MUSCLE SPASM IN POLIOMYELITISA STUDY OF A NEW ZEALAND EPIDEMIC

BY

J. E. CAUGHEY, M.D.(N.Z.), F.R.C.P., F.R.A.C.P., andD. S. MALCOLM, M.D.(N.Z.), M.R.A.C.P.

From the Auckland Hospital(RECEIVED FOR PUBLICATION AUGUST 16, 1949)

The purpose of this article is to record a clinicaland experimental study of muscle changes noted in a

recent epidemic of poliomyelitis in New Zealand.The term muscle spasm has come into general use

to describe those changes which occur in the acutestages of the disease and has to be distinguishedfrom the state of contracture which is a terminalcondition of muscle shortening due to fibrosis. Inthis study we are chiefly concerned with the state ofmuscle spasm encountered in acute poliomyelitis.The subject of muscle spasm has been a controversialone and skilled observers in the U.S.A. havestated that they encounter muscle spasm in allpatients with poliomyelitis, whereas experiencedneurologists and orthopaedic surgeons in theUnited Kingdom and the U.S.A. state that they havenever encountered muscle spasm in the diseasealthough, rather curiously, all agree that spasmoccurs in the muscles of the neck and back, and inthe hamstring muscles.We regard muscle spasm in poliomyelitis as a

state of shortening of muscle, encountered in theacute stage of the disease. Affected muscles arecontracted and usually tender on palpation and onstretching; pain usually develops and the spasmincreases. In some patients the spasm is notapparent in the muscles until stretch is applied.

Clinical ObservationsIncidence of muscle spasm. At the outset of the

epidemic attention was focused on the extensormuscles of the neck and spine and on the hamstringmuscles, those muscles which in the past have beenheld to be affected by so-called 'meningealirritation.' In our first 124 patients, evidence ofmuscle spasm in these muscle groups was detectedin 89 per cent. Thereafter, it was realized that ourmethod of examination for muscle spasm wasinadequate and that a complete examination of apoliomyelitis patient, in addition to the usualexamination of all systems, entailed a search formuscle spasm by a detailed inspection of all musclegroups, and further, big muscle groups should betaken through their full range of movement in order

to observe the effect of stretch on the muscles. Anexamination of forty consecutive patients carriedout in this manner revealed evidence of musclespasm in 100 per cent.

TABLE IINCIDENCE OF MUSCLE SPASM

First 124 Cases Last 40 Cases

No. Percent- No. Percent-age age

Neck rigidity 90 73 25 63Back rigidity 101 81 25 63Kemig sign 96 77 18 45Spasm ofother muscle Not fully Not fully

groups examined examined 25 63Cases havingone or otherof above .. 110 89 40 100

Method of examination. This is best carried outin a warm room, with the patient clad in a pair ofshorts and lying on a plinth, rather than on a bed.The patient is first inspected in the supine positionfor deviation of the head to the right or left or forundue extension of the head. The shoulders areexamined for so-called 'cupping' in which there isupdrawing and rotation forward of the shoulders,and the biceps for spasm which causes flexion atthe elbows. Next the patient is inspected in thelumbar region for exaggeration of the normallumbar lordosis or for scoliosis. On assuming thesitting posture, spasm and pain cause the patientto assume the 'tripod ' posture with the knees andhips flexed, the lumbar region held straight andrigid and the body weight supported by the armswhich are extdnded backwards (fig. 1). Beforesitting up the legs should be carefully straightenedout on the bed so that the internal malleoli aretogether. This may be difficult on account ofspasm in the hamstring muscles. On sitting thepatient up, one leg may shoot forward further thanthe other due to slight protective flexion at the hipon the affected side. The feet are inspected forinversion or eversion and for plantar flexion due

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to spasm of the gastrocnemius muscle. The patientis then turned to the prone position in order toinspect the back muscles and the glutei muscles.After inspection in the above manner major musclesgroups are stretched by taking them through theirfull range of movement. The trapezius muscle istested by separating the head from each shoulderin turn. The usual test for neck rigidity is carried

riG. i.-i ripo posiion wim muscie spasm o0 unelumbar and hamstring muscles.

out by slowly flexing the head. The muscles aroundthe shoulder girdle are stretched by full abductionof the arm, and the biceps and triceps by full flexionand extension at the elbows. The lumbar musclesare stretched by lateral flexion to right and left andby asking the patient to touch the toes with thelegs extended on the bed. Slight scoliosis of thespine may only be apparent when the patient standsand attempts to touch the toes, bending down andcoming up slowly. The quadriceps may be stretchedby full flexion by attempting to place the heel on thebuttock or by turning the patient into the proneposition and again attempting to put the heel onthe buttock. The hamstring muscles are stretchedby the usual Kernig test and the gastrocnemiimuscles by dorsiflexion of the feet.

Manifestations of muscle spasm. Muscle spasmmay be apparent when the patient is in a restingposition. The affected muscles are usually tenderon deep palpation and may be exquisitely so. Tothe touch they appear to be firmly contracted andthe muscle tendons are tight. Stretching has theeffect of increasing the muscle spasm in musclesalready obviously in spasm and it may inducespasm in muscles which are apparently free ofspasm. It is probable that the muscle spasm whichis apparent at rest is brought about by stretch whichis the result of postural change.The effect of stretch is variable. In some patients

muscles pass into painful spasm on the slighteststretch, and in others muscles can be taken almostto the end point of stretch before the patientcomplains of tightness and discomfort and spasm

develops. The increase of spasm or the develop-ment of spasm on stretch usually occurs at the onsetof a phase of painful stretch, but not invariably.It might be suggested that pain had set up anabnormally active stretch reflex. On the release ofstretch to a point just short of pain the spasm passesoff. If muscles are stretched beyond the onset ofspasm resistance to further stretch increases. Thedegree of possible further stretch varies, and islimited at some times by extreme spasm and atother times by spasm and severe pain.The sites of muscle spasnL The extensor muscles

of the head and spine were those most commonlyaffected. In most patients the spasm of thesemuscles was apparent on stretch alone. In severecases extension of the neck and back was apparentat rest and the knees were partially flexed. Onoccasions one side was more affected than the other,causing deviation of the head to one side, a tightligamentum nuchae on one side or a scoliosis.When one lumbar group was more affected thanthe other there was flattening of the muscles on theaffected side with a scoliosis with the concavity tothe side of the flattened tight muscles. Musclesaround the shoulder girdle were commonly affectedcausing the characteristic deformity referred toabove. Spasm of the pectoral and latissimus dorsimuscles prevented complete abduction at theshoulder. The flexors of the forearm were some-times affected and at times the pelvic girdle wastilted by spasm. In the thighs, the quadricepsmuscles at times were partially or completelyinvolved preventing complete flexion at the knee;when tested by flexion of the knee with the patientlying in the prone position, spasm and pain in thequadriceps muscle led to protective elevation of thebuttock caused by flexion at the hip (fig. 2).

.i

FIG. 2.--5paSm 01 quarieps muscle witn proteciveflexion at the hip on attempting to place the heel on the

buttock.

Tightness of the gastrocnemius muscle was apparenton dorsiflexion of the foot, and, in some, spasmcaused inversion or eversion of the foot. Spasmof the plantar muscles produced tightness andnarrowing of the plantar fascia.

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MUSCLE SPASM IN POLIOMYELITISOther clinical features of muscle spasm. Aggrava-

tion of muscle spasm was caused by variousactivities, such as heavy massage or rough handlingof muscles. Premature weight bearing with tooearly ambulation without adequate support (suchas elbow crutches) also caused aggravation. Onoccasion patients were discharged from hospitalapparently well, but after a time at home, as a resultof unsuitable regulation of motor activity, musclespasm developed again, at times necessitatingfurther periods in hospital. For this reason,patients, when discharged, were advised to refrainfrom athletics, cycling, digging or other verystrenuous activities for a few months, and for atime were examined regularly as out-patients.Exposure to cold caused aggravation in con-valescent patients and sometimes was responsiblefor unmasking muscle spasm in mild cases whichotherwise would not have been diagnosed aspoliomyelitis. The effect of fever was apparentwhen an epidemic of influenza occurred. One girl,aged seventeen years, who had marked musclespasm on admission, was almost symptom-free aftersix weeks. She then developed an attack ofinfluenza (Type B. strain Lee), and with the onset ofthis intercurrent infection there was a prompt returnof muscle spasm in the muscles previously affected.No change in the spinal fluid developed during thisrelapse. A similar reactivation of spasm was seenin some children who developed chickenpox andin some with mild upper respiratory infection.No correlation was found between the degree of

muscle spasm and the cell count of the spinal fluid.We encountered marked spasm in the presence of anormal spinal fluid and it was found to persist forweeks after the spinal fluid had returned to normal.During the epidemic many cases presented with atypical history of onset and characteristic musclespasm without paresis or changes in the spinal fluid.Some muscles, apparently devoid of power, werefound to be in a state of muscle spasm. This usuallyoccurred as a result of reflex inhibition, due to fearof pain, and, on relief of the spasm and pain, powerreturned. At times weakness was the result of adisturbance of reciprocal innervation. The effectof effort in relation to the degree of paralysis hasbeen noted by other observers. We have occasion-ally observed extreme aggravation of muscle spasmfollowing strenuous exercise soon after the onsetof the disease. One adult woman, two days afterthe onset of fever, danced for four hours and thefollowing morning presented a picture of extremespasm in many muscle groups, especially in the backand lower extremities.

The Relationship of Muscle Spasm to Paresis

The incidence of muscle spasm in the NewZealand epidemic was very high and occurred in100 per cent. of cases fully examined. The incidenceof paresis in the first 224 patients was 49-1 per cent.(1 10 patients).

Effect of treatment. Treatment of all patients inthe acute stages of the disease was directed to therelief of muscle spasm and pain. Patients werenursed on a firm mattress which gave adequatesplintage to the back muscles, and the feet restedagainst a foot board. The legs were preventedfrom rotating by sandbags and the weight of thebedclothes was taken by a cradle.The relief of muscle spasm was accomplished by

the use of hot packs made of a fine woollen materialdipped in boiling water, wrung dry in an extractor,and applied at a high temperature. These packswere applied at hourly to four-hourly intervalsduring the day, and at night if required. Thismethod of treatment relieved muscle spasm andproduced a marked degree of comfort.The ultimate state of muscles in spasm could not

be predicted with certainty. The usual outcomewas resolution of the muscle spasm without residualweakness or contracture. This resolution some-times occurred within a few days; at other times itwas delayed for many weeks. In some, the spasmpassed into a state of permanent contracture due tofibrosis, which was an important factor in theproduction of deformities such as scoliosis. Somemuscles in spasm passed into a state of partial orcomplete flaccid paralysis.

Electromyographic StudiesIn an attempt to determine the site and nature

of muscle spasm we made electromyographic studieson five normal patients and on twenty patients withpoliomyelitis in various stages.

Method. The muscle action potentials wereamplified by an all-mains operated amplifier. Thiswas a resistance-capacity coupled amplifier, singleended, with a maximum gain which enables a2 cm. oscillograph spot deflection to be obtainedwith an input signal of 100 microvolts. Theamplified potential changes were led to two Cossorcathode ray oscillographs as well as to a loud speaker(Weddell et al., 1944). It was therefore possible toview the action potentials on one oscillograph screenwhile these were being photographed on the otherscreen. As no screened room was available theamplifier was so constructed that the frequencyresponse was substantially flat between 20 cyclesand 2,000 cycles per second. All the records wereobtained by the use of a concentric needle electrodein which the electrodes were threaded through ahypodermic needle so that the tips lay in the bevelof the needle (Adrion and Bronk, 1929). The actionpotential of a motor unit can give rise to a recordableimpulse for a distance of the order of 1 cm. fromthe copper tip of the needle (Weddell et al., 1944)and, in order to sample as large an extent of themuscle as possible, the needle was moved in severaldirections once the tip had penetrated the deepfascia and observations were made of the electricalpotentials in each position. Thus the effects ofphysiological rest, of contraction, and of passivestretch were investigated.

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Observations. The following observations weremade (1) on normal muscles; (2) on muscles inspasm (a) at rest; (b) on passive stretch; and (c) onvoluntary contraction.NoRtmAs. In five normal subjects, on complete

relaxation of the quadriceps muscle and on passivestretching of the muscle, no electrical potentialchanges were heard or seen but, on voluntarycontraction, normal motor unit activity was demon-strated. The complexity of the tracing in respectof amplitude and frequency was dependent uponthe force of the contraction.

discharges from such muscles (figs. 3, 4, 5) asreported by Watkins et al (1943).

(b) ON PASSIVE srrrEcH. Each muscle was thensubmitted to a slow stretch to a point of discomfortor pain at which the muscle spasm developed, andin most cases action potentials developed. This,however, was not invariable. In a few cases, nopotentials developed on stretch either with or withoutpain in spite of the development of spasm. In mostcases, stretch was limited by maximum spasm andpain, in some by spasm alone, and at this pointaction potentials recorded were at a maximum.

jj -,,____

C. 'a m

a..

-r ~~~~~~~~~~~~~~~(b)a)

(c)

FIG. 3.-Electromyographs from patient with acute poliomyelitis with spasm of the right quadriceps muscle.(a) Muscle at rest; (b) effect of stretch which did not cause pain: (c) effect of painful stretch; (d) effect

of voluntary contraction.

(d

MuscLEs IN sPAsM (a) AT REST. When theinsertion action potentials had settled down, in mostinstances but not invariably, in a muscle which wasclinically in a state of muscle spasm, there waselectrical silence while the muscle was at rest. Insome such muscles multiple sampling was carriedout in order to confirm the result. In some muscles,fibrillation potentials were demonstrated, but inothers which had had demonstrable spasm for morethan three weeks, no fibrillation potentials weredetected. We did not encounter spontaneous

These action potentials first appeared as the musclesentered the stage of painful stretch. In general,if some motor power was preserved, the actionpotentials on voluntary contraction were greaterthan those elicited on stretch. In some muscles,apparently paretic and in spasm, no action potentialscould be elicited either on attempted voluntarycontraction or on stretch, even to a point of severepain. On slight relaxation, just to the point wherepain ceased, the action potentials disappeared. Wehave not examined any muscle in which the unit

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MUSCLE SPASM IN POLIOMYELITISactivity on stretch was greater than on full voluntarycontraction as suggested by Watkins et al. (1943).

(C) ON VOLUNTARY CONTRACTION. In muscles inspasm capable of voluntary contraction, thefrequency and amplitude of the action potentialsobtained was in direct proportion to the degree ofvoluntary powert-n_o; 'L __-1-rP1USM16 III Lit;11LIUbAl.

Spinal AnaestheticStudies

Kabat and Knapp(1944) tested fivepatients with spinalanaesthesia, three inthe acute and sub-acute stage of thedisease, and two inthe chronic stage.Those in the acuteand subacute stageshowed relaxation ofthe muscle spasmunder a spinalanaesthetic (heavypercaine). In twopatients, fourteenmonths after the on-set of the disease,spinal anaesthesiaproduced practicallyno change in thelimitation of passivemovement. Cook(quoted by Kabat andKnapp) in twopatients in the firsttwo weeks of thedisease, found thatspinal anaesthesiaeliminated musclespasm. Ini twopatients under spinalanaesthesia, KabatandKnapp found thatwhen sensory anaes-thesia was producedand some motorfunction still per-sisted, the restriction FIG. 4. Electromyographs of aof passive movement muscle clinically showingwas reduced but it spasm (1) at rest; (2) duringwas ~~~~maximum voluntary contrac-was not completely tion; (3) during painful stretcheliminated until of the muscle, demonstratingmuscular paresis had activity similar to motor unit

developed, ~~action potentials.We have studied the effect of spinal anaesthesia

on four patients, two in the acute stage of thedisease twenty and twenty-five days after the onset,and two in the chronic stage eighty-five and sixty-three days after the onset. Our yardstick was thegoniometer, with which was measured the angle of

flexion at the knee joint in checking the hamstringmuscles and quadriceps muscles and the angle offlexion of the spine before and after spinalanaesthesia, using 2 ml. of heavy percaine. In thepatients in the acute phase of the disease, spasm ofthe hamstrings, quadriceps, and back- muscles was

relieved.. In the twopatients in the chronicstage of the illness norelief was obtained.Hence, our observa-tions conform tothose of Kabat andKnapp and otherobservers (table 2).

Curare StudiesIn this our experi-

ence was very limitedbut will be quoted.In two patients in theacute phase of theillness (sixteen andtwenty days from thetime of onset) curare(2 ml. 'intocostrin')failed to relievemuscle spasm. Thecurarized muscleswere still painful onstretch. This smallexperience coincideswith that of others(Kottke et al., 1948;Elkins and Carbin,1947) in respect ofcurare.

DiscussionVarious authors

have focused atten-tion on the wide-spread nature of thelesions throughoutthe central nervoussystem. The mainbrunt of the lesionfalls on the anteriorhorn cells of the

FIG. 5. Electromyographs of a spinal cord, on themuscle clinically showing internuncial cells ofspasm (1) at rest; (2) during the cord and on themaximum voluntary contrac-tion; (3) during painful reticulum formationstretch of the muscle, and tegmentum of thedemonstrating absence of brain stem (Barnhartactivity. et al.). The changes

in the meninges have received little attention.Scheinker (1947) has demonstrated changes in theleptomeninges similar to those in the cord. Themeningeal infiltration varied considerably at differentlevels of the spinal cord and the cerebral meningeswere affected only in the region of the mid-brain

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ARCHIVES OF DISEASE IN CHILDHOODand cerebellum. Freeman (1933) found infiltrationof the meninges by lymphocytes at the base of thebrain and particularly along the cord meninges.More recently changes in the muscles have beennoted. Hassin (1943) has reported parenchymatousswelling and disruption of muscle fibres and alsodiffuse and focal inflammatory infiltration in apatient who died two hours after the onset ofparalysis. Carey (1944) has studied muscles andtheir neuromuscular junctions, and has demon-strated in post-mortem material from three patientsdenervation of the extrafusal fibres within thirty-sixhours of the onset of paralysis.

Older views on the normal mode of action of thespinal cord have to be revised in the light of recentwork. We now have to visualize two opposing setsof impulses, excitatory and inhibitory, playing onthe final common pathway, the anterior horn cell.In man, cortical suppressor bands have been provenin area 4 s. This suppressor system passes via theintemal capsule to the caudate nucleus which relaysto the red nucleus, substantia nigra, globus pallidus,subthalamic body, and the thalamus. From thesenuclei, relays pass down the brain stem to thereticular nuclei, whence the band of suppressorbulbospinal fibres arise, pass to the internuncialpool, and thence to the final common pathway, theanterior horn cell. On available evidence it seemsthat the reticulospinal system constitutes an efferentpathway from the higher centres to the local spinalreflex system whose activity is expressed as suppres-sion of anterior motor neurone discharge.

Various investigators have attempted to correlateexactly the known pathology with the state ofspasm found on clinical examination, and havearrived at widely divergent opinions as to the siteof the lesion responsible for the spasm, rangingfrom the reticulum in the bulbar region, themeninges,the internuncial cells, the anterior horn cells, to themuscle fibres themselves. Moldaver (1944) sug-gested that muscle spasm was made up of threecomponents; meningeal irritation in the acute phase;increased stretch reflex due to paralysis of

antagonists and hyper-irritability of inflamedposterior root ganglia. Kabat and Knapp (1944)have postulated damage of the internuncialneurones as the cause of spasm which results fromrelease of proprioceptive reflexes from inhibition.Bodian (1946) has correlated injury to the bulbarinhibiting mechanism with the appearance ofgeneralized spasticity in experimental poliomyelitisin monkeys, and Pohl (1943 and 1945) states thatthe present Kenny concept of the disease is that itis primarily an affection of peripheral structures,principally the muscles and their fascial coverings,but also including the skin and subcutaneoustissues.

Lesions of the suppressor system at different levelshave been held to be responsible for muscle spasmas a result of the removal of inhibiting impulses andthe resultant activation of the excitatory motorsystem. Relief of spasm by a spinal anaestheticwould support this view. On the other hand, alesion of the suppressor system at the cortex, bulbarregion or internuncial pool, would be expected togive rise to an upper motor neurone type of lesionwith hyper-reflexia and a 'clasp knife' type ofrigidity. We find, however, a different state fromthe hypertonus of the upper motor neurone lesion.A consideration of our own findings suggests that

more than one lesion accounts for the phenomenaof muscle spasm.Menreal irritation The available evidence

lends some support to the theory of so-called' meningeal irritation,' that is, reflex muscle spasminduced by irritation of pain-sensitive structures inthe meninges or dorsal nerve roots such as occursin meningitis or subarachnoid haemorrhage. By aseries of studies Wolff (1947) demonstrates thatnoxious stimulation in any part of the cranium maylead to sustained contraction of the head and neckmuscles. Pathological changes of the spinal fluidand meninges in poliomyelitis are well establishedand we believe that this inflammation causesirritation to the pain-sensitive structures and, as aresult, reflex spasm of muscles of the neck, back,

TABLE 2ANALYSIS OF DEGREES OF RELAXATION OBTAINED UNDER SPINAL ANAESTHESIA

Effect of Spinal Anaesthesia (HeavyPatient No. of Days of fliness Percaine) Comment

Before After

1 85 *Kemig (R) 145- 145- No alteration2 63 tQuadriceps (R) 30' 30: No alteration3 20 Quadriceps (R) 20- 0 Definite relaxation

30 10-4 25 lBack 65: 85:' Definite relaxation

Kernig (R) 120' 150-(L) 110° 155-

Kermg angles were measured as angle between leg and vertical thigh.t Quadriceps angles were measured as angle between leg and thigh when heel was approximated to the buttock.Back angle was measured between honzontal plane of the bed and lumbar region when patient was leaning forward as far as possible.

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MUSCLE SPASM IN POLIOMYELITIS 21and lower limbs. The release of spasm of the lowerlimbs by spinal anaesthesia in the acute phase of thedisease would support this contention. There is,however, no apparent correlation between thenumber of cells in the spinal fluid and the degree ofmuscle spasm, as many cases have been shown topresent with muscle spasm alone and a normalspinal fluid and, in the case quoted above, whenmuscle spasm was reactivated by fever, there wasno evidence from the spinal fluid examination, asjudged by the cell count, of a further meningeallesion.

Peripheral lesion. The available evidence alsolends some support to the suggestion of a peripherallesion in the muscle itself, at the myoneural junction,or in the muscle protoplasm. Some pathologicalevidence has been quoted, and requires carefulchecking. Clinically the muscles are found to betender on palpation and on stretch. The relief ofthe spasm by the application of hot packs mightsuggest a local lesion. It has been noted that attimes the spasm is aggravated by motor activity, afebrile illness, or exposure to cold. These threefactors normally induce muscle stiffness and all havethe effect of increasing the metabolic rate with anincrease of metabolites which may impair thechemical action at a damaged myoneural junction.

Electromyographic studies with our instrumentfailed to reveal motor potentials in spasm in spiteof multiple sampling in some cases, and this suggestsa primary involvement of the contractile mechanismof the muscle. The hyperirritability of the muscleon stretch suggests a sensitivity of the muscle spindlesthemselves. The relief cof spasm in the acute phaseby a spinal anaesthetic could be brought about bythe abolition of pain or by the dilatation of bloodvessels as probably occurs with the application ofhot packs. The failure of curare to give relieffavours the diagnosis of a lesion of the contractiletissue. Spasm may occur in muscles devoid ofvoluntary power and these muscles may go on to aflaccid paralysis suggesting that muscle spasm is notdependent upon the existence of an intact reflex arc.All these factors suggest that spasm in the acutephase is not entirely a function of the ordinarymotor neurone.

SummaryWe have found muscle spasm in all patients with

poliomyelitis. It may be present at rest and isincreased by stretch. It may resolve, or a muscleso affected may pass into a state of flaccid paralysis,or into a state of contracture.

Our electromyographic studies have failed todemonstrate electrical potentials in muscles in astate of spasm. We find increased sensitivity orhyperirritability of the stretch reflex.

Spinal anaesthesia relieved spasm in the acutestage of the illness but not in the chronic stage.Curare failed to relieve spasm in the acute stage ofthe illness.

In the acute phase of poliomyelitis, we believethe muscle spasm is in part the result of reflex spasmdue to meningeal inflammatory changes irritatingthe pain-sensitive structures of the meninges anddorsal roots, and in part to a local lesion in themuscles themselves.

We have to thank Dr. Elizabeth Hughes who hasgiven us access to her cases and has co-operatedwith us in this study; the N.Z. Medical ResearchCouncil for the release of the apparatus; ProfessorJ. C. Eccles for his advice and assistance in thisinvestigation. Mr. E. E. Suckling has given ustechnical advice, and Mr. Litherland has preparedthe photographs.

REFERENCESAdrian, E. D., and Bronk, D. W. (1929). J. Physiol.,

67, 119.Barmhart, M., Rhines, R., McCarter, J. C., and Magoun,

H. W. (1948). Arch. Neurol. Psychiat., Chicago,59, 368.

Bodian, D. (1946). Proc. Soc. exp. Biol., N.Y., 61, 170.Carey, E. J., et. al. (1944). J. Neuropath. exp. Neurol.,

3, 121.Freeman, W. (1933). 'Neuropathology.' Saunders.

Philadelphia.Hassin, G. B. (1943). J. Neuropath. exp. Neurol., 2, 293.K#bat, H., and Knapp, M. E. (1943). J. Amer. med.

Ass., 122,989.,- (1944). J. Pediat., 24, 123.

Kottke, F. J., Teigen, B. S., Seigel, S., and Knapp, M. E.(1948). Arch. phys. Med., 29, 141.

Moldaver, J. (1944). J. Bone Jt. Surg., 26, 103.Pohl, J. F. (1945). Lancet, 65, 265.

, and Kenny, E. (1943). 'The Kenny Concept ofInfantile Paralysis and its Treatment.' Minne-apolis. Bruce Pub. Co.

Richards, R. L., Elkins, E. C., and Corbin, K. B. (1947).Proc. Mayo Clin., 22, 34.

Scheinker, I. M. (1947). Arch. Neurol. Psychiat.,Chicago, 57, 565.

Watkins, A. L., Brazier, M. A. B., and Schwab, R. S.(1943). J. Amer. med. Ass., 123, 188.

Weddell, G., Feinstein, B., and Pattle, R. E. (1944).Brain, 67, 178.

Wolff, H. G. (1947). In MacBryde, C. M., 'Signs andSymptoms.' Lippincott. Philadelphia.

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