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DIAGNOSTIC TESTS IN NEUROLOGY
A SELECTION FOR OFFICE USE

DIAGNOSTIC TESTS
A SELECTION FOR
"Science is simply common sense at its best-

rigidly accurate in observation and merciless
is,
that
to fallacy in logic."
Thomas Henry Huxley (1825-1895)

DIAGNOSTIC TESTS
A SELECTION FOR
"Science is simply common sense at its best-

rigidly accurate in observation and merciless
is,
that
to fallacy in logic."
Thomas Henry Huxley (1825-1895)

IN NEUROLOGY
OFFICE USE
By ROBERT WARTENBERG, M.D.
Forewords by
SIR GORDON HOLMES, M.D., F.R.S.
and by
STANLEY TRUMAN, M.D
THE YEAR BOOK PUBLISHERS, INC.

200 EAST ILLINOIS STREET, CHICAgO
RC 34 b
OPTOMETRY
UBRAflY
TO MY FRIEND
DANIEL EDWARD KOSHLAND

WHO LIVES BY THE MAXIM
ALUS IN SERVIENDO CONSUMOR
1885
Foreword
by Sir Gordon Holmes
THERE has been within recent years an increasing tendency to

rely more and more on laboratory, mechanical and other such
methods of investigation of patients suffering with symptoms of
nervous disorder at the expense of careful clinical observation. That
many of them have contributed to a fuller knowledge of the func
tions and diseases of the nervous system is frankly recognized by
the author of this useful book, but, as he rightly protests, they can
not replace adequate clinical study; they can in fact be properly
used only when brought into relation with the symptoms and signs
presented by the patient. Further, many of them which may not be
essential in a particular case are time-consuming and frequently in
cur considerable expense to the patient or to the public responsible
for his care, and they may not be readily available.
The object of this book, which is written in simple language
and profusely illustrated, is to provide the family doctor and the
physician who does not specialize in neurology with simple methods
of examination which may reveal, without resort to laboratory and
other special services, the nature of the illness or disability with
which his patient suffers, for though the study of nervous disorders
often requires more knowledge of the anatomy and functions of
the nervous system than the ordinary practitioner usually possesses,
he can frequently arrive at a correct diagnosis by accurate observa
7
8 DIAGNOSTIC TESTS IN NEUROLOGY
tion and careful interpretation of the facts as he has observed them.
It is mainly for these that Dr. Wartenberg has written this
small but essentially practical book which will prove suitable for
use both at the bedside and in the clinic.
Many of the tests and methods of examination dealt with here,
though well-known and generally employed, are more minutely
described and more liberally illustrated by excellent photographs
than they are in ordinary textbooks, but a few that are new or not
in general use are included. It can be argued that some of these, and
particularly some in either normal or
reflex reactions obtainable
pathological states, are unnecessary in ordinary clinical practice, but
even they may prove valuable in confirming or supplementing
evidence furnished by other means.
The direct and precise presentation of its subject will make this
book a desirable addition to the libraries of both the neurologist
and the general physician.
London, England
Foreword
by Stanley R. Truman
I WISH that you could know Dr. Wartenberg as I know him.

Here is a scientist who can teach. Here is a professor who realizes
that the doctor on Main Street is the one who sees, diagnoses and
treats the patient. Here is a doctor whose practical experience has
led him to the knowledge that an accurate diagnosis comes before
all else, and that this accurate diagnosis depends upon the skill,
knowledge and thoroughness of the examiner.
Dr. Wartenberg's lectures are among the most popular at the
University of California School of Medicine. On the graduate level
his talks and demonstrations are always enthusiastically received at
medical societies and postgraduate courses. Whether he came by his
talents in pedagogy naturally or by long study of teaching methods
is not important; he has the talent to instruct and inform in a clear,
comprehensible and memorable manner. This book is an expansion

of someof his lecture material. For years to come it will be a valu
able addition to the library of the practitioner, the student and the
teacher. Those of us who have forgotten some of the knowledge we
had when we left medical school will find much refreshing material
in this book and find it presented in a way that will help it stick.
We will also find much that is new and practical.
The practical aspect of Dr. Wartenberg's approach is particu
larly valuable and interesting. I am positive that all who read this
9
book will diagnose more precisely the multitude of neurological
problems we see in practice such as multiple sclerosis, Parkinson's
disease and the little strokes; we will also detect the rarer condi
tions earlier, more readily and with greater confidence. Readers will
welcome the constant attention to the methods and means of differ
ential diagnosis of diseases and signs of organic and psychogenic
origin. The book is packed with valuable suggestions. I recommend
it to all physicians and particularly to my colleagues in general
practice, first for reading and study, and then for later reference
and consultation.
Oakland, California
Preface
THIS book is not a primer, not an outline, not a textbook of

neurological examination, nor is it a substitute for any of these.
Although it is not written for the student, its perusal will do him
no harm. It is written for the general practitioner as a supplement
to the textbooks of neurology and as a postgraduate refresher course
in neurological diagnosis. I do not wish to instruct so much as to
remind the reader; not to lead him, but only to light the road. The
of necessity, condensed. The task has been to pre
is,
presentation
sent short course in today's neurological diagnostics to those who
a
have chosen the most difficult and exacting medical specialty of

all general practice. who must diag
the general practitioner
It
is
nose and treat the majorityof the most common neurological dis
eases. He will not fail when given the tools. The practitioner
is
also the key man with whom and through whom the neurologist
works. Still, has been duly considered throughout the whole work
it
that the patient with an organic disease of the nervous system

is
a
comparatively rare sight in the office of the practitioner.

As the subtitle indicates, the book contains "selection" of tests.
a
of course, purely individual and reflects the inter

is,
This selection
ests and research of the author. As teacher and consultant have
I
by
seen the errors made the senior students and the young referring
physicians and have tried to understand the reason for their diag
11
nostic troubles. I have considered the bitter experience of my own
early mistakes and have laid stress on those tests in which the
novice is likely to err, either in technique or in interpretation. All
tests are practically useful; they have proved particularly suitable
and valuable in office examination. Not completeness, but depend
ability and maximal simplification coupled with brevity are the aim
of this work. The enormous and bewildering accretion of methods
and details of neurological examination makes this imperative. The
simple diagnostic tests presented here can easily be applied in the
office or at the bedside and will serve for the first orientation as to
the neurological status of the patient. The book will help the prac
titioner to answer the often perplexing question: Does this patient
present any signs of an organic disease of the nervous system?
The way in which this book came into being would seem to
justify its publication. In recent years I have had the opportunity to
talk on neurology before staffs of general and Veterans Administra
tion hospitals, in postgraduate and national medical assemblies, in
refresher courses and particularly before county medical societies in
California. The topic which had the greatest appeal was "Diagnostic
Methods for Use in the Office." Invariably after every meeting it
was suggested from the floor that the talk be published. This little
book is the result of those suggestions. The final spur was the recep
tion given my talk on office neurology before the American Acad
emy of General Practice in San Francisco, March, 1951.
Neurological examination is particularly dreaded by the practi
tioner because of its alleged complexities and intricacies. Neurology
has a reputation among students as the most abstruse, remote and
difficult discipline, full of high-sounding terms, with an elaborate
technique of examination. of the outpatient department of
Statistics
one large hospital show a preponderance of neurological cases re
ferred. The physician is ready to tackle any problem in medicine,
however difficult, but shies away from a neurological problem and
PREFACE 1 3
refers As Foster Kennedy brilliantly

the patient to the specialist.
said:"Probably early in life they [the internists] took one horrified
look at the picture of the fifth nerve in Gray's Anatomy and de
cided there and then to have nothing more to do with such
octopodian proceedings; and the metagalaxy of reflexes may have
discouraged many even hardier spirits." However, this well-
entrenched attitude belongs in the category of unreasonable preju
dices. It all a matter of presentation. It is true that modern
is
neuroanatomy and neurophysiology are highly complex and become
more so every day. But little is needed by the physician from all
this in order to establish a workable and helpful diagnosis. And
this little is not complicated. I even dare to say it is simple. The
proof follows.
University of California Hospital

San Francisco
Acknowledgments
Figures 15, 21, 48, 62, A and B, have been made

available by Dr. L. Barraquer Ferre of Barcelona, Figures
1, 3, 4, 12, 13, 20, /J, 22, B and C, 35, /4, 36, B, and 47
by Dr. A. Ornsteen of Philadelphia, and Figure 60 by
Dr. L. Boshes of Chicago.
To Eleanor Little for her intelligent editorial and
secretarial help given unstintedly over a period of 12
years, my appreciative thanks.

Contents
INTRODUCTION 21
Clinic versus Laboratory 21
The Power of Observation 26
Diagnostic Tests 29
Plan of Examination 33
Examination in the Office 34
SECTION I: CRANIAL NERVES

Lateral Deviation of the Eyes and of the Head 36
Acute Unilateral Post-traumatic Mydriasis 36
Paralysis of Conjugate Upward Gaze 38
Doll's Eyes Test 38
Exophthalmic Ophthalmoplegia 39
Convergence Paralysis of the Eyes 40
Nystagmus 42
Startle Reaction on Examination of the Pupil 43
Tests for the Cervical Sympathetic 44
Test for Ptosis 46
Lid Lifting Test 47
Tests for Lateral Bulbar Syndrome 48
15
Tests for Intraoculomotor Associated Movements 50
See-Saw Test in Oculomotor Paralysis 52
Corneal Reflex 55
Jaw- Winking Test 57
Winking-Jaw Test 58
Blinking Test 59
Lid Vibration Test 60

Frontalis Muscle Test 62
Tests for Myasthenia 62
Platysma Test 64
Orbicularis Oculi Reflex 64
Intrafacial Associated Movements in Old Facial Paralysis ... 66
Associated Movements in Hemifacial Spasm 69
Facial Nerve Tapping Test 71
Accessory Nerve Test 72
Hypoglossal Nerve Test 74
SECTION II: PERIPHERAL NERVES

General 77
Paralytic Contractures 78
Test for Upper Brachial Plexus Paralysis 80

Test for Syndrome of C-7 81
Long Thoracic Nerve Test 82
Wrist Drop Test 83

Brachioradialis Test 85
Thumb Abduction Test in Median Paralysis 87
Abduction Position of Little Finger in Ulnar Paralysis 89
Thumb Bending Test in Ulnar Paralysis 90
Muscle Percussion Test 92
CONTENTS 17
Test of the Gluteal Muscles 93

Test for Pendulousness of the Legs 94
Knee Hyperextension Test in Tabes 95
Tendon Palpation Test 97
Test for Play of Foot Tendons 99
SECTION III: PYRAMIDAL SYSTEM

General 101
Posture 103
Hand Pronation Test 105
Arm Deviation Test 106
Everted Position of the Foot 108
Leg Extension Test 109

Knee Dropping Test 110
Pronator Tonus Test 113
Quadriceps Tonus Test 114
Acoustic Tonus Test 115
Tests Based on Weakness of Muscles in Spastic Paralysis .... 1 17
Reflexes: General 119
Jaw Muscle Reflex 120

Snout Reflex 121
Pathological Laughing and Crying 123

Head Retractor Reflex 124
Pronator Reflex 126
Finger Flexor Reflex 126
Superficial and Deep Abdominal Reflexes 127

Dissociation between Superficial and Deep Abdominal
Reflexes 129
Quadriceps Reflex 130

Triceps Surae Reflex 131
Plantar Muscle Reflex 132
Plantar Skin Reflex 133
Unilateral Reflex Changes in Pyramidal Lesion 133
Tests for Unilateral Spinal Cord Affection 135
Associated Movements in a Pyramidal Lesion 136
Associated Movement of the Thumb 137
Wrist Drop Test 138
Trunk-Thigh Associated Movement 138

Knee Bending Test 139
Tibialis Associated Movement 139
Homolateral Mass Flexion Reflex 140
Contralateral Associated Movements 142
Contralateral Identical Associated Movements of Fingers . 145

Contralateral Associated Leg Extension 146
Babinski Reflex 147
History 147
Reported Methods of Elicitation 148
Technique of Elicitation 149
Evaluation 151
Physiology 152
Grasp Reflex 154
SECTION IV: EXTRAPYRAMIDAL SYSTEM

General 156
Head Dropping Test 157
Test for Pendulousness of the Arms 159
Shoulder Shaking Test 161
CONTENTS 19
Arm Dropping Test lol

Push Test 163
Fixation of Position Test 164
Micrographia 165
Tests for Torticollis 165
General 165
Counterpressure Test 170
Test of Resistance Movement 171
SECTION V: CEREBELLAR SYSTEM

General 172
Tests for Hypermetria 174
Arm Stopping Test 174
Line Drawing Test 174
Hyperpronation Test 174
Knee Bending Test 174
Heel-Knee Test 174
Arm Tapping Test 174

Agonist- Antagonist Test 175
Finger Spreading Test 178
Finger-Tips in the Midline Test 178
Shoulder Shaking Test 179
Macrographia 181
Tests for Ataxia 181
Discrepancy Triad in Multiple Sclerosis 182

SECTION VI: SENSORY SYSTEM
General 184
Technique of Examination 185

Algic Neuritis 186
Fleeting Sensory Disturbances 187
Testing for Sensory Mononeuritis 188
Testing Skin Areas for Sensory Change 189

Testing Sensibility of the Mamillary Zone 191
Skin Writing Test 191
Tests for Dissociated Anesthesia 192
Astereognosis 194
Static Ataxia of Hand and Fingers 195
Preferential Choice Test 195
Simultaneous Double Sensory Stimulation 197
Feet Together-Eyes Closed Test 198
Nerve Pressure Test 200
Test for Facial Nerve Tenderness 201
Pressure Test in Scalenus Anterior Syndrome 201
Nerve Tapping Test 203
Nerve Stretching Test 203
Kicking Test in Sciatica 206
Head Bending Test 207
Jugular Compression Test 209

Wet-Dry Test for Causalgia 210
SECTION VII: VASOMOTOR-TROPHIC SYSTEM

Test for Dermography 211
Tests for Arthrogenic Muscular Atrophy 212
Tests for Neurogenic Arthropathy 215
INDEXES 216
Introduction
Clinic versus Laboratory
CLINICAL diagnostic tests exclusively are discussed here, tests

which can be performed easily in the office or at the bedside and
without recourse to any laboratory procedure. For these one needs
only a reflex hammer, a pin or a pinwheel, the five senses (sharp
ened by the gift of observation) and a sixth common sense.
There is a growing and deplorable tendency to overload neuro
logical diagnostics with mechanical, technical and laboratory pro
cedures and to overemphasize their importance. The physician is
more and more inclined to base his diagnosis on the results of these
procedures rather than on the findings on simple neurological ex
amination. He does not have a heart-to-heart talk with the patient
about his present and past, does not talk to relatives, but sends his
patient to the laboratory. The art of diagnosing with the eyes, ears
and finger-tips is steadily losing ground. Too many doctors long for
standardized foolproof methods as a substitute for "clinical sense"
based on observation and judgment. They expect from laboratory
procedures a mathematical formula which will give them the diag
nosis as a deus ex machina. Again, a busy physician, overworked
and pressed for time, uncertain about the diagnosis, confused by the
results of the preliminary examination, is apt to "pass the buck" to
the technician, just to gain time and to postpone his decision on
21
grounds which seem reasonable to the patient. If this be criticism,

it must also be directed against me, since I, too, have been guilty of
such practice.This practice has attained such proportions that one
can, with some reason, speak of "mechanized neurology." The situ
ation has become so grave that Foster Kennedy sagaciously warned
lest doctors become a "Union of Slick Gadgeteers."
Overuse of laboratory procedures and overestimation of their
value in neurology and in medicine in general are so undeniable
and so conspicuous that every physician, whatever his specialty, will
admit it. I have never met the man who maintains that laboratory
procedures are neglected at the expense of the clinical.
The last few decades have given neurology epoch-making tools
for the advancement of laboratory and technical diagnostics, to
mention only electroencephalography, pneumoencephalography,
myelography, electromyography, chronaximetry, suboccipital punc
ture, new serological, chemical and neurohistological tests. It is
hardly possible to overestimate their importance in diagnostics,
physiology, medicine and biology and the promise they hold. The
fact that one generally expects more help from them than they can
provide is no reflection on the methods themselves.
It would be completely inappropriate, nay, absurd, to say any
thing against laboratory procedures per se. However, a critique of
the indications for their use in everyday neurological practice is
justified. It is not a question of whether, but when, to use them.
Moritz Heinrich Romberg (1795-1873) wrote of "the great
aim which we must seek to achieve, of medical
the emancipation
science from the trammels of mere mechanical technicalities" (ital
ics his). This was written in 1840. How much more portentous and
significant are these words today!
Before any technical procedure is used, the following points
should be considered carefully. ( 1 ) Some methods are time con
suming. Valuable and irretrievable time may be lost through their
INTRODUCTION 23
use. (2) Some methods are expensive and to some patients may be
an incommensurate economic burden. (3) Some methods are not
always harmless, are often painful and sometimes fraught with
danger. (4) The objective findings depend on the integrity of deli
cate mechanical apparatus. (5) The interpretation may be equivo
cal. (6) Even if by laboratory procedures the presence of a definite
pathological process has been established, it does not mean that the
finding is clinically significant or that it can account for the pa
tient's present condition. (7) The information obtained, however
interesting, may not influence the clinical diagnosis and may be
completely irrelevant to the actual management of the patient.
(8) The correct evaluation of the most informative and illuminat
ing laboratory findings is possible only when correlated with the
findings of a complete clinical examination, for which there is no
substitute. The laboratory cannot tell the whole story; it can give
only brief passage. (9) The more thorough and exact the neuro
a
logical examination, the more informative and helpful are the re

sults of the necessary laboratory procedures. (10) If the laboratory
findings contradict the clinical findings, it
is,
in the last analysis,

best to base the diagnostic decision on the clinical findings.
These truths, though plain and self-evident, are worth repeating.
Too often they are disregarded.
In considering technical procedure, the most important and
a
most difficult question is: this procedure necessary?

Is
Experience
in neurology of over 35 years has taught me that often not.
is
it
If, for instance, statistic of unnecessary x-rays in neurological con

a
ditions could be compiled, the figures would be staggering.

How disheartening to have patient with clear-cut pic
it
is
ture of myasthenia gravis bring in x-ray films taken from his head
to his toes! Epilepsy, in everyday medical practice, and remains
is
clinical diagnosis, electroencephalogram or not. clinical

If
on
grounds idiopathic epilepsy must be assumed, must be treated as
it
such, whatever the EEG may say if anything. Fortunately these
two procedures cannot harm the patient. They are only expensive.
It is tragic indeed to see a patient with the classical syndrome of
Parkinson's disease, of olivopontocerebellar atrophy, of presenile
dementia or chorea subjected to pneumoencephalography and/or
cerebral angiography. Or to see patients with unmistakable clinical
pictures of multiple sclerosis, poliomyelitis or polyneuritis subjected
to myelography. One patient had far-advanced, long-standing mus
cular dystrophy which could have been diagnosed after a few min
utes' examination in the office. Yet he spent weeks in hospitals,
was subjected to lumbar puncture, myelography, radiography and
finally muscle biopsy! In 1926 in the Outpatient Department of
the Hopital Necker in Paris, I saw Sicard, the originator of myelog
raphy, examine a patient with subacute mild spastic paraplegia of
the lower extremities. The same day the patient was admitted to
the hospital and myelography with Lipiodol immediately per
formed. Later clinical examination revealed a huge visible and pal
pable gibbus due to tuberculous spondylitis. This was clearly seen
by the naked eye and x-ray.
The present popularity of the diagnosis "herniated disk" is re
sponsible for the taking of countless unnecessary myelograms. In
the search for a "disk," one patient was twice subjected to myelog
raphy. Later a short clinical office examination revealed the patient
to be suffering from primary lateral sclerosis of many years' dura
tion. More cruel than helpful is muscle biopsy in muscular dystro
phy, liver biopsy in hepatolenticular degeneration, lumbar puncture
in long-standing cases of multiple sclerosis, when the diagnosis
could have been established clinically beyond any doubt. This ends
a list which could be greatly expanded.
Should these laboratory and technical procedures become rou
tine and be applied indiscriminately, it is quite true that on an
extremely rare occasion a morbid condition might be uncovered
INTRODUCTION 25
that otherwise would have passed unnoticed even by the most exact
clinical examination. However, the price of such a discovery would
be far too high.
There are not, nor can there be, undeviating rules for the appli
cation of laboratory procedures. In some cases they are an absolute
necessity and may be of vital importance to the patient. Yet in
every case it is incumbent upon the physician to consult his medical
and human conscience, to be guided by the two supreme laws of
medical ethics: (1) salus aegroti suprema lex esto, and (2) pri-
mum non nocere. The latter applies not only to therapeutics but as
well to diagnostics. Laboratory procedures should be used only in
carefully selected cases, as the last resort in diagnosis and only after
an exhaustive clinical examination has been made. They should not
be "diagnostic luxuries" at the patient's expense, nor should they be
performed just to satisfy the curiosity of the physician.
Careful history taking and interpreting, minute and repeated
clinical examinations are time consuming. It is particularly the busy
physician who is inclined to delegate the diagnosis to the laboratory
in the vain hope of saving time. Too many irrelevant technical pro
cedures often confuse the issue, cloud the essential point and
broaden the margin for error. Time invested in clinical examination
might have paid greater dividends.
The main point is this: laboratory procedures often seem neces
sary because the clinical examination has not been adequate. They
are all too often superfluous, and a thorough clinical examination
would have provided grounds for correct management of the pa
tient. The more clinical neurology we know, the less need there is
for laboratory procedures and the more valuable these procedures
become when they are necessary.
What Penfield and Kristiansen say of epilepsy applies to the
whole field of clinical neurology: "Our aim is to emphasize the
importance of the critical analysis of seizure patterns. Without it a
physician can hardly treat the patients under his care intelligently.
Without it the surgeon lacks his surest guide to radical therapy in
focal epilepsy. Without it the encephalographer is deprived of his
most helpful collaboration and the neurophysiologist of illuminat
ing clues of function localization."
Cushing, disappointed with the misleading results of a myelog
raphy performed in his clinic by Forestier, remarked: "From now
on we will use less Lipiodol and more neurology."
Whatever place the laboratory may have in diagnostics, it is
clear that the general practitioner needs a better working knowl

edge of clinical neurology. A well equipped laboratory is often not
available to him. He simply must get along with what he can un
cover by clinical examination.
What has been said here about and against the laboratory ap
plies to everyday, routine neurological work in the office and at the
bedside, in the hospital and at home. Only when research is in
volved are the indications for laboratory procedures widened.
The Power of Observation
"All human science is but the incre

ment of the power of the eye."
JohnFiske (1842-1901)
To enhance our clinical acumen we should strive to develop

and cultivate the precious art of observation, which Osler called
"the most difficult of all arts." Observation is the very basis of all
our clinical work. The accent lies on "observation"; to see is not
enough. This applies not only to daily practice of neurology but
also to teaching. The primary object of neurological instruction is
to teach the student to observe.
On the value of the power of observation, the greatest in medi
cine left immortal words. They are classic and bear repeating.
INTRODUCTION 27
"Don't touch the patient state first what you see; cultivate
your powers of observation" (Osler).
"There is a widespread impression that the scientific quality of
medical education and practice is in some fashion dependent upon
the part played by the laboratory. This is not the case. Science is
essentially a matter of observation, inference, verification and gen

eralization" ( Flexner ) .
"I very much doubt if the modern doctor with the laboratory at
his back .... is as good at the bedside .... as those who have
had to trust to their powers of observation" (Balfour).
"We have instruments of precision in increasing numbers with
which we and our hospital assistants at untold expense make tests
and take observations, the vast majority of which are but supple
mentary to, and as nothing compared with, the careful study of the
patient by a keen observer using his eyes and ears and fingers and
a few simple aids" (Cushing).
Our students should at all times strive to apply the infinite
wisdom inherent in these words.
There is no substitute for observation, for the experience gained
by "seeing much, and seeing wisely." "Seeing wisely" is a prudent
integration of seeing locally and generally, with the whole patient
in focus. The danger in neurological examination is that the exam
iner monomaniacally fix too much attention on minute local mani
festations of the disease and so miss more general and more en
lightening signs.
Failure to observe carefully can lead to tragicomic errors and
puzzles. Apatient was referred to Cassirer with the diagnosis of
left-sided brachial monoplegia. It is quite true that this patient
could not move his left arm, but only because on that side he had
an axillary abscess which had been completely overlooked by the
referring neurologist. Another patient was treated for weeks for a
mysterious and undiagnosed disease, until a young doctor inspected
the patient's thighs, discovered numberless scars from injections and
found a case of chronic morphinism. Still another patient was
operated on for a unilateral cerebellopontile angle tumor. Only
after the operation was his skin inspected and generalized neuro
fibromatosis found. The tumor was, as the autopsy revealed, bi
lateral! Numerous x-rays of the cervical spine were made of a
patient who complained of dysesthesias in one thumb. On careful
examination it was found that he suffered from a purely peripheral
affection of the cutaneous branch of the radial nerve, which was
compressed at the wrist by his watchband.
It is true, neurological diagnostics is now more complicated
and more exacting than it was in the time of Babinski and Oppen-
heim. Still, it is fitting to pause briefly and remember that long
before the of "mechanized neurology" there were highly
birth
successful neurologists who worked with simple clinical tools. The
well-trained eye of an experienced neurologist sees what may re
main unnoticed by others. Not knowledge alone, but careful ob
servation throughout the years, combined with profound knowledge,
has made our great diagnosticians in neurology. Here are some
examples of their uncanny gift of observation.
In 1923, as assistant to Nonne in Hamburg, I presented a pa
tient with a diagnosis of epidemic encephalitis. On each of several
ward rounds, without personal examination but after merely glanc
ing at the patient, Nonne objected to the diagnosis, insisting that
the patient "looked tumorous." Suddenly the patient died, and
autopsy revealed bilateral frontal lobe tumor. As an assistant to
Foerster in 1924, after several days of most careful examination I
presented with a diagnosis of right-sided frontal lobe
a patient
tumor. At first glance, Foerster noticed that on walking the patient
tended to fall back and to the left. This had escaped the notice of
all his assistants. Without further examination Foerster suspected
not a frontal but a temporal lobe tumor and so it proved to be.
INTRODUCTION 29
These stories are told not to encourage short-circuit, intuitive,

snap diagnosis by neurologists, young or old, but to show how far
diagnostically a glance "of the wise" may lead.
Diagnostic Tests
We first try to establish a preliminary diagnosis on the symp
toms and signs as they present themselves; then we perform diag
nostic tests to elicit further signs and symptoms. It is here that the
gift of observation comes into its own.
The expression "symptoms and signs" is much used for head
ings in textbooks. But in the text proper the distinction between
signs and symptoms is not always made, and the words are used
interchangeably. However, the distinction is a valid one, though
occasionally a doubt may arise as to which term should be applied.
A symptom is a subjective phenomenon. To uncover it we must
depend essentially on the statement of the patient. For instance,
headaches, dizziness, palpitation of the heart, dysesthesias and pain
are symptoms. Though under certain conditions it is possible to
objectify a symptom, by and large it is and remains a subjective
phenomenon. In their entirety, symptoms constitute the symptoma
tology of a disease.
A sign is an objective phenomenon and can be perceived by the
sensesof the examiner. It is demonstrable. It is signs for which the
examiner looks first of all. As Hordes said: "In diagnosis one physi
cal sign is of more value than many symptoms." Exophthalmos,
tremor, trophic disturbances, abnormal posture, involuntary move
ments, reflexes all are signs. In their entirety signs constitute the
semeiology of a disease.
There are two kinds of signs. The first are discernible immedi
ately and usually on simple inspection of the patient, without con
tact between him and the examiner. The second are those which
must be uncovered by action, either of patient or of examiner. In
this second category the examiner really tests something and ob
serves the results exactly as a chemist does when he notes the
reaction produced by mixing various chemicals. The difference be
tween a sign and a test is the same as between seeing and doing.
A test is a sign in action. We make a test to produce a sign or
symptom. Therefore the well-known signs of Romberg,
Kernig,
Lasegue, Brudzinski and Froment should be called tests. Into the
category of tests fall those signs which require certain maneuvers
to disclose them.
All reflexes belong in the category of tests. We speak correctly
when we say "testing the reflexes." They are signs uncovered by
some maneuver. But since reflexes represent such a large and inde
pendent group, they will be discussed under the heading "Reflexes."
Of the diagnostic tests discussed here, some are new, some so
new that they have not been mentioned in any neurological Bae
deker. Older, time-honored tests which have not found proper rec
ognition are mentioned if they need special emphasis. The constant
endeavor has been "to make new things familiar, and familiar
things new." Tests which not only have local significance but also
colorfully illustrate some general physiological principle of broader
application are given their due.
Definite, decisive, "high-powered" tests have been selected.
However, to these proved tests have been added a few whose diag
nostic significance and value have not fully established.
as yet been
But they are promising and worth trying. Tests which serve to un
cover the inception of a disease, those which alert the examiner,
have been particularly stressed.
Sometimes it has been found advisable to offer a choice of sev
eral tests to demonstrate a single diagnostic phenomenon. The ex
aminer will find that, in order to prove one point, it is advantageous
to have several tests at his disposal. The result of one test may be
inconclusive, but even when it is conclusive, it is always precarious
INTRODUCTION 31
to base final judgment on it alone. The sign usually regarded as
pathognomonic for a certain condition may be absent. The Babinski

reflex, for instance, in amyotrophic lateral sclerosis.
is often absent
It is always well to keep the following simple rule in mind: if
some sign pathognomonic for a morbid condition is absent, the
condition still may be present. It is best to base a diagnosis on the
results of several tests, all of which point in the same direction.
All tests described in this book are simple and can be easily
performed in the office or at the bedside. None is time consuming,
none will make the patient uncomfortable.They are proved tests,
based not on bookish wisdom but on years of practice. Here there
is no borrowed experience; only what I have seen with my own
eyes is reported.
Since the whole structure of our diagnostics is based on the re
sults obtained from the evaluation of symptoms, signs and re
sponses to tests, the technique of these tests will be described in
detail. The minutiae, "the little things" that appear trivial, will be
carefully considered. Upon the accuracy of these minutiae may rest
the final diagnosis.
As in everything else, in the performance of a neurological test
there are many ways to do it wrong, but only one way to do it
right. A slight imprecision in technique may indicate an abnor
mality where none exists. Here lies the source of the gravest mis
takes of the uninitiated, who may regard as pathological that which
is normal. The cumulative power of such mistakes is immeasurable.
One basic precept derived from an inaccurately performed test may
lead to a diagnostic impasse and utter confusion. In 1926 William
Spiller said to me: "Do not try to explain anything that may be
wrong in the first place." The whole examination should always be
guided by this wise admonition.
The newer textbooks outline disease entities in the greatest de
tail but tell little about the technique used to establish their diagno
sis. It highly regrettable that the exposition of such fine tech
is
niques is being neglected. Clinical neurological examination is los
ing ground and is being relegated to a minor position. The recent
neurological literature contains few advances in this field as com
pared with those made by the European schools at the turn of the
century.
For each test discussed here there will be a brief description of
the physiological mechanism involved. It is not enough to memo
rize the name, content, physical happenings and allocation of a
given test. It is essential that the reader understand its physiology.

Only then will he be able to evaluate the result correctly.
In discussion of the physiological mechanism the utmost simpli
fication and synthesis must be achieved, and the main goal of the
physiological interpretation is to reduce diverse tests to a common
denominator. Such an attempt to simplify must, of necessity, lead to
some dogmatism. As John Ruskin said: "It is far more difficult to
be simple than to be complicated." Where opinions differ, one has
been accepted and followed with a minimum of "but's," "on the
other hands's" and "however 's." Such a didactic method of presenta
tion, which bars all controversy, naturally invites criticism but is
used in order that the reader may not become confused.

In neurological literature, texts and records, one is struck by
the number of proper names. A symptom, sign, reflex, test, syn
drome or disease is often not characterized clinically, pathologically
or descriptively but usually bears a proper name. In texts, proper
names alone sometimes constitute chapter headings. There is
in neurology that is not encumbered by an eponym.

scarcely a sign
This "eponymania" is endemic particularly in European countries.
For instance, a leading European neurologist, reporting a case in
1937, in a single paragraph and without further comment used 14
proper names (including his own) to describe the reflexes in his

case. Eponymization of a scientific discovery is often due to the
INTRODUCTION 33
purely personal benevolence of writers, among whom there is no

unanimity. An eponym may denote the man who first described,
introduced, explained or effectively modified something. A phenom
enon may be thus variously termed: A, B, C, A B, B-A, and so on
ad infinitum. Local and national patriotism contributes to this pleth
ora of eponyms. The great confusion which is rampant is under
standable. Indeed, it is well-nigh impossible to attribute a scientific
discovery to a single person. It is rare that single eponyms are his
torically correct.
The disavowal of eponyms may discourage the overambitious
from mass production of unnecessary signs and reflexes.
In this work the eponyms will be kept at a minimum. A fitting
physiological name for a test tells more than any proper name can.
We need more physiology and fewer eponyms, more understanding
of neurology and less memorizing of proper names.
Plan of Examination
The neurological examination should be careful, concise and
complete, the accent being on "complete." It is therefore imperative
always to follow a definite plan, even to the point of pedantry; to
think of everything, to forget nothing. In a formalistic fashion the
minutiae should be scrupulously checked and nothing taken for
granted. The great neurologists were true pedants in their diag
nostic work.
Examination should be complete in every way, every system
covered evenly and without bias. That the examination be done
evenly is all-important. Every physician has his favorite diseases,
so also has his favorite methods, regions, signs, tests. These "special
interests" should never be allowed to prevail. The generally accepted
plan of examination is: (1) cranial nerves; (2) motility; (3) re
flexes; (4) sensibility; (5) vasomotor-trophic system.
But whether we follow this or any other plan, we must realize
that an ideal scheme of neurological examination has never been
devised and never will be. The reason is that all divisions and sub
divisions we make are artificial. The entire nervous system is a
single indivisible unit, and no part of it works independently or in
isolation. In any scheme, some overlapping is inevitable. But it
must be remembered that it is better to repeat than to omit. While
concerned with the minutest part of the nervous system, the exam
iner must not lose sight of the fact that the whole being body,
mind, nervous system This reminder is general, hackneyed,
is one.
outworn and overworked but contains a basic, useful and highly
practical truth. Another reminder, old, but still of value: although
you are interested in neurology or are a neurologist, although a
patient is explicitly for neurological examination and
referred
thinks "a nerve is pinched," his affection still may be arthritic, vas
cular or what not and not neurological. Another, and a last, re
minder: if you are confronted with a "neurological" problem which
seems very complicated and baffling, where signs contradict symp
toms, and symptoms contradict signs; if you have
clinical picture
a
full of unusual and bewildering features, it might be worth while
to remember that the whole problem may be psychiatric.
Examination in the Office

The complete and over-all neurological examination, as prac
ticed by the fourth year student in the hospital, suffers a modifica
tion when he becomes a busy practitioner facing the patient in his
office. Lack of time requires that completeness of examination be
sacrificed to some extent. Increased knowledge and ripened experi
ence make this possible. According to the requirements of the case,
special or local examinations are favored at the expense of the com
plete examination. This specialization and localization are depend
ent on what we assume the lesion to be after taking the history and
a "first glance." The "sense for the essential" arises to compete
INTRODUCTION 35
with completeness. The goal is not only to arrive at a workable

diagnosis but to arrive with a minimal expenditure of time and
effort. It is a compromise, but a bitter necessity. The practitioner
immediately adapts his plan of examination to the requirements of
the case; he focuses his attention on a certain region or on the
leading symptom or sign. He stresses some signs and tests, touches
lightly on some and neglects others. His attention is immediately
directed to the site of the lesion. Certainly the course of an office
examination differs when we suspect a temporal lobe abscess, tabes
dorsalis or meralgia paresthetica. This abbreviation of the complete
neurological examination is acceptable since otherwise the physician
runs the danger of not seeing the forest for the trees.
In view of these requirements of an examination in the office,
which is concerned with localization of the morbid process first of
all, the tests discussed are arranged in the following order:
1. Cranial nerves
2. Peripheral nerves
3. Pyramidal system
4. Extrapyramidal system
5. Cerebellar system
6. Sensory system
7. Vasomotor-trophic system
SECTION I
Crania IN erves
LATERAL DEVIATION OF THE EYES AND OF THE HEAD
WHEN the patient has just suffered a cerebrovascular accident

and lies unconscious with his eyes closed, the eyes should be opened
passively and their position ascertained. If the eyes and sometimes
also the head persistently deviate to one side ( Fig. 1 ) , this consti
tutes a valuable localizing sign. In the first place it means that
there is a focus of irritation (often hemorrhage) in the frontal
lobe, turning the eyes to the opposite side. If and when the irritation
ceases and paralysis supervenes, the eyes turn to the other side: the
patient looks toward his lesion. This is due to the unopposed action
of the lateral rotators of the eyes on the healthy side of the brain.
This deviation of the eyes, however, is transient.
ACUTE UNILATERAL POST-TRAUMATIC MYDRIASIS
Slight anisocoria, i.e., a difference in the size of the pupils, has

no diagnostic significance and may occur in the normal subject. It
may be due to an error of refraction or to imbalance of autonomic
innervation. Marked unilateral mydriasis, however, is of high diag
nostic importance. The dilatation of the pupil may be due to in
creased sympathetic stimulation or it may be paralytic, due to loss
of innervation by the parasympathetic fibers running with the ocu
36
CRANIAL NERVES 37
lomotor nerve. Only post-traumatic oculomotor paralysis is consid

ered here.After a head trauma, particularly to the temporo-parietal
region, which may or may not cause loss of consciousness or skull
fracture, the patient makes an immediate recovery, has few com-
Fig. 1. LATERAL DEVIATION OF THE EYES AND HEAD.

Acute cortical hemorrhage on patient's right. Both eyes deviate to the left;
also the head, but slightly. This is due to irritation of the cortical center for the
contralateral deviation of the eyes and of the head.
plaints. After several hours of this so-called "lucid interval," how

ever, headache and drowsiness develop and he lapses into stupor.
In such cases it is of vital importance to test for unilateral mydriasis.
If
if,
such mydriasis develops on the side of the trauma, and in ad

dition, even the mildest signs of contralateral hemiplegia appear,
there bleeding from the middle meningeal artery: blood clot
is
presses on the third nerve, producing mydriasis. In scarcely any

other acute emergency could an immediate operation removal of
the blood clot and hemostasis be more vital or the effect more
dramatic. Delay in operation means certain death. It is the unilateral
mydriasis with a fixed pupil which points to the gravity of the
situation.
It well to remember that acute unilateral mydriasis may be
is
the most outstanding manifestation of paralysis of the oculomotor
nerve; absence of other signs of oculomotor paralysis does not
speak against involvement of the oculomotor nerve.
PARALYSIS OF CONJUGATE UPWARD GAZE
In examining eye movements we are apt to omit testing of the

patient's ability to raise, on command, both eyes simultaneously
above the horizontal level. His symptoms may not indicate that a
disturbance of such a movement is present. The patient at rest, look
ing straight ahead, is asked to move both eyes upward. If he is
unable to do so and his eyes remain at the horizontal level, there is
paralysis of conjugate upward gaze. The uncovering of such a
paralysis is of great diagnostic significance. It is usually caused by
lesions at the level of the quadrigeminal plate: tumors (particu
larly of the epiphysis, of the hypothalamic region), vascular proc
esses, encephalitis. The quadrigeminal plate may be affected indi
rectly by distant pressure.
Paralysis of conjugate downward gaze occurs much less often.
Its diagnostic significance is not so clear.
DOLL'S EYES TEST
When conjugate paralysis of upward gaze is caused by a lesion

at the level of the quadrigeminal plate, the lesion is supranuclear.
It lies in the pathways between the cortex and the nuclei of the
motor nerves of the eyes. The cardinal characteristic of supranuclear
paralysis is present: the movement cannot be performed spontane
CRANIAL NERVES 39
ously or on command, but it can take place as an associated move

ment unintentionally, reflexly, automatically. This is in contrast to
nuclear or infranuclearparalysis, when the movement cannot be
performed under any circumstances. In supranuclear paralysis, the
patient, though unable to move his eyes upward on command, can
still perform this movement when he fixes an object, e.g., the ex
aminer's finger. He can then follow the object as it is moved upward.
This dissociation between the voluntary and the involuntary
conjugate movements of the eyes can also be demonstrated in the
following manner. The patient is asked to close both eyes. The
examiner keeps them open passively by lifting the upper lids; he
watches the movements of the eyeballs. If the so-called Bell phe
nomenon appears, i.e., if the eyeballs automatically turn upward on
an attempt to close the eyes, the lesion is supranuclear.
The most striking test to demonstrate supranuclear paralysis of
conjugate upward gaze is the following. The patient is completely
unable to look upward on command. He is asked to stare fixedly at
an object before his eyes. His head is then passively bent down
ward. If the lesion is supranuclear, his eyes will turn upward as his
gaze remains fixed at the stationary object, while the position of
his head is being altered. This automatic movement of the eyes, in
reverse direction to that of the head, is seen in some dolls. There
fore the name, Doll's Eyes Test.
In nuclear or infranuclear paralysis this upward turning of the
eyes on bending of the head does not occur; the paralysis is perma
nent under any and all conditions.
EXOPHTHALMIC OPHTHALMOPLEGIA
When multiple palsies of the external ocular muscles insidi

ously develop in middle life, and when simultaneously some dys
function of the thyroid appears, and even the slightest exophthalmos
develops, it is wise to consider the diagnosis of exophthalmic oph
thalmoplegia. There is no fatigability of the muscles, as in myas

thenia, and Prostigmin is ineffective. This condition has only
recently been outlined as a clinical entity and is easily misdiagnosed.
The main characteristics are ophthalmoplegia and exophthalmos
Fig. 2. EXOPHTHALMIC OPHTHALMOPLEGIA.

Multiple palsies of the extraocular muscles with exophthalmos and dysfunc
tion of the thyroid.
(Fig. 2). There is a close relationship to disturbed function of the

thyroid. Careful testing of the eye movements reveals more paraly
ses than seem to exist at first glance.
CONVERGENCE PARALYSIS OF THE EYES
The reaction of the pupil to light and on convergence is rou

tinely checked. However, the important testing of the movements
CRANIAL NERVES 41
of the eyes on convergence is sometimes overlooked. Complete

paralysis of eye movements on attempted convergence is rare. More
often, there is a slight paralysis, and the range is conspicuously
diminished. This can be observed in patients whose symptoms give
no indication of such a disturbance. Since there exists a special

nucleus for the convergence movement of the eyeballs, this move
ment may be affected isolatedly. But usually there are signs of con
comitant involvement of other parts of the brain stem. Convergence
paralysis is common and may be caused by a great variety of condi
tions, ophthalmological or neurological, organic or functional. It is
mentioned here primarily because convergence paralysis may be an
early and valuable sign of idiopathic or symptomatic Parkinson's
disease (Fig. 3). It may even be regarded as characteristic of this
disease. The paralysis, which may be asymmetrical, is not itself
sufficient to establish a diagnosis; but when, on examination of the
head, convergence paralysis of the eyes, an exaggeration of the
orbicularis oculi reflex and the slightest rigidity of the neck muscles
are found, the combination of these three signs will warrant a diag
nosis of Parkinson's disease.
NYSTAGMUS
Next to aphasia, nystagmus is the most complex and difficult

problem in neurology, clinically, physiologically, pathogenetically.
Once, in 1921, 1 of unusual nystagmus.
was about to write up a case
I consulted the famous neuro-ophthalmologist Wilbrand, and he
said half- jokingly: "Never write on nystagmus, it will lead you
nowhere." There is a great variety of types of nystagmus, and there
are many structures in- and outside the nervous system which may
produce nystagmus and may do it in different ways. When the phy
sician encounters a case of intricate nystagmus, it is wise for him to
consult an ophthalmologist.
Fortunately, not every instance of nystagmus which is diagnosed
by the uninitiated proves to be pathological. It is a common occur
rence for a student to diagnose nystagmus when none exists. In the
normal subject there may be a slight fixation nystagmus, and also a
nystagmus which can occur when the eyes are fixed for a long time
in extreme position. Particularly is this latter nystagmus often mis
diagnosed as pathological. In the healthy individual, nystagmus
occurring in extreme positions of the eyes is of short duration and
wanes rapidly. In testing for nystagmus, such positions should be
avoided. Fatigue and barbiturates may also produce nystagmus.
There is one striking form of nystagmus which has great local-
iz'mg value. It is the nystagmus which is different in character when
the patient looks to the right and when he looks to the left. On
CRANIAL NERVES 43
looking to one side, the nystagmus is coarse and slow; on looking

to the other side it is fine and quick. The lesion lies on the side of
the coarse and slow nystagmus, and the first assumption must be
cerebellopontile angle tumor. If on this side there is also an old
history of involvement of the acoustic nerve, weakness of the facial
muscles and loss or diminution of the corneal reflex, the diagnosis
of cerebellopontile angle tumor is well warranted. This form of
nystagmus occurs also in the lateral bulbar syndrome (occlusion of
the posterior inferior cerebellar artery).
STARTLE REACTION ON EXAMINATION OF THE PUPIL

To find an anomaly of pupillary reaction to light is of grave
diagnostic significance. Such a diagnosis should be based on re
peated examinations made with the utmost thoroughness and care.
This will help to avoid embarrassing, ambiguous and meaningless
records such as "slightly impaired reaction to light." Records like
these are about as useful as "slightly pregnant" or "a little cancer."
The term "sluggish reaction" often means an inadequate examina
tion. As Wernicke put it: "Sluggishness of pupillary reaction means
sluggishness of the examiner."
When the reaction of the pupil to light was tested, it was re
peatedly found that the pupil seemingly failed to react. Particularly
was this the case when the testing was done at the beginning of the
examination and strong artificial light was used. However, when
the patient was examined later in a darkened room and milder light
was used, the pupillary reaction was found to be completely nor
mal. A reasonable explanation is that the tense patient was startled
by the strong light and this psychic reflex brought about such a
dilatation of the pupil that it neutralized the normal constriction of
the pupil to light. When, in the course of the examination, the pa
tient becomes less tense and relaxes in the darkened room, when
weaker light is used and when the examiner approaches the eye
slowly and cautiously from the side, the startle reaction is avoided
and a normal reaction of the pupil obtained. Therefore, when a
flashlight is to be used, strong light should be avoided and the light
should not be applied too suddenly.
It also may happen that a pupil which actually does not react to
light seems to do so. This may be caused through faulty technique
of examination. The reaction to accommodation may take place be
cause the patient looked, not into the distance, but at an object near
Fig. 4. PARALYSIS OF THE CERVICAL SYMPATHETIC.

In each patient, the left side is affected. Note ptosis and myosis on that side.
In A, the paralysis is a residual of occlusion of the left posterior inferior cere
bellar artery.
at hand the examiner or the light. A pupillary constriction on ac

commodation may thus be mistaken for pupillary reaction to light.
When the pupils are already constricted because the eyes are
converging, further constriction to light may not take place. It
would thus be wrong to assume that the pupil does not react to
light. Avoid the pupillary constriction on accommodation when you
examine the pupillary reaction to light.
TESTS FOR THE CERVICAL SYMPATHETIC
A deficit in the function of the cervical sympathetic manifests

itself in the eye by the well-known triad of signs described by the
CRANIAL NERVES 45
Swiss ophthalmologist Horner in 1869. It consists of ptosis, myo-

sis and enophthalmos. The last may be absent or inconspicuous. Of
the three signs, ptosis is the most constant, most significant, and its
presence is most easily established. The ptosis may be mild (Fig. 4)
Fig. 5. IRRITATION OF CERVICAL SYMPATHETIC

Patient's left side shows enlargement of the palpebral fissure. The slight
mydriasis and mild vasomotor disturbances are not discernible in the picture.
Pressure on the cervical sympathetic chain by enlarged thyroid ( ? ) .
or considerable (Fig. 7, A) but is not so massive as in oculomotor

paralysis (Fig. 6). The reason for this is that paralysis of the cervi
cal sympathetic affects only the superior tarsal muscle. This consists
of smooth muscle fibers which form but a small component of the
levator of the upper lid. In oculomotor nerve paralysis the more
powerful, striated part of the levator is involved. With sympathetic
denervation there also may be, on the affected side, vasomotor and
secretory disturbances, particularly anhidrosis. However, these are
seldom complete and seldom permanent.
The syndrome may be produced by a lesion along the extended
pathway of the cervical sympathetic from the hypothalamic region,
through the ciliospinal center situated in the lateral horn of C-8,
the anterior roots of C-8, D-l and D-2, the cervical sympathetic
chain, carotid sympathetic plexus, gasserian ganglion, first division
of the trigeminal nerve. The ciliospinal center and roots C-8 and
D-l are the site of predilection for cervical sympathetic injury.
In the cervical sympathetic there may be not only a defect in
the innervation but also a state of irritation. This documents itself
in the opposite syndrome: enlarged palpebral fissure, enlarged pu
pil, exophthalmos. The first two signs are the more important. This
irritation may stem from any place in the long course of the cervi
cal sympathetic. For instance, it may be produced by a tuberculous
infection of the upper tip of the lung or by pressure of an enlarged
thyroid ( Fig. 5 ) .
TEST FOR PTOSIS
Ptosis may be caused by a great variety of organic conditions.

Occasionally, however, it is psychogenic. If the ptosis is organic, the
patient tries to compensate for the affected levator palpebrae muscle
by strong innervation of the frontalis muscle, causing marked
wrinkling of the forehead (Fig. 6, A). The combination of ptosis
and wrinkling of the forehead is highly characteristic of tabes ( Fig.
6, B). This may enable us to suspect the disease at a glance.
When the ptosis is psychogenic, the patient is not interested in cor
recting it: he does not wrinkle his forehead. Even when asked to
open his eyes widely, he makes no effort to innervate the auxiliary
muscles.
CRANIAL NERVES 47
In order to evaluate the of an organic ptosis, the auxil

degree
iary action of the frontalis muscle must be eliminated. The exam
iner pushes the frontalis muscle down to prevent its contraction,
forcing the eyebrows to remain static. Then he asks the patient to
Fig. 6. ORGANIC PTOSIS.

A, ptosis due to oculomotor paralysis on the patient's left. Innervation of
frontalis muscle on upward gaze. B, bilateral oculomotor paralysis with ptosis in
a tabetic. Constant wrinkling of forehead to compensate for the paralyzed
levator of the lid.
look up. The strength of the levator palpebrae is indicated by the

extent to which the eyelid can be raised. Here the frontalis muscle
does not participate.
LID LIFTING TEST
In order to appraise the comparative strength of the muscles

which keep the eyes closed in a comatose patient, and to establish
the side of hemiplegia, the lid lifting test can be tried. The exam
iner lifts both upper lids with his thumbs, then releases them sud
denly. On the paralyzed side, the lid descends more slowly and the
eye closes less completely than on the healthy side. If
in this passive
lifting of the patient's eyelids the examiner meets with resistance,
the patient is not truly comatose and the ptosis is psychogenic: the
patient actively contracts the orbicularis oculi. This is never the case
in organic ptosis.
TESTS FOR LATERAL BULBAR SYNDROME
When a middle-aged person suddenly develops vertigo, vomit

ing, dysphagia and pain or dysesthesias in one side of the face, he
should be tested for the lateral bulbar syndrome. This syndrome is
quite common, but often misdiagnosed. It is usually due to throm
bosis of a branch of the vertebral artery, the posterior inferior cere
bellar artery, which supplies a wedge-shaped section of the lateral
part of the bulbus medullae. In the complete lateral bulbar syn
drome the sympathetic, trigeminal and glossopharyngeal-vagus
nerves, the cerebellar pathways and occasionally the abducent, facial
and acoustic nerves are affected homolaterally, whereas the spino
thalamic tract is affected contralaterally. The components of this
syndrome show great variation. The leading manifestations are: pain
or dysesthesias in the trigeminal area, dissociated anesthesia of
syringomyelic type in this area and in the contralateral extremities,
nystagmus, particularly to the side of the lesion, homolateral ptosis
and homolateral paralysis of the glossopharyngeal-vagus nerve.
Ptosis (sympathetic) may be considerable (Fig. 7, A). Of decisive
importance for the diagnosis is the involvement of the glosso
pharyngeal-vagus nerve. The function of the muscles of the soft
palate should be tested. The patient is asked to say "ah." In uni
lateral disturbance of the glossopharyngeal-vagus nerve the muscles
of the soft palate contract only on the healthy side and move the
Fig. 7. LATERAL BULBAR SYNDROME.
Occlusion of the right posterior inferior cerebellar artery. A, paralysis of the
right cervical sympathetic with marked ptosis. Anhidrosis of the right side of
the face not discernible in photograph. B, same patient; paralysis of the right
glossopharyngeal-vagus nerve. On phonation, only the muscles of the palatal
arch on the left contract and pull the uvula to this side.
49
uvula to that side. However, the position of the uvula is difficult to

evaluate because even in the normal individual it is not always in
the midline. Therefore it is better to observe the movement of the
palatal arch. The affected side remains flat and immobile and only
the healthy side contracts (Fig. 7, B).
Laryngoscopic examination
revealing a vocal cord paralysis on the affected side clinches the
diagnosis.
Since in the lateral bulbar syndrome there is a defect in the
homolateral cerebellar innervation, the following two tests, when
positive, contribute to the diagnosis. When the patient stretches out
his arms and closes his eyes, the arm on the affected side tends to
move outward (vide Arm Deviation Test, p. 106). Pendulousness
of the affected leg is increased, due to cerebellar hypotonia (vide
Test for Pendulousness of the Legs, p. 94).
TESTS FOR INTRAOCULOMOTOR ASSOCIATED MOVEMENTS
When an oculomotor nerve has not recovered completely from

paralysis, a most peculiar and puzzling condition may result. On
checking the eye movements one notes a great and unusual variety
of them. At first glance they seem to be without any order or rule.
However, the situation becomes clear when one considers intra-
oculomotor associated movements, i.e., associated movements among
the muscles innervated by the oculomotor nerve.
At of these muscles with ptosis
rest there is a residual paralysis
and the eye in abduction (Fig. 8, A). The patient is able to correct
his ptosis but slightly. The range of active movements of single
muscles of the oculomotor nerve is very limited. The clinical pic
ture is dominated by associated movements. In these movements the
levator of the upper lid participates strongly, the internal rectus to
a lesser degree. They both contract simultaneously when any other
muscle supplied by the oculomotor nerve is moved, and an associ
ated movement results in which the upper lid rises and the eye
Fig. 8. TESTS FOR INTRAOCULOMOTOR ASSOCIATED MOVEMENTS.
Status after incomplete recovery from left-sided oculomotor paralysis. The
residual ptosis and abducted position of the eye can be voluntarily corrected to
a slight degree only. A, face at rest. B, associated movement of the levator of
the left upper lid on looking inward. C, associated movements of the levator of
the left upper lid and of the left internal rectus on looking upward. D, associated
movement of the levator of the left upper lid and, to a milder degree, of the
left internal rectus on looking down. E, no associated movement of the levator
of the left upper lid on looking outward.
51
moves inward. The ptotic eyelid rises automatically when the pa
tient looks inward (Fig. 8, B). The eyelid rises and the eye moves
inward when he looks up (Fig. 8, C) or down (Fig. 8, D). How
ever, there is no elevation of the upper lid when the patient looks
outward, i.e., when he moves the external rectus innervated by the
abducent nerve (Fig. 8, E).
These associated movements are the clue to the baffling semei:
ology after incomplete recovery from oculomotor paralysis. The
underlying physiology is simple: the slightest impulse sent to any
paralyzed muscle innervated by the injured oculomotor nerve radi
ates to other muscles of this nerve. Associated movements result,
particularly in the levator palpebrae and internal rectus (Fig. 8).
The range of these secondary movements may be greater than the
initial movement.
SEE-SAW TEST IN OCULOMOTOR PARALYSIS
The intraoculomotor associated movements occurring after in

complete recovery from oculomotor paralysis explain another pecul
iar phenomenon found in this condition. It is called the see-saw
sign and has long puzzled investigators. With the patient at rest,
looking straight ahead, the affected side shows ptosis and abducted
position of the eye (Figs. 8, A; 10, A; 11, A). With the paretic eye
closed, the healthy eye is not affected. However, when the patient's
healthy eye is closed, the affected eye moves inward and the upper
lid upward, and the ptosis disappears (Figs. 9, 10, B, and 11, B).
When the healthy eye opens and its lid lifts, the eyeball on the
affected side moves outward, its upper lid moves down the ptosis
reappears. This automatic alternation between the eyelids, one go

ing up and the other going down, accounts for the name see-saw
sign. This is not due to any concomitant involvement of the healthy
eye or to any disturbance in the correlation of both eyes.
The mechanism is simply this. On the affected side there
is,
as
CRANIAL NERVES 53
usual, an associated movement between the internal rectus muscle

and the levator palpebrae muscle. The ptosis disappears when the
patient turns his eye inward. At rest, looking straight ahead, the
Fig. 9. SEE-SAW TEST IN OCULOMOTOR PARALYSIS.

Same patient as in Figure 8. The examiner passively closes the patient's
healthy eye, and the ptosis disappears. Compare with face at rest in Figure 8, A.
patient, with the eyeball on the affected side being held abducted,
fixes objects with his healthy eye. He suppresses the image seen by
the affected eye. However, when the healthy eye is closed, he is
forced to fix objects with his affected eye. In order to do so, he must
first as far as he can adduct the eye to bring it into focus. This
A, face at rest; left-sided ptosis. B, the examiner passively closes the patient's
healthy eye, and the ptosis disappears.

A, left-sided ptosis and abducted position of the left eye, residu
face at rest;
als of oculomotor paralysis. B, examiner passively closes the patient's healthy
eye, and ptosis and abducted position disappear. C, when patient, with right eye
passively closed, is asked to look to the left, the ptosis is not influenced.
54
CRANIAL NERVES 55
brings about the associated movement of lifting of the ptosed lid.

When the healthy eye is reopened, he fixes for near vision with this
eye, does not use the affected eye, which automatically abandons
the position of adduction, and the lid drops.
A crucial test which proves the validity of this conception is the
following. When the patient's healthy right eye is closed and he is
asked to look outward to the left, the ptosis remains (Figs. 8, E;
11, C). The reason is that here he does not converge, does not in
nervate any muscle on the left side supplied by the oculomotor
nerve, therefore no associated movement is induced and the ptosis
remains unaffected.
CORNEAL REFLEX
This reflex is best regarded as a superficial one, a skin reflex of

the orbicularis oculi muscle. This muscle also has its own deep
muscle reflex, elicited by percussion and stretching of the muscle:
the orbicularis oculi reflex. Similar conditions exist in the abdomi
nal muscles, which have a superficial as well as a deep reflex.
The diagnostic value of a diminished corneal reflex is great and
definite. Bilateral diminution or absence of this reflex gives us reli
able information about the depth of coma, anesthesia and sleep. The
corneal reflex is impaired unilaterally in fresh lesions of the contra
lateral cerebral hemisphere. Particularly significant is its diminution
in an ipsilateral lesion of the medulla or the trigeminal nerve. Few
neurological signs have such grave diagnostic import as a unilater
ally absent corneal reflex (Fig. 12). In cerebellopontile angle
tumor the diminution or absence of the corneal reflex on one side is
a leading and early sign. In every
of facial pain or dysesthesia
case
of any kind one should not fail to examine this reflex. The tech
nique is simple. The patient is asked to look to either side; from the
opposite side the examiner cautiously approaches the cornea and
touches it with a glass applicator or a wisp of cotton. Touching of
56 DIAGNOSTIC TESTS IN NEUROLOGY .
the eyelashes or anything that will provoke a startle reaction or a

blink reflex should be avoided. When cerebellopontile angle tumor
is suspected, the patient should be examined while lying on the
The corneal reflex can also be tested without the use
affected side.
of an applicator or any other instrument. The examiner simply
blows air on the eye, which will immediately blink and close. An
empty atomizer may be used satisfactorily for this purpose.
Fig. 12. CORNEAL REFLEX.

The corneal reflex on the patient's left is absent. Touching of the cornea
does not cause blinking of the eye.
Conjunctival reflex. Closing of the eye when the conjunctiva

is touched has less significance than the corneal reflex, since the
former may be absent in the normal individual. Some textbooks
retain the obsolete statement that the corneal or conjunctival reflex;
may be diminished or absent in hysteria, bilaterally or unilaterally,
and that this may constitute a hysterical stigma. This is a myth.
Hysteria is a purely psychic phenomenon, and the diagnosis of hys
teria cannot be supported by the presence of any reflex changes.
CRANIAL NERVES 57
The same, incidentally, applies to the pharyngeal reflex contrac

tion of the pharyngeal muscles when the back of the pharynx is
touched. This is allegedly absent in hysteria. Like the conjunctival
reflex, it has nothing to do with hysteria.
JAW-WINKING TEST
This test was first described by the London ophthalmologist
Fig. 13. JAW-WINKING TEST.

Congenital ptosis on the patient's right. A, the lid cannot voluntarily be
lifted even to the slightest degree. B, the ptotic eyelid rises automatically when
the patient opens her mouth.
Marcus Gunn in 1869. The patient has unilateral, usually congeni

tal, ptosis. The eyelid cannot be lifted on voluntary effort, but it
lifts involuntarily and automatically when the patient opens his
mouth or moves his mandible to the opposite side (Fig. 13). This
is a pathological associated movement. The movement of the jaw
produces, as an associated movement, lifting of the ptotic lid. The
time-honored term "jaw-winking" is not correct, but it is too well
entrenched in the literature to be abolished. The movement is a re
lease phenomenon and is due to a central lesion which has reunited

the innervation of the external pterygoid and levator palpebrae
muscles, that had been separated in the course of phylogenetic
development.
WINKING-JAW TEST
This is an inverted and reversed jaw-winking test. It is not the

mandible that moves first, but the eyelid. The movement consists
not of opening but of closing the eye. This closing automatically
produces movement of the mandible to the opposite side. There is
no ptosis.
When the result of the test is positive, the mandible moves to
one side as the cornea of the other side is touched. Here a reflex
contraction of the orbicularis oculi muscle, incident to the touching
of the cornea, induces an associated movement of the external
pterygoid muscle. The cornea must be touched with some force and
a strong closing of the eye achieved. The same movement of the
mandible may take place, but less strongly, when the patient closes
one eye briskly and forcefully. It is essential that the patient relax
his jaw muscles and allow the mandible to hang loosely. The ex
aminer must watch carefully for the sidewise movement of the
mandible, which may be so quick and of so short a range that it
might easily be overlooked.
A positive result i.e., if touching the cornea causes the mandi
ble to move briskly to the opposite side indicates a lesion of the
corticotrigeminal pathways on the side of the touched cornea. It is
a valuable sign of a supranuclear lesion of the trigeminal nerve and
serves in the differential diagnosis of suprapontile and intrapontile
lesions of this nerve. The response is not positive in all conditions
affecting corticotrigeminal pathways, but can best be demonstrated
in the first few weeks after a hemiplegic attack. In fresh cases of
apoplexy it may be the leading sign indicating the cortical lesion
CRANIAL NERVES 59
and its site. In chronic hemiplegia the response tends to become

negative. A positive result in cases of amyotrophic lateral sclerosis
is an early indication that the pyramidal degeneration has reached
the brain stem and has affected the corticopontile tracts of the tri
geminal nerve. In amyotrophic lateral sclerosis there may be a
strongly positive result when either or both corneae are touched.

The reaction to the test is not positive in the normal subject, or is
positive only to an insignificant degree.
The associated movement of the orbicularis oculi and the ex
ternal pterygoid muscle, which is the basis of the test, is best re
garded as a release phenomenon due to a supranuclear lesion. These
two muscles formerly belonged together, but they have been sepa
rated as differentiation occurred in the course of phylogenetic devel
opment. A supranuclear lesion brings about a functional reunion of
these muscles. The pathological process de-differentiates what phy-
logeny has differentiated. There is hardly a more valuable test than
this to uncover a supranuclear lesion of the trigeminal nerve.
BLINKING TEST
Spontaneous blinking of the patient is carefully observed. The

examiner notes how often and how quickly blinking occurs on each
side. In unilateral facial paralysis, even in its earliest stages, blink
ing occurs less often and less quickly on the affected than on the
healthy side; the eyes blink asynchronously. The same is seen when
the patient is asked to blink rapidly or when the visual blink reflex
is elicited, i.e., when an object is suddenly brought into his visual
field. The difference between the two sides is most marked when
there is not only facial weakness but also some defect in trigeminal
innervation, for instance, in cerebellopontile angle tumor. In such a
case the infrequency and retardation of blinking on the affected
side may be particularly striking and may constitute a most con
spicuous sign, obvious at first glance.
LID VIBRATION TEST
Physiologically speaking, every sustained voluntary innervation

of a striated muscle is not a continuous action. It does not consist
of a static, complete, single contraction of the muscle, but consists
of many fine, interrupted contractions which follow one another
very closely. The action is continual. In other words, it is a tetanus.
On contraction, the muscle vibrates. This vibration can be felt when
the palpating finger of the examiner attempts to lift the closed
upper lid. The palpable vibration of the upper lid is absent in com
plete paralysis of the facial nerve. It is diminished in mild paralysis,
and herein lies the value of this test. The technique follows.
The patient is asked to close his eyes. The examiner places the
ball of his thumb on or above the upper lid and gently attempts to
lift the upper lid against resistance. In so doing the examiner feels
the fine vibration of the upper lid with his thumb. This vibration
can also be felt when the examiner places the tip of his finger on
the patient's temple just lateral to the outer corner of the eye and
pulls it back slightly. The first method is easier. The patient is asked
to close his eyes with varying degrees of force, and the maximum
vibration is sought. It is important to keep in mind that it is not the
strength of the muscle which is being tested, but only the vibration.
This vibration of the muscle is markedly diminished even in
the mildest facial paralysis: the oscillations of the muscle are less
vigorous, less frequent and less extensive. In slowly developing fa
cial paralysis, for instance, in cerebellopontile angle tumor, this
diminished vibration may be the very first sign presaging the on
coming paralysis. The usual signs of weakness of the facial muscle
may be completely absent. In the course of recovery from facial
paralysis, the vibration returns and assumes a normal character
extremely slowly and very late. Thus in the last stage of recovery
from facial paralysis the muscles may, as shown by inspection,
CRANIAL NERVES 61
strength and electrical reaction, have been restored completely. The

orbicularis oculi reflex is normal, yet the lid vibration test shows
diminished vibration. This diminution may be the only remnant of
an old facial palsy. This is particularly striking in cases of old facial
paralysis in which contractures and associated movements appear on
the formerly affected side. At first glance, the opposite side seems to
have been affected by the paralysis. Here, by testing the vibration
of the upper lid, the real condition is revealed at once. Paralysis
originating as long as 20 years previously, and which to all appear
ances no longer exists, can be detected in many instances exclu
sively by this test. In cases of slowly developing facial paralysis
the test reveals the condition at its very beginning, even when all
other signs and symptoms fail. Thus, diminution of vibration seems
to be both the first and the last sign of facial paralysis. The sign is
so reliable and sensitive that it can be said: If on palpation the vi
bration of the upper lid is equal on both sides, facial paralysis
either has never existed or has recovered completely.
The vibration test is useful in cases of both central and periph
eral paralysis. It is of no value for their differential diagnosis.
The test has great value in uncovering old and very mild
cases of hemiplegia involving the face. When such a patient stands
before you, it may happen that hardly anything abnormal can be

detected even on the most careful inspection. There is nothing con
spicuous about the face; facial movements appear to be normal.
And still, employing this test you are able, in a few seconds, to un
cover diminished vibration of the upper lid on one side the side
on which hemiplegia was sustained long ago. It can be said without
exaggeration that this test is the finest method of detecting pathol
ogy of the facial nerve.
The German internist Rosenbach described lid flutter as a sign
of general nervous hyperirritability. This sign consists of visible,
fine, rapid tremor of the upper lids on closing of the eyes. It be
came very popular in Germany, where hardly a hospital chart failed
to mention "lid nutter," "finger tremor" and "dermography" when
a neurasthenia (anxiety neurosis of today) was described. This "lid
flutter," indeed a valuable sign of general nervous hyperirritability,
can be detected more definitely by palpating the upper lid. When
the vibration is marked we should look for other signs of general
nervous hyperirritability. "Lid flutter" is often seen in Parkinson's
disease. Needless to say, "lid flutter," whether found by inspection
or on palpation, is not a sign of hysteria, as even some of the latest
texts would have us believe.
FRONTALIS MUSCLE TEST
It is important to ascertain the full strength of the frontalis

muscle innervated by the facial nerve. A defect in innervation of
the frontalis muscle is not always obvious when the patient per
forms spontaneous movements. On command, he often fails to in
nervate the frontalis muscle to the fullest extent, but he does so
when the following test is applied. He is asked to close his eyes.
The examiner places his finger-tips on the patient's upper lids and
holds them down. The patient is then asked to open his eyes against
the resistance exerted by the examiner. In this attempt, the patient
makes a maximal effort to contract his frontalis muscle. Then the
full strength of the muscle comes into play, as it did not when the
movement was performed on command or spontaneously. The fron
talis muscle is a potent auxiliary muscle for the lifting of the eyelid
and acts as a compensator in ptosis. Its action is more effective when
directed against resistance. This test is helpful in determining the
degree of peripheral facial paralysis.
TESTS FOR MYASTHENIA
The muscles of the eyeballs, of the face, particularly of the eye

lids, and the muscles of mastication are most commonly affected in
CRANIAL NERVES 63
myasthenia. The clinical manifestations of their involvement vary.

There may be marked weakness of the muscles demonstrable on the
slightest movement; there may be no visible manifestation of the
disease. However, the weakness becomes apparent when the move
ment is repeated. Here the outstanding sign of myasthenia fatiga
bility becomes manifest. There are myasthenics with involvement
of the face who, at first glance, may appear completely normal. The
following tests uncover their disability.
The patient is asked to close his eyes several times in rapid
succession and with the greatest possible force. Or, in the same way,
he is asked to open and close his mouth with or without resistance
offered by the examiner or to make smacking or kissing movements
with his lips. These repetitious movements bring out the fatigability.
Ptosis or weakness of the muscles of the lips and of the jaw im
mediately become apparent. The ptosis of the upper lid may also
be brought on when the patient is asked to look steadily and for
some time at the examiner's finger held above the horizontal. To
test the strength of the masticatory muscles, the patient is asked to
hold a tongue blade between the teeth. One is surprised to see how
strong the clenching movement is in normal persons and how weak
it may be even in the early stage of myasthenia. The patient may
be asked to read aloud. He begins normally, but gradually his
speech slows down, longer and more frequent pauses are interjected,
and the speech sounds laborious and indistinct. If the arms are
affected, the patient is asked to perform some movement several
times.The range of the movement diminishes on repetition.
The abnormal fatigability may serve to differentiate myasthenia
from chronic progressive external ophthalmoplegia and bilateral
facial paralysis. The first condition in particular is often misdiag
nosed as myasthenia, and the patients are extensively and uselessly
treated with Prostigmin, etc. In contrast to myasthenia, in progres
sive ophthalmoplegia there is no fatigability and the progression is
slow; there are no remissions, double vision is rare and the eyes are
symmetrically and exclusively affected.
PLATYSMA TEST
Working under stress, a muscle not only manifests its maximal

strength but also exposes its defect. Ordinary muscle activity may
not show such a defect clearly. When, for instance, the platysma is
affected in peripheral or central facial paralysis, this may not be
apparent when the patient moves his facial muscles spontaneously
or on command. However, the weakness of the platysma, particu
larly in peripheral paralysis, may be rendered conspicuous by the
following test. The patient is asked to open his mouth with all his
strength, or to flex his head forward toward his chest; the examiner
opposes this movement by pressing the patient's chin upward. The
deficient innervation of the platysma then becomes visible: the mus
cle fibers are less prominent on the affected than on the healthy
side. In lesser degree this is seen in spastic hemiplegia involving the
face.Failure of the platysma to contract does not mean that the
pyramidal lesion has abolished a normal associated movement. The
contraction of the platysma on opening of the mouth is not an
associated but simply an accessory movement. The test uncovers
only the weakness of the platysma in peripheral or central facial
paralysis. It is well to keep in mind that associated movements are
not abolished in central paralysis but, on the contrary, may be in
creased, and other, new associated movements appear.
ORBICULARIS OCULI REFLEX
Orbicularis oculi, the ring muscle which closes the eye, has, like
any other striated muscle, its stretch reflex. Its fibers contract on
percussion that involves stretching. The threshold for this reflex is
very low. This is particularly true of the muscle fibers of the lower
CRANIAL NERVES 65
lid. The orbicularis oculi also contracts on other stimuli, e.g., visual
and acoustic. But the reflexes produced by these stimuli are of a
quite different and higher order than the response to stretching:

they are cortical reflexes. The most fanciful names have been given
to the orbicularis oculi stretch reflex. These names, chosen for the
most part according to the point of elicitation, cloud the issue.
They do not tell what this reflex really is a deep muscle reflex of
the orbicularis oculi muscle. Each orbicularis oculi muscle can be
stretched by pulling back the skin over the temple with simultane
ous tapping on the pulling finger. The tapping means additional
stretching and elicits the reflex. Since the muscle lies directly on the
bone, and since its reflex excitability is very high, even gentle con
cussion of the bone in the neighborhood of the muscle elicits its
reflex. A textbook published in 1952 still contains the time-honored
statement that this reflex is elicited by "percussion of the supraorbi
tal nerve." The orbicularis oculi reflex, however, has nothing to do
with the supraorbital nerve. When this nerve is tapped, it is the
concussion of the bone, of the insertion points of the muscle, which
evokes this reflex, not the mechanical excitation of the nerve.
What we want to know first of all about this reflex is whether
there is a difference in strength between the two sides. To ascertain
this, equal stimulus must be applied to both sides simultaneously.
The most appropriate spot to assure this is the glabella. The reflex
hammer should be held above the patient's eyes and he should not
be allowed to look at it. The blow should be gentle to avoid a
startle reaction. Such a blow produces a simultaneous reflex on
both sides. On the side of the facial paralysis the reflex is dimin
ished, and herein lies its main value. In spastic paralysis of the facial
muscle the reflex is somewhat exaggerated, but this is not as evi
dent as the diminution in peripheral paralysis. The reflex is absent
in coma and in epileptic stupor. This indicates the depth of un
consciousness.
It is difficult to compare two such heterogeneous phenomena as
palpable vibration of the upper lid and reflex contraction of the
orbicularis oculi muscle. But still there is a definite impression that
the vibration test renders better service than the orbicularis oculi
reflex when a minimal degree of facial paralysis is to be uncovered.
In the of recovery from facial paralysis there may be a stage
course
in which the orbicularis oculi reflex is normal but vibration of the
upper lid remains diminished.
In Parkinson's of the idiopathic and particularly the
disease
postencephalitic variety, the exaggeration of the orbicularis oculi
reflex is a common and conspicuous finding. In the latter type it is
so outspoken that it must be regarded as a pathognomonic sign.
The exaggeration of this reflex is in sharp contrast to the infrequent
blinking and diminished mobility of the facial muscles in Parkin
son's disease. If a triad for this disease were to be established, it
should consist of (1) exaggeration of the orbicularis oculi reflex,
(2) positive head dropping test, (3) diminution of pendulousness
of arms or legs.
INTRAFACIAL ASSOCIATED MOVEMENTS IN

OLD FACIAL PARALYSIS
The common acute peripheral facial paralysis, called rheumatic,

is probably of infectious origin. Its course varies. There may be no
recovery, the paralysis remaining complete and permanent. There

may be complete recovery, without a vestige of the former paralysis
remaining. Not infrequently, however, a peculiar condition results
which has no parallel in neuropathology except in the oculomotor
nerve. This condition, which is permanent and intractable, is char
acterized by partial recovery combined with hyperkinesias. These
hyperkinesias in the formerly paralyzed muscles are (1) contrac
tures, (2) spontaneous spasms, and (3) associated movements in
CRANIAL NERVES 67
which all facial muscles participate. It is these associated movements

which are most characteristic and permit a retrospective diagnosis
of facial paralysis which may have occurred many years before. The
associated movements are exclusively intrafacial; i.e., they occur
only among the muscles innervated by the facial nerve. They do
not occur on innervation of nonfacial muscles. The patient has lost
his ability to contract in a normal way any muscle of the facial
Fig. 14. TESTS FOR INTRAFACIAL ASSOCIATED MOVEMENTS IN

OLD FACIAL PARALYSIS.
Left-sided facial paralysis, partially recovered. A, face at rest. B, automatic
closing of the left eye on wide opening of the mouth. C, automatic closing of
the left eye when the patient makes a sucking movement with her lips.
nerve singly, but has the tendency to innervate them en masse.

These associated movements occur on voluntary and also on reflex
innervation. For instance, tapping the glabella as for elicitation of
the orbicularis oculi reflex may produce a visible contraction of the
medial fascicle of the platysma. This of course, not
is,
reflex but
a
an associated movement of the platysma contingent upon the reflex

movement of the orbicularis oculi muscle.
In some patients the associated movements are so conspicuous

that they are immediately apparent; in some they may be so slight
that they are easily overlooked unless attention is drawn to them.
In testing for these associated movements, one must watch particu
larly for the mutual synchronous activity of the orbicularis oris and
the orbicularis oculi muscles. It consists of closing of the eye on
Fig. 15.TESTS FOR INTRAFACIAL ASSOCIATED MOVEMENTS IN

OLD FACIAL PARALYSIS.
Right-sided facial paralysis partially recovered. A, face at rest. B, automatic
closing of the right eye on slight broadening of the mouth. C, automatic closing
of the right eye on puffing out of the cheeks. On the affected right side the
cheek protrudes less than on the healthy side, due to associated contraction of
the buccinator muscle on the right.
broadening of the mouth or on puffing out the cheeks, and in the

opposite movements lifting of the corner of the mouth on closing
of the eye. Here, sometimes only the mentalis muscle of the chin
comes into action. Such intrafacial movements, if present on one
side, warrant the assumption that the patient has suffered a periph
eral facial paralysis on this side. This paralysis might have healed,
leaving the associated movements as the only evident sequela ( Figs.
14 and 15).
CRANIAL NERVES 69
ASSOCIATED MOVEMENTS IN HEMIFACIAL SPASM
Testing for intrafacial associated movements may be helpful in

differential diagnosis of facial hyperkinesias, of which there are
many confusing varieties. Of these, two must be differentiated with
Fig. 16. ASSOCIATED MOVEMENTS IN HEMIFACIAL SPASM.

Left-sided idiopathic facial spasm, i.e., not preceded by facial paralysis. At
rest the face shows no anomaly. As the patient is asked to puff out the cheeks,
there are simultaneous automatic closing of the left eye and contraction of the
left buccinator muscle. The cheek on the affected side does not protrude as does
the cheek on the healthy side.
particular care: (1) the psychogenic facial tic, and (2) the idio
pathic (cryptogenic) hemifacial spasm. The latter has much in
common with hyperkinesias occurring after facial paralysis, except
that no such paralysis precedes idiopathic hemifacial spasm. It is of
clinical significance that in long-standing cases of idiopathic hemi
facial spasm, associated movements of the facial muscles (Figs. 16
and 17) exist which are identical with those found in postparalytic
FIg. 17. ASSOCIATED MOVEMENTS IN HEMIFACIAL SPASM.
Left-sided idiopathic facial spasm, i.e., not pteceded by facial patalysis.
A, face at rest. B, automatic closing of the left eye when teeth are shown.
C, automatic movement of the left corner of the mouth on closing of the eyes.
D, automatic closing of the left eye on fotceful wide opening of the mouth.
70
CRANIAL NERVES 71
hemifacial spasm. The results of the tests described above are posi
tive in hemifacial spasm and negative in psychogenic facial tic.
They thus may serve in the differential diagnosis of these two
conditions.
Confronted with the differential diagnosis tic or spasm we
may well test also the following two phenomena which are present
in hemifacial spasm and absent in tic. To test oculoauricular associ
ated movements, the patient is asked to move his eyes maximally to
one side. The result is positive when simultaneously the auricle on
this side performs an involuntary movement backward and inward.
This is due to the contraction of the small transversus auris muscle
which is innervated by the facial nerve. The palmomental reflex
consists of contraction of the homolateral mentalis muscle of the
chin on stimulation of the palm of the hand. It is rare to find both
tests positive in hemifacial spasm, but their presence is diagnosti-
cally helpful and physiologically significant.
FACIAL NERVE TAPPING TEST
When this test is positive, the muscles innervated by the facial

nerve show spasmodic contraction when the facial nerve trunk or
its branches are tapped by the hammer or finger. This cannot be
called a reflex of any kind, particularly not a deep muscle reflex,
for it is simply due to increased mechanical irritability of the facial
nerve and perhaps the facial muscles as well. It does not occur in
the normal individual. It is marked in tetany but is by no means
pathognomonic for this disease; it may also occur in many non-
tetanic conditions such as tuberculosis, gastroenteritis, exophthalmic
goiter, myxedema, hypothyroidism, anemia, myasthenia, rickets and
cachexia. It is sometimes erroneously mentioned as occurring in
hysteria. For no reason whatever can it be considered any sort of
hysterical manifestation. Of diagnostic importance also is a mildly
positive response to the test, i.e., when on tapping of the facial nerve
or its branches, there is a slight twitch in the corner of the mouth
only. There is a positive reaction in spasmophylic diathesis, some
times called tetanoid constitution or subclinical tetany. Such patients
also show a general vasolability. With hyperventilation they de
velop tetanoid symptoms and signs more readily than normal indi
viduals. In adults, the following signs of general nervous and vege
tative hyperirritability are often associated with a positive result of
the facial nerve tapping test: hand tremor, wet, clammy palms, der-
mography, tenderness of the ulnar and peroneus nerves to pressure.
A positive response should be considered abnormal in the adult. It
should alert the examiner to seek other signs of nervous hyperirri
tability.
In peripheral facial paralysis it has been found that the facial
nerve tapping test produces a weaker spasmodic contraction of the
facial muscles on the affected side than on the normal side. More
interesting is the finding that in mild spastic hemiplegia affecting
the face, the spasmodic contraction on tapping is slighter on the
affected than on the normal side. Further investigation may show
whether this has any diagnostic significance.
ACCESSORY NERVE TEST
Some muscles help maintain the position of limbs or parts of

limbs against gravity. If the nerve supply to these muscles is dam
aged, the limb drops by the force of gravity. Thus we have wrist
drop in radial paralysis, foot drop in peroneal paralysis. Analogous
to these is the arm drop in lesions of the accessory nerve. This nerve
innervates the upper part of the trapezius muscle, which acts against
gravity to keep the arm up. Even in the most expert surgical hands
the thin accessory nerve, lying superficially, is often damaged in
operations on the neck, especially for the removal of glands. The
branch supplying the sternocleidomastoid muscle may not be dam
aged. Paralysis of the nerve may remain unnoticed for some time.
CRANIAL NERVES 73
It is easily overlooked, since other muscles may compensate and the

real functional defect may be slight. Nevertheless, the patient often
complains of a nagging, deep-seated ache in the arm, due to the
arm drop. This arm drop can easily be diagnosed. The patient
stands with his arms hanging loosely at his sides. The levels at
FIg. 18. ACCESSORY NERVE TEST.

Accessory nerve paralysis on the patient's left. The finger-tips on the af
fected side extend beyond those on the healthy side.
which his finger-tips touch the thighs are compared. On the affected
side the finger-tips touch the thigh at a lower level than on the
healthy side.
The following test is also revealing. The patient is asked to ex
tend his arms, hands and fingers in front of him and slightly down
ward, with the palms touching each other. Due to dropping of the
shoulder, the finger-tips on the affected side extend beyond those on
the healthy side (Fig. 18). A patient complained for years of pain
in one shoulder and arm ever since an operation for the removal of
glands in the neck. The surgeon denied any possibility that the
patient's condition might be due to the operation, contending that
"the brachial plexus could not possibly have been affected by the
Fig. 19- HYPOGLOSSAL NERVE TEST.

Bilateral atrophy of the tongue in amyotrophic lateral sclerosis.
operation." Results of the tests described here were positive, and

subsequent investigation disclosed that the accessory nerve had been
severed at operation.
HYPOGLOSSAL NERVE TEST
Neurogenic disturbances of the tongue may be bilateral or uni

lateral. The normal tongue, with its grooves and fissures, can mis
CRANIAL NERVES 75
takenly be thought atrophic. Real bilateral atrophy of the tongue is

unmistakable (Fig. 19). Fibrillations always accompany the atro
phy. Of even greater aid in diagnosis is the speech disturbance
which always results from the paralysis of the tongue. The speech
is thick, heavy, slow, indistinct and sounds as though the patient
Fig. 20. HYPOGLOSSAL NERVE TEST.

A, paralysis of the hypoglossal nerve on the patient's left. B, paralysis of
the hypoglossal nerve on the patient's right; also, paralysis of the cervical sym
pathetic on the same side. Syringobulbia.
were speaking with his mouth full. The lingual and labial sounds
are affected early and predominantly.
When in unilateral paralysis of the hypoglossal nerve the
tongue is maximally protruded, the genioglossal muscle on the in
tact side pushes the tip of the tongue toward the affected side. This
may be very pronounced (Fig. 20). Lying on the floor of the
mouth, the tongue is straight or its tip deviates toward the healthy
side. This deviation increases when the tongue is forcefully drawn
back. This is due to the unopposed action of the intact styloglossal

muscle. Slight deviation of the ptottuded tongue to one side is diag-
nostically insignificant because complete symmetry of the human
body hardly exists. The common mistake is to diagnose concomitant
hypoglossal paralysis in cases of facial paralysis. When a patient
with marked unilateral facial paralysis protrudes his tongue, it looks
as though it were not being protruded in the midline. This illusion
is due to the deviation of the whole musculature of the mouth

toward the healthy side. The examiner should be guided not by the
position of the tip of the tongue in its relation to the cheeks but by
its relation to the middle of the maxillary arch. If the paralysis
affects only the facial nerve, sparing of the hypoglossal nerve and
straight protrusion of the tongue may be demonstrated. Facing the
patient, the examiner corrects with his fingers the deformity caused
by the facial paralysis by lifting the paralyzed upper lip until it
becomes symmetrical with the healthy side.
SECTION II
Peripkeral Nerves
GENERAL
THE fundamental goal of schools of medicine is to give the

student what the general practitioner will need, a well-balanced
education in all fields of medicine. In this regard, the school has
two disadvantages. The first is that the future general practitioner
is taught by ultraspecialists, and the second that the student gets
his education in the largest hospitals in the country. Such hospitals
have become great centers for diagnosis and treatment of the most
difficult, rare and grave diseases. It is as though a law student read
the law only on Supreme Court cases. A standing complaint of the
newly established doctor is that in practice "it's different." Here he
does not see thekind of patients he formerly saw in the hospital.
Speaking of neurology in particular, the peripheral nervous sys
tem is taught inadequately, and the practitioner is not versed in
"little neurology" seen in every-day practice, with its many neurit-
ides and "neuralgias" due to purely local processes. Influenced by
"big" cases, in the hospital, the young doctor tends to cen
as seen
tralize every process. In his postgraduate work the practitioner

should try to make up for this inadequacy in his education, and in
particular he should gain more knowledge of the peripheral nervous
system. He should learn to "think peripherally." Confronted with
77
a localized neurological condition, he should look first "on the
premises" for the cause and then proceed centralward in his search
for the difficulty.
PARALYTIC CONTRACTURES
These are contractures of healthy muscles whose antagonists are

paralyzed. In the normal individual there is a well-sustained equi
librium between the agonist and antagonist muscles which move a
Fig. 21. PARALYTIC CONTRACTURES.

Extreme pes equinus; maximal bilateral contracture of the plantar flexors of
foot and toes due to complete paralysis of the dorsiflexors. Polyneuritis.
limb in opposite directions. When a muscle or a muscle group is

paralyzed, the unopposed antagonists contract and pull the limb in
their direction. When this lasts a long time, the contracture may
become irreparable. Secondary changes in the contracted muscles
and joints set in against which even the recovered muscles are
powerless. Permanent damage beyond repair is the result. The diag
nostic significance of such a paralytic contracture is great. The exact
analysis of contractures and of muscles involved gives a clue as to
which of the muscles are paralyzed it is always the antagonists of
Fig. 22. PARALYTIC CONTRACTURES.
A, left-sided facial paralysis; contracture of the right facial muscles. B,
severe long-standing right-sided facial paralysis; marked ectropion, sagging of
the paralyzed muscles; patient is asked to close his eyes. C, right-sided facial
paralysis. The cornea of the right eye was so endangered by the ectropion that
a tarsorrhaphy was necessary to close the palpebral fissure.
79
the contracted muscles. Paralysis of a single nerve, such as the facial,

ulnar, median, radial, peroneal, always produces typical contractures
of the antagonists, which are spared.
Therapeutically, paralytic contractures are of great importance.
The treatment of these contractures consists in their prevention. In
any paralysis it is imperative to place the limb at once in such a
position asto prevent contractures (Fig. 21). In poliomyelitis, for
instance, mere pressure of the blanket on the paralyzed feet may
mean irreparable Highly dangerous to the eye (ectro
damage.
pion! ) and most unfavorable for recovery is the contracture of the
contralateral muscles in facial palsy, not to speak of the sagging of
the muscles on the paralyzed side ( Fig. 22 ) . The therapeutic indi
cations in such cases are self-evident.
TEST FOR UPPER BRACHIAL PLEXUS PARALYSIS
The upper part of the brachial plexus, which corresponds to the

fifth and sixth cervical segments, is often exclusively affected since,
mechanically speaking, it is very unfavorably situated and easily
exposed to injury. The lesion may be traumatic or toxi-infectious.
Only the muscles supplied by these two segments are affected; the
lower segments (C-7, C-8 and D-l) are spared. A striking disso
ciated paralysis of the muscles of the arm results. The clinical pic
ture is typical. The arm hangs inertly by the side, adducted and
rotated inward. When the arm is passively supinated, it immediately
reassumes the inward position. Abduction of the upper arm, flexion
of the forearm and supination are markedly impaired. The move
ments, which lift a glass to the lips, are impaired. German students
had a word for this: paralysis of the "nervus poculo-motorius"
(poculus means drinking cup). The test for upper brachial plexus
paralysis consists in searching for defects in these very muscles and
establishing the absence of any defect in the other muscles of the
upper extremity.
PERIPHERAL NERVES 81
TEST FOR SYNDROME OF C-7

In direct or indirect injuries to the vertebral column in general,
or in local injuries to the cervical column by violent movement of
the head, it is the seventh cervical segment which suffers most or
alone. This occurs when the bent head strikes the bottom after a
dive into shallow water. The resulting syndrome is characteristic
and common. The paralyzed patient lies immobile, flat on his back.
Fig. 23. TEST FOR SYNDROME OF C-7.

Typical position in transverse lesion of C-7: arms abducted, forearms flexed
(paralytic contracture). C-6 is intact; flexion of forearm preserved. C-7 pri
marily affected; triceps paralyzed. Spastic paralysis from C-8 down.
He is conscious. His cranial nerves are intact. There is not the

slightest movement in the lower extremities. The upper extremities
assume a characteristic position. The upper arms are held abducted,
and the forearms are flexed (Fig. 23). If the examiner changes this
position, the patient immediately reassumes it. There is spastic pa
ralysis of the finger flexors, with complete flaccid paralysis of the
triceps, but the flexors of the forearm are preserved. This dissociated
paralysis of the muscles acting on the elbow produces the position
of flexion of the forearms. The underlying pathology is a transverse
lesion of the seventh cervical segment which produces spastic paral
ysis from C-8 downward, flaccid paralysis of the triceps, with ab
senceof the triceps reflex, and leaves the flexors of the forearm
(C 6) intact. Clinically, these cases show an amazing similarity.
LONG THORACIC NERVE TEST
The long thoracic nerve lies superficially and is easily exposed

to trauma or infection. This leads to paralysis or weakness of the
Fig. 24. LONG THORACIC NERVE TEST.

paralysis of the serratus anterior muscle in muscular dystrophy.
Bilateral
A, patient at rest. B, displacement of the scapulae becomes more pronounced
when he raises his outstretched arms against resistance. C, "loose shoulders."
anterior serratus muscle which fixes the scapula to the thorax and
moves the arm from a horizontal to a vertical position. In complete
paralysis of this muscle the marked displacement of the scapula
both at rest and on arm motion, the "winging" of the scapula, is
very conspicuous. However, the paralysis may be mild and incom
plete. The displacement is usually greater than the functional defect,
which may be slight. It may be minimal at rest but becomes more
apparent in the following test. The patient stretches his arms hori
zontally in front of him and is then asked to raise them. The exam
iner opposes this movement by placing his hand somewhat heavily
across both of the patient's wrists. Or the patient, his arms out
stretched horizontally, presses his hands against the wall. Thus the
displacement of the scapula, its "winging," becomes very prominent
(Fig. 24, A andB).
Characteristic of paralysis of the anterior serratus muscle, par
ticularly as it occurs in muscular dystrophy, are "loose shoulders."
The shoulders can be passively moved much higher than in the
normal individual (Fig. 24, C).
WRIST DROP TEST
The patient extends his arms horizontally in front of him, his

hands pronated. One hand drops. Such wrist drop is usually caused
by paralysis of the radial nerve. But this is not always the case.
Wrist drop may also be caused by a supranuclear, or central lesion.

In other words, the paralysis of the extensors of the hand may be
spastic and not flaccid. It must be remembered that a cortical lesion
may produce not only hemiplegia or monoplegia but also paralysis
of a small muscle group. A circumscribed cortical lesion, therefore,
may produce paralysis of the dorsiflexors of the hand. On inspec
tion, wrist drop due either to spastic or to flaccid paralysis has the
same appearance. How can a wrist drop caused by a central lesion
be distinguished from one caused by a peripheral lesion? The dis
tinction is easily made if we remember that in central lesions, i.e.,
in spastic paralysis, normal associated movements may be preserved
despite the paralysis and new associated movements may appear.
This documents itself in the following way. The patient with spas
tic paralysis is unable to perform on command an isolated, a single
movement. However, this very movement can be performed as an
associated movement, as part of a greater mass movement. Figure
25,A, shows wrist drop in spastic paralysis of the dorsiflexors of the
hand. In Figure 25, B, the patient is asked to dorsiflex his affected
hand and fingers with all his might. He can do this only to a very
Aflk II
Fig. 25. WRIST DROP TEST.

A, spasticparalysis of the dorsiflexors of hand and fingers. B, on command
the patient can dorsiflex the hand and fingers only to a slight degree. C, patient
is asked to grasp an object in his hand; simultaneous involuntary dorsiflexion
of the hand as an associated movement.
Fig. 26. WRIST DROP TEST.

A, flaccid paralysis of the dorsiflexors of hand and fingers due to lesion of
the radial nerve. B, on command, the patient can dorsiflex the hand and fingers
only to a very slight degree. C, patient is asked to grasp an object in his hand;
volar flexion of the hand increases.
84
mild degree. In Figure 25, C, the patient is asked to grasp an object

in his hand. Like a normal individual, while grasping he simultane
ously performs an involuntary dorsiflexion of the hand by automatic
simultaneous innervation of the spastically paralyzed dorsiflexors of
the hand. This dorsiflexion is quite strong.
It is interesting to note that in spastic paralysis of dorsiflexion
of the hand, even such a remote movement as yawning may set off
extension of the hand as an involuntary associated movement.
Quite different is the behavior of the dorsiflexors of the hand in
peripheral paralysis. Figure 26, A, shows typical paralysis of the
radial nerve due to a lesion of the upper arm. In Figure 26, B, the
patient is asked to extend hand and fingers with the greatest possible
force. He can perform this movement only to a very mild degree.
In Figure 26, C, the patient is asked to grasp an object with his
fingers. No associated movement, no simultaneous dorsiflexion of
the hand takes place as in central paralysis of the dorsiflexors or in
the normal subject. On the contrary, volar flexion increases, and the
wrist drop becomes accentuated as the patient tries to tighten his
grip-
BRACHIORADIALIS TEST
It is easy to diagnose a peripheral radial paralysis. Wrist drop

and adduction position of the thumb are very revealing. After one
has established that the median or ulnar nerve is not involved, the
next step is to find out where, in the long course of the radial nerve,
the lesion lies. The first question is whether the brachioradialis
muscle is involved. One is apt to forget that this muscle, a flexor of
the forearm, is innervated by the radial nerve. Often the patient
does not realize that there is a defect in its function. The defect
does not become obvious when the patient performs every-day ac
tions. However, by the following test, a defect in the brachioradialis
muscle can be made evident. As is the case with testing other mus
The patient
cles, the brachioradialis muscle must be put undet stress.
and the examiner sit facing each other. The patient bends his half-
pronated forearms, and the examiner opposes this movement. In
this way the normal brachioradialis muscle becomes prominent. The
Fig. 27. BRACHIORADIALIS TEST.

Patient has left-sided radial paralysis which involves the brachioradialis
muscle. He bends his forearms against resistance. Brachioradialis becomes prom
inent on the healthy right side but not on the left.
lack of this prominence on the affected side is very conspicuous and

indicates paralysis (Fig. 27). When the test uncovers a defect in
the innervation of the brachioradialis muscle, this immediately
places the site of the lesion not in the forearm but in the upper
arm proximal to the point where the branch for the brachioradialis
muscle leaves the main trunk.
THUMB ABDUCTION TEST IN MEDIAN PARALYSIS
In paralysis, central as well as peripheral, there is not only

weakness, not only a decrease in the rapidity of movement, but also
a decreasein range of movement. Although a movement still can
be performed, its excursion is not so great as normal. Testing the
range of movement in paralysis has been much neglected. The
diminished excursion enables us not only to detect the paralysis but
also, to some degree, to appraise it quantitatively. On this is based
the test for paralysis of the median nerve. If this nerve is damaged
at the wrist, the muscles affected are the opponens pollicis, the ab
ductor pollicis brevis and the superficial head of the flexor pollicis
brevis. The cardinal function of these muscles is the opposition and
abduction of the thumb. In testing these functions we are accus
tomed first to examine the opposition of the thumb, but when the
lesion is at the wrist we may be trapped by these pitfalls. First, the
flexor pollicis longus and the adductor pollicis, to some degree,
may substitute for the muscles primarily responsible for opposition
of the thumb. Second, thenar muscles, which participate in the
opposition and usually innervated by the median nerve, may be
innervated to a varying degree by the ulnar nerve. The compen
sation by other muscles and the innervation of the median muscles
by the ulnar nerve explain why, in a median nerve lesion at the
wrist, the opposition of the thumb can sometimes be performed re
markably well even if this nerve is completely severed. Third, it is
sometimes difficult to determine whether there is real opposition
(rotation of the thumb around its own axis) so that the tip of the
thumb meets the tip of the little finger or whether there is a
"pseudo-opposition" in which the thumb meets the radial side of
the end phalanx of the little finger.
In the thumb abduction for median nerve function, the pa
test
tient is asked to adduct and extend the fingers of both hands and
also to abduct and extend both thumbs maximally, keeping them
on one plane with the palm. He then lifts his hands to the same
horizontal level, palms forward. The radial tips of the index fingers
touch each other and, in the normal, so do the tips of the out
stretched thumbs. It is the position of Oriental prayer ( Fig. 28, A ) .
Another technique of this test is: the patient adducts and
stretches his fingers, brings the finger-tips of both hands together so
FIg. 28. THUMB ABDUCTION TEST IN MEDIAN PARALYSIS.

Left-sided median paralysis. On the affected side the thumb cannot be ab
ducted as far as on the healthy side. Tips of the thumbs are on different levels
and not on the same level as in the normal.
that they form a roof, palms inward. The thumbs are maximally
abducted at right angle to the palms (Fig. 28, B). In the normal
individual, the tips of the thumbs touch each other.
When a lesion of the median nerve is present (Fig. 28), the
thumb on the affected side, owing to defective abduction, remains
above the thumb on the healthy side. The more severe the median
nerve paralysis, the higher is the tip of the affected thumb above
that of the healthy thumb. As recovery sets in, the patient is able to
abduct the affected thumb more and more until its tip reaches the
horizontal level of the thumb on the healthy side.
Thus this test is not only a qualitative but also a quantitative
one.
ABDUCTION POSITION OF LITTLE FINGER IN

ULNAR PARALYSIS
The general tendency to paralytic contracture of the antagonists

to paralyzed muscles manifests itself also in ulnar paralysis. Here
the contracture affects the little finger. Adduction is performed by
the interosseus, abduction by the hypothenar muscles. Both groups
of muscles are innervated by the ulnar nerve. However, in abduc-
ABDUCTION POSITION OF THE LITTLE FINGER IN UL

Flg. 29.
NAR PARALYSIS.
tion of the little finger the extensor digiti quinti proprius also plays
a definite part. It is innervated by the radial nerve. If the muscles
innervated by the ulnar nerve are paralyzed or weak, this extensor
muscle innervated by the intact radial nerve predominates and
keeps the little finger in abduction. In marked ulnar paralysis this
abduction is conspicuous even with the hand at rest. But in mild
paralysis the abduction is not so apparent unless the fingers are
extended. It is seen best when the extensor muscles of the fingers
come into action. The patient is asked to hold up his hands in front
of him, fingers extended. He is asked to keep the fingers together
without exerting any force. On the affected side the little finger,
and sometimes the ring finger as well, shows a tendency to abduc
tion (Fig. 29) owing to the action of the extensor innervated by
the radial nerve which serves as an auxiliary in abduction. In the
normal subject with an intact ulnar nerve which adducts the fingers,
the action of this auxiliary muscle is counterbalanced by the adduc
tor. It becomes apparent when unopposed.
The tendency to abduct the little finger may be an early or late
outstanding feature of ulnar paralysis.
This abduction position of the little finger is simply an expres
sion of weakness of the adductor. When ulnar paralysis is suspected,
this weakness may be tested directly. The examiner places his finger
between the little and the ring finger of the patient, who is asked
to squeeze the examiner's finger. Thus the examiner can appraise
the strength of adduction of the little finger. It is diminished on the
side of the ulnar paralysis.
THUMB BENDING TEST IN ULNAR PARALYSIS
Paralytic contracture of unopposed antagonists is one of the

most characteristic features of a nerve paralysis. The next leading
feature is compensation. When any nerve is paralyzed, the patient
tries to overcome the difficulty by various substitute movements.
He brings into action muscles which normally serve as auxiliaries.
It is amazing how much a patient can achieve by these compensa
tory movements. In paralysis of the accessory nerve, with dropping
of the shoulder, one can see the levator scapulae muscle, hypertro-
phied to several times its size, elevate the shoulder quite satisfac
torily, much more than this muscle does under normal conditions.
In muscular dystrophy the patient puts into action remaining, or
remnants of remaining, muscles and can, to a considerable degree,
make up for lost muscles. All this is valid only if the patient has
the will to recover. This will is often killed when there is a pre
mium on the disease, in cases of pending financial compensation.

as
The following exceedingly reliable test for ulnar paralysis is

based on the fundamental principle of muscle substitution. When a
healthy person holds a flat and thin object between his thumb and
the radial aspect of his index finger, he uses the powerful adductor
pollicis muscle and holds the object with the end phalanx of the
thumb kept straight. If there is the slightest paralysis of the ulnar
Fig. 30. THUMB BENDING TEST IN ULNAR PARALYSIS.

The patient holds a flat object between thumb and index finger of both
hands. The examiner tries to withdraw the object. The end phalanx of the
thumb on the patient's right is bent, indicating ulnar paralysis on that side.
nerve, and consequently weakness of this adductor, the patient sub

stitutes for this adductor the flexor of the end phalanx of the thumb
(flexor pollicis longus), innervated by the median nerve. To hold
the flat object, he bends the end phalanx of his thumb (Fig. 30).
The bending is increased when the examiner tries to withdraw the
object. A markedly positive result of this test means that the ulnar
nerve is damaged and the median nerve intact.
The two foregoing tests, abduction position of the little finger
and thumb bending, are tests of the motor function of the ulnar
nerve and its early impairment. They are particularly valuable for
diagnosis of the common, slowly developing, so-called "late ulnar

palsy" which is caused by constitutional anomalies or by surgical,
orthopedic, degenerative or traumatic conditions at the elbow. Motor
signs may predominate here, and sensory manifestations may even
be absent.
MUSCLE PERCUSSION TEST
This test is performed by tapping the muscle directly with the

reflex hammer. The examiner, with an elastic swing, applies a short,
sharp, bouncing blow. Idiomuscular contraction of the fibers results
when they are struck directly. The contraction is purely local, cir
cumscribed and of short duration. This mechanical irritability of the
muscles is increased in degenerative diseases of the peripheral motor
neuron, as in progressive spinal muscular atrophy and amyotrophic
lateral sclerosis. Here the idiomuscular contraction is quicker,
stronger and is elicited with comparatively mild stimuli. In muscu
lar dystrophy, on the contrary, the idiomuscular contraction is de
creased, and often very early in the course of the disease. The diag
nostic value of this local idiomuscular contraction, however, is not
very great. More important is the contraction of the muscle fibers
when mechanical irritation with a reflex hammer leads to visible
movement. The phenomenon is not seen in the normal person. Only
in myotonia does muscular contraction on percussion become so
prominent as to be of diagnostic value.
The pectoralis, triceps and thenar muscles may be tapped, but it
is best to tap the thenar eminence. In myotonia, percussion of the
thenar eminence causes a slow, prolonged tonic contraction of the
muscles (Fig. 31). The thumb moves slowly toward the palm and
again slowly returns to its original position. The slow, sustained
movement of adduction and opposition, the delay in relaxation and
the gradually subsiding contraction are highly characteristic and un
mistakable. The myotonic muscles react to mechanical stimulation
exactly as they react to voluntary and reflex impulses and to elec

trical stimulation. This mechanic-myotonic reaction is more marked
when the extremity is cold, as is the case with other reactions of
myotonic muscles. The reaction becomes less and less pronounced
Fig. 31. MUSCLE PERCUSSION TEST; MECHANIC-MYOTONIC

REACTION.
A, hand at test. B, thenar eminence was struck with reflex hammer; thumb
has moved toward the palm. Myotonia dystrophica.
when tapping of the muscles is repeated in quick succession. Practi

cally speaking, the mechanic-myotonic reaction is found only in my
otonia, congenital or dystrophic. Here it may decide the diagnosis.
TEST OF THE GLUTEAL MUSCLES
Muscular dystrophy begins with weakness in the muscles of the

shoulder and/or pelvic girdle. The atrophy is not as conspicuous as
in progressive muscular atrophy. This is particularly true of the so-
called late progressive muscular dystrophy which begins in the third
and fourth decade or later and has a most insidious onset. It is often
misdiagnosed. The atrophy of the muscles may be masked by fat
accumulation in the buttocks. The following two tests are useful to
detect a slight weakness of the gluteal muscles.
1. The gait is observed. The weakness documents itself very
early in standing and walking. The slightest weakness of the gluteal

muscles produces a forward tilting of the pelvis on its transverse
axis. To compensate for this, the patient assumes a lordotic posture,
in which the upper part of the trunk is tilted back. The arms then
hang behind the trunk. The weakness in lateral fixation of the pel
vis accounts for the slightly wobbling gait. This posture and gait
are highly characteristic of dystrophy. The picture is most striking
in advanced cases. In late progressive muscular dystrophy the slight
lordosis and the wobbling gait with the arms hanging behind the
trunk are also characteristic, though not as pronounced. This gait
differs from the normal so conspicuously that the slightest intima
tion of such a gait warrants a suspicion of muscular dystrophy.
Another test for the strength of the gluteal muscles is to ask
2.
the patient to pick up an object from the floor. A patient with even
the slightest degreeof weakness in the gluteal muscles rises slowly
and with effort and often uses his hands to climb up his legs. This
is not seen in the normal individual. It is also amazing how little
pressure the examiner need exert on the patient's back to prevent
him from rising.
TEST FOR PENDULOUSNESS OF THE LEGS
In of the motor system, first the status of the

the examination
muscles is appraised by inspection. Next comes examination of the
muscle tonus: the tension in which the muscles are constantly kept
is estimated. There are many ways of doing this: passive movement,
palpation of the muscles, and others. The best method of appraising

the tonus of the muscles which move the knee is based on pendu-
lousness of the legs, i.e., their movement to and fro after they have
been displaced passively.
For this test the patient sits on the edge of a table with his legs
hanging freely. His attention is diverted; he is made to relax. The
examiner lifts both of the patient's legs simultaneously to the same
horizontal level, then releases them, permitting them to swing
freely. Normally, this swinging is regular, precise and equal on
both sides. The range of successive movements diminishes steadily
and evenly. The swinging time depends on the tonus. The pendu-
lousness in its preciseness cannot be produced voluntarily.
In disturbances of the lower motor neuron, from the anterior
horns to the muscle, the tonus is diminished, the swinging time is
increased and the leg on the affected side continues to swing after
the leg on the healthy side has come to a standstill. This difference
in swinging time has proved diagnostically valuable in diseases
such as poliomyelitis, progressive spinal muscular atrophy, spinal
cord tumor, prolapse of an intervertebral disk, postanesthetic spinal
syndrome with radiculitis in the lumbar region, neuritis of the
cauda equina, femoral neuritis, muscular dystrophy and arthrogenic
muscular atrophy (after knee injury). The great value of this test
lies in the fact that it is objective, to a considerable degree. In uni
lateral affections involving the muscles around the knee, quality
and quantity of the swinging are so characteristic as to defy imita
tion. Every attempt of the patient to interfere consciously or un
consciously with the smooth flow of motion is easily detectable.
KNEE HYPEREXTENSION TEST IN TABES
One of the cardinal and early signs of tabes is hypotonia, par

ticularly of the muscles which steady the knee. The hypotonia in
tabes is physiologically significant because it is one of the main
causes of impaired locomotion. There are many ways to demonstrate
this hypotonia, but the simplest is the following. The patient lies
supine, his legs outstretched. With one hand the examiner presses
Fig. 32. KNEE HYPEREXTENSION TEST IN TABES.

A, legs B, positive response to knee hyperextension test; the exam
at rest.
iner is able to lift the patient's heel from the surface of the bed while the
knee is held down. Tabes with hypotonia.
the knee down while with the other he tries to lift the patient's heel
from the surface of the bed. In the normal person this is possible
not at all or only slightly. In tabes one can lift the heel from the
surface and do so without discommoding the patient in any way;
the thigh and lower leg form an obtuse angle (Fig. 32). One is
amazed that marked hypotonia can be demonstrated in this way
while it has not documented itself in corresponding disturbances in
locomotion. Only in some healthy contortionists and acrobats may
the same result be obtained. The test can help differentiate tabes
from polyneuritis.
TENDON PALPATION TEST
Every lesion of the lower motor neuron leading to a defect in

innervation produces hypotonia of the muscles involved. The ten
don palpation test serves to ascertain the existence and to appraise
the degree of this hypotonia. Most muscles terminate in tendons,
and the tension of the tendon reflects the tonus of the muscle. The
test works best on the Achilles tendon. The patient stands on the
examining table or on a sturdy, flat-seated chair, his back to the
examiner. It is most essential that the patient bear his weight
equally on both legs and not favor either leg. The examiner grasps
the patient's ankles from the outside, his thumbs resting on the
Achilles tendons. With the balls of the thumbs, the examiner
presses both tendons simultaneously and judges the resistance they
offer to the compression (Fig. 33). It is advisable to compress the
tendon at different levels. To increase the tension of the tendon, the
patient may be asked to lean forward very slightly.
In unilateral lesions of the sciatic for instance, prolapse
nerve,
of the intervertebral disk or infectious sciatic neuritis, the Achilles
tendon is softer and offers less resistance than the normal one. This
with a normal subject standing flat on his feet,
is easy to feel since,
the Achilles tendon is taut and its resistance very strong. The tendon
is "hard as stone." When the lesion is bilateral, it of course, diffi
is,
cult to estimate the degree of softness of the Achilles tendon. How

ever, in some advanced cases of tabes, alcoholic polyneuritis and
bilateral prolapse of lumbar disk, the tendons on both sides have
a
definitely been found less resistant to pressure. The value of this

test is enhanced by the fact that it may indicate a lesion of the pe
ripheral motor neuron in patients in whom there is no muscular
wasting, no paralysis and even the triceps surae reflex is preserved.
A soft Achilles tendon may thus be a very early sign of "sciatica."
Hypotonia of the sciatic muscles due to unilateral cerebellar disease,
e.g., cerebellopontile angle tumor, can also be detected by palpation
Fig. 33. TENDON PALPATION TEST.

Technique of palpation of Achilles' tendon.
of the tendon. This cerebellar hypotonia is less marked than tabetic

or neuritic hypotonia and tends to subside. The softness of the
Achilles tendon may be of decisive importance in the differential
diagnosis between neurogenic and non-neurogenic affections.
What is said of the Achilles tendon applies to other tendons as
well: hypotonia of the muscles documents itself in softening of the
tendon. However, it cannot be demonstrated as well on other ten
dons as on the Achilles.
It stands to reason that hypertonia, i.e., pyramidal spasticity or
extrapyramidal rigidity, of affected muscles shows itself by increased
tension of the tendons on palpation. Particularly is this true of the

antigravity muscles in a pyramidal lesion. But this increase of ten
sion of the tendons in hypertonia is not as easily demonstrated and
appraised as the decrease in hypotonia.
Time will tell how much value this test may have in the diag
nosis of pyramidal and extrapyramidal disease. Its value in the
diagnosis of peripheral disturbances has been established beyond
doubt. However, this test, like others, has the usual limitations.
When positive, it is useful; when negative, it does not exclude an
organic lesion of the nervous system.
TEST FOR PLAY OF FOOT TENDONS
Partial or complete paralysis of the muscles innervated by the

common peroneal (lateral popliteal) nerve is not uncommon. It
may represent a local condition or may be the expression of a sys
temic disease. It may be the first sign of tabes or polyneuritis. To
find and to evaluate a defect in the innervation of the dorsiflexors
of the foot supplied by the peroneal nerve, the patient is usually
asked to dorsiflex his foot while lying or sitting. Still better, ask
him to stand on his heels. To do this he must maximally innervate
the dorsiflexors of his feet. The most efficient method by which
to gauge the function of these dorsiflexors is to put them under the
stress of an acute emergency. To achieve this, the patient is put in
a position where his dorsiflexors must be innervated suddenly, fully
and automatically. Such an action should not be purely voluntary.
The following test meets these requirements. The patient stands on
a hard surface, both feet firmly planted, his weight equally distrib
uted on both sides. The examiner places his hand on the patient's
chest and gently but unexpectedly pushes him backward or side
ways. To prevent himself from falling, a normal person innervates
the dorsiflexors of the feet immediately, automatically and maxi
mally. Swaying of the body produces an alternating prominence of
the tendons of the dorsiflexors of the feet. This is best seen when
the patient stands on one foot. Here it is not even necessary to push
the patient. The tendons of the paretic or paralyzed muscles partici
pate feebly or not at all in this play which has aptly been called
the "dance of the tendons." This play or the lack of it discloses the
real status of the dorsiflexors. Even a malingerer or a hysteric who
simulates foot drop will show this play of tendons. Such people, too,
automatically innervate their dorsiflexors to prevent falling. They
find, so to speak, no time to display a paralysis in this acute emer
gency. They are caught off guard by this test.
SECTION III
Pyramidal System
GENERAL
THE pyramidal motor system, to put it simply, consists of the

corticospinal pathways, from the cells of the cortex to the nuclei of
the cranial nerves and anterior horns of the spinal cord. It is an
efferent system. The term "pyramidal sign" denotes an objective
manifestation of a lesion of this pyramidal tract with a deficit in its
function. Such a lesion need not necessarily mean destruction of the
pyramidal tract; the slightest damage might suffice.
From a physiological standpoint, it might not be strictly correct
to speak of pyramidal signs as being caused by lesions of the py
ramidal tract. The matter is not so simple. What is called a
pyramidal sign may be caused by lesions of the extrapyramidal, pre-
motor area. In lesions limited to the corticospinal tract, in the
strictest sense of the word, no spastic phenomena the basis of
the pyramidal signs may be present. However, from a practical
clinical standpoint, it is still permissible to speak of pyramidal signs
as manifestations of a lesion of the pyramidal corticospinal tract.
The diagnostic value of a pyramidal sign is very great. A reli

able pyramidal sign (a) is in most cases an objective phenomenon,
independent of any co-operation on the part of the patient, (b)
proves the presence of an organic lesion of the nervous system,
101
(c) shows that the upper motor neuron is affected,and (d) indi
cates not an irritation but a defect in the function of this neuron.
But it does not tell where along the extensive course of the pyram
idal tract the lesion lies.
Of grave diagnostic importance are those signs which help to
uncover early and slight in the pyramidal tracts. Such
changes
changes are often due to a mild "stroke" which leaves insignificant
and transient symptoms and signs in its wake. The patient is afraid
to admit to a "stroke" and inveigles himself and his doctor into
assuming "indigestion," "fainting spell," "gall bladder disturbance"
or the like. The diagnostic situation is cleared up, however, when
presence of a pyramidal sign is definitely established. Osler once
said: "One swallow does not make a summer, but one tophus makes
gout and one crescent malaria." The same may be said of a single
pyramidal sign: it can "make" the diagnosis of an organic affection
of the nervous system.
Although the doctrine of the pyramidal signs is not compli
cated, great confusion unfortunately is rampant when these signs
are discussed in the literature or described for the student in texts.
There is a glaring lack of understanding of the physiological mech
anism involved.
In a popular article it is stated: "The nearest approach to the
Babinski type of reflex in the hands is the Hoffmann sign." No!
The Hoffmann is a plain muscle stretch reflex of the finger flexors,
whereas the Babinski is part of a complicated mass movement,
the homolateral mass flexion reflex. "A positive
(abnormal) re
sponse [to stroking the sole] is a slight dorsiflexion of the great toe,
a spreading of the other toes and a contraction of the tensor faciae
latae." No! Contraction of the tensor faciae latae on stroking of
the sole is a normal phenomenon. "The Rossolimo test involves
tapping of the muscles with the resulting Babinski toe movement,"
says another writer. No! In the Rossolimo reflex there is plantar
PYRAMIDAL SYSTEM 103
flexion, in the Babinski, dorsiflexion. "The reflexes of Mendel-

Bechterew, Oppenheim and Rossolimo of
represent a modification
theBabinski reflex." No! The physiological basis of the reflexes of
Mendel-Bechterew and Rossolimo is completely different from that
of the Babinski reflex. When these heterogeneous phenomena are
confounded, the way to an understanding of the pyramidal signs is
completely blocked.
A lesion of the pyramidal tract produces numerous and varied
changes in the extremity involved. The different signs are based on
completely different physiological mechanisms. To understand the
pyramidal signs better and to evaluate them intelligently and effec
tively, it is imperative to classify, to "pigeonhole" them according
to the mechanism involved. The following scheme may be found
useful. The pyramidal signs may be based physiologically on: (1)
posture, (2) tonus, (3) strength of movement, (4) range and
rapidity of movement, (5) behavior of the deep muscle reflexes,
(6) appearance of latent reflexes, (7) appearance of associated
movements, and (8) the Babinski reflex.
POSTURE
In testing for pyramidal signs it well to begin with those

is
based on posture. The plainly visible posture of the patient and of
his limbs is often overlooked and its study neglected. We are all
apt to jump at the examination of the pupils, the reflexes, the mo
tility and what-not before we look at the patient. First, observe him
and see what can be found by simply glancing at him before he is
even touched or talked to. What Sir George Humphrey said about
surgery applies also to neurology: "Eyes first and most." It is amaz

ing how much we can learn from the tell-tale posture the patient
assumes or tends to assume. There are many factors which can pro
duce abnormal posture. There are, for instance, algogenic postures:
the patient immobilizes a limb in such a position as to avoid stretch
ing or compression of a nerve.In any atrophic or dystrophic muscu
lar process the patient tries to retain his erect posture with the aid of
those muscles which are preserved, hence the lordosis in muscular
Fig. 34. HYSTERICAL PARALYSIS.

Left arm involved, with contracture in extension at the elbow.
dystrophy. There are countless instances of paralytic contracture,

i.e., contractureof muscles which are antagonists to the paralyzed
ones. There is loss of erect posture in Parkinson's disease. There are
posture changes in dystonia. There is also a definite posture in spas
tic paralysis: the forearm, hand and fingers are flexed, the hand
pronated, the leg extended. It is as if the arm and leg were frozen
in that attitude which is one phase of the act of climbing or
running.
The contracture in flexion at the elbow is particularly character
istic of an organic spastic paralysis of the arm. It is invariably pres
ent in this condition. The patient in Figure 34 does not show this
posture. Here there is a contracture not in flexion but in extension
at the elbow. This does not occur in organic spastic paralysis. The
patient has, indeed, hysterical paralysis of the left arm.
Many pyramidal signs are based on this posture and the irre
sistible tendency of the patient to assume it. The following five tests
reveal such pyramidal signs.
HAND PRONATION TEST

This test is based on the tendency of the hand to assume a posi
tion of pronation with the slightest degree of spastic paralysis.
Physiologically speaking, this pronation is a fragment of decere
brate rigidity. It is seen not only in spastic paralysis but also in
chorea and athetosis. But it is most noticeable in pyramidal lesions.
There are many ways in which to uncover this tendency toward
pronation. It is seldom seen in a patient with mild hemiplegia
when he allows his arms to hang loosely by the side. Special tests
are needed tobring out the tendency to pronation. The patient may
be asked to flex his forearms. On the affected side the forearm
assumes a position of pronation, so that the hand approaches the
shoulder not with its palmar but with its dorsal surface. Or the
examiner passively raises the patient's arms to the vertical position,
then drops them. The affected forearm comes down in pronation.
Or the patient is asked to place his hands in a Buddha-like position,
palms up and finger-tips touching each other above the top of the
head. Again, the tendency of the affected forearm to assume a posi
tion of pronation becomes manifest. Pronation is equally evident in

the patient who raises his arms vertically, palms in front (Fig. 35,
A ) . But the best method is this. The patient stretches his arms hori
zontally in front of him, palms up. The examiner tosses them up
several times. The affected forearm slowly assumes the position of
pronation (Fig. 35, B). One must wait a little, since this tendency
Fig. 35. HAND PRONATION TEST.

A, patient with right-sided hemiplegia is asked to raise his arms vertically.
On the affected side the hand assumes a position of pronation. B, patient with
left-sided hemiplegia is asked to stretch her arms horizontally in front of her.
On the affected side the hand assumes a position of pronation.
needs some "incubation time." This test is obviously useless in fully

developed hemiplegia, but is applicable in incipient lesions and can
be positive where there are no contractures.
ARM DEVIATION TEST
This test serves to uncover latent or mild spastic paralysis of

the arm. In fully developed paralysis it is unnecessary. The patient
is asked to stretch his arms horizontally in front of him, keep them
still and close his eyes. The arm on the affected side slowly and
slightly deviates downward (Fig. 36, A). The downward move
ment becomes more rapid on closure of the eyes or soon afterward.

The patient is aware of this downward movement but is surprised
when he opens his eyes to see how far the arm actually has devi
ated. With eyes closed, he can counteract this downward movement
but little; he can do it quite well with the eyes open. The impor
tance of visual control is shown in the following test. When the
Fig. 36. ARM DEVIATION AND HAND PRONATION TESTS.

Tests simultaneously positive in right-sided hemiplegia. A, outstretched
right forearm pronates and the arm deviates downward. B, outstretched arm on
the affected side deviates downward and the hand assumes a slightly more pro-
nated position.
patient keeps his eyes open and the examiner tries to depress the
patient's outstretched arms against resistance, this resistance is the
same on both sides. It becomes much weaker on the affected side as
soon as the patient closes his eyes. In other words, the spastic paraly
sis of the arm manifests itself only, or is more evident, when the
visual control is eliminated.
In these tests the spastic-paretic arm tends not only to drop but
also to bend at the elbow. Passive turning of the head toward the
healthy side may accentuate both dropping of the arm and bending
at the elbow. The tendency to drop is stronger when the out
stretched arms are subjected to the stress of an acute emergency.
The examiner supports the patient's arms so that the latter's hands
rest comfortably on the forearm of the examiner or on a ruler or
stick which the examiner holds. Suddenly this support is withdrawn.
The dropping is more clearly seen in these circumstances, as the
elevators of the arms are called upon to act quickly in an emergency.
The test is useful in the differential diagnosis between organic
and psychogenic paralysis. It is striking how slowly the arm drops
in organic spastic paralysis and how slowly it eventually reaches
the vertical position of rest. Not so in psychogenic paralysis. Here
the arm drops heavily, inertly and reaches the vertical position at
once, in one fell swoop.
Figure 36 shows the hand pronation test and the arm deviation
test simultaneously positive in the same patient. On the hemiplegic
side the outstretched arm deviates downward and the hand is pro-
nated.
EVERTED POSITION OF THE FOOT
The position of the leg of a hemiplegic patient as he lies supine

and relaxes is noteworthy. On the normal side the foot rests squarely
on its heel and the great toe is perpendicular or very slightly
everted. In mild hemiplegia, even before distinct paralysis or clear-
cut pyramidal signs are present, the leg on the affected side lies
rotated outward and the foot spontaneously assumes the position of
eversion (Fig. 37). The examiner attempts to correct this position
by rotating the leg inward, thus achieving a vertical position of the
toes. Every time, however, the leg will slowly move back into its
former position of eversion. The reason is that in an upper motor
neuron lesion the outward rotators of the leg are stronger than the
inward rotators, and prevail. Exactly the same is the case with the
extensors of the knee which, in a pyramidal lesion, are stronger
than the flexors, so that extension prevails. Everted position of the
foot seems to be an early pyramidal sign for which it is worth while
to watch.
It might also be mentioned here that, very early in spastic hemi
plegia, the muscles of the thigh lose their contour and become flat
tened. The result is apparent in the so-called "broad thigh."
Fig. 37. EVERTED POSITION OF THE FOOT.

Left-sided hemiplegia. The left foot spontaneously assumes the position of
eversion.
LEG EXTENSION TEST
In spastic paralysis of the lower extremity the extensors of the

knee are less affected than the flexors and, correspondingly, the
tonus of the extensors is greater than that of the flexors. This, to
gether with the weakness of the dorsiflexors of the foot, causes the
tip of the shoe to wear down more on the affected side, a telltale
"sign" of hemiplegia. The patient keeps his leg extended at the
knee and returns to this position again and again when the knee is
flexed. This is the physiological basis for the leg extension test and
the knee dropping test (following).
For the leg extension test the patient lies prone and is made to
relax. His lower extremities lie extended and slightly separated.
Then he is asked to bend his knees or they are passively bent by
the examiner. The lower legs are brought to a vertical or nearly
vertical position and the patient is told to maintain this position.
In severe paralysis the lower leg drops heavily and at once. In mild
paralysis the leg tends to go down in a few seconds. The patient
repeatedly tries to lift it and to keep it vertical. But eventually the
leg comes to rest flat on the table. The leg on the normal side re
mains vertical. The tendency of the leg to drop can also be demon
strated when it is put under the stressof acute emergency. The pa
tient lies prone, the legs extended. The examiner puts his forearm
under the lower part of each tibia and lifts the legs to an angle of
about 45 degrees. Both legs of the patient rest comfortably on the
examiner's forearm. The patient should not press his legs down
ward against the forearm of the examiner, who should feel merely
the weight of the patient's lower legs. Then the examiner suddenly
lowers his forearm, thus removing the support. On the hemiplegic
side the drop of the leg is much heavier and quicker than on the
healthy side.
In fully developed hemiplegia the of course, useless.
is,
test
Here the patient can hardly keep his leg vertical and drops in
it
stantly, like dead weight. But the test valuable in the detection
is
a
of mild, incipient hemiplegia.
KNEE DROPPING TEST
The physiological basis of the knee dropping test the same

is
as that of the leg extension test. Both tests express the dominant
tendency of the hemiplegic leg to assume position of extension
a
at the knee and to revert to after the knee has been flexed. This
it
to extension strong, constant and immutable. For the

is
tendency
knee dropping test the patient lies supine and relaxed on hard
a
for instance, an examining table. not appropriate

A
surface, bed
is
because too soft. The patient asked to pull his knees to

is
is
it
a
flexed position. It is essential that the friction between the heels and
the surface on which they rest be reduced to a minimum. If the
heels rest on a sheet, and particularly on a soft bed, the friction is
so great that the test loses most of its potency. Something flat, with
a hard smooth surface a polished wooden board, hard cardboard,
a square of metal plate should be placed under the heels. So that
they may slide more easily, the surface should be covered with pow
der and powder rubbed on the heels as well.
In spastic hemiplegia the result is positive: the knee on the
affected side slowly drops as the leg extends (Fig. 38). If this does
not happen and the knee remains immobile, the test can be made
more sensitive when the board or metal plate is pulled away slightly
and the legs are kept more extended. The less the knees are flexed,
the more likely and the easier the knee drops when there is an
upper motor neuron lesion. The patient tries to correct this tendency
of the knee to drop and spontaneously or on request lifts the knee
on the hemiplegic side to the level of the normal side. But he does
not succeed in the long run, and the spastic leg drops more and
more until it has assumed a horizontal position, resting flat on the
surface. In several patients it was found to be the only, or the most
striking, pyramidal sign. In these cases the Babinski reflex was defi
nitely not present. In fully developed hemiplegia this test is super
fluous and even impossible to carry out. The patient is unable to lift
his knee and, when this is done passively, the knee drops immedi
ately like a dead weight.
The comparative weakness of the knee flexors, which underlies
this test, can also be well demonstrated by putting them under the
stressof acute emergency. For this the examiner puts his forearm
under the patient's knees. He lifts them to the same level. The
knees of the patient rest relaxed on the examiner's forearm, and
suddenly and unexpectedly the examiner lowers his forearm or with
draws it. The knee dropping may be more pronounced when this
method is used.
Fig. 38. KNEE DROPPING TEST.
Patient flexes both knees to same horizontal level. His heels rest on a slip
pery, powder-covered metal plate. To extend the legs further and to make the
test more sensitive, the examiner pulls slightly on the metal plate. The left
knee descends slowly. Clock indicates testing time in seconds. Mild spastic
paralysis of the left lower extremity.
112
The test has the advantage that little or no co-operation of the

patient is needed. It has been found to be more sensitive than the
Babinski reflex. In fact, it may well be the most sensitive pyramidal
sign we have. It is by all standards objective, unmistakable and
convincing, and there is nothing ambiguous about it. It deserves
to become a routine test in the neurological examination.
PRONATOR TONUS TEST

The following four tests of pronator, quadriceps and acoustic
tonus and of pendulousness of the legs, all of which serve to un
cover pyramidal signs, are based on the fact that in pyramidal
lesions some muscle groups are particularly prone to exhibit spas
ticity. This is especially true of the pronators of the hand and of
the quadriceps muscle of the leg.
We have how an even slightly spastic upper extremity has
seen
a tendency to pronation. This is due to the comparatively greater
spasticity of the pronators. The spasticity appears very early and

can be demonstrated in patients whose upper extremities are in a
normal position. The increased tension of the pronator muscles as
a forerunner of hemiplegia can best be demonstrated in the follow
ing way. The patient flexes his elbow at a right angle; the exam
iner reassures himself again and again that the patient's muscles are
well relaxed. Holding the patient's hand lightly, he attempts to
bring the forearm into the position of supination with short, brisk,
sudden, repetitive movements. It is essential to make these move
ments sharp and quick. In cases of the mildest spastic paralysis the
examiner feels increased resistance in the pronator muscles. The re
sistance is typically elastic. It is at its height at the beginning of the
passive stretch of these muscles and increases with the briskness of
the movement. It yields quite suddenly despite continuation of the
stretching. Very little or no resistance is felt when the movement is
slowly performed. The spasticity is felt only, or much more, in the
pronators than in the supinators. In contrast to pyramidal spasticity
in the pronator muscles, the resistance felt in extrapyramidal rigidity
of the "lead pipe" type, that leathery, even, never elastic and
is,
is
felt in both agonist and antagonist muscles.
QUADRICEPS TONUS TEST

Since even the mildest spastic paralysis of the lower extremities
documents itself early in spasticity of the quadriceps muscle, the
tonus of this muscle should be examined first when such paralysis
For this purpose the examiner usually flexes and ex
is
suspected.
tends the supine patient's leg at the knee to appraise the resistance
felt and thus to evaluate the tonus. This somewhat crude
is
a
method. The following better. The patient lies supine on the
is
examining table; he made to relax his lower extremities maxi

is
this not done, the test cannot be performed. Approach

If
mally.
is
ing from the side, the examiner slips one hand under the patient's
thigh and the other hand under the lower part of the leg. He lifts
the thigh halfway between horizontal and vertical, keeping the
knee extended. Then he suddenly removes his hand from under
the patient's lower leg. Without support the leg falls of its own
weight. Normally falls inertly; the motion even; falls with
is
it
it
solid sharp thud. In pyramidal lesion as though there were

it
is
a
by
"catch" in the movement. The fall broken up series of

is
a
a
jerky interruptions. The reason for this that the sudden dropping
is
produces of muscle stretch reflexes of the quadriceps

sequence
a
which counteract the even fall. The spasticity facilitates the stretch
by
reflex. In these circumstances the sound produced the falling leg

soft and low, not sharp. In Parkinson's disease the dropping
is
is
slowed up too, but evenly and without the jerky movements seen
in pyramidal lesion. The reason that brisk movement in Parkin
is
a
son's disease does not produce stretch reflex as easily as in spastic

a
paralysis.
ACOUSTIC TONUS TEST
With this test the tonus of the knee muscles is appraised. The
patient lies flat on his back, legs outstretched and slightly separated,
his muscles thoroughly relaxed. Approaching from the side, the ex
aminer slips one hand under the patient's thigh and lifts it to an
angle of about 45 degrees; with the other hand the examiner sup
ports the patient's heel. The leg is held in moderate flexion at the
knee. Quite suddenly the examiner removes the support from the
thigh, and at the same time with his other hand he extends the leg
and allows the knee to drop. At the end of the procedure the leg
is in complete extension, elastically supported at the heel by one
hand of the examiner. In the normal person the sudden approxima
tion of the joint surfaces of femur and tibia produces a character
istic clear, snapping sound, somewhat prolonged and crescendo. In
hypertonia the sound is dulled, muffled and slightly delayed due to
increased resistanceof the hypertonic muscles which tighten the
knee joint. This is more pronounced in extrapyramidal rigidity than
in pyramidal spasticity. In cases of hypotonia, particularly of the
tabetic type, the sound is quicker, sharper, higher pitched. The test,
although interesting, is only of supportive value. No definite diag
nosis can be made on this test alone.
This is a valuable test in the diagnosis of lesions of the pyram

idal, extrapyramidal, cerebellar and peripheral nervous systems.
Here we are concerned with its use in the diagnosis of a pyramidal
lesion.
The patient sits on the edge of a table, his legs hanging freely.
The prerequisite for this test is that the patient's legs be relaxed.
The examiner lifts them simultaneously to the same horizontal
level. It is essential that they be lifted strictly in the sagittal plane,
without sidewise deviation. The examiner then releases them and
allows the legs to swing freely to and fro. In the normal subject,
the swinging takes place in a straight sagittal plane. The movements
Fig. 39. TEST FOR PENDULOUSNESS OF THE LEGS.

An electric light is fastened to the big toe. A, pendulousness in a normal
person. The light pattern indicates that the leg swings to and fro in a straight
sagittal plane. B, pendulousness typical of spastic paralysis. Right side. Mild
clinical signs but no symptoms and no apparent functional defect. Note un
evenly circular light pattern. C, pendulousness typical of spastic paralysis. Left
side. Clinically: pronounced paralysis.
are back and forth, without any deviation to the right or left (Fig.
39, A). Not so with a pyramidal lesion. In spasticity the regular
to-and-fro movements are abandoned. The foot describes a flattened
ellipse, a broken circle, a spiral or an undefinable figure. There is a
marked tendency to rotatory and sidewise movements which do not

occur in the normal (Fig. 39, B). The more severe the pyramidal
lesion, the more does the swinging deviate from the straight line
(Fig. 39, C).
The test is easy to perform and to evaluate. It may reveal spas
tic paralysis of the leg very early. It is particularly valuable if found
on a preliminary examination, when it alerts the examiner to look
for other confirmatory pyramidal signs.
TESTS BASED ON WEAKNESS OF MUSCLES

IN SPASTIC PARALYSIS
In spastic paralysis the voluntary movements of the limbs are

not disturbed to an equal degree. Some are more affected than
others. Some movements are almost abolished, some weak, some
hardly affected. In the forearms, the paralysis is more severe in the
extensors than in the flexors. Supination of the forearm is always
weaker than pronation. The knee flexors are more affected than the
extensors. This dissociated weakness may be used to detect pyram
idal lesions. For this purpose, those movements which are particu
larly weak are tested.
The spastic patient keeps his wrist bent; the extensors of the
hand are weaker than the flexors. This is a striking and early sign
of spastic hemiplegia and can be used as a test. The patient is asked
to dorsiflex his hand at the wrist, and the examiner compares the
strength of this movement on both sides. Weakness of one side is
suggestive of a pyramidal lesion. The same can be said of the weak
ness of abduction of the thumb which becomes manifest very early
in hemiplegia. The patient's thumb therefore consistently assumes a
position of adduction. Weak dorsiflexion and weak abduction of
the foot are very early signs of hemiplegia. Here, the dorsiflexors
of the foot suffer very early. Their weakness is in sharp contrast to
the comparative strength of the plantar flexors of the foot. To test
this weakness, the supine patient is asked to dorsiflex both feet.

The examiner tries, against the resistance of the patient, to flex the
feet plantarward. Unilateral weakness of dorsiflexion is suggestive
of a pyramidal lesion. It must be kept in mind that the dorsiflexors
of the foot are very strong and that a normal individual can resist
almost any attempt at passive plantar flexion. The difference in the
strength of the dorsiflexors and plantar flexors of the foot may be
striking. The patient may not be able to dorsiflex the foot at all, or
do it only feebly, and this movement may be easily suppressed by
the examiner. Yet the plantar flexion on the same side can be car
ried out with such force that the examiner may be unable to
counteract it.
In spastic hemiplegia, not only are the movements weak but
their range is decreased as compared with the normal side. This can
The patient for instance, asked to
is,
be shown by different tests.
abduct his fingers as far as he can. When he brings the palms of
his hands together, the difference in the range between the normal
and the affected side easily seen. The thumb and index finger are
is
abducted more on the healthy than on the affected side. When the
patient lies prone, he bends the leg less on the hemiplegic than on
the healthy side. When he lies supine and dorsiflexes his feet, he
does this more extensively on the healthy than on the paretic side.
This diminution of the range of movement may be very early or
a
residual sign of spastic paralysis. These simple tests can be used

a
easily in the search for pyramidal signs.

In pyramidal lesion, not only are there diminished strength
a
and range of movement but the movements which are preserved

cannot be performed as easily on the hemiplegic as on the healthy
side. Such movements as remain are slow, and the lack of speed
is
practically as important as the lack of power. The retardation of

movement may be found to be out of proportion to the loss of
power.
REFLEXES: GENERAL
The reflexes form an important group of tests for pyramidal

signs. They are therefore discussed here, although reflexes are of
equal value in the examination of other systems.
The two main classes of reflexes are (1) the deep muscle and
(2) the superficial reflexes. The first group are also called tendon,
bone, periosteal, osteoperiosteal, osteotendon, joint, fascial or apo
neurotic reflexes. The most appropriate name, however, is "deep
muscle reflexes" since their origin lies in the stretching of the mus
cles. It is best to name a reflex not after the point of elicitation but
according to the muscle involved, i.e., brachioradialis reflex, finger
flexor reflex, quadriceps reflex, triceps surae reflex, plantar reflex.
The first is sometimes called "radial periosteal reflex (supinator
jerk) ." This term is not appropriate because the radial bone is not
involved, nor is the periosteum; it is neither a jerk nor a supinator
jerk. "Jerk" is a popular, broad, general term. It is not exact and
specific, nor is it scientific enough to be used in physiology. Chore
atic movements and epileptic discharges are "jerks," too, but they
are not reflexes. The "radial periosteal reflex (supinator jerk)" is
a brachioradialis reflex which is produced by sudden stretching of
the brachioradialis muscle. This name is a physiological one and
debars all misunderstanding.
In the examination of the deep muscle reflexes, reinforcement
plays an important role. The usual technique of stretching the mus
cle does not always elicit a perceptible reflex contraction, and the
reflex seems to be absent. No reflex should be declared absent,
unless some method of reinforcement has first been employed.
There is a great variety of such methods. If the reflex is not elicited
on the first stroke, it might be advisable to tap the belly of the
involved muscle with the reflex hammer or to have the patient
squeeze the upper arm of the examiner. The best method consists
of a slight, voluntary contraction of the muscle which is directly

involved in the very reflex to be elicited. Thus an invisible reflex
may become visible and a weak one stronger. To reinforce the
quadriceps reflex, for instance, the patient, with his legs hanging
loosely over the edge of the table, is asked to push one leg slightly
forward against the resistance of the fingers of the examiner. The
moment the patient slightly contracts the quadriceps muscle, the
patellar tendon is tapped and the reflex elicited. The same method
is applied for the triceps surae reflex, the Achilles tendon being
tapped at the moment the patient plantarflexes his foot slightly
against resistance. This method is also very effective when applied
to the flexor muscles of the fingers. The finger flexor reflex may not
be elicitable, yet if the patient is asked to flex his fingers slightly
when the reflex is being elicited, it becomes very distinct.
The second class of reflexes useful in diagnosis of lesions of the
pyramidal system are the superficial reflexes. Here no muscle is
stretched, in the elicitation of deep muscle reflexes, but it con
as
tracts when the skin above or near it is stimulated.

Of all the deep muscle reflexes, only a few will be discussed
here, and these only briefly.
JAW MUSCLE REFLEX
This reflex is sometimes called the masseter reflex. This is not

quite correct, since besides the masseter other muscles which close
the mouth are involved. This is a typical deep muscle reflex, the
sensory and motor arc of which goes through the trigeminal nerve.
It is elicited by briskly tapping the lower jaw in a movement
which depresses it. The mouth should be kept slightly open and the
jaw relaxed. It is sometimes easier to elicit this reflex by tapping a
tongue blade placed on the base of the tongue instead of tapping
the lower jaw directly. The blade must not touch the teeth. With
this method, the jaw muscle reflex may appear on less strong stim
uli and more distinctly than when the lower jaw is tapped directly.
The jaw muscle reflex is exaggerated in diffuse bilateral damage to
the corticotrigeminal pathways. Any kind of bilateral supranuclear
cerebral lesion such arteriosclerosis, progressive paralysis and
as
hypertensive encephalopathy may produce exaggeration of this re

flex, sometimes even clonus.
SNOUT REFLEX
When both pyramidal tracts become affected in their intra
cranial course, some reflexes in the area of the face which are not
found in the normal individual come to the fore. They exist nor
mally in latent form, and become apparent only with a defect in
bilateral pyramidal innervation. One of the most important of these
is the snout reflex. The conditions under which it may appear are
somewhat complicated. It may be elicited by different stimuli. Here
we are concerned with it as a deep muscle reflex due to percussion
and stretching of the orbicularis oris muscle.
With the patient relaxed and completely at rest, the examiner
taps the center of the lips, or only of the upper lip, with the reflex
hammer. The tapping may be done through a tongue blade laid
across or halfway across the patient's lips. Tapped directly or indi
rectly, the lips protrude forming a snout. Except during the first
year of life, this does not occur in the normal subject. The snout
reflex is present in diffuse lesions of the brain such as cerebral ar
teriosclerosis, hypertensive encephalopathy, progressive paralysis of
the insane, senile dementia, chronic alcoholism and idiocy. In the
following two conditions it is striking and diagnostically most valu
able. One is amyotrophic lateral sclerosis, but only in those cases in
which the process has ascended the pyramidal tracts above the
spinal cord into the brain and now involves the corticofacial pyram
idal fibers. The other condition is the so-called pseudobulbar palsy
which, of course, is and should be called supranuclear (spastic)
bulbar palsy. The word "spastic" should be used to distinguish this
type from the rare striatal bulbar palsy which is also supranuclear.
In spastic bulbar palsy the corticofacial pyramidal fibers degenerate
primarily and bring about a lowering of the threshold for elicita-
tion of the snout reflex, i.e., the deep muscle reflex of the orbicularis
oris.
It is sometimes difficult to say how mild a lip protrusion should
be termed a snout reflex, but when the protrusion is marked and
definite, its diagnostic value is considerable. A diffuse brain lesion
if,
can certainly be assumed, all the more so besides the snout reflex,
the head retractor reflex (see p. 124) also present and the jaw
is
muscle reflex exaggerated.
When in lesions of the pyramidal tracts the snout reflex
is
pres
ent, another reflex of the same kind appears. This the reflex of
is
the muscles which elevate the upper lip, particularly the corners of
the mouth (levator labii superioris; levator anguli oris). On tap
ping the bridge or the side of the nose with sufficient force to bring
about concussion of the underlying bone, these muscles come into
a
action, and reflex lifting of the upper lip, particularly at the corner
of the mouth, results. In the normal individual, this reflex cannot
be elicited; its threshold too high. pyramidal lesion lowers the
A
is
is by
threshold removing the central inhibition of this reflex. The

physiology the same as that of the snout reflex.
The snout reflex should be distinguished from reflex much
a
more seldom seen, the "wolfing" reflex ("eating" or "sucking" re

flex). The method of elicitation and the clinical features are differ
ent. In the "wolfing" reflex the lips need not be percussed but are
merely touched. The patient makes of rhythmic tasting, series
a
sucking, chewing, swallowing movements. When an object

is
brought near the lips, the mouth opened and follows the object
is
when moved. This reflex seen in extensive and intensive

it
is
is
damage to the brain, congenital or acquired, particularly in the

young. Traces may be seen in the normal newborn. This sucking

reflex is easy to distinguish from the snout reflex, although the latter
may be a part of the former. It is due to lesions of the frontal lobe.
Fig. 40. PATHOLOGICAL LAUGHING AND CRYING.

Patient with diffuse cerebral arteriosclerosis and spastic bulbar paralysis.
Attacks of crying occur spontaneously, without provocation or accompanying
emotion.
PATHOLOGICAL LAUGHING AND CRYING

This condition, too, is a release phenomenon and manifests it
self in the following manner. The mimic expressions of laughing
and crying start more quickly, are more excessive, more extensive
and intensive and last longer than in the normal person. The face
comes to rest slowly. The threshold for the act of laughing and
crying is extremely low and the art is poorly controlled. There may
be prolonged giggling caused by the most insignificant and harm
less remarks which are hardly tainted by wit or emotion. The
stimuli which provoke the attacks are inadequate and inappropriate.
Added to this, there occur spontaneous, so to speak, propriocep-
tively induced spasmodic attacks of laughing and crying with no
provocation whatever (Fig. 40). The manifestations seem to be
purely psychic, but their genesis is neurological. One should be
familiar with them, lest one run the risk of misinterpreting them as
genuine emotional outbursts. The attacks may start unprompted
and stop abruptly without any emotional residual. The physical
machinery of laughing and crying "runs empty."
Such attacks are often called abnormal, purposeless, episodic,
uncontrolled, spasmodic, forced, unprovoked, inappropriate and ex
cessive. They may also be called "dysmotivated." Although the
word "dysmotivated" is not listed in Webster, it is appropriate as a
term. For this laughing and crying, it is extremely difficult to find

an appropriate adjective comprehensive enough to cover the whole
phenomenon. Nothing remains but to use the general term "patho

logical," although it is not specific enough.
Pathological laughing and crying occurs in cases of diffuse
lesions of the brain, whatever the cause, and in far advanced cases
of amyotrophic lateral sclerosis. Bilateral interruption of the cortico-
fugal pathways for such expressions of emotion may be assumed.
HEAD RETRACTOR REFLEX
Another deep muscle reflex which exists in latent form and is

brought out by a defect in bilateral pyramidal innervation is the
head retractor reflex. This is a reflex of the muscles which retract
the head, i.e., bendit back. As in the case of all other deep muscle
reflexes, we need brisk stretching of the muscles for its elicitation.
This is followed by their reflex contraction. To elicit the reflex, the

patient is made to relax his neck muscles as much as possible. The
head is kept slightlybent forward by the fingers of the examiner
placed on the patient's occiput. With a reflex hammer a sharp,
quick, elastic tap is applied to the patient's upper lip, the blow
being directed downward. The purpose is to cause a brisk further
bending of the head. When the reflex is present, the patient reacts
with a brisk, involuntary retraction of the head.
This reflex must be regarded as essentially normal, but it cannot
be elicited in the normal individual because its threshold is very
high. However, when a bilateral lesion of the pyramidal tract re
moves the central inhibition from this reflex, it can be elicited. Its
presence indicates a bilateral lesion of the corticocervical pyramidal
tract. Its diagnostic value is very great. Generally it is easy to dis
tinguish the slight concussion of the head, which results when the
hammer taps the upper lip of the normal person, from the retrac
tion of the head of patients in whom the reflex is present. In diffuse
encephalopathies, in some far-advanced cases of amyotrophic lateral
sclerosis and of bilateral spastic paralysis, this reflex has been seen
very distinctly. The retraction of the head after tapping was unmis
takable. The reflex is helpful in the differential diagnosis between
amyotrophic lateral sclerosis and upper cervical cord tumor. In the
latter condition the reflex is never observed. It is not uncommon to
find a marked snout reflex and a head retractor reflex in patients
with no definite pyramidal or cerebral signs. Such patients may not
have a dramatic history of "strokes" or cerebral manifestations like
aphasia, hemianopia, dysarthria. They may have suffered unrecog

nized occlusions of small cerebral arteries. However, on psychiatric
examination these patients usually show some personality changes,
particularly some mental deterioration and memory defect. The
elicitation of a snout reflex or head retractor reflex in such cases
may be of decisive value in diagnosis.
PRONATOR REFLEX
The importance of this reflex lies in the fact that it is distinctly

and very early exaggerated even in a mild pyramidal lesion. It is a
reflex of the pronators of the hand. The patient sits with his relaxed
forearms resting with their ulnar surfaces on his thighs. The exam
iner, swinging the reflex hammer loosely, applies an elastic blow to
the volar side of the lower end of the radius. The blow brings about
a sudden mechanical supination of the hand, and reflex pronation
follows. Unilateral exaggeration of this reflex is one of the most
delicate and early of all pyramidal signs.
FINGER FLEXOR REFLEX
The best method of eliciting this reflex follows. The patient's

half supinated hand rests with its dorsum on his knee, the fingers
slightly bent. The examiner places his extended index and middle
fingers across the tips of the patient's four fingers. The examiner
then taps the dorsum of his own fingers with the reflex hammer.
A reflex flexion of the patient's four fingers,
as well as of the end
phalanx of the thumb, takes place. This indicates that the reflex is
present. The reflex is often very weak or hardly perceptible. To
little more
it,
reinforce the patient asked to bend his fingers

is
when the blow applied. The result of this reinforcement some

is
is
times very striking. The so-called Hoffmann and many other re

flexes carrying various eponyms are based on the same mechanism,
i.e., stretching of the finger flexor muscles. In some texts the Hoff
mann reflex still listed as pathologic reflex and mentioned in
is
the same breath with the Babinski reflex. The physiologic mech
anism of the finger flexor reflex entirely different from that of
is
the Babinski reflex; simple muscle stretch reflex like the

it
is
a
quadriceps reflex. normal reflex, though sometimes difficult

It
is
a
to elicit. When this reflex greatly exaggerated, may, but need

is
it
not, indicate a pyramidal lesion. It may be only an expression of a

purely functional increase of reflexes. Only a difference in the
strength of this reflex between right and left should be regarded
as pathological.
SUPERFICIAL AND DEEP ABDOMINAL REFLEXES
The textbooks use the term "abdominal reflexes" to designate

the superficial abdominal reflexes. This is not correct, since there
Fig. 41.
PINWHEEL FOR EXAMINATION OF THE SUPERFICIAL RE
FLEXES AND OF SENSIBILITY.
are two kinds of abdominal reflexes, the superficial and the deep.
Physiologically, they are completely different.
The superficial abdominal reflex is a skin reflex, a skin-muscle
reflex or extrinsic muscle reflex. Here, on stimulation of the skin,
the abdominal muscles contract. The muscles are not directly af
fected, they react to the stimulation of the skin. To stimulate the
skin, one should not use a pin or any other sharp instrument, but a
pinwheel (Fig. 41). Such a pinwheel is nothing else than a pattern

tracer used by tailors and pattern makers. It can be purchased for

less than $1.00 in any department store or tailor shop. The pin-
wheel is rolled over the abdomen with light or no pressure. For
elicitation of the superficial abdominal reflex, the pinwheel has
great advantages over the pin and should be used exclusively. It
may happen that the reflex cannot be elicited by the use of a pin
but will appear distinctly when the pinwheel is used.
The importance of the superficial abdominal reflex lies in the
fact that its loss is highly indicative of a lesion of the pyramidal
tract. It must be remembered, however, that this reflex may also be
absent in non-neurological conditions and may be preserved or re
turn in pyramidal lesions.
The abdominal muscles have not only a superficial, or skin,
reflex but also a deep muscle reflex of their own. This deep muscle
reflex is elicited on brisk stretching of the muscles. Since the line
of insertion of the abdominal muscles is extremely long, in fact
longer than the insertion line of any other muscle of the human
body, there are many places from which a stretching of the muscles
can be effected, and there are different ways to do this. The reflex
can be elicited by tapping a ruler pressed on the abdomen in front
or on the side. The ruler is pressed down and tapped with the re
flex hammer. When the reflex is present, the muscles contract and
"jump up" powerfully in response to the blow which stretches them.
The ruler may also be placed above the symphysis pubis, pressed
down and tapped.
To reinforce this reflex, the same method is used as in the re
inforcement of any other deep muscle reflex, namely, slight volun
tary contraction of the muscle involved. For this purpose, the pa
tient is asked to say "putt-putt" briskly, to bend his head forward or
to make a slight attempt to rise. The examiner opposes this move
ment by placing his fingers on the patient's forehead or chest. All
this brings about increased tension in the abdominal muscles and
facilitates the appearance of the reflex. The same method, by the

way, may be used for elicitation of the superficial abdominal reflex.
This reflex can be more easily obtained while the patient stands
than while he lies. This might be due to the fact that when the
patient stands the viscera sag and exert some tension on the abdomi
nal muscles.
This deep abdominal muscle reflex, elicited by direct stretching
of the abdominal muscles, must be strictly distinguished from the
long-known superficial abdominal reflex, briefly called abdominal
reflex.
The behavior of these two completely different types of reflexes
is as follows.
1. In the normal: superficial reflexes present, deep muscle re
flexes present, but may be very weak.
2. In lesions of the spinal cord affecting the sixth to twelfth
thoracic segments directly: both types of reflexes absent.
3. In bilateral lesions of the pyramidal tract situated above
T 6, the highest level of segmental innervation of the abdominal
muscles: superficial reflexes lost, deep muscle reflexes exaggerated.
Dissociation between Superficial and Deep

Abdominal Reflexes
This third possibility of behavior of the abdominal reflexes is

of great diagnostic significance. Here there is a striking dissociation
of the two types of abdominal reflex. The superficial reflexes cannot
be elicited from any place or by any means, whereas the exaggera
tion of the deep muscle reflexes is pronounced. The muscles actually
"jump," even on the slightest percussion of a bone to which they
are attached, e.g., the costal margin, the anterior superior iliac crest,
the symphysis pubis. The muscles react briskly to both direct and
indirect stretching. This dissociation is not so striking in a unilateral
pyramidal lesion, although the superficial reflexes may be com

pletely lost. In examining a patient with spastic paralysis of the
lower extremities, one must look first for this dissociation. If it is
present, this definitely places the lesion above the sixth thoracic
segment. Such a dissociation speaks decidedly against a lesion af
fecting the thoracic segments 6-12, whereas the loss of both
types of reflexes will speak for such a lesion. In amyotrophic lateral
sclerosis, when the lesion does not reach below the sixth thoracic
segment, this dissociation is very striking. Cases of this disease are
not rare in which the Babinski reflex is absent but the dissociation
very pronounced. In the diagnosis and localization of spastic paraly
sis, a careful for dissociation of the abdominal reflexes is
search
most helpful. When present, it may decide the issue.
In the evaluation of the two components of this dissociation, the
increase of the deep abdominal reflexes has more weight than the
loss of the superficial. The reason is that the latter are inconstant
and may be easily exhausted or even absent owing to a non-neuro
logic condition. Although originally absent in a pyramidal lesion,
they may return, even though the lesion persists.
Thus one may say without exaggeration that among neurologi
cal tests there are few which, in significance and importance, can
compete with the dissociation of the superficial and deep abdominal
reflexes.
QUADRICEPS REFLEX
This term is physiologically sound and more appropriate than

the terms "patellar tendon reflex," "patellar reflex" and "knee
jerk." It is not a reflex of the patella or of its tendon. It can be
elicited without touching the tendon. It is also more than just a
"jerk." It is a muscle stretch reflex of the quadriceps muscle and

should be so called. This reflex is easily examined by the following
procedure. The examiner sits facing the patient, who sits on the
examining table with his legs hanging loosely over the edge. The
examiner palpates the upper edge of the patella and strikes it
lightly with a downward tangential blow of the hammer; or the ex
aminer may strike his palpating finger put on the upper edge of the
patella. This stretches the muscle and elicits its reflex. When the
patient lies supine the reflex may be elicited when the examiner
places his bent finger above the upper edge of the patella, presses
the patella downward and then taps his own finger. It is interesting
to observe that when the reflex is absent, the blow on the patellar
tendon produces a peculiar dull sound, quite different from the high
sound heard when the reflex is present.
TRICEPS SURAE REFLEX
This term is physiologically, didactically and practically more

correct than the old terms "Achilles' tendon reflex" and "ankle
jerk." Again, it is not a reflex of the tendon and can be elicited even
without touching the tendon. The Achilles tendon acts only as a
transmitter of the stretch impulse to the muscle. It is a muscle

stretch reflexof the triceps surae and should be so called, regardless
of the point of its elicitation. This reflex can be elicited in three dif
ferent ways. ( 1 ) By tapping the Achilles tendon. Here it is neces
sary that the foot be held elastically dorsiflexed.Without prelimi
nary stretching of the muscle, no reflex appears. The tendon can be
tapped on a patient supine, prone or kneeling. The last procedure
may be used but is somewhat complicated and uncomfortable. The
following method is preferable. With the patient sitting on the ex
amining table, the legs hanging loosely, the examiner places his left
hand under the ball of the foot, lifts it up and with the hammer in
his right hand strikes the Achilles tendon. (2) In a supine patient
with his knees slightly bent, the examiner elastically dorsiflexes the
foot with one hand, while with the hammer in the other he strikes
the lower part of the tibia. By depressing the tibia and thus increas
ing the dorsiflexion of the foot, the blow indirectly stretches the
Achilles tendon and the attached triceps surae muscle. (3) On a
patient lying supine, legs outstretched, the examiner dorsiflexes the
foot and taps the ball of the foot with the reflex hammer, thus pro
ducing an additional brisk passive dorsiflexion.
The method of reinforcement is the same regardless of the way
in which the reflex is elicited: the patient is asked to plantarflex
the foot slightly, and the blow with the hammer is applied at the
same moment.
PLANTAR MUSCLE REFLEX
There are number of deep muscle reflexes in which the thresh

a
old for elicitation is so high that they can seldom be elicited in the
normal individual. They can, however, be obtained when a pyra
midal lesion, by removal of inhibition, lowers the threshold for the
deep muscle reflexes. This is clearly exemplified by the plantar mus
cle reflex. The plantar muscle of the sole of the foot is not easily
accessible to stretching. This mechanical condition accounts for the
fact that the deep muscle reflex of the plantar muscle is only rarely
seen in the normal person but becomes clearly visible with the
slightest defect in the pyramidal tract. From a physiological stand
point it is essential to realize that elicitation of the plantar muscle
reflex does not mean that a new pathological reflex is being elicited.
It only a pathological exaggeration of a normal deep muscle
means
reflex. When this reflex is observed, a pyramidal lesion may be
suspected but need not necessarily exist.
There are many ways in which to stretch the plantar muscle
and elicit its reflex. The result is always the same plantar flex
ion of the toes. This can be obtained by tapping the plantar surface
of the toes, the sole, the heel or the dorsum of the foot. When a
defect in the corticospinal tract exists, concussion of the bones of
the foot produces this reflex. The plantar muscle reflex drastically
exemplifies the multiplicity of points from which a deep muscle

reflex can be elicited. Regardless of the various points from which
this may be done, and notwithstanding the different mechanics, it
is always the same reflex the deep plantar muscle reflex elicited
by stretching of the same muscle. The literature lists over 20 re
flexesof the foot, most of which carry single or compound epo-
nyms. All of them represent the plantar muscle reflex. This is
sometimes regarded as a variation of the Babinski reflex. It certainly
is nothing of the sort, for the Babinski is not a muscle stretch reflex,
whereas the plantar muscle reflex undoubtedly is.
PLANTAR SKIN REFLEX
When the sole of the foot is stroked, the toes flex. This is the
normal plantar skin reflex. The flexion of the toes may be very
slight, hardly perceptible, and has even been reported absent bi
laterally in up to 10 per cent of normal people. Therefore, scarcely
any diagnostic conclusion can be drawn from the bilateral absence
of this reflex alone. It may be easily exhaustible, as is the case with
all other skin reflexes. Unilateral absence of this reflex, the so-called
"dumb sole," may, however, indicate slight damage to the pyram
idal tract and may be regarded a predecessor of the Babinski reflex.
UNILATERAL REFLEX CHANGES IN PYRAMIDAL LESION
Perfect symmetry of the human body does not exist. In fact, it

has been shown again and again how great the differences are be
tween the two halves of the body. However, neurological examina
tion is based on the assumption that the two halves of the human
body are equal. In fact, the main object of the neurological exami
nation is to uncover the differences between them. This is particu
larly true of the reflexes, and it is assumed that every difference
between the two sides is pathological. We must be on the most
careful lookout for differences between reflexes on the right and

left, particularly for an increase on one side. Such an increase is
diagnostically more significant than the findings of any specific test.

Diagnostically, a general increase of reflexes is of little signifi
cance. It cannot be emphasized strongly enough that in neurotics
there may be marked exaggeration of the reflexes in general, with
out the slightest indication of any pyramidal affection. Every single
deep muscle reflex may be bilaterally exaggerated; multiple reflexes
may be elicited on a single tap. On tapping of the patellar tendon,
the contralateral adductor reflex may appear (through concussion
of the pelvis! ) . There may be a strong contraction of the tensor
fasciae latae on stimulation of the sole, and still all this need not
in itself mean a pyramidal lesion.
What really counts is a difference between right and left. While
both sides are being compared, it is important to keep the patient's
head straight.
To compare the triceps reflex on each side, the patient is asked
to put his arms akimbo, his hands resting at the waist above the
hips. The examiner, standing behind him, can easily compare the
triceps reflex on each side.
For the diagnosis of a slight hemiplegia with a difference in the
adductor reflex, the following method is useful. The examiner places
a ruler or a tongue blade on the symphysis pubis and taps it exactly
in the middle. This brings about a concussion of the pubic arch
from which the adductor muscles originate. The concussion pro
duces a slight stretching followed by reflex contraction of the ad
ductors, equal force acting on each side. If there is a unilateral
pyramidal lesion, the adductor reflex on the affected side is stronger.
As the ruler, placed above the symphysis pubis, is tapped with less
and less force, the reflex finally appears only on the affected side.
This difference may constitute one of the finest signs of a pyramidal
lesion affecting the legs.
The quadriceps reflex can be examined on both sides simultane

ously when a stick, placed above or below the patellae, is tapped
in the center. However, this method is not reliable, because it is
difficult to strike the blow exactly in the middle, and the slightest
deviation off center causes the reflexes to appear unequal. The same
applies to a stick put across the balls of both feet for simultaneous
examination of the triceps surae reflex. However, to compare this
reflex on either side, the following method can be employed. The
extended legs are placed together. First one foot, then the other, is
passively dorsiflexed and kept elastically in this position. The ball
of each foot is tapped in quick succession, or, when both feet are
kept in dorsiflexion simultaneously, the lower part of the shin is
tapped. The strength of plantar flexion on each side can thus be
compared easily.
TESTS FOR UNILATERAL SPINAL CORD AFFECTION
When a difference in the deep muscle reflexes of the legs has

been found, one should not forget to test the sensibility of both
For instance, the reflexes may be exaggerated on the left, and,
legs.
when the pain sensation in both legs is tested, the patient says: "The
left leg is stiff, but I feel the pin better on that leg than on the
right." Such a statement is highly significant and should lead to
further investigationof the sensibility of both lower extremities.
An effort should be made to determine the highest level of sensory
deficit. Such a statement by a patient may indicate the presence of
a lesion on the left half of the spinal cord somewhere above the
lumbar segments. A unilateral lesion situated in a thoracic or cervi
cal segment of the spinal cord, and damaging the left half only,
would produce spastic paralysis of the left lower extremity due to
the lesion of the ipsilateral pyramidal tract, and at the same time
would cause loss of pain and temperature sensations in the right
leg due to a lesion of the crossed spinothalamic tract. The touch
sensation on the right leg is essentially preserved. These are the
outstanding features of the syndrome which carries the name of
Brown-Sequard ( 1849). Briefly, it is characterized by the following
changes: one lower extremity is spastic, but in the other the sensa
tions for pain and temperature are lost. There may be incomplete,
abortive clinical pictures of this syndrome. It must be remembered
that the spinothalamic tract crosses the spinal cord obliquely, i.e.,
after ascending a few segments. Therefore the upper level of the
sensory dissociation is much lower than the unilateral lesion of the
spinal cord.
ASSOCIATED MOVEMENTS IN A PYRAMIDAL LESION
The pyramidal tract has many and varied functions. There is a

great diversity of combinations in which the functions of the pyra
midal tract may be qualitatively and quantitatively disturbed. This
makes the semeiology of a lesion of the pyramidal tract so ex
tremely rich. Spastic paralysis has many components: static, dy
namic, tonogenic. To the question What is the outstanding, the
leading sign in a pyramidal lesion? there are many answers, de
pending on the angle from which the disturbance is viewed. One
well-founded answer is: It is the loss of ability to perform fine, iso
lated movements, instead of which mass movements are performed.
In a pyramidal lesion the motor power may be almost normal, the
gross mass movements preserved; yet the use of the hand restricted
because of inability to perform fine movements. A patient of mine,
a young rancher, was operated on for focal epilepsy which always
began in the right fingers. The cortical hand center was extirpated
and the attacks ceased. The patient stated that after the operation he
could use his hayfork nearly as well as before but could not button
his shirt. In order to perform fine, isolated movements, the integrity
of the corticospinal tract must be preserved. Many signs of a pyra
midal lesion are based on this physiological principle.
Associated movement of the thumb. With his left hand the

examiner tightly grasps the patient's supinated hand at the wrist
from below. With his right hand he hooks his four bent fingers into
Fig. 42. ASSOCIATED MOVEMENT OF THE THUMB.

A, the patient bends his last four fingers against the resistance of the four
hooked fingers of the examiner. The thumb moves toward the palm. Mild spas
tic paralysis of the hand. B, with his fingers hooked over a horizontally fastened
rod, the patient is asked to pull it down. The right thumb performs an associ
ated movement toward the palm. Right-sided spastic hemiplegia.
the four bent fingers of the patient. The patient is asked to bend
his four fingers further against those of the examiner and to exert
all his strength. The examiner pulls against the patient's fingers
(Fig. 42, A). By another method, with his fingers hooked over a
horizontally fastened stick, the patient is asked to pull it down

(Fig. 42, B). The forceful bending of the four fingers brings about,
as an associated movement, bending of the thumb. When the slight
est spastic paralysis of the hand exists, the patient's thumb is ad-
ducted, flexed and moved inward across the palm (Fig. 42). This
constitutes a very early pyramidal sign. In the normal individual the
thumb remains immobile or its end phalanx bends very little.
The pathological associated movement of the thumb toward the
palm often starts slowly and only after the patient has exerted his
full strength for some time. Therefore, it is essential that the pa
tient's efforts be continued and the test not be given up prematurely.
It is particularly the marked difference in the behavior of the
right and left thumb that makes the test valuable. A positive result
may indicate a pyramidal lesion in patients who have no functional
defect in the use of the hand and arm, and even when the patients
themselves are unaware of any change.
Wrist drop test.This is discussed in the section on peripheral
nerves (p. 83). A patient has paralysis of the dorsiflexors of the
wrist. He is asked to grasp an object with his affected hand. When
the lesion is peripheral, the wrist drops still further. When the
lesion is central, there is a simultaneous dorsiflexion of the wrist as
an associated movement contingent on the bending of the fingers.
The normal associated movement is preserved.
Trunk-thigh associated movement. The patient lies supine on
the examining table. A soft bed is not appropriate for this test. His
hands are folded across his chest, his legs slightly separated. He is
asked to sit up. On this attempt, the leg affected with spastic paraly
sis will rise. The same happens when the patient lies down from
the sitting position. If both legs go up, the paralyzed leg rises
higher. This is due simply to an associated movement of the flexors
of the thigh, contingent upon the innervation of the flexors of the
trunk. This tendency to associated movements exists on the affected
but not on the healthy side. A patient with hysterical hemiplegia

will raise the normal leg but not the paretic one. If necessary, the
test may be enhanced when the examiner opposes the effort to sit
up by placing his fingers against the patient's chest. This test is of
value only if there is a pure pyramidal lesion. Lesions of the cere
bellum or of the lumbosacral nerves may interfere with this test.
The same associated movement of lifting the hemiplegic lower
extremity occurs also on coughing and in other forms of straining
the abdominal muscles. This was reported as early as 1837 by
Marshall Hall: "whenever he [the hemiplegic] coughs, the leg is
thrown involuntarily upwards."
KNEE BENDING TEST
While standing erect, the patient is asked to try to touch the

floor with his finger-tips without bending his knees. On the side
with spastic paralysis he bends his knee, while on the normal side
the leg remains stiff. The mechanism is the same as in the trunk-
thigh associated movement. On bending, i.e., on innervation of the

flexors of the trunk, a simultaneous involuntary associated move
ment of the flexors of the thigh takes place.
TIBIALIS ASSOCIATED MOVEMENT
This is a particularly valuable test. The patient, lying supine

with his legs outstretched, is asked to lift the affected leg against
resistance. The examiner opposes the movement by placing his hand
on the patient's knee. In spastic paralysis the foot assumes a posi
tion of dorsiflexion and supination, and the tendon of the tibialis
anterior muscle becomes prominent ( Fig. 43 ) . The greater the pa
tient's effort to lift his leg, the more prominent the tendon becomes.
It for the associated movement to develop fully.
takes some time
It may occur, though not very distinctly, in the normal individual
who, in contrast to the hemiplegic, can easily suppress it. This asso
ciated movement, when pronounced and unilateral, may give sub
stantial aid in diagnosis.
It may, though to a lesser extent, also exist in reverse form;
is,
that flexion at the hip and knee may occur when the patient
is
by
asked to dorsiflex his affected foot against resistance the examiner.
Fig. 43. TIBIALIS ASSOCIATED MOVEMENT.

Spastic paralysis of the right lower extremity. At rest the position of both
feet the same. The patient asked to lift the affected leg against resistance
is
is
offered by the examiner, who presses down on the knee. The foot assumes
a
position of dorsiflexion and supination.
HOMOLATERAL MASS FLEXION REFLEX
The spastic lower extremity has tendency to combined flexion

a
in all its joints when any one of variety of external stimuli

is
a
applied. In the ankle this flexion

by
carried out the so-called ex

is
tensors tibialis anterior, extensor hallucis longus and extensor

digitorum longus. These muscles are extensors in name only. Physi
ologically speaking, they are flexors. They flex, they shorten the
extremity exactly as do the flexors of the hip and knee. The litera
ture contains many terms and eponyms designating this flexion of
the spastic lower limb on peripheral stimulation, but the most ap
propriate term for it is homolateral mass flexion reflex. The mass

flexion movement is not equal in all its components. Some may be
very pronounced, some appear only in traces. Generally speaking,
pIg. 44. HOMOLATERAL MASS FLEXION REFLEX.

Spastic paralysis of the lower extremities. A, patient's legs at rest. B, passive
forceful plantar flexion of the left toes elicits the homolateral mass flexion re
flex: dorsiflexion of the foot, flexion of the knee and hip. Simultaneously the par
tial contralateral mass extension reflex is elicited: plantar flexion of the right
foot and toes. There may be also a slight extension of the whole right leg,
judging from the fold in the sheet in front of the heel.
movement is strongest in the joint closest to the applied stimulus.

For instance, when the sole is stimulated, the movement in the
ankle is stronger than that in knee and hip. This mass flexion reflex
occurs on any stimulus, particularly a painful one, applied to the
sole of the foot. It can appear on compression of the foot or on
pinching, or any other irritation, either of the sole or of the dorsum.
The best method of eliciting the homolateral mass flexion reflex
is passive, brisk, forceful plantar flexion of the toes. Then the pa
tient performs an automatic and irrepressible bending in all joints
of the lower extremity ( Fig. 44 ) . The movements occur slowly and
with monotonous regularity. They are not a reaction to pain or dis
comfort and are easily distinguishable from the defensive move
ments a patient makes to protect himself and to prevent pain. A
strongly positive homolateral mass flexion reflex may occur even
when there is complete paralysis of the lower extremity on volun
tary innervation. I have seen many a patient referred with the diag
nosis "hysteria" based on the following argument: "The patient
could not move his leg on command but could move it on needling
of the foot."
When in the course of his disease a patient with hemiplegia or
paraplegia in extension shows an increase in the homolateral mass
flexion reflex, i.e., when this reflex can be elicited by milder stimuli
and even occurs spontaneously, without external stimulation, it is
an ominous sign of great significance. It means that the lesion of
the spinal cord progresses and slowly eliminates the resisting vestib
ulospinal tract, the very tract that keeps the legs in extension. In
multiple sclerosis, such flexor spasms of the lower extremity, occur
ring on slight stimulation or spontaneously, mean the end of para
plegia in extension and the beginning of the very distressing
paraplegia in flexion.
CONTRALATERAL ASSOCIATED MOVEMENTS
Among the many and different contralateral associated move

ments occurring in spastic paralysis, some are rare, inconstant and
more important physiologically than clinically. For clinical diagno
sis the following have certain value.
Fig. 45. CONTRALATERAL IDENTICAL ASSOCIATED MOVEMENTS
OF FINGERS.
Right-sided hemiplegia of mildest degree, without symptoms. A, hands at
rest. B, patient squeezes the examiner's hand with his affected right hand; no
associated movements of the left. C, patient squeezes the examiner's hand with
his healthy left hand; simultaneous bending of the fingers of the affected right
hand. Associated movements were the most conspicuous pyramidal sign.
143
FIg. 46. CONTRALATERAL IDENTICAL ASSOCIATED MOVEMENTS
OF FINGERS.
Spastic paralysis of the left hand. A, patient squeezes the examiner's hand
with his healthy right hand; simultaneous bending of the fingers on the left.
B, patient extends fingers of his healthy right hand against resistance offered by
the examiner; simultaneous extension of the fingers on the left.
144
Contralateral Identical Associated

Movements of Fingers
The patient with hemiplegia is asked to squeeze the hand of
the examiner with his healthy hand, and with great force. When
exertion is at its height, a slight involuntary bending of the fingers
Fig. 47. CONTRALATERAL IDENTICAL ASSOCIATED MOVEMENTS

OF FINGERS.
Boy with left-sided infantile spastic hemiplegia. A, fingers at rest. B, making
a fist with the healthy right hand produces flexion of fingers on the left.
on the affected side takes place (Figs. 45, C, and 46, A). Or the
patient is asked to extend the fingers of his healthy hand against
the resistance offered by the examiner. The fingers of the affected
hand to a slight degree simultaneously perform the same move
ment of extension (Fig. 46, B). It must be assumed that on the
affected side the corticospinal tract is no longer isolated as it is in
the normal. Impulses destined for the opposite healthy side, spring
to the affected side and evoke similar movements. These identical
"mirror" movements often escape the attention of the
associated,
examiner who, testing the strength of a patient's hand, naturally
concentrates on that. Such movements occur predominantly in
young people, for instance, in those who have had mild spastic
hemiplegia during infancy ( Fig. 47 ) . These movements may consti
tute a conspicuous, helpful and often surprising pyramidal sign.
Contralateral Associated Leg Extension
In a pyramidal lesion, one of the most common contralateral

associated movements is observed in the following maneuver. The
patient sits on the examining table with his legs hanging over the
edge. He is asked to make a strong movement with his unaffected
hand or arm against resistance. Each such exertion brings about an
increase of extension of the leg on the affected side. Any physical
strain increases the extensor tonus of the hemiplegic leg. This may
occur even when the patient coughs, yawns, cries, laughs or sneezes.
Any strain also increases the flexor tonus of the affected arm, but
this is not as conspicuous as the increase of the extensor tonus of
the leg. The phenomenon is physiologically interesting but of no
great practical value because it appears only when other and more
reliable pyramidal signs are already present.
In unilateral or, more so, in bilateral spastic paralysis of the
legs, the following associated movements can sometimes be ob
served.
a) When the homolateral mass flexion reflex is elicited on one

side by stimulation of the sole or by passive flexion of the toes, a
contralateral mass extension reflex may appear. This consists in ex
tension of the hip and knee and plantar flexion of foot and toes.
This reflex usually appears in abortive form, i.e., as plantar flexion
of the foot and toes or of the toes alone (Fig. 44, B).
b) On such unilateral stimulation, not the contralateral mass

extension reflex but the mass flexion reflex may appear and also in
the abortive form: there may be dorsiflexion of the big toe only.
c) In spastic hemiplegia, when the healthy leg is abducted or
adducted against resistance, a contralateral identical movement of
the affected leg may take place.
d) When the patient presses one extended leg downward, the
other has a tendency to rise, and vice versa.
The appearance of these phenomena is so capricious and in
constant that, from a practical neurological standpoint, they do not
deserve the attention given them in textbooks. Their physiological
significance, however, is great.
BABINSKI REFLEX
History
On Feb. 22, 1896, at the meeting of the Societe de Biologie de
Paris, the 39 year old Joseph Babinski described a reflex of dorsi
flexion of the great toe on stimulation of the sole. The same phe
nomenon had been described by the London physician Marshall
Hall in 1841, and by the Berlin neurologist E. Remak in 1893.
But it was Babinski who first realized the significance of this reflex.
The international literature on this little sign and its physiology is
tremendous, and to the Babinski reflex justly may be applied the
words of Mark Twain: "There is something fascinating about sci
ence. One gets such wholesale returns of conjectures out of such a
trifling investment of fact." The Babinski reflex did not immediately

gain recognition as a "pyramidal sign" or, let us say less specifically,
as an "upper motor neuron sign" that it now enjoys throughout the
world. German, French, American, Italian, Russian and Swiss au
thors thought its diagnostic importance to be "quite minimal." They
regarded this reflex as "inconstant," "uncertain," "without diagnos
tic value," and stated that they found it in hysterical patients.
Reported Methods of Elicitation

For Babinski, his reflex was essentially a plantar skin reflex, a
modification of the normal reflex: owing to a pyramidal lesion,
stimulation of the sole evokes not a plantar flexion but a dorsi-
flexion of the big toe. Now we know that it is more than this. The
dorsiflexion of the big toe is part of a complex reflex, namely, a
mass flexion reflex of the whole lower extremity. We know also
that this flexor mechanism springs into action on stimuli of many
kinds, not just on stimulation of the sole.
Here are some of the methods by which the Babinski reflex
has been elicited.
a) By stimulation of superficial sensibility: stroking the ball

of the foot, particularly the sulcus hallucis; stroking the inner side
of the big toe; pricking and stroking the dorsum or the lateral
margin of the foot; pricking the lateral aspect of the toes, of the
big toe; tapping the dorsum of the foot with the reflex hammer;
stroking the dorsal surface of the ankle, the skin around the exter
nal malleolus; thermal or electrical stimulation of the foot; strok
ing the lower part of the leg, thigh, inguinal region, abdomen,
chest, the whole side, including the face.
There is even a conditioned Babinski described: a stroking
movement in the neighborhood of the sole without touching it may
elicit dorsiflexion of the toe.
b) By stimulation of deep sensibility: pressure on the dorsum
of the foot over the fourth interosseus interspace; compression of
the plantar arch; release of pressure on the foot or sole; compres
sion of Achilles' tendon; pressure on the tibia, the fibula, the calf
muscles; depressing the patella distalward; pinching the adductor
muscles of the leg, the quadriceps; pressure on a testis, on abdomi
nal muscles, on the ribs; pinching and releasing a skin fold below
a transverse lesion of the spinal cord; pinching the thoracic mus
cles, the neck muscles; pressure on the eyeball; pinching the ear
lobes; pressure on the occiput.
c) By passive movements: shaking the foot; moving the foot;
bending one or all of the toes; tapping the plantar surface of the
toes, as in the elicitation of the plantar muscle reflex; abduction of
the little toe; pronation and supination of the foot; lifting of the leg
extended at the knee; inward or outward rotation of the leg at the
hip; flexion of the arm in all joints, beginning with the joints of
the fingers; tilting of the head.
d) By active movements: spreading of the little toe or toes
against resistance; plantar flexion or dorsiflexion of the foot; press
ing the homolateral or contralateral heel downward; flexion or ex
tension of the knee; flexion of the hip with or without resistance;
innervation of the abdominal muscles; attempt to rise from the
supine position; bending of the fingers against resistance; bending
of the head; yawning.
The list of these so-called "modifications" of the Babinski reflex
could be enlarged ad infinitum. Some of these modifications have
such fanciful names "joint," "paradoxical," "resistance," etc., re
as
flexes; "tibial phenomenon," "calf pressure phenomenon." Some

are adorned with single or double eponyms. Strictly speaking, there
are no modifications of the Babinski reflex; there is only one Babin
ski reflex but there are numberless variations of the technique of
elicitation of the dorsiflexion of the big toe.
Technique of Elicitation
The most reliable method is still the old method of Babinski.
The best results are achieved by the following technique.
The patient lies supine, relaxed, with legs extended. The Babin
ski reflex may be reversed when the patient lies prone, with legs
flexed. The foot should be warm; if it is not, it should be immersed
in warm water before examination or the patient should be asked
to walk first. Babinski kept a basin of warm water ready in his
examination room. Some prefer the leg fully extended. Some prefer
it slightly flexed at the hip and knee, and the thigh slightly rotated
outward. This does not make much difference; still, extension is
preferable. With one hand at the ankle, the examiner holds the
foot in place. To stimulate the sole it is best to use a toothpick, a
match, a blunt nail file, letter opener or the fingernail. Stroke the
outer border of the sole slowly from the heel upward. If the sole
is callused or the patient is ticklish, the outer border of the foot
should be stroked. Do not stroke the sole at the base of the big toe.
One should apply minimal stimuli which do not produce pain and
violent protective withdrawal of the whole extremity. Such move
ments may obscure the dorsiflexion of the toe. Gentle stroking will
avoid the elicitation of a movement other than that of the toes.
Repeat the strokes in quick succession, increasing the stimulus, try
ing first the outer edge of the sole, then the lateral border of the
foot.
of the Babinski reflex is the immediate, slow,
Characteristic
tonic dorsiflexion of the big toe and the slight spreading of the
other toes. Turning the head of the patient away from the paralyzed
side may facilitate the appearance of the reflex. To reinforce the
reflex, stroking of the sole may be combined with simultaneous
pressure on the tibia orwith compression of the calf muscles.
Of the numerous techniques for elicitation of the Babinski re
following may be mentioned in particular. As has been
flex, the
shown before, the homolateral mass flexion reflex of the lower ex
tremity can be elicited by passive flexion of the toes. It stands to
reason that, since the Babinski reflex is but a part of this mass re
in the same way. For this it is obviously
flex, it too can be elicited
necessary to flex not all the toes but only any one of the smaller
toes and let the big toe move unhindered. Thus forceful flexion,
snapping and sudden release of the second, third, fourth and fifth
toes singly or all four outer toes simultaneously will produce dorsi-
flexion of the big toe. It is sometimes advisable to keep the toe or
toes bent for 15 or more seconds. This is nothing else than a partial
homolateral mass flexion reflex. If a stronger and longer lasting
stimulus is used in flexing the smaller toes, not only isolated dorsi-
flexion of the big toe but other components of the mass flexion
reflex, such as dorsiflexion of the foot, flexion at the knee and hip,
come to the fore. This method gives good results but has no abso
lute superiority over the old method of Babinski, and the same can
be said for any other "modification" of the Babinski reflex.
Evaluation
In evaluating the significance of the Babinski reflex, the follow
ing points should be considered:
1. The Babinski reflex is present in the normal child during
the first year and often to the end of the second.
2. It may not be present in patients with definite, indubitable
lesions of the pyramidal tract, for instance, amyotrophic lateral
sclerosis.
3. Presence of the reflex does not mean destruction of the
pyramidal tract, as is sometimes maintained. The slightest damage
to the pyramidal tract is sufficient to produce it. The reflex may
appear transiently after drugs, infections, autointoxications, after
exertion, shortly after epileptic or artificially induced convulsions,
in sleep, in apneic conditions, during insulin coma.
4. The Babinski reflex is compatible with normal function of
the leg andwith complete absence of symptoms. It may be found
in people who have no complaint. Babinski himself once (1926)
showed me such a patient and said: "You see, the reflex is present,
yet the function of the leg is completely normal." This fact is of
particular importance in legal medicine.
5.The strength of the Babinski reflex has no bearing on the

severity of the lesion. Extension of the reflexogenous zone for the
Babinski reflex, for instance, its elicitation from the dorsum of the
foot and leg, may indicate a severe lesion of the spinal cord, but
not necessarily so. Nor is it a gauge of the severity of a cerebral
lesion.
6. Despite the great amount of investigative work that has
been done on the subject, the Babinski reflex does not in itself tell
anything about the place where, in the long course of the pyram
idal tract, the lesion lies. Nor is it even of help in differentiating
between a cortical and a subcortical lesion.
7. It is not possible to answer the question, why in some cases
the Babinski reflex is easier to elicit with one method than with
another. There is no valid reason to assume that this has any defi
nite localizing significance.
Physiology
The Babinski reflex is only a small integral fragment of the

mass flexion reflex with which the animal reacts to stimuli of many
kinds, when its pyramidal tract is damaged. The movements of this
mass reflex are preparatory to flight in the horizontal level,
flight
running, jumping; and in the vertical level, climbing. The move
ments have two main components. The first consists of shorten
ing of the extremity, with flexion at the hip and knee and
dorsiflexion at the ankle. This constitutes the first step in running,
jumping or climbing. The second component is the spreading of the
toes. This is an essential movement preparatory for running and
climbing. It increases the surface and friction of the sole and ren
ders more secure the hold of the foot on the running surface or on
the tree. Thus viewed, the fanning of the toes, described by Babin
ski in 1903, is more significant pathophysiological^ than the dorsi
flexion of the big toe. The opinion has even been expressed that
dorsiflexion of the big toe, unless associated with spreading of the

other toes, is consistent with an intact pyramidal system. If spread
ing of the toes is such an essential part of the "flight reflex" and if
this reflex is the basis for the Babinski reflex, the question arises:
Why does the great toe not abduct like the other toes? The answer
Fig. 48. BABINSKI REFLEX.

Spreading of the toes; dorsiflexion and slight abduction of the big toe.
is: the movement of the great toe ought to be abduction, and it was
so primarily in the earlier stages of phylogenetic development. But
in the course of this development, as the human foot adapted itself
more and more to the function of the erect position, the metatarso
phalangeal joint of the great toe gradually lost its ability to allow
a lateral movement of the toe and preserved only the essential up
and down movement. As far as the reflex is concerned, dorsiflexion
of the great toe has become a substitute for abduction, which is
performed but poorly. On stimulation of the sole, the great toe
should abduct like all the others. But the acquired configuration of
the joint prevents any major degree of abduction, and the big toe
performs the next best movement possible, that of dorsiflexion. On
careful examination one can sometimes observe this primitive tend
ency toward abduction, which is discernible despite the pronounced
dorsiflexion (Fig. 48).
GRASP REFLEX
This reflex is rare but, when unmistakably present, has a defi

nite and important value for the diagnosis of frontal lobe lesions.
The reflex, usually present on one side only, is tested in this way.
The patient lies on the healthy side; with an elongated object for
instance, the handle of the reflex hammer or his fingers the ex
aminer casually touches the patient's palm, preferably between
thumb and index finger. This maneuver should be made out of
sight of the patient. At the slightest touch, the patient grasps the
object and is unable to relax his grasp. He holds it firmly and con
tinues to do so even when the examiner tries to remove it. Any
attempt to pull the object away only increases the strength of the
grip. Sometimes it is even possible to raise the patient from the bed,
The grasp reflex may be spontaneous. The
so strong is his grasp.
recumbent patient holds tightly to anything within his reach. The
patient shown in Figure 49 was such a one. A woman, aged 30,
with bilateral athetosis, lying in bed, clung with all her might to
the blanket or sheet, seemingly in an effort to raise herself. At
times she clawed at the wall. While sleeping, she was found clutch
ing the blanket with both hands. She showed a grasp reflex on the
right side when anything touched her palm. Figure 49 shows the
position in which she was often found in bed, with fingers and toes
on the right holding firmly to the bed rail and pulling it forcibly.
Removed from this position, she assumed it again and again. This
is a spontaneous grasp reflex.
Besides the grasp reflex, there is sometimes another, a groping
reflex: when an object is removed from the patient's hand he tends
to grope after it. The hand follows the object as though magnetized.
The grasp reflex is pathognomonic for a contralateral premotor
FIg. 49. SPONTANEOUS GRASP REFLEX.

Lying in bed, the patient's right hand and foot spontaneously grasp the bed
rail with force, cling to it and hold it indefinitely. (From Wartenberg, R.:
Ztschr. ges. Neurol, u. Psychiat. 83:303, 1923.)
lesion, but at the same time the pyramidal tract must not be com
pletely destroyed. The reflex may also appear in lesions of parts of
the brain in the neighborhood of the frontal lobe. In hydrocephalus
the reflex may appear when damage has been done to the anterior
part of the brain in general. The grasp reflex is normal in infancy.
In adults it is due to an automatic subcortical mechanism released
by a lesion of the frontal lobe. It is best conceived as a release of
the act of climbing where grasping is essential.
SECTION IV
Extrapyramidal System
GENERAL
DISEASES of the central ganglia, of the extrapyramidal motor

system, though ill-defined, may be divided into two main groups:
(1) the choreatic group, in which hyperkinesias predominate, i.e.,
chorea, athetosis and dystonia, and (2) the Parkinson group, in
which rigidity and hypokinesis predominate. The striking hyper
kinesias of the choreatic group render the diagnosis comparatively
easy. Only a few diagnostic tests are applicable for this group.
Cases of the Parkinson group are much more common than those
of the choreatic group. In fact, next to multiple sclerosis and tu
mors, Parkinson's probably ranks as one of the most common dis
eases of the nervous system. The term "Parkinson" is used here as
a generic one and includes parkinsonian states of every origin.
Paralysis agitans is called idiopathic Parkinson's disease, while par
kinsonian states of other origin are called postencephalitic, post
traumatic, toxic, etc.
It is easy to diagnose a fully developed parkinsonian state of
any variety. However, it is sometimes difficult to diagnose incipient
or abortive cases, the so-called formes frustes. The insidious begin
ning and the slow course render the diagnosis in some cases particu
larly difficult.
156
EXTRAPYRAMIDAL SYSTEM 157
The differential diagnosis, too, may not be easy, since many and
diverse conditions come into consideration: degenerative and non-
degenerative diseases of the brain, intoxications, arthritis, neuroses.
Cerebellar tremor may be particularly difficult to distinguish from
Parkinson tremor. Mistakes on this score are bound to occur. Still,
the diagnosis should and can be made on purely clinical grounds.
What is the outstanding characteristic of a parkinsonian state
that can serve as a basis for early diagnosis? As we have seen, the
outstanding characteristic in pyramidal lesions is associated move
ments. In Parkinson's it is rigidity. There is Parkinson's dis
disease
ease without tremor, but there is no parkinsonian state without
rigidity. And if there is no rigidity, Parkinson's disease should not
be diagnosed. If a person has tremor which closely resembles that
of Parkinson's disease but has no rigidity, the tremor is not parkin
sonian but most probably cerebellar.
Ithighly significant that rigidity, the leading sign, starts very
is
early in this disease and first of all affects the neck and shoulder
muscles. Several tests are based on this fact.
HEAD DROPPING TEST
The patient, lying supine on the examining table, is made to

relax as much as possible. The surface on which his head rests
should be padded, but no pillow should be used. The patient is
asked to close his eyes and his attention is diverted. He should not
try to raise his head from the table. The examiner places one hand
under the patient's occiput, the dorsum of the hand resting on the
table, so that the patient's head rests on the examiner's palm.
Suddenly, unexpectedly, and briskly, the examiner with his other
hand lifts the patient's head and drops In the normal individual,
it.
the head drops immediately, with force and momentum as dead

a
weight, as there were no tonus in the neck muscles at all. The

if
sharp impact of the falling head and the inertness of the fall are
very striking. The test should not be evaluated unless the patient is
completely relaxed. In any case, the test should be repeated several
times, and the heaviest drop is the one that counts.
In this test the most striking change from the normal is seen
in Parkinson's disease, even in its earliest stages. Here the drop of
the head is merely a "downward movement," slow, deliberate, al
most reluctant. It maintains an even flow from beginning to end,
like a rigid extremity being stretched. Not only by sight, but by
Fig. 50. HEAD DROPPING TEST.

Advanced case of Parkinson's disease. Rigidity of the neck muscles and flexed
position of the head the basis for this test are so marked here that the pa
tient, lying supine, keeps his head off the supporting surface indefinitely.
touch as well, can the examiner appraise the character of the head
drop. In the normal subject, the impact upon his hand is sharp,
with a resounding slaplike note; in Parkinson's disease the drop is
slow, dull and almost soundless. This test is decisive in the differ
ential diagnosis of Parkinson's versus senile tremor. In senile tremor
the head drops normally. The test has never failed to be of help in
differential diagnosis of Parkinson's disease. Here it has proved
superior to any other test.
Figure 50 clearly illustrates the physiological basis for the head
dropping test in Parkinson's disease: the flexed position of the head
caused by rigidity of the neck muscles. In advanced stages it is so

pronounced that when the patient is asked to lie supine, he keeps
his neck flexed and his head off the surface indefinitely.
The characteristic response to the head dropping test in Parkin
son's disease is seen also in other extrapyramidal affections in which
there is a rigidity of the neck muscles, i.e., hepatolenticular degen
eration, striatal torticollis, pallidal degeneration, and others.
Although in Parkinson's disease the changes in head dropping
are marked, they are minimal in pyramidal lesions, even when these
lesions are bilateral and involve the corticocervical tracts. Here head
dropping may show some elastic resistance, but is not essentially
affected. In of amyotrophic lateral sclerosis or diffuse hyper
cases
tensive encephalopathy there may be signs of brain involvement
such as a head retraction reflex or a snout reflex. Yet the head drop
ping test may be essentially normal. This normal finding helps to
differentiate between pyramidal and extrapyramidal lesions and to
assess the extrapyramidal component in mixed affections. When the
dropping of the head is slow in a patient with a brain lesion with
pyramidal signs, it points to concomitant involvement of the extra
pyramidal motor system.
TEST FOR PENDULOUSNESS OF THE ARMS
It is a truism that no neurological examination is complete un

less a record of the gait is included. The examiner should observe
how the patient walks at different speeds, on his toes, on his heels,
with knees bent, backward, around a chair and in the "tight rope"
position along a straight line with his arms horizontally abducted.
He should note how the patient stops quickly; how he turns around
quickly. It might even be advisable to begin the examination by
observing the patient's gait. Pathological gait may lead at once to a
certain line of diagnostic thought. The final diagnosis may to an

amazing degree be influenced by observation of the patient's gait.
Here we are concerned with but one facet of the gait which is often
overlooked: the swinging of the arms.
Parkinson's disease early and markedly reduces the automatic
pendulousness of the arms in walking. This is most conspicuous in
unilateral Parkinson's disease and may be a decisive factor in the
diagnosis. To examine for pendulousness of the arms, the patieat
should walk where he has more space than in the usual examining
room, for instance, in a hall. Heavy outer garments should be re
moved. The patient should hold nothing in his hands. He should
be asked to walk at different speeds. If some anomaly is found, the
examination should be extended or repeated at another time. It is
surprising how often changesin pendulousness of the arms are
found at first but cannot be confirmed later. Only deviations found
on repeated examinations are of value, but their value is funda
mental.
Since in the examination for pendulousness of the arms thf ex
cursion is all-important, this can be appraised more easily if the
examiner, keeping pace with the patient, walks abreast of him and
watches him from the side. The degree of pendulousness is best
judged by noting the forward excursion of the arms. This can be
seen more distinctly from the side. Every person has his character
istic pendulousness of the arms in walking. It varies both in charac
ter and in range from person to person. It is of no particular
importance if the range is short on both sides, unless there are other
definite signs of Parkinson's disease. More important is the differ
ence in range between right and left. In Parkinson's disease, pendu
lousness of one arm, particularly the forward excursion, may be
diminished very early. For some time this may go unnoticed by the
patient. A peripheral or a pyramidal lesion affecting the side with
the diminished range can easily be excluded. No other disease of the
nervous system reduces the pendulousness so early and so obviously
as does Parkinson's disease.
SHOULDER SHAKING TEST
The examiner, facing the standing patient, places his hands on

the patient's shoulders and moves them with brisk jerks alternately,
to and fro, around the long axis of the body. He varies the force,
range and intervals of the jerks. Swinging of the patient's arms re
sults. In unilateral Parkinson's disease, swinging is diminished on
the affected This test enables us to appraise the diminution
side.
quantitatively, to some degree. Keeping the movements of both
shoulders equal, the examiner gradually and slowly reduces the
force and range of the jerks. Thus the shoulder motion, and with it
the pendulousness, diminishes. In unilateral Parkinson's disease, the
examiner reaches a point when only one arm swings, while the
other remains static. The arm that swings is normal, or less affected.
Another technique of shoulder shaking sometimes gives even
better results: instead of rotating the patient's shoulders, the exam
iner gently rocks them back and forth. Here the movement is not
alternate, right and left, but both shoulders are moved simultane
ously in the same direction. This produces simultaneous swinging of
both arms in the same direction. The arm that describes the greater
excursion is the healthy one or the one less affected.
The shoulder shaking test is useful to confirm the findings of
pendulousness of the arms in walking or, in doubtful cases, of help
in making a diagnostic decision.
ARM DROPPING TEST
This test, too, helps in the diagnosis and quantitative appraisal

of parkinsonian rigidity of the shoulder muscles. With both arms
hanging loosely by his sides, the patient stands before the examiner.
The patient is made to relax his arms as much as possible. The ex
aminer slides his hands between the patient's trunk and arms, so
that the dorsa of his hands touch the inner surfaces of the patient's
wrists. The attention of the patient is diverted. Suddenly and un
expectedly, with a quick, forceful outward movement of both his
arms simultaneously, the examiner throws the patient's arms up
ward and allows them to drop, meanwhile bringing his
quickly
own hands back to their former position at the patient's flank. The
examiner's hands receive the impact of the patient's arms as they
fall. Thus the examiner can see, feel and hear the difference in the
way the arms fall. In unilateral Parkinson's disease, the fall of the
arm on the affected side is retarded. It hits the examiner's hand less
heavily, less inertly and the sound is duller than that on the normal
side.When this test is compared with the head dropping test, one
has the impression that in Parkinson's disease rigidity of the neck
muscles exceeds that of the shoulder muscles.

This test has been discussed in the sections dealing with the
peripheral and the pyramidal system. It has been shown that in a
lesion of the peripheral nervous system, the pendulousness of the
affected leg is increased. It has also been shown that in a pyramidal
lesion the affected leg does not swing in a straight line to and fro
asin the normal subject but carries out a somewhat circular motion.
This constitutes a valuable pyramidal sign.
In Parkinson, pendulousness is altered in a quite different way.
The patient sits on the examining table with his legs hanging freely
over the edge of the table. When the examiner lifts the patient's
legs and drops them, they swing to and fro. In Parkinson, this
swinging is of extremely short duration. It is particularly conspicu
ous in unilateral Parkinson's disease. When both legs are simul
taneously lifted to the same level and allowed to drop, the leg on
the affected side stops swinging almost at once, whereas the healthy
leg continues to swing. In far advanced cases, this pendulousness
may be completely abolished. However, in contrast to what is seen
in pyramidal lesions, in Parkinson's disease the swinging legs move

in a straight line, strictly in a sagittal plane, and never sidewise.
This disease shortens the swinging time of the legs with such regu
larity, and so definitely, that it can be said without reservation: if a
patient shows normal head dropping and normal pendulousness of

the legs, Parkinson's disease of any type can be excluded. Diagnos-
tically it is highly significant that in unilateral Parkinson's disease,
diminished pendulousness of the leg may be the only manifestation
of involvement of the lower extremity. The leg may give the patient
no reason for complaints, it may show no defect in function, no
other sign of Parkinson's disease may be present and still the
pendulousness may be diminished and by itself indicate the spread
of the disease to the lower extremity. This statement is based on
many observations.
PUSH TEST
The patient with Parkinson does not change positions readily.

This is the basis for the push test, which is carried out in the follow
ing way. The patient stands erect. The examiner, his fingers on the
patient's sternum, pushes him gently backward. The patient should
not be thrown completely off balance. In order to preserve his equi
librium and not fall backward, a normal person innervates the
dorsiflexors of the toes and feet. First he lifts the big toe slightly
from the floor and then the other toes, according to the strength of
the push. He shifts his weight to the heels. When the push is
stronger, the tension in the dorsiflexors of the toes and feet, par
ticularly the tibialis anterior, becomes greater and the contraction
of the muscles may extend upward to the quadriceps and the ab
dominal muscles. But with a slight push, only the dorsiflexors of the
toes and feet come into action. This does not occur in patients with
Parkinson's disease. The feet remain flat on the floor. The toes are
not elevated, and the tendons do not become prominent, or only
slightly The action of all the muscles in this push test is ex

so.
tremely retarded and diminished. This is particularly well seen in

unilateral Parkinson's disease and can serve as an aid in diagnosis.
FIXATION OF POSITION TEST
A patient with Parkinson's disease tends to fix his limbs in

any new position he assumes and to maintain that position for an
excessive length of time. When points of origin and insertion of a
muscle are passively approximated, the muscle contracts and re

mains in the state of tension. Shortening of the muscle acts here as
a stimulus for tonic contraction. This does not occur in the healthy
person or with lesions of the pyramidal, cerebellar or peripheral
nervous system. This phenomenon can be demonstrated in any
muscle but is best seen in the biceps.
To perform the fixation of position test on the biceps, the ex
aminer places his thumb on the patient's biceps tendon and, with
the other hand, in jerky movements passively bends the patient's
forearm. He holds it in flexion for a few seconds. The examiner
feels the biceps tendon become tense under his thumb and sees it
become prominent. This test can also be shown on the foot, where
it was first demonstrated by Westphal in 1877 as "paradoxic muscle
contraction." The examiner dorsiflexes the patient's foot. When he
removes his hand, he can observe that the tendon of the tibialis
anterior muscle has become tense and prominent, and the foot re
mains in dorsiflexion for some time. Then very slowly it drops
plantarward. The fixation of position test can also be shown in the
extensors of the wrist. The examiner passively dorsiflexes the pa
tient's hand and then lets it go. The patient keeps the hand in
extension for some time, and only slowly does the hand resume the
normal position of volar flexion. This test is very interesting physio
logically, but in practical diagnosis is only confirmatory. The degree
of rigidity of the palpated tendon is a matter of subjective appraisal.
ARM DEVIATION TEST
It of the extrapyramidal motor system

seems to be the function
to inhibit the inward movement of the extremities. When this sys
tem is damaged, adduction prevails. This is the physiological basis
of the arm deviation test. In Parkinson, when the patient stretches
his arms horizontally in front of him and closes his eyes, the arms
have a tendency to deviate slowly inward and downward. Even
patients with severe tremor show the tremulous hands moving in
ward and downward. In some cases this is very pronounced. How
ever, it is by no means constant and is seen clearly only in cases of
severe postencephalitic Parkinson's disease.
MICROGRAPHIA
It must be assumed that there is a definite physiological antag

onism between the cerebellar and the extrapyramidal motor system.
This documents itself, among other ways, in the difference in size
of handwriting. Patients with cerebellar lesions tend to write large
characters, and the amplitude of their strokes tends to increase. The
patient with extrapyramidal disease, particularly Parkinson, on the
contrary, tends to decrease the size of his characters, so that they
constantly become smaller, or he begins with small characters and
continues to write in the same manner. As there is macrographia in
cerebellar disease, so is there micrographia in Parkinson's disease.
TESTS FOR TORTICOLLIS
General
Formerly it was assumed that every spasmodic torticollis, the
disease characterized by involuntary movements of the neck muscles,
was a psychogenic affection. The French had a word for torti
it,
collis mental. Now can be regarded as an established fact that

it
torticollis can be of. organic origin, caused by a lesion of the extra

pyramidal motor system. This lesion is usually degenerative or en-
cephalitic. Torticollis as a component of a postencephalitic extra
pyramidal syndrome is not uncommon. The fact that torticollis may
be the first and, for some time, the only manifestation of a more
diffuse extrapyramidal lesion, namely torsion dystonia, is of great
diagnostic importance. Peculiar to this disease is the fact that it may
FIg. 51. TORTICOLLIS. Retrocollis.
affect the neck muscles first or most severely. The movements of the
head are usually sideways. Backward movements retrocollis (Fig.
51) are rare.The muscles of the pelvic girdle, too, may be af
fected, and tortipelvis result. Torticollis and tortipelvis are best
regarded as athetosis of a certain localization. The distal parts of the
extremities, the hands and feet, are rarely affected. Extrapyramidal
torticollis deserves to be better known to the physician. It is rarely
diagnosed correctly, and patients are subjected to long and intensive
psychotherapy and costly psychoanalysis.
The existence of extrapyramidal torticollis should not lead us
to the other extreme denial of the existence of psychogenic torti

collis. Both types occur and must be strictly differentiated. When
mistakes are made, it is usually the extrapyramidal torticollis which
The differential diagnosis of extrapyram
is considered psychogenic.
idal from psychogenic torticollis is generally easy. Psychiatric ex-
Flg. 52. TORTICOLLIS. Beginning stage.
amination revealing the history, the beginning and the course of the
disease and, further, the theatrical manifestationsof psychogenic tor
ticollis usually provide the clue. The patient and his family, in their
quest for a cause of this puzzling condition, often unconsciously
falsify the history to relate the beginning of the disease to some
external happening, usually of an emotional character. All the more
so, since the disease often strikes in puberty, the time of conflicts.
However, on careful and critical analysis this motivation proves
168
169
woefully inadequate. Extrapyramidal torticollis develops slowly, in

sidiously, and at the beginning the motor movements are inconspic
uous and not impressive (Fig. 52). This is particularly true when
an extremity is first involved. This lack of impressiveness speaks
against a hysterical origin. Later the violent, strong movements are
too uncomfortable to be hysterical (Fig. 53). When hysterical pa
tients want to show the world their illness, they are very choosy in
their technique. They do not demonstrate anything that will be very
uncomfortable for them. And the movements of organic spasmodic
torticollis certainly are.
The coexistence of signs of extrapyramidal involvement in an
area outside the involved neck muscles is very helpful in the diag
nosis of organic torticollis. The arm on the side to which the head
is turned is sometimes involved early. If this arm shows the slightest
extrapyramidal sign, the diagnosis is clinched (Fig. 54).
There are few special tests for organic torticollis. They are not
always positive. Their mechanism is poorly understood but is of
great physiological interest. These tests are based on the fact that
some stimuli can automatically, reflexly inhibit or relieve the spas
modic movements of torticollis.
COUNTERPRESSURE TEST
This test is based on the so-called counterpressure phenomenon.

It is best seen in dystonia involving the distal parts of an extremity.
Take, for instance, a dystonic mobile spasm of the flexors of the
hand and fingers. On account of these spasms, the patient is unable
to dorsiflex his hand and fingers on command. When asked to do
this, not only is he unable to perform this movement but there is a
"derailment" of the impulse: the patient, instead of extending his
hand and fingers, flexes them still more. But when the examiner
holds his fingers against the dorsum of the patient's fingers and
then asks the patient to dorsiflex his fingers and hand against the
resistanceof the examiner, the patient can easily perform this move
ment. This is a paradoxical phenomenon in that the movement can
only be performed against resistance, when counterpressure is ex
erted. The same occurs in torticollis. The patient's head turns to one
side by continual spasmodic contractions of the neck muscles. On
command, he is unable to turn the head to the other side, or he
performs this movement imperfectly and is able to keep the straight
position only for a very short time. He can, however, perform the
desired movement -and keep his head straight for a longer period if
he himself opposes this movement with his fingers. The counter-
pressure he exerts need be only very slight. This is the basis for
many puzzling maneuvers which patients discover for themselves
to alleviate the spasmodic movements. To the uninitiated, these
maneuvers seem to prove that torticollis is psychogenic.
Test of Resistance Movement

In torticollis the patient's head is pulled, let us say, to the
right; he is unable to keep his head straight on command. But when
his left shoulder muscles are lifted actively and with force, when they
are abducted or adducted against resistance offered by the examiner,
the patient is able simultaneously to straighten his head. As soon
as the resistance ceases, the patient's head snaps back into the
twisted position. But only the innervation of neighboring muscles is
helpful. Innervation of remote muscles is ineffective. Only forceful
movement against resistance is effective.
Dystonic movements, including torticollis, may also be influ
enced by other, sensory stimuli, e.g., those affecting the deep sensi
bility in neighboring But such tests are less effective than
areas.
the counterpressure test and the test of resistance movement.
SECTION V
Cerebellar System
GENERAL
ALTHOUGH objections may be raised against any gross gen

eralization, it still can be maintained that the cardinal disturbance
in cerebellar lesions is dyssynergia, i.e., lack of co-ordination. This
means that the various muscle groups of the body do not collabo
rate normally in time, speed and strength, when a movement is
attempted which requires collaboration of many and distant groups
of muscles. We see this in gross movements, as when the patient
stands, walks, bends or moves a whole extremity. Dyssynergia is
further manifested in defective collaboration of neighboring muscle
groups, when a simple movement is performed, such as pronation
and supination of the forearm.
Of the numerous expressions of dyssynergia, two in particular
deserve to be stressed: (1) decomposition of movement, and (2)
hypermetria.
A complex body movement is decomposed when one compo
This happens through no fault
nent fails to participate normally.
of its own. There may be no lesion of the executive organ; the
nerve-muscle unit is intact; there is no paralysis, no tonus change,
yet the limb fails to collaborate with the rest of the body. Here
the fault lies only in defective transmission of innervation signals
172
CEREBELLAR SYSTEM 173
to auxiliary and subauxiliary muscle groups. For instance the nor

mal person, bending backward, simultaneously flexes his knees and
thus keeps his balance. Bending his trunk backward, the cerebellar
patient keeps his legs stiff and is in danger of falling. Yet there is
no local lesion affecting the flexors of the knees. In unilateral cere
bellar disease, the affected arm does not perform the normal pendu-
lar movements when the patient walks. Yet the motility of the arm
is normal. The disturbance lies only in the defective collaboration
of the arm with the other extremities.
Hypermetria only one part of the broader disturbance of
is
movement called dysmetria which is seen in cerebellar affections.
In dysmetria, generally speaking, the movement is not appropriate
or accurate in range, route or speed. The patient with cerebellar
disease does not follow the axiom that "the shortest distance be
tween two points is a straight line." Hypermetria is seen in walking,
where the up and down movement of the leg is excessive. It is also
manifest in movements on command, in which the performing
limb overshoots the mark. The hypermetria documents itself pre
dominantly in a striking tendency to hyperflexion. The lower ex
tremities are much more affected than the upper. Tests for cerebellar
function are based essentially on dyssynergia, decomposition of
movement and hypermetria.
When the diagnostic significance of cerebellar tests is evaluated,
one should always keep in mind the fact that all signs of cerebellar
deficit become less evident as time passes. Typical signs are found
only in acute affections of the cerebellum. In no other system does
compensation work as vigorously as in the cerebellar. This is true
both of man and of the experimental animal. It must be assumed
that there are brain centers which can take over functions of the
cerebellum. Practically, this means that even the most dependable
cerebellar sign, present in an acute lesion, may not be present in an
old one.
TESTS FOR HYPERMETRIA
Arm stopping The patient is asked to raise his arms and

test.
to hold them in the vertical position. Then he is asked to lower
them quickly to the horizontal position. The cerebellar arm stops at
a lower level than the normal one.
Line drawing test. The examiner draws two vertical lines on
either paper or blackboard and asks the patient to draw a horizontal
line connecting them. The cerebellar patient starts correctly but
draws beyond the confines of the second vertical line.
Hyperpronation test. The patient stretches his arms in front of
him horizontally, palms up. He is then asked to pronate both fore
arms. On the affected side, the pronation is much more extensive.
Knee bending test. The patient, lying supine, is asked to bend
his knees. On the cerebellar side the bending is more excessive. Or,
the healthy knee is passively bent and the patient is asked to bring
the cerebellar knee to the same angle. His tendency is to overflex it.
Heel-knee test. The patient, lying supine, is asked to lift one
heel and place it on the other kneecap. In doing so, the patient lifts
the heel too high, flexes the knee too much and touches the thigh
far above the patella. On successive trials he may correct this and
reach the patella directly.
Although the patient with cerebellar disease is generally in
clined to pass the point at which he is aiming, it may also happen
that he stops before the goal is reached. To prevent hypermetria, he
exhibits hypometria. This is seen particularly in rapid movement
and can be regarded as overcompensation.
ARM TAPPING TEST
The patient, facing the examiner, stands with his arms out
stretched horizontally. The examiner suddenly and briskly taps both
arms at the wrist downward with the same force, either simultane
ously or one after the other. On the cerebellar side the displacement
caused by this tap is much greater, and the arm swings up and
down for a longer time in flail-like fashion. On the healthy side the
displacement is less and the arm comes to a standstill earlier. On
the affected side hypotonia and dyssynergia bring about more ex
cessive and longer swingingof the displaced arm. The shoulder
muscles the agonists and the antagonists fail to stabilize the dis
placed extremity as quickly as they do in the normal.
AGONIST-ANTAGONIST TEST
This term is better than "adiadochokinesis," which is Greek and
remains so to most of us. The test is most valuable to uncover cere
bellar deficit. Here cerebellar dyssynergia documents itself dras
tically. In performing rapid agonistic and antagonistic movements,
the muscles involved do not work as smoothly and efficiently as in
the normal. With each arm separately, the patient is asked to per
form pronation and supination as rapidly as possible. In evaluating
the test, one has toallow for the fact that the ability to perform
agonistic and antagonistic movements in brisk succession differs
from one person to another, and that normally there may also be
considerable difference between the movements on the right and on
the left. On the affected side, alternating movements of pronation
and supination are performed slowly, awkwardly and irregularly.
The interval between pronation and supination is longer; a move
ment may cease abruptly; the antagonists may not relax rapidly
enough; the rhythm of movement is disturbed and conspicuously
jerky. The patient performs unnecessary, adventitious movements.
The elbow is not properly steadied; the whole arm may participate.
The cerebellar deficit is brought clearly to the fore when there is no
involvement of other systems: no weakness, no pyramidal spasticity
or extrapyramidal rigidity. When there is an associated involvement
of other systems, evaluation of the test is difficult.
ARM DEVIATION TEST
The cerebellum assists in adduction and flexion of the extremi

ties. The extrapyramidal motor system assists in abduction and
extension of the extremities. These two systems are antagonistic.
When one system is damaged, the other system has the upper hand,
and its functions predominate. Thus, when the cerebellar system is
damaged, adduction and flexion of the extremities are inhibited,
abduction and extension of the extremities prevail. The abductor
tonus outweighs the adductor tonus. This is best seen in the upper
extremities. On this fact is based the arm deviation test, particularly
valuable in diagnosis of cerebellar affections.
The examiner and the patient stand facing each other, their
arms outstretched horizontally in front of them, their finger-tips in
contact.The patient closes his eyes. The examiner removes his sup
port but allows his fingers to retain their position and remain im
mobile. He watches whether one or both of the patient's arms
deviate,' in which direction. It may be advisable to ask the
and
patient, when he closes his eyes, to move his arms from the hori
zontal to the vertical position and back, up and down several times.
The deviation may be stronger when the test is performed as a
kinetic rather than a static test. On the side of the cerebellar lesion,
the patient's arm tends to deviate out and up. Sometimes it may
deviate out and down, but the most characteristic movement is out
ward (Fig. 55).
Whether up or down deviation depends on a lesion of the

anterior or posterior lobe cannot be decided with certainty, but is
of no great practical importance. Although the upward deviation
may be regarded as characteristic of cerebellar lesions, deviation
downward certainly occurs. The unilateral deviation outward is
often very striking. Patients have been observed in whom arm devia
tion was the leading sign and decisive for the diagnosis. Pronounced
Fig. 55. ARM DEVIATION TEST.
A and B, in olivopontocerebellar atrophy. A, position of patient's and ex
aminer's hands at beginning of test. B, examiner breaks contact with patient's
fingers, and patient's left arm deviates outward. C, in lateral bulbar syndrome;
occlusion of left posterior inferior cerebellar artery. Left arm deviates outward
slightly.
177
deviation is seen in cerebellopontile angle tumors and olivoponto
cerebellar atrophy. This test may help to differentiate cerebellar
from parkinsonian tremor. The test may be helpful also in the di
agnosis of chronic cerebellar degeneration, of which there are many
varieties. This disease is not uncommon, but its diagnosis particu
larly in the early stages may be extremely difficult; characteristic
are its insidious development and the triad of cerebellar speech,
ataxic gait and ataxic writing.
FINGER SPREADING TEST
The sign revealed in this test was observed in but a single

patient. However,- it was so constant on repeated examination and
under such a variety of arrangements that it is worthwhile report
ing. All the more so, since physiologically it seems significant. The
patient had multiple sclerosis with cerebellar and pyramidal signs
on the right side and astereognosis of the right hand. When asked
to press down on a solid object with all his strength, he invariably
spread his fingers on the affected side and, in particular, moved his
little finger outward (Fig. 56). Since in cerebellar lesions the ab
ductor tonus predominates, the deviation of the affected extremity
is almost always outward; since spontaneous abduction of the little
finger is also seen in cerebellar lesions, a positive finger spreading
test may be regarded as a cerebellar sign.
FINGER-TIPS IN THE MIDLINE TEST
In unilateral cerebellar disease, the tendency of the affected arm

to deviate outward is demonstrated in the following way. The pa
tient, with his eyes closed, is asked to stretch his arms and to bring
his right and left middle finger-tips together in a wide arc in front
of him. The finger-tips of the normal person meet exactly in the
midline; the affected arm of a patient with a cerebellar lesion lags
behind and does not reach the midline. Consequently the middle
finger-tip on the healthy side goes far beyond the midline in order
to meet the lagging finger-tip of the hand on the affected side.
Fig. 56. FINGER SPREADING TEST.

Patient with pyramidal and cerebellar signs on the right. A, patient puts his
fingers over a stick. B, when forcefully flexed the fingers on the affected right
side are automatically abducted.
SHOULDER SHAKING TEST
In Parkinson's, as in other extrapyramidal diseases, the rigidity

affecting the shoulder muscles may early lead to diminished pendu-
lousness of the arms in walking. When this diminution is unilateral,
it becomes a most valuable sign of incipient Parkinson's disease.

However, diminished pendulousness on one side may not be due
only to extrapyramidal rigidity. It may be due to an ipsilateral cere
bellar affection. The lesion leading to this diminished pendulous
ness may lie either within the cerebellum itself or in the restiform
body. This structure may have been damaged by brain concussion.
Since each cerebellar hemisphere is under the influence of the con
tralateral frontal lobe, diminished pendulousness of one arm in
walking may also be due to a lesion of the contralateral frontal
lobe. Whether the cerebellar involvement be direct or indirect,
there is on the affected side no rigidity as in extrapyramidal disease,
but cerebellar hypotonia instead. Still, the affected arm swings less.
Watching the patient's gait, one cannot say whether the diminished
pendulousness stems from an extrapyramidal or from a cerebellar
lesion. The diminished pendulousness appears the same whether the
patient has, for instance, incipient Parkinson or a cerebellopontile
angle tumor. But the physiological mechanism involved is not the
same. Extrapyramidal lesions diminish pendulousness through rigid
ity of the affected muscles. Cerebellar affections produce diminution
of pendulousness through "decomposition of movement." Here the
arm, though hypotonic, does not move synchronously with the con
tralateral leg in walking, because of cerebellar dyssynergia, i.e., the
lack of co-ordination of movements among different parts of the
body.
If a patient shows diminished pendulousness of one arm in
walking, the shoulder shaking test will decide whether this is extra
pyramidal or cerebellar in origin. In this test (described on p. 161),
the examiner, with hands on the patient's shoulders, rotates him
briskly on his vertical axis, alternately to and fro. Swinging of
the arms results. In Parkinson, of this swinging is dimin
the range
ished on the affected side. It is normal or increased in affections of
the cerebellum. As is true of all signs of cerebellar deficit, the dimi
nution of pendulousness of the arm in walking becomes less and

less evident as time goes on, since some compensation takes place.
MACROGRAPHIA
In cerebellar affections there is a tendency for movements of the
extremities to be expansive, to overshoot their mark. This is clearly
shown in the writing of the cerebellar patient, who uses large
characters which may become even larger as he continues to write.
These overexpansive movements may lead him to break the point
of his pencil and to tear the paper. This is the exact opposite of the
micrographia seen in extrapyramidal affections, particularly in
Parkinson's disease, a further proof that the effect produced by cere
bellar diseases is the opposite of that of extrapyramidal diseases.
TESTS FOR ATAXIA

There are numerous tests to demonstrate ataxia in cerebellar
disease.They are too well known to bear repetition. However, the
following two techniques deserve brief mention. In examining for
ataxia of an arm, it is worthwhile to put a long rubber band around
the patient's wrist. One end of the band is held by the examiner.
The ataxia may become manifest more easily if the movement is
performed against the resistance offered by the rubber band. For
ataxia of the leg, the following simple test is the best. The patient
lies supine and is asked to raise an extended leg slowly and to re
turn it slowly to its original position. In cerebellar ataxia, the move
ment of raising is not performed in a straight line. The leg moves
sideways and rotates outward or inward. It is brought in a jerky
motion from one position to another. At its maximum height it
wavers, particularly sideways. The downward movement takes a
lowering is not performed smoothly, and the foot
zig-zag course;
may hit the surface with great force and often miss its initial
position.
DISCREPANCY TRIAD IN MULTIPLE SCLEROSIS
Cerebellar functions should be particularly tested when there is

a suspicionof multiple sclerosis. In this disease, cerebellar signs may
appear early and play an important role in the clinical picture. The
famous triad of Charcot nystagmus, intention tremor, scanning
speech leans heavily on the cerebellar aspect of multiple sclerosis.
There has always been a tendency to squeeze the semeiology of a
triad. It
is,
common disease into a however, difficult to condense
the diverse clinical features of multiple sclerosis into any triad.
If
this must be done, the following triad, though more general,
is
more helpful than that of Charcot. based on
It
diagnostically
is
discrepancies in the clinical picture of multiple sclerosis rather than
on any particular signs of this disease, which does not lend itself to
any schematization of semeiology. This discrepancy triad does not,
strictly speaking, consist of tests. "smuggled in" here because
It
is
of the importance of multiple sclerosis in neurological practice.

The first discrepancy, disproportion or incongruity, between
objective signs and functional Judging from the signs, we
defect. is
expect much greater disturbance of function than we find. The

a
by
defect much less serious than were caused gross macro

if
is
it
scopic lesion. A patient may have definite signs of hemiplegia and

still be able to use his affected hand or leg well; he may even be
unaware of any change. Or patient, aware of his hemiplegia, may
a
declare that his other leg "all right." Yet on examination, this
is
leg, while not showing any gross functional abnormality, may show
Babinski reflex.
a
The second discrepancy between clinical signs and general or

is
local manifestations. The latter may be lacking or may fall short

of This incongruity
one's expectations. seen particularly in the
is
acute onset of multiple sclerosis or in acute exacerbations of the

disease. The patient may have severe and extensive hemiplegia or
complete paraplegia of the lower extremities and yet may not show
any corresponding general or local signs and symptoms such as one
might find were the underlying lesion not a patch of multiple scle
rosis but a macroscopic one, i.e., tumor, hemorrhage, thrombosis.
Multiple sclerosis patients have been seen with severe hemiplegia
or paraplegia alone without any symptom attributable to the site
of the lesion, such as sensory disturbances. In many instances this
differential consideration has proved very helpful.
The third discrepancy is between the attitude of the patient and
his physical defects. He does not express the complaints one would
expect in view of the effects of the disease. There is a peculiar lack
of concern regarding his incapacity. Patients with similar functional
defects arising from other neurological disturbances are much more
concerned about their condition. The often striking indifference and
aloofness the multiple sclerosis patient shows toward his disease is
due to the fact that he has, withal, an actual feeling of physical
well-being.
SECTION VI
>ensory System
GENERAL
The two fundamental and immutable laws for examination of

sensibility are: (1) Never suggest anything in any way to the
patient. (2) Never deceive yourself.
Every physician is apt to forget the tremendous power of sug
gestion his words and actions exercise upon the patient. The patient
believes that a doctor knows everything and knows it better.
Seeking aid, the patient often wishes to avoid contradicting his
physician, and will affirm the doctor's questions, answering them in
the way which he thinks will please the physician. An adroit exam
iner, using an appropriate technique, can extract from a gullible
patient practically any history he desires. The patient, the true "yes
man," will answer anything the doctor seems to expect. The doctor,
for example, suspects myasthenia. In order to round out his diag
nosis, he needs the symptom of fatigability. So he bombards the pa
tient with highly suggestive questions regarding fatigability. Finally,
the patient confesses to it. Critical examination proves there is none,
nor is there myasthenia.
The patient is particularly open to suggestion while his sensi
bility is being tested. The examiner's slightest and most harmless
remark may result in fancied sensations felt by his patient. The
184
SENSORY SYSTEM 185
more .complete the sensory disturbances, the more profound, for

instance, the analgesia, the more likely are they to be iatrogenic,
i.e., caused by the physician. Some neurologists maintain that 90
per cent of massive disturbances in sensibility are psychogenic.
In testing the sensibility, the examiner is apt to deceive himself
and thus make grievous mistakes. This is particularly the case when
he starts the examination with some preconceived idea about its
results or arrives at hasty conclusions before the examination is
complete. Examination of the sensibility requires the utmost objec
tivity, sober impartiality and .... patience.
Once the changes in sensibility are mapped out on the patient's
skin, particular care should be taken in transferring these markings
to the printed sensibility chart. Such charts show segmental or
peripheral nerve areas. The danger is that the original boundaries
made on the skin may be changed unconsciously in order that they
conform to the schematic chart. Therefore it is better to indicate
the sensory changes on a simple outline figure of the human body
and not use a schematic chart showing the sensory areas.
TECHNIQUE OF EXAMINATION
In examination of sensibility for touch, the following must be

considered: the stimulus applied to the skin must be as small and
fine as possible, preferably pinpointed; pressure and stimulation of
the sense of temperature should be avoided. It is best to use a piece
of cotton drawn out to a fine point on a wooden stick or match,
or the corner of a handkerchief which has been tightly rolled, or a
piece of paper may be used.
In examination of the sensibility for pain it is best to employ a
pinwheel (p. 127), rolling it over the skin under light pressure or
allowing it to exert its own weight. The patient should not be asked
whether he feels sharp or dull, but whether he feels pain or not.
To determine the boundaries of an area with altered sensibility,
it is advisable to apply minimal stimuli at its border areas. It fre

quently happens that sensory impairment is detected only when
mild stimuli are applied. As far as possible, the stimuli should be
equal in intensity, distance and time interval. The pinwheel helps
to fulfill these requirements.
Since in testing sensibility much depends on the collaboration of
the patient, the examination should not tire him. It is better to stop
when he shows signs of fatigue and repeat the examination at an
other time. Indeed, in repetition itself lies the validity of all tests
for sensibility.
As to the nomenclature of sensory disturbances, the terms
"dysesthesia" and "paresthesia" are often used incorrectly and inter
changeably. They are not identical. Distinction is made on the
grounds that the prefix "para-" in paresthesia means "beside," "be
yond," "accessory to," "apart from." Therefore the word paresthesia
should be used only when some external stimulus produces abnor
mal sensations instead of the normal. Abnormal sensory reactions
which appear in response to a stimulus should be called paresthe
sias. Abnormal sensory disturbances which appear spontaneously
should be generally called dysesthesias.
ALGIC NEURITIS
It may happen that a patient, according to all his symptoms,
has a disturbance of a single peripheral nerve, sensory or mixed.
The leading symptom is severe localized pain. On examination of
the sensibility, however, nothing pathological can be found. This
does not militate against the presence of an organic affection of the
nerve, traumatic, toxi-infectiousor degenerative. Even the smallest
nerve is a complicated structure with afferent and efferent systems
conducting many kinds of sensibility. Any of the multifarious con
ductive systems of the nerve can be qualitatively affected in two
ways. There may be paralysis with deficit of function or irritation
SENSORY SYSTEM 187
with increase of function. The reaction of the nerve to a morbid

agent may thus be quite varied. Some conductive system or systems
may be affected, and in a different manner or to a different degree;
some may be completely spared. There is a pathoclisis, i.e., a specific
affinity for certain morbid agents not only of certain elements of
the brain but also of the peripheral nervous system. Thus it can
happen that a morbid process, attacking the peripheral nerve, selec
tively affects the pain-conducting system, producing irritation and,
consequently, pain but nothing else. Such a condition is best
called algic neuritis. There are, accordingly, other selective neu-
ritides such as motor, sensory, ataxic, vasomotor and many combi
nations of these.
FLEETING SENSORY DISTURBANCES

It may also happen that a patient definitely and credibly main
tains that he had on several occasions, circumscribed dysesthesias or
pain, even with complete anesthesia, and still on examination of
the sensibility nothing definitely abnormal can be found. What
might have caused such complaints? In cases of sudden, transient,
localized pain one must consider that the patient, through an awk
ward movement, might have brought about a brisk, violent stretch
ing of a slightly diseased nerve. It is an established fact that in such
a case the affected nerve may react with violent but fleeting pain to
brisk stretching {vide Nerve Stretching Test, p. 203). There may

be insignificant or no signs or symptoms of a nerve lesion except
for this acute pain on stretching. This pain may even be the first
signal of a nerve affection. The fleeting attack of pain does not
leave an objective or subjective aftermath.
Fleeting dysesthesias, pain with complete anesthesia and anal
gesia occur particularly in the arms. This condition is called brachi-
algia statica paresthetica or nocturnal arm dysesthesias. It is com
mon, but hardly ever correctly diagnosed. The patient complains
bitterly that he often awakens during the night with dysesthesias,
mostly in the distal ulnar part of the forearm; some mornings he
finds on awakening that the ulnar side of the hand is completely
anesthetic. "It feels like leather." The aroused patient shakes his
arm, and the discomfort quickly vanishes. On examination later the
same morning, no trace of any sensory disturbance can be found.
We with a complete or partial compression
are dealing here usually
of the brachial plexus. In most cases only the lower part of the
plexus is compressed, rarely the whole plexus. The following are
the contributory factors for these nocturnal arm dysesthesias: relax
ation of the muscles; immobilization of the limb during sleep;
dropping of the shoulders in middle age; slight anomaly of the
thoracic outlet and of the brachial plexus. Even the anatomy of the
is,
normal brachial plexus shows that it from an orthopedic stand

point, most unfavorably located. The compression of the plexus
during transient, and the symptoms disappear when the
is
sleep
by
continuous pressure on the plexus removed shift of position.

is
TESTING FOR SENSORY MONONEURITIS
not so well nor so generally known should be that

It
as
is
it
a
neuritic process, toxi-infectious or metabolic in origin, may involve
single sensory nerve. Thus there may be clinical picture of iso
a
lated sensory mononeuritis. The same process may involve several

nerves in separated areas scattered over the entire body and in
volve them at various times. Disseminated migrant sensory mono
neuritis results. "broken up" sensory polyneuritis. This has
It
is
a
practical application when we are confronted with sensory disturb

ances in circumscribed area, suggesting the involvement of
a
single sensory nerve. may be due not to any local, mechanical

It
or orthopedic condition but to some general factor, i.e., to some

toxi-infectious or metabolic process with specific affinity for the
a
SENSORY SYSTEM 189
sensory nerves. Thus, one should not be surprised to find an isolated

spot of diminished sensibility with dysesthesias and/or paresthesias
in any part of the body. And this without any indication of local
causation! In searching for such local pathological process one must
realize that a general factor may be at work. Every single super
ficial sensory nerve of the human body, not excluding the trigemi
nal, can be affected isolatedly or in conjunction with others. The
lateral cutaneous nerve of the thigh is affected most often, produc
ing meralgia paresthetica. Next in frequency are the superficial
branch of the radial nerve, producing cheiralgia paresthetica; pos
terior cutaneous nerve of the forearm; anterior cutaneous nerve of
the thigh; saphenous nerve; deep peroneal nerve; calcaneal nerves,
digital nerve branches of the fingers and toes. The prepatellar
branch of the saphenous nerve may also be isolatedly affected, pro
ducing gonyalgia paresthetica.
TESTING SKIN AREAS FOR SENSORY CHANGE

In examination of the extent of sensory change in disturbances
of the peripheral nerves, the following two facts always must be
considered.
Textbooks usually outline the areas of skin innervation by single
nerves. These are maximal areas, i.e., areas corresponding to the
greatest extent of innervation of the skin by a certain single nerve.
When this nerve is damaged, we should not expect that the dam
aged area will correspond exactly to that given in textbooks. Besides
this large area, every nerve has a much smaller one which is its
own province, its bailiwick. It shares innervation of the remaining
portion with its neighboring The area of damaged sensi
nerves.
bility may thus be very small and constitute only a part of the area
attributed to a certain nerve. In some nerves, for instance the radial,
it may be extremely small (Fig. 57), indefinite or even absent.
In outlining the boundaries of damaged sensibility of a single
nerve one must remember also that the sensory areas of the various
nerves differ greatly from one person to another. For instance, the
area of the lateral cutaneous nerve of the thigh in one person may
extend like a wide band along most of the entire lateral aspect of
the thigh, while in another it may be but the size of the palm of the
hand, or even smaller. The area of distribution of the ulnar nerve,
too, may vary greatly. .
In testing the segmental boundaries of the dermatomes one must
Fig. 57. TESTING FOR SENSORY MONONEURITIS.

Area of sensory disturbance on the ulnar surface of the thumb in a lesion of
the superficial branch of the radial nerve.
remember that the area of the cervical segments extends to the

face and that it is the cervical segments, not the trigeminal nerve,
which innervate the skin over the angle of the mandible. Therefore,
if the sensory disturbance extends over the whole face, the lesion
must involve more than just the trigeminal nerve. It should also be
remembered that the second dorsal segment extends to the inner
part of the forearm, so that the sensibility of this area is preserved
even if the whole brachial plexus is so severely damaged that com
plete anesthesia of all the rest of the arm has resulted. Another im
SENSORY SYSTEM 191
portant segmental boundary is on the anterior aspect of the chest at

the level of the second rib where C-4 and D-2 meet.
In of the segmental sensory innervation of the skin, the
tests
sequence of the dermatomes may easily be visualized by the follow
ing imaginary picture. A manikin, representing the human body,
walks on all fours, with thumbs turned forward. The legs, bent at
the hips, are in extreme outward rotation, so that the medial malle
olus faces forward. The segments are "cut" from head caudalward
in vertical slices perpendicular to the long axis. In this position the
segments of the radial aspect of the arm, C-5 and C-6, are "cut"
first and therefore are higher than the ulnar segments, C-7, C-8,
D-l. Similarly, the segment of the inner aspect of the leg, L-4, is
higher than those of the outer aspect, L-5, S-l.
TESTING SENSIBILITY OF THE MAMILLARY ZONE
When tabes is suspected it is advisable to check the sensibility

of the mamillary zone. In the very early stages of the disease this
zone may show hypesthesia for touch. The affected area is at the
level of the mamillae (D-4, D-5). It may even extend from the
second rib down to the umbilicus. Pain sensation may be partially
preserved. The zone of hypesthesia may take the form of a girdle
or appear as islands and patches. Hypesthesia may also be found in
other regions such as that of the ulnar nerve, peroneal nerve and
sole of the foot; but in the mamillary zone it seems to be most
frequent and most severe. The finding of mamillary tactile hypes
thesia is important for differential diagnosis between tabes and poly
neuritis. It is not present in polyneuritis.
SKIN WRITING TEST
The sensory conduction system of the posterior columns is quite

complex and concerned with the vibratory sense, position sense,
sense of discrimination, two-point discrimination, etc. When this

column is damaged, the various modalities of sensibility may not be
affected to the same degree. Clinically important among these possi
bilities is the condition in which the sense of discrimination is par
ticularly involved. This occurs often in the first stages of compres
sion of the spinal cord.
The best method of testing discriminative sensibility is to write
numerals on the skin with any blunt instrument and ask the patient
to name them. The examiner writes a numeral from 0 to 9 below
and above the suspected level of compression. The patient thus
becomes acquainted with the procedure. The patient with a trans
verse lesionof the spinal cord easily recognizes the numerals writ
ten above the level of the lesion, while he makes inaccurate guesses
or does not recognize at all those written below the level of the
lesion. It is amazing how easy it is for a normal person, and even
one of lower intelligence, to recognize numerals written on the
skin. It is also striking to what extent this ability is impaired in
lesions of the posterior columns. The test is used to the greatest
advantage in transverse lesions of the spinal cord affecting the
lower extremities. It helps to uncover the mildest degree of disturb
ancein the conduction of sensibility in the posterior columns. In
compression of the spinal cord these columns may suffer earlier and
more than the spinothalamic tracts.
Another and much cruder test is to put a moist finger-tip or the
eraser tip of a pencil on the skin of the affected area and move it in
various directions which the patient must identify. Mistakes or fail
ure in this task also point to a lesion of the posterior columns.
TESTS FOR DISSOCIATED ANESTHESIA
Lesions of the spinal cord may affect predominantly or exclu

sively certain sensory qualities, leaving other qualities more or less
intact. So-called dissociated anesthesia results. Of course, there is not
SENSORY SYSTEM 193
always anesthesia, there may be hypesthesia; the essential point here

is that the different sensory systems are not affected to an equal
degree.
The most important is the dissociated anesthesia of the syringo
myelic type. It occurs particularly in syringomyelia and hematomy-
elia. Here sensibility to pain and temperature is lost, while the other
sensibilities are more or less completely preserved. Particularly strik
ing is the contrast between the lost pain-temperature sensibility
conducted by the spinothalamic tract and the completely preserved
discriminative sensibility conducted through the posterior columns.
In the affected area the patient may have no sensibility whatever for
pain and temperature, and still may recognize numerals written on
the analgesic skin. This loss of sensibility for pain and temperature
with preservation of the ability to recognize numerals written on
the analgesic skin is striking. It is more characteristic of dissociated
anesthesia of syringomyelic type than the loss of sensibility for pain
and temperature with preservation of sensibility for touch. It indi
cates that the posterior columns are preserved and the spinothalamic
tract is damaged.
The syringomyelic cavity which leads to dissociated anesthesia
of this type most commonly occurs in the cervical region. But it is
well to remember that it may also, though rarely, occur in the
lumbosacral cord. Failure to realize this simple fact may cause grave
diagnostic mistakes. I remember a patient with typical lumbosacral
syringomyelia who for a year had been treated for leprosy.
Among the kinds of dissociation of sensibility that may be found
in tabes is loss of vibratory and position sense with preservation of
sensibility for pain, temperature and touch. This combination may
also be found in multiple sclerosis and dorsolateral sclerosis. In
tabes, again, there may be marked diminution of sensibility to deep
pressure with relative preservation of superficial sensibility. The
eyeball, with the lid closed, is pressed downward from above.
Normally there is typical pain, which is lacking in tabes even in

the early stages. Pain may be absent or diminished on compression
of muscles, particularly of the calf, or the nerves, the testis or the
Achilles tendon. Withal, the superficial sensibility may be com
pletely or comparatively preserved.
In alcoholic polyneuritis a quite different kind of dissociated
anesthesia occurs. In contrast to tabes, the skin may be hypesthesic
while the deep structures are hyperesthesic. Even mild pressure on
the muscles, particularly those of the calf, may be very painful.
Other diseases produce dissociated anesthesia but rarely. If they
do, it is the sense of position and vibration which suffers most.
Sensory disturbances in half-sided lesions of the spinal cord are
discussed in the section on the Pyramidal System.
ASTEREOGNOSIS
In lesions of in other loca
the parietal lobe and much less often
tions, a peculiar condition results. Patients in acute stages of multi
ple sclerosis show it not infrequently. The patient complains bitterly
that he cannot use one hand. The search for pyramidal signs gives
negative results or is unrewarding, for there is little here to explain
the functional loss. But the patient's peculiar behavior betrays the
condition. Let us say the left hand is affected, and the patient wants
to take something from his left pocket. He puts his left hand there
in order to pick it out. Then, with his right hand, he grasps the out
side of his left pocket, fumbles with it and, through the cloth,
pushes the desired object into his left hand. This indicates astereog-
nosis. To test for this condition, the patient is asked to close his
eyes; he is given in turn a variety of small objects coins, key,
button, pencil, and the like and asked to name them by touch
and by moving his fingers around the object. Failure to do this is
astereognosis. If the disturbance is incomplete, the recognition of
objects is delayed. It is astereognosis, and not the mild pyramidal
SENSORY SYSTEM 195
lesion that may accompany which at the root of his complaints.
it,
is
The term "astereognosis" should be used cautiously. implies
It
central, cortical or subcortical lesion leading to disturbance of
a
a
one of the highest gnostic functions. Here recognition disturbed.
is
The term also implies that the primitive sensory perception, the
essentially intact. not, the
If
sensibility for touch and position,
is
it
is
condition not astereognosis but stereoanesthesia. When the periph
is
eral apparatus for vision, the optic nerve, damaged we do not
is
speak of visual agnosia. Nor do we speak of astereognosis when the
peripheral sensibility abolished. This, too, may lead to inability of
is
by
the patient to name objects touch.
STATIC ATAXIA OF HAND AND FINGERS

When the sense of position (postural sensibility) of hand and
fingers disturbed because of cerebral, spinal or peripheral lesion,
is
static ataxia results. This dramatically demonstrated by the fol

is
lowing test. When the patient stretches his arms, hands and fingers
forward and closes his eyes, the affected hand and fingers perform
"pseudo-athetotic" movements of which the patient unaware
is
(Fig. 58). When he opens his eyes, he surprised at the position

is
his hand and fingers have assumed. These involuntary movements

range from restlessness to "tabetic athetosis." They are also aptly
called "piano-playing fingers." When there concomitant mild
is
a
pyramidal lesion, the arm drops. This sensory static ataxia together
with astereognosis occurs in the acute state of multiple sclerosis.
This simple test reveals the real
So-called "useless hand" results.
nature of the disturbance which had often been thought to be
hysterical.
PREFERENTIAL CHOICE TEST
In lesions of the parietal lobe, although there are no conspicu

ous changes in the strength of the hands and arms and no marked
Fig. 58. STATIC ATAXIA OF HAND AND FINGERS.
Acute multiple sclerosis involving the patient's left upper extremity. A and
B both show involuntary changes of position of hand and fingers, "piano play
ing fingers." A and particularly B also show downward deviation of the left arm
due to a mild pyramidal lesion.
196
SENSORY SYSTEM 197
reflex changes, still the functional defect may be considerable. The

popular term "useless hand" is quite appropriate. Whether right-
handed or left-handed, the patient prefers to use the unaffected arm.
It is in small, everyday actions that this preference manifests itself,
and the patient is unaware of it. This can be demonstrated in the
following way. The patient is asked to pick up an object or to put
his hand in his pocket, to squeeze the examiner's hand, to put on a
slipper. Unconsciously and invariably he chooses to perform these

acts or to perform first with his unaffected extremity.
SIMULTANEOUS DOUBLE SENSORY STIMULATION
When we examine for any modality of sensibility such as touch,

pain, astereognosis, vision or hearing, we usually apply a single
stimulus to a chosen sensory field. When we wish to compare the
two sides or different parts of the body, we apply a stimulus first to
one, then to the other, consecutively. A much more delicate method
is to apply stimuli to both places simultaneously.
A patient with a brain lesion has diminished sensibility, let us
say, on the left side. When the sensibility is examined in the usual
manner, first on the right and then on the left, the patient can rec
ognize the stimulus on the affected side. But when this very stimulus
is applied to both sides simultaneously, the sensory perception on
the normal side is relatively so strong that it completely "sup
presses" that on the affected side. The patient is not aware of the
time,
if,
sensory stimulation on the affected side at the same

a
sensory perception arises from the healthy side. This healthy per
ception "extinguishes" the perception on the affected side. To this
perception the patient inattentive; he neglects it. In this way we
is
may disclose sensory defect which does not manifest itself when
a
stimuli are applied singly.

This procedure can be useful in examination of the visual fields
the finger confrontation test. The examiner uses his fingers on
by
both sides simultaneously when confronting the patient. It is helpful
also in testing astereognosis. A coin put into each hand separately is
identified. But with a coin in each hand at the same time, the pa
tient may be unaware of its presence on the affected side, or he may
recognize it tardily. In other words, when astereognosis is tested by
putting identical objects into each hand, the strength of the sensa
tion in the healthy palm impairs the appreciation of the simultane
ous sensation in the affected palm. This impairment may go so far
as to extinguish the sensation from the affected side altogether.
As soon as the object is removed from the healthy side and the
"competitive" sensation is eliminated, the patient may recognize
the object he holds in his affected hand.
When the lesion is in the spinal cord and not in the brain,
stimuli are simultaneously applied at different levels of the body.
In this manner it might be possible to detect early a transverse
lesion of the spinal cord and its level.
FEET TOGETHER-EYES CLOSED TEST
Firm stance requires complete integrity of deep sensibility of the

trunk and lower extremities. Mild impairment of this sensibility
may pass unnoticed when the patient simply stands or walks. It
may, however, become apparent when the patient is put under
acute stress while standing erect. This is done by asking the patient
to place his feet parallel and together, to close his eyes and stand
immobile. Thus his stance is taxed in two ways: the width of the
ground surface for support is diminished, and closure of the eyes
deprives him of the ability to correct his position by fixation of
Under these conditions a defect in deep sensibility makes
objects.
him sway. This is the physiological basis for the time-honored
Romberg test. To make the test more delicate, the patient's atten
tion must be diverted. Instead of asking him to close his eyes, the
examiner may close them for him casually during the eye examina
SENSORY SYSTEM 199
tion, while the patient is standing with his feet together. To divert
his attention the examiner may ask the patient to count backward
or to show his tongue, or he may press lightly on the eyeballs and
ask the patient to describe the entoptic phenomena he perceives.
He may also ask the patient to lift both arms forward, to stand on
tip-toe with his knees bent, to bend over and straighten up or to
perform the finger-to-nose test. Standing on one leg makes the test
particularly delicate.
Evaluating this test, we must realize that the stance of a normal
person with his feet together and his eyes closed is not perfect. Mild
degrees of swaying on the part of the patient are not always patho
logical. The degree may be judged best by the "dance of the ten
dons" on the dorsum of the foot the tendons of the anterior tibialis
and long extensors of the toes. Needless to say, the examiner should
beware of the malingerer, who may start to sway violently and
ostentatiously even before closing his eyes and topple like a felled
tree. There is a good method by which the hysteric or malingerer is
made to betray himself. The genuine patient, with or without
ataxia, in order to keep his balance and to prevent himself from
falling backward tries to immobilize his knees. He does this by
innervating the quadriceps muscle; he displaces the patellae up
ward. Not so the malingerer or hysteric, who sways and falls with
out trying to prevent it. It
is,
therefore, advisable to watch the

patient's patellae while this test being carried out.
is
The general value of the Romberg test not as great as for

is
merly assumed. hardly ever the only manifestation of the dis

It
is
turbed deep sensibility. When the result positive, as in tabes or

is
polyneuritis, there are usually more reliable signs which help to

diagnose these diseases.
Intelligent patients with tabes occasionally report that, when
stooping over basin and covering their eyes while washing their
a
face, they sway and even strike their heads against the basin, mirror
or wall. This is
a positive response to the Feet Together-Eyes Closed
Test performed spontaneously.
NERVE PRESSURE TEST
We have a tendency to limit our sensory examination to the

skin the superficial sensibility forgetting to check the deep sen
sibility, particularly that of the nerve trunks themselves. A time-
honored test for sensibility of the nerves is the examination of the
pressure points of Valleix, 1841). Nowadays
(points douloureux
these points are not considered so significant diagnostically as in the
past. In testing the tenderness of nerves to pressure, one is apt to
deceive oneself. The nerve is usually pressed where it lies on the
bone. This procedure may be painful even in the normal subject.
Simultaneous unavoidable pressure on muscles may be causing the
pain. Healthy people, particularly neurotics, may experience pain
on pressure on the nerves. Besides this, some nerves are difficult to
palpate. It is hard to avoid suggestive questions, and the patient's
reaction as well as the evaluation by the examiner are highly sub
jective. Therefore, one cannot be too cautious. In the past, pressure
points were made the shibboleth in diagnosis of neuralgia and in
ruling out neuritis. Here the test has failed completely.
Although the test of nerve tenderness to pressure has a re
stricted value, it should nevertheless be tried. In some cases the
nerve tenderness is definite and strictly localized. The pain does not
radiate into the area supplied by the nerve. Such pain may be re
garded as due to perineuritis or interstitial neuritis. Every accessible
nerve should be tested, particularly the ulnar nerve at the elbow,
the peroneal nerve behind the head of the fibula and the first and
second branches of the trigeminal nerve at their exit from the skull.
But, again, in all these instances, painful pressure on the bone may
give false results.
Occasionally, pressure on a nerve produces not strictly localized
SENSORY SYSTEM 201
pain but paresthesias in the whole area of its distribution. The pa

tient has difficulty in describing the feeling and usually calls it
"tingling" or "electric shock." In mild degrees this may occur in
the normal individual. Stronger paresthesias may indicate tetany or
a tetanoid constitution. One should not fail to use this test when the
facial nerve tapping test gives a positive result. When results of
both are positive, it is advisable to search for further signs of tetany
or stigmata of general nervous and vegetative hyperirritability.
TEST FOR FACIAL NERVE TENDERNESS

Acute "rheumatic" paralysis of the seventh nerve, so-called
Bell's palsy, is often preceded by pain in the mastoid region. The
pain may persist for a few days after the paralysis has set in. In
such cases the facial nerve may be found tender to pressure. The
place to test for this tenderness is at a point below and slightly in
front of the ear lobe. An attempt should be made to reach the
nerve at its point of exit from the skull cavity. If there is definite
unilateral tenderness of the nerve to pressure, differential diagnosis
is in favor of "rheumatic" facial palsy as against palsy of other etiol
ogy. Of course, such a finding is highly subjective, and only a
marked difference between the two sides should be considered.
PRESSURE TEST IN SCALENUS ANTERIOR SYNDROME

There is a comparatively common disturbance of the lower part
of the brachial plexus caused by compression at the insertion point
of the scalenus anterior muscle on the first rib. It is usually called
the scalenus anterior syndrome. Pain starts early in the course of the
disease and radiates from the neck into the arm and forearm in the
region of the ulnar and median nerves. There may be motor and
sensory defects in the area of the lower cervical plexus; vascular
disturbances are less common. The differential diagnosis of this en
tity may be difficult since the same manifestations may herald a
variety of other diseases. A
constant finding in scalenus anterior syn
drome is tenderness to pressure above the clavicle near the insertion
point of the scalenus anterior muscle (Fig. 59). The patient experi
ences pain radiating down the upper extremity. Care should be
taken to press on the insertion point of the scalenus and not later
ally, for here pressure may affect the whole brachial plexus. Caution
should be used in making a diagnosis of scalenus anterior syndrome,
with its therapeutic surgical indications should response to the pres-
FIg. 59. PRESSURE TEST IN SCALENUS ANTERIOR SYNDROME.

Crosses mark the spots which are tender in this syndrome.
sure test be negative. The response to this test has been positive in
all cases observed; in patients operated on, diagnosis was' confirmed.
Speaking of pain in the arm, it is worth while to point out that
when it occurs in an adult and his x-rays show cervical spondyl
arthritis, this does not automatically mean that the spondylarthritis
is responsible for the pain. X-ray findings alone are not sufficient to
justify this assumption. Weighty clinical findings must lend their
support. Generally speaking, cervical spondylarthritis, as demon
strated by x-ray, rarely gives rise to any neurogenic clinical symp
toms or signs. It is a common experience that marked changes in
SENSORY SYSTEM 203
the cervical vertebrae can be found accidentally by x-ray. These may

represent the normal wear and tear on the vertebrae seen in nearly
every person. The nerves are much less apt to be damaged in the
intervertebral foramina than they are at the thoracic outlet. Here
the brachial plexus is most unfavorably situated. It passes over the
first rib beneath the clavicle in the tight triangle between the
rib and the scalenus muscles. Brachialgia statica paresthetica, a
common condition in which the patient has pain and dysesthesias

in the arm during sleep, is often mistaken for spondylarthritis. The
lesion, however, lies at the brachial plexus where it crosses the first
rib and where it is easily subject to pressure or stretching.
NERVE TAPPING TEST
To uncover even the mildest local irritation of a superficially

situated nerve and to determine its site, the nerve tapping test is
useful. The cutaneous nerves are particularly suited to this test. The
examiner follows the course of the nerve, tapping it with his finger
or rolling it gently. When the tapping finger reaches the spot
where the nerve is damaged, the patient experiences paresthesias in
the area supplied by the nerve. Traces of these may be found even
after clinical recovery has taken place. When the lesion is traumatic
and the nerve fibers regenerate, the point of maximal tenderness of
the nerve migrates distalward as the regeneration of the fibers
progresses.
NERVE STRETCHING TEST
It can be regarded as an established fact that any traction or

stretching is injurious to a peripheral nerve. Violent and sudden
stretching of an extremity plays an important role in the etiology
of neuritides. This is particularly true of the brachial plexus. From
both a static and a dynamic standpoint most unfavorably located,
this plexus operates under strong tension even in normal conditions.
Comparatively slight trauma which produces sudden, violent stretch

ing of the arm may damage the brachial plexus severely even with
out injuring the skin, muscles or joints. Such traumas may give rise
to long-standing, stubborn pain in the arm. It is the suddenness
and speed of movement rather than its wide range which produces
an algic neuritis of the brachial plexus.
If a normal peripheral nerve is easily damaged by stretching,
the reaction of a diseased nerve to stretch is even greater. It then
reactswith dysesthesias and pain not present when the nerve is re
laxed and at rest. Traction is a much more potent factor than pres
sure in causing damage and irritation, pain and dysesthesias. Since
every diseased peripheral nerve, mixed and particularly sensory, re
acts to passive brisk stretching with pain and paresthesias, the use
of nerve stretching as a test is therefore as logical as it is simple.
The response to the test becomes distinctly positive very early in the
course of neuritis and remains so even when the neuritis has sub
sided clinically. In performing the test, the examiner visualizes the
courseof the nerve and brings the extremity into a position that will
cause maximal elongation of the nerve. It is essential that the
stretching be performed suddenly and briskly. If pain and paresthe
The sensory manifestations may be
sias result, the test is positive.
very mild and may consist only of a sensation of tingling in a small
area innervated by the affected nerve. It is hardly necessary to de
scribe this test in detail as applied to every single nerve. A few ex
amples will suffice.
The best known of all nerve stretching tests is the straight-leg-
raising test, the so-called Lasegue. Historically this eponym is not
correct. It is true that Lasegue introduced this test, but he never
described it. This was done by his pupil Forst in 1881. Earlier, in
1880, the test was described by the Serbian clinician Lazarevic of
Belgrade. It is self-evident that in a patient lying supine with legs
extended at the knees, flexing of the thigh at the hip brings about
SENSORY SYSTEM 205
a stretching of the sciatic nerve. When the nerve is diseased, this

causes pain in its distribution. On this maneuver the patient not
only has pain but will also automatically attempt to bend his knee
and thus prevent further stretching of the sciatic nerve. When the
knee is bent, the nerve is relaxed. This automatic bending of the
leg on straight-leg raising is the basis of the Kernig test. Exactly
the same stretching of the sciatic nerve can be accomplished when
the patient lies supine with his legs stretched flat and the examiner
lifts the patient's trunk by placing the palm of his hand against the
patient's upper back. The patient's body is bent at the hips. Since
the legs are extended, this means traction of the sciatic nerve and
produces pain. Again, the patient counteracts the pulling on the
nerve by the most effective method at his disposal, namely, by bend
ing his knees. This constitutes the Brudzinski test.
Another technique to stretch the sciatic nerve is this. The pa
tient lies prone on the examining table, with the affected leg close
and parallel to the edge. The examiner passively abducts this leg
beyond the edge of the table so that it is no longer supported.
When the unsupported leg drops over the edge of the table, such
dropping of the extended leg means, of course, stretching of the
sciatic nerve as in the Lasegue test. Because of pain, the patient tries
to prevent the leg from dropping. This test may serve to uncover
malingerers who, being familiar with the Lasegue test, complain of
pain when the heel is hardly lifted from the surface. Unfamiliar
with the test described here, malingerers allow the leg to drop,
which shows that no pain is caused by stretching of the sciatic nerve.
The superficial branch of the radial nerve provides another ex
ample of the nerve stretching test. This nerve may be isolatedly af
fected, producing the syndrome of cheiralgia paresthetica. The pa
tient may have only slight dysesthesias and paresthesias in the area
of the nerve. To perform the stretching test here, the arm is ex
tended, elevated and maximally brought backward, then pronated;
still there is no discomfort. However, the moment the thumb is

maximally flexed, adducted and brought across the palm, the super
ficial branch of the radial nerve is stretched and the patient experi
ences sharp and painful paresthesias. In affections of the brachial
plexus, the following maneuver should be tried. The arm is ex
tended at the elbow, rotated inward, elevated and brought back
maximally. At the same time the head is bent and rotated to the
other side. Thus a position of the head is assumed as in shaving.
This position stretches the plexus and invariably produces pain
when the plexus is affected. If the sensory nerves of the dorsum of
the foot are affected, the patient has similar paresthesias when, with
the legs extended, the foot is briskly and passively plantarflexed.
Such examples could easily be multiplied, but the physiological
principle is the same. The nerve stretching test has proved most
valuable and of decisive importance in diagnosis and in differential
diagnosis of disturbances of peripheral, sensory or mixed, nerves.
It can be stated without reservation that if the result of this test is
negative, an affection of the nerve has never existed or else has
completely healed. A positive response may constitute the last
remnant of a neuritis. There may be complete clinical recovery from
neuritis, but the nerve, even months afterward, may still react with
paresthesias to stretching. For the diagnosis of peripheral nerve in
is,
volvement, the nerve stretching test no doubt, more valuable than

the nerve pressure or nerve tapping test. Not all peripheral nerves,
however, can be effectively subjected to brisk stretching, and in such
cases the test not applicable or must be evaluated with caution.
is
KICKING TEST IN SCIATICA

Stretching of nerve causes pain and paresthesias
in
diseased
a
its area. The more sudden, abrupt and forceful the stretching, the
sooner will these symptoms appear, the more acutely will they de
velop and the more pronounced will they be. This the basis for
is
SENSORY SYSTEM 207
the kicking test in sciatica. It is nothing more than a brisk and vio
lent straight-leg-raising test. While standing, the patient is asked to
keep a leg extended at the knee and to kick it forward from the hip
several times with brisk, jerky movements. In sciatica the range of
these movements is markedly diminished as they cause violent pain.
In patients with herniation of an intervertebral disk these move
ments are particularly restricted and painful, and patients complain
that the movements cause a "catch" in the back.
HEAD BENDING TEST
The pull we exert in the nerve stretching test extends beyond

the peripheral nerve and even its plexus. It may extend to the nerve
roots and the spinal cord. That this is the case with the straight-leg-
raising test has been shown experimentally. Raising the leg ex
tended at the knee means stretching not only of the sciatic nerve
but also of its roots and of the spinal cord. The cord may show a
displacement of several centimeters. The effect of traction on the
outstretched arm may extend centralward far beyond the brachial
plexus. This is shown by the fact that in accidents to the arm, such
stretching has been known to tear the nerve roots at their attach
ment to the spinal cord. In the same way as straight-leg-raising
exerts a pull on the lower part of the spinal cord, a similar pull can
be exerted on the upper, or cervical, portion of the cord. This is
done in the head bending test.
The examiner bends the head of the patient lying supine or sit
ting or standing and asks him whether and where he has any ab
normal sensations. The bending should be performed forcibly and
quickly. The patient must be assured that no great pain will result
from the test and must be made to relax his neck muscles maxi
mally. This passive bending of the head means considerable elonga
tion of the spinal cord, meninges and roots. This is the basis for the
well-known Brudzinski neck sign: involuntary flexion of the legs at
the knees on passive bending of the head. It is obviously not a tonic
reflex of any kind, but a mere pain reaction. In meningitis the nerve
roots and the meninges are inflamed and adherent. They react to
stretching in the same way as does any inflamed nerve with pain.
The pull caused by head bending may extend downward along the
whole cerebrospinal axis. The patient immediately and uncon
sciously tries to counteract this elongation by the two means at his
disposal : ( 1 ) by stiffening his neck muscles to prevent bending of
the head and, since this cannot always be effected, (2) by bending
his knees. Through this maneuver he relaxes the lower part of the
tense cerebrospinal axis and allows some slack to the upper part.
In the normal person the mobility of the spinal cord, meninges
and roots is such that no discomfort, particularly no radiating pares
thesias, are felt on head bending. If there is any lesion of these
structures, head bending produces pain or paresthesias exactly in
the affected area. This is most dramatically seen in compression or
stretching of a root by a tumor or herniated intervertebral disk, but
is seen also in diffuse involvements of the roots, i.e., polyradiculo
neuritis. Patients usually describe the sensation as "electric shock"
or "tingling." Patients with a localized disturbance of the nerve
roots caused by tumor or herniated disk avoid bending of the head
since this evokes localized pain. This reaction of the patient consti
tutes a valuable diagnostic aid. In infectious polyneuritis of any kind
the painful sensations on head bending may be felt in legs, heels
or fingers. In multiple sclerosis and dorsolateral sclerosis the ab
normal sensations are, when present, felt in the upper part of the
back. In multiple sclerosis this may be one of the earlier, or even
the earliest, symptom. Even if the response is negative, i.e., if there is
no complaint on head bending, this has significant diagnostic value.

It means that the spinal meninges and roots are free or at least not
grossly involved. This simple, harmless and brief test is highly rec
ommended as routine in everyday neurological examination.
SENSORY SYSTEM 209
The head bending test may be reinforced by combining it with

the straight-leg-raising test. This can be performed while the patient
islying or sitting. With one hand the examiner bends the patient's
head, while with the other he lifts the patient's legs and "doubles
him up." The last stage of head and leg flexion should be done
briskly. This "jack-knifing" of the body means a tremendous trac
tion on the cerebrospinal axis, particularly if the knees are held
stretched as much as possible. If the response to this combined test
is negative, any gross involvement of the sensory system, spinal
cord or roots can be excluded.
The test may also be of value when applied in reverse. When
the patient in a sitting position, with his head bent, has pain or
paresthesias and retraction of the head brings relief, we may con

clude that it was the bending position that brought on the pain and
paresthesias.
JUGULAR COMPRESSION TEST
When a patient has a gross space-consuming intradural lesion

which causes radicular pain by tension or traction on a sensory
root, this pain is increased by coughing, straining at stool, sneezing
or any exertion. All these factors increase intracranial pressure and
thus cause traction, displacement and irritation of the nerve roots
involved. This is particularly true of tumors of the cauda equina.
A sudden pain-producing of intracranial pressure may also
increase
be effected by compression of the jugular veins in the neck. The
procedure is the same as in the Queckenstedt test. Both jugular
veins are compressed and the pressure suddenly released. The re
sulting increase and fluctuation of intracranial pressure produce
sharply localized radicular pain. The site of the pain so produced is
of great localizing value. A positive result speaks first of all for irri
tation of a root by an intradural tumor.
WET-DRY TEST FOR CAUSALGIA
Causalgia is brought about by injury, often slight, to a nerve,

particularly the median or sciatic nerve. It is characterized by severe
burning pain and extreme hyperalgesia. As Weir Mitchell said, it is
"the most terrible of all tortures which a nerve wound may inflict."
There is a marked local and general dysfunction of the sympathetic
Fig. 60. TEST FOR CAUSALGIA.

Causalgia after nerve injury to the left arm. The patient's reaction as the un
affected right arm is touched, A, by a wet hand and, B, by a dry hand.
nervous system. The pain is not limited to the area of the affected
nerve. The whole personality is involved. A slight emotional, visual
or auditory stimulus may precipitate a paroxysm of pain. Character
istic of causalgia is the extreme susceptibility of the patient to dry
ness of the skin. He will resort to anything in order to keep the
affected limb wet. It is reported that in war, soldiers moistened the
extremity with their own urine. Figure 60 shows the patient's re
action as a remote area of skin, which was not even affected, was
being touched with a wet hand and a dry hand.
SECTION VII
Vasomotor-Xropliic System
TEST FOR DERMOGRAPHY
Even the shortest neurological examination should include the

testfor dermography. Here the reaction of the skin vessels to me
chanical irritation is tested. The examiner simply strokes the skin of
the patient's chest with his finger-nail or a blunt instrument such as
the handle of the reflex hammer. At the site of stimulation there

appears a white line followed by a red line or, more often, a red
line only. This line widens. Its periphery may be pale. Among nor
mal individuals this reaction varies from person to person. If the re
action is more intense, involves a wider area, is prolonged for more
than two to three minutes, it must be regarded as abnormal, particu
larly if attended by an urticaria-like elevation. Such abnormal re
action is found in cases of imbalance of the autonomic nervous
system. As Osler put it: "Dermatographia is an outward and visible
sign of an inward and hidden instability." It

is,
however, not pos

sible to define exactly where the normal ends and the abnormal
begins.
Even definitely abnormal dermography has no pathognomonic
significance for any particular disease. However, does give valu
it
able hint to the vegetative constitution of the patient. re

It
as
is
markable how often dermography occurs together with other signs

211
of vegetative hyperirritability increased mechanical irritability of
the nerves and clammy, wet hands and also with signs of general
nervous hyperirritability tremor of the outstretched fingers, in
crease of reflexes, increased vibration of the upper lid, and so on.
TESTS FOR ARTHROGENIC MUSCULAR ATROPHY
In for the site of a lesion around the joints, it is good

a search
practice to start at the periphery and to proceed proximally. The
prevalent tendency to hold cervical spondylarthritis responsible for
many disturbances in the area of the upper extremity is completely
out of proportion with the clinical significance of this condition.
Spondylarthritis starts early and is very common. If it produces
pain, this may be arthrogenic and not neurogenic. Spondylarthritis
is all too often unjustly held responsible for affections of the upper
extremity when, in truth, the lesion lies distally to the spinal column
in a nerve, muscle or more peripheral joint. The tendency to "cen
tralize" a morbid process should be curbed. Morbid conditions in
the neighborhood of joints which seem to be central in origin are
sometimes purely arthrogenic, and one must look first of all upon
the neighboring joints as the source of pathology. This is particu
larly true of the shoulder. Many of its affections, to mention only
arthritis, periarthritis, bursitis and tendinitis, may simulate organic
nervous diseases. An orthopedic examination should precede the
neurological in such cases. It is amazing how much discomfort
arises from a harmless calcareous tendinitis with minimal calcium

deposits and how promptly it reacts to deep x-ray therapy. Even a
brief examination of the shoulder may point to an orthopedic origin

of the condition. There may be a tender spot around the joint, the
scapula may move with the forearm, the movement of placing the
dorsum of the hand on the back may be restricted, etc. In arthritis
of the hip there may be pain when the heel is placed on the patella
of the opposite side and the knee is pushed down.
VASOMOTOR-TROPHIC SYSTEM 213
Not only in painful conditions in and around the joints but also
in atrophy of the muscles we must first suspect the joint as the
source of pathology, particularly after trauma. There is a definitely
established clinical entity called arthrogenic muscular atrophy. In
FIg. 61. TEST FOR ARTHROGENIC MUSCULAR ATROPHY.

Marked atrophy of muscles of the shoulder girdle, right more than left, due
to arthritis of the shoulder joint.
non-neurogenic diseases of the joints, acute as well as chronic,

particularly after trauma, the surrounding muscles may undergo
considerable and rapid atrophy (Fig. 61). This atrophy may not be
merely the result of inactivity but may be caused by some patho
logical reflex arising at the joint. The following muscles are par
ticularly affected: deltoid (shoulder), triceps (elbow), gluteal
VASOMOTOR-TROPHIC SYSTEM 215
(hip) and quadriceps (knee). The small muscles of the hand may
undergo atrophy in chronic arthritis deformans of the hand and
fingers. It is in the deltoid and quadriceps that the atrophy is most
conspicuous. This arthrogenic atrophy is a source of many errors in
diagnosis, since it is usually considered to be neurogenic. In cases of
atrophy of the deltoid, a patch of anesthesia on the outer side of
the upper arm, however, points to involvement of the axillary
nerve, to a neurogenic and not to an arthrogenic atrophy.
TESTS FOR NEUROGENIC ARTHROPATHY
Neurogenic arthropathies are produced by tabes, syringomyelia

and lesions of peripheral nerves. But tabes is by far the most com
mon cause. A few brief tests for tabes examination of pupils,
reflexes and sensibility may quickly solve the mystery of some
puzzling case of arthropathy. Some of these tabetic arthropathies
are mistakenly assumed to be traumatic, but careful analysis always
shows that trauma was completely inadequate to produce the dam
age. Monstrous in joints, particularly the knee (Fig. 62, A
changes
and B), with marked swelling, effusion, dislocation, destruction of
cartilages and bones and new bone formation should raise the sus
picion of tabetic arthropathy, especially when pain and signs of
inflammation are absent and the disability is slight in proportion to
the damage. Any joint may be affected, including the joints of the
vertebral column and ankle (Fig. 62, C).
Special Index
Morbid Conditions Pertinent Tests

A Brachialgia statica paresthetica
Abducens paralysis fleeting sensory disturbances, 187
for lateral bulbar syndrome, 48
tests
pressure test in scalenus anterior
Amyotrophic lateral sclerosis syndrome, 201
Babinski reflex, 147 Brain trauma
dissociation between superficial and acute unilateral post-traumatic my
driasis, 36
deep abdominal reflexes, 129
head dropping test, 157
C
head retractor reflex, 124
hypoglossal nerve test, 74 Cerebellar affections
muscle percussion test, 92 agonist-antagonist test, 175
arm deviation test, 176
pathological laughing and crying,
arm tapping test, 174
123
snout reflex, 121
discrepancy triad in multiple scle
rosis, 182
winking-jaw test, 58
Anisocoria finger spreading test, 178
acute unilateral post-traumatic my finger-tips in midline test, 178
driasis, 36 fixation of position test, 164
Arthrogenic muscular atrophy macrographia, 181
pendulousness of legs test, 94 micrographia, 165
tests for, 212 shoulder shaking test, 179
Astereognosis, 194 tendon palpation test, 97
simultaneous double sensory stimu tests for ataxia, 181
lation, 197 tests for hypermetria, 174
Athetosis tests for lateral bulbar syndrome, 48
grasp reflex, 154 Cerebellopontile angle tumor
tests for torticollis, 165 arm deviation test, 176
blinking test, 59
B corneal reflex, 55
Brachial plexus paralysis lid vibration test, 60
test for upper brachial paralysis, 80 nystagmus, 42
216
SPECIAL INDEX OF MORBID CONDITIONS 217
shoulder shaking test, 179 posture, 103

tendon palpation test, 97 test of resistance movement, 171
Cerebral arteriosclerosis tests for torticollis, 165
jaw muscle reflex, 120
E
snout reflex, 121
Cerebrovascular accident Encephalopathies (diffuse)
lateral deviation of eyes and head, head retractor reflex, 124
36 snout reflex, 121
Cervical spondylarthritis Epilepsy
nerve stretching test, 203 Babinski reflex, 147
pressure test in scalenus anterior orbicularis oculi reflex, 64
syndrome, 201 Exophthalmos
tests for arthrogenic muscular atro exophthalmic ophthalmoplegia, 39
phy, 212 tests for cervical sympathetic, 44
Cervical sympathetic External ophthalmoplegia

tests for cervical sympathetic, 44 tests for myasthenia, 62
tests for lateral bulbar syndrome, 48 Eye paralysis
Cheiralgia paresthetica convergence paralysis of the eyes, 40
nerve stretching test, 205 doll's eyes test, 38
testing for sensory mononeuritis, 188 exophthalmic ophthalmoplegia, 39
Coma, see also Unconsciousness lateral deviation of eyes and head,
corneal reflex, 55 36
lid lifting test, 47 lid liftingtest, 47
orbicularis oculi reflex, 64 paralysis of conjugate upward gaze,

38
D see-saw test in oculomotor paralysis,
Deltoid muscle affection 52
tests for arthrogenic muscular at startle reaction on examination of
rophy, 212 the pupil, 43
Dermography tests for intraoculomotor associated
facial nerve tapping test, 71 movements, 50
lid vibration test, 60 tests for myasthenia, 62
Dissociated anesthesia
test for unilateral spinal cord affec
F
tion, 135 Facial paralysis
tests for lateral bulbar syndrome, 48 associated movements in hemifacial
Dorsolateral sclerosis spasm, 69
head bending test, 207 blinking test, 59
tests for dissociated anesthesia, 192 facial nerve tapping test, 71
Dysesthesias frontalis muscle test, 62
corneal reflex, 55 hypoglossal nerve test, 74
fleeting sensory disturbances, 187 intrafacial associated movements in
nerve stretching test, 203 old facial paralysis, 66
tests for lateral bulbar syndrome, 48 lid vibration test, 60
Dystonia nystagmus, 42
counterpressure test, 170 orbicularis oculi reflex, 64
paralytic contractures, 78 counterpressure test, 170
platysma test, 64 feet together-eyes closed test, 198
test for facial nerve tenderness, 201 homolateral mass flexion reflex, 140
tests for lateral bulbar syndrome, 48 lid vibration test, 60
tests for myasthenia, 62 posture, 103
Fatigability test for play of foot tendons, 99
exophthalmic ophthalmoplegia, 39 tests for torticollis, 165
tests for myasthenia, 62
Femoral neuritis affections I
pendulousness of legs test, 94 Intervertebral disk protrusion
Frontal lobe lesions head bending test, 207
grasp reflex, 154 kicking test in sciatica, 206
lateral deviation of eyes and head, pendulousness of the legs test, 94
36 tendon palpation test, 97
shoulder shaking test, 179
L
G Lateral bulbar syndrome
Glossopharyngeal-vagus nerve paraly tests for, 48
sis Leprosy
tests for lateral bulbar syndrome, 48 tests for dissociated anesthesia, 192
Gluteal muscle paralysis Lid flutter
test of gluteal muscles, 93 lid vibration test, 60
tests for arthrogenic muscular atro Lordotic posture
phy, 212 test of gluteal muscles, 93
H M
Head trauma Malingering
acute unilateral post-traumatic my feet together-eyes closed test, 198
driasis, 36 nerve stretching test, 203
Hematomyelia test for play of foot tendons, 99
tests for dissociated anesthesia, 192 Median nerve paralysis
Hemifacial spasm brachioradialis test, 85
associated movements in, 69 paralytic contractures, 78
Hemiplegia, see Spastic paralysis testfor causalgia, 210
Horner's syndrome thumb abduction test, 87
tests for cervical sympathetic, 44 thumb bending test in ulnar pa
Hydrocephalus ralysis, 90
grasp reflex, 154 Meningitis
Hypertensive encephalopathy head bending test, 207
head dropping test, 157 Meralgia paresthetica
head retractor reflex, 124 testing for sensory mononeuritis, 188
jaw muscle reflex, 120 testing skin areas for sensory change,
snout reflex, 121 189
Hysteria Multiple sclerosis
Babinski reflex, 147 astereognosis, 194
corneal reflex, 55 discrepancy triad, 182
finger spreading test, 178 O

head bending test, 207 Oculomotor paralysis
homolateral mass flexion reflex, 140 acute unilateral post-traumatic my
static ataxia of hand and fingers, driasis, 36
195 see-saw test, 52
for dissociated anesthesia,
tests 192 tests for intraoculomotor associated
Muscular dystrophy movements, 50
long thoracic nerve test, 82 P
muscle percussion test, 92
Paresthesias
pendulousness of legs, 94
head bending test, 207
posture, 103
nerve stretching test, 203
test of gluteal muscles, 93
nerve tapping test, 203
Myasthenia
Parietal lobe lesions
exophthalmic ophthalmoplegia, 39
preferential choice test, 195
facial nerve tapping test, 71
Parkinson's disease
tests for myasthenia, 62
Mydriasis
arm dropping test, 161
acute unilateral post-traumatic my
convergence paralysis of the eyes, 40
driasis, 36
fixation of position test, 164
tests for cervical sympathetic, 44
Myosis
micrographia, 165
testsfor cervical sympathetic, 44
orbicularis oculi reflex, 64
Myotonia
posture, 103
muscle percussion test, 92
push test, 163
N quadriceps tonus test, 114
Nervous hyperirritability shoulder shaking test, 161
facial nerve tapping test, 71 tendon palpation test, 97
lid vibration test, 60 test for pendulousness of arms, 159
nerve pressure test, 203 test for pendulousness of legs, 162
test for dermography, 211 Peroneal nerve paralysis
Neuritis accessory nerve test, 72
algic neuritis, 186 paralytic contractures, 78
nerve pressure test, 200 test for play of foot tendons, 99
nerve stretching test, 203 Poliomyelitis
pendulousness of legs test, 94 paralytic contractures, 78
tendon palpation test, 97 pendulousness of legs test, 94
testing for sensory mononeuritis, Polyneuritis
188 feet together - eyes closed test, 198
tests for neurogenic arthropathy, head bending test, 207
215 knee hyperextension test in tabes,
Nystagmus 95
discrepancy triad in multiple scle tendon palpation test, 97
rosis, 182 test for play of foot tendons, 99
nystagmus, 42 testing sensibility of mammillary
tests for lateral bulbar syndrome, 48 zone, 191
testing for sensory mononeuritis, agonist-antagonist test, 175
188 arm deviation test, 106
tests for dissociated anesthesia, 192 associated movement of the thumb,
Polyradiculoneuritis 137
head bending test, 207 associated movements in a pyrami
Progressive paralysis dal lesion, 136
jaw muscle reflex, 120 astereognosis, 194
snout reflex, 121 contralateral associated leg exten
Progressive spinal muscular atrophy sion, 146
muscle percussion test, 92 contralateral identical associated
pendulousness of legs test, 94 movements of fingers, 145
posture, 103 corneal reflex, 55
Ptosis discrepancy triad in multiple sclero
frontalis muscle test, 62 sis, 182
jaw-winking test, 57 dissociation between superficial and
see-saw test in oculomotor paralysis, deep abdominal reflexes, 129
52 everted position of foot, 108
test for ptosis, 46 facial nerve tapping test, 71
tests for cervical sympathetic, 44 finger flexor reflex, 126
tests for intraoculomotor associated finger spreading test, 178
movements, 50 fixation of position test, 164
tests for myasthenia, 62 hand pronation test, 105
Pupillary reaction head retractor reflex, 124
startle reaction on examination of homolateral mass flexion reflex, 140
pupil, 43 knee bending test, 139
R knee dropping test, 110
Radial nerve paralysis leg extension test, 109
accessory nerve test, 72 lid lifting test, 47
brachioradialis test, 85 lid vibration test, 60
paralytic contractures, 78 orbicularis oculi reflex, 64
wrist drop test, 83 plantar muscle reflex, 132
S plantar skin reflex, 133
Scalenus anterior syndrome platysma test, 64
pressure test, 201 posture, 103
Sciatic neuritis pronator reflex, 126
kicking test, 206 tonus test, 113
pronator
nerve stretching test, 203
quadriceps tonus test, 114
tendon palpation test, 97
superficial and deep abdominal re
test for causalgia, 210
flexes, 127
Spastic bulbar palsy
tendon palpation test, 97
snout reflex, 121
Spastic paralysis (hemiplegia) test for pendulousness of legs, 115
acoustic tonus test, 115 test for syndrome of C-7, 81
acute unilateral post-traumatic my test for unilateral spinal cord affec
driasis, 36 tion, 135
tests based on weakness of muscles, test for syndrome of C-7, 81

117 test for arthrogenic muscular atro
tibialis associated movement, 139 phy, 212
trunk-thigh associated movement, Trigeminal nerve paralysis
138 testing for sensory mononeuritis,
unilateral reflex changes in pyrami 188
dal lesions, 133 testing skin areas for sensory change,
winking-jaw test, 58 189
wrist drop test, 83, 138 tests for lateral bulbar syndrome, 48
Spinal cord compression tests for myasthenia, 62
head bending test, 207
U
jugular compression test, 209
Ulnar nerve paralysis
pendulousness of legs test, 94
abduction position of little finger,
skin writing test, 191
89
Syringomyelia
brachioradialis test, 85
tests for dissociated anesthesia, 192
paralytic contractures, 78
tests for neurogenic arthropathy,
thumb abduction test in median
215
paralysis, 87
T
Tabes thumb bending test, 90
acoustic tonus test, 115 tests for dissociated anesthesia, 192
feet together - eyes closed test, 198 Unconsciousness, see also Coma
knee hyperextension test, 95 acute unilateral post-traumatic my
tendon palpation test, 97 driasis, 36
testing sensibility of mamillary zone, lateral deviation of eyes and head,
191 36
tests for dissociated anesthesia, 192 lid lifting test, 47
tests for neurogenic arthropathy,
V
215
Tetany Vasolability
facial nerve tapping test, 71 facial nerve tapping test, 7 1
nerve pressure test, 200 Vocal cord paralysis

Thyroid dysfunction tests for lateral bulbar syndrome, 48
exophthalmic ophthalmoplegia, 39 W
Torticollis "Winging" of the scapula
counterpressure test, 170
long thoracic nerve test, 82
Writing
test of resistance movement, 171
tests for torticollis, 165
macrographia, 181
Tremor
micrographia, 165
discrepancy triad in multiple scle Y
rosis, 182 Yawning
general, 156 contralateral associated leg exten
test for dermography, 211 sion, 146
Triceps muscle affection wrist drop test, 83
General Index
A associated movements of fingers, 144,

abdominal muscles, 163 145
abdominal reflexes, 127, 128 astereognosis, 178, 194, 195, 197, 198
abducent nerve, 48 athetosis, 105, 154, 156, 166, 195
accessory nerve, 72, 74, 90 B
accessory nerve test, 72
Babinski reflex, 28, 31, 102, 103, 111,
Achilles' tendon, 97, 98
113, 126, 130, 133, 147, 148,
acoustic nerve, 43, 48
150, 151, 182
adductor reflex, 134
Balfour, 27
adiadochokinesis, 173
barbiturates, 42
alcoholic polyneuritis, 97
Bell phenomenon, 39
algogenic postures, 103
blink reflex, 59
amyotrophic lateral sclerosis, 31, 59,
brachial monoplegia, 27
92, 121, 124, 125, 130, 151,
brachial plexus, 79
159
brachialgia statica paresthetica, or noc
anhidrosis, 46
turnal arm dysesthesias, 187,
anisocoria, 36
203
anterior cutaneous nerve of the thigh,
brachioradialis muscle, 85, 86
189
"broad thigh," 109
anterior serratus muscle, 82
Brown-Sequard syndrome, 136
anxiety neurosis, 62
Brudzinski, 30, 205, 207
aphasia, 42
buccinator muscle, 68, 69
arm stopping test, 174 C
arteriosclerosis, 121 calcaneal nerves, 189
arthrogenic muscular atrophy, 95, 212 Cassirer, 27
arthropathy, 214 causalgia, 210
associated movement(s), 39, 50, 52, cerebellopontile angle tumor, 28, 43,
53, 55, 57, 58, 59, 64, 67, 68, 55, 56, 59, 60, 98, 178, 180
69, 70, 71, 83, 84, 85, 136, cerebellum, 48, 50, 165, 172, 176,
137, 138, 139, 140 178, 180, 181
222
GENERAL INDEX 223
cerebral arteriosclerosis, 121, 123 dysmetria, 173

cerebrovascular accident, 36 dysphagia, 48
cervical spondylarthritis, 202, 212 dyssynergia, 172, 173, 175
cervical sympathetic, 44, 45, 46, 49, dystonia, 104, 156, 166, 170, 171
75
E
cheiralgia paresthetica, 189, 205
chorea, 24, 105, 156 "eating reflex," 122
chronic alcoholism, 121 encephalitis, 38
chronic cerebellar degeneration, 178 encephalopathies, 125
chronic progressive external ophthal enophthalmos, 45, 46
moplegia, 63 epidemic encephalitis, 28
ciliospinal center, 46 epilepsy, 23, 65, 136, 151
coma, 47, 48, 55, 65 eponyms, 32
compression of the spinal cord, 192 exophthalmic ophthalmoplegia, 39, 40
confrontation test, 197 extensor digitorum longus muscle, 140
conjugate downward gaze, 38 extensor hallucis longus muscle, 140
conjugate upward gaze, 38 external pterygoid muscle, 58
conjunctival reflex, 56 extrapyramidal motor system, 165,
contralateral associated leg extension, 166, 169, 170, 176, 180, 181
146
F
contralateral associated movements, 142
contralateral mass extension reflex, 146 facial muscle (s), 43, 60
convergence of the eyes, 40, 41, 42 facial nerve, 60, 62, 71, 72, 201
cord tumor, 125 facial pain, 55
corneal reflex, 43 facial paralysis, 59, 60, 61, 62, 63, 64,
counterpressure, 171 65, 66, 67, 68, 76, 78, 79, 201
Cushing, 26, 27 facial tic, 69,71
fanning of the toes, 152
D
fatigability, 63
"dance of the tendons," 100 fatigue, 42
decerebrate rigidity, 105 femoral neuritis, 95
decomposition of movement, 172, 173, finger flexor reflex, 119, 120
180 finger spreading test, 179
deep peroneal nerve, 189 Flexner, 27
deltoid, 213 flexor spasms of the lower extremity,
dermatomes, 190, 191 142
dermography, 62, 72, 2 1 1 "flight reflex," 153
deviation of the eyes, 36 Forestier, 26
digital nerve, 189 Foster Kennedy, 15, 22
dissociated anesthesia, 48, 192, 193 Froment, 30
dissociation between superficial and frontal lobe, 28, 36, 123, 154, 180
deep abdominal reflexes, 129 frontalis muscle, 46, 47, 62
dorsolateral sclerosis, 208
"dumb sole," 133
G
dysesthesia (s), 28, 29, 48, 55, 186, gait, 159
187, 188, 189, 204, 205 glossopharyngeal-vagus nerves, 48, 49
gluteal muscles, 93, 94, 213 K
groping reflex, 155
Kennedy, Foster, 15, 22
Kernig, 30, 205
H
knee bending test, 174
Hall, Marshall, 139, 147 Kristiansen, 25
hand pronation test, 105, 107
head dropping test, 66 L
head retractor reflex, 122 laboratory procedures, 21, 24, 25
head trauma, 37 Lasegue, 30, 204, 205
heel-knee test, 174 lateral bulbar syndrome, 43, 48, 49, 50,
hematomyelia, 193 177
hemifacial spasm, 69, 70, 71 lateral cutaneous nerve of the thigh,
hemiplegia, 37, 48, 58, 61, 64, 83, 105, 189, 190
106, 107, 108, 109, 110, 111, levator palpebrae muscle, 45, 46, 47,
113, 117, 118, 137, 139, 140, 50, 52, 53, 58
142, 143, 145, 147, 182 levator scapulae muscle, 90
hepatolenticular degeneration, 24, 159 lid flutter, 61, 62
herniated disk, 24, 208 line drawing test, 174
Hoffmann, 102, 126 Lipiodol, 26
homolateral mass flexion reflex, 142, "loose shoulders," 82
146, 150 lordosis, 94
Horner, 45 "lucid interval," 37
hydrocephalus, 155
hypermetria, 172, 173 M
hyperirritability, 72, 201 malingerer, 100, 199, 205
hyperpronation test, 174
mamillary zone, 191
hypertensive encephalopathy, 121, 159
Marcus Gunn, 57
hyperventilation, 72 Marshall Hall, 139, 147
hypoglossal nerve test, 74, 75
masseter reflex, 120
hypoglossal paralysis, 76
mechanic-myotonic reaction, 93
hypothalamic region, 38, 46
median nerve, 79, 85, 87, 91
hypothyroidism, 71
median paralysis, 87, 88
hysteria, 56, 57, 62, 71, 100, 105,
Mendel-Bechterew, 103
142, 147, 170
mentalis muscle, 71
meralgia paresthetica, 189
I
middle meningeal artery, 37
idiocy, 121 Mitchell, Weir, 210
idiomuscular contraction, 92 monoplegia, 83
internal rectus, 50, 52, 53 multiple sclerosis, 24, 142, 156, 178,
182, 183, 194, 196, 208
intervertebral disk, 97, 207
muscle tonus, 94, 97
J muscular dystrophy, 24, 82, 83, 90,

92, 93, 94, 95
jaw muscle reflex, 122 myasthenia, 23, 40, 62, 63, 71, 184
jaw-winking test, 57 mydriasis, 36, 37, 38, 45
GENERAL INDEX 225
myelography, 24 pendulousness of arms or legs, 66, 116
myosis, 44, 45 Penfield, 25
myotonia, 92, 93 peroneal nerve, 72, 79, 99, 191, 200
pharyngeal reflex, 57
N
pinwheel, 127, 128
nerve stretching test, 187 plantar muscle, 132, 133
nervous hyperirritability, 61, 62, 72, plantar reflex, 119
212 plantar skin reflex, 148
neurasthenia, 62 platysma, 64, 67
neuritis, 186, 200, 203, 204, 206 "points douloureux," 200
neuritis of the Cauda equina, 95 poliomyelitis, 24, 95
neurology, 14, 22 polyneuritis, 24, 78, 97, 99, 191, 194,
nocturnal arm dysesthesias, 187, 188 199, 208
nystagmus, 42, 43, 48, 182 polyradiculoneuritis, 208
postanesthetic spinal syndrome, 95
O
posterior columns, 191, 192
observation, 26 posterior cutaneous nerve of the fore
oculomoror nerve, 37, 38, 50, 52, 55, arm, 189
66 posterior inferior cerebellar artery, 43,
oculomotor paralysis, 37, 45, 47, 52, 44, 48, 49, 177
53, 54 posture, 103, 105
olivopontocerebellar atrophy, 24, 177, prepatellar branch of the saphenous
178 nerve, 189
Oppenheim, 28, 103 presenile dementia, 24
orbicularis oculi muscle, 55, 58, 59, primary lateral sclerosis, 24
64, 65, 66, 67, 68 progressive paralysis, 121
orbicularis oculi reflex, 42, 61, 66, 67 progressive spinal muscular atrophy,
orbicularis oris, 68, 122 92, 94, 95
Osier, 26, 27 prolapse of intervertebral disk, 95, 97
psychogenic paralysis, 108
P
ptosis, 44, 45, 46, 47, 48, 49, 50, 52,
pallidal degeneration, 159 53, 54, 55, 57, 58, 62, 63
palmomental reflex, 71 pupil, 44
"paradoxic muscle contraction," 164 pupillary reaction, 40, 43, 44
paralytic contracture ( s ) , 78, 79, 81, pyramidal lesion(s), 115, 116, 117,
90, 104 126, 127, 128, 130, 132, 134,
paraplegia in extension, 142 139, 148, 160, 162
paraplegia in flexion, 142 pyramidal sign(s), 101, 102, 103,
paresthesia (s), 186, 189, 201, 203, 105, 108, 113, 119, 125, 126,
205, 206, 208 138, 143, 147, 159, 179
parietal lobe, 195
Parkinson's disease, 24, 41, 42, 66, Q
114, 156, 157, 158, 159, 160, quadriceps, 215
161, 162, 163, 164, 165, 179, quadriceps reflex, 135, 163
180 quadrigeminal plate, 38
pectoralis, 92 Queckenstedt test, 209
R semeiology, 29
radial nerve, 79, 83, 84, 85, 90, 189 senile dementia, 121
radial paralysis, 72, 85, 86 sensibility (examination for) , 185
radiculitis, 95 sensory mononeuritis, 190
range of movement, 87, 118 sensory polyneuritis, 188
reflex (es) sensory system, 184
Babinski, 147 sign, 29
corneal, 55 skull fracture, 37
dissociation between superficial snout reflex, 125
and
soft palate, 48
deep abdominal, 129
finger flexor, 126 spastic bulbar palsy, 122, 123
spastic paralysis, 72, 82, 83, 85, 105,
grasp, 154
106, 107, 109, 113, 114, 116,
head retractor, 124
125, 130, 135, 136, 137, 139,
homolateral mass flexion, 140
jaw muscle, 120 140, 141, 142, 144
orbicularis oculi, 64 Spiller, 31
spinal cord, 95, 207
pathological laughing and crying,
sternocleidomastoid, 72
123
plantar muscle, 132 "sucking" reflex, 122
plantar skin, 133 superior tarsal muscle, 45
pronator, 126 supraorbital nerve, 65
sympathetic nerve, 48
quadriceps, 130
snout, 121 symptom, 29
superficial and deep abdominal, 127 symptomatology, 29
triceps surae, 98, 119, 131, 132, 135 syringomyelia, 193
unilateral changes in a pyramidal

lesion, 133
T
reflexes, 30, 102, 133, 134 tabes, 46, 47, 95, 97, 98, 99, 115, 191,
reflexes (deep muscle), 119, 120, 121, 193, 199
122, 124, 134 temporal lobe, 28
reflexes (superficial), 119, 120 test(s)
reinforcement, 119, 126, 128 abduction position of little finger
Remak, 147 in ulnar paralysis, 89
retrocollis, 166 accessory nerve, 72
rickets, 71 acoustic tonus, 115
Romberg, 22, 30, 198, 199 acute unilateral post-traumatic my
Rossolimo, 102, 103 driasis, 36
Ruskin, 32 agonist-antagonist, 175
arm deviation, 106, 165, 176
S
arm dropping, 161
saphenous nerve, 189 arm stopping, 174
scalenus anterior syndrome, 201 arm tapping, 174
sciatic neuritis, 97 arthrogenic muscular atrophy, 212
sciatica, 98, 206 associated movements in hemifacial
see-saw sign, 52 spasm, 69
GENERAL INDEX 227
astereognosis, 194 lid lifting, 47

ataxia, 181 lid vibration, 60
blinking, 59 line drawing, 174
brachioradialis, 85 long thoracic nerve, 82
cervical sympathetic, 44 macrographia, 181
contralateral identical associated micrographia, 165
movements of fingers, 145 muscle percussion, 92
contralateral leg extension, 146 myasthenia, 62
convergence paralysis of the eyes, 40 nerve pressure, 200
counterpressure, 170 nerve stretching, 203
demography, 211 nerve tapping, 203
dissociated anesthesia, 192 neurogenic arthropathy, 215
doll's eyes, 38 nystagmus, 42
everted position of the foot, 108 paralysis of conjugate upward gaze,
exophthalmic ophthalmoplegia, 39 38
facial nerve tapping, 71 pendulousness of the arms, 159
facial nerve tenderness, 201 pendulousness of the legs, 94, 115,
feet together-eyes closed, 198 162
finger spreading, 178 platysma, 64
finger-tips in the midline, 178 play of foot tendons, 99
fixation of position, 164 preferential choice, 195
frontalis muscle, 62 pressure in scalenus anterior syn
gluteal muscles, 93 drome, 201
hand pronation, 105
pronator tonus, 113
head bending, 207
ptosis, 46
head dropping, 157
push, 163
heel-knee, 174
homolateral mass flexion, 140 quadriceps tonus, 114
hypermetria, 174 resistance movement, 171
hyperpronation, 174 see-saw in oculomotor paralysis, 52

hypoglossal nerve, 74 sensibility of the mamillary zone,
intrafacial associated movements in 191
old facial paralysis, 66 shoulder shaking, 161, 179
intraoculomotor associated move simultaneous double sensory stimu
ments, 50 lation, 197
jaw-winking, 57 skin areas for sensory change, 189
jugular compression, 209 skin writing, 191
kicking in sciatica, 206 startle reaction on examination of
knee bending, 139, 174 the pupil, 43
knee dropping, 110 static ataxia of hand and fingers,
knee hyperextension in tabes, 95 195
lateral bulbar syndrome, 48 syndrome of C-7, 81
lateral deviation of the eyes and of tendon palpation, 97
the head, 36 thumb abduction in median pa
leg extension, 109 ralysis, 87
thumb bending in ulnar paralysis, triceps surae reflex, 98, 119, 131, 132,
90 135
tibialis associated movement, 139 trigeminal, 48, 55, 58, 59, 120, 189,
torticollis, 165 190, 200
triceps, 79, 82, 92 trunk-thigh associated movement, 138,
trunk-thigh associated movement, 139
138 tumor, 208, 209
unilateral changes in pyramidal Twain, Mark, 147
lesion, 133
unilateral spinal cord affection, 135 U
upper brachial plexus paralysis, 79
ulnar nerve, 72, 79, 85, 87, 89, 90,
weakness of muscles in spastic pa
190, 191, 200
ralysis, 117
ulnar palsy (late), 92
wet-dry for causalgia, 210
ulnar paralysis, 89, 90
winking-jaw, 58 uvula, 50
wrist drop, 83, 138
tetanus, 60 V
tetany, 71, 72, 20i
thyroid, 39, 40, 45, 46 Valleix, 200
tibialis anterior, 140 vasolability, 72
tonus (of muscles), 97, 114, 115 vertigo, 48

torticollis, 159, 166, 167, 168, 169, vibration test, 66
170, 171 vocal cord paralysis, 50

"torticollis mental," 165 vomiting, 48
transversus auris muscle, 71
trapezius muscle, 72
W
tremor, 61, 62, 72, 157, 158, 165, Westphal, 164
178, 182, 212 Weir Mitchell, 210
triad of Charcot, 182 "winging" (of scapula), 82, 83
triceps, 82, 92, 213 "wolfing" reflex, 122
triceps reflex, 134 wrist drop, 83, 84, 85, 138

WARTENBERG Diagnostic Tests in Neurology - Cópia

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3^ 71S

A SELECTION FOR OFFICE USE

"Science is simply common sense at its best-

Thomas Henry Huxley (1825-1895)

"Science is simply common sense at its best-

Thomas Henry Huxley (1825-1895)

By ROBERT WARTENBERG, M.D.

STANLEY TRUMAN, M.D

THE YEAR BOOK PUBLISHERS, INC.

DANIEL EDWARD KOSHLAND

by Sir Gordon Holmes

THERE has been within recent years an increasing tendency to

I WISH that you could know Dr. Wartenberg as I know him.

comprehensible and memorable manner. This book is an expansion

THIS book is not a primer, not an outline, not a textbook of

have chosen the most difficult and exacting medical specialty of

that the patient with an organic disease of the nervous system

comparatively rare sight in the office of the practitioner.

of course, purely individual and reflects the inter

refers As Foster Kennedy brilliantly

University of California Hospital

Figures 15, 21, 48, 62, A and B, have been made

secretarial help given unstintedly over a period of 12

years, my appreciative thanks.

Clinic versus Laboratory 21

The Power of Observation 26

Examination in the Office 34

SECTION I: CRANIAL NERVES

Doll's Eyes Test 38

See-Saw Test in Oculomotor Paralysis 52

Jaw- Winking Test 57

Lid Vibration Test 60

Accessory Nerve Test 72

Hypoglossal Nerve Test 74

SECTION II: PERIPHERAL NERVES

Test for Upper Brachial Plexus Paralysis 80

Long Thoracic Nerve Test 82

Wrist Drop Test 83

Test of the Gluteal Muscles 93

SECTION III: PYRAMIDAL SYSTEM

Arm Deviation Test 106

Everted Position of the Foot 108

Leg Extension Test 109

Pronator Tonus Test 113

Quadriceps Tonus Test 114

Acoustic Tonus Test 115

Test for Pendulousness of the Legs 115

Tests Based on Weakness of Muscles in Spastic Paralysis .... 1 17

Reflexes: General 119

Jaw Muscle Reflex 120

Pathological Laughing and Crying 123

Finger Flexor Reflex 126

Superficial and Deep Abdominal Reflexes 127

Quadriceps Reflex 130

Trunk-Thigh Associated Movement 138

Contralateral Associated Movements 142

Contralateral Identical Associated Movements of Fingers . 145

SECTION IV: EXTRAPYRAMIDAL SYSTEM

Arm Dropping Test lol

Push Test 163

Fixation of Position Test 164

Arm Deviation Test 165

Tests for Torticollis 165