How Manipulation Works

CHRISTOPHER SO

nociceptors

Introduction

Physiotherapist, Manipulative Therapist

Manipulation is an ancient art dating back to the time ofHippocrates, and use of it by the medical profession to relievepain, swelling and muscle spasm, and to restore the functionaluse of impaired joints, has waxed and waned (Lomax, 1978) .Various schools of thought have been developed to explainhow manipulation works, but despite its long-standing history,there are still many contending ideas regarding its use . Watson-Jones has written that there is no place for manipulation inorthopaedic practice related to spines (Mennell, 1975), whereasWiles has suggested that manipulation should always be triedbefore any surgery on back problems (Mennell, 1975) . Afterreviewing the available literature and research, many notedphysicians and scientists have come to the conclusion that"There is no justification for the use of manipulative therapy"(Nachemson, 1975; Pearce and Moll, 1967; Sham, 1974) .On the other hand, practitioners of manipulation feel thattheir clinical results are positive and their treatments effective(Gitelman, 1975 ; Maitland, 1977 ; Mennell, 1960) . In view ofthese contradictions, I would like to attempt to explain

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GATE CONTROL SYSTEM

Fig. 1 Gate Control Theory`how manipulation works' in terms of neurophysiology andbiomechanics .

1 . The Effect of Manipulative Procedures with Reference toNeurophysiology

a . The Gate Control Theory (Fig . 1).

actionsystem

Melzack and Wall (1965) put forward the "Gate ControTheory" . They specified that the site of sensory interactionis in the substantia gelatinosa (SG), which acts as a gate forpain transmission . Afferent input through the large fibrestends to close the gate and input through the small fibretends to open it, therefore modulating pain transmission,The output from the target cell (T) is influenced by thepassage of these impulses through the SG . Melzack and Wallalso suggested the mechanism of presynaptic inhibitionwhereby if the T cell's output exceeds a certain thresholdit will activate the action system and pain will be perceived

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The gate system is also connected to the Central NervousSystem (CNS), whose activities may influence the outputof the system .

As more research was done, Melzack (i973) and Wall(1978) admitted the shortcomings of the theory andrecognised that modifications would be necessary . They alsodiscovered the existence of a postsynaptic inhibitionmechanism in addition to their postulated presynapticinhibition mechanism .

b . Articular Neurology

Wyke (1980) stated that "articular neurology is one of thefundamental sciences of manipulative therapy ."

The following is the classification used for receptors insynovial joints and their function .

i . Type I Mechanoreceptors are :

numerous in the outer layers of capsular tissues of alllimb joints and apophyseal joints .more densely distributed in the proximal joints andcervical apophyseal joints.6 to 9 u in diameter .subject to static and dynamic response to changes ofjoint position, pressure, direction, amplitude andvelocity of active or passive joint movement .slow in adapting ; their frequency of resting dischargerises in proportion to the degree of change in jointcapsule tension .

ii. Type II Mechanoreceptors are :

- embedded in the deeper layers of fibrous joint capsules.- relatively more numerous in distal joints .- 9 to 12 u in diameter .- inactive in immobile joints.- fast adapting, with a dynamic response to acceleration

or deceleration of joint movements .

iii . Type III Mechanoreceptors are :

present in joint ligaments (both extrinsic and intrinsic),but absent in the ligaments of the vertebral column .active, when considerable stress is applied towards theextremes of active or passive movement or by a hightraction force .13 to 17 u in diameter .They have a high threshold to mechanical pressurewith a slowly adapting response .

iv . Type IV Painreceptors are :

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2 to 5 u in rnyelinated fibres and less than 2 u inunmyelinated fibres .a plexus of unmyelinated nerve fibres that weaves inthree dimensions throughout the fibrous capsule,adjacent periosteum, fat pads and advential sheaths ofthe articular blood vessels .individual free unmyelinated nerve endings that weavebetween the fibres of ligament .entirely inactive under normal circumstances.only active when irritated by the development ofabnormal mechanical or chemical (histamine, bradykininor 5HT) changes in the tissue .absent in synovial tissue, intraarticular menisci, articularcartilage and intervertebral discs .

c. Joint Trauma

Mennell J . (1960) provided us with a concise clinicalexplanation ofjoint trauma . Both the capsule and the ligamentsof a joint are extremely sensitive structures, having a richnerve supply, and even minor assaults on their integrity canbe very painful. The reflex action to capsular pain is spasm .If this spasm is strong enough, the joint can be immobilisedby it . Spasm initiates fatigue, which may cause further spasmand more pain . At a later stage following disuse, the articularsurfaces seize up, as a result of a loss of the normal amount oflubricating synovial fluid between them . Attempted movementgives rise to pain and sets off a vicious circle of pain, spasmand fatigue . This often results in locking of the joint .

The cause of joint pathology is controversial . In traumaticcases, all tissues around the joint can be affected . In severecases the bone may be fractured and ligaments may be torn -incorporating bony avulsion . In minor injury, differentstructures around the joint are affected to a varying extent .However, three things invariably occur : pain, spasm and lossof function (decrease in range of movement or increasedresistance to movement).

In the early stage of injury, resistance experienced onpassive movement of the affected joint is probably due tovoluntary and involuntary muscle spasm . Muscle spasm maybe set up by nociceptive afferents from Type IV receptorsystems in joint tissues . They project polysynaptically toalpha motoneurones in the motoneurone pools of the musclesrelated to the joint in question, thereby giving rise to abnormalreflexes in such muscles (Wyke, 1980) . This may be of aprotective nature . Trauma leads to excitation of the Type IVnociceptive system, pain is perceived and muscle spasm occursand this produces resistance to movement .

d . How Manipulation Works

The essential prerequisite for evoking pain is transmissionof nociceptive afferent activity . This arises from the irritatedType IV receptor system and travels through the gateway or

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collateral branches which synapse in the basal spinal nucleus.This is transmitted up to the brain via the anterolateral spinaltracts . This transmission can be modulated by all peripheralmechanoreceptors (not just the articular mechanoreceptors).They synapse on the apical spinal nucleus whose axons runanteriorly into the basal spinal nucleus, wherein theyterminate in axo-axonic synapses on the presynaptic terminalsof nociceptive afferents that are subtended upon the basalnuclear neurones . Activation of peripheral mechanoreceptorsby joint or soft tissue manipulation will produce presynapticinhibition of nociceptive afferent activity and lead to painsuppression or reduction.

Different grades of mobilisation according to Maitland'sconcept (Maitland, 1977) will produce selective activation ofdifferent mechanoreceptors :

i . Mobilisation

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Grade I

: activates Type I mechanoreceptors with a lowthreshold and which respond to very smallincrements of tension

activates cutaneous mechanoreceptors

oscillatory motion will selectively activate thedynamic, rapidly adapting receptors, ie .Meissner's and Pacinian Corpuscles . The formerrespond to the rate of skin indentation and thelatter respond to the acceleration and retractionof that indentation .

Grade II

: similar effect as Grade I

by virtue of the large amplitude movement itwill affect Type II mechanoreceptors to agreater extent .

Grade III : similar to Grade II

selectively activates more of the muscle andjoint mechanoreceptors as it goes intoresistance, and less of the cutaneous ones asthe slack of the subcutaneous tissues is takenup .

Grade IV : similar to Grade III

with its more sustained movement at the end ofrange will activate the static, slow adapting,Type I mechanoreceptors, whose restingdischarge rises in proportion to the degree ofchange in joint capsule tension.

Grade V

: in the premanipulative position it has the sameeffect as a sustained grade IV

in the snapping action, manipulation certainlyactivates Type II and Type III (high threshold)mechanoreceptors .

Clinically, resistance due to spasm melts under mobilisationor manipulation . This may be due to the stimulation of Type Iand Type II mechanoreceptors (Wyke, 1980). They havedynamic and static responses to changes of pressure, and like

the cutaneous mechanoreceptors, project polysynaptically to- fusimotor (not alpha) neurone pools within the central nervoussystem, thus contributing to the continuous modulation ofactivity flowing around all the fusimotor muscle spindle loopsystems. They exert reflexogenic influences on muscle tone .Fisk (1978) attributed the immediate decrease in pain aftermanipulation to a reflex decrease of muscle spasm .

2. The Effect of Manipulative Procedures with Reference toBiomechanics .

a. Joint Mechanics

Joint mobilisation is primarily indicated for reversiblejoint hypomobility, but is also useful for maintainingmobility, delaying progressive stiffness and relieving pain .The degree of freedom of a joint depends on its configuration

In a normal ball and socket joint, there are six degrees offreedom namely flexion, extension, abduction, adduction,internal and external rotation .

These directions of movement can be carried out by thepatients . Their range of movement is large. They are termedas gross, voluntary, or angular movements (Fig . 2) .

EXTERNALROTATION

FLEXIONGLENOIDCAVITY

Fig. 2

Voluntary or angular movements of shoulder joint

However, there are involuntary movements which canncbe performed by the patient at will . They occur as the joinsmoves, especially towards the end of range . They give extrayield to joint movements. Otherwise, such movements canonly be done by a third party or therapist . These movementsare termed as involuntary, accessory or linear movements(Fig . 3), as distinct from the gross or angular movements,

It is these accessory movements which will be affected toa greater extent by trauma and which will be regained last .Without proper treatment by mobilisation, they may neverreturn to normal .

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f

AP

Fig . 3

Involuntary or linear movements of shoulder joint

Volume 8, 1986.

CRUD

ANTEROPOSTERORGLIDE

Fig . 4

Ankle dorsiflexion with anteroposterior glide

b. How Manipulation Works --Related to BiomechanicsManipulative therapy lays stress on treatments to regain

both angular and linear movements. Exercises are given mainlyto help the patient to regain the gross or angular movements .There are a few weight-bearing or self resisted exercises whichmay help in gaining accessory movements, but compared topassive mobilisation they are far from ideal . Examples includelunging exercise for ankle dorsiflexion and extension exercisesfor the wrist (Figs . 4 and 5) .

EXTENSION

POSTEROANTERIOR GLIDE

Wrist dorsiflexion with posteroanterior glide

Manipulative procedures constitute various manual ormechanical techniques (Maitland's Peripheral & VertebralManipulation, 1977) . Their effects on the biomechanics ofjoints are clear cut and direct, as explained previously . Traumawill bring about a loss of function . In the acute phase, itmay be caused by pain, swelling, muscle spasm andmalalignment of joint configuration . Manipulative therapyaims to reduce pain, swelling and spasm . There are a numberof pain relieving techniques . Other conventional physiotherapytreatments will be beneficial as well. In the chronic phase,problems will be caused by the malalignment of joint con-figuration . In addition, adhesions and contractures plusweakness of the supportive joint structures, namely theligaments and muscles, can also lead to joint dysfunction .In the chronic phase stiffness is a bigger problem as comparedto pain . Manipulative procedures play a major part in regainingthe range of movement or function of the joint . Exercises helpto maintain the range of movement gained from mobilisation .

The signs and symptoms of the patient are analysed beforethe treatment . Possibilities of pain referred from joints otherthan those underlying the painful areas are considered,assessed and cleared . Pain or stiffness of the joint is relatedto the mechanism of the injury and activities that cause the

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PA posteroanterior glideFig . 5

AP anteroposterior glide

CEP cephalic glide

CAUD caudal glide

MED medial glide

LAT lateral glide

pain . These are termed as 'aggravating activities' . The move-ment and direction of these activities is analysed according tothe anatomy and biomechanics of the joint concerned .Components of soft tissue around the joint that might beaffected by such activities are considered . A joint and itssurrounding soft tissue cannot be separated functionally ."Normal joint physiology requires that the surroundingmuscles and relevant blood vessels, nerves and connectivetissues are functioning properly" (Kaltenborn, 1976) .Lehto (1985) found that mobilisation seems essential for thequicker resorption of scar tissue and better structuralorganisation of the healing muscle .

The importance of passive mobilisation and manipulationlies in the restoration of gross movements and accessorymovements, which cannot be gained by patients throughexercises alone, and certainly not by rest . The essence of theapproach of manipulation lies in the integration of all theinformation gained from subjective and objective assessmentsin order to arrive at a logical conclusion of what structures ofthe joint are involved and which techniques are best for suchjoint dysfunction .

Nowadays, orthopaedic surgeons and physiotherapists aremore 'aggressive' than before . In Australia, the mobilisationof recent fractures (Jull, 1979) and mobilisation of non-uniting fractures (McNair, 1985) has produced good results.(It must be stressed that an 'aggressive' approach does notnecessarily mean rough handling.)

Recent research has supported the idea of the existence ofa meniscus in the spinal apophyseal joints as hypothesisedby Wolf (Goldstein, 1975) . Moreover, the narrowing of thedisc space is found to be the result of subchondral fracturesrather than actual thinning of the disc . On the contrary,the disc thickens as it ages (Twomey and Taylor, 1985) . Suchknowledge of joint biomechanics helps us to decide whichstructures within a joint are the more plausible cause of theproblem in certain conditions . It also helps the therapist tochoose the most appropriate technique for each condition.

SummaryIn conclusion, there seems to be a sound scientific basis for

manipulative therapy in the treatment of joint problems.As more knowledge of joint physiology and biomechanicsunfolds, the effect of manipulative therapy may become moreconvincing. Even at this stage, the importance of manipulativetherapy for joint problems should not be ignored .

References

Articles1. Fisk, J.W. (1978)

3. Goldstein, M. (1975)The Research Status of Spinal Manipulative Therapy. NINCDS

Monograph No . 15 DHEW

4. Jull, G. (1979)The role of passive mobilisation in the immediate management ofthe fractured neck of humerus. Aust. J. Physiother., 25 :3 July .

5. Lehto, M., Duance,V.C. and Restall, D. (1985)Collagen and fibronectin in a healing skeletal muscle injury . Animmunohistological study of the effects of physical activity on therepair of injured gastrocnemius muscle in the rat. The Journal ofBone and Joint Surgery, 67-B(5), p. 820-828.

6. Lomax, E. (1978)Manipulative Therapy: An Historical Perspective . In : Approachesto the Validation of Manipulative Therapy . Buerger A.A . & TobisJ.S. Ed ., Charles C. Thomas, p. 205-216.

7. McNair, J. (1985)Non-uniting Fractures Management by Manual Passive Mobilisation .Proceedings of Fourth Biennial Conference . M.T.A.A. Brisbane .

8. Melzack, R. and Wall, P.D . (1965)Pain mechanisms : a new theory . Science 150, p. 971-979.

9. Mennell, J. McM. (1975)

History of the Development of Medical Manipulative Concepts :Medical Terminology. In : The Research StatusofSpinal ManipulativeTherapy. Ed . M. Goldstein, NINCDS Monograph No . 15 DREW,p. 19-24.

l0.Nachemson,A. (1975)A critical look at the treatment for low back pain . In : The ResearchStatus of Spinal Manipulative Therapy. Ed. M. Goldstein, NINCDSMonographNo. 15 DHEW, p. 287-293.

II .Pearce, J. and Moll, J.M.H. (1967)Conservative treatment and natural history of acute disc lesion.J. Neurol. Neurosurg. Psychiat ., 30:13-17 .

12 . Sham, S.M . (1974)Manipulation of the lumbosacral spine. Clinical Orthop . RelatedRes., 101:146-150.

13.Taylor, J.R . and Twomey L.T. (1985)Vertebral Column Development and its Relation to Adult Pathology.Aust. J. Physiother., 31 :3, 83-88.

14.Twomey, L.T . and Taylor J.R . (1985)Age Changes in the Lumbar Articular Triad. Aust. J. Physiother.31 :3,106-114 .

15 .Wall, P.W . (1978)The Gate Control Theory of Pain Mechanisms : a re-examinationand re-statement . Brain, 101 :1-18 .

16 . Wyke, B.D . (1980)Articular Neurology and Manipulative Therapy. In : Aspects o)Manipulative Therapy. Ed . Idczak, R.M . Lincoln Institute ofHealth Sciences, p. 67-72.

Books1 . Kaltenborn, F.M . (1976) Manual Therapy for the Extremity Joints.

An Evaluation of Manipulation in the Treatment of the Acute Low Wellington New Zealand, University Press.

Back Pain Syndrome in General Practice . In Approaches to the 2. Maitland, G.D . (1977) Vertebral Manipulation, 4th Ed ., London,Validation of Manipulative Therapy. Buerger A.A . & Tobis J.S ., Butterworth.Ed . Charles C. Thomas, p. 236-270.

3. Maitland, G.D . (1977) Peripheral Manipulation, 2nd Ed ., London,2. Gitelman, R. (1975) Butterworth.

The treatment of pain by spinal manipulation . In : The ResearchStatus of Spinal Manipulative Therapy. Ed . M. Goldstein, NINCDS 4. Melzack, R. (1973) The Puzzle ofPain, Penguin Education.

Monograph No . 15 DHEW, p. 277-285. 5. Mennell, J. McM. (1960) Back Pain, Boston, Little, Brown and Co

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