mckenzie spinal rehabilitation

7/27/2019 Mckenzie Spinal Rehabilitation

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Second Edition

A Practitioner's Manual

Craig Liebenson, Editor

Lippincott Williams & Wilkinsa Wolters Kluwer businessPhiladelphia • Baltimore • New York • LondonBuenos Aires • Hong Kong • Sydney • Tokyo

Rehabilitation

of the Spine



15McKenzie SpinalRehabilitation Methods

Gary Jacob, Robin McKenzie, and Steve Heffner

IntroductionThe Three Syndrome Patterns and

ExplanationsPostural Syndrome

Dysfunction SyndromeDerangement Syndrome

Acute Spinal Antalgia Paradigms of McKenzie Method DerangementManagement

Kyphotic Antalgia Management—ExtensionPrinciple—Posterior DerangementAcute Coronal Antalgia Management:Lateral-Then-Extension Principle—RelevantPostero-Lateral DerangementAcute Lordotic Antalgic Management—FlexionPrinciple—Anterior Derangement

Learning Objectives After reading thi s chapter you should be able to

understand

• McKenzie Method descriptions of patterns of mechanical and symptomatic responses tomovement and positioning

• McKenzie Method classification of mechanicaland symptomatic response patterns into threesyndromes: the postural, dysfunction, andderangement syndromes

• McKenzie Method pathoanatomical explanationsof the syndrome patterns

• Management of the postural, dysfunction, andderangement syndromes

330



Chapter Fifteen: McKenzie Spinal Rehabilitation Methods 331

Introduction

The goal of rehabilitation is independence in self-care. To serve that purpose, spinal rehabilitation pro-motesself-efficacy. However, such efforts are often delayedwhen clinicians provide passive, palliative comfortcare while waiting for things to "calm down" before the"good stuff" (rehabilitation) is introduced. Thecombined fears of patient and practitioner may beroadblocks to the exploration of patient self-generatedmovements for therapeutic purposes. The specter of dependency and deconditioning of physique andpsyche is raised when patients are passive receptaclesof care. Any delay in patient active participation is adelay in developing patient empowerment throughself-management skills, the ultimate goal of rehabilitation.

This chapter introduces McKenzie Method man-agement of common lower cervical and lower lumbarspinal symptoms, which uses patient-generatedmovements for acute and chronic symptoms. Whetheracute or chronic, McKenzie Method concepts andskills promote independence in self-care from day one,without passive therapy detours on the rehabilitationroad to recovery. The McKenzie Method educatespatients regarding movement and positioningstrategies that have the potential to rapidly amelioratecomplaints if the practitioner and patient choose tomake self-generated movement and positioning thecenterpiece of care.

This chapter attempts to enrich the reader's ap-preciation of the conceptual foundations of theMcKenzie Method to promote facility with its practicalapplications. Our consideration of McKenzie Methodmanagement of common lower cervical and lowerlumbar symptoms is but a slice of the McKenzieMethod "pie" and does not include appropriateMcKenzie Method management of headaches, theextremities, adherent nerve root (epidural fibrosis),nerve root entrapment, and other conditions. Furtherstudy is encouraged by means of the texts authoredby Robin McKenzie (5—7) and postgraduate study within the McKenzie Institute International (1). Weclose the chapter with only a brief consideration of theresearch literature and the reader is directed to theLiterature Relevant to the McKenzie Method on theMcKenzie Institute International web site (2) to perusethe expansive literature regarding the McKenzieMethod.

The Three Syndrome Patterns and Explanations

The McKenzie Method recognizes three clinicalpat-terns (syndromes) of mechanical andsymptomatic responses to loading that areamenable to mechanical (movement and positioning)

therapies. The constructs of these three syndromesoccur on two levels. The first level is the description of phenomenological patterns of mechanical andsymptomatic responses to spinal loading. The secondlevel is the pathoanatomical explanations of those

phenomenological patterns. The syndromes are namedafter the pathoanatomical explanations, but this shouldnot detract from the phenomenological observations onwhich those explanations are based.

We first consider the phenomenological patterns(the what) of the syndromes, after which we considerthe pathoanatomical models proposed to make senseof what occurs (the why). Phenomenology gives equalimportance to subjective and objective data and resiststemptations to conjecture what the pathoanatomicalunderpinnings are. A phenomenological accounting formechanical and symptomatic responses to loadingincludes a meticulous description of objective

phenomena that can be observed and measured by clinicians (ranges of motion, antalgic posturing, etc.)and subjective phenomenon reported by the patient(symptom location, frequency, quality, duration,provocations/ palliations, etc.). Consideringphenomenology before pathoanatomy permits a betterappreciation of phenomena, permits the reader to posithis or her own pathoanatomical explanations toexplain the why of what's going, and enables one toappreciate how McKenzie Method pathoanatomicalexplanations account for phenomenon.

The three syndrome patterns of mechanical andsymptomatic responses to loading for which therapeutic

movement and positioning strategies may be used areas follows.

The Postural Syndrome The Dysfunction Syndrome The Derangement Syndrome

Although the syndromes are named according toMcKenzie Method pathoanatomical explanations, wewill, for each syndrome, first consider how the patternsbehave and then consider the explanation for thosebehaviors.

Postural Syndrome

Postural Syndrome: Phenomenological Pattern Exam-ination of the postural syndrome patient reveals full andpain-free range of motion. Symptoms are only elicitedwith sustained end range loading, a "finding" typically obtained from history versus the examination.



332 Part Four: Acu te Care management (first 4 weeks)

Figure 15.1 The bent finger.

Symptoms are intermittent because they only occurwith sustained end range loading, a position typically only assumed intermittently. There are no responsesat beginning or middle range. There is nopractitioner-observed or patient-perceived range of motion loss or deviation from intended movementplane directions. There is no particular "curative"direction to load in.

It takes time for the end range loading to be

provocative, i.e., the end range loading must bepro-longed and static. The symptoms at themechanically unimpeded end range are in response toan abnormal amount or (more commonly) duration of load at that end range.

Symptoms cease once the end range loading ceases. The reaction occurs only at the end range being loaded.Loading in other movement plane directions has noeffect on the reaction at the mechanically unimpededend range, nor does loading at the mechanically unimpeded end range affect other movement planedirections.

The remedy is to avoid loading at the provocative

mechanically unimpeded end range, which eventually results in resolution of its symptomatic effects.Although the postural syndrome can occur in any

movement plane direction, the movement planedirection most commonly culpable for lower cervicaland lower lumbar postural syndrome symptoms isflexion.

Postural Syndrome:Pathoanatomical Explanation

Postural syndrome patterns are the result of anexcessive amount or duration of end range loading

of normal articular containing or restraining elemen The solution is to avoid the excessive end rangloading, i.e., to adopt new postural habits that do nochallenge restraining or containing elements. Normtissue can be symptomatic in response to abnormforces without there having to be something wronwith the tissue. If the tissue is normal but the load "wrong" (i.e., abnormal), symptoms may result.

The McKenzie Method uses the "bent finger" astool to educate about the postural syndrome (Fi15.1).

If a healthy finger is hyperextended far enough, aabnormal amount of force is brought to bear on nomal structures, causing discomfort. If the finger werhyperextended to the point of pain and then backeoff to the first point of no pain, sustaining that postion over time would result in discomfort caused bthe abnormal duration of force brought to bear onormal structures.

Postural Syndrome: Clinical Intervention

The most common postural syndrome provocateufor the lower cervical and lower lumbar spine is sutained flexion. For many, flexion is the most frequenposture assumed throughout the day as it is prmoted with sitting slouched and other activities (Fi15.2).

Figure 15.2 Slouched posture when sitting.



Certain patients report pain absent any range of motionloss or painful examination findings (e.g., mobility andorthopedic tests). What mechanical explanation would

account for this if psychological and systemic factorshave been excluded?

Sitting is frequently reported by patients to becausing, perpetuating, or aggravating lower cervicaland lower lumbar symptoms. Reports of aggrava-tion from sitting should raise suspicions that cor-rection of sitting posture has clinical relevance. As aresult of common relaxed slouched sitting, theupper cervical spine is at extension end range,whereas inferior spinal levels (i.e., the rest of thespine) are at as much flexion end range as slouchedsitting position permits.

For the lower cervical and lower lumbar spine,aggravation from sustained flexion would cause oneto consider the maintenance of lordosis (beginning

range extension positioning) as a remedy. Consider-ing the amount of time people spend sitting symp-tomatically slouched, McKenzie Method posturalcorrection most often concerns correction of theslouched sitting posture. The McKenzie Method usesthe slouch-overcorrect-relax strategy to help patientsfind appropriate lordotic sitting posture. The patientbegins from the slouched, provocative sitting postureand then "overcorrects " by simultaneously hyper-extending the lumbar spine andhyper-retracting the head and neck. The patient then"lets go 10%" to find the neutral sitting posture (Fig.15.3).

Postural syndrome principles are consistent withstabilization philosophies of avoiding excessive endrange loading and remaining safe within a neutralzone. The postural syndrome theme may thereforebe characterized as end range loathing.

Dysfunction Syndrome:Phenomenological Pattern

There is loss of range of motion with a new, premature,limited symptomatic end range being established.Loading at the premature, limited symptomatic endrange results in a beneficial reaction at that end range

only.Repetitive loading at that end range results in nosignificant changes during the examination, other thana temporary increase in discomfort every time loadingat the limited mechanically impeded end range occurs.It takes days, weeks, or months of repetitivemechanically impeded end range loading to achieve abeneficial effect. Benefit is not derived from avoidingany movement plane direction in particular.

The dysfunction syndrome pattern is one where-inloading at a mechanically impeded end range results insymptoms at that end range only, with symptomsceasing once the end range loading ceases. Thebehavior (symptoms, range of motion) of themechanically impeded end range does not

substantially change in response to repetitive loadingduring the course of the examination. The reactionoccurs at the same end range that is loaded.Movements in other movement plane directions have

no effect on the reaction that occurs from loading atthe mechanically impeded end range, nor does loadingat the mechanically impeded end range affect thebehavior of other movement plane directions.

Symptoms occur as soon as the mechanically impeded end range is reached. They are intermittent asthey only occur at end range without responses toloading within the beginning or middle range in thesame or other movement plane directions. Correction isachieved by loading at the mechanically impeded end

range on a frequent basis.


A B C

Figur e 15.3 Slouched (A), overcorrect (B), let go 10% to neutral lordotic sitting (C).

Practice-Base Problem



334 Part Four: Acute Care management (first 4 weeks)

Dysfunctions are named after the movement planedirection within which the mechanically impeded endrange occurs.

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 normalloads on abnormal tissue. The solution is to promoteflexibility by means of frequent end range loading toremodel tissue. Improvement is increased flexibility,congruent with strategies to "stretch" or remodel shorttissue.

Clinical PearlFor the postural syndrome, the motto "if it hurts don't doit" applies; the remedy is to avoid loading at thesymptomatic mechanically unimpeded end range. Theprincipal is one of end range loathing. For thedysfunction syndrome, the motto "no pain no gain"applies; the remedy is to pursue loading at thesymptomatic mechanically impeded end range. Theprincipal is one of end range loading.

Dysfunction Syndrome: Clinical Intervention

Treatment of the dysfunction syndrome uses the rem-edy of "stretching."

For the McKenzie Method, an appreciation of howshort tissue behaves is important to avoid treatingshort tissue that does not exist and to permit one tohave greater success in identifying and treating shorttissue when it does exist. Shortened muscular tissue isoften the target of treatment when mechanical andsymptomatic response patterns do not support theexistence of the short tissue claimed. If the muscle isnot "short," laboring toward making it long may not beprudent.

Clinical Pearl

Shortened tissue is often erroneously assumed to be thecause of symptoms. A careful evaluation often fails to

demonstrate the expected painful loss of motion.

There are various terms used to describe muscleshortening, one of the most extreme being "spasm."Medically defined, spasm is the violent involuntary

sustained contraction of muscle that prohibits jointmotion in the direction opposite the afflicted muscle'saction. Therefore, if a particular muscle were claimedto be in spasm, that claim would predict a specificpainful range of motion loss. Detection of the painfulpreclusion predicted by a specific spasm claimedwould confirm that claim. When range of motionpatterns fail to support the existence of the spasmsclaimed, or are the opposite of what is predicted, theclinical relevance of the claim can no longer beentertained.

Spinal antalgias are good examples of how spasm isinappropriately claimed. Consider the patient whopresents with an acute lumbar kyphotic (Fig. 15.4) orthe patient who presents with an acute lumbar scoli-otic antalgia away from the side of pain (Fig. 15.5). It isnot uncommon for these antalgias to be explainedaway as being caused by paravertebral muscle spasmdespite the fact that the explanations predict antalgias

opposite of the patient presentations.Regarding kyphotic antalgia, paravertebral muscle

spasm would result in fixed hyperextension of thespine, not the fixed flexion of kyphotic antalgia.Flexion positioning of the spine could not be attrib-uted to spasms of muscles that extend the spine. Forthe acute left lumbar scoliotic antalgia away from apainful right side, right paravertebral muscle spasmis often blamed for the situation. Spasm of muscles tothe right side of the spine would not permit anantalgia to the left but would result in an antalgia tothe right. As these two cases demonstrate, discomfortlocalized to a muscle does not a spasm make.

Figure 15.4 Lumbar kyphotic antalgia.

Clinical Pearl

Clinical Pearl



Other terms, such as hypertonicity, hyperactivity,contracture, scar, myofascitis, etc., are used to describemuscle shortening. These terms imply a lesser degree of shortening than spasm. With spasm, motion restriction isso great that the spine is "held" in the direction of themuscle action (pull) and neutral positioning cannot beachieved towards the movement plane direction oppositethe muscles action (pull). With muscle shortening lesssevere than spasm, movement may be permitted beyondneutral, into the movement plane direction opposite theshortened muscle's pull, but a painful restriction is stillpredicted in that opposite direction. In summary, if ashortened muscle is culpable for symptoms, a specificpainful range of motion restriction is predicted.Interventions designed to lengthen tissue have betteroutcomes when the short tissue targeted is really there.

Table 15.1 indicates the painful range of motion lossespredicted if particular muscles were "short." One could notconclude that any of the listed muscles were short if thepainful motion restrictions predicted did not exist or werethe opposite of what is predicted.

When Dysfunction Syndrome patterns are identified,procedures are instituted to improve flexibility, i.e., astretching routine is instituted. There are numerous waysto "stretch" inflexible spinal joint complexes and mostconservative spinal care specialists have expertiseregarding stretching instruction. The McKenzie Methoduses "stretches" for dysfunctions that are the same endrange movements used to "compress" derangements.

Derangement Syndrome

Derangement Syndrome:

Phenomenologic al Pattern

Table 15.1 Predicted Painful Motion Restrictions Based on Particular Muscles Being Short

Muscle Shortened Motion Painfully Restricted

ParavertebralSuboccipitalUpper trapeziusSCMLevator scapulaeRhomboidsQL PsoasPiriformisGluteus maximus

FlexionCervical flexion and lateral flexion to opposite sideCervical flexion, rotation to opposite sideCervical extension, rotation to same sideCervical flexion, rotation to opposite sideRaising of the arm on the same sideLumbar flexion, lateral flexion to opposite side

Thoracolumbar and hip extensionHip adduction and internal rotationHip flexion and internal rotation

Figure 15.5 Left scoliotic antalgia.

Chapter Fifteen: McKenzie Spinal Rehabilit ation Methods 335

Is the location of symptoms or palpation findings

adequate to determine the presence of shortened

muscular tissue? What other information might be

important?A mechanically unimpeded end range is an endrange of motion that is not restricted by mechanical factors.

Practice-Based ProblemPractice-Based Problem



336 Part Four: Acute Care Management (first 4 weeks)

Any loss of motion toward that end range would becaused by symptoms or factors other than mechanicalfactors. A mechanically impeded end range is apremature, early end range, before normal end range,

caused by mechanical factors versus symptoms, andmay be perceived by the patient to be a mechanicallimitation (stiffness or obstruction) with or withoutpain.

For the Derangement Syndrome, excessive loadingtoward, or at a mechanically unimpeded end rangeincreases symptoms and promotes a mechanically impeded end range in another direction. The promotionof instability in one direction promotes rigidity in another.Conversely, loading in the direction of rigidity diminishesthat rigidity and also diminishes the provocative power of the direction without restriction. The reduction of rigidity in one direction decreases the instability in another.

These are some of the most important McKenzie Methodobservations. The Derangement Syndrome patterns are complex

co-reactions between movement plane directions pre-cipitated by loading at beginning range, middle range,and/or end range (the latter being mechanically impeded or not). Treatment strategies involve avoiding adetrimental mechanically unimpeded end rangedirection (end range loathing) while pursuing a beneficialmechanically impeded end range (end range "loading").Symptoms may be intermittent or constant. Changesmay be slow and temporary or rapid and maintained, i.e.,there is a high degree of reactivity to loading.

Unique to derangements are constant symptoms andadverse mechanical and symptomatic responses duringmotion occurring in the direction of a detrimentalmechanically unimpeded end range. Not only do adverseresponses occur at the mechanically unimpeded endrange, as with the postural syndrome, but they alsooccur during motion in the same movement planedirection as the mechanically unimpeded end range. Inaddition, symptoms may centralize (retreat toward thecenter of the body) or peripheralize (away from the centertowards the periphery, often into the extremities).Centralization is an optimistic prognosticator even whenit is associated with increased central symptoms.

Peripheralization is a dire prognosticator even when it isassociated with a relative diminution of the level of symptom intensity.

There are three derangement syndrome subtypes,each with a unique pattern of potential mechanical andsymptomatic responses to loading. The differencebetween the three subtypes concerns the movementplane directions within which the responses occur. Whatthey have in common is that they all involve at least onepotential "direction of detriment" and one "direction of correction," the former being a mechanically unimpeded,the latter a mechanically impeded, end range. The termpotential signifies that there are

multiple possible mechanical and symptomaticresponses to loading for each derangementsyndrome subtype and that all of the potentialresponses may or may not be present. In other

words, partial patterns may exist.

When a patient presents acute, how does one determinethe appropriateness or inappropriateness of movementand positioning therapies, including which end rangesto load at and which end ranges to avoid?

The full palette of potential derangement phenom-ena is described, below, concerning what can occur

when loading in the direction of detriment and in thedirection of correction. Two qualifiers must be men-tioned. The patterns, as described, represent casesthat are amenable to mechanical therapy. Cases notamenable to mechanical therapy would evidence adifferent pattern. In addition, the patterns, asdescribed, may require a few repetitions of movementto become established and clearly displayed.

Direction of Detriment

• A mechanically unimpeded end range(MUER) movement plane direction

• Adverse mechanical and/or symptomaticresponses during motion towards and/or atthe MUER

o Increased symptoms in the same movementplane direction

o Promotion of a mechanically impeded endrange in another movement plane direction.

Direction of Correction

• A mechanically impeded end range (MIER)movement plane direction

• No mechanical and/or symptomatic responsesduring motion

• Beneficial mechanical and symptomaticresponses at the MIER only

o Diminution of the MIER in the samemovement plane direction

o Diminution of the provocative power of theMUER direction of detriment

The three derangement subtypes are namedaccording to conclusions about the pathoanatomicalmechanism, i.e., according to the direction of movement of intradiscal nuclear Derangement that

When a patient presents acute, how does onedetermine the appropriateness or inappropriate-ness of movement and positioning therapies,including which end ranges to load at and whichend ranges to avoid?

Practice-Based Problem



best explains the patient's mechanical andsymptomatic responses to loading as follows.

1. Posterior derangements

2. Relevant posterolateral derangements

3. Anterior derangements

The examples considered for the three subtypes of derangements will be three spinal antalgias, whichserve as excellent examples of derangements becauseall of the potential derangement features are presentin these "extreme" cases.

An acute kyphotic antalgia (Fig. 15.4) would be anextreme example of a posterior derangement. An acutecoronal antalgia (lumbar scoliosis or acute cervicaltorticollis) (Figs. 15.5 and 15.21) would be extremeexample of a relevant posterolateral derangement.An acute lordotic antalgia (Fig. 15.24) would be anextreme example of an anterior derangement.

Derangement Syndrome:Pathoanatomical Explanation

Intradiscal nuclear derangement is the model used toexplain the dramatic and long-lasting detrimental orbeneficial responses to movement and positioningexhibited by lower cervical and lower lumbar derange-ment syndrome patterns.

The intradiscal nuclear derangement model con-siders compression rather than stretching forces toexplain mechanical and symptomatic responses.Habitual loading in one movement plane directioncompresses and displaces intradiscal nuclearmaterial in another, often opposite, movement plane

direction. Loading in directions that promoteintradiscal derangement of nuclear material may cause adverse mechanical and symptomaticresponses in the beginning, middle, and end range of that movement plane direction as the derangementprogresses as movement progresses. The end rangeof the detrimental direction is mechanically unimpeded as intervertebral disc material has beendisplaced or "pushed out of the way," thus offeringless resistance to compression of the intervertebraldisc (approximation of vertebral end plates) in thatdirection.

The accumulation of displaced/deranged intradis-cal 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. Theaccumulated intradiscal nuclear material offers a

greater resistance to compressive forces(approximation of vertebral end plates). Mechanicaland symptomatic responses in the movement planedirection within which the accumulated intradiscalnuclear material has deranged are not realized untilthe obstruction offered by that material is met, i.e., at

the mechanically impeded end range. Mechanicaland/or symptomatic responses do not occur during motion in the direction of the obstructed endrange—the movement that caused the nucleardisplacement is being avoided and the accumulatedderanged nuclear material has yet to beencountered.

The remedy is to compress the accumulatedde-ranged nuclear material (the obstruction tomovement), to reduce the derangement, i.e., to senddisplaced 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 migratein similar directions. If loading strategies cause

nuclear material to migrate to a more central orperipheral location, the topography of symptomsfollows suit. Changes in symptom location may bereferred to as centralization and peripheralization,respectively. A response to loading involving anincrease of central symptoms with diminution of peripheral symptoms (centralization) has a positiveprognosis and is appreciated as reflecting the returnof deranged intradiscal nuclear material to a more

central location. As intradiscal nuclear materialreturns to a more central location, so do symptoms.As intradiscal nuclear material returns to a central,more confined, more highly pressurized environ-ment, 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 anegative prognosis, even if symptom intensity lessens, and is appreciated as reflecting intradiscalnuclear material deranging peripheral from itsnormal, central location.

The positing of the intervertebral disc nuclearderangement model fleshes out phenomenologicalobservations, as follows.

Posterior Derangement Pathoanatomical

Explanation

Posterior Derangement Direction

of Detriment: Flexion

• Flexion is the mechanically unimpededmovement plane direction. Loading inflexion displaces intradiscal nuclearmaterial posterior resulting in less intra-discal resistance to flexion. If flexion isnot possible, it is because of increasedsymptoms of, not mechanical resistance




338 Part Four: Acute care management (first 4 weeks)

from, deranged intradiscal nuclearmaterial.

• Flexion loading has adverse mechanicaland/or symptomatic responses at beginning,middle, and end range (includingperipheralization) as nuclear material is

progressively deranged posterior.• Flexion loading promotes an obstruction to

extension caused by the accumulation of deranged intradiscal nuclear material in thatdirection.

Posterior Derangement Direction of Correction: Extension

• Extension is mechanically impeded because of the accumulation of, and resistance tocompression from, deranged intradiscal nuclearmaterial.

• Extension loading has no responses during

motion because it does not promote thederangement and has yet to meet theobstruction to movement from thederangement.

• Extension loading has beneficial mechanicaland/or symptomatic responses at themechanically impeded end range only (includingcentralization), the point at which theaccumulated intradiscal nuclear material iscompressed and returned to a more centrallocation.

• Extension mechanically impeded end rangeloading results in flexion becoming less

provocative. As nuclear derangement isreduced to a more central location, moreflexion would be required to achieve the degreeof posterior intradiscal nuclear derangementthat existed before extension loading.

Clinical PearlIn a posterior derangement, mechanically restrictedex-tension is increased by flexion loading. Extensionloading diminishes the provocative effect of flexion.

Relevant Posterolateral Derangement Pathoanatomi-cal Explanation

A lateral component is "relevant" or not depending onwhether loading outside the sagittal plane (i.e.,loading laterally) is necessary to reduce thederangement. "Relevance" refers to the relevance of alateral loading strategy. If there are symptoms that

are "lateral" but the derangement is reduced withloading in the sagittal plane, any lateral component tothe intradiscal derangement is not considered rel-evant (to loading strategies).

Unilateral symptoms, including sciatica, are oftenadequately addressed with sagittal extension motions

without having to resort to lateral techniques. A rele-vant lateral component is, therefore, not exhibited forthese cases despite MRI that may demonstrate lateralintradiscal derangement. If symptoms are centraland a lateral loading strategy is required for resolu-tion, a relevant lateral component is considered toexist even though unilateral symptoms did not.

With relevant posterolateral derangement, exten-sion loading is initially detrimental but after a courseof coronal loading becomes beneficial. The initialphase of treatment, wherein lateral loading was re-quired, represents a relevant lateral component. Afterlateral loading is successfully used, the relevant lateral

component no longer exists.A relevant posterolateral derangement may be

thought of as a posterior derangement that has pro-gressed to develop a relevant lateral derangementcomponent as well. In the presence of a relevant lat-eral derangement, extension strategies fail to captureand return the lateral derangement to a more centrallocation and, to the contrary, often promote the lat-eral component of the derangement. Treatment of therelevant posterolateral derangement is a two-stepprocess. The first step reduces the lateral derange-ment with coronal (non-sagittal) loading strategies.

The second step is to proceed with posterior derange-

ment management, already considered above. Therelevant lateral derangement must first be reduced toa more central location by means of lateral tech-niques, after which extension is transformed frombeing detrimental to being beneficial by reducing theposterior derangement that remains after the rele-vant lateral derangement is reduced (eliminated). Wewill now consider the case of an individual whosespinal symptoms are right-sided and whosemechan-ical and symptomatic responses areconsistent with a relevant right posterolateralderangement.

Relevant Right Posterolateral DerangementDirections of Detriment: Flexion, LeftLateral, Extension

• Flexion and left lateral movements are themechanically unimpeded movement planedirections. Loading in flexion and left lateralmovements derange intradiscal nuclearmaterial posterior and right lateral (i.e., rightposterolateral) resulting in less intradiscalresistance to flexion and left lateral movements.If flexion or left lateral

Clinical Pearl



movements are not possible, it is because of increased symptoms of, and not themechanical resistance from, derangedintradiscal nuclear material.

• Flexion and left lateral loading have adversemechanical and or symptomatic responses atbeginning, middle, and end range (including

peripheralization) as nuclear material isprogressively deranged right posterolateral.

• Flexion and left lateral loading promote anobstruction to extension and right lateralmovements caused by the accumulation of deranged intradiscal nuclear material in thosedirections.

• Extension is a mechanically impeded movementplane direction that is initially detrimental toload at end range. Although extension ismechanically impeded because of accumulationof intradiscal nuclear material, intradiscalnuclear material has accumulated both posteriorand right lateral. Extension end range loading

fails to capture and return the relevant rightlateral component to a more central location andpromotes right lateral derangement of intradiscal nuclear material. It is the failure of extension to reduce the derangement that causesthis type of derangement to be classified asrelevant posterolateral.

Relevant Right Posterolateral DerangementDirection of Correction: Right LateralLoading

• Right lateral loading is mechanically impededbecause of the accumulation of, and

resistance to compression from, derangedintradiscal nuclear material.

• Right lateral loading has no responses duringmotion because it does not promote thederangement and has yet to meet theobstruction to movement from thederangement.

• Right lateral loading has beneficialmechanical and/or symptomatic responses atend range only (including centralization); thepoint at which the accumulated derangedintradiscal nuclear material is compressedand returned to a more central location.

• Right lateral loading results in flexion, leftlateral, and extension loading becoming lessprovocative as a result of a reduction of right

lateral derangement of nuclear material.Because nuclear derangement is reduced to amore central location, a greater degree of

flexion, left lateral, and/or extension loadingwould be required to achieve the degree of

lateral intradiscal nuclear derangement thatexisted before right lateral loading reduction of derangement.

• After right lateral loading is recovered,extension is no longer detrimental, but is

transformed into something beneficial after therelevant lateral component is reduced, i.e.,once the "lateral" component is taken out of theposterolateral derangement. Extension loadingno longer promotes lateral derangementbecause there is no lateral derangement topromote. From this point on, the progression isas for posterior derangement, which essentially is what is left without the relevant lateralcomponent. Extension results in furtherimprovement as the remaining posteriorcomponent is

reduced.

Anterior Derangement Pathoanatomical Explanation

Anterior Derangement Directionof Detriment: Extension

• Extension is the mechanically unimpededmovement plane direction. Loading inextension deranges intradiscal nuclearmaterial anterior resulting in less intradiscalresistance to extension. If extension is notpossible it is because of increased symptoms of,and not the mechanical resistance from,deranged intradiscal nuclear material.

• Extension loading has adverse mechanical

and/or symptomatic responses at beginning,middle, and end range (including

peripheralization) as nuclear material isprogressively deranged anterior.

• Extension loading promotes an obstruction toflexion because of the accumulation of derangedintradiscal nuclear material in that direction.

Anterior Derangement Directionof Correction: Flexion

• Flexion is mechanically impeded because of the accumulation of, and resistance to,compression from deranged intradiscalnuclear material.

• Flexion loading has no responses during

motion as it does not promote thederangement and has yet to meet theobstruction to movement from thederangement.





• Flexion loading has beneficial mechanicaland/or symptomatic responses at themechanically impeded end range only (including centralization), the point at whichthe accumulated intradiscal nuclear material iscompressed and returned to a more centrallocation.

• Flexion mechanically impeded end rangeloading results in extension becoming lessprovocative. As nuclear derangement isreduced to a more central location, moreextension would be required to achieve thedegree of anterior intradiscal nuclearderangement that existed before flexionloading.

limitation versus significant pain.For introductory educational purposes, the McKen-

zie Method management of spinal antalgias offersexcellent examples of derangement managementbecause the derangement subtype is easy to identify as opposed to the significant investigative efforts

required when antalgia is absent. Appreciation of thepresentation and management of the three acutespinal antalgias informs the process of learning how todetect, evaluate, and manage derangements whenthere is no antalgia, because most derangement pre-sentations can be construed as partial patterns of thefull antalgia patterns.

Acute Spinal Antalgia Paradigms of McKenzie Method Derangement

ManagementWith the McKenzie Method, antalgia is typically resolved within a few visits with self-generatedmovement initiated as the centerpiece of carebeginning with the first visit. A prudentprogression of forces is used to reverse theantalgia while being mindful of centralization

and peripheralization phenomena to judge theappropriateness of the strategy.

Delay of movement therapy for spinal antalgiaoften results from the misconception that acutespinal antalgia represents the "wisdom" of thebody avoiding a position that is deleterious. Thesituation, so conceived, precludes the

exploration of movements to reverse the antalgia.Antalgia is rarely caused by neural or otherpernicious pathological processes; standardhistory and examination procedures rule outthese infrequent contributors.

Patients presenting with acute spinaldeformities are unable to achieve neutral spinalpositioning in the movement plane directionopposite the antalgia. It is as if the precludedmovement plane direction has "col-lapsed" intothe opposite movement plane direction withinwhich the patient is "trapped." The McKenzieMethod management strategy is to first achieveneutral spine positioning and then to "recover" the precluded movement plane direction, guided

all the time by centralization andperipheralization phenomena.

The criteria for the preferred loading strategy are not only centralization phenomena but alsothe degree to which adverse mechanicalresponses resolve. Although the McKenzieMethod is known for being mindful of

symptomatic responses, mechanical responsesare equally important and may, at times, be theonly sign that a positive response to loading hasoccurred. For some patients, the presentingsymptom may be perception of a mechanicalrestriction to motion, perceived as a stiffness

Kyphotic AntalgiaManagement—ExtensionPrinciple—Posterior Derangement

Lumbar Kyphotic AntalgiaManagement—Extension Principle—Posterior Derangement

The patient presenting with a lumbar kyphotic antalgia(Fig. 15.6) typically has symptoms that are central orsymmetrical and do not radiate beyond the knee,consistent with a central, posterior derangement thatdoes not affect more lateral articular or neurologicstructures.

There are detrimental responses within the mechan-ically unimpeded flexion movement plane direction, bothduring motion and at end range. For extension there areresponses at that mechanically impeded end range only.

There are no responses "during motion" for extension

because extension motion is not possible (there is no

Figure 15.6 Lumbar kyphotic antalgia.




Figure 15.7 Prone patient on plinth with pillow.

extension); the mechanically impeded extension endrange is met in the flexed position. As the patientimproves, extension movements become possible butstill evidence a mechanically impeded end range withresponses continuing to occur at the mechanically impeded extension end range only.

When a patient presents with a lumbar kyphoticantalgia, the first step is to achieve neutral (0 degreesof flexion) positioning of the spine, which is difficult toaccomplish in the erect standing posture. The patientis placed prone on the plinth with a bolster pillowunder the abdomen (Fig. 15.7) to relax in a position

accommodating the antalgia.After some time, the pillow is removed and the

patient is flat prone (Fig. 15.8) and may experiencecentralization discomfort as a result.

After achieving prone 0-degree flexion (neutralpositioning), the next step is to recover extension. Thepatient is asked to rise up on elbows (Fig. 15.9) and torest in that position for a few moments; again, anincrease of centralization discomfort may beexperienced.

Next, the patient is asked to perform a proneextension (Fig. 15.10).

From what may be described as a push-up position,the elbows are extended in an attempt to passively extend the trunk over the pelvis. Instruction is given torelax the buttocks because contraction of the gluteus

maximus flexes the lumbar spine, a roadblock toextension. For patients having difficulty relaxing thebuttocks, it is useful to assume a knocked-kneed,pigeon-toed positioning of the lower extremities to

Figure 15.8 Prone patient on plinth.



342 Part Four : Acut e Care management (first 4 weeks)

Figure 15.9 Prone on elbows.

stretch-relax the gluteus maximus. The patientis given the verbal cue to let the pelvis "sag" to thetable. There is a momentary rest/pause atextension end range and then again at thestarting position. The exercise is performedapproximately 10 times.

When performing any end range loadingexercise or mobilization, patients are asked toreport when discomfort is perceived to change inany fashion. The clinician monitors whetherthese changes occur during

motion or at end range. Although the mostimportant criteria is patient status subsequentto the performance of any exercise, during theexercise there is special interest as to what isoccurring at the moment of end range loadingand whether symptoms centralize orperipheralize at the moment of end rangeloading. Centralization and/or peripheral-ization reactions at the mechanically impededextension end range herald whether benefit ordetriment

Figure 15.10 Prone extension.




will be experienced after end range loading ceases. It isan optimistic prognosticator if symptoms becomemore central or diminish at each extension end rangeloading. If radiation to the extremity occurs every time loading at end range is achieved, this wouldraise concerns that loading at that end range may not

be the most prudent strategy.After the patient is able to achieve extension from

the prone position they should, within 1 or 2 days, beable to tolerate and benefit from extension in stand-ing (Fig. 15.11) as an alternative self-treatment, inaddition to prone extension.

Flexion postural syndrome principles of avoidingdeleterious flexion end range and maintaininglumbar lordosis are used. Self-treatment for theposterior derangement centers on avoiding flexion,maintaining lumbar lordosis while sitting (and mak-ing transitions between postures) and periodically pursuing extension end range loading, either prone

or standing (the former usually being more effec-

Figure 15.11 Extension in standing.

Figure 15.12 Cervical kyphotic antalgia.

tive). Education would be conducted concerningcentralization and peripheralization phenomena.

One of the goals of care is the achievement of fullpain-free extension, appreciated to represent thereduction of the posterior derangement. Subsequentto this, flexion would be revisited for two reasons.

The first would be to confirm that flexion is no longerprovokes derangement; the second is to explorewhether a flexion dysfunction developed due to for-mation of scar tissue or avoidance of flexion duringthe course of care. Flexion would continue to be

avoided if it was determined that it still had the powerto promote posterior derangement. Flexion would bepursued if the pattern of reaction was consistent withflexion dysfunction. Flexion loading to remodel dys-function would be followed by extension as aprophylactic measure to ensure that the recentreduction of the posterior derangement stayed thatway.

Cervical Acute Kyphoti c AntalgiaManagement—Extension Principl e—Posterior Derangement

For cervical kyphotic antalgia (Fig. 15.12), the patientis unloaded in a supine position with additionalunloading introduced by means of manual axialtraction. Even though this requires "hands-on,"patients are soon able to self-treat with techniquesthat resemble, and can replace, clinician manualmethods used to get them "going."

The patient is initially made comfortable in theantalgic position. The supine patient's head rests ona pillow supporting the flexed antalgic position.

To achieve 0 degrees of flexion, manual axial trac-tion is used (Fig. 15.13).



344 Part Four: Acute care management (first 4 weeks)

The therapist places the index and middle finger of one hand anterior and inferior to the chin, respec-tively. The thumb and index finger of the other handabuts the inferior border of the occiput. The patient isasked to occlude (not clench) the teeth to avoid bitingthe tongue or disturbing the TMJ. Axial traction isthen applied along the vector of the flexion antalgia.While maintaining the axial traction, cervicalretractions are performed in a slow, gentle, repetitivemanner to achieve beginning range lower cervical

extension (lordosis) and neutral head and neckpositioning (Fig. 15.14).

A momentary rest occurs at end range retractionand at the starting point for each repetition. Appro-priateness is monitored by means of centralizationand peripheralization.

Next, extension is introduced from the retractedposition. As soon as extension is initiated, retractionforces are withdrawn, with axial traction forcesmaintained throughout (Fig. 15.15).

As always, centralization and peripheralizationphenomena judge appropriateness. The head and

neck are extended within tolerance. With eachrepetition further extension is attempted. Atextension end range, gentle very small rotations of

Figure 15.14 Manual supine cervical

traction-retraction to introduce lordosis.


traction.



the head are performed to facilitate further extension.As always, feedback from the patient is essential toevaluate what is occurring during motion and at endrange. Responses at end range are of particularinterest.

Patients are shown how to perform self-treatmentexercises to the degree they are capable. Options in-clude sitting retractions followed by sittingretraction-extension (Fig. 15.16).

For sitting cervical retractions, instruction to keep

the head level to avoid nodding is helpful. Mainte-nance of lumbar lordosis is essential to achievemaximum cervical retraction or extension end rangeloading in the sitting position. Sitting extension is

performed from the retracted position to achievemaximum extension end range. Once extension isintroduced, the retraction is not maintained (theretraction is "lost"). Gentle mini-rotations areperformed at end range to permit further extension.

As with lumbar Kyphotic antalgia, self-treatmentinvolves the flexion postural syndrome treatmentprinciples of avoiding flexion and maintaining lumbarand cervical lordosis (the former required for thelatter) while sitting and making transitions between

postures. Periodically throughout the day, cervicalretraction extensions are performed. Educationregarding centralization and peripheralization wouldbe conducted.

A B



traction-retraction-extension.

Figure 15.16 Sitting cervical retraction and sitting retraction-extension.




As with the lumbar spine, subsequent to the achieve-ment of full pain-free extension, flexion would be revis-ited to confirm whether flexion is still provokedderangement or if a flexion dysfunction developedbecause of avoidance of flexion. Flexion would con-tinue to be avoided if it was determined that it still pro-

moted posterior derangement. Flexion would bepursued if the pattern of reaction was consistent withflexion dysfunction and would be followed by exten-sion as a prophylactic measure to ensure the recentreduction of posterior derangement stayed that way.

Acute Coronal Antalgia Management:Lateral-Then-ExtensionPrinciple—Relevant Postero-LateralDerangement

Unilateral and extremity symptoms are more commonwith coronal antalgia than with sagittal antalgias.

As with kyphotic lumbar and cervical antalgias,unloading tactics are used to initiate treatment forcervical coronal antalgia (acute torticollis) but may ormay not be necessary for lumbar coronal antalgia(acute scoliosis). Acute lumbar scoliosis can often becorrected in the loaded standing position with strate-gies that may prove more effective than unloadedalternatives.

As with the kyphotic antalgias, the acute coronalantalgias can be visually identified. The coronalantalgias (lumbar scoliosis or cervical torticollis) may be associated with a kyphotic antalgia or not. Whethera kyphotic component is visualized or not, the

treatment progression for coronal antalgia involves thetwo-step progression of recovering motion in thecoronal plane opposite the antalgia (the relevantlateral component) followed by recovery of motion inthe extension (sagittal) plane. The progression is thelateral-then-extension principle.

With coronal antalgia, if extension end rangeloading is performed before recovery of the coronalmovement in the direction opposite the antalgia (i.e.,reduction of the relevant lateral component), thepatient may worsen. However, after recovery of motionin the coronal movement plane direction opposite theantalgia, extension end range loading is transformed

from detrimental to beneficial. In fact, the tolerance of,and/or benefit from, extension is a sign of progress.

For our examples of lumbar and cervical coronalantalgias, we will consider a patient with right-sidedsymptoms and a coronal antalgia to the left, inter-preted as a right posterolateral derangement. The goalis to first recover movement in the right coronalmovement plane direction (i.e., to reduce the rightlateral component of the derangement) and then torecover extension (to reduce the posterior derange-ment that remains).

Lumbar Acute Scoliosis An talgia Management

When considering acute lumbar scoliosis, two termsare useful, those being lateral shift and side gliding.

The term "lateral shift" is equivalent to antalgia and isreferenced as right or left depending on the direction

of the coronal deviation of the trunk over the pelvis.Someone with a left antalgia has a left lateral shift (Fig.15.17).

If lateral shift refers to a position in the coronalplane, side gliding is the movement that gets you to,or away, from that position. Side gliding is movementof the trunk relative to the pelvis in the coronal planewith the shoulders kept level.

For our patient with a left lateral shift, the firstintervention to explore is side gliding against the wall,which permits self-correction in the loaded standingposture without need to visit the plinth (Fig. 15.18).

Our left lateral shift patient is positioned with the

left side of the body toward the wall. The medial epi-condyle of the left elbow remains in contact with theleft rib cage on the axillary line. The patient leans thelateral aspect of the left arm against the wall. The feetare placed together a few feet away from the wall. Thepatient places the right hand on the superior aspect of

Figure 15.17 Left lumbar lateral shift.



Figure 15.18 Right side-gliding against the wall to cor-rect a left lateral shift.

wall, therapist overpressure may be required. If thisdoes not turn out well, the therapist may have to offereven more assistance by manually inducing side glidingmaneuvers absent benefit of the wall. In essence, thetherapist becomes a wall with arms (Fig. 15.19).

The patient stands with feet shoulder width apartwith the left arm positioned as it would be to leanagainst the wall. The therapist is on the patient'sleft-side, oriented in the patient's coronal plane andadopting a three-point stance with the forward footbehind the patient. The angle of the therapist'sneck/shoulder girdle contacts the patient's left arm justabove the elbow. The therapist reaches around thepatient, inter-lacing fingers just below the crest of theright ilium. Therapist mobilizations are then applied by simultaneously pulling the pelvis (with the interlacedhands) and pushing the trunk (with the angle of neck/shoulder girdle against the patient's arm) in the coronalmovement plane. Use of a mirror helps ensure that thepatient's shoulders remain level so that side glidingcorrection is used as opposed to lateral flexion. As withthe wall side gliding, adverse reactions often indicatethe need for a slight degree of flexion. As with wall sidegliding, if significant benefit is experienced, extensioncan be added at the point of coronal end range in thedirection opposite the antalgia. To do this, our patient'sright hand would be placed on the therapist's right wrist(behind the patient) and used as a fulcrum to lean backon.

Should standing side gliding strategies prove futile,prone extensions from a lateral shift position may beexplored. For our patient with a left lateral shift, this

the lateral right ilium and pushes the pelvis towardthe wall until the painful obstruction is met; thisend range loading is maintained for a moment. Thepelvis is then backed off to the first point of tolerable discomfort; there is a moment of rest andthe procedure is repeated. With each repetition,further progression to the wall should be achieved.If the feet are placed a proper distance from thewall, contact between the pelvis/hip and the wallshould not occur, even as side gliding improves.

The appropriateness of the intervention, as always,is judged by centralization and peripheralizationphenomena.

If considerable improvement is noted, extensionmay be performed at the end range of the coronalmovement opposite the antalgia; however some,patients do not benefit from extension until somedays have passed. Should side gliding not bewell-tolerated, the introduction of a slight degree(e.g., 10 degrees) of flexion may transform themaneuver into something of benefit. As the patientprogresses, the need to flex should resolve andtolerance and benefit from extension should evolve.

If the patient cannot adequately achieve coronal Figure 15.19 Therapist-assisted right side-gliding to cor- end range movements with side gliding against the rect a left lateral shift.

Chapter Fifteen: McKenzie Spinal Rehabilit ation Methods 347



348 Part Four: Acu te Care Management (firs t 4 weeks)

would be prone extensions from a right lateralshift position (Fig. 15.20).

In the prone position, the pelvis is positionedat coronal end range in the direction opposite thepresenting coronal antalgia. Our patient placesthe pelvis to the left (essentially performing aright lateral shift as the trunk is now to the right of

the pelvis) and prone extensions are performedfrom the right lateral shift position. Benefit ismonitored by centralization as well as the ability of the exercise to diminish the antalgia, onceperformed.

Self-care would include use of flexion posturalsyndrome principles (avoiding flexion and main-taining lumbar lordosis while sitting and makingtransitions between postures) with the periodicperformance of the preferred coronal end rangeloading strategy. Although extension end rangeloading initially fails to benefit, or is of detriment,maintenance of a minimal lordosis (beginningrange extension positioning) is usually tolerated

and avoids the deleterious effects of flexion.Education regarding centralization andperipheralization would he conducted.

After recovery of movement in the coronalmovement plane direction opposite thepresenting coronal antalgia, self-treatmentcontinues by using the extension principle for theposterior derangement that remains once therelevant lateral component of the postero-lateral

Figure 15.20 Prone extension from a right lateral

shift position to correct a left lateral shift.

Figure 15.21 Torticollis: left coronalantalgia demonstrated.

derangement is reduced/eliminated.

Cervical Acute Torticolis Antalgia

Management

As with lumbar scoliosis, cervical antalgia in thecoronal plane (i.e., torticollis) (Fig. 15.21) may ormay not be associated with kyphotic antalgia. Aswith lumbar scoliosis, whether a kyphoticcomponent is visible or not, after the coronalmovement plane direction opposite the antalgia is

recovered, the extension principle is explored. Aswith cervical acute kyphotic antalgia, manualaxial traction is required to get things going.Soon thereafter, the responsibility of treatmentis transferred to the patient using techniquesresembling what the clinician used.

The patient is placed supine with the headcomfortably placed on a pillow in a manner thatdoes not challenge the antalgia. The therapist 'smanual contacts are the same as were used withthe cervical kyphotic antalgia. Axial traction isapplied, at first in the direction of the antalgia.While maintaining axial traction, a lateral flexionmobilization is conducted in the directionopposite the antalgia until the painful obstructionis met at which point there is a momentary pause(Fig. 15.22). The therapist then backs off to thefirst point of tolerable discomfort, pauses amoment (traction maintained throughout), and

repeats the procedure, gaining lateral flexion inthe direction opposite the antalgia with eachrepetition. If lateral flexion fails, the coupledmotion of rotation may be attempted in its place,using the same protocols.

As with the lumbar spine, premature attemptsto recover extension may be detrimental. Unlikethe lumbar spine, combined lateral and extensionmovements are not used. As is occasionally thecase with the lumbar spine, cervical coronal

antalgia more often requires a degree of flexion bemaintained when recovering lateral movements.As with the lumbar spine, subsequent to the



Figure 15.22 Correction of left torticollis.

recovery of coronal movement in the direction oppositethe antalgia, extension end range loading istransformed from detrimental to beneficial. As always,the appropriateness of any loading strategy is auditedby centralization and peripheralization.

Patient self-care includes the employment of flexionpostural syndrome principles as well as self-generatedlateral flexion mobilizations in the direction oppositethe coronal antalgia. Education regarding

centralization and peripheralization is provided. Atfirst, lateral flexions may only be possible supine withthe head on a pillow. As the patient progresses, theability to perform and benefit from lateral flexionmobilizations in a seated, retracted head and neckposition (which promotes lower cervical lordoticextension) is of benefit (Fig. 15.23).

Subsequent to the achievement of end range in thecoronal movement plane direction opposite the coronalantalgia, treatment progress is to the extensionprinciple whether there is a visible acute kyphoticantalgic component or not.

Acute Lordotic Antalgic Management—

Flexion Principle—Anterior Derangement

Clinical PearlConsidering the lower cervical and lower lumbar flexionstressors in everyday life (e.g., prolonged sitting, bend-ing), one would predict that flexion as a treatment of lower cervical and lower lumbar symptoms would be theexception rather than the rule. It has been our experiencethat conditions requiring flexion are less common thanthose requiring extension.

Figure 15.23 Sitting cervical retraction/lateral flexion to

recover coronal motion.

Regarding the kyphotic and coronal antalgias, asimilar mechanical "deformity " occurs in both thelumbar and cervical areas. Lordotic antalgia differsinasmuch as it occurs for the lumbar spine but not forthe cervical spine. Nonetheless, patients presentingwith cervical symptoms amenable to flexion end rangeloading strategies have many of the same mechanicaland symptomatic responses to loading as those

presenting with an acute lumbar lordotic antalgiaexcept, of course, for the lack of an antalgia that can bevisualized.

In addition, the lumbar lordotic antalgia has aunique feature. Whereas most low backs that respondto the extension principle do not present with an acutelumbar kyphosis, most low backs that respond to theflexion principle present with an acute lordotic antalgia(Fig. 15.24).

Manual therapists are usually more adept at pro-moting flexion end range loading than they are atpromoting extension end range loading strategies. Typically these skills have been acquired and usedaccording to the notion that short posterior muscularstructures are culpable for symptoms and need to be

stretched. The McKenzie Method more often uses flexionloading strategies to compress deranged intradiscalnuclear material that has accumulated within theanterior intervertebral disc space to return that materialto a more central location as opposed to promoting the

flexibility of posterior extra-articular structures. Figs.15.25 and 15.26 demonstrate lumbar and cervicalflexion strategies.

Self-treatment involves education regarding cen-tralization and peripheralization but there would be


Clinical Pearl




Figure 15.24 Lumbar acute lordosis antalgia: attempting

flexion.

no education regarding flexion postural syndrometreatment principles, because flexion is not of detri-ment. The patient would be dissuaded from any extension end range loading postural habits or any

extension end range loading for that matter, including"McKenzie prone extensions!"

CONCLUSION

McKenzie Method clinical reasoning would predict

that a majority of individuals with spinal symptomswould benefit from minimizing flexion and periodi-cally pursuing extension, considering the amount of time we spend flexed in everyday life. The McKenzieMethod predicts that loading in one movement planedirection may be more beneficial than loading inother movement plane directions whether symptomsare acute or chronic. These predictions have beenverified within the recent peer-reviewedevidence-based literature.

Snook (8) demonstrated how controlling lumbarflexion in the early morning serves as a form of self-care for reducing pain and costs associated withchronic, non-specific low back pain. The McKenzie

Method predicts that avoiding flexion would mini-mize low back pain for most patients. Early morningflexion is perceived to be particularly provocative

because of imbibition of fluid by intradiscal nuclearmaterial over a night of unloading. Theoretically, if the patient has posterior derangement of nuclearmaterial, the imbibition of fluid makes intradiscalnuclear pressures and the risk of debilitating de-rangements even greater.

Larsen, Weidick and Leboeuf-Yde (3) demonstratedit may be possible to reduce the prevalence of backproblems and use of health care services duringmilitary service, at a low cost, using lumbar proneextensions with a back/ergonomic school includingMcKenzie Method disc theories. Military recruits

A B

Figure 15.25 Promotion of lumbar flexion.




Figure 15.26 Promotion of cervical flexion.

were taught McKenzie Method extension principles(including lumbar lordotic body mechanics and proneextensions were performed periodically throughout theday) resulting in the favorable outcomes noted.

Long, Donelson, and Fung (4) showed that a McKenzieassessment could identify a large subgroup of acute,subacute, and chronic low back patients with a directionof preference ("an immediate, lasting improvement inpain from performing either repeated lumbar flexion,extension or side glides/rotation tests"). Regardless of the direction of preference, "the response to contrastingexercise prescriptions was significantly different."Exercises matching the patient's direction of preferencesignificantly and rapidly decreased pain and medicationuse and improved disability, degree of recovery,depression, and work interference outcomes. Of theoriginal 312 subjects who underwent assessment, 53.5%demonstrated a directional preference for pure sagittalextension, the remainder required prone extensions froma lateral shift position or movements in other planes. Themajority of subjects, therefore, required an extension

component to their preferred loading strategy.

A u d i t P r o c e s sSelf-Check of the Chapter's Learning Objectives

•

What are the three syndromes as defined by theMcKenzie 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.

REFERENCES1. 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 passiveprone extensions of the back prevent back problems? Arandomized, controlled intervention trial of 314 military conscripts. Spine 2002;27(24):2747-2752.

4. Long A, Donelson R, Fung T. Does it matter whichexercise? A randomized control trial of exercise forlow back pain. Spine 2004;29(23):2593-2602.

5. McKenzie R. The Cervical and Thoracic SpineMechanical Diagnosis and Therapy. Waikanae, NewZealand: Spinal Publications, 1990.

6. McKenzie R, May S. The Lumbar Spine MechanicalDiagnosis & Therapy, volume one and volume two.Waikanae, New Zealand: Spinal Publications, 2003.

7. McKenzie R, May S. The Human Extremities Diagno-sis & Therapy. Waikanae, New Zealand: SpinalPublications, 2000.

8. Snook SH, Webster BS, McGorry RW. The reduction of chronic, nonspecific low back pain through the controlof early morning lumbar flexion: 3-year

follow-up. J Occup Rehabil 2002;12(l):13-19.

Audit ProcessSelf-Check of the Chapter’s Learning Objectives

mckenzie spinal rehabilitation

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