spasmodic torticollis: a combined clinical study · (protein-bound iodine (pbi) in 1971). in 1976...

Journal ofNeurology, Neurosurgery, and Psychiatry, 1978, 41, 485-492

Spasmodic torticollis: a combined clinical studyW. B. MATTHEWS, PATRICK BEASLEY',WILLIAM PARRY-JONES, AND G. GARLAND

From the University Department of Clinical Neurology, Churchill Hospital,and the Department of Psychiatry, The Warneford Hospital, Oxford

SUM M AR Y The prognosis in 30 patients with spasmodic torticollis proved to be unexpectedlybad, only one patient making a full and sustained recovery. Investigation did not confirmpreviously reported reflex influences on the degree of spasm. Detailed otological investigationdid not suggest that spasmodic torticollis originates in vestibular dysfunction. Psychologicalassessment of the patients showed no deviation from normal in premorbid personality butconfirmed the severe adverse effects of the condition.

Spasmodic torticollis remains an essentially intrac-table and disabling condition of unknown cause.Opinion is still divided on whether it is an organicor psychogenic disease or whether two forms exist(Meares, 1971a). In this study particular attentionhas been paid to this aspect-to the natural historyand relation to other forms of neurological dis-order, the relevance of vestibular disease (Svienand Cody, 1969), the relation to thyrotoxicosis(Gilbert, 1971), and the effect of movement andother stimuli on the degree of spasm (Podivinsky,1968).

Clinical material

In 1971 an attempt was made to trace all patientsdiagnosed as having spasmodic torticollis in theindex of the Radcliffe Infirmary since 1954. Ofthese 37 patients seven could not be traced andtwo are known to have died. Eight patients eitherdid not wish to be seen or their general prac-titioners advised against further interest in theircomplaint. Of these, four were known still to havetorticollis in 1971 and four claimed to have re-covered. Data from these eight patients have notbeen included in the survey, largely because of thedifficulty in assessing the real extent of recovery.Detailed study was limited to the 20 patients tracedfrom the diagnostic index and personallyexamined, and to 10 further patients seen inclinical practice between 1971 and 1973.

'Present address: Royal Devon and Exeter Hospital, Exeter.Address for reprint requests: Professor W. B. Matthews, University ofOxford, Department of Clinical Neurology, The Churchill Hospital,Headington, Oxford OX3, 7LJ, England.Accepted 26 January 1978

Methods

A detailed medical history and examination wererecorded. Investigations carried out on a propor-tion of patients included radiographs of the skulland cervical spine, and tests of thyroid function(protein-bound iodine (PBI) in 1971). In 1976 allpatients seen in the original survey were againfollowed up either by interview or postal enquiry.The EMG was recorded either on an ink-writing

EEG machine from surface electrodes over thesternomastoid, trapezius, and deep cervicalmuscles, or from the sternomastoid muscles usinga two-channel Medelec electromyograph. Theeffects of eye closure, lifting a weight with eitherhand, cutaneous stimulation on the neck and face,and of the patient's own "antagonistic gesture"were observed.Routine otological examination was carried out,

and, in addition, electronystagmography (ENG)was recorded from electrodes at the outer canthusof each eye with a central reference electrode onthe forehead. Spontaneous nystagmus was soughtwith the eyes open and closed, and with gazedirected ahead and to either side. The effect ofpassive neck torsion with the patient seated wasalso examined. Postural nystagmus was sought inthe supine, prone, and both lateral positions.Caloric labyrinthine stimulation, either singletemperature cold stimulation or bithermal stimu-lation was carried out as follows:

1. left ear r at30°C2. right ear f t30

3. left ear } at 440C4. right ear f

with the head raised 300 from the horizontal and485

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W. B. Matthews, Patrick Beasley, William Parry-Jones, and G. Garland

the eyes closed. The number of beats of nystagmusin the period 60-90 seconds after the beginning ofstimulation was recorded and counted, and usedin the calculation of preponderance (Hinchcliffe,1968). Labyrinthine preponderance (LP) was cal-culated according to Jongkees' formula (Jongkeesand Philipszoon, 1963):

LP= (1+3)-(2+4) X 100%1+2±3+4

For single temperature caloric tests the differencebetween the two sides was expressed as a per-centage of the total response of the two sides.

Directional preponderance of nystagmus (DP)was calculated from Jongkees' formula:

DP=(1 +4)-(2+3) X 100%D= 1+2+3+4

Values of less than 30% are not considered assignificant deviations from normal.

Psychological and psychiatric investigation wasparticularly directed towards the assessment, as faras possible, of the premorbid state, the possiblerelevance of stress to the onset of torticollis, andthe psychological and social effects of the chronicdisorder. Particular attention was paid to thepossibility of detecting a psychogenic group witha better prognosis than that of the presumedorganic form of torticollis. Investigations com-prised a structured clinical interview with thepatient and, whenever possible, with the spouse orclosest other person. Special attention was focusedon social and marital adjustment, the psychiatrichistory, and the subject's life situation at the timeof the onset of the disorder. Specific investigationsincluded the Eysenck Personality Inventory, formA, the Leyton Obsessional Inventory, and theHostility and Direction of Hostility questionnaire(HDHQ). Married subjects and their spouses com-pleted the Ryle Marital Patterns Test and a simplemarital adjustment rating scale.

Results

Of the 30 patients investigated, nine were maleand 21 female. The age of onset is seen in Table 1.

Table 1 Age of onset

Age ofonset Number ofpatients(yr)

0-10 011-20 321-30 331-40 841-50 951-60 661-70 1

Total 30

There was a marked preponderance in the fourthand fifth decades. In 12 patients the torticollisturned the chin to the right and in 15 to the left.One patient had retrocollis, and in two patientswho had sustained more than one episode thedirection of turn had altered.

In no patient was a history of epidemic encepha-litis obtained, and there was no evidence thattorticollis was drug-induced. No patient gave afamily history of torticollis or of any form oforganic nervous disease other than stroke, withthe exception of one patient who had a familyhistory of essential tremor.

In two of the 25 patients x-rayed, a congenitalanomaly of the cervical spine was seen; in one,spina bifida occulta of C6 and 7 vertebrae and inthe other, fusion of the bodies of C5 and 6 verte-brae. Significant asymmetry of the skull was notdetected in any of the 10 patients in whom satis-factory radiographs could be obtained. Thyroidfunction (PBI) was normal in the nine patientsin whom this was examined.

Additional neurological signs were present insix patients. Two patients had dystonic movementsof one upper limb, probably developing at thesame time as the torticollis but without subsequentprogression. One patient had writer's cramp. Onepatient developed widespread torsion dystonia 24years after the initial episode of torticollis. Onepatient had slight signs of Parkinson's disease whenfirst seen with torticollis. One patient had bothhereditary essential tremor and a mild infantilehemiparesis. In the remaining 24 patients torti-collis was the only neurological abnormality. Noassociation with any systemic disease wasrecognised.

OUTCOMEAt the time of the survey in 1971-73 only onepatient was entirely free of symptoms relevant tospasmodic torticollis. A further four patients wereclassified as having made a substantial recoveryin that no torticollis was present, but these patientswere still aware of some abnormality, and foundthat, under even mild stress, pain and tensionwould develop in the neck muscles in a mannerrecognisably related to their original symptoms.Three patients gave a history of complete remis-sion followed by relapse, although, as they werenot seen during the symptom-free period, itis not known whether remission was indeed com-plete. The details of the eight patients in whomsubstantial or complete remission had occurred atsome stage are shown in Table 2. In general, re-mission occurred relatively soon after the onsetbut relapse might occur after many years of free-

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Spasmodic torticollis: a combined clinical study

Table 2 Cases with remission

Case Sex Age at Age at Duration of Age at Duration of Results Commentsinitial onset first attack relapse relapsesurvey (yr) (yr) (yr) (yr) 1971-73 1976(yr)

I F 56 41 4/12 - - Rc Rc2 M 46 35 2 49 2/12 SRc SRc Relapse after initial survey with remission3 F 26 18 1 - - SRc SRc4 F 52 35 1 37 3/12 SRc SRc Relapse after initial survey with remission

54 4/125 F 57 52 1 61 2- SRc P Relapse after initial survey without remission6 M 47 15 2 38 14+ P P Dystonia began with relapse7 F 45 39 4 45 5 + P P Disabled after surgery8 M 64 39 1 53 13 + P P Writer's cramp

Rc recovery; SRc = substantial recovery; P = persistent torticollis

dom. The caution exercised in distinguishing"substantial" from "complete" recovery in theoriginal survey was justified by the further relapseof three of these four patients between 1971 and1976, one being left with persistent torticollis.At the time of the initial survey 22 patients had

had persistent torticollis from between a fewmonths to 40 years (Table 3). By 1976 threepatients had died of cardiac disease. Torticollis hadbeen present to the end in two of these patientsand probably in the third. No necropsy was ob-tained. In 11 patients the torticollis had notchanged but in six there had been significant im-provement, although in one of these Parkinson'sdisease had become increasingly disabling. Nopatient had recovered.The type of movement present at the onset,

whether jerking or turning, and the presence of

Table 3 Cases with persistent torticollis at the time oftile initial survey

Case Sex Age at Age at 1976 Commentssuirvey onset Result(yr) (yr)

9 F 48 28 Unchanged10 M 48 47 Unchanged11 F 67 52 Unchanged Dystonia of one arm12 M 57 52 Died 197413 F 64 51 Died 197414 F 66 49 Improved15 M 46 43 Unchanged Dystonia of one arm16 M 59 36 Unchanged17 F 64 24 Unchanged18 F 42 37 Improved Parkinson's disease19 F 45 43 Unchanged Infantile hemiparesis

Essential tremor20 F 63 61 Improved21 F 31 29 Improved22 F 44 43 Unchanged23 M 49 48 Unchanged24 F 37 36 Unchanged25 F 37 35 Unchanged26 F 44 41 Improved27 F 53 52 Improved28 M 34 16 Unchanged29 F 34 31 Improved30 F 76 65 Died 1974

pain have been thought to be of prognostic signifi-cance (Tibbetts, 1971; Mears, 1971 a). Of thosewho experienced a partial or complete remissionthe onset was judged, in retrospect, to have beenjerking in one, turning in six, and with a fixedposture in one. In those with persistent torticollisthe onset was jerking in six, turning in 14, andwith a fixed posture in two. Pain was rememberedas being present at the onset in 10 of the 22 withpersistent torticollis, and four of the eight in whomremission had occurred.

ELECTROMYOGRAPHYThis was carried out in 16 patients. The resultsconfirmed the widespread contraction of the neckmuscles even when the posture of the head sug-gested relatively isolated corltraction of one sterno-mastoid muscle. The antagonistic gesturehabitually used by each patient to restrain thetorticollis was observed to inhibit muscular con-traction in five (Fig. I) and to have no effect inthree, but in seven patients, under the condition ofthe test, spasm was enhanced (Fig. 2). Eye closurehad no effect on the spasm in 13 patients, butregularly induced inhibition in one patient (Fig. 3).In another patient, however, eye opening wasregularly followed by reduction of spasm.The effect of lifting a weight with the hand on

the same or opposite side to the direction of headturning was recorded, but no consistent resultswere obtained. In six patients lifting a weight witheither hand increased the EMG activity recordedfrom the neck (Fig. 4a, b), and in three no effectwas observed. In three, using the ipsilateral handincreased spasm while use of the contralateralhand resulted in inhibition or had no effect, but intwo patients these responses were reversed. Inone patient using either hand inhibited spasm ofthe neck muscles (Fig. 5a, b). Light touch withcotton wool on the side of the neck and face hadno recordable effect on spasm in the 10 patients inwhom this was examined.

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Fig. 5 Electrode placements as in Fig. I in case 22 showing inhibitory effect of lifting a weight with right (a)or left (b) hand.

OTOLOGICAL EXAMINATION (PB)Sixteen patients were examined, but not alltechniques were applied in every case (case num-bers refer to Tables 2 and 3).Case 3 had inactive right chronic suppurative

otitis media. Pure tone audiometry was normal incases 28, 15, 7, and 10. There was symmetricalpresbyacusis in case 8 and 11, and case 19 had abilateral sensorineural deafness around 4 kHz withan audiographic curve characteristic of minoracoustic trauma.Spontaneous nystagmus with eyes closed was

recorded in five of the 15 patients in whom it wassought (cases 4, 6, 7, 8, and 12). In each casenystagmus was to the right. Neck torsion nystag-mus was not elicited in any patient and positionalnystagmus only in case 15 in whom it occurred tothe left in the supine and left lateral positions.

Six patients were examined by single tempera-ture caloric stimulation and nine by bithermalcaloric tests. Assuming a level of significance of30%, only case 8 showed labyrinthine preponder-ance at 44%, the left labyrinth being the pre-ponderant and the direction of turning being tothe left. In the remaining 15 cases showing minordegrees of labyrinthine preponderance the direc-tion of torticollis was away from the preponderantlabyrinth in 11 cases and toward it in three. In nopatient was significant directional preponderanceof nystagmus found, but in nine cases showingminor degrees of such preponderance it was op-posite in direction to the torticollis in eight and inthe same direction in one.

PSYCHOLOGICAL AND PSYCHIATRIC EXAMINATION(WLP-J AND GG)Twenty-nine patients were examined, one beingexcluded because of severe deafness due to oto-sclerosis (this patient was not examined otologi-cally). Two patients had received psychiatrictreatment at some time before the onset oftorticollis, in both cases for depression.

It was originally hoped to be able to comparea group of recovered patients with those with per-sistent torticollis for such features as neuroticism,obsessional manifestations, intropunitive hostility,and marital disharmony, considered to be impor-tant factors in other studies (Meares, 1971a;Tibbetts, 1971) but the number of those in sub-stantial remission was small at the time of theoriginal surveys, and any comparison based onthis grouping has since been invalidated by thesubsequent relapse of three of the patientsin this category. Evidence of neuroticism, ob-sessional symptoms and traits, and intropunitivehostility in the group as a whole was, therefore,assessed by comparing the group with the normalpopulation.Group mean scores were as follows: EPI-

N,9.93; Leyton Obsessional Inventory Symptom12.03 and Trait 7.20; HDHQ Hostility 10.60 andDirection of Hostility -0.5. Separate analyseswere done for males and females in the group forLeyton and HDHQ since these have separatenorms for males and females. There were nosignificant differences between this group andthe normal population.

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Sixteen of the 29 patients described factors thatcould have influenced the onset of torticollis orimportant environmental events coincident withthe onset. These included, for example, exacerba-tion of severe marital discord, stress from a changeto night shift work, an abortion, hysterectomy,and a road traffic accident in which the neck waspossibly injured. The assessment of the significanceof such reported events often many years later isclearly difficult.Of the 21 married subjects, 13 were women and

eight men. Marital adjustment measured on afive-point scale indicated severe or moderatelysevere marital discord in nine subjects, a majorfactor being unsatisfactory sexual adjustment.

All but six patients claimed adverse social effectsfrom torticollis at the time of examination. Four-teen thought that, at the worst period in the courseof their disorder, the disability had been severeand 11 moderately severe. Fear of ridicule andreluctance to leave the home were almost uni-versal. Two men and one woman were too dis-abled to work.

TREATMENTAt the time of the original survey these patientshad been subjected to a great variety of differenttreatments. A common pattern was that of referralby the general practitioner to a psychiatrist underthe impression that spasmodic torticollis was anhysterical disorder. Eight patients had receivedpsychiatric inpatient treatment and a further sixas outpatients. Two patients had been treated withcourses of electroconvulsive therapy. Anothercommon sequence was referral from the generalpractitioner to an orthopaedic surgeon, perhapsbecause of some confusion with congenital torti-collis or because it was thought that there mightbe some abnormality of the cervical spine. Suchreferral commonly led to manipulation of theneck, sometimes under anaesthesia, or immobilisa-tion in an elaborate plaster. Reference direct toa neurologist did not lead to more successfultreatment, varied forms of physiotherapy being themost popular. This ranged from local heat andexercises directed against the direction of turn toimmobilisation in bed with sandbags and continu-ous traction. Injection of local anaesthetic intothe motor point of the more accessible cervicalmuscles was also practised. Drug therapy includedanticholinergic agents, phenothiazine derivatives,antidepressants, barbiturates, and diazepam. Thislast drug was frequently reported as affordingsome slight relief but was certainly not curative.Five patients had been treated by peripheral sur-gery to the muscles of the neck or their nerve

supply, varying from section of one sternomastoidmuscle to extensive anterior nerve root section.Three patients had been treated by stereotacticthalamotomy, but in each case treatment waslimited to making a lesion on the side contralateralto the direction of turn. The only patient whowas regarded as being completely cured had re-ceived treatment by hypnosis and had recoveredfrom severe torticollis within three months. Oneother patient, as far as could be ascertained, hadbeen treated in this way with only limited andtemporary improvement.At the time of the second review some patients

had also received more recently developed formsof treatment including amantadine, levodopa, halo-peridol, and feedback from the neck muscles, butthe improvement noted in six patients was con-sidered to be spontaneous and not related totreatment.

Discussion

Few neurologists believe spasmodic torticollis tobe hysterical, and yet the evidence for organicdisease remains problematical. Claims that dys-tonic movements of the neck can be distinguishedfrom hysterical spasm have been based on thewidespread nature of the contractions, includingantagonistic muscles (Herz and Glaser, 1949; Herzand Hoefer, 1949) and the combination of sustainedand rhythmic activity. It is undeniable that themovement of spasmodic torticollis differs in manyrespects from the normal action of turning thehead, but it is also possible voluntarily to effectthis movement in an abnormal manner accom-panied by widespread fluctuating muscular con-tractions. The inhibitory and enhancing effects ofdifferent forms of movement and sensory stimula-tion reported by Podivinsky (1968) are of greatinterest but are inconsistent. For example, we wereunable to confirm his observations that slighttouch on the side of the neck towards which thechin is turned reduces the spasm while contra-lateral stimulation causes enhancement. He alsoreported that supporting a weight in the ipsilateralhand aggravated the spasm in 87% of patientswhile using the contralateral hand reduced spasmin 78%. We could find no consistent effect. Theantagonistic gesture, in which sometimes a verylight touch prevents the movement, has been inter-preted both as an indication of reflex inhibitionand of hysteria. In our test conditions spasm wasmore often enhanced than inhibited.

In the only thorough neuropathological exam-ination of a patient with isolated spasmodic torti-collis, adequately investigated in life, no lesion was

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found (Tarlov, 1970). Attempts to detect a dis-order of neurotransmitter mechanisms have alsoso far proved negative (Curzon, 1973). There is astrong association with other forms of involuntarymovement, essential tremor (Couch, 1975), writer'scramp (Meares, 1971c), and torsion dystonia(Marsden and Harrison, 1974), all represented inthe present series, but the anatomical basis ofthese conditions is also unknown. Patterson andLittle (1943) reported motor abnormalities in noless than 33% of their patients including 4% withParkinsonism. It is not easy to determine fromtheir account how much weight should be attachedto the 7% of patients who had a tremor of thehands and the 6% with masked facies. Neverthe-less the association with disorders of functioneither certainly or probably involving the basalganglia is impressive.The nature of any possible underlying structural

disease of the brain naturally remains obscure. Itis now extremely improbable that encephalitislethargica plays any part. Hassler and Dieckmann(1970) suggested that brain damage in infancymight be an important factor, basing this conten-tion on asymmetry of the lateral ventricals seen onpneumoencephalography, sometimes reflected inthe shape of the skull. One of our patients had amild right infantile hemiparesis with torticollis tothe right. No skull asymmetry was found in heror in the other nine patients in whom satisfactoryfilms could be obtained.Because of the close relationship of the ves-

tibular system to posture of the head it has beennatural to suspect that disturbance of this systemmight be responsible for torticollis, but there hasbeen no systematic investigation. Detailed neuro-otological examination in our patients producedno evidence in support of this contention.The approach from the psychological aspect

presents similar difficulties. Paterson (1945) re-ported successful results from psychotherapy, butthose patients whom she regarded as hystericalwere not among those who recovered. Herz andGlaser (1949) considered that 50% of theirpatients had an abnormal personality pattern butquantitative assessment had not at that time beendeveloped. This problem also arose with Tibbetts'(1971) recognition of an organic and a psycho-genic group. Cockburn (1971) using the Maudsleypersonality index and other indications of pre-morbid stability found no difference from controlsubjects. Meares (1971a) also distinguished twocategories. Those with greater evidence of pre-existing neuroticism and psychosexual problemshad a much improved chance of recovery. BothTibbetts (1971) and Meares (1971a) thought that

the type of movement also afforded evidence ofcausation and prognosis. It is not easy to equatetheir descriptive categories but both regardedsustained tonic spasm as evidence of a bad progno-sis. Tibbetts thought that those with mild spasmor with irregular movements were more likely torecover while Meares emphasised the relativelygood prognosis where the onset had been "jerking"or painful. Our original intention of comparing arecovered with a persistent group was thwarted bythe remarkably low rate of full recovery. In thewhole group no evidence of pre-existing person-ality disorder or neuroticism beyond that of thenormal population was discovered. Clearly thismethod would not be capable of recognising oneor two patients in whom psychological factorswere indeed important or even responsible for thetorticollis but our findings are further strong evi-dence against an hysterical cause in most patients.In those with relatively good prognosis, in thatsubstantial or complete remission occurred at somestage of the disease, there was no importantdifference in the mode of onset remembered bythe patient compared with the group with per-sistent torticollis. The exceedingly adverse effectof spasmodic torticollis on the life and happinessof many of the patients was, however, amplydemonstrated.The association between the onset of torticollis

and some form of stress has been noted in otherseries (Paterson, 1945; Meares, 1971a). It isscarcely possible to exclude the natural tendencyof the patients to associate the onset of unpleasantsymptoms with physical or mental trauma. Thepossibility that stress might distort the pattern ofneurotransmitter regulation in the central nervoussystem is attractive as a link between mutuallyexclusive "organic" and "psychogenic" disease,but remains unsubstantiated. Certainly the lack ofevidence of premorbid personality disturbance ismost unlike what would be expected in a conven-tional psychogenic disorder.The prognosis in our patients was unexpectedly

poor, only one being thought to have made a com-plete and lasting recovery. The tendency to relapsepersisted even in those in whom spasm was re-garded as minimal at the time of the initial follow-up examination. In general, our findings confirmedthose of Meares (1971 b) who recognised threestages: progression for five years, but with possi-bility of remission; a static stage for the next fiveyears; and a final stage during which slight im-provement might occur. This pattern is, of course,only an approximation to which many patients donot conform and, in particular, relapse may occurmany years after the onset. Our study was not

B

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specifically concerned with treatment. In agree-ment with Shaw et al. (1972), we did not find thatmedical treatment influenced symptoms signifi-cantly, and surgery, which did not in our seriesinclude bilateral thalamotomy, was either ineffec-tive or palliative. We found no indication of anyform of curative treatment and the outcomeappears to have changed little since Gowers (1893)stated that "the prognosis must be grave in everydeveloped case."

PB would like to acknowledge the assistance ofMrs M. MacDonald in performing electronystag-mography.

References

Cockburn, J. J. (1971). Spasmodic torticollis: a psy-chogenic condition? Journal of Psychosomatic Re-search, 15, 471-477.

Couch, J. R. (1975). The relationship between spas-modic torticollis and essential tremor. Transactionsof the American Neurological Association, 100, 181-183.

Curzon, G. (1973). Involuntary movement other thanParkinsonism. Proceedings of the Royal Society ofMedicine, 66, 873-876.

Gilbert, G. J. (1971). Spasmodic torticollis healedeffectively by medical means. New England Journalof Medicine, 284, 896-898.

Gowers, W.- R. (1893). A Manual of Diseases of theNervous. System. Second edition, Vol. 2, p. 671.Hofner Pbblishing Company: Darien.

Hassler, R., and Dieckmann, G. (1970). Stereotactictreatment of different kinds of torticollis. ConfiniaNeurologica, 32, 135-143.

Herz, E., and Glaser, G. H. (1949). Spasmodic torti-collis. II: clinical evaluation. Archives of Neurologyand Psychiatry (Chicago), 61, 227-239.

Herz, E., and Hoefer, P. F. A. (1949). Spasmodic

torticollis. I: physiologic analysis of involuntarymotor activity. Archives of Neurology and Psy-chiatry (Chicago), 61, 129-136.

Hinchcliffe, R. (1968). Nystagmus rate as an index ofcaloric test response. Acta Otolaryngologica (Stock-holm), 65, 311-315.

Jongkees, L. B. W., and Philipszoon, A. J. (1963). Thecaloric test in Menieres disease. Acta Otolaryngo-logica Scandinavica, Supplement 92, 168-170.

Marsden, C. D., and Harrison, M. J. G. (1974).Idiopathic torsion dystonia (dystonia musculorumdeformans). A review of forty-two patients. Brain,97, 793-810.

Meares, R. (1971a). Features which distinguish groupsof spasmodic torticollis. Journal of PsychosomaticResearch, 15, 1-11.

Meares, R. (1971b). Natural history of spasmodic torti-collis and effect of surgery. Lancet, 2, 149-151.

Meares, R. (1971c). An association of spasmodic torti-collis and writer's cramp. British Journal of Psy-chiatry, 119, 441-442.

Paterson, M. T. (1945). Spasmodic torticollis: resultsof psychotherapy in 21 cases. Lancet, 2, 556-559.

Patterson, R. M., and Little, S. C. (1943). Spasmodictorticollis. Journal of Nervous and Mental Diseases,98, 571-599.

Podivinsky, F. (1968). Torticollis. In Handbook ofClinical Neurology, Vol. 6. Edited by P. J. Vinkenand G. W. Bruyn. North-Holland: Amsterdam.

Shaw, K. M., Hunter, K. R., and Stem, G. M. (1972).Medical treatment of spasmodic torticollis. Lancet,1, 1399.

Svien, H. J., and Cody, D. T. R. (1969). Treatment ofspasmodic torticollis by suppression of labyrinthineactivity: report of a case. Mayo Clinic Proceedings,44, 825-827.

Tarlov, E. (1970). On the problem of the pathologyof spasmodic torticollis in man. Journal ofNeurology, Neurosurgery, and Psychiatry, 33, 457-463.

Tibbetts, R. W. (1971). Spasmodic torticollis. Journalof Psychosomatic Research, 15, 461-469.

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