (SD) :
Muscles used to elevate exhalation rib SO
Scale nes ............................................ ................. Ribs 1 -2

Pectoralis Mi nor ....... ... .. . Ribs 3,4,5 (6) Ribs 3,4,5
Serratus Anterior .......... . . . Ribs 6,7,8,9,10
Latissimus Dorsi - Ribs 9,10, 1 1 , 12
(Quadratus Lumborum) R i b 12 (Indirectly) Ribs 6,7,8
Intercostals ..................................................... Forced inhalatio n
Muscles used to depress inhalation rib SO Ribs 9,10

1 1 ,12
Quadratus Lumborum Rib 12 (directly)
I ntercostalis ······························· · ··· ····· ······
Forced exhalation
A. Scalene Muscles
B . Pectoralis Minor Muscle
C. Serratus Anterior Muscle
D. Latissimus Dorsi Muscle
THE ILEUS PREVENTION TREATMENT: ("RIB RAISING" AREAS

WITHOUT RIBS)
Producing the effects of rib raising in these segments could not be performed
through rib heads. The following describes an inhibition technique for the LI to
L2 spinal area, but the same technique can be used to treat the effects of
hypersympathetic outflow in the thoracic area.
o . . The patient is supine and the physician is seated at the side of the patient.
o . . The physician passes both hands under the back the patient to a point where
the finger tips are on one side and the thenar and hypothenar eminences
are on the other side of the erector spinae mass (ESM).
o . . The hands are then closed, pulling the two erector spinae mass muscles
toward each other between the fingers and the thenar/hypothenar
eminences of the operator.
o This maneuver automatically lifts or backward bends the spinal region
_ .
located above the hands. If the operator's hands were in an area of ribs,
this backward bending would be enough to perform effective rib raising.
198
o . . The pressure on the operator' s fingers and heel of the hands is equalized by
altering the pressure on these structures, resulting in a slight rotation of
the patient' s body to the right or left.
o . . Further balance between the hands and the patient' s back is adjusted by
pushing or pulling one forearm away or toward the operator' s body until
the pressure on the two hands is about equal.
0 When pressures are balanced, the hands remain gripping the ESM until
• .
there is a sense of relaxation (usually about 60-90 seconds) .

o . . Re-gripping the ESM should reveal less resistance of the tissues indicating
that there has been a favorable response to the treatment.
�
This is a description of the soft tissue techni ue called the "ileus prevention
treatment. " This technique has been proven in the clinical arena, preventing
and treating postoperative ileus.
c. ABDOMINAL COLLATERAL GANGLIA:
There are three main sympathetic �::':,:l----:"" CEUAC

collateral ganglia in the abdominal
area; these are the celiac, the 1---- SUPERIOR
MESENTERIC
superior mesenteric, and the inferior
mesenteric ganglia. These ganglia INFERIOR
MESENTERIC
are located in the immediate
preaortic area and posterior to an
imaginary line drawn from the
xiphoid process to the umbilicus.
The celiac ganglion is usually separated into a right and a left ganglion.
Functionally the celiac ganglion innervates the upper GI tract (stomach,
duodenum, liver, gallbladder, pancreas and spleen) . The superior mesenteric
ganglion is located around the base of the superior mesenteric artery and
innervates the entire small intestine below the duodenum , the right side of the
colon, and also the kidneys, adrenals and the gonads. The inferior mesenteric
ganglion, located around the base of the inferior mesenteric artery, supplies the
left colon and the pelvic organs (except for the gonads) .
199
DIAGNOSIS OF FACILITATION OF AN ABDOMINAL COLLATERAL
GANGLION:
o . . The extended fingers of both hands are placed over the midline of the
abdomen between the xiphoid process and the umbilicus
o . . The longer fingers are bent slightly to produce fingers of equal length and
therefore fingers that will make equal depth of penetration when pressure
is applied
o . . Objective sensation of a rapid increase in residence as pressure is directed
by extended fingers applied against the abdominal wall and directly over
the ganglion
o . . Subjective complaint of increased tenderness with mild to moderate
pressure
o . . Positive responses to questioning of the patient regarding signs and
symptoms related to the organ or organs innervated by the tender
ganglion
GANGLION INHIBITION TREATMENT TECHNIQUE:
o . . The extended fingers of both hands are placed over the midline of the
abdomen and over the tender involved (facilitated) ganglion
o . . The longer fingers are bent slightly to produce fingers of equal length and
therefore fingers that will make equal depth of penetration when pressure
is applied
o . . The patient takes a half-breath in against the operator' s finger resistence and
holds it as long as possible
o . . With exhalation, the operator follows the tissues in until a new point of
resistence is met; the breathing cycle is repeated
o . . Posterior pressure is applied and increased to a point where the resistance is
evident and the pressure is tolerable to the patient
o . . This pressure is held until the relaxation of resistance is experienced by the
physician or the pressure has been maintained for about 90 seconds.
o . . Recheck diagnostic pressure over the ganglion should indicate significant
reduction in subjective complaint and a palpable reduction in tissue
resistance
D. CHAPMAN'S REFLEXES: DIAGNOSIS
Chapman ' s reflexes were recorded by Owen in a book entitled Chapman

Reflexes: Owen 's Endocrine Inte[pretation . The points seem better related to
the sympathetic system than to the endocrine system. Chapman charted anterior
and posterior myofascial points where tenderness to mild to moderate pressure
was related to organ dysfunction in a predictable organ. (See charts on pages
232 and 233). Like any diagnostic system, positive findings in this non
invasive system of diagnosis must be correlated and interpreted with other
200
historical and physical findings of visceral dysfunction. Their presence should
also be correlated with other findings of sympathetic hyperactivity. Since the
anterior points are more sensitive and more spread out than posterior points,
they are usually used for diagnosis and the posterior points are used for
treatment. A tender anterior Chapman point indicates a possible organ
dysfunction requiring further history and physical evaluation. The anterior
points are also used to evaluate the success of treatment of that organ
dysfunction or disease .
Diagnostically, Chapman ' s reflex points should be sought prior to any

manipUlative treatment which might modify their presence. Most physicians use
the anterior Chapman points for an aid to diagnosis of systemic diseases but do
not use the original Chapman treatment techniques.
CHAPMAN'S REFLEXES: TREATMENT
3
In the original Chapman method , after treating pelvic somatic dysfunction , the
posterior points were treated first using a circular type of soft tissue
manipulation. The anterior points were only used for treatment if the posterior
treatment was unsuccessful. Some physicians proposed that the treatment of all
points related to the same visceral system be utilized to enhance homeostatic
function of that system.
Using the original treatment method, posterior Chapman ' s points were treated
by performing circular soft tissue treatment over the tender posterior point for
20 to 30 seconds. The anterior Chapman ' s points are usually too tender to treat
with this soft tissue procedure. The anterior tibial bands (relating to the colon)
are an exception to this. These points are very susceptible to circular soft tissue
or rapid mechanical pressure to produce reflex autonomic normalization in the
colon for such syndromes as irritable bowel syndrome, post-viral diarrhea and
ulcerative colitis.
Posterior myofascial points by Chapman were treated with a circular soft tissue
technique to produce reflex changes in the viscera and improve organ function.
This is effective, but the paraspinal soft tissue used by most osteopathic
physicians during their manipulative management of a patient produces similar
results and could be directed to the areas of somatic change. Charts of
Chapman ' s reflexes are available through the Department of Osteopathic Theory
and Methods at the Kirksville College of Osteopathic Medicine. 4
E. THE CERVICAL GANGLIA:
The cervical sympathetic ganglia are not in the thoracolumbar outflow and they
certainly do not fit into the rib raising mechanisms; but they are important in
sympathetic responses in the body, especially the heart and structures of the
201
head (sinuses) and neck. Eight original cervical paraspinal ganglia have
coalesced to form 2 or 3 cervical ganglia (the superior, middle, and sometimes
the inferior). They would be just like any other paraspinal ganglia except that
the cell bodies for these cervical ganglia are located at spinal levels TI-4.
The inferior cervical ganglion lies on the

ventral surface of the head of the first rib
and is frequently fused with the first
thoracic ganglion to form the stellate
"+=::::¥- Superior Ganglion
ganglion. It serves C7, C8, and TI (and
sometimes C6). The middle cervical
ganglion lies approximately at the level of
the C6 vertebra and has connections with
C5 and C6 (and sometimes C4 and C7).
The superior cervical ganglion is a long
ganglion that lies anterior to the transverse \��iddle Cervical
processes of C2, C3, and C4 and sends Ganglion
sympathetic fibers to cervical nerves C I -4. ---... nl••nnr Cervical
Ganglion
Each of the three cervical ganglia sends a
cardiac nerve to one of the cardiac Subclavian Artery
plexuses.
The fascias around these ganglia are closely related to the cervical joints and the
fascial planes of the neck. The cervical ganglia and their activity can be
compromised by somatic dysfunction in the cervical joints or by abnormal
tensions in the cervical fascias. Sinusitis, ear or eye dysfunctions, cardiac
tachyarrhythmias, and other cardiac dysfunctions may be altered by freeing
cervical pathways and treating cervical joint somatic dysfunctions. This is
especially true in the C I -4 and the cervicothoracic junction areas.
ill. TREATMENT FOR LYMPHATIC SYSTEM DYSFUNCTION:
A. BASICS: Goals of Treatment and General Manipulative Treatment

Plan:
o . . To promote the free flow of lymph through its lymphatic vessels and fascial
pathways. These pathways extend from interstitial tissue spaces to the
venous circulation in the upper chest via the right and left lymphatic
ducts.
o . . To improve function of the abdominal diaphragm, the extrinsic pump for
the lymphatic system.
o . . To reduce sympathetic outflow.
202
o . . The cervicothoracic diaphragm is a common pathway in the course of
lymph drainage from any place in the body. For this reason, the
thoracic inlet is diagnosed for fascial rotational preference and treated as
indicated.
o . . Tensions in fascial planes and the other regional myofascial diaphragms
located at the junctions of structural change also hinder the flow of
lymph. For this reason, the other three fascial and muscular diaphragms
may be diagnosed and treated as indicated (craniocervical, abdominal
and pelvic).
The paraspinal musculature at the thoracolumbar junction is relaxed by

soft tissue, stretching, and/or myofascial treatments. The abdominal
diaphragm is then redomed.
The pelvic diaphragm works synchronously and passively with the

abdominal diaphragm to produce optimal pressure gradients between the
thoracic and abdominal cavities.
o . . Lymphatic pump techniques are used to encourage lymphatic flow through

the pathways
o . . Rib raising in areas of major venous and lymphatic vessels is often
necessary because hypersympathetic tone will constrict the larger veins
promoting congestion of tissues in that vein' s region of drainage;
hypersympathetic tone also constricts the larger lymphatic vessels and
restricts the drainage of lymph from their regions.
B. SYMPTOMS OF FASCIAL DYSFUNCTION:
POSTURAL SYMPTOMS:
Whenever there is dysfunction or disease, the body 's tissues and systems must
participate in the establishment of a new homeostatic level for body function.
The type, severity and site of the stress determines which systems will need to
compensate the most; the neuromusculoskeletal system is involved in all
dysfunctions and disease processes.
Postural diagnosis provides an uncomplicated, non-invasive access to the

obvious expression of the function of the entire person. Structurally, the AP
and lateral curves are affected by gravity. Lateral curves may develop and are
particularly affected by inequality of the sacral base from such conditions as a
short leg or a sacral shear, or from an unlevel cranial base as may occur with
birth injury or certain somatic dysfunctions in this region. When no cause for
scoliosis is found its etiology is termed idiopathic; Osteopathic recognition of
these postural causes allows re-classification of some previously diagnosed
idiopathic scolioses. Rotational curvatures are often maintained by regional
203
fascial plane rotations or torsions. It is well known that the emotions may be
mirrored in the posture of a person. It has been clinically observed that postural
imbalance which initially affects any one of the three cardinal planes of the
body will also affect the remaining two body planes and the total posture of the
patient.
A " short leg" may result from a congenital developmental defect or it can be
produced by a leg fracture, by muscle spasm, or by physiologic or
nonphysiologic joint somatic dysfunctions. Sometimes the myofascial
compensation is so good that a spine appears to be straight even when there is a
very obvious short leg. With time, however, the person will develop lateral
scoliotic curvatures of the spine. Since sidebending motion of the spine is
always accompanied by rotation, these lateral curves are often said to exhibit
rotoscoliosis.
SYSTEMIC CHANGES:
In the supine position, normally the motion generated by quiet breathing should
be observed "down to the pubic symphysis. " Failure to observe this in a patient
suggests that the diaphragm is not contracting from a well-domed starting
position , is contracting poorly, or is demonstrating asymmetrical of contraction
between the right and left hemidiaphragm. Poor respiratory function results in a
wide range of congestive symptoms which vary some depending upon which
tissues or system of tissues are congested. Healthy tissue and good function
depends upon adequate circulation and removal of excessive interstitial fluids
from the tissues and their return to the venous system and the heart. Venous
and lymphatic drainage depend on good abdominal diaphragmatic action and
effective pressure gradients between the abdominal and thoracic cavities.
Examples of symptoms and signs from various areas of congestion are listed
below:
PELVIS LEGS BEAD ( CHS )
hemorrhoids edema malaise

varicosities night cramps confusion
diz ziness
SPINE ( CHS ) BOWEL nausea
irritability
Backaches constipation headaches
204
Whenever fascias are subjected to prolonged abnormal physical or chemical
stress they become thickened and reinforced by fibroblastic activity. The large
non-aqueous molecules of the interstitial edema will also stimulate
fibroproliferation and subsequent fibrosis if it they are not properly reabsorbed.
Fibrosis shortens the supporting tissues and impairs joint and general body
motions. The chronic pull of shortened fascias on bony attachments may result
in excessive proliferation of bone called spurs which can be seen on x-ray.
Chronic congestion also results in contractures and/or calcification as well as
generally compromising the intercellular environment of the tissues involved.
OTHER SYMPfOMS AND SIGNS OF FASCIAL DYSFUNCTION:
fascial preference tissue congestion thickened fascias

tissue contracture restricted motion ticklishness
tenderness shortness of breath faulty posture
poor circulation myofascial points strains / sprains
limitation of motion trophic skin changes muscle cramps
" not breathing down to the pubes "

costal breathing by a relaxed person
increased lumbar lordosis in the supine relaxed patient
pain on palpation over fascial dysfunction especially near
areas of fascial attachments, at points of fascial
calcification,and where forces of stress converge
general fatigue or malaise with no physical or laboratory
tests indicate disease.
C. DIAGNOSTIC AREAS INDICATING

REGIONAL TISSUE CONGESTION:
Because of the arrangement of regional lymphatic and venous drainage

channels, fascial stress is revealed in body fascial patterns, preferences in
regional fascial plane motion and congestive changes in the soft tissues,
especially in spinal areas where there is a change in structure or function from
one region to the next.
Tissue congestion in certain key areas of the body provide a clue to congestive
dysfunction in designated body regions. Regional congestion can be suspected
by palpating tissue texture changes at these specific sites.
o . . Bogginess or edema in the supraclavicular area indicates evidence of tissue

congestion from poor lymphatic drainage and dysfunction somewhere in
the head and neck.
205
o . . Fullness and tenderness on palpation of the posterior axillary fold indicates
congestion, poor lymphatic drainage, and dysfunction somewhere in the
upper extremity.
o . . Bogginess in the epigastric area around the xiphoid process means
congestion, poor lymphatic drainage, and dysfunction somewhere in the
abdomen.
o . . Bogginess in the inguinal area means congestion, poor lymphatic drainage,
and dysfunction somewhere in the lower extremity.
o . . Bogginess in the popliteal space--problem is in the knee, leg, or foot.
o . . Bogginess just anterior to Achilles tendon or thickening of the Achilles
tendon itself--problem is in the ankle or foot.
Sites of Terminal Lymphatic

Drainage Dysfunction
A. Supraclavicular Space
B. Posterior Axillary Fold "Arm"
C. Epigastric Area
"Abdomen and Chest"
D. I ngui nal Area

"Lower Extremity"
E. Popliteal Space "Leg"
F. Achilles Tendon
"Ankle and Foot"
Inhalation, with contraction of the abdominal diaphragm, produces negative

intrathoracic pressure and positive intra-abdominal pressure because of fascial
compartmentalization. With diaphragmatic relaxation, intrathoracic pressure is
relatively increased and intra-abdominal pressure is relatively decreased. This
reciprocal action of the diaphragm produces pressure gradients between the two
cavities of the body and along with the one-way valves in the veins and large
lymphatic vessels, aids venous return and provides an extrinsic pump
mechanism for the movement of lymph through the lymphatic vessels, back to
the central circulation and the heart.
206
Diaphragmatic action is most efficient when the diaphragm is well domed, its
nerve supply via the phrenic nerve (C3, 4, 5) is not compromised, and the
lymphatic pathways are unhindered. Fascial restrictions and torsions of fascial
pathways and diaphragms can lead to passive congestion and dysfunction of the
lymphatics, the lungs, and other body systems and tissues.
Clinical Principle: The most common site for relative obstruction to

lymphatic flow, no matter what tissue of the body is congested , is the
fascial diaphragm at the thoracic inlet, the cervicothoracic diaphragm
(Sibson ' s fascia) .
D. FASCIAL PATTERNS FOR DIAGNOSIS OF REGIONAL FASCIAL

DYSFUNCTION:
Fascias are affected by a person ' s structural and functional stresses even when
that person believes that he/she is healthy. Gravity is one of the significant
natural stressors affecting upright body posture; and the fascias can be examined
for evidence of compromised homeostatic mechanisms.
COMPENSATED PATTERN �f UNCOMPE NSATED PATTERN 1

r OA
- ALTERNATI NG NOT ALTERNATING
FASCIAL PATTERNS
ACCORDING TO GORDON ZINK, D.O.
207
r. Gordon Zink, D.O. , FAAO, (formerly at the University of Osteopathic
Medicine and Health Sciences at Des Moines, Iowa) popularized the use of
fascial diagnosis and treatment. Zink had clinically studied postural patterns
and observed that almost all of the people who thought that they were well had
alternating fascial patterns rather than the ideal, in which no fascial preference
was palpated. Fascial direction alternated at anatomical " transition" sites: the
occipitoatlantal area, the cervicothoracic area, the thoracolumbar area, and the
lumbosacral area. Alternation of fascial patterns is a homeostatic postural
response providing compensation when the ideal cannot be reached.
Alternating patterns are termed compensatory fascial patterns. Zink then found
that 80% of the "well people" had a particular compensatory pattern in which
there was preference for its rotation to the left at the occipitoatlantal area, to the
right at the cervicothoracic area, to the left at the thoracolumbar area and to the
right at the lumbosacral area (i.e. leftlrightlleftlright or L,R,L,R). Because this
pattern was so common he named it the "Common Compensatory Pattern
(CCP) " and the clinicians often add the words, "of Zink" in recognition of his
contribution.
Most of the 20% remaining who thought they were well also had a compensated
fascial pattern but it was just the opposite of the Common Compensatory
Pattern. The motion preference of the fascias at the four reference areas in
these subjects was rightlleftlrightlleft (i.e. RlLIRlL). Dr. Zink termed this the
"uncommon compensatory pattern. II
Those people who do not have the ideal fascial pattern and who are not
homeostatically capable of reaching one of the compensatory patterns are said to
have an uncompensated fascial pattern. This means that fascial preferences do
not alternate in direction from one reference area to the next. Non-compensated
patterns often have a traumatic origin.
Rather than list the preferred fascial plane motion at each area when recording
structural findings on a physical examination or talking to someone about a
person I s fascial patterns, the student or physician may write or state something
like one of the following:
o . . the fascial pattern is ideal.
o . . the fascial pattern is in the common compensatory pattern of Zink.
o . . according to the Zink patterns, the fascia is out of the CCP at. . . (and then
names the area or areas that do not fit the CCP.)
o . . the uncommon compensatory pattern according to Zink is present. .
208
Dr. Zink observed that if a person' s fascias fit the ideal pattern (equal
preference to sidebending and rotation right and left in all of these body areas or
had one of the compensatory patterns identified as the CCP of L,R,L,R
rotations respectively or the uncommon compensatory pattern of R,L,R,L), they
tolerated stress, somatic dysfunction, illness, and disease better, responded to
medical care more predictably, and recovered quicker and more completely than
persons who had an uncompensated fascial pattern.
E. THE FASCIAL DIAPHRAGMS, OTHER PATHWAYS, AND THEIR

TREATMENTS:
SOFT TISSUE DIAGNOSIS OF THE THORACIC INLET:
The anatomical thoracic inlet is defined as being outlined by the manubrium, the
right and left first rib and the first thoracic vertebra. The functional thoracic
inlet is the clinical thoracic inlet and is defined as being the manubrium with the
angle of Louis, the first two ribs on each side and the first four thoracic
vertebrae. When an osteopathic physician talks about the thoracic inlet he/she
almost always means this functional thoracic inlet.
This diagram illustrates the thoracic inlet and illustrates the important static
landmarks that are used in the diagnosis of fascial rotational preference (torsion)
of the thoracic inlet.
Infraclavicular Space
/ "'
LBft Right
L R
left Rib HeadlNeck Area

1st Rib
The thoracic inlet is divided into two parts by the mediastinum with the
remaining spaces (one on each side of the mediastinum) providing an opening
through which the apex of the right and left lungs project upward into the
209
cervical area to a height of about 2.5-3 cm above the clavicles. The apices of
the lungs and the thoracic inlet are covered by Sib son ' s fascia.
These thick cupolae are formed from fascias from the longus coli muscle deep
in the cervicothoracic area and from the fascias on the inner surfaces of the
scalenus anticus, medius and posticus muscles laterally. Both the left and the
right lymphatic ducts of the body must pass through this diaphragm. The
rotational preference of these fascias should be evaluated mechanically
whenever there is an upset of fluid homeostasis anywhere in the body.
The thoracic duct (the left lymphatic duct) passes through the cervicothoracic
diaphragm once, travels 3-4 cm up into the neck to a level approximately lateral
to the left transverse process of the C7 vertebra, makes a U-turn, and comes
back down through this fascial diaphragm the second time into the thoracic cage
where it empties into the venous system at the junction of the left subclavian and
left internal jugular veins. The right lymphatic duct also passes through the
thoracic inlet, but only once. ([he site at which the lymphatic ducts empty into
the venous system may vary slightly. They enter into the region of the
brachiocephalic vein.)
When palpating the thoracic inlet of a seated patient, the palpating fingers must
be close enough to the vertebral column at Tl so that they are over the
costovertebral and costotransverse area of the first rib. Is one side higher than
the other? If one rib head seems to be elevated in relation to the other, it may
indicate somatic dysfunction of the first rib. It may also mean that the fascias
of the cervicothoracic junction (the thoracic inlet) are holding the
cervicothoracic region of the body, sidebent and rotated to the side opposite the
elevated rib. The first thoracic vertebra may also exhibit a neutral type somatic
dysfunction which will be sidebent to the opposite side and rotated to the same
side. In all of these cases, the rib head will be tender to the patient on the side
of the palpable "elevated rib head ; " differential diagnosis is then necessary.
If the infraclavicular spaces near the manubrium are equal in depth, there could
be an elevated rib or the first thoracic vertebra could be sidebent to the opposite
side, producing a secondary elevation of the first rib head. If the infraclavicular
space is more shallow on the same side as the elevated first rib head then a
rotational fascial preference of the thoracic inlet is present.
Examples: (x = one direction and y is the opposite direction)
An elevated and tender first rib on side x and a shallow infraclavicular

space on side x indicates that the fascial pattern of the thoracic inlet is
sidebent and rotated y.
2 10
An elevated and tender first rib on side x with an equal depth to the
infraclavicular spaces on side x and y, indicates that this is not due to
fascial dysfunction of the thoracic inlet. These changes could mean an
elevated first rib on side x orland a neutral type first thoracic vertebral
somatic dysfunction with sidebending y.
As with all diagnoses of somatic dysfunction, motion testing is the final

and most reliable verification.
The thoracic inlet of a patient whose general body fascias are in the Common
Compensatory Pattern of Zink will have the left first rib elevated and the right
infraclavicular space will be deeper (the left infraclavicular space near the
sternum more shallow).
The apex of the coracoclavicular angle on the left will be more anterior than on
the right. The following diagram illustrates the fascial rotational preference of
the thoracic inlet as it would be found in a patient whose total body fascial
pattern agrees with the CCP of Zink.
Infraclavicular Spaces
� "
Left Right
Shallow Deeper
-- R
L
Left Rib HeadlNeck Area

1st Rib Elevated
It is important to remember that the fascial patterns from all of the four
junctional areas must be diagnosed before one knows if any one fascial pattern
is in agreement with a compensated or uncompensated pattern. The following
diagram illustrates fascial patterns that are pulling the inlet into sidebending left
and rotation left as would be found in a patient who had the other patterns
compatible with the uncommon compensatory pattern of Zink.
211
� Fascial Ease Fascial Drag -..
o Rib Resilience CD Rib Resistance
L R
MANIPULATIVE TREATMENT OF THE THORACIC INLET

(CERVICOTHORACIC DIAPHRAGM) :
MANIPULATION OF THE THORACIC INLET WITH INDIRECT

MYOFASCIAL UNWINDING TREATMENT:
o . . The patient may be sitting or supine.

o . . The operator' s hands bridge each shoulder with the fingers anterior and the
thumbs posterior.
o . . The tissues are followed in their preference for sidebending and rotation
and held in that position as the patient breaths in and out.
o . . The operator follows the tissue preferences until the tissues approach the
midline again.
MANIPULATION OF THE THORACIC INLET BY TWO-STEP DIRECT

TECHNIQUE:
o . . The patient is supine.
2 12
Step One (correction of sidebending component) :
o . . The operator's MP joint of one hand is placed at the posterolateral

cervicothoracic junction and will be used as a fulcrum for direct method
sidebending.
o . . The head and neck is taken as a unit and sidebent to the restrictive barrier.
o . . The patient' s head is turned to the opposite side to lock the cervical spine.
o . . Adjustment of the sagittal plane localizes the forces at the cervicothoracic
junction and a thrust is carried through the fulcrum hand toward the
opposite axilla while the cephalic hand counters the sidebending thrust.
(Rx sidebending component)
Step Two (correction of rotational component):
o . . A fulcrum is placed at the cervicothoracic junction (CT) on the other side

and the head and neck is rotated to the rotational barrier at the
cervicothoracic inlet, without sidebending the neck.
o . . The sagittal plane and sometimes a slight sidebending adjustment is made to
localize well and a rotational thrust is made through the rotational barrier
at the CT junction.
MANIPULATION OF THE THORACIC INLET IN SITTING ONE STEP

TECHNIQUE:
o . . The patient is sitting.

o . . The operator's hand on the side of the patient's somatic dysfunction is
placed on the patient's shoulder.
o . . The operator' s foot on the side opposite the somatic dysfunction is placed
on the table next to the patient and the patient' s arm on that side is
draped over the operator's thigh.
o . . The operator's thumb is placed on the spinous process of TI , the opposite
hand is placed along side the patient's head and neck on the opposite
side, and the patient's head is sidebent toward the side of the CT somatic
dysfunction; the head is extended to localize and the patient' s body is
directed into a posterior and sidebent away position by guidance through
the operator's knee.
o . . When all forces are localized there is a thrust with the thumb on the T l
spinous process away from the side of somatic dysfunction (this reverses
the rotation) and at the same time, (because of position of the patient' s
neck) sidebending is reversed.
2 13
DIAGNOSIS AND TREATMENT OF THE ABDOMINAL DIAPHRAGM
DIAGNOSIS OF THE THORACOABDOMINAL DIAPHRAGM (THE

EXTRINSIC PUMP FOR THE LYMPHATIC SYSTEM):
The thoracoabdominal diaphragm at the thoracolumbar region (TL) is the main

extrinsic pump for the lymphatic system. Diaphragmatic dysfunction is
suspected when respiratory effort does not produce movement of the abdominal
tissues down to the level of the pubic symphysis. Elements of this dysfunction
can be diagnosed indirectly through the fascias using one flat hand in the
epigastric area and the posterior hand at the thoracolumbar junction to examine
for palpatory preference of rotation about an anterior/posterior (AP) axis.
Other elements can be diagnosed by directly attempting to rotate the
thoracolumbar "tube" right and then left. Once the diagnosis of the myofascial
preference is known, treatment can be effectively applied. Lasting effect from a
redoming manipulative technique to the thoracoabdominal diaphragm often
depends on removing dysfunction of its attachments and functional extensions.
This includes proper treatment of somatic dysfunction of LI-3, the lower six
ribs, and reduction of lumbar lordosis. The role of quadratus lumborum
dysfunction in inhibiting the effectiveness of these techniques should be noted
and it is important to remember that the diaphragm is innervated by the phrenic
nerve, C3,4,5. It seems prudent to manipulate any somatic dysfunction found
in the lumbars, lower ribs, quadratus lumborum muscle, pelvis, and the
iliopsoas muscle first.
MANIPULATIVE TREATMENT IN PREPARATION FOR DIAPHRAGM

REDOMING:
If there is increased tone in the thoracolumbar paraspinal musculature and

increased lumbar lordosis, utilize any and all methods of soft tissue kneading,
stretch, and/or myofascial treatment to relax the region.
TREATMENT FOR QUADRATUS LUMBORUM SPASM OR LUMBAR

PARA VERTEBRAL MUSCLE SPASM:
The primary intent of treatment is to stretch the quadratus lumborum and re
establish normal 12th rib motion. The following example of a direct method
treatment uses respiratory cooperation of the patient.
o . . The patient is prone; the arm on the side of dysfunction is resting by the
side of the head.
o . . The lower extremities are moved to the edge of the table away from the
side of myofascial dysfunction.
2 14
o . . The operator stands on the side opposite the dysfunction and contacts the
shaft of the 12th rib with the full length of the thumb on the cephalic
hand, to stabilize the rib.
o . . The pelvis is grasped with the fingers of the caudal hand by curling the
fingers around the anterior superior iliac spine (ASIS).
o .. The operator's contacts are separated by lifting the pelvis and carrying the
rib anterior and superior.
o . . The patient is instructed to inhale as the operator maintains tension at the
contacts. Muscle energy is applied by having the patient pull the ASIS
toward the table against resistance.
o . . Traction/separation is increased to take up slack when the patient exhales
and relaxes; the same procedure with respiratory cooperation is repeated.
Stretching of the quadratus lumborum can also be performed with the patient in
the lateral recumbent position. With the patient in this position, the side of
dysfunction is up and there is a pillow under the opposite side. Increased
stretch can be achieved by dropping the patient' s feet off the side of the table.
Sometimes, spray and stretch of quadratus lumborum myofascial trigger

point(s), as described by Travell, is necessary in recurrent or recalcitrant
dysfunction. 5
TI...IOPSOAS RELEASE TREATMENT:
See Jones Strain/Counterstrain indirect method for treatment applicable to acute

situations. Example: The lower extremities of the supine patient are flexed
externally rotated, and sidebent until 70% or more of the subjective tenderness
over the iliacus counterstrain point is relieved. This position is held 90 seconds
and then passively returned to a neutral position. If not acute, direct stretch
using muscle energy and exercise is very appropriate.
DIRECT (STRETCH) METHOD TREATMENT OF THE ABDOMINAL

DIAPHRAGM:
o . . The patient is supine and the operator stands at the head or at the side of
the table
0 • • The margins of the lower rib cage are gently grasped and pulled and/or
pushed to its rotation restriction and held as the patient deeply breathes
in and out
o . . Sometimes a superior or inferior vector is added to the direct rotation of
the thoracic cage so that there is good palpable movement of both sides
of the diaphragm during deep breathing, i.e. both leaves of the
diaphragm are moving well.
2 15
o . . This position is held for about three big breaths so that the fascial
preference is eliminated and the respiratory effort has redomed the
diaphragm.
INDIRECT METHOD OF TREATMENT FOR THE ABDOMINAL

DIAPHRAGM:
o . . The patient is supine and the operator stands at the side of the table.
0 . . The operator' s caudal hand is placed on the abdomen with the fingers
immediately below the xiphoid process (the anterior attachment of the
abdominal diaphragm); the cephalad hand contacts and bridges the
paraspinal regions from LI-3 (posterior attachment of the abdominal
diaphragm).
o . . The operator' s caudal hand produces clockwise and counterclockwise
motion in the abdominal fascias to determine direction of fascial
freedom.
o . . The abdominal fascias are held in the direction of freedom with one hand
and the fascias of the paraspinal tissues at the thoracolumbar junction are
held in the opposite direction. The tissues are balanced in this position
until release is appreciated.
DIAGNOSIS AND MANIPULATIVE TECHNIQUES OF THE PELVIC

DIAPHRAGM:
The pelvic diaphragm is diagnosed by pressing extended fingers into the lateral
side of the ischiorectal fossa; or placing the thumbs into the upper posterolateral
margin of the ischiorectal fossa; or through evaluation of the muscles of the
pelvic diaphragm during a rectal or vaginal examination. The pelvic diaphragm
can be treated through the perineum, through the rectum, or through the vagina.
Daily pelvic coil or Kegel exercises by the patient at home helps to maintain
pelvic tone after a successful manipulative treatment.
ISCHIORECTAL FOSSA TREATMENT: (a fascial release treatment)
o . . The patient is lateral recumbent with the fossa to be treated away from the
table; or the patient could be supine. In either of these positions, the
patient has the hips and knees flexed 90 degrees. The patient could be
prone but in that position the hips could not be flexed 90 degrees.
o . . The operator stands behind the table or at the foot of the table, identifies the
ischial tuberosity and the coccyx, and then uses the extended fingers to
contact the lateral margin of that ischiorectal fossa (the interphalangeal
joints are fully extended and the metacarpophalangeal joints slightly
flexed; the wrist is held rigid) .
o . . The operator sometimes sits on the table and braces the elbow aginst his/her
own ilium.
216
o . . The operator' s cephalic hand may be placed on the patient' s hip for
counterforce.
o . . The fmgertips are gently inserted to compress the fat of the fossa as far as
allowed by the fascias and as is tolerated by the patient.
o . . Tension (and direction of treatment) will be slightly more posterior if rectal
problems are present, more anterior (but still in the ischiorectal fossa) if
bladder problems are present, and just superior if ovarian and/or broad
ligament congestion is present.
o . . The patient is asked to breathe in and exhale; the fmgers drift more
superiorly as the fingers follow the diaphragm with exhalation; the push
of the pelvic diaphragm is resisted when the patient inhales.
INTRAVAGINAL FASCIAL RELEASE:
o . . The muscle and fascia of the pelvic diaphragm and their areas of tension are
identified by sweeping laterally over the pelvic wall.
o . . The fingers are spread in the transverse plane of the vagina to hold the
orifice open
o . . The patient is then asked to cough shan>ly 2 or 3 times and the fascia and
pelvic muscular diaphragm are automatically stretched by contact with
the operator's fingers.
o . . The pelvic diaphragm is again palpated to evaluate the treatment's effect on
.
the tense tissues.
INTRARECTAL FASCIAL RELEASE: The principles for stretch of pelvic

diaphragm are similar to those used in the intravaginal treatment but are carried
out through the rectum using a single gloved finger and a good lubricant. The
pelvic diaphragm is palpable through the rectal wall and the location of tension
is mentally recorded. Cough is not used to activate; rather, the fingers press
firmly and steadily without hurting the patient, until relaxation of the pelvic
diaphragm is palpable.
MANIPULATION OF THE CRANIAL DIAPHRAGM:
Not all physicians are able to utilize cranial diagnosis and treatment; but
condylar decompression and muscle energy to stretch the OA fascia can be
performed easily by any physician with manipulative skills.
Diagnosis and cranial treatment can be studied by taking specific undergraduate

or postgraduate courses in this field. An important reference text is Harold
Magoun 's book, Osteopathy in the Cranial Field. Contact the Sutherland
Cranial Teaching Foundation, the American Academy of Osteopathy or the
Cranial Academy for postgraduate CME courses.
2 17
IV. OTIIER SOFT TISSUE TREATMENTS TO AID IN LYMPHATIC
DRAINAGE
LYMPHATIC PUMP TECHNIQUFB:
THE GOALS OF LYMPHATIC PUMP PROCEDURES:
o .. to accentuate negative intrathoracic pressure

o .. to increase venous and lymphatic return
o .. to increase homeostasis (immune function)
o .. to mobilize fluids
o .. to mobilize thick plugs of mucus (vibratory treatment)
TREATMENT WITH USE OF LYMPHATIC PUMPS:
THORACIC LYMPHATIC PUMP TREATMENT: This works by

increasing the positive pressure in the chest through direct pressure on the chest
alternating with negative pressure which is increased by the release of this chest
pressure.
o . . The patient is passively supine throughout the entire treatment with the
head turned slightly aside to avoid breathing in the operator' s face.
o . . The operator stands at the head of the patient and applies both hands to the
sides of the patient' s chest cage bilaterally (usually in the upper ribs at
about the mid-clavicular line).
o . . A steady pressure is applied during the patient' s exhalation phase; this is
directed in a functional pattern for the ribs to aid in exhalation. A
vibratory component may be added during exhalation to assist in moving
secretions.
0 . . The application and release may be rhythmic at about 90-120 times per
minute; or the operator may hold pressure until shortly after the patient
initiates a breath and then suddenly release the chest pressure (this last
method is repeated with each exhalation/inhalation of the patient). The
operator must be sure that the patient does not have gum, candy or loose
dentures in the mouth.
IMPORTANT: If the patient is very short of breath (as in COPD), their

own intrinsic rate of respiration should not be disturbed. In more vital
patients, this procedure is optimally performed with a rhythm or while
directing the patient through the exhalation and inhalation portions of the
cycle.
PEDAL LYMPHATIC PUMP (DALYRIMPLE): This technique works

through fascial pumps and by the massage of the diaphragm (and indirectly the
lung bases) utilizing the intermittent movement of the abdominal contents up
2 18
against the diaphragm. This "intermittent motion" aids in increasing the range
of positive/negative pressure gradients.
o . . The patient is passively supine throughout the treatment

0 The operator stands at the'patient's feet and intermittently and rhythmically
• .
applies activating force through the feet at a rate determined by watching

the reaction of the patient' s abdomen. A rate of 90- 120/min is common.
Dorsiflexion of the feet with the operator' s hand on the plantar surfaces
and the fmgers over the toes stretches the posterior fascias of the leg and
is primarily directed into the lumbar and lumbosacral regions.
Plantar flexion of the feet stretches the anterior fascias and is directed
primarily to the thoracic region, ribs, and cervical areas.
PECTORAL TRACTION: This works by helping to elevate the first 6-7 ribs
during inhalation and thereby increasing the negative pressure during that phase
of respiration. Two minutes of pectoralis traction treatment is believed to
provide as much assistance to lymphatic flow as five minutes of thoracic pump
treatment.
0 The patient is supine with knees drawn up and hands on the abdomen.
• •
0 ., The operator is at the head of the patient and gently grasps the anterior
axillary fold (pectoralis muscles) with the fingers carefully conforming
to the patient and not gouging.
o . . Gentle traction is applied in a medial, anterior and cephalic direction and
held for 1-3 minutes while the patient breathes normally or with slight
increase in volume. The grasp is reapplied as needed to permit patient
comfort.
Family members can be taught this method of moving fluids with

relative safety compared to some of the other techniques described in this
section.
SPLENIC PUMP:
This technique is effective in patients with systemic infections and anemic

patients with low resistance to infection. The spleen stores red and white cells
and screens the blood of damaged blood cells.
o . . The patient is supine; the operator stands on the left side and places his/her
hands opposite each other on the lower left rib cage.
o . . Gentle alternate compression and release is applied until tissues release.
The amount of pressure depends upon the patient' s condition and the
judgement of the physician, Avoid in cases with friable splenomegaly.
2 19
LIVER PUMP:
This procedure is performed much the same as the splenic pump except it is
applied over the liver. The liver has a rich bed of lymphatic vessels. Its
decongestion aids in detoxification and helps to relieve visceral congestion.
POSTERIOR AXILLARY FOLD TECHNIQUE:
The goal is to reduce local tenderness and induration in the myofascial tissues of
the posterior axillary fold; if the patient is able to sense the warmth that
accompanies good lymph flow, the desire is to treat so that the "warmth"
encompasses the entire arm to the fingers. Concomitant myofascial trigger
points in the posterior axillary fold may also be addressed with this technique.
o . . patient supine and operator facing the patient

o . . grasp superior portion of the posterior axillary fold with thumb anteriorly
and the index, middle and ring fingers posteriorly, both the thumb and
fingers are next to chest wall
0 . . apply steady, gentle but firm squeeze pressure for 10-15 seconds and
inquire about "sensation of warmth in fingers or arm"
o . . if warmth is sensed by the patient, it can be accentuated by having the
patient clench and unclench the fist to accentuate the peripheral muscular
lymphatic pumps.
WWER EXTREMITY FASCIAL PATHWAY TREATMENT:
o . . patient is supine with the treatment leg off the table and knee bent
0 . . the operator straddles the leg just above the ankle and grasps the patient' s
leg b y clasping the hands together just below the knee joint (thumbs are
often right over the medial and lateral margins of the joint space)
0 . . operator leans backward applying gentle upward , outward, caudal and
rotational encouragement until the forces are centered (stacked in all
motions) at the femoroacetabular joint, knee and ankle. This technique
frees the fascial pathways of the leg, thigh , and hip and improves
lymphatic flow from the lower extremity.
o . . if the patient is able to sense the warmth that accompanies good lymph
flow, it should gradually move to the foot; if the warmth does not
progress, specific OMT to that site would be beneficial.
2 20
VENTRAL ABDOMINAL MANIPULATIVE TECHNIQUES:
ASCENDING AND DESCENDING COWN MESENTERIC RELEASE:

The accessible parts of the colon are palpated to detect tension increases,
congestion, and/or restriction in the motion of their mesenteries. In these
techniques, the bowel is gently taken at right angles toward its mesenteric
attachments and to the extent allowed by its motion barrier. Gentle tension is
then applied to its attachments. The technique is activated by having the patient
take a shallow breath and hold it until a breath is needed. When the patient has
to breathe again there will be a slight give to the mesentery. This technique is
repeated 2-3 times.
RELEASE OF AN ENTRAPPED CECUM:
0 the patient is supine and the operator at the patient' s side

• •
0 . . the patient's knee is slightly bent on the right side to relax the abdominal
musculature over the cecum
o . . the operator applies the heel of his/her right hand to the right lower
quadrant of the abdomen (RLQ) of the abdomen
o . . the operator attempts to gently lift the cecum from the pelvic entrapment
and toward the hepatic flexure of the colon
0 . . the opposite hand (optimal) may be used for inhibition to the
thoracolumbar junction where cecal sympathetic cell bodies of the spinal
cord are located
This technique is a slow maneuver allowing for release of the cecum

from its entrapment in the pelvis. The patient may complain of fullness
and some pain in the ascending colon as well as the hepatic flexure as
the operator' s right hand releases the entrapment and moves the fecal
mass and intestinal gas along the ascending colon.
ABDOMINAL MESENTERIC FASCIAL RELEASES:
o . . the patient is supine; the operator stands on the side of his dominant eye
and facing partially toward the head of the table
0 starting at the right lower quadrant (RLQ) , the operator uses one hand on
• .
top of the other to gently move the abdominal wall and the underlying
intestine in the direction of most ease and holds it until there is a release.
This same procedure is repeated in the RUQ, the LUQ, and the LLQ, in
that order.
LIVER FLIP:
This procedure is performed to release a liver "entrapped" by the diaphragm; it

frees the liver and aids in the decongestion of the right lung base and the
221
superior portion of the liver. Too vigorous an application or a friable liver are
contraindications to this procedure.
o . . The patient is supine; the operator stands on the right side of the patient.
o . . The operator's left hand is placed under the right rib cage about the level
of the 6th, 7th and 8th ribs posteriorly and the right hand is placed on
the anterior rib cage just superior to the anterior-inferior margin of the
right rib cage at the mid-clavicular line.
o . . The patient is instructed to inhale deeply and follow this with a full
exhalation; the operator' s hand follows the rib cage down, compressing
over the rib cage as the patient exhales.
0 . . The compression is maintained as the patient is instructed to inhale deeply;
as the rib cage elevates with forced inhalation, the operator suddenly
releases the compression with the right hand. (The patient must have
his/her mouth open during this procedure.)
0 .. The procedure is repeated 2-3 times
BASIC WCAL SOFf TISSUE TREATMENTS: kneading, stretching,

massage and wringing of soft tissues.
EFFLEURAGE: moderately light stroking of skin and subcutaneous tissues to

move lymph through their small vessels toward the heart. Treatment always
employs a stroking from distal to proximal.
FASCIAL RELEASE TREATMENTS:
o . . Intrinsic Activation: determine direction of rotation of the tissues and then

hold them in that direction until they release (indirect method); follow
tissue balance as dictated by palpation.
o . . Direct Method Fascial Treatment: move tissues in the direction of

restriction and hold the fascial plane at that barrier. Traction is usually
used as the activator but if this is painful, compression is tried.
PETRISSAGE: (used to break fascial adhesions)
o . . grasp skin and subcutaneous tissues in the region of the adhesions; lift and
twist them clockwise and then counter clockwise
0 .. at the resistance barrier in each direction, have the patient take a deep
breath and give a deep, explosive cough
(Continued with charts of ventral abdominal, fascial, and lymphatic treatments

on page 227.)
222
IV. TREATMENT FOR PARASYMPATHETIC NERVOUS SYSTEM
DYSFUNCTION:
The parasympathetics often seem to be overlooked in osteopathic manipulative

management because the hypersympathetic and lymphatic dysfunctions seem to
be more clinically evident and demanding. It also seem s that there have been
less research and clinical reports regarding the results of modifying systemic
disease through manipulative influence upon the parasympathetic system.
Parasympathetic influence to the body viscera is supplied by cranial nerves III,

VII, IX, and X, and by the parasympathetic outflow through the pelvic
splanchnic nerves from S2, 3, and 4. Parasympathetic fibers synapse in the
autonomic ganglia in the head (ciliary, sphenopalatine, otic, submandibular,
submaxillary) , the cervical ganglia of the uterus, and the myenteric
(Auerbach's) and submucosal (Meissner' s) plexuses of the GI tract.
The parasympathetic fibers from eN III supply the eye; eN IX and eN X

supply the carotid body and carotid sinus. eN VII synapses in the
sphenopalatine ganglion to supply the glands in the mucous membranes of the
sinuses, pharynx, Eustachian tubes, and the lacrimal glands. eN X also
supplies the GI tract distally to the transverse or right colon. The pelvic
splanchnic nerves (S2,3,4) supply parasympathetic fibers to the left colon and
pelvic organs. A more complete chart is found on pages 192 and 193.
A. TREATMENT THROUGH THE SPHENOPALATINE GANGLION:
The sphenopalatine ganglion is located in the sphenopalatine fossa of the skull.

It hangs from the maxillary division of the trigeminal nerve and cannot be
reached directly by the palpating finger. It may be reached indirectly, through
the open mouth of the patient by influencing the fascias of the pterygopalatine
muscles. These fascias then manipulate the sphenopalatine (the pterygopalatine)
ganglion. Parasympathetic fibers reach this ganglion from the greater petrosal
nerve, a branch from the geniculate ganglion of the VII cranial nerve.
o . . Purpose: Treatment encourages establishment of a more normal cellular

ratio between the goblet and the ciliated columnar epithelial cells in the
nasal and sinus epithelium. Parasympathetic impulses reduce the goblet
cells and increase the proportion of ciliated columnar cells to thick
mucus producing goblet cells. Parasympathetic activity is a primary
influence in the production of a thin saliva-like nasal secretions.
o . . The operator passes a cotted finger over the molars of the upper jaw on one
side, then lateral and posterior to the maxillary ridge.
o . . From there the finger is moved cephalad over the pterygoid plates (just
posterior to the maxillary ridge) to the extent permitted by the buccal
mucosa in the mouth.
223
o . . The patient is then asked to nod toward the palpating finger. Two or three
repetitions on each side of the mouth will provide an adequate treatment
by indirectly applying pressure on the ganglion through the fascias of the
pterygoid muscles.
o . . Effective treatment is signaled by unilateral "tearing of the eye on the side
of treatment" produced by effective stimulation of the lacrimal gland
which shares the same parasympathetic nerve supply.
B. TREATMENT THROUGH VAGUS NERVE INFLUENCE:
o . . Purpose: to balance parasympathetic influence to viscera of the neck, heart,

lungs, kidneys, and the glands and OI tract (excluding the left colon).
o . . Soft tissue, condylar decompression, and manipulation of specific somatic
dysfunction of the occipitomastoid, OA, AA, and C2 joints will benefit
parasympathetic influence through CN X.
o . . The vagus nerve may possibly be influenced by inhibitory pressure over the
celiac and superior mesenteric collateral ganglia.
C. TREATMENT THROUGH PELVIC SPLANCHNIC INFLUENCE:
o . . Purpose: to balance parasympathetic influence to the viscera (left colon and

pelvic areas).
o . . Direct inhibition to the inferior mesenteric ganglia influences
parasympathetic supply to the left colon and pelvis.
o . . With the patient prone, the operator can place one hand over the sacrum
and enforce its application with the other hand. Encouragement of the
motion of the sacrum with respiration or the enhancement of the
craniosacral motion will help to balance sacral splanchnic output.
(Technique: Rocking the sacrum)
o . . With the patient supine, the operator can place one hand under the sacrum
with the fingers directed cephalad and the sacral body resting in the palm
of the operator. The operator senses the preference indicated by the
craniosacral motion and follows this motion. Sometimes the operator's
cephalad hand and forearm are placed across the two ASIS so they can
be pulled toward approximation, to encourage separation of the
sacroiliac joints and improve the realization and action of the
craniosacral impulse.
o . . Treatment of sacral and innominate somatic dysfunction is also important.
It is especially important to remove any non-physiologic sacral shear or
superior innominate shear if present.
V. TREATMENT OF THE SOMATIC SYSTEM:
Spinal somatic dysfunction is especially important in the T l -L2 area. This is

true because dysfunction here can directly influence the cord segments
224
containing the primary sympathetic cell bodies by establishing facilitation of
those divisions. It should be recognized that if there is a facilitated segment,
somatic dysfunction anywhere may produce impulses that will cause that distant
segment to fire. In general, the rotational component of the somatic dysfunction
related to visceral dysfunction will usually be toward the same side as the organ,
especially if that organ is paired. If there is a non-neutral segmental somatic
dysfunction in an area it is more likely to influence or be connected with
dysfunction of a organ connected to the sympathetic innervation at that cord
level.
Treatment is designed to remove the somatic dysfunction and is based mainly

upon the problem, the condition of the patient, and the skill of the physician. It
must be stated that, clinically, high velocity, low amplitude methods of
activation (HVLA) are often unsuccessful, especially when palpation of the
paraspinal tissues has a "rubbery" texture.
VI. SUMMARY :
In most viscerosomatic reflexes, treatment of the visceral component with

medications, diet, surgery, or some other modality is utilized if the structural
component warrants that level of intervention. Treatment of the soma in a
viscerosomatic reflex arc is often helpful in breaking this reflex cycle and is
beneficial for the functional component. Reduction of stressors at physical,
mental, spiritual, and environmental levels (etc.) is a great benefit as well,
regardless of whether the primary problem is visceral or somatic.
In designing a manipulative approach in a patient with a facilitated segment,

strongly consider removing this "neurologic lens" prior to instituting any other
osteopathic manipulative treatment or introducing any other stressor. Recall
that any osteopathic manipulative treatment will initially raise sympathetic tone
slightly but will be followed by a clinically more important gradual, prolonged
decline. The degree of rise will depend upon the amount of neurologic input.
For this reason select the proper technique for the patient' s condition.
Remember that high velocity, low amplitude techniques will often be ineffective
in removing somatic dysfunction that is secondary to visceral dysfunction and an
alternative activating force must then be chosen.
225
REFERENCFS:
1. Patterson MM: Model mechanism for spinal segmental facilitation. JAOA

Sept 1976; 76: 121-13 1 .
and Patterson MM: The reflex connection: History of a middleman.
OsteQpathic Annals Sept 1976; 357-367.
and Patterson MM: Louisa Bums memorial lecture 1980: The spinal cord-
Active processor but not passive transmitter. JAOA Nov 1980; 80(3) :
210-2 16.
2. Herrmann, Edward; The D.O. Oct 65 ; 163- 1 64
3. Owens C An Endocrine InteIl!retation of Chapman's Reflexes. Carmel CA,
1963.
4. Kirksville College of Osteopathic Medicine; Department of Osteopathic
Theory and Methods; 800 West Jefferson Street, Kirksville, Missouri
63501
5. Simons D.O. , Travell JO: Myofascial origins of low back pain: Part 2.
Torso muscles. Postgraduate Medicine February 1983; 73(2) : 85-89.
226
TABLE: VENTRAL ABDOMINAL, FASCIAL RELEASE; LYMPHATIC PUMPS AND VISCERAL TREATMENTS A
TECHNIQUE PHYSIOLOGIC GOAL ATTEMPTED INDICATIONS CONTRAINDICATIONS
VENTRAL ABDOMINAL RX:
Liver Flip free diaphragm; decreased diaphragm motion; friable, enlarged liver
(p 221) milk right lung base rales in right lower lobe I
Celiac Ganglion
Tension Release calm sympathetics TS-9 upper GI dysfunction aortic aneurysm
(pp 199-200) palpable subxiphoid tension open surgical wound
Superior Mesenteric calm sympathetics T10-l1 dysfunction of sm intestines aortic aneurysm

Ganglion Release below duodenum, right colon, open surgical wound
(pp 199-200) upper GU; palpable tension
midway between xiphoid and
umbilicus
!'V
!'V
..,J
Inferior Mesenteric calm sympathetics T12-L2 lower GI/pelvic dysfunction aortic aneurysm
Ganglion Release palpable tension just above open surgical wound
(pp 199-200) the umbilicus
Cecal Release improve bowel function complaints of constipation appendiceal inflammation

(p 221) (mechanical release) or RLQ pain of mechanical open surgical wound
etiology; visceroptosis
Mesenteric Colon Release

(ASCending/Descending) improve bowel function complaints of constipation open surgical wound
(p 221) (mechanical release) of mechanical etiology colitis
Mesenteric Small improve bowel function abdominal cramping and/or open surgical wound
Intestinal Release (mechanical release) tenderness; altered stool
(p 221) texture
(continued)
TABLE: VENTRAL ABDOMINAL, FASCIAL RELEASE; LYMPHATIC PUMPS AND VISCERAL TREATMENTS continued B
VENTRAL ABDOMINAL cont.
Abdominal Fascial to decrease intra-abdominal abdominal tenderness; hernia open surgical wound
Release (p 221) pressure; improve bowel
function (mechanical)
Splenic Pump (p 219) improve immune function infection, fever enlarged spleen,
mononucleosis
Liver Pump (p 220) detoxification; passive hepatomegaly, friable liver

mobilize lymph epigastric lymphatic congest.
r-J chronic toxic conditions
r-J
(X)
(Ischiorectal Fossa) improve pelvic diaphragm bloated feeling; hernia; perineal abscess !
(pp 216-217) mobility; decongestion; re- lower extremity varicosities (patient incontinence)
duce intra-abdominal press.
FASCIAL TREATMENTS:
Rib Raising improve lymphatic/venous visceral dysfunction; region of spinal fracture

(pp 195-198) return and immune function; respiration not extending to region of spinal surgery
calm sympathetic hyper- pubic symphysis; tight region of rib fracture (s)
activity; improve thoraco- paraspinal muscles; fever; (pleurisy)
abdominopelvic pump lymphatic congestion
Redoming Thoracic improve lymphatic/venous respiration not extending to tubes, incisions, etc.
Diaphragm return and immune function pubic symphysis; lymphatic
(pp 215-216) congestion (anywhere)
(continued)
TABLE: VENTRAL ABDOMINAL, FASCIAL RELEASE; LYMPHATIC PUMPS AND VISCERAL TREATMENTS (continued) C
FASCIAL TREATMENTS cont.
Intravaginal/Intrarectal improve pelvic diaphragm spasm of pelvic floor on rectal or anal abscess
rectal or anal malignancy I
I
Fascial Release motion; decongestion; vaginal and/or rectal exam;
(pp 216-217) decrease pelvic floor vaginitis, prostatic spasm;
spasm if poor results with
ischiorectal fossa treatment
LYMPHATICS/LYMPH PUMPS:
Liver Pump (see section passive hepatomegaly;

"8" of this table) detoxification; epigastric lymphatic friable liver
(p 220) mobilize lymphatic fluid congestion
N rib fracture;
N
U) Lymphatic Pump (thoracic accentuate negative intra- rales and rhonchi; congestion too severe;
classic and rhythmic) thoracic pressure; productive cough; lymphatic incisions, subclavian
(p 218) increase lymphatic return congestion; fever, infection lines etc. COPD unless Rx
only at respiratory rate.
Lymphatic Pump: thoracic same as above but uses same; used in hopes of same; (COPD patients only
classic with vibratory vibratory component during loosening plugs of mucus at intrinsic respiratory
modification (p 218) pressure to loosen mucus rate)
Lymphatic Pump: thoracic same as above; but during same as above loose dentures, gum,
classic with accentu- patient's inhalation, there medication etc. in mouth
ation of negative is sudden release of
phase (p 218) thoracic pressure
Pedal lymphatic Pump accentuate negative intra- may be able to use when venous thrombosis;
(pp 218-219) abdominal pressure; thoracic pump can not; lymph lower extremity problems;
increase lymphatic return congestion; fever; infection abd. surgery (post-op)
(continued)
TABLE: VENTRAL ABDOMINAL, FASCIAL RELEASE; LYMPHATIC PUMPS AND VISCERAL TREATMENTS (continued) D
LYMPHATIC/PUMPS cont.
Lymphatic Pump (seated) same as pedal pump same as pedal pump unable to sit ,
congestion (anywhere)
Pectoral Traction accentuate negative intra- (can be taught to tubes, lines, incisions
(p 219) abdominal pressure; in- a family member); lymphatic on the chest
crease lymphatic/venous congestion; fever; infection
return
Posterior Axillary Fold increase lymph drainage shoulder dysfunction; hand excessive ticklishness
(p 220) from upper extremity; calm and arm paresthesias; cool
� sympathetics T2-6; Rx for and clammy hand
\..J some myofascial points
o
Breast "Drainage" decrease lymphatic Fibrocystic breasts; post- mastitis;

congestion of breast partum breast engorgement; malignancy in the
breast tenderness breast
SPECIAL CLINICAL (OTHER)
surgical wound or
Fascial Release: cough break superficial and deep scar tissue adhesions; incision not completely
activation (p 222) fascial adhesions restricted range of motion healed
Ileus Prevention treat- decrease sympathetic ileus or reduced bowel local infection;
ment: thoracolumbar hyperactivity to GI and sounds; prevent ileus from incision;
inhibition (p 198) restore normal bowel funct. recent surgery or planned thoracolumbar fracture
------ ----L-_____ �-�--
(continued)
TABLE: VENTRAL ABDOMINAL, FASCIAL RELEASE; LYMPHATIC PUMPS AND VISCERAL TREATMENTS (continued) E
TECBH IQUE PHYSIOLOGIC GOAL ATTEMPTED INDICATIONS COHTRAINDICATIONS
SPECIAL CLINICAL cont.
Sacral Inhibition improve parasympathetic Dysmenorrhea; make patient local infection;

(p 224) activity in left colon; more comfortable in second local incisions
decongest uterus; calm and third stage of labor;
hyper-parasympathetic Diarrhea; (constipation)
activity; calm visceral
afferents from left colon;
reduce pain from cervical
dilation (in labor)
Sphenopalatine Ganglion thin mucosal secretion thick nasal secretions; trigeminal neuralgia;
N Treatment (pp 223) via parasympathetic nasal-lacrimal syndrome patient unable to cooper
\..J
.... influence ate, i.e. may bite you
Supra-/Infra-Orbital decrease sensitivity of sinus headache; sinusitis; neuritis of the supra

Treatment (p 28) visceral afferent receptors tenderness over the and infra-orbital nerves
from mucous membranes of innervation of the supra- or
the head area infra-orbital nerves
Myofascial Spray and decrease input to SA node supraventricular tachy if unable to rule out
Stretch of Right from somatovisceral aff. arrhythmias not responsive primary cardiac disease
Pectoralis Major to decrease supraven to usual medications in a or if have not treated
(p 57) tricular tachyarrhythmias patient with this trigger pt. the cardiac disease
Chapman's Reflex decrease sympathetic tone history of symptoms of organ

treatment produced by afferent dysfunction; palpable
(pp 200-201, 232-233) visceral bombardment from Chapman myofascial point;
soma to associated other physical confirmation
visceral tissues
CHAPMAN'S REFLEXES: anterior points
Middle Ear
Nasal Sinuses
Pharynx
Tonsils
Tongue
Retina.
Conjunctiva ---+-. ��:::=�
,�
-- Esophagus. Bronchus
__
Thyroid. Myocardium
/,��y---- Upper Lung. Upper Umb
Neck ---'
'O""")'�"�f--- Lower Lung
(D
...G��:"';"---- Uver R
Ii
Stom� (acidity)
Larynx ---
PyIoris
�_��:t"l!�---- Stoma
---�
(peristalsi�(D
Uver. Gall Bladder \!!2
Spleen(D. Panaeas@
��'7�,r=+---_
Small
Intestines -----e::::3::jI�
Adrenals
��-�
--- dn�
Appendix �
N:III�--
__
__ Bladder
Intestine:
Abdomen
peristalsis
Ovaries
�-=k----- Urethra
��---- �erus
r-,---- __ Rectum
Prostate or
Broad Ugarnent
\-\- +-
_ ______ Colon
�
WlftlV1J
Original ( 9180 )
�
All points are bilateral
Pt where ind�t�
R for right and�or
OT&M Dept. Ie
Reid Taylor. Fellow
232
CHAPMAN'S REFLEXES: posterior points
Retina.
Conjunctiva CEREBELLUM
Middle Ear ---.....:i�S;;�
q:::: ____ NASAL SINUSES
Pharvnx.TonQU8
�.�nu�.Anns _ ��--- CEREBRUM
Neck
_
Esophagus. Bronchus.___
.Thyroid
Upper Lung. Uyocardium -
-===:::��tj�r,:?i��-- ARMS
(also pectoralis minor)
Upper Umb
Lower Lung NEURASTHENIA
StomagL.{acidity) CD (also pectoralis major
Uver @
Stomach (peristalsis) L�___-
Uver. Gall Bladder R
Spleen(:!;). Panaeas R
PYLORUS @
SmaJl lntestines --.....e=::...-=W\ e:��:.�"-+-
...-:: -- OVARIES
Adrenals _____ ...':ttt��lc!:.-_---:---
��f-��-.,: .. INTESTINES peristalsis
APPENDIX ®
Kidneys -----:::fl&'l..
Abdomen. Bladder ---
-
-:'],
'7......
Urethra __ _- 10.---4---- LARGE INTESTINES
Uterus -----taJ
Vagina. Prostate "'�+--7"f1f---=- SCIATIC NERVE (posterior)
Uterus. Broad Ugament
Rectum. Groin Glands ----��
Fallopian Tubes
Seminal Vesides
-....01�-��,..T(��J-%---- HEMORRHOIDAL PLEXUS
Oitoris -----ttl
Vagina
I:1:.::::::�� SCIATIC NERVE (anterior)
All points are bilateral

t where indicated
�
Original (9/80 ) as @ for right and
OT&M Dept. (9 for left
Reid Taylor. Fellow
233
INDEX FOR OSTEOPATIllC MANIPULATIVE TECHNIQUES
IN SYSTEMIC DISEASE
CONTENTS
Treatment Plan For The Use Of Osteopathic Manipulative Treatment in

Systemic Disease................................................................. 189
Goals ...................................................................................... 189

A Diagrammatic Illustration Of A Plan For OMT ................................. 190
Sympathetic/Parasympathetic Innervation Chart ............ ................. ....... 192
Treatment For Sympathetic Nervous System Dysfunction ••••••••••••••••••••••••••• 194
Treatment Goals And General Manipulative Treatment Plans .................... 194

Rib Raising Techniques........................... .. .. .............. .......... . ... .. .. . . 195
The Ileus Prevention Treatment (Rib Raising, Even For Areas Without
Ribs) .. . ... . ..
................. . ....... ........ ..
. . . . ... ......
. ..... .. . ..... . . 198
Abdominal Collateral Ganglia ..... ........................................ .. ... .
. . . .. . 199
Diagnosis ........ ...................... .. .................................. .
. . . . .. . 200
Treatment . .. .. . .... . . ..... ......................... ............. ...
. ... . .. .. . . .. .. . 200
Chapman's Reflexes . .. . .... . ................. ... ..................
........ ......... . . .. 200
Diagnosis .......................................................................... 200
Treatment.......................................................................... 201
Treatment Around Cervical Sympathetic Ganglia . ...................... ........ . . . 201
Treatment Of Lymphatic System Dysfunction ••••••••••••••••••••••••••.••••••••••••••. 202
General Goals And Treatment Plan............. ........................ ... ... .... . . .. 202
Symptoms Of Fascial Dysfunction .......... . . . ......... . .. . . ....... .. . . . . ............ 203
Postural Symptoms ..... . ............. . .. ......... .......... .. . .. . . ....... . . ... .. . 203
Systemic Symptoms .... ...... ............. .. ... ............. ..
. . . ..... . . ....... . . 204
Other Related Symptoms . .. . ... ....... . ..... ..... .... ... . ........ .............. . 205
Anatomical Regions of Congestion ........ . .. ... ............. ... ..
...... .. .. ... .. .. .. 205
Fascial Pattern Diagnosis . . . . ......... ...... .. .. .. ..............
.... ....... ... . . .. . ... . . 207
Fascial And Musculoskeletal Diaphragms ......... ... . . .. ............ . .. . ... . .. . .. .. 209
Thoracic Fascial Inlet............................................................ 209
Diagnosis ................................................................... 209
Treatment.. .......................... .....
. ...................... .. .. . .... . . 212
Abdominal Diaphragm ... ... ...................... . ................... ...
. . .. .. . 214
Diagnosis ....... .... ........... . . . .................. .. . , ...
. ...... . ... . ... . . 214
Preparation For Redoming ............. . ........ .......... ... ....... .. . .. 214
Treatment. .................................................................. 215
Pelvic Diaphragm .... . .. .. ........ . . ...
. .... . . . ....... ..
......... . . . .. ..... . .. .. . 216
Diagnosis ................................................................... 216
Treatment. .................................................................. 216
Cranial Diagnosis And Treatment.............................................. 217
234
Lymphatic Pumps ....................................................................... 218
Goals ............................................................................... 218
Treatment.. ........................................................................ 218
Thoracic Lymphatic Pump. .... ... ... .. ... .. .... ...
... . . ... .. ... . ... ..... 218
Pedal Lymphatic Pump (Dalyrimple) ... .... ..... ....... .... . . . . .. . .... 218
Pectoral Traction ..
......... .. .. .. . ..... .. . . ...... .......
...... .. .. .. .. . ... 219
Splenic Pump . ..... ... ..... ... .. .. ... ... .... .. .. .... ...
.... . . .. .. .. ... . . . . . 219
Liver Pump . ..
..... ... .. ... .. . .. .. . .. .. .... .......
....... . ... .. .. .. . .. . .. ... 220
Other Soft Tissue Treatments For Lymphatic Drainage .... ... .... . . .. . ..... . .. . . . 220
Axillary Fold Technique .. . .. ... . .. .. . .....
. . ... . . ... . . . ... ... ............ .. .... 220
Lower Extremity Fascial Pathway ............................................. 220
Ventral Abdominal Techniques .... . . ...... . .... ... ... ...... . .
... .. .... . .. .. . .. . 221
Ascending And Descending Colon Mesenteric Releases . ......... . . 221
Entrapped Cecum Release Technique .................................. 221
Abdominal Mesenteric Release... . .... .... ... ...... ... . . ... . . .... ...... . 221
Liver Flip. .................................................................
. 221
Basic Soft Tissue Treatments ................................................... 222
Effleurage . ...........
. . .. .. .... .. .... ... ........
....... . . ..... . . .. .. ....... 222
Fascial Release Techniques .............................................. 222
Petrissage.. ................................................................. 222
Treatment Of Parasympathetic Nervous System Dysfunction ••••••••••••••••••••••• 223
Sphenopalatine Ganglion Influence................................................... 223

Vagal Nerve Influence Influence .... ...... ... .... ... . .... ......
.. . . ... .... . . . . .. ..... . 224
Pelvic Splanchnic Nerve Influence.. . ..... ... .. ........ ..... .
. . ... .. . . .. ... . .. .... . .. . 224
Treatment Of Joint Somatic Dysfunction •••••••••••••••••••••••••••••••••••••••••••••••• 224
Summary........................................................................................ 225
Cbarts or Fascial Treatments .............................................................. 227
235
THIS PAGE INTENTIONALLY LEFT BLANK
A - allergic etiology - EENT 16
- allergic manifestation 1, 24, 166
Abdomen 150, 151, 174 - antigen 171
Abdominal - hay fever 48,85
- aneurysm 102 Altitude changes causing ear pain 10, 15
- bloating 104 Alveoli 189
- distension 97, 104, 109, 1 15-1 16, 1 17, - air sacs 34 (diagram), 35,38
138, 139 - hyperinflation 48
- dysfunction 206 - surfactant 36
- guarding 86 Amblyopia 7, 14
- pain 1 04, 109, 1 10, 1 15, 1 16, 1 17, Amebiasis 1 10
120, 127, 132, 139, 141 Amine compounds 1 15
- recurrent pain 11 0 Amoeba 1 10
- rigidity 86 Anal
- tenderness 227,228 - abscess 229
- wall 151 - cancer 229
- surgery 101 - digital inhibition 105
Abruptio placentae 152 - triangle 99
Abscess 102,228,229 Analgesia 23, 138, 140
Accidents 153 Anatomical disturbance 99
Accommodation spasm 4 Anatomy 79, 107, 1 17, 1 7 1
Acetominophen 177 Anemia 1 10,2 1 9
Acetylcholine 59 Aneurysm 7 , 102, 227
Ache 127, 164, 188 Angina 58, 60, 185
Achille's tendon 206 Angiography 59
Acid secretion 93 Angiotensin 62 (diagram)
Acidosis 95 Angle of Louis 209
Action potential 71 Ankylosis 162
Activity level 173 Anorexia 176
Activity-of-daily-living (ADL) 57, 165 Anovulation 132
Adhesion 222,230 Antacids 1 16
- pharyngeal 10, 15 Anterior axillary fold 219
Adipose tissue 184 Anterior chest wall syndrome 57-58
Adrenal 4,65, 133, 151, 152, 155, 165, Anterior cranial fossa 7
188, 192, 193, 199 Anterior sacral base 1 5 1 , 157
- Chapman's reflex 65 (diagram), 67 Anti-infla mmatory medication 1 3 1 , 159,
- corticoids 152 167
- function 65, 165 Antibiotic medication 15, 16,23,40,4 1,
- hormones 1 5 1, 152, 155 42,87, 106, 127, 135, 136
Adrenaline 188 Anticholinergic medication 1 16
Adrenergic blockade 185 Antihistamine medication 15, 4 1
Aging 149, 1 5 1 Antispasmotic medication 1 16
- developmental stages (pediatric) 178- Anus 99
179 Anxiety 6, 1 10, 1 14, 1 16, 173
- geriatrics 40 Aorta 85, 192
Air hunger 89 - aneurysm 227
Albuminuria 123 Aphrodisiac 132
Alcohol 78, 153 Appendix 192
Aldosterone 62-63 (diagram), 65 Aqua-cize 166
Allergic factors 15 Arm 59,193
- allergen 1 Arousal 143
Arrhythmia 50,54,56,57,59,60 -sinoatrial block 67
(diagram) , 6 1 ,67-7 1,85, 172, Atrophic vagina 144
185 Atropine 1 16
-bradyarrhythmia 59,67,68,70,85, Attention deficit disorders 172
172 Axillary folds
- ectopic foci 50,60,185 - anterior 2 19
-extrasystole 67 -posterior 164, 206,220,230
-malignant arrhythmia 69 -OMT 1 64,220,230
-paroxysmal atrial tachycardia 67 Auerbach's plexus 223
-paroxysmal ventricular tachycardia 67 Autonomic
- pathogenesis 7 1 -activity 1 1 1, 120
-sick sinus syndrome 56, 72 - balance 88,95
-sinoatrial block 67 - nerve plexi 120
-supraventricular 50,57 (diagram) , 23 1 - nervous system 66, 91, 142, 190
-tachyarrhythmia 4,50,57 (diagram) , - Chart 187-188
67,69,70,202,23 1 -Extrinsic 1 17, 1 1 8, 121
-ventricular 50,60, 69,70, 185 -Intrinsic 120, 121
Artery/arteriole 50, 125, 149 -Upper GI 83-85
- blood 89, 150 -response 195
-carotid 187 Azotemia 135
-constriction 133
-inferior mesenteric 199 B
-left circumflex coronary artery 69
-wall 7 1
Arthralgia 136 Backache 79, 128, 139, 204
Arthritis 1 6 1 , 162, 167 - See also Pain -Back
-lower extremity 1 6 1 Bacteria 72,80,95, 1 14, 1 34, 136, 137,
-morning stiffness 164 172
-spine 1 6 1 -bacteremia 136
- see also Rheumatoid arthritis & -bacteriology prologue
Osteoarthritis - Campylobacter pylori 87
- see also under Rheumatology - endocarditis 72
Articular cartilage 159 -infection 68, 72
Articular mobilization 175 - proliferation 10, 25
Articular surface 1 6 1 -prostatitis 134
Ascending colon 1 1 1 - secodary infection 3,24,25
- OMT: How to treat 22 1 - toxins 80
Ascites 56, 66, 70,73 Barium GI study 1 10
Aspirin 1 1, 140, 177 Baroreceptors 62
Asthma 2,5,48,49,85 Barral , IP 89, 102
-length of hospital stay 49 Barrel chest 48
-OMT 49 Bartholin gland 129
Atherosclerosis 50, 56,7 1 , 184 Basement membrane -Multilamination
- pathogenesis 7 1 161
Atrial Bed rest 40
-action potentials 7 1 Bedside manner 172
- atrioventricular (AV) node 50,55,68 Bedwetting 129
-atrioventricular block 67,72 Behavior modification 77
-atrioventricular conduction 72 Belch 100, 1 15
-fibrillation 67 Bell's palsy 7
-flutter 67 Bicarbonate 84, 1 16, 1 17
Bile 186 Bogginess 205
Bile duct 93, 187, 192 Bone
Biochemical factor 109, 188, 189 - erosion 1 6 1
-changes 6 - growth 184, 185
-homeostasis 189 -mass 1 66
-kinins 24 - spurs 166
-lactic acid accumulation 95 Bowel 165
- mechanism 109 -altered contractions 1 14
-reaction 33 - changes 109, 1 10
- stressor 1 12 - frequency 109
Biofeedback 66 -function 227,228,230
Biological 155 - gas odor 1 15
Biological stress 152 -handling 100, 101
Biomechanical dysfunction -Primary 82 -hyperactivity 1 16
-stress/strain 165, 166 -irregular habit 109
- see also Physical stress , Trauma -narrowing 1 14
Birth canal 157 - threshold to distension 1 14
Birth trauma 172,203 - sounds 101,230
Bladder (Urinary) 124, 126 (diagram) , - See also GI contraction
129, 132, 137, 138, 188, 193,2 1 7 Bradyarrhythmia 59,67,68,70,85, 172
- autonomic 126 Brain 1 12, 183
-capacity 129 - see Central nervous system; Nervous
- dysfunction 132 system

- external sphincter 126, 133 Breast
-hyper-/ hypotonic 126 - cancer 230
-incomplete emptying 125, 133, 134, -congestion 157, 230
135 - engorgement 157,230
-infection (See cystitis) - examination 158
-internal sphincter 126, 134 -hypertrophy 155, 156
-irritation 132 -mammary gland 192
-neurogenic 126 (diagram) -OMT 230
-sphincter 126, 1 33, 134, 193 -tenderness 28,230
-tone 133, 1 34 Breathing 33, 34, 35, 38,43,44, 136,
-wall 124, 125, 126, 133, 1 34 1 95,204
Blindness 14 -costal 205
Bloating 109, 141,228 -exhalation 33, 43 (diagram) , 198
Blood 149 - ineffective 205,228
-cultures 40-4 1 - inhalation 33, 35,40,43 (diagram) ,
- flow 55,60,9 1 ,95, 1 15, 159, 1 6 1, 44, 195, 198, 206
164, 181, 184 - intermittent positive-pressure breathing
-pressure 54,62,64,70, 124, 125, 133 41
-hypotension 68 -rapid 38
-supply 123 - shallow 38
-vessel 187 -splinted 44
-volume 155 - See also Respiration , Chest motion ,
- See also Artery, Circulation and specific Diaphragm
topics Broad ligament 1 30,217
Blush 56 -Chapman's reflex 125, 130,232-233
Body fluid shift 66 Broncru 23,25,35,36,37,192
Body mechanics 123 - constriction 50
Body unity iv , 12,93, 142,152, 163, 175 -dilation 41,50
- gland 187 - see also specific disease or cardiac
- muscle/muscle tone 35,48,49,187 condition
- secretions 35 - see Myocardial infarction, Congestive
- spasm 48 heart failure, Subacute bacterial

Bronchitis - Chronic 48 endocarditis
Bronchodilators 40 Cardio-cardiac reflex 60,69,70,185
Brunner's glands 84 Cardiovascular system
Bruxism 8 - abstract summaries 68-73
BUN 135 - disorders 53-78
Burning pain 81 - function 50
Burping 100 - OMT 50,60,61,66,67,89
- parasympathetics 55
c - shock 60 (graph)
Carotid
- artery 187
C2 38,60,85 - body 34 (diagram), 35,38,54,55,
- Vagal connection 59,85 192,223
C3- 5 34 (diagram), 35,81,124,207,214 - plexus 25
Calcification 205 - sinus 34 (diagram), 54,62,67,183,
Calculus (GU) 123,125,134,137 192,223
- calyceal 138 - sinus massage 67
-silent 138 Carsickness 11
Campylobaeter pylori 87 Cartilage 159, 161,167,171
Cancer 110,114,124,229,230 - regeneration 161
-colon 110,114 Catecholamines 69
- renal 124 Cathie, Angus DO 17
Capillaries 149 Cause/effect 79
Carafate 87 Cecum 111,221
Carbon dioxide 117 -OMT: How to treat - Cecal release 227
Cardiac Celiac ganglion 80 (diagram), 90,92,
- arrhythmia (See Arrhythmia, 107,112,165,192,199,224
Bradyarrhythmia, Cell bodies 225
Tachyarrhythmia) Cellular level 88 ,98
- cardio-cardiac reflex 60,69,70,185 - dysfunction 79,95
- chronotropic effect 54,69 - nutrition 98
- conduction deficit 67 Center of gravity 151
- disease/dysfunction 202, 231 - See also Gravity, Posture, Postural
- electrical instability 69 disorder
-function 57 Central nervous system 80,81,150,151,
- inotropic effect 54,69,183 152,183,195,204
- innervation 54- 55 (diagram) Central venous pressure 68,73
- irritability 68,71 Cephalgia 2,6,7,14,16,17,40,44,85,
- ischemia 185 93,104,139,204,231
- lymphostasis 71,72 - occipital 85,93
- muscle 183 - sinus headache 16,231
- output 39,48,57,62,66,88 Cerebellum 183
- pathology 59 Cerebrospinal distribution 81
- plexus 50,202 Cerebrospinal tract 80
- resuscitation 61 Cervical spine 154
-workload 60,68 - disk disease 2
- joints 202
- lordosis 166, 171 Chemical stress 205
- lymph nodes 172, 174 Chemoreceptor 183
- spondylosis 2 Chest 202
- strain 155 - barrel 48
- sympathetic ganglion 2, 25, 26 - �ge motion/excursion 38, 44, 48, 49
(diagram), 50, 54 (diagram), 183, - compression 61
184, 192, 194, 201, 202 (diagram) - incision 230
- OMT 67 - pain 40, 44, 57, 58 (diagram)
Cervical vertigo 2 - pressure, intermittent 102
Cervix 129, 132, 139, 188, 189 - volume 156
- anteverted 139 Children 129, 171-175
- dilation 231 - failure to thrive 7
- environment 144 - osteopathic considerations 171- 180
- ganglion (Uterus) 223 Chills 136, 13.8
Cervicothoracic junction 202, 203, 207, Cholecystectomy 87, 115
208, 210, 212, 213 - post-cholecystectomy syndrome 87
- See also Sibson's fascia, Thoracic inlet Cholecytokinin 115
Chain ganglion 25, 194, 195, 202 Cholelithiasis 82 (diagram), 110, 115
Chapman's reflex 3, 37, 82, 83, 90, 91, Cholinergic fibers 59
92, 119, 134, 194, 200-201, 232- Chronic bronchitis 48
233 (diagrams) Chronic disease 123, 159
- adrenal 65, 77 Chronic obstructive pulmonary disease
- diagrams 65, 232-233 (COPO) 39, 48, 218, 229
- bladder 125 -GMT 45, 48
-diagrams 125, 232-233 ChTonicity 161, 163, 228
- broad ligament 125, 130 Chronotropic effect 54, 69
- diagrams 125, 232-233 Ciliary ganglion 4, 223
- colon 96, 104, 119 Ciliary muscle 4, 5 (diagram), 187
- diagrams 96, 232-233 Ciliated:goblet cell ratio (See
- EENT 3, 17, 26 Goblet:ciliated cell ratio)
- diagrams 3, 232- 233 Ciliosplnal center 18
- GI 86, 90, 96, 165 Circulation 88, 95, 120, 149, 151, 162,
- diagrams 90, 96, 232-233 165, 176, 184, 189, 202, 204,
- gonads 125, 130 205, 206
- diagrams 125, 232- 233 Cisterna chyli 85
- GU 125, 139 Clavicle 86
-diagrams 125, 232-233 Clidinium 116
-heart 37, 59 Clopping. 41
- diagrams 37, 232-233 Cloudy swelling 95
- kidney 125, 126 Coccyx 216
-diagrams 125, 232-233 Cochlea 183
-lung 37 Codeine 41
- diagrams 37, 232-233 Cold (temperature) 8
-OMT: How to treat 92, 104, 201 Colic 82, 100, 172
-prostate 125, 130 Colitis 97, 98, 161, 186, 227
- diagrams 125, 232-233 Collateral circulation 54, 56, 60, 68, 184
- small intestine 90, 119 Collateral (sympathetic) ganglion 80, 82,
- diagrams 90, 232- 233 83 (diagram), 86, 91, 92
Charcot-Leyden crystals 48 (diagram), 107, 112, 118, 134,
Cheek - Tingling 7 192, 194, 195, 199 (diagram), 200
Chemical mediators 188 - diagnosis 200
- OMT: How to treat 200 - terminal lymphatic regional sites 206
- see also Celiac ganglion; Superior (diagram)
mesenteric ganglion; Inferior - venous 6,70, 116,118,120,140,149
mesenteric ganglion (diagram), 151, 152
Colon 84,85,95,96,98,99,100,104, Congestive heart failure 50,56,66,71,
105,107,115,143,192,193, 72,85, 185
199,201,221,223,224,227,231 - right-sided 48
- ascending 111,221 Conjunctiva
- cancer 110,114 - conjunctivitis 14
- colitis 97,98,161,186,227 - reddening 8,14
Common cold 23-31,31 (chart), 48, 79 - vascular engorgement 8
- OMT 25,29 Connective tissue 151
Compensatory mechanism 63,72,121, -disease 186
152,153,156,204,207 - pathway 89
- Common compensatory pattern 154, Conservative treatment 165
156, 208,209,211 - see also Rational osteopathic treament
- compensatory fascial pattern 207 Constipation 45,93,97,98,104,105,
(diagram), 208,209,211 109,114,204,227,231
- compensatory musculoskeletal problem - incomplete emptying 109
57 Contacts 13
- uncommon compensatory pattern 208, Contracture 161,1663,183, 186,205
209,211 Convulsion 177
Complication 93,139,144 Coordination 178
- post operative 46- 47 COPD (See Chronic obstructive pulmonary
Compression 161,164,165, 219,222 disease)
Compression fracture 166 Coracoclavicular angle 211
Concentration of urine 127 Cord memory 93,112
Conception 144 Cornea 6,7
Concussion 11 Coronary
Conductive hearing deficit 10,11 - artery 58,59,69
Condylar decompression 102,105,120, - left circumflex coronary artery 69
217 - artery disease 59,61,69
Confusion 204 - artery occlusion 69
Congenital defect 204 - blood flow 60
Congestion 18,27,31,33,36,38,39, - vascular resistance 69
42,68,88,93, 95,98,99,116, - vasospasm 54
118,120,131,134,135,140,149 - see also Myocardial infarction,
(diagram), 150, 151,155,157, Myocardial ischemia
162,164,186,189,203,204, Corpora cavernosa 130,193
205,206 (diagram), 207,217, Cortical influence 142
221,228,229,230 Coryza 12
- abdominopelvic 99 Cost 144
- congestive symptoms 149,204,206 Costal examination 105
- local 24 Costochondritis 58
- lymphatic 6,8,12,40,105,116,118, Cough 2,4,36,39,40,44, 45,46,48,
120,140,149 (diaphragm), 151, 85,127,229
162,228,229,230 - activation for OMT 222
- passive 123, 207 - non-productive 45
-pelvic 105, 131,186 - paroxysmal 48
- in pregnancy 149 (diagram), 155- 156 - productive 46, 229
- reflex 2,36
Counselling 139, 144 CV4 technique (See OMT - CV4 technique)
Countercurrect exchange 127, 134 Cyanosis 186
Cowper gland 129 Cystitis 134; 136
Cramp (muscle) 204 , 205 Cystoscopy 129, 139
Cramping 81, 104, 105, 139, 188, 227 - basket extraction 139
Cranial
- base 60, 171 (See also OA, Occiput) D
- craniosacral mechanism 140, 144, 154,
156, 224
- "diaphragm" 203 Dalrymple technique (Pedal pump) 44,
- dural strain/stress 7, 15, 172 46, 102, 218-219, 229, 230
- extension mechanics (CRI) 48, 140, Deafness 15
157 Debilitated patient 196
- lambdoidal suture 120 Decongestant 23, 25, 135
- mobility 105 Decongestion 34, 142, 176, 220, 221,
- occipitomastoid suture 6, 92, 120 229, 231
- jugular foramen 84, 92, 105, 120, - interstitial· tissues 34
150 - uterus 14�
- occipitotemporal motion 105 Deformity 161, 164
- rhythmic impulse (CRI) 15 Degeneration 161
- strain patterns 8, 15, 172 Dehydration 176
- see specific bones; OMT -Cranial Delivery 7, 153, 156-158
Cranial nerve - difficult 7
- dysfunction 7, 8, 9, 10, 172 -labor 156- 157, 231
-I (Olfactory) 7 - pre-delivery care 156
- III (Oculomotor) 4, 7, 190, 192, 223 - post-partum period 152, 157
- IV (Trochlear) 7 - "blues" 157
-V (Trigeminal) 5, 7, 9, 10, 15, 16, - breast engorgement 230
28, 29 - treatment 157
- VI (Abducens) 7 - uterine inertia 157
-VII (Facial) 7, 18, 31, 190, 192, 223 Demerol 138
- geniculate ganglion 5 (diagram) Denervation 69
- superior salivatory nucleus 5 Dental
- VIII (Vestibulocochlear) 7 - dentures 8, 229
- IX (Glossopharyngeal) 7, 10, 15, 56, - trauma 7, 8
190, 192, 223 Depression 110, 116, 131, 139, 157, 162
-X (Vagus) 5, 7, 10, 11, 35, 38, 44, Dermatome 101, 143
48, 50, 55, 67, 68, 84, 85, 92, 93, Detoxification 42, 45, 163, 166, 220,
97, 98, 105, 107, 112, 120, 133, 228, 229
141, 190, 192, 223 Developmental
- XI (Spinal accessory) 9 - defect 204
- XII (Hypoglossal) 7 - stages (pediatric) 178- 179
Crawling 171 Diabetes mellitus 7, 130
Cremasteric muscle 127 Diagnosis
Crepitus 162 -abdominal collateral ganglion 200
Crohn's disease 97, 98, 110 - acumen - GI 109
Cross-talk 189 - Chapman's reflexes 200-201, 232-233
Cruciate ligament 164 - diaphragm 214
Cnishing pain 188 - fascial patterns 207- 212
Cultural stress 137 - pelvic diaphragm 216
Cultures 40-41 - regional tissue congestion 205
- soft tissue 209 - sodium benzoate 166
- somatic dysfunction 211 - wheat bran 117
- system 200 Differential diagnosis v, 11, 87, 88, 190
- See Somatic clues - Visceral dysfunction - cardiac 57
Dialysis 135 - EENT 7, 9(chart)
Diaphragm 33 (diagram), 35, 81, 85, - GI 79, 90, 110
100, 124, 127, 128, 130, 150, - GU 128, 131
151, 152, 156, 202, 203, 204, - inguinal hernia 129, 138
206, 207, 214, 216, 218, 221, 227 -ureterolithiasis 129, 138
- attachment 31, 38, 50, 104, 105, 156, - UTI 134
214, 216 Diffusion 159, 161, 162
- flattened 33 (diagram), 38, 39, 86, 156 Diffusion gradient 162, 163
·
- function 39, 48, 50, 99, 105, 152, Digestion 112
202, 204 - acids/enzymes 84, 111 (See also
- motion 38, 130 specifics)
- OMT: How to treat 215-216 Digital massage of prostate 136
- redoming 43 Diplopia 14
- pump 123 (See also Extrinsic/intrinsic Disease process 117, 172, 209 (See also
pump) specifics)
- well domed 33 (diagram), 43, 90 Dizziness 2, 8, 11, 204
(defined), 105, 156, 207 - differential diagnosis 11
Diarrhea 93, 97, 98, 100, 104, 105, 109, Dorsal hom of spinal cord 24, 188, 189
110, 139, 201, 210, 231 - lamina V 188
- idiopathic diarrhea 97 Drainage
- post-viral 210 - cardiopulmonary system 56
Diastolic pressure 65 (See also Blood - .colon 105
pressure, Hypertension) - decongestion 34, 142, 176, 220, 221,
Diet 13, 40, 50, 78, 116, 117, 121, 135, 229, -231
139, 153, 165, 166, 172, 176, 225 - EENT 6-8
- alcohol 78, 153, 166 - GU 123
- bulk in diet 116, 117 - lymphatic 6-8, 18, 25, 26, 27, 31, 33,
- non-absorbable 117 39, 43, 48, 50, 56, 86, 105, 120,
- chewing gum 8, 229 127, 139, 140, 156, 163, 164,
- citrus fruit 166 167, 176, 203, 204, 205, 206
- coffee 153, 166 - pathways 162 (See also specific)
- considerations 13, 78, 166 - surgical tubes 101
- cranberry juice 135 - thoracic 48
- eating habit 153 - venous 6-8, 25, 33, 43, 89, 140, 166,
- fasting state 113 204, 205
- fat restriction 117 Dribbling 136
- fat storage 155 Drug use 153
- flour 166 Duodenum 84, 107, 192, 199
- fluid intake 101, 102 - duodenal ulcer 86, 110
- food 190 Dupuytren's contracture 186
- food allergy 166 Dural strain/stress 7, 15 (See also listings
- food intolerence 100 under Cranial)
- lactose/milk 117, 166 Dysarthria 7
- linoleic acid 166 Dysmenorrhea 131, 132, 139-142, 231
- meal 113, 116, 165 - osteopathic approach to treatment 139-
- precipitating pain 109 142
- sugar 166
Dyspareunia 143-144 - development 171
-OMT 143 - epiblastic origin 129
Dyspepsia 110 - fetal development/growth 144, 149,
Dyspnea 48 153
Dysuria 129, 134, 136, 137 - germ theory iv
- Mullerian duct 129
E - origin 80, 124, 129
- Wolffian duct 129
Emergency treatment 79
Ear 5, 8, 9, 11, 12, 23, 174, 202 Emotion 172, 181, 185, 189, 190, 204
- abnormal sensation 8, 9, 11, 12 - disorder 181
- dysfunction 11, 12, 202 - factor 132, 142
- differential diagnosis 11 - growth 172, 190
- external canal 174 - instability 131
- hearing disorders 8, 9, 10, 12, 15 - stress 8, 69, 115, 125, 137, 138, 144,
- conductive 10, 11 189, 225
- deafness 10, 15 Empirical treatment 136
- decreased 11 Endocardial
- diminished 9, 10, 15 - endocarditis 68, 72
- high-pitched sound 9 - fibroelastosis 72
-low-pitched sound 9, 12 -fibrosis 72
- differential diagnosis 11 Endocrine system 184, 200 (See specific
-sensineural 11 organs)
- middle ear function 10 Endolymphatic
- wax plug 2 - channel/duct 6, 18
Ectopic foci - Heart 50, 60, 185 - hydrops 6
Ectopic pregnancy 152 - pressure 18
Edema 4, 10, 13, 36, 38, 71, 73, 80, Endothelium - Vascular 71
105, 116, 150, 155, 162, 186, Energy 153
204, 205 Enuresis 129
Edinger-Westphal nucleus 5 (diagram) Environmental factors 15, 49, 61, 112,
Education 144, 165, 166 113, 120, 225
EENT dysfunction 1-21 - external environment 112, 114, 120
-OMT 18 (chart) -smoking 15, 36, SO, 153
Efficiency 121 - See also Diet, Cold (temperature)
Effleurage 13, 18, 31, 66, 93, 222 - internal environment 113
Ejaculation 130, 133, 143, 188 - host factors iv, 10, 15, 24, 69, 106,
- disorder 130 113, 135, 177
- duct 129 - intracellular environment 205
EKG changes 56, 69, 72, 185 - uterine environment 144
- long Q-T interval/syndrome 69, 185 Enzymes 80, 84, 111
- prolonged P-Q interval 72 - cholecytokinin 115
- sick sinus syndrome 56, 72 - digestive enzymes 84, 111
Elavil 116 - see also specific enzymes
Electrolytes 127 Eosinophils 48
- balance/imbalance 34, 40, 45, 56, 66, Epigastric area 86, 206, 214, 227
101, 135 - diagnosis of abdominal collateral
- electrochemical gradients 111 ganglion 200
- electrophysiologic mechanisms 111 - subxiphoid fullness/tension 86, 227
- in hypertension 62 (diagram) - see also Celiac ganglion
Embryologic Epiglottis 175
Epiphoria 85 - chart 13
Epithelium - contact 173-174
- bronchial 36, 42 - entropion/extropion 14
- ciliated columnar 16, 23, 29, 223 - exercise 13
- hyperplasia 25, 37, 38 - failure of lid to follow cornea 4
- inflammation 24 - fatigue/strain 7, 14
- pseudostratified ciliated columnar cells - focus 13
35 - foreign body 13
- respiratory 24, 27, 28, 35 - glaucoma 6, 14, 18, 186
- sinus 223 - acute closed angle 14
- stratified squamous 16, 24 - chronic open angle 14
Erben's reflex 67 - narrow angle 4
Erectile dysfunction 142-143 - Horner's syndrome 3
- erection 130, 142, 188 - intraocular pressure 4, 14
Erogenous zone 132 - lens - innervation 4
Esophagus 192 - lymphatic drainage 6
- esophageal hernia 128 - GMT: How to treat 13-14
Essential hypertension 55, 61, 70, 125 - pain 8, 9, 14
- blood pressure 54, 62, 64, 70, 124, - pressure 55, 67
125, 133 - protrusion of eyeball 4
- labile phase 62 - symptoms 5, 8, 9
- pathogenesis 64 - visual disturbances
Estrogen 151, 152, 155, 157 - blindness 14
- cream 144 - blurred 4, 7, 8, 14
Ethmoid bone 16, 28 - diminution of perceived light 4, 8
- pump 28 - diplopia 7, 14
Eustachian tube 11, 17, 31, 223 - far-sighted/near-sighted 13
- dysfunction 8, 9, 10, 11, 15 - jumpy print 8
Exanthema 176 - visual development 178-179
Excitation 187 - watery 5
Excretion 124, 165 - widening 4
Exercise 13, 50, 140, 141, 164, 165, 166,
171, 215, 216 F
- Aqua-cize 166
- eye (Richardson) 13-14
- Kegel 216 Facial anhidrosi& 3
- knee-chest position 141 Facilitation 25, 44, 64, 130, 132, 143,
- pelvic coil 216 144, 164, 165, 183, 185, 189,
Exophthalmic goiter 4 190, 196
Expectorant 41 - altered reaction to stimulus 113-114,
Extraocular muscle 117, 125, 138, 183
- innervation 7, 14 (See also Cranial - deceased threshold 113, 183, 189, 196
nerves III, IV, VI) - facilitated segment 3, 18, 26, 27, 31,
- dysfunction 7 36, 37, 38, 44, 48, 50, 60, 64, 67,
- strabismus 7, 14 80, 82, 83, 84, 88, 90, 91, 93, 95,
- tone 14 97, 101, 102, 107, 118, 130, 133,
Extremities 185, 186 141, 144, 164, 165, 167, 189,
Extrinsic pump 206, 214 190, 194, 195, 225
Exudate 24, 25, 36 Failure to thrive 7
Eye 6, 18, 171, 174, 202, 223 Fallopian tube 129, 131
- angle of the anterior chamber 6 - disorder 144
Falls 140, 153 Floating kidney 123, 124
- ice/roller skating 140 Flu epidemic of 1918 41, 42
Family history 15, 153 Fluid 127, 139, 176, 210
Fascia 120, 123, 164, 171, 194, 195, - fluid intake 101, 102
205, 207, 210, 219 - mobilization 140
- anterior/posterior body 219 - retention 70, 125, 131, 151, 152, 155
- anterior cervical 174 - volume 64
- adhesions 230 Fluori-Methane 165 (See Spray &
- diaphragm 209 *etch; Trigger point»
- pathway 89, 156, 189, 202 Focal point (lens) 4
- pattern 88, 89, 154, 203, 205, 207-212 Fracture 24, 58, 100, 166, 204, 228, 229,
- Compensated 208, 209, 211 230
- Ideal 208, 209 - vertebral 100, 166, 228, 230
- Uncompensated 208, 209, 211 Frequency (See Urinary frequency)
- plane 202, 203 Friable liver .222, 227, 228, 229
- preference 203, 205 Friction 80
- restriction 207 Friction rub 37
- symptoms 203-203 Frigidity 132, 143
- tension 92, 205 Frontal bone 16
- torsion 86, 105149, 151, 204, 207 Frowning 8
- treatment 208 Fryette motion 171
- OMT 66, 90, 167, 176, 216, 230 Functional
- OMT (fascial release) 101, 102, 222 - change 161, 165
- OMT (fascial unwinding) 164 - definition 109
- upper GI 89-90 - disorder 85, 109, 123, 142, 207
Fatigue 4, 40, 105, 157 - obstruction - GI 113
Fatty acids 186 - reaction 117
Febrile seizure 177 - retention of salt/water 125
Fecal mass 221 - scoliosis 175
Fecal movement 111, 113 - structure-function interrelationship iv ,
Fertility 144 1, 12, 141 49, 50, 68, 93, 117,
Fetus 151, 153 131, 152, 161, 172, 175
- growth & development 144, 149, 153
Fever 3, 40, 41, 45, 46, 110, 136, 138, G
176, 228, 229, 230
- OMT 172
Fibroblastic activity 205 Gag reflex 175
Fibrocystic breast disease 230 Gait 57
Fibromyalgia syndrome 167 Galbreath technique 17
Fibroproliferation 205 Gallbladder 87, 93, 98, 116, 187, 199
Fibrosis 6, 18, 40, 72, 98, 161, 162, 175, - cholecystectomy 87, 115
205 - cholecytokinin 115
WFight or flightW 83 - cholelithiasis 110, 115
- see Sympathetic response, - disorder 86, 87 (diagram) , 93, 115
Hypersympathetonia - pain 115
Finger surgery 15 - post-cholecystectomy syndrome 87
First rib 209-213 - secretions 116
Fitst trimester 152, 153-155 - study IH.I
Flank pain 127, 131 Ganglion nodosum 85, 92, 105
Flatulence 97, 104, 109, 114, 115 Gas 109, 114, 116, 117, 221
Flexibility 166 - absorption 115
- bowel odor 115 - GYN examination 158
- excessive (GI) 114-115 - infection li8
- flatulence 97, 104, 109, 114, 115 - neurologic function 126 (diagram)
- hydrogen (GI) 114 - sphincter 188
- lung excretion 115 - treatment 133-144
Gastric acid 24 - (See also specific disorders and
Gastric ulcer 110 functions)
Gastrin 111 Geriatrics 40
Gastritis 165 - aging 149, 151
Gastrocolic reflex 111, 113, 116 Germ theory iv
Gastrointestinal (GI) tract 116, 161, 192, Glans penis i 31
199, 224 Glaucoma 6, 14, 18, 186
- bacteria 114 - acute closed angle 14
- cancer 229 - chronic open angle 14
- Chapman's reflex (diagrams) 90, 96, - narrow angle 4
232-233 - OMT study 14
- contraction 111, 116 Glomerular filtration rate (GFR) 125,
- gastrocolic reflex 111 133, 138, 185
- mass movement 111 Glomerulonephritis 135, 163
- non-propulsive 111 Glycogen
- propulsive/retropulsive 111 - glycogenolysis 184, 187
- segmentation 114 - synthesis 187
- slow wave ratio 113 Gnawing pain 81
- dysfunction 79, 93 (chart), 165, 195 Goblet cells 3, 18, 23, 29, 31, 38
- function 109 - goblet:ciliated cell ratio 23, 25, 29, 35,
- gas (See Gas) 38, 42, 223
- glands 85 Gonads 131, 199
- greater omentum 81 - gonadal deficiency 144
- haustra 111 - gonadal tissue 130
- headache 93 Gravity 142, 149, 203, 207
- hyperchlorhydria 84, 85 Gripping pain 188
- hypermotility 85 Groin pain 129, 131
- lesser omentum 80, 81 Guarding 86
- lower GI disorders 92, 95-107 Gyinnastics 140
- mechanisms 87, 115-116 GYN examination 157
- motility 98 - vaginal examination 100, 216, 229
- OMT 79, 89-93, 95, 101-106 Gynecologic dysfunction 132
- perforation 82
- polyps 110 H
- ulcer 86, 87, 110
- upper GI disorders 79-93
Geniculate ganglion 5 (diagram), 223 H2 blocker medication 87
Genitoiliopsoatic syndrome 132 Habitual factors 61, 149, 153
Genitourinary (GU) tract Haemophilus influenza 25
- bladder function 126 (diagram) Hay fever 48, 85
- Chapman's reflex diagrams 125, 232- Head 11, 153, 192, 202, 204, 205
233 - trauma 11, 153
- disorder/dysfunction 123-147, 217, Headache (See Cephalgia)
227 Healing process 118
- genital tissue 193 - healing rate 19, 34, 40, 95, 98, 135,
- genitoreproductive disorder 132, 143 209
Health v, 153, 171 91, 93, 106, 117, 123, 135, 139,
Hearing disorders 8, 9, 10, 12, 15 149, 152, 153, 156, 159, 162,
- conductive 10, 11 172, 189, 196, 201, 203, 208,
- deafness 15 210, 218
- decreased 11 - cardiovascular 68
- diminished 9, 10, 15 - mechanism 159, 177, 189, 207
- high-pitched sound 9 Hormones 151, 152, 155, 156, 157, 165
- low-pitched sound 9, 12 - adrenal 4, 65, 133, 151, 152, 155,
- differential diagnosis 11 165, 188, 192, 193, 199
- loss 10 - corticoids 152
- sensineural 11 - function 65, 165
Heart 149, 150, 156, 173, 187, 192, 201, - hormones 151, 152, 155
204, 206, 222 - adrenaline 188
- block 67, 72 - basis 131
- chronotropic effect 54, 69 - deficiency 144
- failure (See Congestive heart failure) - influence 115
- innervation 54-55 (diagrams) - mechanism 142
- inotropic effect 54, 69, 183 - pineal gland 184
- muscle 69 - pituitary 4, 17, 144, 165
- rate (See Bradyarrhythmia, - pituitary-ovarian axis 144
Tachyarrhythmia) - secretion 130
- rhythm (See Arrhythmia) - steroids 165
Heat 40 Homer's syndrome 3
Heel lift treatment 140, 165 Hospitalization 45, 176
- See also Short leg syndrome, Postural - intensive care unit (lCU) 60
disorders - length of stay 42, 49
Hematuria 136, 138 - patient 49
Hemidiaphragm 204 Host factor iv, 10, 15, 24, 69, 106, 113,
Hemodynamics 101 135, 177
Hemoglobin-oxygen dissociation curve 33 - host defenses . 136, 177
Hemophilus influenza 15 Humidification 23
Hemorrhage 72, 186 Humoral factors 61
Hemorrhagic necrotizing pancreatitis 84 Hydrogen 93, 114, 116
Hemorrhoid 204 Hydronephrosis 123, 124, 127
Henshaw 46-47 Hydrostatic pressure 71
Hepatic flexure 221 Hyoid bone 15, 17, 31, 61, 174
Hepatomegaly 56, 73, 227, 228, 229 - OMT 31
Hereditary factor 1, 61 Hyperchlorhydria 84, 85
Hering-Breuer reflex 38 Hyperlordosis (See Lumbar hyperlordosis,
Hernia 128 (diagram), 129, 228 Cervical hyperlordosis)
Hesitancy (Urinary) 137 Hypermotility of the intestines 85
Histology 161, 164, 184 Hyperparasympathetonia 231
History iv, 41, 79, 153, 154, 172-3, 177, Hypersympathetonia 44, 56, 64, 83, 84,
190 88, 91, 92, 104, 114, 118, 125,
- family history 15, 153 135, 137, 138, 161, 176, 183-188,
- pediatric history 172-3 194, 195, 198, 201, 203, 223,
- trauma history 6, 153, 172 228, 230, 231
Hoarseness 2, 85 - facilitation 25, 44, 64, 130, 132, 143,
Homeostasis iv, v, 1, 6, 12, 15, 16, 19, 144, 164, 165, 183, 185, 189,
28, 29, 34, 38, 39, 42, 44, 46, 48, 190, 196
49, 50, 56, 62, 65, 79, 84, 85, 87,
- altered reaction to stimulus 1 1 3-1 14, Implantation 144
1 17 , 125, 138, 1 83 Impotence 130, 132, 134, 142-143
- deceased threshold 1 1 3, 183, 189, Incision 101, 102, 227, 228, 230, 23 1
196 Incontinence (Urinary) 127, 228
- facilitated segment 3, 18, 26, 27, Induration 220
3 1 , 36, 37, 38, 44, 48, 50, 60, 64, Inertial injury 2, 7
67, 80, 82, 83, 84, 88, 90, 9 1 , 93, Infant 100, 1 7 1-175
95, 97, 101, 102, 107, 1 18, 130, Infection 6, 10, 24, 27, 34, 36, 40, 56,
133, 1 4 1 , 144, 164, 165, 167, 72, 85, 88, 95, 98, 102, 1 10, 123 ,
1 89, 190, 194, 195, 225 127, 132, 134, 135, 144, 163 ,
Hypertension 50, 55, 56, 6 1 , 64, 70, 1 84 172, 176, 177, 1 82, 219, 228,
- classification 6 1 229, 230, 23 1
- fixed 63 - bacterial 24, 36, 68, 172
- mechanism diagrams 62, 64 - bronchial 36
- OMT 62-63 - EENT 16, 27
Hyperthyroidism 1 1 - focus 163
Hypogastric plexus 129 - lower respiratory tract 40
Hypoperfusion 95 - measles 1 82
Hypotension 68, 155 - nasal 10, 24
Hypothalamus 52, 69, 1 14 - OMT 172
- hypothalamic "tuning" 1 14 - pharyngeal 6, 10
Hypothyroidism 1 1 - predisposition 72, 85, 88
Hypoxia 40, 4 1 , 48, 161 - prodrome 176
- prostate 136-137
I - upper respiratory tract 23-3 1 , 48
- urinary tract 134-135
- viral 10, 24, 36, 4 1 , 42, 172
Idiopathic diarrhea 97 Inferior cervical ganglion 202
Ileus 97, 100, 103 , 104, 199, 230 Inferior mesenteric ganglion 92, 97, 104,
- OMT 103 , 198, 230 107, 1 12, 125, 129, 130, 192,
Iliac fossa 127, 1 3 1 199, 224
Iliolumbar ligament 128, 129, 1 3 1 Inferior thoracic outlet (See Thoracic
- pain pattern diagram 128 outlet)
- strain 128, 1 29 Infertility 132, 144
Iliopsoas tenderpoint 139 - fallopian tube disorder 144
- See Muscle - Iliacus, Psoas, Psoas - genitoreproductive disorder 132, 143
syndrome - impotence 130, 132, 134, 142-143
- See also OMT -Counterstrain - OMT 142
Iliotibial band 96, 104, 130, 201 - spermatic count 144
- diagram 96 - work-up 144
- See also Chapman's reflex (Colon, Infiltration 80
Broad ligament, Prostate) Inflammation vi, 14, 24, 36, 37, 72, 84,
Illness 209 98, 1 3 1 , 132, 134, 137, 163, 188
Immune system 172, 218, 228 - EENT 27
- complex 159, 16 1 , 162, 163, 165, 166 - epithelium 24
- deposition 165 - eye 14
- function 2 1 8 , 228 - inflammatory arthritis 164
- reaction 163 - inflammatory cells 137
- response 3, 177 Influenza 24, 4 1 , 42
Immunization 171 - epidemic ( 1 9 1 8) 4 1 , 42
Immunology 1 82 - virus 24
Infraclavicular space 2 10, 2 1 1 Ischiorectal fossa 99 (diagram), 100, 130
Inguinal area 206 (diagram), 216; 229
- hernia 128 (diagram), 129 , 228 - OMT technique 105, 136, 2 16-217
Inherent functional property 1 83 (how to treat), 228, 229
- mechanism 1 2 1 - pelvic floor 99 (diagram), 128, 130,
Inhibition 1 87 134, 136, 143, 229
Inhibition 88, 9 1 , 1 87
- pressure 42 J
- reflex 196
Injection 165
Injury (See trauma) Joint 161
Innominate somatic dysfunction (See - arthralgia 136
Somatic dysfunction - Innominate ) - arthritis 1 6 1 , 162, 167
Inotropic effect 54, 69, 183 - lower extremity 1 6 1
Insomnia 4 - spine 161
Intercellular environment 189 - cartilage 159
Intercostal - damage/deformity 162, 166
- muscle 39 - description 161
- neuritis58 - destruction 163
- spaces 92 - effusion 166
Internal jugular vein 86 - function 164
Interstitial - minor motions 161
- edema 7 1 , 205 ... nutrition 162 (diagram), 164
- fluid 98, 149, 1 5 1 , 176, 189 - range of motion 162
- pressure 134 - structure 166
- space 127, 149, 202 - surface 159, 164
Intertransverse spaces 92 - tenderness 162
Intestinal tract (See Gastrointestinal tract) - see also Rheumatoid arthritis &
Intra-abdominal pressure 127, 128 Osteoarthritis
(diagram), 206, 228 - see also under Rheumatology
Intracellular environment 205 Jones' points
Intralumenal pressure 1 16, 1 17 - iliopsoas 139
Intraocular pressure 4, 14 - See OMT - Counterstrain
- See Eye, Glaucoma Jugular foramen 84, 92, 105, 120, 150
Intrapelvic pressure 128 - occipitomastoid suture 6, 92, 120
Intrathoracic pressure 195, 206, 2 1 8 Jugular vein 6
Intrinsic activation 222
Irritability 1 3 1 , 139, 204 K
Irritable bowel 85
- syndrome 97, 98, 109-122, 186, 201
- Diet 1 17 Kegel exercise 216
- medication 1 16-1 17 Kidney 42, 55, 62, 65 , 70, 123, 124,
- OMT 1 17-121 126, 127, 133, 134, 138, 165,
- personality type 1 10 1 85, 1 88, 192, 199, 224
- treatment 1 16-121 - calyceal calculus 1 3 8
Irritation - damage 1 34
- bronchial epithelium 36 - function 65, 1 24
- intercostal nerve 37 - glomerular filtration rate (GFR) 125,
Ischemia 56, 84, 1 85, 1 86 133, 1 3 8 , 1 85
- ischemic heart disease 69 - glomerulonephritis 135, 163
Ischial tuberosity 216 - in hypertension 63
- infection 134 Lightheadedness 11
- Lloyd' s punch test 127, 134 Linoleic acid 166
- nephrosclerosis 63, 64 Lipolysis 1 84
- polycystic kidney di sease 124 Lithotomy position 157
- ptosis 123, 124 Liver 42, 8 1 , 98, 107, 123, 165, 166,
- uremia 135 1 86, 1 87, 192, 199, 220, 221 ,
- See also GU tract; Urine 222, 227, 228, 229
Kinins 24 - Glisson' s capsule 8 1
Kneading 214, 222 - hepatomegaly 56, 73, 227, 228, 229
Knee 206 - OMT (Liver flip) 221-222, 227
Knee-chest position 140, 141, 142 - OMT (Liver pump) 45, 86, 166, 167,
(diagram) 220, 228, 229
Korr, I.M. 1 83 - portal venous congestion 70
Kyphosis 148, 15 1 , 155 - tenderness 73
Lloyd' s punch test 127, 134
L Local environment 1 12, 120, 137, 144,
1 89
- control 1 1 1
Ll -2 132, 143 - factors 137
Labia 127, 142 - nutrition 164
- pain 127 Long Q-T interval/syndrome 69, 185
Labor 156-157, 23 1 Lordosis
Laboratory data 1 10, 173, 205 - cervical 148, 166
Labyrinthitis 1 1 - lumbar 38, 1 15, 148, 15 1 , 166, 1 7 1 ,
Lacrimal gland/ Lacrimation 5 (diagram), 2 14
8, 29, 1 87, 192, 223, 224 - byperlordosis 124, 139, 151
Lactase 1 17 - Levitor orthosis 165
Lactic acid accumulation 95 - See Posture, Postural disorders, Gravity
Lambdoidal suture 120 Low back pain 127, 132, 136
Lamina V 1 88 Low energy 157
Larynx 55, 85 Lower extremity dysfunction 206, 228,
Learned reflex pattern 1 12 229
Learning disorder 172 - edema 155
Leg 155, 193, 204, 206, 219 - fracture 204
- edema 155 - leg 155, 193, 204, 206, 219
- fracture 204 Lubrication 143, 144
Length of stay 42, 49 Lumbar region 219
- asthma 49 - See Lordosis
Levitor orthosis 165 - lumbosacral angle 171
- See Lordosis, Postural disorders, - lumbosacral junction 104, 105, 154,
Gravity 208, 219
Librium 1 16 Lung 33, 34 (diagram), 86 , 173, 1 89,
Lifting 127, 128 192, 207 , 209, 2 10, 218, 224, 227
Ligament 128, 129, 130, 140, 157, 164, - base 2 1 8 , 22 1 � 227
166 - capacity 48
- iliolumbar 128 (diagram) - hypoperfusion 37, 38
- strain 140 - innervation/reflexes 34 (diagram)
- tension 157 - See Respiratory tract
- weakened 1 5 1 , 152, 155, 164 Lymphatic system 149, 150, 155, 172,
Ligamentum pectinatum 6 190
Light stroking of skin 222 - change in pregnancy 151
- congestion 105, 1 16, 1 1 8, 120, 140, Lymphaticovenous communication 70,
15 1 , 162, 228, 229, 230 7 1 , 86 (diagram)
- Ear 8 - return 3 , 6 1
- constriction/dysfunction 150, 223 Lymphoid infilitration 4
- obstruction 152 Lymphoplasmaphoresis 163
- drainage 3, 1 8 , 25, 26, 27, 3 1 , 33, 39, Lysis of nasopharyngeal adhesions 15
40 (diagram), 43 , 50, 56 Lysozyme 23
(diagram), 86, 120, 127, 139,
140, 156, 163, 164, 167, 203 , M
204, 205, 206
- Colon 105
- EENT 6-8 Malaise 204
- Eye 6 Manipulative treatment (See OMn
- GI 85-86, 89 Manubrium 105, 209, 210
- GU 127 Mass movement 1 1 1
- Heart 56 Massage 222
- Lungs 56 Mastoid air cells 7
- Reproductive tract 130-13 1 Maternal homeostasis 149
- Thoracic 48 Maxillary pain 12
- duct 27, 56, 86, 202, 210 Maxillary sinus 28
- Thoracic duct 56, 70, 73, 86, 99, - pain 9, 16
127, 210 - secretions 12
- distension 66, 70, 73 Mayo Clinic 82 (diagram)
- surgical drainage 163 Meal 1 13 , 1 16, 165
- effect 1 8 , 3 1 , 50, 93, 141 - precipitating pain 109
- Cardiovascular 68 Measles 1 82
- GU 134 Mechanical
- element 132, 135 - change 151
- flow 1 8 , 3 1 , 34, 50, 70, 7 1 , 72, 85, - decompensation 156
86, 95, 99, 102, 1 17, 120, 127, - 'stress/strain 15 1 , 152, 155, 1 6 1 , 164
1 3 1 , 1 34, 150, 1 5 1 , 156, 157, Medial strabismus 7
195, 202, 203 , 207, 2 1 9 Mediastinum 6 1 , 209
- flow capacity 85 Medical treatment 14, 60, 67, 69, 86, 87,
- rate 66 93 , 136, 153
- renal hilar 127 - failure 86
- stasis 7 1 , 72, 1 3 1 - ineffective 40, 7 1 , 98-99
- fluid 1 89, 229 Medication 1 1 , 4 1 , 50, 79, 88, 106, 1 16-
- goals 164 1 17, 1 3 1 , 135, 138, 140, 159,
- Rheumatology 162-163 16 1 , 163 , 165, 167, 1 89, 225, 23 1
- nodes 172, 174, 176 - alcohol 78, 153
- cervical 6, 172, 174 - amitriptyline 167
- lymphadenopathy 172 - antacids 1 16
- pathways 27, 28, 85, 88, 152, 164, - antibiotic 15, 16, 23 , 40, 4 1 , 42, 106,
207 127, 135, 136
- production 70 - anticholinergic medication 1 16
- pump 1 3 , 33, 39, 43 , 44, 46, 105, - antidepressant medication 1 16, 167
152, 156 - antihistamine medication 15, 41
- Extrinsic 120, 150 - anti-inflammatory 131, 159, 167
- return 66, 124, 196, 218, 228, 229 - antipyretic 1 77
- vessel 150, 1 5 1 , 162, 202, 203 , 206, - antispasmotic medication 1 16
220 - antitussive 4 1
- aspirin 1 1 , 140, 177 - OMT (mesenteric lift, release, stretch)
- salicylate toxicity 11 89 (how to treat), 93, 102, 107,
- Carafate 87 1 15, 190, 221 (how to treat), 227
- codeine 41 Mesocolon 80
- concentration 3, 88, 99, 1 35, 136, 159 Metabolic
- demerol 138 - acidosis 33
- dextromethorphan 41 - changes 98
- dosage 48, 49 - dysfunction 79
- drug use 153 Metabolism 95, 124, 1 5 1 , 159, 163, 177,
- estrogen cream 144 190
- expectorant 41 - metabolites 155
- Flexeril 167 Metallic taste 7
- H2 blocker Metastatic di sease 28
- homeostasis and 79 Metatarsal varus 173
- ineffective 23 1 Methane 1 14
- morphine 138 Microorganism 177 (See Bacertia, Virus)
- NSAIDs 1 3 1 , 140, 165 Micturition 126 (diagram)
- OMT and 79, 86, 88, 93 Middle cervical ganglion 202
- penicillin iv Middle cranial fossa 7
- pseudoephedrine 15 Middle ear function 10
- side effect 1 1 , 159, 16 1 , 163 , 165 Milk 1 17, 166
- sulfa compounds 1 15 Misalignment
- sulfamethoxazole 1 36 - lower extremities 161
- sympathetic blocker 167 - spine 161
- sympathomimetic 41 - See also Postural disorders
- tranquilizers 1 16 Mitral stenosis 72
- trimethoprim 1 36 Mitral valve prolase 58
Medulla 34, 35 Morbidity 19, 54, 56, 69, 72, 1 84
- medullary center 34 (diagram), 196 Morning stiffness 164
Megacolon 1 86 Morphine 138
Meissner's plexus 223 Mortality 40, 4 1 , 42, 50, 56, 60 (graph) ,
Melatonin 1 84 6 1 , 72, 84, 95, 1 84, 1 85, 1 86
Membrane permeability 159 Motion testing 154
Memory pattern 195 Motor vehicle accident 7, 153
Meniere's disease 6, 1 1 , 15, 1 8 Mouth 174, 175
- OMT 15, 1 8 Mucolytic expectorant 41
Meninges 150 Mucorrhea 1 17
Menstruation 139, 144 Mucosa
- dysmenorrhea 1 3 1 , 132, 139-142, 23 1 - barrier 87, 93
- osteopathic approach 1 39-142 - defenses 84
- irregular cycle 144 - mucous buffer 84
Mental factor 142 - GI · 9 1
- mental health 153 - mucous blanket 35, 36
- mental need 190 - bowel 1 16
- stress 144, 1 89 , 225 - irritation/ulceration 24, 27
Mesentery 80, 86, 89, 98 (diagram), 1 15, - mucous membrane
1 16 , 120, 221 - Defense mechanisms 3
- attachments 98 (diagram) - Driness 3
- congestion 1 16 - Engorgement 5
- GI 84
- mucous gland 1 87
- Swelling 1 0, 27 - orbicularis oculi spasm 8
- mucus plug 2 1 8 , 229 - orbicularis oculi TP 8, 9, 1 2
- mucus secretion - paraspinal 90, 9 2 , 1 0 1 , 102, 104, 1 3 1 ,
- Excessive GI 1 14 1 7 1 , 228
- Thick 24, 28, 42 - pectoralis 1 97, 2 1 9
- Thin 24, 27, 28, 42, 23 1 - Pectoralis major 4, 5 7 , 23 1
- sensitivity 93 - diagram 57
- sloughing 24 - Pectoralis minor 198
Mullerian duct 129 - pilomotor 1 87
Mullerian orbital muscle 4 - psoas 124, 128, 132 (diagram)
Multipara 157 - OMT 2 1 5
Muncie Technique 1 5 - pterygoid 1 7 , 29, 224
Muscle - trigger point 8, 9
- contraction 1 7 1 - See Muscle - Lateral & Medial
- inhibitory pressure 42 pterygoid
- metabolism 69 - pterygopalatine 223
- rigidity 1 3 1 - quadratus lumborum 90, 124, 198
- smooth muscle 138 - OMT 2 14-2 15
- of bowel 1 1 1 - rectus abdominus 1 39
- spasm 25, 86, 1 32, 16 1 , 204 - rotatores 82
- spindle 1 83 - scalene 39, 198, 2 1 0
- strengthening 140 (See also Exercise) - serratus anterior 198
- sympathetic effect on 1 83 - splenius cervicis TP 8, 9
- tone 101 - sternocleidmastoid, sternal division TP
- weakened 151, 152, 155 8 , 9, 12
Muscle - Specific - sternocleidomastoid (Clavicular portion)
- abdominal 86, 127, 1 3 1 11
- accessory respiration 48 - trigger point 9, 1 1
- bronchial 35, 49, 1 87 - tensor veli palatini 12, 1 7
- cardiac 1 83 - trapezius TP 8, 9, 1 2
- ciliary 4 Musculoskeletal stress 153
- cremasteric 127 - complaint 154
- digastric TP 9, 1 2 - dysfunction 109, 1 5 1
- erector spinae 42, 127, 1 7 1 , 1 9 8 , 199 - See also somatic dysfunction
- extraocular 7, 14 Myalgia 1 36
- hip 1 7 1 Myasthenia gravis 163
- iliacus/iliopsoas 2 14, 2 1 5 Mydriasis 4, 1 8
- See slso Muscle - Psoas Myenteric plexus 223
- intercostal 35, 39, 198 Myocardial damage 1 85
- lateral pterygoid TP 7 , 9, 16 - infarction 50, 54, 59, 60, 66, 68, 70,
- lateral rectus 7 72, 1 84, 1 85
- latissimus dorsi 197, 198 - Anterior wall 59, 68
- levator palpebrae 4 - differential diagnosis 58
- longus coli 2 1 0 - Inferior wall 59, 60, 68
- masseter 1 1 - Morbidity 69
- trigger point 8, 9, 12 - Posterior wall 59, 70
- medial pterygoid 1 1 , 12, 17, 1 8, 3 1 - ischemia 70
- trigger point 9 , 10, 12, 15 - palpatory fmdings 59 (diagram)
- Mullerian orbital 4 - See also under listillgs Angina, Cardiac,
- occipitalis 1 1 Coronary
- occipitalis TP 8, 9, 12 Myofascial points 205
- See under listings Trigger point, - preganglionic fiber 125, 129
Counterstrain - ramus communicans 1 85
Myofascial trigger points (See Trigger - somatic 50, 1 15
point) - sensory afferent 8 1 , 1 88, 1 89,
Myotome 101 194
- speed (fast, very fast, slow, very
N slow) 195, 1 96
- visceral afferent 2, 3 , 24, 34, 35,
83, 89, 90, 95, 97, 1 1 1 , 1 15, 1 19,
Nails - Thickened 1 86 1 26, 143, 1 88, 1 89, 194, 195, 23 1
Narrow angle glaucoma 4 - primitive 1 12
Nasal - receptors 62, 80, 8 1 , 1 83
- congestion 24 - segmental 79
- cycles 24 - See also Segmental facilitation,
- discharge 85 Facilitated segment
- disorder 2, 16, 24 - supply 95, 123
- mucosa 7 - thresholds 1 13 (See also Facilitation)
- passages 23, 24 Nervous system - Specific Nerve
- secretions 2, 3, 4, 5, 16, 223 - abducens 7
- Thick 4, 16, 23 1 - buccal (Trigeminal branch) 9
- Thin 5, 1 6 - cardiac 202
- septal deviation 1 6 , 24 - deep petrosal 25
- sinus function 16 - facial S, 7, 190, 223
- turbinates 23 - genitofemoral 124
Nasolacrimal syndrome 23 1 - glossopharyngeal 7, 10, 15, 190, 223
Nasopharyngeal - greater petrosal 2, 5 (diagram), 223
- adhesions 6 - greater splanchnic 107, 192
- mucosa 5 - hypoglossal 7
- nasopharyngitis 15 - inferior laryngeal 5
Natural defences 1 36 - infraorbital 23 1
- host factors iv, 10, 15, 24, 69, 106, - OMT: how to affect 28
1 1 3 , 135, 177 - intercostal 35, 37
Nausea 8 1 , 85, 104, 138, 139, 204 - least splanchnic 107, 192
Neck 1 92, 202, 205 - lingual 56
- pain 5, 59 - lumbar splanchnic 107, 192
- See also listings under Cervical and - occipital 85
OMT - oculomotor 4, 7, 190, 223
- veins (distended) 73 - olfactory 7
Nephrosclerosis 63, 64 - pelvic parasympathetic 106
Nervous system 172 - pelvic splanchnic 84 (diagram), 93, 98,
- central nervous system 150, 1 5 1 , 152, 100, 107, 1 12, 1 19, 126, 129,
172, 1 83 , 195, 204 1 3 3 , 1 4 1 , 190, 193, 223
- cerebrospinal distribution 81 - OMT: How to affect 224
- spinothalamic tract 80 - phrenic 27, 3 1 , 35, 46, 8 1 (diagram),
- endings 80 105, 124, 133, 196, 207, 214
- fibers - pterygoid canal 25
- efferent fibers (sympathetic) - pudendal 100, 106, 126, 127, 133, 142
- lumbar sympath. splanchnic 83 - sciatic 1 32
- thoracic sympathetic 83 - small petrosal 56
- pathways/plexi 111 - spinal accessory 9
- post-ganglionic fiber 83, 129 - splanchnic 80
- superior laryngeal 5 Non-absorbable bulk 1 17
- supraorbital 23 1 Normoblasts 1 84
- OMT: How to affect 28 Nose 174
- trauma 172 - fracture 24
- trigeminal 2 (diagram), 7, 9, 10, IS , - pain 5, 1 2
1 6 , 28, 29, 223 - rhinitis I S , 1 6 , 3 1 (chart)
- geniculate ganglion 5 (diagram) - rhinomanometry 16
- trochlear 7 - runny 5
- vagus 2, 5, 7 , 10, 1 1 , 35, 3 8 , 44, 48, - See also Sinus
50, 55, 67, 68, 84 (diagram), 85, Noxious somatic input 161
92, 93, 97, 98, lOS , 107, 1 12, NSAIDs 1 3 1 , 140, 165
120, 1 3 3 , 1 4 1 , 190, 223 Nutrient 93, 95, 1 6 1 , 167
- OMT: How to affect 224 - concentration 159
- See also Vagal afferents, Vagal - supply 3, 6, 25, 68
connections, Vagal tone; Vagal Nutrition 88, 95, 120, 14 1 , 149, 159,
hyperactivity 16 1 , 164, 166 , 167, 1 7 1
- vestibulocochlear 7 - See also Diet
- vidian 2 (diagram), 5 (diagram) Nystagmus 7
Neural
- control o
- bladder 126 (diagram)
- EENT 6-8
- GI extrinisic/intrinsic 1 1 1 -1 12 02 exchange 141
- pUlmonary 34 (diagram) OA 154, 208
- element 1 35 OA-AA 85, 105
- foramen 166 Obstetrical
- function 156 - cases 28
- mechanism 142 - patient 149-158
- symptoms 166 - OMT 157-158
Neuritis 23 1 Obstructive uropathy 134, 135
Neuroanatomy 79 Occipital
Neurogenic factors 6 1 , 132 - bone 6, 84
- obstruction 1 37 - compression 8
"Neurologic lens" 144, 225 (See - headache 85, 93
Facilitated segment) - level 154
Neuromuscular - occipitomastoid suture 6 , 92, 120
- splinting 1 0 1 , 102 - jugular foramen 84, 92, lOS , 120,
- transmission 1 83 150
- neuromusculoskeletal system 17 1 , 190, - occipitotemporal motion 105
203 Occlusal disharmony 8
Neuronal pool 1 89 Occult blood 1 10
Neurophysiology 79 Ocular
Neurovascular compromise 48 - oculocardiac reflex 55
Nervousness 1 16 , 1 3 1 - oculocervical reflex 2
Nervus erigens 56 - stroking 18
Neurotic personality type 1 10 Olfactory apparatus 183
Newborn 1 7 1-2 Omentum 80, 81
Night cramPS 204
Nitrogen 1 14 OMT (Osteopathic ManipUlative
Noctural enuresis 129 Treatment) 40, 136, 1 89
Nocturia 1 36 , 137
[Note: Section subdivisions/or OMT OMT: GENERAL EFFECT
include: - Circulation improvement 89
OMT:AUTONOMIC FUNCTION - Congestion relief 89
OMT:GENERAL EFFECT - Fever modulation 172
OMT:GOALS - Homeostasis 63
OMT:MANIPULA TIVE - Pain relief 88
PRESCRITION - Preventative medicine 135
OMT:MOBILIZE FLUIDS - Range of motion increase 175
OMT:RESEARCH STUDIES OMT: GOALS 88, 106, 1 2 1 , 133, 1 89,
OMT:REGIONAL 194-195, 202, 227-23 1 (chart)
APPLICA TION - Asthma 49
OMT:SOFI' TISSUES & - Cardiovascular 61
MUSCLES - Congestive heart failure 66
OMT:SYSTEMIC COMPLAINTS - Ear 14-15
OMT:TECHNIQUE - EENT 6
DESCRIPTION - GI 87, 9 1
- GU 123 , 1 3 8
OMT: AUTONOMIC FUNCTION - Irritable bowel syndrome 1 17-1 1 8
- OMT: PARASYMPATHETICS 18, - Lower respiratory 45
3 1 , 50, 93, 107, 133, 140, 1 4 1 , - Lymphatic pump 218
1 9 0 , 223-224 - Myocardial infarction 60
- to GI tract 92-93, 1 19-120 - Obstetrics 153-158
- Pelvic splanchnic influence 224 - Physiologic goal addressed 227-23 1
- See also OMT - Sacral , Sacroiliac, (chart)
S2-4 - Pneumonia 42
- Sphenopalatine ganglion 16, 17, 1 8 , - Prevention 1 12
3 1 , 49, 223, 224, 23 1 - Rheumatology 163-164, 167
- Vagal influence 49, 224 - Systemic di sease 88
- See aso OMT - OA-AA-C2, - Upper respiratory tract 25
Cranial, Occipitomastoid - Uterus 140
- OMT: SYMPATHETICS 1 8 , 3 1 , 50, OMT: RESEARCH STUDIES
93 , 107, 1 1 8-1 19, 1 3 3 , 1 4 1 , 164, - Asthma 49
190, 194-202 - Cardiovascular 50
- Cervical ganglion 67 - Chronic bronchitis 48
- Collateral ganglion (Ventral - COPO 48
abdominal) 9 1 , 93, 102, 107, - Fibromyalgia 167
1 1 8, 120, 1 3 3 , 1 4 1 , 190, 200, - Glaucoma 14
221-222, 224, 227-228 - Historical 41 -42
- Celiac ganglion 227 - Hypertension 65
- Inferior mesenteric ganglion 133, - Lymphatic pump 28
1 4 1 , 200, 227 - Meniere's di sease 15
- Superior mesenteric ganglion 141, - Nose 16
227 - Pneumonia 41-42
- Chain ganglion 190 - Post-operative ileus J03
- Rib raising 1 8 , 26, 27, 3 1 , 42, 44, - Postoperative respiratory complication
45, 46, 50, 67, 88, 9 1 , 93, 102, 46-47
104, 107, 1 1 8, 1 3 3 , 1 3 8 , 14 1 , - Renal disease 135
176, 190, 195-199, 201 , 203 , 228 - Uterine contractions 157
- Chapman's reflexes 17, 1 8 , 3 1 , 50, Ol\IT: MANIPULATIVE
66, 67, 92, 93, 104, 107, 1 19, PRESCRIPI'ION 121
133, 190, 201 , 23 1 , 232-233 - Choice of technique 164, 225
- Dosage 154, 164, 175 - Pectoral traction 28, 44, 6 1 , 102,
- General 1 , 152 156, 2 19, 230
- Indicatior;ts for 227-23 1 (chart) - OMT: LOCAL TISSUE
- Ineffective 17 MOBILIZATION
- Length of treatment 91 - Ascending colon release 227
- Mechanisms postulated 66 (chart) - Breast drainage 230
- Modifications needed 101 - C.ecal release 227
- OMT and medication 79, 86, 88, 93 - Descending colon release 227
- ·OMT" by family member 157, 176, - Eustachian tube 1 5 , 17
2 1 9 , 230 - Gallbladder pump 167
- Order of treatment 44, 60, 9 1 , 201 - Hyoid 31
- Hypersympathetonia treated first - Liver flip (lung bases) 221-222, 227
- (Relative) contraindications 6, 1 3 , 4 1 , - Liver pump 86, 166, 167, 2 1 8 , 2 1 9 ,
79, 102, 1 39, 152, 164, 166, 176, 220, 228, 229
2 1 9 , 222, 227-23 1 (chart) - Mandibular drainage technique 17
- Side effects 164, 1 7 1 - Mesenteric lift 89, 102
- Therapeutic trial 144 - Mesenteric release 89, 93, 107, 190,
- Treatment frequency 101 22 1 , 227
- When to start 88 - Mesenteric stretch 1 15
OMT: MOBILIZE FLUIDS - Ocular muscle energy 14, 1 8
- OMT: MAXIMIZE THORACO - Ocular stroking 14, 1 8
ABDOMINO-PELVIC PUMP - Posterior axillary fold 164, 220, 230
- Thoracoabdominal diaphragm 13, - Ruddy technique 14
1 8 , 27, 3 1 , 43 , 50, 67, 85 , 90, 93, - Small intestine mesenteric release 89,
1 0 1 , 105 , 107, 120, 133, 1 4 1 , 227
176, 190, 2 14-2 16 - Small intestine mesenteries 89
- Abdominal fascial release 228 - Splenic pump 219, 220, 228
- Diaphragm redorning 6 1 , 105, - Somatic component 118
120, 176, 214, 228 - Supportive 104-106
- Thoracic cage - Symptom relief 87
- Costal 1 8 , 3 1 , 44, 50, 6 1 , 66, 90, OMT: REGIONAL APPLICATION
93 , 107 , 1 3 3 , 1 4 1 , 190, 198 - OMT: ACTIVATING FORCES
- Sternum 50, 6 1 , 90, 102 - Direct 90, 105, 222
- Pelvic diaphragm 107, 190, 216-2 1 7 - HVLA 43 , 49, 82, 164, 166, 1 7 1 ,
- Intrarectal release 105, 229 176, 225
- Intravaginal 105, 217, 229 - Muscle energy 14, 1 8 , 49, 157,
- Ischiorectal fossa 105, 136, 216- 198, 2 1 5 , 2 1 7
2 1 7 , 228, 229 - Muscle energy for eyes 14
- OMT: LYMPHATIC PUMPS - Pillow technique 154
- Lymphatic pumps 1 8 , 28, 3 1 , 46, - Resistive duction (Ruddy) 18
49, 50, 66, 67, 88, 93, 102, 120, - Indirect 43 , 49, 60, 6 1 , 90, 1 0 1 ,
1 3 3 , 1 4 1 , 176, 1 82 , 190, 203 , 102, 105, 1 5 7 , 164, 167, 212,
2 1 8-2 19, 229-230 2 1 5 , 222
- Dalrymple (Pedal pump) 44, 46, - Counterstrain 1 39, 157, 165, 167 ,
102, 21 8-219, 229, 230 215
- Thoracic pumps (various - Stacking 164, 167
modifications) 28, 176, 229, 230 - Joint pump 164, 167
- Lymphatic techniques 120, 162, - Myofasciallfascial unwinding 164,
167, 1 76, 202-222, 2 1 8-222, 229- 212, 214, 222
230 - Fascial release 1 0 1 , 102, 222
., Respiratory cooperation/force 89, - Iliopsoas 215
215 - Medial pterygoid 1 8 , 31
- OMT: CERVICAL - Paraspinal 88, 90, 1 0 1 , 102, 104,
- Suboccipital 92 1 3 8 , 201 , 214
- OA 1 3 , 1 8 , 3 1 , 44, 46, 50, 66, 67, - Quadratus lumborum 214-215
88, 93, 104, 120, 1 3 3 , 1 4 1 , 190, - Soft tissue 1 8 , 27 , 3 1 , 43, 45, 46,
224 90, 9 1 , 104, 105, 1 1 8, 1 19, 120,
- AA-C2 1 8 , 3 1 , 44, SO, 6 1 , 67, 88, 157, 164, 167, 175, 176, 201 ,
93, 104, 107, 120, 133, 141, 190, 2 14, 2 1 8 , 222, 224
224 - Clopping 41
- C3-5 1 8 , 3 1 , 190 - Compression 165
- Cervical 12, 44, 46, 1 0 1 , 102 - Effleurage 1 8, 3 1 , 93, 222
- OMT: CRANIOSACRAL 144, 224 - Inhibition 43, 46, 9 1 , 1 0 1 , 102,
- Condylar decompression 16, 30, 92, 104, 138, 224
102, 105, 120, 217, 224 - Kneading 104
- Cranial 7, 1 3 , 14, 16, 1 8 , 28, 3 1 , - Vibratory 218
50, 67, 77, 88, 92, 93, 105, 107, OMT: SYSTEMIC COMPLAINTS
1 3 3 , 140, 144, 157, 165, 190, 224 - Asthma 49
- CV4 46, 49, 6 1 , 66, 102, 140, 157, - Cardiovascular 67 (chart)
166, 167 - Common cold 25-29
- Frontonasal suture spread 28 - Dysmenorrhea 139-142, 141 (chart)
- Infraorbital nerve 16, 28, 23 1 - Dyspareunia 143
- Occipital decompression 30 - EENT 18 (chart)
- Occipitomastoid suture 66, 104, 224 - GI dysfunction 95
- Supraorbital nerve 16, 28, 23 1 - Colon dysfunction 101- 106, 107
- OMT: SACRAL (chart)
� S2-4 93, 107, 133, 1 4 1 , 190 - Ulcer 79
- Sacral inhibition 140, 23 1 - Upper GI dysfunction 89-93, 94
- Sacral rocking 1 19, 140, 224 (chart)
- Sacroiliac 93, 107, 1 19, 133, 135, - GU dysfunction 133 (chart)
1 4 1 , 142, 190 - Hypertension 62-63
- OMT: THORACIC - Ileus 103 (chart)
- Thoracic inlet 12, 1 8 , 3 1 , 46, SO, - Ileus prevention 198, 230
67, 93, 1 0 1 , 107, 133, 1 4 1 , 176, - Infection 172
190, 2 1 2 - Obstetrical patient 158
- Tl-12 3 1 , 190 - Postpartum patient 157
- T l-4 12, 1 8 , 3 1 , 46 - Pediatric 1 7 1 , 175-177
- Tl-6 50, 67 - "Tick-tock" method 176
- T5-9 93, 107 - Pulmonary dysfunction 3 1 (chart), 34,
- TlO- l l 93, 107, 133, 141 SO (chart)
- OMT: THORACOLUMBAR - Rheumatology 163-167
- Tl2-L2 93, 107, 1 3 3 , 141 - Sexual dysfunction 142
- Thoracolumbar junction 1 8 , 27, 3 1 , - Sinus dysfunction 16
50, 66, 67, 90, 93, 1 18 , 120, 135, - Systemic dysfunction 1 89-233 , 190
140, 1 4 1 , 230 (chart)
OMT: SOFT TISSUES & MUSCLE - Urologic disorders 1 33-134
- Fascia 66, 90, 167, 176, 216, 230 - See also Rational osteopathic treatment
- Anterior cervical fascia 17, 46 plans
- Anterior/posterior body 219 OMT: TECHNIQUE DESCRIPTION
- Cervical fascia 17, 1 8 , 46 (How to treat)
- Muscles - Abdominal diaphragm 215, 216
- Direct stretch 2 15-2 16 Orbeli effect 1 83
- Indirect 216 Orbital tenderness 23 1
- Ascending colon mesenteric release Organ function 150
221 Organ hypertrophy 151
- Cecal release 221 Organic disorder 88, 109, 142, 144
- Chapman's reflexes 65, 92, 201 Orgasm 1 30, 143
- Colon 104 Ortalani 's test 175
- Collateral ganglion inhibition 200 Orthodontic treatment 140
- Dalyrimple technique 2 1 8-219 Orthosis 165
- Descending colon mesenteric release - heel lift 140, 165
221 - Levitor orthosis 165
- Eye exercises 13-14 - shoe 165
- Fascial release 222 Orthostatic albuminuria 123
- Ileus prevention 198-199 Osmotic gradient 127
- Infraorbital nerve 28 Osteoarthritis 166, 1 85
- Intrarectal release of pelvic floor 217 Osteopathic considerations vi, 152
- Intravaginal release of pelvic floor 217 - GU tract 123-147
- Ischiorectal fossa 2 16-2 1 7 - irritable bowel syndrome 109-122
- Liver flip 221-222 - obstetrical patient 149-158
- Liver pump 220 - pediatric patient 1 7 1 - 1 80
- Lower extremity unwinding 220 - rheumatology 159-168
- Lymphatic pump 2 1 8 , 219 - treatment plan model 1 8 , 3 1 , 50, 93,
- Thoracic 218 107, 1 3 3 , 1 4 1 , 190
- Pectoral traction 219 - See also Rational osteopathic treatment
- Pedal 2 1 8-219 - See also OMT for patients with
- Mandibular drainage 17 SYSTEMIC COMPLAINTS
- Mesenteric release/lift 89, 221 Osteopathic manipUlative treatment (See
- Ocular 14 OMT)
- Pectoral traction 219 Osteopathic principles application (See
- Pedal pump 2 1 8-219 Rational osteopathic treatment)
- Pediatric 1 76 Osteoporosis 28, 1 6 1 , 166, 1 86
- Pelvic diaphragm 216-217 Ostial occlusion 16
- Pelvic splanchnic nerves 224 Otalgia 10, 15
- Petrissage 222 Otic ganglion 223
- Posterior axillary fold 220 Otitis media 10, 15, 172
- Quadratus lumborum 2 14-215 Otologic examination
- Rib raising 42, 196, 197 - abnormal 10
- Debilitated patient 196 - otoscope 174
- Seated patient 197 Ova & parasites 1 10
- Supine patient 197 Ovarian
- Rib Twelve (R12) 2 14-215 - congestion 217
- Sphenopalatine ganglion 223-224 - cyst 131
- Splenic pump 219-220 - inflammation 1 32
- Supraorbital nerve 28 - ovaries 130, 132, 1 4 1 , 1 8 8 , 192, 2 1 7
- Thoracic inlet (Indirect) 212 - ovulatory cycle 139, 144
-" Thoracic inlet (Direct, 2-step) 212-21 3 Oxygen 3 3 , 34, 38, 40, 48, 88, 93, 95,
- Thoracic inlet (Seated) 213 98, 1 14, 120, 1 4 1 , 16 1 , 1 84, 1 85
- Vagal influence 224 - consumption 161
Oocotic pressure 134 - saturation 48
Ophthalmoscope 174 - oxygenation 88, 98, 120, 155
Oral fluids 101
p - maxillary sinus 9, 1 6
- menstrual 139
- neck 5
Pacinian corpuscle 80, 183 - nose 5 , 12
Pain 86, 162, 164, 173, 1 83 , 1 86, 1 88 - orbit 8
Pain factors/qualities - pelvic 105, 1 3 1 , 132, 137
- amplification 1 6 1 - penis 1 3 1
- characteristics 8 1 - perineum 1 36
- excruciating 139 - phrenic 8 1
- fibers 85 - pleuritic 37
- mechanisms 80-81 (diagram) - post-auricular 12
- medication 1 3 8 (See Analgesics, - prostate 137
Specific Rx) - rectum 1 3 1
- pain-insensitive structures 8 1 - retro-orbital 5 , 8
- pain-spasm-pain cycle 163 - right-sided abdominal 1 16
- perception 1 6 1 , 164, 1 83 - sacral 1 3 1
- precipitated by meals 109 - shoulder pain 59, 8 1
- quality 1 88 - sinus 7 , 9, 1 2 , 2 8
- radiation 1 3 1 - somatic 8 1
- receptors 80, 8 1 - somatic localization 8 1
- location 80 - substernal 57
- reduction/relief 104, 163, 23 1 - suprapubic 1 3 8
- swallowing 12 - temple 5
- threshold 141 - thigh 1 3 1 , 1 3 8 , 1 39
- visceral 80-8 1 (diagram) - thoracolumbar 127, 1 3 8
Pain location - throat 12
- abdominal 109, 1 14, 1 15 , 1 16, 1 17, - urinary bladder 129
120, 127, 132, 138, 139 - uterus 1 3 1
- abdominal distension 1 15-1 16 - vascular 1 88
- arm 59 - visceral 80, 8 1
- back 1 3 8 , 139 Pain pattern 79 , 82, 86, 132
- low back 127, 1 32, 1 36 - cardiac 58, 81 (diagram)
- cervical 59 - cardiovascular system 58
- chest 40, 44, 57, 58 (diagram) - duodenum 81 (diagram)
- colon 105 - gall bladder 8 1-8 1 (diagram)
- ear 5 , 9, 10, 1 1 , 15 - iliolumbar ligament diagram 128
- with altitude changes 10, 15 - Mayo 01 surgical diagram 82
- eye 8 , 9 , 1 4 - peptic ulcer 82
- eyebrow 7 - peritoneocutaneous reflex (Morley) 81
- fallopian tube 1 3 1 - somatic 8 3
- flank 13 1 , 138 - ureterolithiasis 1 3 8
- gallbladder 1 15 - visceral 8 1 -82 (diagram)
- 01 104, 109 - viscerosomatic 80 (diagram), 87
- compression (01) 1 16 Pain referred 8 , 9, 8 1 , 87, 129, 188
- contraction (G1) 1 16 - cardiovascular pattern 58, 8 1
- groin 1 29 , 1 3 1 - segmental 1 3 1 (See Facilitated
- head (See Cephalgia) segment)
- iliac fossa 1 3 1 - see also Pain pattern
- iliolumbar ligament 1 3 1 Painful urethral syndrome 137
- localization 80, 8 1 , 1 88 Palate shape 48
- maxillary 1 2 Pallor 8 1
Palpation 1 2 1 , 154, 165 - respiratory 23, 27 , 29, 35, 3 8 , 44, 48
- accuracy 59 - rheumatology 163
- change 127, 1 3 1 , 1 3 8 - sinuses 28
- examination 4 1 , 8 2 , 154, 190, 225, Paresthesia 230
23 1 Parietal peritoneum 80
- prostate 1 36, 137 Parotid gland 56, 1 87
- "rubbery" 225 Paroxysmal atrial tachycardia 67
- tissue texture change 82, 83, 9 1 , 102, Paroxysmal ventricular tachycardia 67
172, 1 8 8 , 205, 225 Passive range of motion 1 6 1
- touch 173 Patllogen 1 36, 1 37
Palpitations 4 Patnogenesis
Pancreas 93, 107, 1 16, 1 86, 1 87 , 192, - arthritic change 1 6 1
199 - G I di sease 87 (diagram), 109
- pancreatitis 84, 86, 1 1 3 , 1 86 - GU calculi 139
Panic 1 14 - rheumatoid athritis 161
Pap smear 157 - rheumatologic disease 159, 1 6 1
Paralytic ileus 100 Pathophysiologic changes 1 3 5 , 161
Paraspinal inhibition 60 - cardiac 59
Paraspinal tissues 225 (See also Muscles - - GI 87 (diagram), 1 1 3
paraspinal) - pathology 109, 11 1 , 164
Parasympathetic characteristics - pathophysiology v, 2, 38, 50, 79, 99,
- activity 23 1 1 1 8 , 124, 163, 167
- balance 190 - cardiovascular 50
- dominance 104-105 - extraocular muscle disorder 7
- effect 1 8 , 3 1 , 50, 93, 141 - eye 14
- Cardiovascular 68, 70 - GU 133-134
- Lower GI 104-105 - respiratory 24, 36
- see also specific organs - rheumatology 159-160, 167
- hyperactivity 98, 23 1 - upper GI 79-87
- hypoactivity 98 - syndromes 85
- imbalance 1 39 Patient
- influence 1 16 - comfort 87, 1 17 (see also symptomatic
- influence - Chart 187-188 care)
- nerve ending 1 1 1 - education 163
- reflex 85, 126, 142, 144 - patient-physician relationship 155,
- supply 1 89 172-177
- symptoms 104-105 (See also effect) - rapport 153
- tone 130 Patterson, Michael 93, 193
Parasympathetics 1 1 8, 190 (diagram), Pectoral traction See OMT 44, 6 1 , 102
19 1-193 (chart), 194, 223-224 Pectoralis trigger point 57, 58, 59, 67,
- cardiovascular 60 23 1
- diagrams 5 , 55, 84, 97 Pedal pump 46
- EENT 4-6, 28, 223 Pediatric
- Eye 223 - EENT 1 5 , 172
- GI 48, 84 (diagram), 85, 89, 97 - growth (Chart) 17 8
.
(diagram), 98, 100, 1 12-1 1 3 , 1 19, - immune system 17 1-172

120, 223 - nervous system 172
- GU 124, 126 - OMT 1 7 1-2, 175-177
- mucous membrane 223 Pelvic 140, 154, 192, 204
- OMT (See OMT: Autonomic) - coil exercise 216
- pelvic organs 1 12 , 1 19 - congestion 1 3 1 , 1 86
- diaphragm 99, 100, 105, 123, 127, - nerve 27, 46
128, 130, 137, 143 , 2 16-2 1 7 , 228, - pain 81
229 Physical examination 154, 165, 172, 208
- dysfunction 92, 195, 227 - kidney 124
- floor 99 (diagram), 128, 130, 134, - pediatric 172-172
136, 1 43 , 156, 229 - physical finding 201
- p. floor tension myalgia 128 Physical needs 163
- organ 98, 100, 107, 140, 143 , 199, Physical stress 1 12, 1 89, 205, 225
223 , 224 Physiological
- pain 105, 1 3 1 , 132, 137, 139 - basis prologue, 109
- tone 216 - change 151
Penicillin iv - function 144
Penis 56, 130, 1 3 1 , 143 - massage 1 36
Peptic ulcer disease 82 (diagram), 86 - mechanism 99, 106, 109, 132, 142,
Percussion hammer 1 19 144
Perforated viscus 82 - reaction 1 17
Periarticular tissues 164, 167 - relief 121
Pericarditis 58 - stress 1 5 1 , 152, 153
Perineum 100, 129, 216, 228 Physiology 1 17 , 149, 189
- abscess 228 - GI tract 1 1 1-113
Perineural edema 105, 106 Pilomotor muscle 1 87
Peripheral arteriolar vasculature 55 Pineal gland 1 84
Peripheral edema 56, 66, 73 Pituitary 4, 17, 144, 165
Peripheral resistance 62-63 (diagram), 64 - pituitary-ovarian axis 144
Peripheral vascular disease 1 86 Plagiocephaly 15, 172
Peristalsis Placenta 151
- GI 90, 93
- ureter 125, 126, 133, 134, 135, 139, Pleura 192
1 85 - pleural friction rub 37
Peritoneocutaneous reflex of Morley 81 - pleurisy 58, 228
(diagram) - pleuritic pain 37, 38
Peritoneum 80, 8 1 , 124 Pneumonia 38, 40-46, 85
- irritation 134 - bronchial 45
Periumbilical palpatory change 125 - hospitalized patient 45
Perpetuating factor 8, 57, 134, 144, 165 - lobar 45
Personality type - viral 85
- in irritable bowel syndrome 1 10 Pneumotaxic center 34 (diagram)
- neurotic 1 10 Polycarbophil tablet 1 17
Petrosphenoidal ligament 7 Polycystic kidney disease 124
Pharmacologic treatment 1 16- 1 17 , 1 2 1 , Polymorphonuclear leukocytes 161
1 24, 127 Polyps - GI 1 10
- pharmaceutical by-product 124, 127 Popliteal space 206
Pharynx 23 , 223 Portal venous congestion 70
- dysfunction 17 Post-concussion syndrome 11
- hyperesthesia 4 Post-nasal drainage 16
- secretions 2-5 Post-operative
- pharyngitis 16, 3 1 (chart) - complication 46-47
Philosophy iv, xvi, 149 - conditions 28
- of treatment 87 - ileus 103 , 199
Photophobia 4, 5 - patient 95, 229
Phrenic - postcholecystectomy syndrome 87
- protocol - OMT 101-102 Premature ejaculation 1 3 3 , 143
Post-partum situation Premature labor 1 52
- "blues" 157 Premature rupture of membranes 152
- breast engorgement 230 Premenstrual syndrome 131
- OMT 157 Prenatal care 1 5 1 , 156, 158
- period 152, 157 Pressure 80
- treatment 157 - change - intermittent 86
Posterior axillary fold 164, 206, 220, 230 - gradient 33 (diagram), 3 8 , 39, 105,
Posterior pharynx 23 , 24 150, 1 5 1 , 152, 156, 195, 203,
Postural clopping 41 204, 206, 2 1 8 , 229 , 230
Posture 167, 1 7 1 , 175, 204, 207 - ear 10
- Postural analysis 165 - intermittent compression 161
- autonomic nervous system 139 - oncotic pressure 134
- cervical lordosis 166 Preventative medicine 93, 103 , 1 12-1 13 ,
- crossover 57 135, 139, 157, 166 , 1 7 1 , 195
- diagnosis 1 7 1 , 175, 203 Primary vs secondary 82
- iliac crest level 154 Primipara 157
- lumbar lordosis 38, 1 15, 1 5 1 , 166, Prognosis 87, 136
1 7 1 , 214 Prolonged P-Q interVal 72
- pattern 208 Proprioceptive input 1 89, 196
- shoulder level 154 Prostaglandins 87, 1 3 1 , 140
- symptoms 203-204 - prostaglandin inhibitor Rx 1 3 1 (See
- thoracic kyphosis 57, 1 5 1 also list under Medication)
- treatment 165 Prostate 128, 129, 1 30, 1 3 1 , 132, 133,
- heel lift 140, 165 136, 137 (diagram), 193
- Levitor orthosis 165 - congestion 134
- trochanteric level 154 - digital massage 136
- Postural disorder 8, 57, 1 1 8, 123, 128, - dysfunction 132
1 32, 137, 139, 144, 149, 1 6 1 , - physiologic massage 1 36
165, 167, 1 7 1 , 203 , 204, 205 - prostatitis 128, 1 34; 1 36-137
- lumbar hyperlordosis 124, 139, 1 5 1 - prostatodynia 1 36, 1 37
- short leg syndrome 128, 132, 140, - reflux 133
154, 16 1 , 1 7 1 , 203 , 204 - secretion 136, 1 3 7 (diagram)
Preaortic region 199 - spasm 229
- preaortic ganglion 194 - wall 1 36
- preaortic nodes 127 Protective reflex 36, 127
Predisposing factor 10, 15, 134, 1 35 Protein 162
- otitis media 10, 15 - balance 66
Preeclampsia 152 Pseudoephedrine 15
Pregnancy 144, 149-158 PSIS level 154
- congestive stage 149 (diagram), 155- Psoas
156 - contracture 124
- contraindications to OMT 152 - spasm 1 24, 128
- ectopic 152 - See also Muscle - Iliopsoas, Psoas;
- labor and delivery 157 OMT - Iliopsoas; Trigger point -
- mUltipara/primipara 157 Iliopsoas
- OMT 152, 157-158 Psychiatry
- preeclampsia 152 - care 162
- premature rupture of membranes 152 - depression 1 10, 1 16, 1 3 1 , 139, 157,
- preparatory stage 156 162
- structural stage 153-154 - illness 1 10
- neurosis 1 10 Rational osteopathic treatment protocol
- personality type 1 10 163
- psychogenic disturbances 49 - Arrhythmia 67-68
- schizophrenia 181 - Asthma 48-49
Psychologic factor vi, 109, 1 12, 132, - Cardiovascular 67-68
1 37 , 142 - Common cold 25-29
- needs 163 - Congestive heart failure 66
- support 156, 163 - COPD 48
- psychoemotional level 162 - Dysmenorrhea 141
Pterygoid plate 223 - Ear 14-15
Pterygoid venous plexus 17 - EENT 12-19
Ptosis 3, 8 - EENT Summary 1 8
Pubic bone 130 - ENT Unit 17
Pubic symphysis 204, 2 14, 228 - Eye 13-14
Puboprostatic ligamnet 129 - General prologue, v, 19, 29-30, 50
Pubovesicular ligament 129 - GI dysfunction 93, 107
Pulmonary branches of vagus 55 - GU dysfunction 133
Pulmonary - Hypertension 6 1 -66
- Chapman's reflex 37, 232-233 - Myocardial infarction 60-6 1
- dysfunction 50 (chart), 85 - Nose 16, 3 1
- OMT 34 - Pharyngitis 31
- edema 56, 72 - Pneumonia 40-46
- embolism 58 - Post-op pulmonary complications 46-
- hypertension 48 47, 101 -102
- lymphatic system 72 - Respiratory 25-29, 48, 50
- mucosal irritation 36 - Rheumatologic 163
- staging 45 - Sinuses 16-17, 3 1
- toilet 40 - Throat 17
- postural clopping 41 - Pediatric 175-177
- vascular resistance 48 Receptor
Pupil 1 87 , 192 - baroreceptor 62
- constricted 3, 4 - chemoreceptor 1 83
- dilation 4 - pain 80, 8 1
- Homer's syndrome 3 Rectosigmoid region 99, 1 1 3 , 1 3 1 , 216
- innervation 4 - abscess 229
Pyelonephritis 135 - bleeding 1 10
Pylorus 98 - cancer 229
- examination 100, 216, 229
Q - sphincter 1 88
- ulceration 1 10
Red blood cell 124
Q-T interval 1 85 Red reflex 174
Quadratus lumborum spasm 124, 2 1 4 Reference organs 194
Referred pain 8 , 9, 8 1 , 87 , 129, 188
R - arm 58
- cardiovascular 58
- gallbladder 87
Rales 48, 227, 229 - groin 129
Range of motion 16 1 , 162, 163, 167, - jaw 58
1 7 1 , 195, 205 - neck 58
Rash 176
- segmental referred 1 3 1 (See Facilitated - pathway 93
segment) - pattern
- shoulder 81 - Genitoreproductive 131
- ureterolithiasis 138 - Learned 1 12
- viscerosomatic 87, 1 8 8 - response 195
Reflex 1 89 - symptoms
- Cardio-cardiac 60, 69, 70 - EENT 16
- Cardiocardiac 1 85 - Upper respiratory tract 26
- Chapman's 37, 82, 83, 90, 9 1 , 92, Reflex sympathetic dystrophy 16 1 , 1 86
1 19 , 1 34, 194, 200-201 Reflux
- Chapman's (adrenal) 77 - gastric 58
- Chapman's (bladder) 125 - urinary 125 , 1 3 3 , 135
- Chapman's (broad ligament) 130 Refractory period 71
- Chapman's (colon) 104 Regional fascial dysfunction 207-212
- Chapman's (GI) 86, 165 - See Fascial patterns, Compensation
- Chapman's (gonads) 130 Regurgitation 172
- Chapman's (GU) 139 Relaxation 27, 66, 87 , 88, 1 2 1 , 195, 214
- Chapman's (heart) 59 Renal
- Chapman's (kidney) 126 - blood flow 138
- Chapman's (prostate) 130 - calyces 138
- Cough 36 - capsular lymphatics 127
- Erben's 67 - capsule 127
- Gag 175 - circulation 135
- Gastrocolic 1 1 1 , 1 16 - colic 138
- Hering-Breuer 38 - damage 139
- Intraprostatic 137 - disease/dysfunction 132, 135, 1 3 8
- Oculocardiac 55 - failure 135
- Oculocervical 2 - fat pad 123 , 124
- Parasympathetic 48, 85, 126, 142, 144 - function 70
- Protective 36 - parenchyma 127
- Red 174 - renal pelvis 127, 1 3 8
- Somatosomatic 34 - See also Kidney
- Somatovisceral 26, 34, 36, 49, 57, Renin 64
100, 1 12, 1 15, 1 1 8, 1 1 9, 167, 23 1 - Renin-Angiotensin 66
- Sympathetic 142 Reproduction 1 84
- Uterus 131 - function 144
- Visceromotor 125, 127, 165, 167, 225 - organ 188
- Viscerosensory 127 - tract 129-132
- Viscerosomatic 33, 35, 36, 37, 38, 49, Residual urine 129
79, 83, 86, 90, 100, 1 0 1 , 109 Resistance - Host 106
1 15, 1 1 8 - resistance to infection 88
- Viscerovisceral 25, 3 3 , 69, 70, 85 Respiration 26, 33-35, 38, 42, 50, 70, 86,
- Vicious cycle 118 90, 1 30, 164, 228
Reflex parameters Respiratory
- activity 135 - acidosis 3 3 , 35
- center - Rostral 125 - alkalosis 33
- connections - EENT 2 - axis of sacrum 105
- cycle 225 - center 38
- dysfunction 88 - complication 46-47
- mechanisms vi, 19, 36 - depth 196
- neurophysiology 79 - disorders/dysfunction 33-52
- efficiency 196 Ruddy resistive duction technique 14, 1 8
- effort 1 50
- epithelium (See Epithelium) s
- function 66, 204
- infection 40
- innervation 34 (diagram) S l-3 1 19
- internal/external 26 (diagram) S2-4 98, 100, 1 12, 1 19, 124, 126, 129,
- mucosal functions 23-24 1 30, 1 3 3 , 135, 136, 140, 142,
- plexus 25 143 , 193 , 223
- pump 164 Sacral 154, 224
- symptom 40 (See also Specific - axis 105
symptoms) - base anterior 140, 157
- therapy 40 - base unleveling 203 (See also: short leg
- postural clopping 4 1 syndrome)
Restricted motion 1 7 1 (See Somatic - diagnosis 157
dysfunction) - Sacral shear 140, 154, 203 , 224
Retention - SaltlWater 1 85 - Sacral somatic dysfunction (See
Reticular formation 1 83 Somatic dysfunction - Sacrum)
Reticuloendothelial system 26, 1 84 - rocking 1 19
- Reticulocytes 1 84 - sacroiliac joint 1 19
Retina 1 83 - sacroiliac strain 140
Retrograde ejaculation 133 Salicylate toxicity 1 1
Retroorbital pain 5 Salivary gland 192
Rheumatoid arthritis 159, 1 6 1 , 164, 166, - salivation 7
1 85 Salt retention 62, 70
Rheumatic fever 72 Scar tissue 40, 98, 230
Rheumatology - scarring 40, 98
- diagrams 160, 162 Schizophrenia 1 8 1
- OMT 163-166 Sclera 6
- pathophysiology 159-160 Scoliosis 57, 154, 1 7 1 , 175, 203 , 204
Rhinitis 15, 16, 3 1 (chart) Screening examination 157
Rhinomanometry 16 Scrotal pain 127
Rhinovirus 24 Seasickness 1 1
Rhonchi 229 Second trimester 155
Rhythm assimilation reaction 1 83 Secretion 1 8 , 3 1 , 50, 1 87 , 223
Ribs 9 1 , 123, 1 56, 195 - secretion rate - GI glands 85
- fracture 58, 228, 229 - secretions - Thick 48
- head 9 1 , 194, 195 Sedimentation rate 1 10
- hump 175 Segmentation 79, 1 14
- motion 194, 196 Seizure 152, 177
- bucket handle 196 Self-breast examination 157
- rib 1 105 Self-centered 162
- rib raising - effect 42-44 Self-regulatory mechanisms 152 (See
Richardson eye exercises 13-14 (chart) homeostasis)
Risk factor 135 Seminal vesicle 129
- cardiac 69 Sensation of "warmth" 220
- gallbladder 93 Sense of smell 7
- hypertension 78 Sensineural hearing loss 1 1
Rotatores muscles 82 Serosa 8 1
Rotoscoliosis 154, 204 (See scoliosis) - stretch 1 15
"Rubbery " palpatory finding 225 Serum laboratory measurements
- aldosterone levels 65 Small intestine 84, 89, 107, 1 14, 1 15 ,
- serum lipid 71 1 17 , 192, 199
- serum pC02 3 3 , 35, 48 - dysfunction 227
- serum pH 33, 34 - mesentery 89
Sexual - small bowel study 1 10
- aphrodisiac 132 - See also OMT
- desire 132 Smoking 36, 50, 153
- development 1 84 Smooth muscle 138
- dysfunction 142-144 - bowel 1 1 1 , 1 12
- OMT 142 - cyclic activity 111
- function 142, 143 (diagram) - GU 130
- intercourse 142 - spasm 81
Shallow breathing 38 - stretch 81
Shock 60 Sneezing 10, 1 6 , 127
Short leg syndrome 128, 132, 140, 154, Social growth 172
16 1 , 1 7 1 , 203, 204 Sodium benzoate 166
- heel lift 140, 165 Sodium resorption 64
Shortness of breath 205, 2 1 8 Soft palate 175
Shoulder dysfunction 230 Soft tissue 155
- pain 81 - swelling 162
Sibson's fascia 207, 210 (See Thoracic - See also OMT; Tissue texture change
inlet) Solitary nucleus 34, 35
Sigmoid colon 111 Somatic afferent referral 161
- sigmoidoscopy 1 10 Somatic and cardiovascular system 57-59
Sinoatrial (SA) node 50, 55, 68, 7 1 , 23 1 Somatic clues v, 1 , 25, 28, 37, 59
- automatism 71 - Cardiovascular 59
- block 67 - Colon dysfunction 104
- bradyarrhythmia 55, 67, 70 - Congestion 205-207
- tachyarrhythmia 67, 70 - EENT 28
Sinobronchial syndrome 17 - General 152
Sinus 5, 192, 202, 223 - GI 90
- attack 12 - GU 138
- disorder 2 - Lower GI 97
- drainage 28 - Lower respiratory tract 44
- headache 16, 23 1 - Lung dysfunction 37
- infection 28 - Upper respiratory tract 25
- OMT 16 - Visceral dysfunction 82, 83 , 85, 86,
- pain 7 , 9 , 12, 16, 28 1 1 8 , 130, 165, 1 89, 225
- sinusitis 12, 15, 16, 202, 23 1 - See also Visceromotor patterns
- acute 16 Somatic complaints 1 10
- chronic 16 Somatic component 100, 144
Sitz bath 136 Somatic dysfunction v, 1 8 , 3 1 , 50, 93,
Skin 1 87 , 222 107, 1 1 8, 123 , 125, 1 3 3 , 1 4 1 ,
- change 205, 1 8 8 1 6 1 , 1 6 7 , 1 7 1 , 1 89, 190, 194,
- ·clammy· hand 230 195 , 209, 225
- See Tissue texture change
Skull 223 [See also Somatic Dysfunction
- base 150 - See also Cranial Subdivisions -
Sloughing 36 SD:CERVICAL REGION
Slow wave activity 111 SD:CRANIUM
- slow wave GI contraction ratio 1 13 SD:EXTREMITIES
SD:GENERAL FACTORS - Ll-3 2 1 4
SD:LUMBAR AREA - Lumbosacral 105
SD:SA CRAL & PELVIC AREAS - Psoas 2 1 4
SD:THORA CIC & CHEST CAGE - Quadratus lumborum 2 1 4
Somatic dysCunction:
Somatic dysCunction: SACRAL & PELVIC AREAS
CERVICAL REGION - Innominate 105, 154, 224
- Suboccipital 104 - Pelvic floor 1 34
- OA 1 1 , 27, 44, 55, 66, 85, 92, 120, - Pelvis 1 32, 144, 201 , 214
1 89 - Pubic symphysis 129, 1 34, 154
- AA 10, 55, 92, 120 - Sacral 105 , 1 19, 132, 1 39, 140, 157,
- C2 55, 59, 85 1 89, 224
- C3-5 46-47, 105 - Sacral shear 1 19, 140, 154, 203 ,
- Cervical 2, 4, 27, 44, 58, 59, 92, 202 224
- Hyoid 1 7 , 6 1 - Superior innominate shear (upslipped)
Somatic dysCunction : 1 19, 224
CRANIUM Somatic dysCunction:
- Cranial 7 , 8, 10, 14, 15, 48, 49, 120, THORACIC & CHEST CAGE
1 65, 17 1 , 172, 1 89, 203 - Collateral ganglion 200
- Cranial nerve involvement 7, 9 - Diaphragm 66, 196, 214
- Extraocular muscles 14 - Rib 36, 38, 39, 44, 49, 58, 66, 82,
- Lambdoidal suture 120 124, 195, 198, 210, 2 1 1 , 214
- Occipitomastoid 66, 92 - First rib 39, 154
- Sphenobasilar symphysis 10, 49 - Sternal 58, 196
- Temporal bone 8 , 9, 10, 1 1 , 15 - Thoracic 4, 38, 58, 82, 196, 210, 2 1 1
Somatic dysCunction: - Thoracic cage 43 , 66
EXTREMITIES - Thoracic inlet 27, 43 , 6 1 , 105
- Lower extremity 206 - Thoracolumbar 66, 124, 143 , 144
- Posterior axillary fold 206
- Upper extremity 206 Somatic elements
Somatic dysCunction: - effect of viscerosomatic reflex 1 15
GENERAL FACTORS - efferent fibers 83
- Diagnosis of Somatic Dysfunction 2 1 1 - innervation 161
- Fascia 105, 1 89, 205 - input 142
- Fascial pattern 207-2 12 - pain 8 1 , 83
- Fascial symptoms 203-205 - pain localization 8 1
- Joint 204 - predisposing to dysfunction 1 0 , 15,
- Lymphatic 205, 207 1 35, 172 (See also specific
- Myofascial 162, 165 factors)
- Non-neutral 82, 225 - segmental distribution 8 1
- Non-physiologic 154 Somatic system
- Predisposing factor 1 35 - EENT 8-12
- Primary 1 12 - Genitoreproductive 1 32
- Contributing factor (GI) 109 - Lower respiratory 3 8
- Recurrent 82, 153, 154 - Renal 127-129
- Regional tissue congestion 205 - Rheumatology 161 -162
- Segmental 86, 1 34, 154 - Upper GI dysfunction and 86-87
- Sidedness 80 Somatosomatic reflex 34
- Secondary 82 Somatovisceral reflex 167, 23 1
Somatic dysCunction: Somatovisceral reflex 26, 34, 36, 49, 57,
LUMBAR AREA 100, 1 12, 1 15, 1 1 8, 1 19
Sonic disruption 1 39 Stabbing pain 1 88
Soreness 171 Staging - Pulmonary disease 45
Spasm 132, 1 6 1 , 204 Stance 173
- bowel 1 15, 1 17 Staphlococcus pyogens 25
- intercostal muscle 58 Staphylococcus bacteria 25, 95
- orbicularis oculi 8 Stellate ganglion 69, 70, 202
- pain cycle 163 Sternum 105, 196
- paraspinal 1 0 1 , 228 Steroids 165
- pelvic diaphragm/floor 99, 128, 143 , Stethoscope 173, 174
229 Stiffness 164
- psoas 124, 128, 1 32 Stiles, E study 60 (diagram)
- quadratus lumborum 124, 214 Still, AT quote prologue, xvi, 53
- receptors 80 Stimulus
- reflex 138 - altered reaction to 1 13-1 14, 1 17, 125,
- smooth muscle 81, 138 138, 183
- sphincter (GU) 129 - bronchial tree 24
- vagina 143 - cardiac 69
Spasmogenic action 140 - cervical somatic dysfunction 10
Spastic colon 85 - cranial somatic dysfunction 10
Spastic constipation 1 14 - dermatomal 143
Spermatic count 144 - emotional 1 14
Sphenoid bone 7 - "erogenous" 132
Sphenopalatine fossa 223 - esophagus 10
Sphenopalatine ganglion 16, 1 8 , 25, 28, - external/internal 1 17
3 1 , 49, 223 - U-2 143
- diagrams 2, 5, 29 - lung 2, 36, 44
- sphenopalatine syndrome 5 - penis 143
Sphincter 124, 126, 127, 133, 134, 1 88, - renal sympathetic 1 25
193 - sinus 24
- tone 127 - somatic 88
Spike potential 1 1 1 - teeth 10
Spinal - thigh 1 32
- cord 1 12, 143, 150, 183, 1 89, 194, - TMJ 1 0
195 - tongue 10
- learning 195 - tonsils 10
- membranes 1 5 1 - tympanic membrane 2
- motion pattern 17 1 - upper Gl 2
Spinothalamic tract 80 - upper respiratory tract 25
Spiritual factor 142 - ureter 125
- spiritual need 190 - visceral 3
- spiritual stress 225 82, 23 1
- visceral afferent
Splanchnic nerve 80 Stirrups129
Spleen 8 1 , 1 87, 192, 199, 219, 228 Stomach 24, 84, 98, 107, 1 1 1 , 1 87, 199
- splenic pump 45 - See also Specific disorders or
- splenomegaly 219, 228 dysfunction
Sprain 205 Stool 1 16, 1 17
Spray and stretch technique 165, 215, 23 1 Stool changes 227
- See also Trigger points; Fluori-Methane - stool laboratory tests 1 10
Spurs 205 Strabismus 7, 14
Sputum - Frothy 48 - medial 7
Squinting . 8 Strain 128, 129, 205
Strept p neumonia 15 Subxiphoid fullness/tension 86, 227
Stress/stressor 8, 24, 49, 50, 61, 64, 66, Suckling disorder 7, 172
69, 85, 88, 90, 98, 109, 1 12, 1 1 8, Sudden death 69
1 2 1 , 125, 1 32, 138, 139, 144, Sudden infant death syndrome 1 85
149, 153, 155, 165, 1 89, 196, Sugar 166
203, 205, 207, 209, 225 Sulfa compounds 1 15
- emotional 8, 49 Sulfamethoxazole 136
- environmental 49 Superior cervical ganglion 1 83, 1 84, 202
- pathogenesis of hypertension 64 - diagrams 2, 26
(diagram) - OMT 67
- physical 49 Superior mesenteric ganglion 90, 92, 107,
- pregnancy 1 5 1 , 152 1 12, 125, 192, 199, 224
- reduction 50, 64 - OMT 141 , 227
- stress-relaxation response 66 Superior transverse axis of sacrum 105
- visceral pathology 1 1 1 Superior vena cava 150
Stretch 1 15, 166, 214, 222 Superoxide 95
- receptors 80 Supraclavicular
- stretching 104 - edema 205
Structural - region 6
- abnormality 154 Supraventricular tachyarrhythmia 50, 57,
- balance 156 23 1
- change 1 35, 1 5 1 , 1 6 1 , 164, 165 - treatment (See Trigger point - Pectoralis
- component 225 major)
- effect 155 Surgical treatment 14, 16, 17, 46-47, 69,
- examination 157, 1 7 1 , 208 72, 87, 95, 100, 101, 102, 106,
- factor 139 1 12, 129, 136, 139, 163, 166,
- (see also somatic dysfunction, 167, 225, 228, 230
postural disorder) - cholecystectomy 87, 1 15
- scoliosis 175 - complications 46, 47, 87, 103, 199
- stress 144, 1 5 1 , 207 - Congestive heart failure 72
Structure-function interrelationship iv, 1 , - GI 46-47
12, 14, 49, 50, 68, 93, 1 17, 1 3 1 , - post-operative OMT 46-47, 101- 103,
152, 1 6 1 , 172, 175 198, 230
- Cardiovascular 68 - site 101
Subacute bacterial endocarditiis 68 - sympathectomy 16 1 , 1 84, 185, 1 86
Subclavian line 229 - tubes 228, 230
Subclavian vein 86 - wound 101 , 102, 227, 228, 230, 23 1
Subcortical activity 1 83 Swallowing 10, 15
Subcutaneous tissue 222 - disorder 7, 9
Sublingual gland 1 87 - pain 12
Subluxation 164 Sweat 1 86
Submandibular ganglion 223 - sweat gland 1 87
Submaxillary ganglion 223 - sweating 4, 8 1
Submaxillary gland 56, 1 87 Sympathetic supply 83 (diagram), 1 1 8,
Submucosal plexus 223 162
Suboccipital - Adipose tissue 1 84
- headache 93 - Bladder wall 124
- OMT 92 - Blood vessel 1 84
- strain 155 - Bone 1 84
Substance abuse 1 8 1 - Bronchial tree 26
Substernal pain 57 - Cardiovascular 53-55
- Central nervous system 1 83 - mechanism 1 37
- Collateral circulation 1 84 - nerve ending 111
- Colon 104, 1 6 1 - nervous system - general 37
- EENT 2-4 - OMT (See OMT: Autonomic)
- Endocrine 1 84 - outflow 194, 202
- Extremity 1 86 - reflex 142
- Fallopian tube 129 - reflex pattern 90
- Genitoreproductive 129, 130 - response 143 , 190
- GI 83-84, 89 - segments 1 6 1 (See Facilitated
- GU 1 85 segments)
- Heart 1 85 - stimuli 62
- Liver 1 86 - tone 225
- Lower respiratory 36, 42, 49 - venous response 55
- Nasal mucosa 26 Sympathetic-parasympathetic hyperactivity
- Pancreas 1 86 coexisting 70
- Pediatric 1 85 Sympathomimetic drug 41
- Penis 130 Symptomatic care 15, 19, 23 , 25, 29, 4 1 ,
- Peripheral sensory mechanism 1 83 42, 45, 87, 88, 1 00 , 1 16, 1 1 7,
- Reticuloendothelial system 1 84 121 , 129, 134, 139, 140, 152, 166
- Rheumatology 160- 1 6 1 Symptomatology v, vi, 40, 44, 45, 85,
- Sinuses 26 188, 204
- Skeletal 1 85 - Genitoreproductive tract 132
- Skeletal muscle 1 83 - GI 109
- Structural involvement 3 - GU 138
- Thoracic duct 56 - Respiratory 40, 44
- Urinary tract 124, 125-126 Synapse 1 1 1 , 125, 1 89
Sympathetics Synovial
- activity 165 - cell 163
- blockade 167 - crepitus 162
- cell bodies 221 - fluid 159, 1 6 1 , 163
- chain ganglion 90, 91 - membrane 159, 1 6 1
- dominance 104 - synovium 1 6 3 , 154
- effect 18, 50, 93, 1 14, 141 Systemic disease/dysfunction 79, 106,
- Cardiovascular 68, 70 1 09 , 159, 1 89
- GU 133 - OMT 1 89-233
- Kidney 70 - systemic effects 163
- Lower GI 104 - systemic infection 1 35, 219
- fibers 83 - systemic involvement 164
- ganglion - systemic toxicity 40, 4 1 , 43, 44, 45
- diagrams 26, 9 1 Systemic lupus erythematosus 163
- (See Sympathetic chain ganglion; Systolic pressure 65 (See Blood pressure;
Collateral ganglion; and specific Hypertension; etc)
ganglia by name)
- ganglion block 1 85 T
- hyperactivity 68 (See
Hypersympathetonia)
- imbalance 139 Tl-12 35, 3 8 , 45, 166
- influence - Chart 1 87-188 Tl-4 2 (diagram), 3 , 24, 25, 59, 105,
- see also Sympathetic supply 192, 202, 209
- innervation 1 0 1 , 192-193 (chart), 194 Tl-6 24, 25, 34 (diagram), 36, 37, 38,
- see also Sympathetic supply 42, 50, 59
T2-8 1 6 1 , 193 - cage (thorax) 123
T3 1 85 - mechanical impediments 42
T5-9 82, 83, 84, 90, 9 1 , 92, 107, 1 12, - duct 56, 70, 73, 86, 99, 127, 210
1 6 1 , 165, 192, 227 - distension 66, 70, 73
TlO- 1 1 83, 84, 90,9 1 , 92, 107, 1 12, 130, - surgical drainage 163
1 3 1 , 192, 227 - ganglion 202
TlO-12 135 - inlet 27, 86 (diagram), 89, 154, 156,
T lO-L2 1 6 1 203 , 207
T l 1 - 1 2 129 - defined 209
T 1 1-L l 135 - diagrams 27, 209, 2 1 1 , 212
T l2-L2 92, 1 12 , 107, 124, 125, 126 , 130, - See OMT
136, 140, 193, 227 - kyphosis 57, 1 5 1
Tachyarrhythmia 4, 50, 57 (diagram), 67, - outlet (Inferior) 89
69, 70, 202, 23 1 - outlet (Superior) 48
- Paroxysmal atrial tachycardia 67 - pain 59
- Paroxysmal ventricular tachycardia 67 - pump 219
Tachypnea 3 8 , 40 - See OMT, Lymphatic pump
Tactile receptor 183 - thoracoabdominal pump efficacy 156
Target organ/tissue 125, 1 83 - thoracoabdominopelvic pump 228
Taste - Metallic 7 - See OMT for thoraco-abdomino-
Taste receptor 1 83 pelvic pump
Tea 166 Thoracolumbar junction 38, 100, 104,
Team approach 1 67 105, 1 15, 127, 130, 140, 154,
Tears 5 , 14, 29, 224 156, 194, 201 , 208, 214, 230
Teeth - Clenching 8 Threshold 183, 1 89, 196
Teeth - Worn 8 - decreased 1 13
Temperature - Decreased 172, 177 - See Facilitation
Temperature - Increased (See Fever) Throat pain 12
Temperomandibular joint 7 Throbbing pain 1 88
- temperomandibular joint dysfunction Thrombosis 1 84, 229
161 Thyroid 4, 1 1 , 1 87, 192
- temporomandibular joint syndrome 8 - dysfunction 17
Temporal bone 6, 7, 14, 84 - hyperthyroidism 11
Tender points 1 62, 167 - hypothyroidism 11
Tenderness to palpation 82, 172, 205, - innervation 5, 6
206, 220 - secretion 4
Tendon sheath 162 - thyrotropic hormone 4
Tenosynovitis 162 Tibial torsion 173
Tentorium cerebelli 7 Tic douloureux 7
Terminal lymphatic drainage 86 Ticklishness 205, 230
- diagram 206 Tietze's syndrome 58
- dysfunction 205-207 Time efficacy iv
- lymphatic ducts 27 Tinnitus 4, 6, 7 , 8 , 9 , 10, 1 1 , 12, 14, 15
Testes 1 30, 1 8 8 , 192 - differential diagnosis 11
- ache 128 Tissue
- dysfunction 132 - congestion 93, 95, 98, 135, 1 4 1 , 149,
Therapeutic trial v, 1 , 14, 19, 144 155
Thickening - Achilles tendon 206 - damage 1 39
Thigh pain 131 - defense 135
Third trimester 1 5 1 , 152, 154, 155-156 - hypoxia 161
Thoracic - tissue response to OMT 154
Tissue texture change 82, 83, 9 1 , 102, - See also Rational osteopathic treatment;
172, 188, 205, 225 OMT
- See Somatic dysfunction; specific Treatment protocol 163 , 196
changes Treatment response 1 35
Tobacco 15, 36, 50, 153 Tricyclic medication 1 16
Tongue 56, 174, 175 Trigeminal neuralgia 7, 23 1
- tongue blade 174-175 Trigger point 10, 15, 67, 86, 1 32, 162,
Tonsillectomy 10 165, 194, 220
Total peripheral resistance 55, 60, 6 1 , 62, - Abdominal 100, 129, 1 32
63 (diagram) - Digastric 9, 12
Touch 173 - Ear symptoms 12
Toxemia of pregnancy 152 - EENT symptoms 8 , 9 (chart)
Toxicity 40, 4 1 , 43 , 44, 45, 163, 165, - Lateral pterygoid muscle 7, 9 , 16
167, 228 - Masseter 8, 9 , 12
Toxins 80, 120, 165 - Masseter (Deep) 11
Trachea 36, 192 - Medial pterygoid 9 , 10, 1 1 , 12, 15
Traction 80, 222 - Occipitalis 8, 9, 1 1 , 12
Tranquilizer medication 1 16 - Orbicularis oculi 8, 9, 12
Transition zones 208 - Pectoralis major 57, 58, 59, 67, 23 1
Transverse colon 111 - Pectoralis minor 58
Trauma 6 , 1 1 , 95, 100, 1 12, 1 1 8, 140, - Pterygoid 8, 9
153, 1 83 , 1 86, 203 , 208 - Quadratus lumborum 215
- falls 140, 153 - Rectus abdominus 1 3 2 , 139
- head trauma 1 1 , 153 - Splenius cervicis 8, 9
- history 6, 153 - Spray and stretch technique 14
- motor vehicle accident 7, 153 - Fluori-Methane 165
- post-concussion syndrome 11 - Sternalis 58, 67
- whiplash injury 2, 7 - Sternocleidomastoid
Travell 100, 162 (See Trigger point) - clavicular portion 9, 1 1
Treatment - sternal division 8 , 9, 12
- General goal 1 16 - Trapezius 8 , 9, 12
- See also Rational osteopathic Trigone 124, 193
treatment Trimethoprim 136
- Medical (See Medical treatment) Trophic change 85, 88, 1 86, 205
- See OMT Tumors - GI 1 10
- Surgical (See Surgical treatment) Twelfth rib 214
- Tender points 162 Tympanic membrane 174
- See also Spray & stretch; Fluori- - abnormal light reflex/retraction 10
Methane; OMT; Inhibition - fluid level 10
Treatment plan 1 8 , 3 1 , 50, 93, 107, 133, - perforation 15
141, 190 - poor insufflation 10
- Cardiac dysfunction (Chart) 67-68
- Common cold 31 u
- Dysmenorrhea 141
- EENT 18
- GI dysfunction 93, 107 Ulcer 82 (diagram), 86, 87 (diagram),
- GU 133 1 10
- Pharyngitis 31 Ulceration 84, 165
- Pulmonary dysfunction 50 Ulcerative colitis 1 10, 1 1 3 , 201
- Rhinitis 31 Umbilicus 89, 92, 97, 104, 1 15 , 1 1 8,
- Upper respiratory tract infection 31 125 , 155, 199, 200, 227
Uncommon compensatory pattern 208, - flow 133
209, 2 1 1 - formation 127
Unsteadiness 4 - volume 125
Upper extremity 48, 164, 206 Urogenital diaphragm 129, 1 30, 1 3 1
- afferents 161 - (See also Pelvic diaphragm)
Upper GI tract 161 Urogenital triangle 99, 130 (diagram)
- disease 8 5 , 8 7 (diagram) Uropathy 134, 135
- see Specific dysfunction, Innervation, Uterus 129, 140, 1 4 1 , 142, 155 , 188,
etc 1 89, 23 1
Upper respiratory tract (Chart) 31 - contraction 140, 1 4 1 , 157
- infections 23-3 1 , 48 - fundus 139, 1 8 8
- symptoms 17 - growth 155
Uremia 135 - hypertrophy 151
Ureter 124, 126, 133, 137, 138, 1 85, 193 - inertia 157
- kinked 123 - inhibition 140
- dysfunction 132 - pain 131
- flow 1 85 Uvula 175
- function 124 - asymmetrical elevation upon phonation
- obstruction 127, 134 10
- orifice 124
- peristalsis 125, 126, 133, 134, 135, v
1 39
- reflux 133
- stone 123, 125 Vagal (See also Cranial nerve X (Vagus»
- ureterocolic 127 - afferents 2
- ureterolithiasis 137-139 - See Nerve - Visceral afferent
- ureterospasm 125, 133, 138 (diagram) - hyperactivity 60, 68
Urethra 124, 129, 137 - vagal tone - Techniques to modify 67
- dysfunction 1 32 - See OMT, OA-AA-C2,
- hypertonia 1 37 Occipitomastoid
- sphincter 126 - vagal-C2 connection 59, 85
- tone 137 Vagina 129, 142, 143, 144, 216
Urinary - examination 100, 157, 216, 229
- culture 136 - leukorrhea 131
- dribbling 1 36 - vaginitis 229
- frequency 128, 1 3 1 , 1 34, 136, 137, Val salva manuever 67
138, 139 Valves - One way 206
- hematuria 136, 1 3 8 Varicosity 204, 228
- hesitancy 137 Vas deferens 1 29
- incontinence 127 Vasa recta 127
- obstruction 125 Vascular factors 61
- output 1 3 3 , 135 - di sease 1 86
- pH 1 3 5 , 1 39 - element 132, 135
- stasis 123 - mechanism 142
- stream - weak 1 37 - occlusion 1 84
- urinary tract infection (UTI) 128, 134- - tone 93
135, 136 - vasculature 1 87
- OMT 1 33-134 Vasoconstriction 3, 15, 18, 25, 3 1 , 37,
- urgency 128, 129, 136, 137 50, 54, 55, 64, 68, 84, 125, 140,
Urine 124, 127 1 4 1 , 1 86
- concentration 134 - venoconstriction 62
Vasodilation 54, 55, 140 Viral infection 23 , 24, 4 1 , 42, 85
Vasomotor tone - change 48, 1 88 - lymphadenopathy 172
Vasovasorum 7 1 - measles 1 82
Vegetative nervous system 1 12 - pneumonia 85
Vein 89, 203 - post-viral diarrhea 201
- azygos 150 - replication 177
- bracbiocephalic 2 1 0 - upper respiratory tract 24
- communicating 150, 152 - virus 24, 172, 177, 201
- hemiazygos 150 - inflenza virus 24
- inferior vena cava 155 - rhinovirus 24
- internal jugular 86, 150 - varicella (herpes) zoster 5 8
- jugular 150 Viscera 1 88 , 192-193 (chart), 194
- left internal jugular 210 Visceral
- left subclavian 210 - afferents (See Visceral afferent under
- lower extremity 155 specific nerves)
- one-way valves 206 - component 144, 225
- renal 127 - dysfunction 82, 83, 95, 100, 109, 1 1 8 ,
- spinal membrane 152 1 19, 152, 1 6 1 , 1 6 3 , 165, 1 89,
- subclavian 86 , 127 194, 20 1 , 225 , 228
- valveless vertebral plexus 150, 152 - secondary 93, 1 12
- vertebral 150, 152 - function 89, 163
Venous - innervation 83, 194
- anastomosis 150 - irritation 95
- capacity 68 - manipUlation 89, 200, 220-222
- change 1 5 1 - pain 80 (diagram) , 8 1 , 188
- circulation 202 - peritoneum 81
- congestion 6, 70, 1 16, 1 1 8, 120, 140, - pleura 192
1 5 1 , 152 - serosa 8 1
- drainage 6-8, 25, 33, 43 , 89, 140, 166, - stimulus effect 3
204, 205 Visceromotor reflex 125
- EENT 6-8 - Cardiac 5 8
- flow 1 52 - Genitoreproductive 1 3 1
- plexus 150, 206, 2 1 8 , 228 - G I 79-82, 100
- return 66, 124 - GU 127, 1 3 1
- stasis 1 3 1 - Uterus 1 3 1
- system 149, 150, 155, 204, 210 Visceroptosis 120, 123
- thrombosis 229 Viscerosensory pattern
Ventricular - diagram 80
- arrhythmia 50, 60, 69, 70, 1 85 - GI 79-82, 100
- fibrillation 50, 60, 69, 70, 1 85 - GU 127
- output 54 - Genitoreproductive 1 3 1
- repolarization 69 - Gonads 1 3 1
- subendocardial hemorrhage 72 - Uterus 1 3 1
- tachycardia 70 Viscerosomatic dysfunction 82
Vertebral column 150, 151 - pain diagram 80
- fracture 100, 166, 228, 230 Viscerosomatic reflex 33, 35, 36, 37, 38,
Vertigo 2, 4, 6 , 7, 8 , 9, 10, 1 1 , 14, 15 49, 79, 8 3 , 100, 101, 109, 1 15,
- differential diagnosis 1 1 1 1 8 , 165, 167, 225
Vessel wall 64, 7 1 , 166 Viscerosomatic-Somatovisceral cycle 103
Vicious cycle 1 1 8 , 123, 163 Viscerovisceral reflex 25 , 33
Vision
- Blindness 14 z
- Blurred 7, 8 , 14
- Diminution of perceived light 8
- Diplopia 7, 14 Zink, J. Gordon 154, 208
- Disturbance 8, 9 - see also Fascia - pattern; Compensatory
- Far-sighted 13 mechanism - Common
- Jumpy print 8 compensatory pattern
- Near-sighted 13
- Visual development 178-179
Vomiting 8 1 , 85, 100, 104, 1 3 8 , 172
Walking 1 66
Warm slide preparation for amoeba 1 10
Waste product 98, 120, 124, 127, 159,
162, 164
- removal 88, 95
Water retention 62, 70
Wax plug (ear) 2
WBC increase 45
Weight control 166
Weight gain 1 3 1 , 153, 1 6 1
Weight loss 1 10
Well-baby 171
Wheat bran 1 17
Whiplash injury 2, 7
White blood cells 95
Wolffian duct 129
Work absence 79
X Ray 4 1 , 166, 205

Xiphoid 92, 104, 105, 1 1 8, 155, 199,
200, 206, 227
Yawning 10, 15
ISBN 1 -57074- 1 54-9
GREYDEN
...·
:: == PRESS
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Osteopathic Considerations

Michael L. Kuchera, D.O., F. A. A.O

William A. Kuchera, D.O., F.A. A. 0

Michael Kuchera, D.O., F.A.A.O.

Greyden Press, LLC

Osteopathic Considerations in Systemic Dysfunction

Printer/ Binder: Greyden Press, LLC

A.T. Still, M.D.

"The inevitable result of the rapid strides in the study of bacteriology,

"(Neuroscience) studies are establishing the physiological bases for

Horace W. Magoun, Ph.D.

Osteopathy is relatively a young profession in the history of medicine. Slightly

Osteopathic physicians are educated to use and understand all current

o .. support the patient's body systems that will be stressed by the

By studying anatomy and physiology from the philosophical vantage point

"Variability of symptoms is the rule in clinical medicine, a fact which

"It is not only necessary to understand that symptoms produced by a

"Most of the important symptoms arising from diseases of internal

1. Pottenger F M Symptoms of Visceral Disease. St Louis, CV Mosby Co,

��1r J)1{��C:1rI()� ••.•••••.•••••••••••••••••.•.•••••••••.•.••••••••••••••.•••••.•.••••..••• 1

Sympathetics ... ...

Venous And Lymphatic Systems . . . 6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

The Eye . .. . . . . . . . ... .

The Nose ... . .

The ENT Unit . .. . . . .

Additional EENT Bibliography.......................................................... 19

1rII� <:()�()� <:()� .......................•••............................................. 23

WWER R.ESPIR.ATORY DISORDERS ...............................................•... 33

Normal Functional Respiration .......................................................... 33

Reflex Action During Infection . . . .. . . 36 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CARDIOVASCULAR DISORDERS ........................................................ 53

Introduction ...... . . . ....................................................................... 53

UPPER GI DISORDERS ...................................................................... 79

Introduction ........... . ........... . ... . . ...................... . ............... . .. . . . . . . . . .. 79

Introduction ............................................................................ ... 95 .

Pathophysiology ..................................... .................. .................... 96

Other Complaints................................................................. 105

References. ............................................................................... 106

IR.R.ITABLE BOWEL SYNDROME- ...................................................... 109

Introduction .............................................................................. 109

GENITO'URIN'ARY TRACT DISORDERS ............................................. 123

Introduction .............................................................................. 123

TIlE OBSTETRICAL PATIEN'T .......................................................... 149

Existing Stresses Aggravated By Pregnancy......... .... .. .... .. . .. .... . . . . . . . . . . . . . 149

��" ()If ����])( ••.••..••••••.•••••••••••••••••••••••••••••••••.•.......•.••••••...... 169

Manipulation In The Pediatric Patient................................................ 171

PRACTICAL �EX FOR OSTEOPATHIC

Figure 1 All Parasympathethic Ganglia of Head and Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Figure 3 Anterior Chapman Points to Head, Neck, Bronchi . . . . . . . . . . . . . . . . . 3 .. . .. . . . . . . ..

Figure 4 Ciliary Ganglion to Eye (parasympathetic) . . . . . . . . .. .. . ... 5

Figure 5 Parasympathetic Innervation to Head and Neck . . . . .. . . . 5

Figure 6 Sphenopalatine Ganglion to Nasal Mucosa and Lacrimal Gland . . . . . . . . . 5 . ... . .

Figure 7 Richardson's Eye Exercise Chart . . . . . . . .. . .

Figure 8 Cervical Sympathetic Ganglia . ..

Figure 9 Important Landmarks of Normal Thoracic Inlet . . . .. . . . . 27

Figure 10 Sphenopalatine Ganglion (parasympathetics to Lacrimal Gland

Figure 11 Diaphragmatic Action (A Major Lymphatic Pump) .. . . .. . . . . . . . . . 33 .. . . .. . ... . .

Figure 12 Innervation of the Lung

Figure 13 Anterior Chapman Points of Cardiopulmonary System . . . .. . . . . . . . . . . . . 37 . . . . . .

Figure 14 Diaphragmatic Action (A Major Lymphatic Pump) . . . . . . . . . . . . . . . . . . . . . . 39 . . . . .

Figure 15 Common Lymphatic Drainage of the body . . . . . .

Figure 17 Sympathetic Innervation of Heart . . . .. .. ... . . . .... ...

Figure 18 Diagram of Sympathetic Innervation of Body . . . . . .... .... . . .. 54

Figure 19 Parasympathetic Innervation of the Body . . . . . . . ...

��" ()If ��])( ••.••..••••••.•••••••••••••••••••••••••••••••••.•.......•.••••••...... 169

in the upper thoracic or cer