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REHABILITATIONOF THE SPINEA PRACTITIONER'S MANUAL

EditorCRAIG L1EBENSON, DCLos Angeles, California

-Q)~.JWilliams & Wilkins

A WAVERLY COMPANYII,\[T[MORE' I'H[!.\DEI.I'H[A 1.0~DO~ 1',1[\[$ IIASGKOK

HONG KONG. MUNICH SYDNEY TOKYO' WROCL\W

1996

Practice (Blending Active and. 13

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Contents

Seclioll I. Basic Principles1. Guidelines for Cost-Effective Management of Spinal Pain

CRAIG UEBENSON

2. Integrating Rehabilitation into ChiropracticPassive Care) .CRAIG UEBENSON

. .. ........}

3. Training and Exercise ScienceJEAN P. BOUCHER

.......... .45

()6: Evaluation of Muscular Imbalance 97

VLADIMIR JANDA

Sectioll ll. Assessment ofMusculoskeletal Function4. Pain and Disability Questionnaires in Chiropractic Rehabilitation 57

HOWARD VERNONC)

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5.. Outcomes Assessment in the Small Private PracticeCRAIG UEBENSON and JEFF OSLANCE

7. Diagnosis of Muscular Dysfunction by InspectionLUDMILA F VASILYEVAand KAREL LEWIT

8. Evaluation of LiftingLEONARD N. MATHESON

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............... .113

................ 143

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Sec/ion 111. Patient Education9. Back School 153

PAUL D. HOOPER

10, Patient Education ' .CRAIG UEBENSON and JEFF OSLANCE

Appendix IO.l How to Care/or Your B(J(:k "lid Neck: A Sec/ioll Addrc.'i.\"cd J(J thePatient __ . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . 169

Section IV. Functional ReslOrariollll~ Role of Manipulation in Spinal Rehabilitation 195

KARELLEWIT

)l;iii

CONTENTS

20. PatientIDoctor Interaction A05WILLIAM H. KIRKALDYWILLIS

17. Lumbar Spine Injury in the Athlete 341ROBERT G. WATKINS

.225

. . .21.)3

. AI9

. ..............316

......................... All

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Index .

21. Place of Active Care in Disability PreventionVERT MOONEY

18.- Active Rehabilitation ProtocolsCRAIG LIEBENSON

16. Postural Disorders ofthe Body Axis 329PIERREMARIE GAGEY and RENE GENTAZ

Sectioll \~ Psycho.weial and Sociopolitical Aspects of Rehabifiwrioll19. Psychosocial Factors in Chronic Pain....... ., 391

GEORGE E. BECKER

15. Sensory Motor Stimulation 319VLAOIMIR JANDA and MARIE vA vRovA

14: Spinal Stabilization Exercise Program .JERRY HYMAN and CRAIG L1EBENSON

Appendi.\' 14.1 Ex.ercise Checklist .

13. -Manual Resistance Techniques and Self-Stretches for Illlproving FlexibilitylMobility 253CRAIG L1EBENSON

12. 'Spinal Therapeutics Based on Responses to LoadingGARY JACOB and ROBIN McKENZIE

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IBASIC PRINCIPLES

1 GUIDELINES FOR COST-EFFECTIVEMANAGEMENT OF SPINAL PAINCRAIG L1EBENSON

MISDIAGNOSIS AND MISMANAGEMENT OFTHE PROBLEM

Em'crging evidence indica(c~ the problem of low bad:pain has been mismanaged on a gr;md scale. From over-prescription of bed rest to overuse of surgical interven-tion and advanced imaging techniques. the costs related[0 low back pain afC unccilwincd. The U.S. govcrnmcnl re-ccntly issued federal guidelines on .acme low back painaimed at promoting a quoJlit)' care modeL I RC Most of these individualsrecover within 6 weeks, but 5 to 15% arc unresponsive totreatment and have continued disabili ty7-'O (Fig. 1.1). Theminority of patients who do not recover within 3 months aecount for up 75 to 90% of the total expenses related to thishealth care problem,1l-17 which exceed $60 billion peryear in the United Slates. 11 The 7.4% of patients who arcout of work for 6 momhs account for 75.6% of the 101'11cost lll (Fig. 1.2). The majority of these costs (60%) are attrib-utable to indemnity. with only 40% related to treatlllcm ll . 15(Table 1.1).

Among those patients whose symptoms resolve. recur-rences arc COllllllon. In some studies. recurrence rates were aslow as 22 to 36%.I'}-21 BerquistUllman and Larsson foundIhat 620/c; of patiellls with acute back pain suffered at least onerecurrence during I year of follow-up. 10 A longterm study re-vealed that 45% of patients had at least onc significant recur-rence within 4 years. 22

The incidence rate. cost of chronicity and disability,and high recurrence ralC add up lO a problem of epidemicproportions. In his Volvo award winning paper. \VaddclJstated. "Convcmional medical treatment for low-back painhas failed. ~md lhe role of medicine in the present epidemicmusl be critic::llly eXtllnined:~.\ The cause of this epidcmicinvolvcs a number of f"ctors. The reasons for this failure or treatment .md potcntial solutions .are presenteu inTable 1.2.

Ovcrcmphasis on a Structural [)iclgnosisArtcr ivtixtcr and Barr's, discovery that compn::ssiol1 of anerve root by a hcrnialc

REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL

Table 1.2. The Low Back Pain Epidemic

Adnplcd wilh permissIon from Pope MH, Frymoyer JW. Andersson G (~cls):Occupational low Back Pain. New YOlk, Pracgcf. 1984. p 107"

33

67

100

Percent

11114322

2245

Early, aggresive conservativelherapy

Ac!ive care lor subacute casesEarly JD of disability predictors

The Solulion

10 deconditioning syndrome

Percent

Overuse of surgeryIgnoring abnormal illness

behavior

Thc Problem

Overemphasis on slrucu!raldiagnosis

Overprescription of bed res!

Back Pain Costs

Medical costsPhysician's feesHospital costsDiagnostic testsPhysical therapyDrugsAppliances

OisabilityTemporaryPermanentTolal costs

Table 1.1. Percentage of Costs by Type of Treatmentand Compensation

cause of their symptoll\s.Jb For this re

l,;HAt-' I t:K 1 : uU'UtLII\lt:~ FOR COSTEFFECTlVE MANAGEMENT OF SPINAL PAIN 5

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Prolonged lx:d resl may be counleq)roduc(ivc."l~ Dcyo andcolleagues p~rformcd a controlled clinical lrial comparing] d'lys ;.lg;lin:-:l ::! weeks or bed n.::.;(. They concluded lhal nolonly was 2 days of bed fC.'a as crfc.:ctivc as 2 wc.:eks. but alsothe negmivc effecls of prolonged immohilizatioll wcre also

lil1litcd:~'~

Overuse of Su rgcry

The t)\'crus.... ()f surgery has he..... 1 perl laps tllc single lliost dam-aging medical intervention for b'H:k pain sufferc.:rs. Bigos andBaltic said. "Surgery seems helpful for ,It most 2~~ of patientswith back problem:;. and its inappropri:'ltc IJSC can have .1 grealimpact on increasing the chance of chrOllic back pain disabil-ity.l'ln his Volvo award rape.!'. W..lddcll said, "Such dramaticsurgical successes unfortunately only ;:\pply to approximatelyl'lc of palit;llls with low back disorders. Ou.r failure involvesthe remaining 999'0 .. for wholll the problem has becomeprogressively worse."=' Saal and Saal supervised care for agroup of patiClllS referred by neurologists for surgery. They

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Because most patients do not have a diagnosable struc-tural cause of their symptoms, a functional disorder should bcassumed. Pain in the locomotor system should be viewed as asign of impaired function. Nonspecific or idiopathic back painmost likely has to do with muscle or joint dysfunction with rc-

. sultant soft tissue irritation and pain generation. Treatmentsdesigned for injury states or disk lesions inevitably fail. thusCll:-.!:ig r~p:-~(,"!0rt. desp~ir. and illness bchavior.n-JI:>

Abnonnal illness behavior was dehllct..i by PiI0wsk~.'Jl as apatient's inappropriate or maladaptive rcsponse to a physic

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CHAPTER 1 : GUIDELINES FOR COSTEFFECTIVE MANAGEMENT OF SPINAL PAIN 7

PROBABILITY OF RETURNING TO WORK ulations over a I-month period.s" Certain studies excludedfrom the meta-analysis were those such as Meadc's, whichincluded other therapies. the effects of which could notbe disentangled from those of manipulation.&4s5 The studyby Meade and co-workers was one of a select few thatsuggested manipulation was beneficial for chronic lowback paill. R5 Triano et at reported recently that in patientswith low back pain over 7 weeh, an avemge of 10.)treatments with chiropractic manipulation resulted in im-proved function and significantly reduced pain.l Erhardand Delitto demonstrated that patients receiving manipu-lation and exercise outpcrfonned those receiving ex.ercisealone.'u

EARLY RETURN TO WORK IS A KEY

Secondary Functional Restoration

Prolonged passive care in an attempt to ameliorate the suffer-ing of back pain patients can lead to patient dependency. Inthe acute stages of an injury. such care is nccessary; however.when the chemical signs of innammation arc missing. a moreactive. patient participatory type of care is required. Olandand Tveiten said, "... resources from the health servicesshould be used in the subacute stage to enhance diagnosis,treatment, and rehabilitation and to inform the public of thebenign. self-limiting course of low~back pain and the positiveeffect of physical training."'))

Secondary functional restoration care that focuses on spe-cific functional goals and patient education should be themode of care for subacute or recurrent pain, paticn(s~Comprehensive rchabilitation involves functional capacitytesting. physical training. education about biomechanics andergonomics. and identification of psychosocial predictors ofdisability (Table 1.5).

Aggressive care gives the best chance for early return towork. Litigation neurosis is easy for disabled workers to ac-quire. Promoting bed rest and prolonged inactivity only in- .creases the likelihood of prolonged disability. Treatments thatmobilize the patient and auempt to return them to workquickly are advantageous. Communication between doctorand employer is essential because certain job modificationsmay be necessary to ensure worker safety on return to work.Deyo and associates said, "Our data support a recent trend to-ward earlier mobilintion of patients with back pain .... earlyreturn to work may help to prevent the emergence of chronicback pain syndromes, with their enormous human and mone-tary costs."~s Cats-Baril and Frymoyer also said. "It wouldseem that people who 3re able to work through the acutephase of a low back pain episode or those who go back towork even if the pain has not disappeared after a period of restarc unlikely (0 become disabled .... keeping people al workis vcry effective thcrapy."n Waddell succinctly stated that,"Prolonged time away from work in itself makes recoveryand return to work progressively less likcly."~J

24__. __c ~ ~====d

oo 6 12 1B

TIME OuT OF WORK (MONTHS)

Fig. 1.3. The probability of recovering from low back pain. (FromFrymoyer JW: Epidemiology of spinal disorders. In Mayer TG,Mooney V, Gatchel AJ (eds): Contemporary Conservative Carefor Painful Spinal Disorders. Philadelphia, Lea & Febiger, 1991.)

MANIPULATIVE THERAPY RESULTS IN LESS DISABILITY ANDINCREASED PATIENT SATISFACTION

times lower in the Early Active Intervention group than in thetraditional group. Many doctors consulting in managed caresituations today wrongly conclude that care should be mini-mized for back pain sufferers because most will get better re-gardless of carc.

Manipulative therapy has clearly established its cost cfrcc~tivcncss in patients with acute and subacute low back

pain.'~-'~"~ Jarvis and colleagues found. in comparing medi..:alversus chiropractic treatment for identical diagnoses, that"COSI for care \Va... significantly more for medical claims. andcompensation costs were lO~fold less for chiroprac~tic claims."S(J Authors of a recent meta-analysis looked atstudies comparing spinal manipul

REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL

Table 1.5. Functional Restoration

Functional capacity evaluationRehabilitation of the motor systemPatient educationIdentification of psychosocial factors (disability predictors)

FUNCTIONAL CAPACITY EVALUATION

Functional reactivation requires .lsseSSll1cnt of the fUllctiom,1status of the patient's 010101' system, EvalmHion of pos-ture and movement or static and dynamic function is essen-tial and should include assessmcnl of joint mobility. mus-cle strength. coordination. cndUl

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CHAPTER 1 : GUIDELINES FOR COSTEFFECTIVE MANAGEMENT OF SPINAL PAIN

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important than biomechanical ones.68--rn:7-l1.75 Frymoyer said.'There is increasing evidence from the general field ofdisability, and specifically low back disability, that a 'disabil-ity prone profile' can be identified and used to predict po-lential disability before the condition becomes trulychronic....., Job dissatisfaction is one of th~ only provenpredictors of disabling back pain. m According to Cats-Bariland Frymoycr,Il6 other predictors of low back disability in-clude work status and job satisfaction~ injury being viewed ascompensable: past hospitaIi7...,tion; and the patient's educa-tional level.

Recent studies indicate that it may be possible to idcmifyacute back pain patients with psychologic predispositions tobecoming chronically disabled. ll7m In the MinnesotaMulliphasic Personality Inventory (MMPI), responses indi-cating increased catastrophizing as a painMcoping strategy aswell as emotional distress appear to be promising discrimina-tor5.111-122 D~prcssion. anxiety. hypochondriasis, and hysteriaarc related to poor surgical outcomc.n.1l6 The "bio-psychoso-cial" model has been proposed by Waddell to address the dis-ability problem in patie",s with low back pain"(Table 1.6).

Tertiary Multidisciplinary Functional Restoration

Tertiary treatment of the chronic. disabled patient with multi-disciplinary junctional restoration has demonstrated its costeffectiveness. A combination of technically advanced func-tional capacity evaluation. exercise training. iid psy.::liV-social intervention are essential to the program's succcss.With a functional restoration approach. Mayer et al. allowed87% of chronically disabled people to return 10 work com-pared to only 41 % of a comparison group.12) Hazard et al. rc-ported that 81 % of the treatment group returned to work com-pared to only 21 % of lhe conuol group.I~4 \Vhen Sachs et at.used less psychologic intervention. 73% returned to workcompared with 38% in the control group. This approach wasless costly than that used by Mayer or Ha7.md and their col-

Icagues.l~j Oland and Tvciten aUemptcd a modified programin Europe. but they had difficulty achieving similar results.9 .'Alaranta et al. compared a multidisciplinary functionalrcslOration program to a primarily passive care approach anddocumented improved function, pain, and disability Icvcls.I~('In contrast to most other multidisciplinary approaches, theirapproach lnvalved the use of low cost. "low-tech" functionalcapacity measures.

Multidisciplinary functional restoration includes the com-ponents described in Table 1.7.

Table 1.6. Blopsychosocial Approach to lowBack Disability

Restore functionPromote return 10 workDecrease painReduce distressReduce abnormal illness beh~'::;:::

9

CONCLUSION

\Vith consensus-based guidelines emerging as the best chanceto cut costs associated with diagnosis and treatment of lowback pain. it is incumbent on us to be aware of the directionin which new findings lead. Quality care will result in bcHerpatient satisfaction and reduced costs. Manipulation and ex-ercise both appear to be of value if our beliefs arc based on[he scicntitlc literature. Future studies will hopefully nush outwhich patients respond better to what type of care and whatarc appropriate timelines for transfening from passive to ac-tive care.

Table 1.7. Multidisciplinary Functlonat Restoration

Quantifiable, functional capacity evaluationPhysical reconditioning of the impaired "weak linkMWork hardeningBehavioral disability managementOngoing outcome assessment using objective criteria

REFERENcr~I. Riga... S. Bowyer O. Brnen G. ct :11: Acute Low B;\ck Problems in

Adults. Clinical Pmctice Guideline. Rockville. MD. U.S. Departmentof Hcallh and Human Services, Public Health Service. Agcoc)' forH{'allh Care Policy and Rcsc

REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL'.

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18. Sri,,,, wo. Lc Oboe FE. i)urul, M." ,,, S,I,,,,llk "ppn""h IU Ih';\s:>cs~mcnt and man3~.:mO:IlI of :lCli\ II~ -rdalc,l spillal disort!crs: ArtlOllognlph for diniciallS. R~pUI1 lit" llw

...... ,..., ~n I uUIUt:LINt:.~ FOR COST-EFFECTIVE MANAGEMENT OF SPINAL PAIN 11

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101. Mayer TG. Gatchel RI. Kishino NO. et at: Objective :lSsessmentof spine function following industrial injUl)': A prospective studywith comparison group and one-ycar follow-up. Spine 10:482.1985.

102. Linton SJ. Dndlcy LA.Jensr.n I. el al: TIlc secondary prevention of lowbad: p3in: A controlled study with follow-up. Pain 36: 197, 1989.

103. Kdlct KM. Kellett DA. Nordholm LA: Effccts of an exercise programon sick Ic M. ct al: ManipulOltivc therapy versuseducalioR programs in chronic low back pain. Spine 20:948. 1995.

91. Erhard RE. Delino A: Relative effectiveness of an extension programand a combined program of manipulalion and nexion and extension ex-ercises in patients with acute low back syndrome:. Phys Thcr 74:1093,1994.

92. Cats-Baril WL, Frymo)'cr JW: Identifying patients at risk of becomingdisabled becausc of lowback pain. Spine 16:607. 1991.

93. Oland G, T\'cilen GT: t\ lri:ll of modem rehabilitation for chronic low-back pain and disability. Spine 16:457. 1991.

94. Alaranta H, Hurri H, Hcliovaara M.el al: Non-dynaffietric trunk perfonm.ncc tests: Rciiability and nonnative data. Scand J Rchab Mcd26:211,1994.

95. Rissanen A, Alaranta H, Sainio P, ct OIl: Isokinelic and nondynametrictests in low-back pilin patients rdated to pain and disability index.Spine 19:1963, 1994.

96. Mitchell RI, Camlcn GM: Results of 3 multiccnter trial using an inten-sive active cxercise program for the treatment of acute soft tissue andb.:lck injuries. Spine 15:514, 1990.

97. Lindstrom A, Ohlund C. Eel. C. ct :1.1: Activation of subaCUle low backpaticnts. Phys Ther 4:279.1992_

98. Faas A, Chavannes AW, van Eijk J Th M. et OIl: A randomi1.ed, placebo-controlled trial of exercise thcr.lpy in patients with acute low back pain.Spine 18:1388, 1993.

99. Catchlove R, Cohen K: Effccts of a dircctive return to work approachin the tratmcnt of workmens' compensation patients with chronic pain.Pain 14:181. 1992.

100. Fordyce WE, Brockway JA, Bergman lA. et al: Acutc baek pain: A con-trol group comparison of behavioural vs. lradilionallllanagement methods. J Behav Med 9:127,1986.

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Integrating Rehabilitation into ChiropracticPractice (Blending Active and Passive Care)CRAIG L1EBENSON

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Exerciseintolerance

live motion or continuous passive motion prevented SUl,'h ad-hesion forlllation.Y

The remodeling phase involvcs lysis of adhesions and r~orientation of coll,lgcn fibers along the lines of impos.~dstress. Again, prolonged immobilil.ation is. a negative fal,'(or inproper healing. In studies of rhesus monkcys. Noyes studiedthe effects of 8 weeks of immobilization on ligament stiffnessand failure ~~!e.;' Ligmncnt stiffness was reduced (0 69(';'".. of

Fig. 2.3. Effects of musculoskeletal immobllization. (From TroupJDG, Videman T: Inactivity and the aetiopathogenesis of muscu~loskeletal disorders. Clin Biomech 4: 175. 1989.)

I

Inactivity

/~Decreased

Muscle pain content ofmitochondria

recurrent pam

Enzyme defectacquired diseaseviral infection

mental depression

~ static & dynamic muscular performance

jointsliffness

illnessbehavior

muscle pain avoidance /hypertonicity \ ! beh.,ior --.. depression / /

,.-..~ ~ /& disuse ~

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Table 2.1. Negative J::ffer.t~ nf Immobilization

JointsShrinks joint capsules:.)Increases compressive loading'Leads to joint contracture~GIncreases synthesis rate of glycosaminoglycans"';'Increase in periarticular librosis'o-':Irreversible changes after 8 weeks immobilization')"

LigamentLowers failure or yield poinFH> '5-"Decreased thickness of collagen libers'l'I_~

Disk biochemistryDecreases oxygen~'Decreases glucose~lDecreases sullate2 'Increases lactate concentralion~.l'Decreases proleoglycan cooteotn

BoneDecreases bone density:n-3'Eburnation"

MuscleDecreased thickening of collagen fibers18.3.l'Decreased oxidative polential1....3~Decreased muscle mass::'2.3C>-3?Decreased Sarcomeres'oDecreased cross-sectional areatl -4)Decreased mitochondrial contenr"Increased connective tissue librosis"~Type 1 muscle alroph~2.,o."TType 2 muscle atroph~e.~20% loss of muscle strength per weekUl

CardiopulmonaryIncreased maximal heart rate~'Decreased va: max,"lDecreased plasma volume'"'

(From liebensoo C: Pathogenesis of chronic back pain. J ManipulativePhysiol Ther 15:303, 1992,)

nonnal after 8 weeks. After 5 months of reconditioning. stiff-ness was reduced to only 7% of nonnal levels.} Five monthsof reconditioning improved the tissue failure rate to 80% ofnormal. and after 12 months of reconditioning, the ratc wascompletely nonnal.}

FUNCTIONAL DEFICITS ARE PROSPECTIVELY CORRELATEDWITH LOW BACK PAIN

Patients typically become inactive when they cxperiencepain, and this inactivity promotes dcconditioning. \Vith de-conditioning comes greater susceptibility to typical posturalor occupational repetitive strains. A chronic cycle of recurringpain is easily established unless function is restorcd./lf painrelief is the only goal of treatment. and functional restora-tion is ignored, painful recurrences arc more likely". Sponsmedicine specialist Stanley Herring says, "signs and symp-toms of injury abate. but these functional deficits persist. ' . ,adaptive patterns develop secondary to the remainingfunctional dcficits,"~ Focusing on function helps patientsto develop control over their symptoms and to preventrecurrences.

In many retrospective studies, investigators have docu-mented that various functional changes in musculoskeletalperformance arc associated with episodes of bnck pain. al-

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though tht:y C:l 11 1l0t dctcrminc if (hcse changcs are a causeor :1 rc:,uh of lhc pain. Prospcclivc studies come closer to

id"'lltiryin~ clioll\gic factors. Thc goal of such research is toidctltify what factors are causally linked to low back painepi:'Olks in a prcdictivl: manner. The following studies arc allpnlspCl:liw,

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pectcdl)' applied oul'ing their vulncrable. recovcry pk,~~."MAccording to Andcrsson ...It is generally believed thai r~pe!itive loading causes failure becausc of faligue of the varioustissues: I .\ Brinckmann and Pope condudc under repet-itivc loading. the yield strc~s of thesc l1lillcriilb .tIld thestrength of struclllres buill from these matcrials i:-: n:duccdwith respect to the stress or strength obscrved under a singleload cyclc..f .... (Fig. 2.7). l?educillg ('xjJo.mre 10 high /t.\.e/.\" ofload-sllch as trunk flexioll wilh eilher CO/1//u(!.uiofl or rota-tion-is Ol/e! of 1he 1110.\1 i/1/{Jorlwll le/1('I.\" (~rpre vclII ioll oj 1011'

STRESS

Microlailure

Fig. 2.5. Stress-strain curve lor a ligament. (From Bogduk N,Twomey LT: Clinical Anatomy of the Lumbar Spine. 2nd Ed.Melbourne. Churchill Livingstone. 1991.)

Functional capacity

Fig. 2.4. Relationship between exte.rnal demand and functionalcapacity.

(fatigue) and eventunl injury arc the result (Fig. 2.4). Thestress! strain curve explains the mech:Jnics of the relationshipbetween extemalload (~aress) and lissue deformation (strain).The applied or elongming force is termed slress. The amountor percent of elongation is the strain. Stress is measured innewtons and strain in percent (%) elongation.

Loadittg of biologic tissues produces a characteristicstress/slrain curve demonstrming the amount of stress (load~iog) required to produce a set amount of strain (percent ciongation or deformation)I"- (Fig. 2.5). Thc initial concave por-tion of thc curvc is lhe "toc" region, which corresponds [0 theinitial tissue distraction involving a structural changc from acrimped. wavy fibril organization [Q a morc straightened, paralleI arrangement.~ In the toe region, little force or energy isrequired to lake the slack out of the tisslle. but the tissuequickly becomes stiffer, resisting further dong..Hion. If greater

forc\"~ arc prescnt. tissue dcform

11

CONTROL

50

250

200 -19\ --------

LOAO 150INI 100

tS THERE A PAtN CYCLE?

Th~ existence of a pain-spasmpain cycle has been a \vell-acccpted concept of physical therapy and chiropractics. As acriteria for therapeutic decision making. it is one of the mostil\lluel\tial "" priori" assumptions of many practitioners. espcdally aillong those who lise extensive passiv~ techniquesand/or soft tissue manipulation. Its validity is unproven. how-cver. and currently. it is often ignored. The litemture docsshow thm prolonged or intense pain can lead to both psycho-logic (abnormal illncss behavior) and neurologic (dorsalhorn sensitization) consequences. Either or both of thesebehavioral and physiologic dysfunctions arc at the heart of thetransition frolll :.111 .\cutc to a chronic pain syndrome.Significant external loading that exceeds intrinsic functionalcapacity leads to tissue fatigue and altered biomechanics. Tomaintain spinal stability following biomechanical changes,.such as can occur after creep and hysteresis, type I and typeII affcrcllls arc stimulated to maintain accurate proprioceptionCrable 2.3). The initial firing from the joint mcchanorecep-tors, muscle spindle affcrents. ilnd Goigi tendon organ affer-Cllts allows ad'lptation to occur so the fatiguing tissues canavoid failure. Because these receptors arc adaptive. they donot continue to discharge if the biol1lechanical changes :lr~

Neuroph)'siologic FactorsAs tbc activc component of our locomotor system. musclesarc often called on consciously or by reflex to protect othcrtissues' under stress. Compcns3lOry adaptations (facilitative;llld inhibitory) typically follow any strain, whether or not it ispainful. \Vhat may begin as a segmcntal, reflex muscular'Idaptalion to pain may become "programmed" in the form of

present for a long period of time. As a result, repetitive strainseventually exhaust the adaptive capacity of the body's dc vfenses and lead to painful injury.

Once tissue failure occurs, inflammation, mediated bybradykinin. substance P, and prostaglandin E2, lead to stimu-lation of nonadaptive, types III and IV nociceptive affcrcnts.Various changes in the muscular system occur automaticallywhen injury occurs. For instance, muscle inhibition followsacute low back pain or knee injury/inflammation. 67.(,~Additionally, increased neuromuscular tone also results fromstrong nocic.:.ip;iVt .Hiiiiulation,!,9-71 Protective mechanisms-nonnal illness behavior-to immobilize an injured area areusually appropriate in the acute stage. If they become memorized as a "pain-motor program," however, they can lead to achronic state. Abnormal illness behavior, such as excl!ssive orprolonged stress, fear, or anxiety, will affect the neuromuscular system behaviorally via canditialling alld ph.lfSiologicalJ.vfrom the limbic center, thus providing an ideal terrain forchronic pain.

Testing with evoked potentials of patients with chronicback pain revealed lower pain thresholds and higher than nor-mal evoked responses at thresholds than are noted in normalsubjects.72 Magnetocnccphalographic study with sub, supra,and standard intracutancous electric shock stimuli in chronicback sufferers also revealcd a higher than normal pain-evokedmagnetic field.n It was concluded that this heightcncd re-sponse was attributable to central nervous system hyperre-sponsiveness in the primary somatosensory cortex.

Acute pain involves biomcchanical insult (i.e., injury,repetitive strain), biochemical mediation (inflammation), fa-cilitation of algesic pathways, and finally neuromuscularadaptation. If repetitive biomechanical insult is not avoided;abnormal illness behavior is present; or deconditi~ning oc-curs, resulting in inadequate neuromuscular adaptation, thenchronic pain with central nervous system involvement (corti-calization) can be expected.

To prevent the transition from acute to chronic pain, threethings should ocq~r once the initial acute, inflammatoryphase has passed: (1) patietll educaricm about how to idenllfy

Table 2.3 Nerve Types and Functions

II

Low Threshold/Adaptive

REPETITIVE STRAININJURY

~Swelling &

Inflammation

~Soft Tissue

~~('oPain ~Gradual 'VO/ MuscularM~ru,,,~ ~09'""'~:

Joint StiffnessFig. 2.9. The pain cycle.

THE PAIN CYCLE:

and limit external SOlfl"ces of [);o/lll'chan;nt! ovcrlo(ld; (2)early idelllificatioTl of psychosocial j{zctors (~r abnormal iffIless behavior; and (3) idellfijicatio/l and rehabilitatioll (~ftlu'functional pathology of the motor system (i.e., dl'COlldit;ollill~

.~~vlldro/llc). This third aspect involves looking for specificjoint and muscle dysfunctions so that patient reactivation canbe promoted and deconditioning prevented. Figure 2.9 showshow chronic pain can arise from dccol1ditioning syndrome.

, Pain is dcrived from the Latin term "poena" mcaningpenalty or punishment... Unfortunately, pain docs not alwaysserve as a good early-warning system, but/oftell arises onlyafter damage is done,. Pain alone is just a symplOm-the COIl-scious perception of nociceptive aClivity. If [Jain relilf is the01l/Y goal of care, thell decollditiolling afld variollsfulIctiOfwlpathologies will remain as precursors to future bio/llccJ/(mi-cal failures. Functio/lal re:"'toratio/l ill additio" to paill relielare appropriate goals because prevellfion of recurrent orchronic pain is the ultimate goal of a cost cOlllainmellt-oriellled approach. In as much as we can identify specificfunctional pathologies that are causally linked-trigger pointsor overactive muscles, weak muscles or abl1of!lIal movementpatterns, and joint dysfunction-we can then not only providesymptomatic (pain) relief, but also restore function. Evcn inthe absence of uncovering a clear chain of functional patllo-logic changes. identifying deficits in functional capacity candrive the reactivation of the patient by rcrnediating painavoidance behavior.

MUSCULAR PAIN, TENSION, AND INHIBITION

Muscles are often ignored while joints or disks receive themajority of recognition as potential pain generators. For

C

Chronic pain,postganglionicautonomic,dorsal root af-ferents

IV

SLOWUNMYELINATED

SMALL

High ThresholdlNonadapting

III

Acutepain

Adelia

Secondary musclespindle, gammaefferent to intra-fusal musclespindle

A beta and g~mma

FASTMYELINATED

LARGE

A alpha

Golgi tendon,primarymusclespindle, allerenls toskeletalmuscle

\,.,on""r I t:.M .:: . In 1 cur"'", I 11\l1I Ht::HAtjllllAllUN INTO CHIROPRACTIC PRACTICE 19

High gamma

Muscle length

/ !/LOW___ } gamma

AfferentIimpulsefrequency

......-_._-_..._----_.

patients with low back disability.'" In addition. sustainedEMG activity has been found in the nidus of trigger points.'9It has also been noted that when pressure is applied to an ac-live trigger point. EMG activity increases in musclcs in thc re-ferred pain zone.l;O

Static overstrain. such as from prolongcd sitting or slump-ing, has often been suggested as a high risk activity for indi-viduals with a back problem. Sustained contractions of only4% of thc maximum voluntary contraction possible have beenshown to lead to negative cffccts.(,~111 Metabolites are pro-duced that stimulate groups 1II and IV aUerents and increasegamma motor neuron activity. It has also been shown that in-creased interstitial potassium concentrations sensitize thegroups III and IV muscle afferents.,n resulting in an increasein the sensitivity to stretch of muscles with convergent affer-ent inpu(Sj (Figs. 2.11 and 2.12).

Study of muscle fibers has shown that conditions of con-stant 10,1'1 affect the ability of a ltlusde to achieve efficient rc-laxation.'4 As a result. tension and pressure build up in themuscle.'J The more the muscle contracts. the greater the en-ergy expenditure. Local ischemia is another key factor in-volved in increased muscle tone. Under conditions of is-chemia. groups III and IV muscle affcrents become moresensitive to strelchX-l (Fig. 2.13).

Ischemia itself is not painful; however. if II musclecontracts under ischemic conditions. pain develops wilhinI minute.lI~ Br~ldykinin is released during ischemia and istherefore thought to be associated wilh ischemia-producedpain."lJ Under eccentric muscular conditions. mild over-load may swell muscle fibers without inflammation.!((;Heavy eccentric exercise leads to swelling and necrotic in-flammation.1I7

Joint receptors. if stimulated. cause both facilitation andinhibition of muscles. Low intensity stimulation of joint af-ferents in the knee have been shown to influence the sensitiv-ity to stretch of Illuscles around Ihe kncc.w.llt-91J Also. rellcx in-hibition of muscles has been noted when joints and ligaments;,ue

._." ~ vr- Inc: .:)rll\lC: "'" t'HAl.; 1IIIONER'S MANUAL

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CHAPTER 2 : INTEGRATING REHABILITATION INTO CHIROPRACTIC PRACTICE 21

i . -->. ~ -.

Leclon

IARc le4se o[v4soneuTo~ctivesubstances

Fig. 2.13. local vicious cycles in damaged muscleas a possible peripheral mechanism for chronic mus-cle pain. The right-hand cycle is assumed to bestarted by a tissue lesion that releases vasoneuroac-live substances (path A). The centrallactor of the cy-cles is ischemia, which can be produced by venouscongestion, local contracture. and tonic activation ofmuscles by descending motor pathways (path 8).(From Mense S: Nociception from skeletal muscle inrelation to clinical muscle pain. Pain 54:241.1993.)

hibition of certain muscles required for a task is a likely con-tributor to overload injury or pain.9.,.I1~

Hides et al. documented/unilateral wasting of the multi-fidus muscle in patients with acute low back pain/"~ With real-time sonography. they measured cross-sectional area (CSA)of the muscle and determined that the wasting was isolated toone vertebral segment. The wasting occurred rapidly in a 10'calized area and was thus not considered to be the result ofdisuse atrophy. The authors were abk to correlate the area ofwasting with a dysfunctional segment identified on clinicalmanual examination (i.e .. motion palpation) ....ln patients withchronic back pain. CT scanning demonstrated generalized at-rophy but a relative increase in the CSA on the symptomaticside~~ Such a relative increase in the CSA could be explainedby Ihe findings of increased paraspinal muscle activity% andhi..ologic evidence of type I fiber hypcl1rophy on the symp-tomatic side and type II fiber atrophy bilaterally in personswith chronic back pain.!H

BullockSaxton et al. described gluteus maximus andmedius inhibition during gait. and their subsequent facilila-tion after a brief course of propriosensory retraining."ll Jandaalso reported r~ciprocal inhibition of the abdominal mus-cles as a result of stiff. overnctivc erector spinae musclcs.r~)He showed that the abdominals became spontaneouslystronger following inhibition and stretching of the erectorspinae. Headley successfully demonstrated inhibition of the100ver trapezius muscle during shoulder Oexion or abduc-tion when active trigger points in the upper trapezius are pres-cnt.lI~ Simons also reported inhibition of the deltoid muscleduring shoulder flexion when infraspinatus trigger poilHs arcprescnt.!!!)

;

IIII1

~

1,

i )I~ C)1 ~

I ;.JII (,)I ~;--""-J.;.J}! (}-~! f}iII!

Fa Hure o[Col++ pu:~p

\Contracture

LOCo'llischo'lemia

Jt'II18II

Increase inmuscle toncvia descendinqpathways

Venousconqcstion

OedemA

TIIP ;/lirhtl muscular reactioll to pain alld injury has tra-t/itional/y been as.mlllct/to be im:reased tell-fie", ami slijJ"ess.Data ill Ihe lilerlllure indicate ilihibiliull is at least as signifi-callt. Tissue immobilization occurs secondarily. which leadsto joint stiffness and disuse muscle atrophy. Such changes be-come a habit. mediated by central motor regulatory pathwaysas a new "pain-motor program" forms.

The combination of trigger points. muscle inhibition, andjoint dysfunction arc kcy peripheral components of the func-tional pathology of the motor system. If sustained over a pe-riod of time. these components 1ll.1Y outlive the elimination ofwhat caused them in the first place. This f

_ ....... ' , ............ ,,

vNr\1"' I tH ;.::: ; IN I tUHAIINl,;i REHABILITATION INTO CHIROPRACTIC PRACTICE 23

J 1r~

IMMOBILIZATION ....--

~ FlJxI:::/CONTRACTURE

an "irritable focus" in specific spinal cord segments, II", Perlcl al. lOi and Kcnshalo and co_workcrs lt1lt made the initialexperiments that showed that noxious sensory :-;tlmuli produccd heightened sensItivity 01 dorsal horn neurons to futurestimuli.

A new concept called "ncu1"Opmhic pain" iJ being pitt for.ward to explain the common clinical prescuwlioll of persis[e/lf pain. hY{Jer.w!ll.'iitil'jry, alld poor motor cOlltrol ill the ab-::('II('e of a pallia-til/atomic or Ileurologic expJlIIull;01l.Bcc

REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL

,j

. (

Ji;

lUres. Stimulation of viscera docs not .tlways producepain. btU \'isccral aftcn::nts projecting into the dorsal horndo lypicciceptivc neurons have convergent input from mcchanorcccptors. their responses to both innocuous and noxious me-chanical stimuli will then be increased.... Sensitization thencauses formerly subthreshold responses to rench thresholdand trigger disehargcs."'u, According to Mayer and col-leagues. "Overwhelming evidence suppons the conclusionthat a change in the central processing of input from low-threshold mcchanorcccptors is responsible for secondary hy-peralgesia to light touCh."I~lI Silent nociceptors that arcmechano-insensitivc also can become mechanoscnsitive oncesensitized. 1flo Table 2.4 lists the neural changes associatedwith sensitization and Figure 2.17 depicts the p::Hhophysiol-ogy of sensitiz'ltion.

How Do Mechalloreceptor A[[ereflts Cause Pain? TheNeurochemistry of Neuropathic Paill. The p:'lthophysiologyof neuropathic pain involves peripheral ilnd central neural

- Small d'OmeTer ,npvl

To osccnd,nQsyslem!>

(ommon pool orCOnnC(lor neuronsWith thruhold K

o

De'!.cend,nQsysl~ms

I

Poor 1'..lotor Contro'-lncoordin~lIi{ll1()r POD( balance.Test: Incoordinatcd !novcmClH pallcrns or gait; ro~ilj\,c

Rhombcrg or Hamanl tcstReferred Pain or Sccondur)" H),JlCnllgcsia-Sprc:ld of p

CHAt-' I cH Z : 11'1 I I::UNAllNli Ht:HAI:ULlIAIIUN INTO CHIROPRACTIC PRACTICE

Repetitive strain

1Hysteresis and deformation

I -T

Decreased tissue fatigue/failure point

1Sustained aHerent barrage in types III and IVMechanoreceptorslnociceptors

~Sensitization of dorsal horn neuronsI

Neufopathic pain

) IItc

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c\'~nts. Sustained activity in types III and IV (small diameter)primary affcrcnts leads to a rclcflse of excitatory amino acids(gl~t,;!.7 Secondary neuron hyper-responsive-ness after repeated stimulation is called "wind-up" and isoften short term. Inhibitory amino acids such as GAB A arcpresent to dampen this exaggerated response. but. over time.segmental inhibition is deactivated by the flood of cxciuttory

nc.nMOIL.llf\IIUN OF THE SPINE: A PRACTITIONER'S MANUAL

)

,,

TIbialis anleriorGluteus maximusGluteus mediusRectus abdominusLower/middle trapeziusLongus capitus & colliDelloidsDigaslrics

Phasic (Tend 10 hypoactivily)

Triceps suraeHamstringsAdduc(orsReclus femorisTensor fascia latae (TFL)PsoasEreclor spinaeQuadratus lumborum (QL)PeCloralisUpper trapeziusSternocleidomastoid (SCM)SuboccipitalMasticalories

Postural (Tend to hyperactivity)

Table 2.5. Postural and Phasic Muscles 13S

Fig- 2.19. Pathways for cerebellar "error'" control of involuntarymovements. (From Guyton A: Basic Neuroscience. Philadelphia,we Saunders. 1987.)

RETICULARfORMATION

SUBSTANTIANIGRA ---

Sherringtol1'S Law of Rcciproc~1I Inhibition (Fig. 2,20). Thus,ifCl TU/'ilum{ mllscle SllC" as the iliop.WlJ.\' become.\ .'ihortemdfrorfloverusc. flot olily will it lJu!(:lumically {imit Ihe rang('\/tlf motion of it,'I {Jlltllgolli.'it 'fie 81weus max;mus. bw also iT

. wifl 'leurolO);ically illh.i11ir.j1S_GCI,h}!l as well. This combin:ltion of biomcchanical and neurophysiologic influences is astrong stimulus to the creation and maintenance of muscularimbalances.

Electro'myographic (EMG) data (Fig. 2.21) show th;:tt atight erector spinae muscle will be active during its rever:,\::lction. trunk flexion. and thus inhibits the action of the ago-

CorticospinalIrocl

Reliculospinol - and Rublospinol

IIoels

\

MESENCEPHALON,~-~--11 PONS, oml

MEDULLA

Spinoc.etcb~UolhoC I

Fig. 2.18. Pathways lor cerebellar control 01 volunlary move-ments. (From Guyton AC: Basic Neuroscience. Philadelphia. weSaunders. 1987.)

Clinical FeaturesMUSCULAR IMBALANCE

RED NUCLEUS \r.:::J..+-r

MOTORCORTEX

\Vhen muscles reacl lo protect the body from harm or lo re-duce pain, certain muscles become overactive while othersare inhibited. As a result. joinl stress is altered and greaterlIluscie fatigue results. For such prolective reactions, [he pos-lural or anligravity muscles arc activated most easily,Conversely. muscles wilh a primarily dynamic or phasic func-tion tend to be inhibited when physical Slress is prescnt. jandlland co-workers. who studicd thcse typical musclc rcactions inboth neurologic and onhopcdic patients. call this commonclinical phenomena "muscle i111balancc,"I~~-I,I~

Janda l11ul co/{eaglles (.'x"llIined that the basis for mostt1lflscle ;ml)(llallces comes from our predicwble respot1se tostressfttl cnvironmetltal demands (constrained pO.'iIUreS,reperiiive tasks, gravity stre,'iS, inactivity). They identifiedthat the pO!'itural muscles tend toward overuse and eventualshortening, whereas the ph'1Sic muscles tend toward disuseand weaknessl~-l~l (;rable 2.5). These muscles arc oftcllgrouped as paired antagonists and appear to be affected by

onen enough arc learned by the cerebellum. This new centralprogramming is called an "engram." In regard to this programming. Pail lard says. "The existence in all animals of aconsolidated rcperloirc of motor capacities. either inherited orsecondarily acquired. is now all incomrovcrlible fact of con-tempof

Fig. 2.21. Electromyographicactivity before and alter stretch-ing light muscles. (From JandaV: Muscles. central nervousmotor regulation and back prob-lems. In Korr 1M (ed): Neu-robiologic Mechanisms in Ma-nipulative Therapy. New York.Plenum. 1978.)

27

Fig. 2.20. Reciprocal inhibition 01 motor neu-rons to the opposing muscle. Impulses lromttle contracted muscle .e.xcite motor .unit:!,(the same muscle (faclhtory synaptic)nllu-ence designated with a plus sign) and inhibit.through an interneuron. motor units in theopposing muscle (inhibitory synaptic influ-ence designated wilh a minus sign). (FromLehmkuhl LD. Smith LK: Brunnstrom'sClinical Kinesiology. PhilEldelphia. FA Davis.1983.)

E..lcnsornlusdcttdeeps)

An intermediale muscle type is FR::::':J~I~!_~~y.itch fatigue~sistant:'This typt: resists fatigue but illS0 has f,lst COlli rac-tion nnd relaxation speeds. The FR type has both aerobic andt1naerobic metabolic e

REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL

Fig. 2.22. The lower crossed syndrome. (From Jull G. Janda V:Muscles and Motor Control in Low Back Pain. In Twomey LT.Taylor JR (eds): Physical Therapy for the Low Back. Clinics inPhysical Therapy, New York, Churchill livingstone. 1987.)

",

,,

.~,

ih;

Phasic "fight or m9ht~-. -".'.

Low

Type FF -Fast-TwitchFatigable"

Type IIEasyAnaerobicGlycogenMinimal

(MUSCle shorteningJFast

Type I

Posture "antigravity"

Constant musclelength

Slow

Type S "Slow-Twitch"

Resistant""OxidativeMitochondriaJATPExtensive

Characteristics

FatigabilityMetabolismEnergyCapillary

networkMetabolic

preferenceSpeed 01 can

traction,relaxationand forcegeneration

Metabolism alrest

Function

Table 2.6. Characteristics of Muscle Types"'ill20

Muscle imbalances alter the performance of related move-ments. Repeated performance of abnormal movements leadsincvitably to further strain, which can perpetuate muscularimbalances andjoim dysfunction. In the work place, the com-bination of muscle imb~ This dumge occurred rapidly lllld thlts

'was nor considered 10 be a di.Hl.\'C arroph,,: Stokes eI al. !owufgeneralize,! atrophy in paticlIIs with dmmic back pain. but (lrd(ltive increase ill the CSA was noted 011 the symplOmafic

-",yide. 9J Type I Jiber hypertrophy on the symptomlJlic side and........... tYl!!. II fiber atrophy bilarerallv have been documented in

c~roTllc back pai" patients.,}7Muscles housing trigger points have been shown to have

dramatically different levels of EMG activity within the samefunctional muscle unit. Hubbard and Berkoff showed EMGhyperexcitability in the nidus of the trigger point in a tautband that had a characteristic pattern of reproducible referredpain. 79 Case studies. havc also revealcd that trigger points inone muscle are related to inhibition of another functionally rc-Imed muscle.7l19!i In particular. Simons showed thalthe deltoidmuscle.can bc..inbibl~d _~Y!lc~1JlLcre arc infr~~p)'na1Us triggerpoints.ll(t HC~ldley has .ghown that lower trapezius inhibitio~ isrelated to trigger points in the upper trapezius:;:

Fig. 2.23. Depiction of the layer syn-drome. (From Jul1 G, Janda V: Musclesand Motor Control in Low Back Pain. InTwomey LT. Taylor JR (eds): PhysicalTherapy for the Low Back, Clinics inPhysical Therapy. New York, ChurchillliVingstone. 1987.)

Thofaco1urnblll

Elector Splnu

The gcneral crfects or llluscular imbalance ..Irc listed inTahle 2.7. Muscular imbalance is lypic

'-.,,.... ..... , ... , ''"''1 tUN UI- rHE SPINE: A PRACTITIONER'S MANUAL

SCM. sternocleidomastoid.

Table 2.8. Muscle and Joint Functional Chains'''~

--------------

,)'

\

MuscleJoint

CoccyxHip

certain. stcrcotypit: 1ll0vem~lH patterns. The Ilcgatin: rela-tionship bctwct=n various individual functional p~uhologicchanges and the abnormal pcrfonllanct:: of basic m(l\t::mclltpatterns is self-perpetuating. Ahcred or f;'llIlty movemcnt pat-terns thcmsch'cs place new slrains 011 the locomotor systellland lead to the spread or a local problcm beyond a singlercgion.

Slid, mm'emellt paltcms ira, ji,.st n:co}.tlli;('d clinicallyby Jonda. who noticed tlla! til(' do......i

\,,;n/"\I'" I en G . ,,~ .....vn/"\. II"\): H.t:Hf't:SlLlIJ\IIVN INIU

32 nL..",.... ... '~, ...... " ... , .,. __ .

i~III1i~

I

III,I

medicine model directed at rapid safe return tu work l:oupkJwith ergonomic intervention h

CHAPTER 2 : IN I "GRATING REHABILITATION INTO CHIROPRACTIC PRACTICE 33

Table 2.12. Goals of Treatment

Acute Intervention Remobilization Rehabilitation and Reconditioning Lifestyle Adaptations

Reduce inflammalionNo pain at restMinimal pain with unstressed

daily activitiesDecrease muscle ~spasm~

Increase painfree mobilityMinimize ClecondllioningPromote tissue repair/regeneration

Increase muscle strength/enduranceImprove coordinationIncrease flexibility'InCrease aerobic capacityPromote tissue remodeling

Improve ergonomic factorsEducation about biomechanicsAddress psychosocial lactors

PAIN RELIEF

Table 2.15. Factors that May Predict a Longer Recovery(from the Mercy Guideline)History of more than 4 episodesLonger than 1 week of symptoms before seeing a doctorSevere painPre-existing structural pathology or skeletal anomaly (i.e .. spondy-

lolisthesis) directly related to new injury or condition(From Haldem.:.n S, Ch

Yes --1 Increase Activity I

Ves +-I Return to Normal Activity

yes...... Return to Normal Activity

Yes +-I Return to Normal Activity

INo

Is pain settling withinIhe first 13 days

(2 weeks if nerve root pain),even if still present?

No

Is function improving within12 weeks. even if still

with some pain?

Time1ine: 3-6 monthsConsider Second Opinion:

- Active Rehabilitation Specialist(reconditioning, functional outcomes, behavioral principles)

Simple Backache orNerve Root Complaint

Timeline: 6-12 weeksContinued Primary Management:

- Active Rehabilitation (active care> passive care)- Id of factors which may predict a longer recovery(table 2.15) or risk factors of chronicity (table 2.16)

- Alternative symptomatic measures (muscle relaxants .antidepressant, injections. supports)

- Objective outcomes utilized'

No

+

Yes Yes

+ +Timeline: 1-3 Days LI_R_e_,_e..,rr_a_'-J

Reassurance:- No serious pathology /C-

- P~ive prognosis. but possibifity 01 recurrence ( +Symptom Control:

Analgesics. NSAIOs- Heat or lee

Activity Modillcatlon:\. Bed resl 13 days (

----- -- ----

Table 2.J7 ~ulnmarizcs the pnlglHl~i~ for tll~ \'ari(lll~ g~n~raltyp~s of cases, Th~ algorithm in Fi.surc 2.24 is llsd'ul for UIl-dcrst;:lIldin!.! the indicati()n~ for bed rest, m

REPORT TO THIRD PARTY PAYOR

vnM.rlt:r14!; 11\1 I tUN1\1 INu Ht::HAl::.iIUIAIIUN INTO CHIROPRACTIC PRACTICE

J_1:,.~ ,'~".J

,

Ii

After the patient has been given the working diagnosis. iiis important to explain that although most {Xoplc gel bcltcrwithin 6 weeks. recurrences nrc the rule rather than the cx-ceptionY' For this reason, it is prud.:nl to spend some timetcaching paticnrs how to reduce further strain on their backand how to increase their intrinsic capacity to handle extemaldemands. If a patient is "disability prone:' psychosocial aswell as biomcchunical issues will need to be

Trunk Flexion andDate ---;: SLR (degree) ---:7' VAS (low back) (%)-:7 Extension ROM ----7 Oswestry (/0)

"),

".'

,,

i

78543004

INCREASING PATiENT ADHERENCE, COMPLIANCE.AND MOTIVATION

trauma" from prolonged overuse and/or constrained posturesI~ads '0 gradual dcconditioning o( the strained soft tissues.This deconditioning weakens the various musculoskelct3.1

stnJcturc..~ to the extent that painful injury can result withoutany trauma. Such pain ean occur without the innaml1l

l'HAI-' I t:H ~ : IN I t:t:iHAIING REHABILITATION INTO CHIROPRACTIC PRACTICE 39

I(EFERENCES

plained that this tightness or weakness is what leads to irrilU-tion and pain with activity. They must learn that rchabilitationOf restor,ilion of function will prevent pain from arising in thefirst place. and although such rehabilitation Illay be morepainful in the shon term, improving function is the key tolong-tenn pain relief. Always seeking tcmpormy pain reliefwill do nothing to prevent the problem from sHIrting again.

\Patients can be re.!2~jJ.hY. __

4U REHAtilLllAllUN UI"" I HI:: :::it"INt:: A I""tiAl;IIIIUNl::H-:::; MANUAL

S. Akcson WHo WOO SLY, Amici D. ct al: Biomcch:lIIical and biochemi-cal changes in the periarticular conllective tissue during contracture de-velopment in the immobilized rabbit knee. COllnect Tissue Res 2:315.1974.

6. WOO SLY, l>'1athcws JV, Akcsoll WH, ct "I: Connective tissue respollseto immobility: Correlative study of hiomcch:mical and biochemicalmeasurements of normal and imlilobilized "lbhi! knees. ArthritisRhc\llll 18:257, 1975.

7. Vidcman T. MidH~lss(1l1 JE, Rauh:lIl1aki R, ct al: Changes in 355-5UI-ph:llC uptake in differ"111 tissues in the knee :md hip regions of rabbitsduring irnllwbilizalion. rClllOhilizalion and the development of os"teoarthritis. Acta Orthop ScamI47::!90. 1976.

8. Eronen I, Videman T, Frimon e. et al: Glycosaminoglycan metabolismin experimental osteo;Jrlhrosis c

l.Jn .....t' I t:H ~ tN I t:bHAIINli HEHABILITATIUN INTO CHIHUt-'HA{.; lie I-'KA{.; II{.;!:: 41

)

~ ".,-;"

i,,

,),IJl ."v!,

,)Ii

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~i~

I ()",.,,

.)! \,I 0i

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51. Katz DR. Kumar VN: Effects of prolonGed bed rCSl ,'n l;.rdiojlul.monary condilioning. Onhop Rc\' 11:89.1982.

52. Chaffin DR. Park KS: A longiludinal sludy of lo.....-b3d I\,~in;\s ;\ssod-::Ited wilh occupalion31 weighl liflin~ beloo>. Am Iml Hy~ t\~soc J34:513.1973.

53. Chaffin DB. Herrin GD. Keyscrling WM: Preemploymcnl "tn:ngth lCsting: An upd::l!ed position. J Occup Moo 20:403. 1978.

54. Cady LO. Bischoff LP. O'Conncl ER. et 31: SlrclI1;th and litness;Jnd suhsequcnt b.:Id: injuries in firefighters. J Occup ~kd 21:269.!C)?9

55. Rowe ML: Low hack pain in induslry. J Occup Med 11:1!ll. 1969.56. Bicring-Sorcnscn F: Physical mC3surcmcnts :1... risk indicators for low.

back trouhle ovcr a ollc-year period. Spine 9: 106. 1984.57. Troup JOO. M::lrtin JW. Lloyd DCEr: Bnek p:lin in indust!'}: A prospec-

tive slud). Spine 6:61. 1981.58. Dehlin O. Berg S. Andersson GB1. ct ;1.1: Effcct of physical training and

ergonomic counseling on the psychological perception of work and onthe subjectivc assessmenl of low-back insufficiency. Scand J RehahilMod 13: I. 1981.

59. Gundewell B. Liljeqvisl M. Hansson T: Primnry prcvcnlion of backs)'mploms :lIld 3bsence from work. Spine 18:587. 1993.

60. Vidcman T, Rauhala S. Asp K, Cl Oil: Patient-handling ~kilL back in-juries. and back pain. Spine 14:148. 1989.

61. B3t1ie MC. Bigos SJ. Fisher LO. et "I: The role of spinal ncxibility inback p;'lin complaints within industr)': A prospeclive slUdy. Spine15:768. 1990.

62. Dcyo RA. B:lSS JE: Lifcstyle and low baek p;lin: -nlC influencc ofsmok-in~, cxcrcisc nnd obesity. Clin Rcs ~5:577A. 1987.

63. Frymo)'er JW: Epidcmiolo~y. In F!'}'moyer JW, Gordon SL (cds):Symposium on New Perspective... on Low Back P;!in. Park Ridge.American Academy of Onhopaedic Surgcons. 1989. pp 19-:U.

64. Bogduk N. Twomey LT: Clinical Analomy of the LUllln:tr Spine. 2ndEel. C'hurdlill Livlllgslone. Mdbounll.:. 1991.

65. Anderssoll GBJ: Occupmion;11 biOnll.:chanics. In Weinstein J:-;. WicselSW (cds): The Lumbar Spinc: the Imem:llional Society fur the Study ofthe Lumb;lr Spine. Philadelphia. W8 Saunders, 1990. p 213.

66. Brinckll1ann p. Pope MH: Effects of repeated loads and ,'ibratioll. InWeinstein IN. Wiesel SW (cds): the Lumbar Spinc: the Im.:mation:L1Society f()r the Study of the Lumbilr Spine. Phil:ldclphhl. WB Saunders.1990. p 171.

67. OcAndrad..: JR. G...nt C. Dixon ASJ: Joinl dislension and rdkx muscleinhibition in lhc knce. J Bone Joint Sur ,17:313.1965.

68. Hides J,'. Slokes ~H. Saide M. CI al: Evidence of lumhar mullilit.lusmu.''Cks waslinl; ip\ilatcrallo symplolll!i- in p:llicnts wilh :Kutdsub:lCUIClow back pain. Spine 19: 165. 1994.

()9. Johanssl1Jl H. Sjolander p. Sojk;J P: RCCeplOT'S in thc knee joill1 lig.n-mcnts ;tndlh.:ir role in the biomechanics of the joint. Crit RCl' "iollledEng UU41. 1991.

70. Woolf CJ: Long tcnn aller.llions in the cxcitabilil)" of lhe fk~ion reflexproduced hy pcripherallissuc injury in lhe chronic decerebratc r.lt. l'ilill18;3'25. 1%4.

71. D

nt:.nl"\u ..... ' ,n."VI"" vr I nt >;)"'1I~r::.: 1\ t"HAl.,; IllIUNl::.HS MANUAL

100. SchIud). Ilhy.. Ther 7-':216. 1~t}3_

152. Schwar1.er AC ,\pril CN. Bogduk N: '1111.: :o.'lcrllili;I': joilll il1chmnic lowback pain. Sjlille 2(1::\ I. ]lJIJS.

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155.

156.

157.

ISS.

159.

160.

161.

162.

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16S.

169.

B:lmslc)' L. Lord SM, Wallis 61, et al: The prevalence of chronic cervic,; zyt:arophyseal joinl p:,in :Ifter whip!a~h. Spine 2n:20, 1')95,Nordin }.I: E:..!r1y lilldinfs of NIOSH/CDC model b:ld clinic n:n.'al sur-prising obser\'ations Oil work-related low h:lck p:lin prcdicl\\r:-. SpincLettcr 1:5,6. 1994.Kellett J: Acute soft tissue injurks-a rC\'iew of the litcralull:. Ml'O SdSports Excre 18:489, 191\6.():Ikes U: AculC SOflli.~suc injuries: Nalull: and managcment. AUSlr p,lInPhysici:lII Suppl 10::'1. 19S2.Va:: Dcr~ktllill HIC: !'~I.'::;:": :i,:;:(' ,If kmlwkJgc Oli p;a;;cs~., .,:. :i':;1\'ing in col:agl.:'11 stnlClures. Ill! 1 Sports ~kd 3(Suppl 1):9, 1982,Waddell G: to. new c1inic:ll model for Ihe lrt::lllnent of low-h:ICk pain.Spine 12:634, IllS7.Tarola GA: Whiplash: COnlCl1IrXWJry considerations in asS('ssmelll,In:lnagemell1. trcallllelll :md prognosis, JNMS 4:156, 1993.M:lycrT, Galchel R, Maycr H, et oJ: A prospective r:llldomized two yearstudy of functional restoration in industri:ll low back injury utilizingobjeclh'c :L~se~Sll1enl. JAMA 258: 176:'1, 1987.Reis S, Borkiln J. Hcnnoni 0: Low back p3in: More Ih:m an:\tom)'.Film Pmct 35:509, 1992.Kirkaldy-Willis W: Managing Low Oack Pain. New York: ChurchillLivingstone, 1983. pp 75-128.Bosh K. Cowan NK. Kml, DE, et :II: Thc nalur;)1 history of sd::llica :'.~.s()ci:llcd wilh di~l' n:llhnln~y: r\ pros['lCclive study with clinical and in-depcndclll T:ldiologic follOW-Up. Spine 17: 120S. 1992.FT)tl1o)'cr JW: Prediclinf disahility from low hack p:lin, Clin Onhop221:121. 1987.C:tI.\-E3:1ril WI. FrY11lo}'cr lW: Idelllifying p:l\iCnl.~ 011 ri~k of I:Jccomin!!disabled because of low h:td: ~in. Spine 16:605. 1991.Waddell G, Ne\~1on M. Henderson L ct al. A fear-amidance t>clicfsquestionnaire and lhe role of fCaT-

".' 3 Training and Exercises ScienceJEAN P. BOUCHER

L

Human behaviors ;Ire dictated by many laws. constr.lims, anddcgrees of freedom. In other words, (hI: human s)'stcm has

limilalions. Many IimjtJlions in rcgartllo mOlar bcha\iors. ormovcments. are wcll dOCUl11cnL~d in the field of excrcise sci-ence or kinesiology. defined as the science of movement in bi-ologic syslcms. Such limilations liS the muscle dynamics lindthe fundamental facLors of performance arc discusscd in thiselI,j!)(cr.

THE LOCOMOTOR SYSTEM

The locomotor system. which is responsible for all motor be-haviors involved in locomotion. is composed of fundamcntal\lnits that must be controlled to achieve complex movcments.such as walking or runni~g. Understanding the locomotorsystcm rcquires then a knowledge of the fundamcntal unitscomposing il (e.g.. boncs. joints. and musc.:les); of the quali-ties characterizing these units: and of the operations im'olvingthem. Concentr

;;

JFig. 3.1. Neuromuscular slruc-tures and pathways or tracts im-plicated in motor control.

Muscle Fibers

Cerebellum

STRUCTURES

The fccdforwarJ conlrol ml"l'h:llli'Ill, also n:fCITl'd ((1 ;1-. Cl'll-tral or supras~gmenlalcontrol. i... d~:"nihcd ,I:" Ihe dir~l'l L'()ll-trol {)f effector" by the cel\tral na\'Olls sy:"h:m withOlIl ill{cr-aClion with thl.': information fwm Ihe I..':llvironlHclH. i.~ .. Ihl..':moving limb or segmel\t. UnJ~r this type of control. move-mel1ls arc carried oul by the excnl\ion of 11lotor COmll1alKls orprograms whik the :-;ystem is nol concerned by the feed hackcoming from the afferencc:-; ;lCli";'llcd during the mOWIHCtlb.The motor commands arc sent d\)WJ1 dilTerell! ~lru(llIr~" ;mdthrough pathways or tracls rl."prescl1lcd :"Chclll;lticall~ inFigure 3.1. Such a I11cdwnislll j, useful for underslanding Ih~execution and control of fasl. hallistic movements that arl' :"0rapid thaI fcedbck contraction, cannot modify the llHl\'C~ment. Learning or modification or (hi:" type of 1Il0VCllh:1H {':Hloccur only by modifying the motor commallds after thl" fact.by using the knowlcdge of response inform;,nion. InfoflU:llionabout the error committed can be incorpor~ted through ~Xleroceptors or proprioceptors and the ccntral (ol1l1nand elll bemodified as to reduce lhe alTIOUIl1 of error detccted. Thi:-; lypeof learning or plasticity is then (arricd out in ;,ttl 01Jt:n loop

CENTRAL CONTROL IFEEDFORI'IARD)

..:onifO! ;.11\: .Il"~' ii.,J;t;~,il;d:~, .~fI.':IT~Ll to a:" {lpJ:H hhlp ;llIddosed loop cClntn,ll. Till..' (halkllg~ is to umkr:-;t:IlHI not onlyIhe different I1ll'l'hanis1H:", hm abu how Ihe:-=c l11edl;ll1i:"I1ISinteract 10 ;Khicn: hKOIlHlli\\n or any oth..,!" i.:oordillal~dmovemenlS.

MCMI-\OILIIf\1 tUIIi ur I Ml: -=:.t'll'H:: 1-\ t"HAL; 1llIUNI:H ~ f\.iANUAL

---- Cerebral Cortex

'-----,'---- Red Nucleus

1------Thalamus

-+----- Reticular Fonllation

.f4------ Spinal Cord

TRACTS

RubrospiJlal-------~==='1Ioi

Conicospinal-------'.\

Reticulospinal-------_.I'

Vestiblllospinal--------Itt- 01

Motor ControlFollowing the siudy of the units composing the human sys-tem, a greater challenge is to understand how this system canproduce and comrol voluntal')' movements, In general. move-ment comrol C;;1Il be divided into two mechanisms: (I) fecd-forward conlrvl and (2) feedback control. These modes of

as any discrepancies revealed between the paltcms of the uut~put parameters (c.g., forces. muscle aCii\'ity) from onc side tothe other. Such discrep.mcics arc quantilicd by determiningthe difference between the pilucrns. or by establishing sidc-[{)-side ratios on specific discrete variablc~.

According to these definitions. all three f;Jctors penainto mutually exclusive sets of struct\m::s. Anatomic factor!"reveal the staWS of the hones. the mechanical factorsreveal the status of the Iig.aments hulding the bones to-gether, and the functioll

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H~HA~llIIAlION OF THE SPINE: A PRACTITIONER'S MANUAL

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ORGANIC QUALITIES

The organic qualities can be presented on a cUlHinuulll basedon the type of metabolic processes underlying lhe productionof energy needed.Q These qualities ;Irc: C/UlltrtlIlCC, rcsiSf(l/lcc.and POWCI: The aerobic processes. underlying the cnduf,anccquality, are those realized in the presence of (l,Xygl:ll. On till.:otlter hand, resistance and power arc based on the (///(/('fof,icprocesses available when the oxygen is not presenl.

MUSCULAR QUALITIES

TIle muscular qualities of force.

CHAPTER 3 : TRAINING AND EXERCISES SCIENCE 49

Fig. 3.2. Summary of themotor unit types and char~acterlstics. (From Ed~ington OW, Edger-Ion VR: The Biology ofPhysical Activity. Boston.HoughlonMifflin. 1976.)

la EPSP

muscle is the immediate source stored in the muscle

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A schematic representation of a typical force ...elocity curvc isshown in figure 3A. This curve shows clearly that the grt:at-cst amount of force is produced in the eccentric condition.Thb faCl could he explained by t\\to distim.:t mechanisms ac-tivc simultancou ..ly during muscle lcngthening ecccntric con-tractions. One mechanism is lht: \tretching of the clastic COI11-poncl\ls in the muscle. In fact. the muscle acts panly OIS anclastic: it is able to si(lre energy while being stretched. Thisstorage of energy automaticillly increases the force outputmonitored. The \ccono mcclw.ni\1l1 is based 011 the ncuromlls-cul;'lr control jJvail~lblc to Ihe muscle, Receptors. the musclespindle specilically. arc sensitivc to stretch. When the mu:.dcis being stretched. the spindle is excited. the Ia afferent libel'Sthai connect directly on lhe alpha motoneuron respollsiblt.: forthe ongoing contraction ,Ife soliciled. and thc nerve output tothe muscle is increased. producing gre;'ltcr force. These (womechanisms arc speed dependent. Accordingly. the forcc-velocily curve Ic\cb off at greater levels of negative velocity.

As soon as movement starts in the desircd direction (Le..concentric contraction). the capacily of the muscle to produceforce is drastic

~", ;

vHAt" I t:H ;j: I HAININ\j ANU EXERCI::iES SCIENCE 51

Torque (Nm) Fig. 3.4. The force-veiocifyrelationship.

100% (nux L'iOI1H.1riC)

TRAINING SPECIFICITY

FORCEANGLE RELATIONSHIP

VelocityConcentric

cilk painfrce

Torque(I'm)

100%. (pc:lk 1\'f'IUC UlIll'lIt)

Nt:n.... OlL.. ll .... 1 IVI'I vr I nt: "r-1I'1t:; 1-\ t"HA~ t IIIUNt:H':::; MANUAL

Fig. 3.5. The forceangle relationship. Ii '.!,,,!l

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Full Extension Joint Angle Full Flexion

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Dysfunctions are often associated with usc. overuse. misus('.or immobilization. It appears that too much or too little move..ment brings aboul a functional problem.

Movement in men and women is neither accidental nor in ..cidental. Movement is cenainly csselltialto heahhy life. if notits essence. Realizing that both use and immobilization. twoopposites. can or will cause functional problems leading todiscomfon. dysfunction. or dys..e'lse. highlights the need todefine what can be called a u'ilU/ou' of ol'lima/ a

CHAPTER 3 : TRAINING AND EXERCISES SCIENCE 53

LEVELS ofh'lTERVENTION

REUADIUTATION REACTIVATiON ACfIVATION

TYPES of II\TERVENTION

Incrensing Pcrformun(:c

Fig. 3.6. Performance continuum including the relalive position of the levels of intervention (rehabilitation. reactivation, and activation)and the different phenomena responsible for increasing and decreasing performance.

..

LEVELS of

PERFORMANCEINCREASED"NORMAL"

Performanu

REFERENCESI. OcSI1l,lr:tis F, Boucher lP: t\ Illwer limh a'YlIlIll..:lry modd: /\nalAll exercise science appro;'lch outlined in this chapter shouldbe useful in guiding functional cvalu

b4 REHABILITATION OF THE SPINE: A PRACTITIONER'S MANUAL

J

14. Bcnder JA. K:lplan HM: 111e llluhipic anglc test ill. rnelhod forlhe evalualion of muscle stren~th. J Bone Joint Surf: lAm) 45,\: I 35.1963.I~. ~k)'C;rs C: Effects of 2 isometric roulincs on sln=nglh. size and endur-

:llIce uf excr~'i~ed :md lion-exercised anns. Res Q JSA30. 1967.16. Boucher JI'. Cyr A. King MA. el "I. )ltOUlClnc t(:linin/; ll\"er!ltlw: Dc

lerlllin;l\ioll of :1 ll(lIl':"I~ciliciIY winuow. ML:d Sci SPllriS EXL:n.:. 2:':SD4.19

C) IIASSESSMENT OF

MUSCULOSKELETAL FUNCTION

'I:1,

4 Pain and Disability Questionnaires inChiropractic RehabilitationHOWARD VERNON

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"An old joke: \Vhich is better to have. a watch that'sslOpped. or a watch that's always five minutes fast? Answer:T.!!c wmch that's slOpped-because m Icast it's dght twice aday!"

[[valuation is the cornerstone of clinical mcdicin,flNo di-agnosis can be reached and no effective treatment can be ren-dered without conducting a clinical evaluation. which allowsfor the identification. of salient signs and symptoms 9f lhe pre-senting disorder. This fOfm of clinical assessment is con-ducled by using a time-honored system comprising a patientintervic\\' or history. obscrv~Hion. and clinical examinationprocedures. These procedures often include established andtraditional "tests" 10. for eX

H~HA~ILIIAIION OF THE SPINE: A PRACTITIONER'S MANUAL

i"leasurcment Scales

Table 4.1. Attributes of Tests in Clinical Rehabilitation

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Yes/No1 2

QuestionnairesNominal Scale:

~Do you have painT

Table 4.2. Scaling in Pain and Disability

Ordinal Scale:wHow severe is your painT

o 2 4 6 8 10none awful

TestingInterval Scale:

Determine Ihe thermal pain threshold in a pain patient (Range:40 to 55)

Ratio Scale:Determine the pressure pain threshold in a pain patient(Range: 0 to 10 kg,'cm l )

other words, whether 2 really represents twice as much of thevalue as one. or, on a scale from I to 5. whether each intervalreally represents 25% of the tOlal value is. at best. uncertain.Nonetheless, this relationship of ::In ordinal scale to the valuemeasured is often assumed by users, prompting some inap-propriate conciusions.

In the ;ll1en'al scllic. numbers do not merely n:prcselltunits of value. they constitute the units of \'aIUl~, Thi.;. ,;,c;lk j..;synonymous with a type of data known as "continuous daw.On the interval scale. data points arc true numeric rcprcsenla~tions of the value of tht.: parameter in questiollUI,ese data(X?i nts c::ar~..~~~~l~~~51.{~t J

CHAPTER 4 : PAIN AND DISABILITY QUESTIONNAIRES IN CHIROPRACTIC REHABILITATION 59

:"\._-~

Sources of Bias

One funuallleiHal premise tllltkrlying dinil.::d lllC;lSllrl.'l11t.:nl isIhe notion Ihall'lTOr and bias Ill.,)' l..'.\i,q at :lll len::ls and from.111 sources throughoUl Ihe measun::mcnt pnH;ess.: I :: Thcscsources include lhe subject. the instrullh.'IIt. ;Iud till..' l..'.\alllincr.

THE SUBJECT

Emotional. f'."ycIJ%gic. ami pl'rsollalily jt'C!o"x illl..',ilahlypl;t)' a p;U1 in lhl' :-uhjel:I's n,:spOllSl' hI lllcaSlirCIllCIll.:; bc itsclf-r.tting qucslionnaires or physi":

may be placed upon the test; what do the results mean !"21 Thisdefinition also Lt7 (Fig.4.1). a standardized self-report measurement of the location.extent, and, to some degree, the quality of pain. As well asthese descriptive features, the manner in which a patient de~piets his or her pain has been shown to reveal a grei.1t dealabout interpretations of the pain experience, mood, and psy-chologic state and behavior while in pain. In this respect. till-ing out the pain diagram becomes a pain behavior, and it candemonstrate an appropriate as opposed to an inappropriatemanner on the pan of the patient..1~

Outcomes are derived from the pain diagram in a numberof ways. First. subjective ratings by trained observers Gill bemade from the appearance of the diagrams. These ratings. infacL can be system~tized, using rankings from more 01'-g:'ll1ic/more realistic to less organiclless realistic and, perhaps.psychogenic or inorganic."'" Second, scores from a checklistof penalty points, which rate the anatomic fidelity, the pres-cncc of cxtraneous markings within and outside the body. etc.,arc compiled. The higher the score, the more likely it is to re-flect inappropriate pain behavior:''

V.,.... ,.. I r:n .. : r-'f\Il'l AI\lU UI::>At::HLlTY QUESTIONNAIRES IN CHIROPRACTIC REHABILITATION 61

PAIN DIAGRAMINSTRUCTIONS

PAIN DIAGRAMINSTRUCTIONS

Fig. 4.1. Pain diagram. A, Example of a well-delinealed, analomically correcl depiction. B, Example of a poorly delineated. anatomi-cally incorrect. exaggerated depiction.

8

-xxxx- /I /I-0000

painstiffnessnumbnessother(specify)

Quality

In 1975. Melzack introduced the McGill Pain Questionnaire(MPQ).~1 "lIId it has since been llsed in numerous studies ormusculoskeletal and other pain syndromes. It has undergonea great de;'ll of rcplicmion ,,1I1d is acknowledged :ls onl' of thegold standards in the field of pain assessment. Tht: MPQ con-sists of 20 category scales of vcrbal descriptors of pain.,'I.l5~ranked in order of severity and clustered into four ~ubscales:st::nsory. affective. evaluative. and misccllaneol1:-i scales. uswell as a five-poinl "present p;'Iin rating index." Scores can beobtained on the rank scores added for the total instrument orfor each of the subscales. or grealest inlerest to researchershas been the ability to distinguish the scn~ory and the affec-live domains of the pain experience.

Test/retest reliability had been confirmed as high from theoutset. with Melzack's lirst report indicating .1 70% consis-tency of responses of three trials over a 3-day period.~1Aikll

Concurrent validity among these scales and with mhermeasures of p.tin ;md loss of function is reponedly high. SCOltand Huskisson~7 reponed comparisons of the VAS and theVDS-t)'pl' sc.alcs that correlated at 0.75, where:'ls a coefficientor 0.63 was reponed betwecn the VAS scores and MPQ

scores.~7 The VAS tli.lS been shown time and again to be sensitivl' 10 treatment cffccts.~s although Scott ;,md Huskissont::.Iutioned that providing lhe original scorc or using a VAS forrelief or improvement may be more appropriate.~ojOther au-thors disagree with this stf

Ht:.NAt'ILIIAIIUN UI" IHt:. ~I""INt:.: A PRACTITIONER'S MANUAL

2. ACTIVITY INCREASE (walking, standing, working, exercising, etc)

Please try to remember back to the first day when you started thesetreatments and tell us how much you have improved since that first day.Please do this page before today's treat~ent begins.

Make a mark (I) along the line which you think rGprese;,~:; y~.;; CUi;en~ :l;:ve; vi IJdill in youlmajor area of injury, somewhere between ~No Pain At AII~ and ~Pain As Bad As It Could Be",

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DOESN'T APPLYTO ME

WORSE

DOESN'T APPLYTO ME

Completerecovery of

- all activitysincetreatmentsbegan

Complete relief- of pain since

treatmentsbegan

Pain As BadAs It Could Be

Date

lots of .

relief

increase.

lots of

relief

moderate

moderate

torial structure, especially of the sensory and the affectivescales.:>1'{,(J The concurrent validity has been confirmed be-(ween the MPQ and the MMPI and many other instrumcntsthat measure pain intensity. mood state in pain. and psy-chosocial disturbance. Phillips and Hunter reported an inter-esting and significant correlation between MPQ scores andthe pain diary in headache subjects.~

With regard to discriminant validity. Dubuisson andMelzack!>-l found that 77% of 95 pain p;.nients could be cor-rectly classil1cd into diagnostic groups on Ihe basis of theirMPQ score alone. Reading~7 studied patients with acute ilild

slight

slight

relief

increase. increase

o 1 2 3 4 5 6 7 8 9 10

ABF YOU RETTER SI~CE YOUR EIRSTIREATMENIl

No increasein activitysince -treatments 0 1 2 3 4 5 6 7 8 9 10began

No relief ofpain since ~treatmentsbegan

1. P~IN RELIEF.

B

No PainA AtAIi

Nam~

and Weinmann~~ reportcd similar results over four tri.tlswithin I week. Phillips and HUlllcr~(o studied tcst/retest rcli'l-bilily of the MPQ in patients with headache and reponed cor-relation coefficicilts as follows: for the Presclll Pain Index.which is the total scorc. an R of 0,94; for tbe sensory scale.0.83; and for the affective scale, 0.95. These findings indicatethut people can, wilhin a rel.ltively short period of timc. re-member their pain state from one measuremcnt intcrval toanothcr.

Thc greatest imcrest with the MPQ has bcen in the area ofvalidity, Numerous factorial analysc~ have confirmed the fac~

Fig. 4.2. Visual analogscales for rating pain (A) andvisual analog scale for ratingimprovement (B).

:1

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I1iII

IIIIIII,~,

I~iIIi

'vM/"\t"j t:H 4 : t"AIN ANU UI~At:HLlI'Y UW:.::> IIUNNAIRES IN l,;HIHUI-'HAL; IlL; Ht:.HABILlTATIQN 63

Patient Directions:On 8 scale of 1 10 place 8Jl X In your current pain level

NORMAL LOW PAIN MODERATE PAIN INTENSE PAIN EMERGENCY

( ) 0 ( ) 1 ( ) 4 ( ) 7 ( ) 10

( ) 2 ()S ( ) 8( ) 3 ( ) 6 ( ) 9

Fig. 4.3. Borg verbal rating pain scale (A) and ver-bal pain rating scale (6) (from the Roland-Morrisscale).

()

A

Course

Uttle pain

Quite bad pain

vals; the sevcrity and actual dUrFinally. the MPQ has been used in a many treatment trials(lnd h.ls been found to be sensitive to treatment effects.f'l Itsusefulness lies ill its relative case of administration. Also, itis casy to score and rich in data, particularly with regard tothe sllbsc;llcs and how their scores may apply to the thc-(Hetie

K\::HAt:SILIIAIION OF THE SPINE: A PRACTITIONER'S MANUAL

PAIN DIARY PAIN MAP

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firmed the high dcgn:e of reliability of th(; prolOeo!. They re-ported inter-rater agreement Kappa c(xflicicl1ts betwecn O.SOand 0.93. Test/retest correlations over I ~ days were al O.7};.

\\lilh regard 10 validity. Kecl"c c! al'''' n.:portcd scnsili\'ily 1.0treatment changes

,~n '1' rM."" M.liV UI;::.1\t:SILII Y UUESTfONNAIRES IN CHIROPRACTIC REHABILITATION 65

Nonctheless. lhe link between pain behaviors and pain sevcr-ily i~ not lirlllly estahlished. evcn at the thcorctil:al levcl.Observers haw noted a grcal dcal of pain behavior in (he ab-sence of high lc\'cl~ of pain severity ilsclf. ns well as dimin-ished pOlin beh~l\'i()r

uu HtHAt::lILIIA1IUN Of THE ~PINI::: A PRACTITIONER'S MANUAL

r:aase late (he st:vt:1iiy 0: yvv,' :ow back pain by circling a number below:

No pain Unbearablopain

Name Date __-"-__1-__ ' File #

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"':>1):

Pain prevent!;. all fOlms of lr,wel ~I(Cepllh.il1 dono lying down

Pain tCSfticlS mq 10 shorl flUCP.ssary journeys under30 minutes

P.ilin ICSttictS alllollTls 01 It.ilvel

I get no p.ilin when 1r::Jvehn\J

I gel SO'TlC pnin when It;lvehng bUI none at my usuallormsof travel m.,kc II any worse

I have hard1-, any socinillfe because of the polin.

My soaal hie IS normal ;lnd gives me no pain.

My soci

()

..._._... ........ ,u~ ..... n~.;:J 11" ..,. "nurn/'\"" I I"" t1t:.NAI:HLlTATION

o 1. I stlly home most of the time because of my back.

o 2. I change position frequently to try and get my back comfortable.o 3. I walk more slowly than usual because of my back.I:} 4. Because of my back, I am not doing any of the jobs that I usu-

ally do around the house.o 5. Because of my back, I use a handrail to get upstairs.o 6. Because of my back, I lie down to rest more.

o 7. Because of my back, I have to hold on to something to get outof an easy chair.

o 8. Because of my back, I try to get other people to do thingsfor me.

o 9. I get dressed more slowly because of my back.o 10. I only stand up for short periods of time because of my back.o 11. Because of my back, I try not to bend or kneel.o 12. I find it difficult to get out of a chair because of my back.o 13. My back is painful almost all of the time.o 14. I find it difficult to turn over in bed because of my back.o 15. My appetite is not very good because of my back.o 16. I have trouble putting on my socks {stockings} because of my

back.

0 17. I only walk short distances because of my back pain.

0 18. I sleep less well because of my back pain.

0 19. Because of my back pain, I get dressed with help from someoneelse.

0 20. I sit down for most of the day because of my back.

0 21. I avoid heavy jobs around the house because of my back..0 22. Because of my back pain, I am more irritable and bad tempered

with people than usual.0 23. Because of my back, I go upstairs more slowly than usual.0 24. I stay in bed most of the time because of my back.

Fig. 4.6. RolandMorris Back Pain Scale.

67

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NECK DISABILITY INDEX

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Section 6 Conccntr3Lion

=Ican concentrate fully when J want to with nodifficulty.

= I can concentrate fully when I want to with slightdifliculty.

= I Mve a fair dcgroc of difficult,y in concentratingwhen I want to. 0= J have a lot of difficulty in concentrating when 1W,1ntto.

-

= I have a great dC3.l ofdimculty in concentratingwhen I w;mt to.

= 1cannot concentratc at all.Section 1 Work

c::::J I can do as much work as I want to.C=:J I can only do my wual work,. but no mot"C..c::J I can do most of my ust.J.a.l work,. but no more.c::::J I cannot do my usual work.c:::J I can hardly do any 'work at all.c::J Jcan't do any work at all.

Section 8 - Drivingc::J I can drive my car without any neck pain.c:::J I can drive my car as long as I want with slight

pain in my neck.

=I can drive my car as long as I want with moderatepain in my neck.

= I can't drive my car as tong as I -want because ofmoderate pain in my nock.= I can hardly drive at all bcc:auscaf severe pain inmy neck.= J can't drive my car at aU.

Stion 9 Siupingc::J I have no troublesJccping.c::::J My sleep is slightlydisturbOO (less than 1 hr. sleepless).c::J My Sleep is mildly disturbed (\-2 hrs. sl~less).

=My sleep is mooCr.ttcly disturbed (2-3 hI'S. slc:cplcss).

c:::::l My sleep is greatly disturbed (3-5 hrs. sleepless),c::J My sleep is completely disturbed (5-7 hrs. sleepless).

Section 10 ~ R~.1;tionc::J I am able to engage in all my f'CCl'C4ltion activities ....;th

no neck pain at all.

= J am able to engage in all my I"CO'C.1tion ;]ctivitic:s, ....;lhsome pain in my f\CCk..

= I am able to engage in most, but not all of my usualrecreation activities bocausc of pain in my neck.= I am able to engage in a few of my usual recreationactivities because of pain in my neck.= I ca.n hardly do any recreation activities becauseof pain in l-:ly neck.= I can'l do any rccreJtion activities

I' , ...... ~- 1I'lIt::. M rNA"" 1IIIUNt:H'::; MANUAL

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28. Vemon HT. Mior 5: 1llc neck disabilil), indc),: A slody of rcli:lhility and\ali,Iity. J J\.'lanipul'l\i\'c Physiol TIlcr 14:409, 1991.

29. Guyal! G. Walt..:r S, Nunllan G: Mca...uring changc ovcr lim..:: Ass:.=.ssingu.~dulne ...s of cV:llu'llion inslrul1lCnl.". J Chronic Di$ .JO: 171. 19X7.

30. Bombardier C, Tugwell P: McdlOdologica! considerations in fum:lion:llassessment. J Rhcumatol 14(Suppl 15):(1. 1981.

31. Kirsdmer H, Guy:m G: A IlIclhndologic:lI fralllcwnrk fm ils~cssinghcalth indices. J Olronic Dis 38:27. 1985.

.12. Kl'-dc K1>: 'nlc pain chan. L...ncet 2:(1, 194M.JJ. 1\!.lrgl)lis RH. Chihn:llt IT. T;dr RC: I\.. strl'l";~;l n:!i::bilil}" Ill' lh~' p;d;,

drawing. inslfUlllcnt. Pain n:49, 19Htt:,\-I. Marg.olis Ril. Tail RC. Krause SJ: R'l1ing !'ysh~m for usc with p:ttielll

p:lin drawings. Pain 2+:57, 1%6.;\5. Tail RC. Chibn'lll n. Margolis RB: P'lin C:(lcnt: RelaliOlll' Wilh psycho

It1gic:!1 stme. polin sc\'crity, pain histnry anu uisability. Pain 41 :295. 1990.36. R:lIl.~fmd BV, Caims D. Mooney V: 'n,C pain umwing :1S .m aid 10 PS)

dlUlugical c\'aluation of paliellts with low hack pain. Spine I: 127, ItJ76.;\7. Uden A. Hstrom M. Bcrgcnudd H: P.lin dr:!wings in chronie hack pain.

Spinc 13:389, 1988.J8. I-luskisson cC: r-,1t.'asurelllClll "fpain. LUlcc, 2:127, 197..1.39. RC:lding Ac: CompOlrison (If pain ralill~ scales. J Psychosolll Re ... 2J: 1/9.

1980..JO. Ohllhaus EE. Adter R: Melhouologkal prohkms inlhc lI1e'l...urcIllClll.~)r

pain: A c(Jl\lparisol1 between the vcrp:l1 r.ltil1t: scale and the visual 'lIlaloguc scale. I);lin 1:379. 1975.

41. Duncan Gil. Bu.shndl MC, Lwignc GJ: CornpOlri:.:on of verbal ;llid ,i!'ua1 analog.ue scales (or mcasuring. lhe il1lCllSity and unp!c;\s:tlllncss {)fcxperimental pain. Pain 37:295. 191'19.

42. Jensen MP. Kamly p. Bravcr S: 11,c meOlsurC1\lcnl (If "lini":11 pain inlen~ity: A comparison o( six methods. fl"in 21: 117. 19$6.

.J3. Downie WW. Leatham PA, Rhim.l VM. ct .11: StuJies with pOlin r:ltin;;scales. Ann Rheum Dis ~1::n8. 197X.

44 Huskisson EC: Mea....urement Ilf pOlin. J Rhcum:11(I1 9:7(lloi. 19X2..J5. Husldsson EC: Visual :lIlalll~ue sla!c!'. In Md/.al.:k R (cd): P'lin

Mea~uremcnt :HIlI A~sc'"melll. New York. 'Raven Prcs!'. 1910.4(1. Dixon JS. Bird tit\: ReprodUl... ihiliIY ailing" Ilh'nt \-....nkal visual ana

logue Calc. Alln Rheullll)i.~ .JfI:R7. 19HI.47. Scott J. Huskisson EC: Verticalm 1I\)ri7.(1I1I;11 \'i~ual ;mall1gue scales. Ann

Rheum Dis J8:560. 1979.48. Ma.'( .....ctl C: Scn... iti\'it)' and a1.:curm:y of Ihe \'isual all;JlllplC s{a!c. Br J

Clin Pharlllaeol (d5. 197R.49. Seem J. Huski!'s(lll EC: Accur

CHAPTER 4 PAIN AND DISABILITY QUESTIDNNAIRES IN CHIROPRACTIC REHABILITATION 71

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61. llurkh;lrt.1t ('$: Tho: usc ui the t\ktllii 1';1111 Vl....:-lh'llll.":.: III a,~",'.. ,in;:anhritis P:lill. I):lin 19;305. 19SJ.6~. Alldr:lssik F. Bbnchard EB. 1\llk:- T.":I al: Ass ...ssin;: Ih~' rc.h.:ti,c;I' WC'1l

:IS lho.: s...nSUf) comjlnno.:nl of hcad;l.:h~ pain. 1k;lIl:ldl': : I'~ IS. IIJS I.63. Fairh;l1lk JCT. Couper J. Davio.:s JB. n Ill' r;l1n h....ha\'il)r inlow b:u.:k p:lin palicol\ls durin~ phy:-kal cX:lIuinatiun. 1';1111 ~n:~'it). It)X4.

(17. JcIl~CIlIU. llr:.Jdk) LA. Linton 5J: \'alidatioll (If:1II \lh:-.:n;ltiuII m,,:thtldof pain a:"s.....~slIlcnl in nonchrunil' h:ld: pain. Pain .31J::to'!. 19S1).

IS. Triano JJ. SchultJ. A[J: Corrd:nion or" ohjeclh''': 1Il":':I.~ur....~ "I' trunk lIIutinlland muscle funClion wilh low h:ld disahility r:llil\~~. Spino.: 12:5C,1.1987.

69. Hsieh CJ. Phillips RB. Adams AU. ct al: FlIllclilln:lI ("IUI;:OI1\CS of lowb':lck pain; COlllp"rison of four treatment ~roIlP,~ in a r;ml!ol1\ll.o.:d cuntrolled lrial. J Manipulative Ph}'siol Ther 15:4. 199~.

70, Tait Rc' I'tlilard CA. ~targolis Ril . ..:t al: IllC Pain Di,ability Imk... :Psychometric and v,didil)' data. Arch Phy~ Med Rch:lbiI6S:-l3S. 1987.

71. Tail RC, Chibnall JT. Kr:1USC s: 'nK' P':lin Di.~:lhi1iIY Illd~": P~ych(llll~'lrkproperties. Pain 40:171. 1990.

72, Lcavin F. Garron DC: Validil)" (If:l Bal'k P;lin C1a~... iliC.lIl(ln St.:;lk ;UlIilllp: ,\I:lIllltd f"1 lh' Illtt~'" l\,,:h:I\ltlr Q\lco~ti(1l1n;\ircOBC)). :ull Ell. Addaitk. AIISlra!l;I: Lnn .... r:-ll} uf :\ddaitk. 19S.~.

it,. :"bill CJ. W.,.I,ldl G: A t.:1l111l'ari~(ln ,'Il")~l\ili\'c lll~':hllrcs ill Inw 1':I..:kp:lin: SI:IIl~II~.11 ,trtKlllrC ;tnt! dinicli \:=Iidil\' ;11 initial ;1':-CSSlllCIll. I'':lin.1(,:~:n. !,JIlI

i7 l'ilo\\":-k~ I. Ch:q'l1l;1ll CR. lh'lli c';1 JJ !':Iill. do.:Pl\~~itl!l :lI\d illl\\.'~'; b..:11;\l"i"r ill ;I P:\l1l dini.: p'lplllatillil. I',llll -l: I :-\:;-. l'n7.

'So W;lddcll (i.I'lllll\,ky I. BlInd t'....IR: CI:lli,:tl a~"~',~~I1\':111 :Illd illl ...ql1.:t:llillllor abnpl'l1l:11 illll"" h.:ha\'illr in 101, 1'.,.. " paill. 1':lill ,,1):-11, IIlX'J.

il). W;ultkll G.