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Rehabilitation of The Spine: A Practitioner's Manual
Rehabilitation of The Spine: A Practitioner's Manual
of the Spine
Second Edition
A Practitioner's Manual
Craig Liebenson, Editor
15
McKenzie Spinal
Rehabilitation Methods
Gary Jacob, Robin McKenzie, and Steve Heffner
Introduction
The Three Syndrome Patterns and
Explanations
Postural Syndrome
Dysfunction Syndrome
Derangement Syndrome
Acute Spinal Antalgia Paradigms of
McKenzie Method Derangement
Management
Kyphotic Antalgia ManagementExtension
PrinciplePosterior Derangement
Acute Coronal Antalgia Management:
Lateral-Then-Extension PrincipleRelevant
Postero-Lateral Derangement
Acute Lordotic Antalgic ManagementFlexion
PrincipleAnterior Derangement
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Learning Objectives
After reading this chapter you should be able to
understand
Introduction
The goal of rehabilitation is independence in self-care.
To serve that purpose, spinal rehabilitation pro-motes
self-efficacy. However, such efforts are often delayed
when clinicians provide passive, palliative comfort
care while waiting for things to "calm down" before the
"good stuff" (rehabilitation) is introduced. The
combined fears of patient and practitioner may be
roadblocks to the exploration of patient self-generated
movements for therapeutic purposes. The specter of
dependency and deconditioning of physique and
psyche is raised when patients are passive receptacles
of care. Any delay in patient active participation is a
delay in developing patient empowerment through
self-management skills, the ultimate goal of
rehabilitation.
This chapter introduces McKenzie Method management of common lower cervical and lower lumbar
spinal symptoms, which uses patient-generated
movements for acute and chronic symptoms. Whether
acute or chronic, McKenzie Method concepts and
skills promote independence in self-care from day one,
without passive therapy detours on the rehabilitation
road to recovery. The McKenzie Method educates
patients regarding movement and positioning
strategies that have the potential to rapidly ameliorate
complaints if the practitioner and patient choose to
make self-generated movement and positioning the
centerpiece of care.
This chapter attempts to enrich the reader's appreciation of the conceptual foundations of the
McKenzie Method to promote facility with its practical
applications. Our consideration of McKenzie Method
management of common lower cervical and lower
lumbar symptoms is but a slice of the McKenzie
Method "pie" and does not include appropriate
McKenzie Method management of headaches, the
extremities, adherent nerve root (epidural fibrosis),
nerve root entrapment, and other conditions. Further
study is encouraged by means of the texts authored
by Robin McKenzie (57) and postgraduate study
within the McKenzie Institute International (1). We
close the chapter with only a brief consideration of the
research literature and the reader is directed to the
Literature Relevant to the McKenzie Method on the
McKenzie Institute International web site (2) to peruse
the expansive literature regarding the McKenzie
Method.
The Three Syndrome Patterns and Explanations
The McKenzie Method recognizes three clinical
pat-terns (syndromes) of mechanical and
symptomatic responses to loading that are
amenable to mechanical (movement and positioning)
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Postural Syndrome:
Pathoanatomical Explanation
Postural syndrome patterns are the result of an
excessive amount or duration of end range loading
Dysfunction Syndrome:
Phenomenological Pattern
Practice-Base Problem
333
Figure 15.3 Slouched (A), overcorrect (B), let go 10% to neutral lordotic sitting (C).
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Dysfunction Syndrome:
Pathoanatomical Explanation
The model for the dysfunction syndrome is that of
"short" tissue," i.e., tissue resistant to flexibility
demands. It involves the adverse reaction of normal
loads on abnormal tissue. The solution is to promote
flexibility by means of frequent end range loading to
remodel tissue. Improvement is increased flexibility,
congruent with strategies to "stretch" or remodel short
tissue.
Clinical Pearl
Clinical
Pearl
For the postural syndrome, the motto "if it hurts don't do
it" applies; the remedy is to avoid loading at the
symptomatic mechanically unimpeded end range. The
principal is one of end range loathing. For the
dysfunction syndrome, the motto "no pain no gain"
applies; the remedy is to pursue loading at the
symptomatic mechanically impeded end range. The
principal is one of end range loading.
Clinical
Pearl
Clinical
Pearl
Shortened tissue is often erroneously assumed to be the
cause of symptoms. A careful evaluation often fails to
demonstrate the expected painful loss of motion.
Practice-Based Problem
Problem
Practice-Based
Is the location of symptoms or palpation findings
adequate to determine the presence of shortened
muscular tissue? What other information might be
important?
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Derangement Syndrome
Derangement Syndrome:
Phenomenological Pattern
A mechanically unimpeded end range is an end
range of motion that is not restricted by
mechanical factors.
Table 15.1 Predicted Painful Motion Restrictions Based on Particular Muscles Being Short
Muscle Shortened
Paravertebral
Suboccipital
Upper trapezius
SCM
Levator scapulae
Rhomboids
QL
Psoas
Piriformis
Gluteus maximus
Flexion
Cervical flexion and lateral flexion to opposite side
Cervical flexion, rotation to opposite side
Cervical extension, rotation to same side
Cervical flexion, rotation to opposite side
Raising of the arm on the same side
Lumbar flexion, lateral flexion to opposite side
Thoracolumbar and hip extension
Hip adduction and internal rotation
Hip flexion and internal rotation
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and
1. Posterior derangements
2. Relevant posterolateral derangements
3. Anterior derangements
The examples considered for the three subtypes of
derangements will be three spinal antalgias, which
serve as excellent examples of derangements because
all of the potential derangement features are present
in these "extreme" cases.
An acute kyphotic antalgia (Fig. 15.4) would be an
extreme example of a posterior derangement. An acute
coronal antalgia (lumbar scoliosis or acute cervical
torticollis) (Figs. 15.5 and 15.21) would be extreme
example of a relevant posterolateral derangement.
An acute lordotic antalgia (Fig. 15.24) would be an
extreme example of an anterior derangement.
Derangement Syndrome:
Pathoanatomical Explanation
Intradiscal nuclear derangement is the model used to
explain the dramatic and long-lasting detrimental or
beneficial responses to movement and positioning
exhibited by lower cervical and lower lumbar derangement syndrome patterns.
The intradiscal nuclear derangement model considers compression rather than stretching forces to
explain mechanical and symptomatic responses.
Habitual loading in one movement plane direction
compresses and displaces intradiscal nuclear
material in another, often opposite, movement plane
direction. Loading in directions that promote
intradiscal derangement of nuclear material may
cause
adverse
mechanical
and
symptomatic
responses in the beginning, middle, and end range of
that movement plane direction as the derangement
progresses as movement progresses. The end range
of the detrimental direction is mechanically
unimpeded as intervertebral disc material has been
displaced or "pushed out of the way," thus offering
less resistance to compression of the intervertebral
disc (approximation of vertebral end plates) in that
direction.
The accumulation of displaced/deranged intradiscal nuclear material causes a painful obstruction to
end range loading (mechanically impeded end range)
in the movement plane direction it has deranged into.
An example would be flexion causing derangement of
intradiscal nuclear material posterior, which then
obstructs (get in the way of) extension. The
accumulated intradiscal nuclear material offers a
337
greater
resistance
to
compressive
forces
(approximation of vertebral end plates). Mechanical
and symptomatic responses in the movement plane
direction within which the accumulated intradiscal
nuclear material has deranged are not realized until
the obstruction offered by that material is met, i.e., at
the mechanically impeded end range. Mechanical
and/or symptomatic responses do not occur during
motion in the direction of the obstructed end
rangethe movement that caused the nuclear
displacement is being avoided and the accumulated
deranged nuclear material has yet to be
encountered.
The remedy is to compress the accumulated
de-ranged nuclear material (the obstruction to
movement), to reduce the derangement, i.e., to send
displaced nuclear material back from whence it came,
i.e., to a more " central " intervertebral disc location.
As nuclear material migrates through posterior,
lateral, or anterior annular tears, symptoms migrate
in similar directions. If loading strategies cause
nuclear material to migrate to a more central or
peripheral location, the topography of symptoms
follows suit. Changes in symptom location may be
referred to as centralization and peripheralization,
respectively. A response to loading involving an
increase of central symptoms with diminution of
peripheral symptoms (centralization) has a positive
prognosis and is appreciated as reflecting the return
of deranged intradiscal nuclear material to a more
central location. As intradiscal nuclear material
returns to a more central location, so do symptoms.
As intradiscal nuclear material returns to a central,
more confined, more highly pressurized environment, an increase of the intensity of central
symptoms (at times, a pressure-type pain) may
occur. A response to loading causing an increase of
peripheral symptoms (peripheralization) has a
negative prognosis, even if symptom intensity
lessens, and is appreciated as reflecting intradiscal
nuclear material deranging peripheral from its
normal, central location.
The positing of the intervertebral disc nuclear
derangement model fleshes out phenomenological
observations, as follows.
Posterior Derangement Pathoanatomical
Explanation
Posterior Derangement Direction
of Detriment: Flexion
Flexion is the mechanically unimpeded
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Clinical Pearl
In a posterior derangement, mechanically restricted
ex-tension is increased by flexion loading. Extension
loading diminishes the provocative effect of flexion.
339
340
Kyphotic Antalgia
ManagementExtension
PrinciplePosterior Derangement
Lumbar Kyphotic Antalgia
ManagementExtension PrinciplePosterior
Derangement
The patient presenting with a lumbar kyphotic antalgia
(Fig. 15.6) typically has symptoms that are central or
symmetrical and do not radiate beyond the knee,
consistent with a central, posterior derangement that
does not affect more lateral articular or neurologic
structures.
There are detrimental responses within the mechanically unimpeded flexion movement plane direction, both
during motion and at end range. For extension there are
responses at that mechanically impeded end range only.
There are no responses "during motion" for extension
because extension motion is not possible (there is no
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344
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As with the lumbar spine, subsequent to the achievement of full pain-free extension, flexion would be revisited to confirm whether flexion is still provoked
derangement or if a flexion dysfunction developed
because of avoidance of flexion. Flexion would continue to be avoided if it was determined that it still promoted posterior derangement. Flexion would be
pursued if the pattern of reaction was consistent with
flexion dysfunction and would be followed by extension as a prophylactic measure to ensure the recent
reduction of posterior derangement stayed that way.
Figure 15.18 Right side-gliding against the wall to correct a left lateral shift.
347
348
antalgia demonstrated.
derangement is reduced/eliminated.
Cervical Acute Torticolis Antalgia
Management
As with lumbar scoliosis, cervical antalgia in the
coronal plane (i.e., torticollis) (Fig. 15.21) may or
may not be associated with kyphotic antalgia. As
with lumbar scoliosis, whether a kyphotic
component is visible or not, after the coronal
movement plane direction opposite the antalgia is
recovered, the extension principle is explored. As
with cervical acute kyphotic antalgia, manual
axial traction is required to get things going.
Soon thereafter, the responsibility of treatment
is transferred to the patient using techniques
resembling what the clinician used.
The patient is placed supine with the head
comfortably placed on a pillow in a manner that
does not challenge the antalgia. The therapist's
manual contacts are the same as were used with
the cervical kyphotic antalgia. Axial traction is
applied, at first in the direction of the antalgia.
While maintaining axial traction, a lateral flexion
mobilization is conducted in the direction
opposite the antalgia until the painful obstruction
is met at which point there is a momentary pause
(Fig. 15.22). The therapist then backs off to the
first point of tolerable discomfort, pauses a
moment (traction maintained throughout), and
repeats the procedure, gaining lateral flexion in
the direction opposite the antalgia with each
repetition. If lateral flexion fails, the coupled
motion of rotation may be attempted in its place,
using the same protocols.
As with the lumbar spine, premature attempts
to recover extension may be detrimental. Unlike
the lumbar spine, combined lateral and extension
movements are not used. As is occasionally the
case with the lumbar spine, cervical coronal
antalgia more often requires a degree of flexion be
maintained when recovering lateral movements.
As with the lumbar spine, subsequent to the
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Clinical Pearl
Clinical Pearl
Considering the lower cervical and lower lumbar flexion
stressors in everyday life (e.g., prolonged sitting, bending), one would predict that flexion as a treatment of
lower cervical and lower lumbar symptoms would be the
exception rather than the rule. It has been our experience
that conditions requiring flexion are less common than
those requiring extension.
350
" McKenzie
CONCLUSION
McKenzie Method clinical reasoning would predict
that a majority of individuals with spinal symptoms
would benefit from minimizing flexion and periodically pursuing extension, considering the amount of
time we spend flexed in everyday life. The McKenzie
Method predicts that loading in one movement plane
direction may be more beneficial than loading in
other movement plane directions whether symptoms
are acute or chronic. These predictions have been
verified
within
the
recent
peer-reviewed
evidence-based literature.
Snook (8) demonstrated how controlling lumbar
flexion in the early morning serves as a form of
self-care for reducing pain and costs associated with
chronic, non-specific low back pain. The McKenzie
Method predicts that avoiding flexion would minimize low back pain for most patients. Early morning
flexion is perceived to be particularly provocative
because of imbibition of fluid by intradiscal nuclear
material over a night of unloading. Theoretically, if
the patient has posterior derangement of nuclear
material, the imbibition of fluid makes intradiscal
nuclear pressures and the risk of debilitating derangements even greater.
Larsen, Weidick and Leboeuf-Yde (3) demonstrated
it may be possible to reduce the prevalence of back
problems and use of health care services during
military service, at a low cost, using lumbar prone
extensions with a back/ergonomic school including
McKenzie Method disc theories. Military recruits
A
Figure 15.25 Promotion of lumbar flexion.
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Audit Process
Audit P r o c e s s
Self-Check of the Chapter's Learning Objectives
What are the three syndromes as defined by the
McKenzie Method?
What are the responses during motion and at end
range for each syndrome?
What is the role of pursuing or avoiding end range
loading for each syndrome?
According to the McKenzie Method, what are the
possible reasons a patient might experience
increased discomfort with sitting versus standing
and vice versa? Consider each syndrome and
subtypes to account for the phenomena.
REFERENCES
1. McKenzie Institute International home page
http://www.mckenziemdt.org. Accessed May 9, 2005.
2. Literature Relevant to the McKenzie Method @
http://www.mckenziemdt.org/libResearchList.cfm?
pSection=int. Accessed May 9, 2005.
3. Larsen K, Weidick F, Leboeuf-Yde C. Can passive
prone extensions of the back prevent back problems? A
randomized, controlled intervention trial of 314 military
conscripts. Spine 2002;27(24):2747-2752.
4. Long A, Donelson R, Fung T. Does it matter which
exercise? A randomized control trial of exercise for
low back pain. Spine 2004;29(23):2593-2602.
5. McKenzie R. The Cervical and Thoracic Spine
Mechanical Diagnosis and Therapy. Waikanae, New
Zealand: Spinal Publications, 1990.
6. McKenzie R, May S. The Lumbar Spine Mechanical
Diagnosis & Therapy, volume one and volume two.
Waikanae, New Zealand: Spinal Publications, 2003.
7. McKenzie R, May S. The Human Extremities Diagnosis & Therapy. Waikanae, New Zealand: Spinal
Publications, 2000.
8. Snook SH, Webster BS, McGorry RW. The reduction of
chronic, nonspecific low back pain through the control
of early morning lumbar flexion: 3-year
follow-up. J Occup Rehabil 2002;12(l):13-19.