Focal dystonia diagnosis of unilateral jaw masticatory · J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.49.6.651 on 1 June 1986. Downloaded from Focaldystonia ofthejawandthe

Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:651-656

Focal dystonia of the jaw and the differential diagnosisof unilateral jaw and masticatory spasmPD THOMPSON, JA OBESO,* G DELGADO,t J GALLEGO,f CD MARSDEN

From the University Department ofNeurology, Institute ofPsychiatry & King's College Hospital MedicalSchool, London UK, the Movement Disorders Unit, Department ofNeurology, Clinica Universitaria, UniversityofNavarra,* and the Neurology Service, Hospital Provincial de Navarra,t Pamplona, Spain.

SUMMARY The clinical features, differential diagnosis and treatment of unilateral spasms of the jawand masticatory muscles are discussed and illustrated by eight cases of unilateral jaw spasms ofvarious aetiologies. These include focal dystonia of the jaw, hemimasticatory spasm with and with-out facial hemiatrophy, paroxysmal events in multiple sclerosis and tetany. Attention is particularlydrawn to four cases of unilateral dystonia of the jaw which has not been described before.

In a discussion of the "masticatory spasm ofRomberg", Gowers described several conditionswhich were associated with tonic or clonic jawspasms.1 He referred to tetanus, trauma, tetany,facial pain, hysteria, pontine lesions and coldexposure as causes of tonic spasm or trismus; he listedconvulsions, rigors, paralysis agitans, facial pain, andchorea among the causes of clonic jaw spasm. Suchspasms must be distinguished from the involuntarymovements of the jaw which occur in a number ofother conditions. These include generalised and cra-nial dystonia,2 acute dystonic reactions to neurolepticdrugs,3 tardive dyskinesia,3 tardive dystonia,4 dys-kinesias induced by levodopa and related drugs, andpost-encephalitic Parkinsonism.5 Trismus and bru-xism or teeth grinding may also be encountered inpseudobulbar palsies due to cerebrovascular disease.6Bruxism is also considered to be a manifestation ofanxiety.7 In addition, a variety of complicated masti-catory movements may be seen in epileptic automa-tisms and in response to oral or facial stimulation inpatients with severe damage of the cerebral hemi-spheres or brainstem.8 Finally, masticatory spasmmay occur in peripheral neuromuscular disorders thatresult in muscle spasms or cramp, and is a prominentlate feature of the clinical syndrome of progressivemuscle spasm, alopecia and diarrhoea.9

In most of these disorders, the jaw spasms are bilat-eral and occur as one facet of a generalised disorder of

Address for reprint requests: Professor CD Marsden, Department ofNeurology, Institute of Psychiatry, De Crespigny Park, LondonSE5 8AF, UK.

Received 1 October 1985. Accepted 18 November 1985

movement. In contrast isolated unilateral jaw spasmsare distinctly unusual. Apart from a number of casereports of masticatory spasm, most occurring in asso-ciation with facial hemiatrophy,10 -12 few referencesto unilateral jaw spasms are to be found in the litera-ture.The purpose of this report is to describe the clinical

features of eight patients with unilateral jaw spasmsof differing aetiologies causing unilateral deviation ofthe jaw and to discuss the clinical and electro-myographic differential diagnosis of this condition.

Methods

Four of the eight patients described in this report were seenin the Department of Neurology at the Maudsley Hospital,three in the Department of Neurology, University ofNavarra Medical School, Pamplona, Spain and one in theDepartment of Neurology, Sir Charles Gairdner Hospital,Perth. The patients were all females and their ages rangedfrom 24 to 60 years. Detailed electromyographic recordingsand electrophysiological studies of the facial and masti-catory muscles were performed in selected patients. TheEMG recordings were made using silver/silver chloride sur-face electrodes, placed over the muscles of interest, and con-centric needle electrodes were used to sample the motor unitdischarge pattern in the masseter, pterygoid and orbicularisoris muscles. The EMG signals were amplified (Devices 3120amplifier; band width from 80 Hz to 2 5 KHz, -3 dB, forboth surface and needle recordings) and recorded on a PDP12 computer (sampling rate 40 KHz). In patients 1, 3 and 5the EMG signals were recorded directly on magnetic tape(Racal store 7DS) for later analysis. In patients 4, 6, and 7the EMG recordings were made using a Medelec MS6 sys-tem. Exteroceptive suppression in the masseter muscles dur-ing masseter contraction (the masseter silent period), and theblink reflex and its recovery cycle were measured according

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Fig I EMG recordings (concentric needle electrodes) fromthe masticatory muscles in unilateraljaw dystonia (case 1).In the position ofmaximaljaw deviation, activity wasrecorded in the contralateral lateral pterygoid, while themasseter muscles were silent (right halfofrecord). Ifthepatientforcibly returned herjaw to the midline, and held it inthat position by clenching her teeth, the activity continued inthe pterygoid and was co-contracting with the masseter (lefthalfofrecord).

to the methods described by Berardelli et al.13 The latency ofthe masseter reflex was measured following mechanical stim-ulation of the jaw with a tendon hammer.

Case reports

Case I Isolated unilateraljaw dystoniaA 24-year-old woman first became aware of abnormal jawmovements at age 14 years when her jaw began to deviate tothe left. This would persist for several weeks at a time beforeresolving spontaneously. Over the following years the jawdeviation recurred intermittently, often lasting for severalmonths at a time before returning to normal. Each episodevaried in duration and the extent of lateral jaw deviation.During them she found it difficult to chew or talk. At timesshe experienced pain and tingling in the region of the leftmandible. The disfigurement produced by the jaw deviationcaused considerable embarrassment. She underwent severaltreatments including a variety of dental procedures and hadbeen prescribed a number of drugs, without benefit. Therewas no significant family history and she took no regularmedications. Examination during an attack revealed sus-tained deviation of the jaw to the left, giving the face anasymmetric appearance. When free of symptoms the exam-ination was normal. A number of investigations includinghigh resolution computed tomography of the brain and pos-terior fossa, cerebrospinal fluid examination and visual andauditory evoked responses were normal. EMG recordings ofthe motor unit potentials in the jaw muscles indicated thatsustained activity in the right lateral pterygoid was

Thompson, Obeso, Delgado, Gallego, Marsdenresponsible for the (contralateral) jaw deviation (fig 1). Themorphology of the motor units appeared normal. In thedeviated position activity was recorded only from the ptery-goid muscle. However, when the jaw returned to the mid-line(which the patient was able to achieve with some effort),co-contraction of the masseter and pterygoid muscles on theright was present (fig 1). The masseter reflex latencies werenormal (9 ms; R= L) as were the latencies of the early andlate components of the blink reflex (RI = l0ims, R2 =40 ms,R= L). The recovery cycle of the blink reflex was normal.

Benzhexol, in daily doses of 20 to 30mg, was initiallyeffective in almost completely abolishing the prolongedperiods of jaw deviation, although short episodes havesince reappeared.

Case 2 Unilateraljaw dystonia preceded by temporarytorticollisA 37-year-old woman developed torticollis with the chindeviated to the left, at age 30 years. This became increasinglytroublesome over a period of 2 years before resolving aftervigorous neck manipulation. A short time later she devel-oped involuntary opening of her mouth and deviation of thejaw to the left. She found chewing difficult and would oftenbite her tongue. These movements were painful and thesource of considerable embarrassment on account of the

Fig 2 Deviation ofthejaw to the right, producing anasymmetricface and giving the impression offacial weaknessin a patient withjaw dystonia and torticollis (case 3).

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Focal dystonia of the jaw and the differential diagnosis of unilateraljaw and masticatory spasm

Fig 3 Jaw dystonia in a patient with cranial and segmentaldystonia (case 4). Note the deviation ofthejaw to the left,left sided blepharoclonus, drawing ofthe lips to the left anddeviation ofthe protruded tongue to the left.

facial disfigurement they produced. Two years later shebegan to develop sustained spasms ofjaw opening, particu-larly when eating. She was also aware of a numb sensationaffecting the left side of the face. She had tried numeroustherapies and drugs without benefit. There was a family his-tory of retinitis pigmentosa. Examination revealed a pig-mentary retinopathy with constriction of the peripheralvisual fields. Intermittent spasms of the jaw muscles pro-duced jaw opening and/or deviation of the jaw to the left.Facial sensation, the corneal reflexes and the jaw jerk werenormal, as was the remainder of the examination.

Benzhexol, in a dose of 15 to 20mg per day, reduced butdid not abolish the involuntary movements.

Case 3 Unilateraljaw dystonia with torticollisA 42-year-old woman developed painful movements of thejaw with deviation of the jaw to the right following a dentalextraction, at age 35 years. The movements and the degree ofjaw deviation fluctuated during the 7 year history but neverdisappeared completely. The movements interfered withchewing and she often bit her tongue. A variety of dentalprocedures were performed without benefit, includingextraction of her remaining teeth. She had not been aware ofany other involuntary movements. There was a past historyof depression but she had not received any drugs before the

onset of the jaw movements. There was no significant familyhistory. Examination revealed sustained deviation of thejawto the right, producing an asymmetric face which gave theimpression of facial weakness (fig 2). Facial movements andsensation were normal. There was intermittent torticollis tothe right. The remainder of the examination was normal.Investigations including computed tomography of the brainwere normal.EMG recordings revealed normal motor unit morphology

and patterns of discharge in the masseter muscles. The mas-seter reflex latencies were normal (8 5 ms bilaterally) as wasthe masseter silent period on both sides. The blink reflexlatencies were also normal (RI = 12 ms and R2= 29ms;R= L) but the recovery cycle of the blink reflex following aconditioning stimulus was enhanced in a manner similar tothat described in patients with oromandibular dystonia andblepharospasm. I3Treatment with benzhexol in daily doses of between 25

and 35 mg lessened the severity of the jaw movements. How-ever, she became depressed and the treatment was graduallywithdrawn. The movements worsened but later improvedwith amitriptyline 100mg per day.

Case 4 Unilateraljaw dystonia with cranial and segmentaldystoniaA 22-year-old female developed deviation of the jaw to theleft and intermittent closure of the left eye, associated with atingling sensation of the left forehead. These symptomsresolved spontaneously over a period of 3 weeks butrecurred 4 weeks later. She has continued to experienceattacks, each lasting for weeks at a time, before settling, withsymptom free intervals lasting several weeks. There was nosignificant past history and no history of drug ingestion.Examination during an attack revealed intermittent blepha-roclonus of the left orbicularis oculi and sustained deviationof the jaw and lips to the left (fig 3). On protruding thetongue, it too deviated to the left. There was a torticollis withthe chin turned to the left and dystonic inversion of the out-stretched left arm. The remainder of the examination wasnormal. Investigations including computed tomography ofthe brain, vertebral arteriography and cerebrospinal fluidanalysis were normal. Visual and somatosensory evokedresponses were normal as were EMG recordings from theleft masseter and blink reflex latencies.Treatment with anticholinergics, carbamazepine, clonaze-

pam, haloperidol and tetrabenazine did not provide anyrelief.

Maswter aLL k L l6-L LL 16 L,50 uV

Fig4 Electromyographic (concentric needle electrode)recordingfrom masseter in hemimasticatory spasm withfacial hemiatrophy (case 5) illustrating the sudden onset andoffset ofbursts ofspontaneously discharging motor units.Note the variable burst duration lastingfrom 50 to 300ms asillustrated in thefirst three bursts. The next briefdischarge(20ms) isfollowed by two longer bursts each approximatelyof400 ms duration, punctuated by another short discharge.

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Case S Unilateral hemimasticatory spasm withfacialhemiatrophyA 38-year-old woman had been aware of abnormal pig-mentation of the right side of her neck, lower face and jawsince childhood. During her teens she was aware ofprogressive atrophy of these regions and a series of skinbiopsies revealed changes consistent with morphoea. At age31 years she developed spasms of the muscle of the right jawwhich caused it to close forcibly. Each spasm would beginwith a series of small "warning" contractions which she feltas a tightening of the face, and last for a second or two. Theywere often precipitated by mouth closure or movement ofthe jaw while eating. Opening the jaw would interrupt thespasm. If a prolonged spasm developed it would last forseveral minutes. She had bitten her tongue on numerousoccasions and at times the spasms woke her at night. Theyhad been temporarily abolished by mandibular anaesthesiaduring the fitting of a dental plate. A masseter myotomy didnot improve her symptoms but carbamazepine and phen-ytoin had greatly reduced the severity of attacks. She wasalso aware of spasm of the right lower lip which pulled thecorner of her mouth down on that side for several seconds ata time. Examination revealed patchy pigmentation of theskin and atrophy of the subcutaneous tissue of the right sideof the neck and face. The masseter was visibly hypertrophiedand repetitive contractions of it could be seen and palpatedduring a spasm ofjaw closure. The jaw jerk was present andthere was no weakness of jaw opening or closure. Facialsensation was normal as were facial movements when therewas no spasm of the lower facial muscles. Spasm and devi-ation of the lower lip down and to the right were presentintermittently and could be induced by stretching the lip.The remainder of the neurological examination was normal.EMG recordings from both masseter muscles revealed

spontaneous activity in the right masseter while the leftremained silent except during voluntary contraction. Thespasms in the right masseter consisted of repetitive, sponta-neous bursts of motor unit discharges, varying in durationfrom 20 to 400 ms (fig 4). Similar bursts were recorded in theright orbicularis oris muscle. The latency of the masseterreflex on the right (11Ims) was prolonged in comparison tothat on the normal side (7 ms). Blink reflex latencies werenormal (R1 = 10 ms, R2 = 35 ms; R = L) following stimu-lation of the right supraorbital nerve, as was the recoverycycle of the reflex following a conditioning stimulus. Theterminal latency of the facial nerve to the orbicularis orisfollowing stimulation anterior to the mastoid process wasnormal (3-4ms). She continues to take carbamazepine andphenytoin.

Case 6 Hemimasticatory spasm without facial hemiatrophyA 60-year-old woman presented with a 3 year history ofpainful spasm of the left temporalis and masseter muscles,the details of which have been reported previously.12 Thespasms were similar to those described in case 5, with repet-itive brief contractions of the masseter and temporalis mus-cles. They occurred spontaneously and were induced by jawclosure but interrupted by jaw opening. There was no evi-dence of facial hemiatrophy and there was unilateral hyper-trophy of the masseter and temporalis muscles involved.Numerous drugs were tried without benefit, and extensiveinvestigation failed to reveal any underlying structural

Fig 5 Complexfacial and masticatory movements inpossible multiple sclerosis (case 7). Note the spasm ofadduction of the left eye, contraction ofthefrontalis on thatside, with closure of the right eye and elevation of the rightcorner of the mouth and closure of thejaw which was deviatedto the right.

abnormality of the brain. The jaw jerk was absent on the leftand EMG recordings of the spontaneous activity were simi-lar to those described in case 5, with repetitive short bursts(20-100ms) of motor units and longer spasms lasting up to1 s.

Case 7 Paroxysmal unilateral spasms of thejaw, associatedwith possible multiple sclerosisA 28-year-old woman developed difficulty closing the righteye and deviation of the mouth to the left, which recoveredover several weeks. Two months later she developed shortattacks in which the mouth and jaw would deviate to theright and the right eye would close forcibly. These would lastfor 1 to 2 minutes and often recurred in bouts lasting severaldays. No precipitating factors were identified. There was nopast history of significance and she took no regular medica-tions. Examinations during an attack revealed that it wouldbegin with closure of the right eye followed by elevation ofthe right corner of the mouth and closure and deviation ofthe jaw to the right, accompanied by spasms of the rightorbicularis oculi, oris, mentalis, left frontalis and adductionof the left eye (fig 5). The remainder of the cranial nerveswere normal. When walking the right foot would adopt aposture of plantar flexion and inversion which would last aminute or so and subside with rest. There was no muscleweakness but the deep tendon reflexes were exaggerated,especially in the legs. The superficial abdominal reflexes wereabsent and the plantar responses were flexor.

Investigations including computed tomography of the

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Fig 6 Spasms in tetany (case 8) involving theface,jaw andlimbs. In addition to the bizarre distortion of thefacialmuscles and spasm of thejaw muscles, typical carpopedalspasm also is present.

brain, antinuclear factor, serum and urinary copper levels,visual and somatosensory evoked potentials and cere-brospinal fluid analysis were normal. EMG recordings fromthe orbicularis oculi and oris during an attack showed motorunits of normal morphology.

Brief attacks have continued without any obvious precip-itating factors.

Case 8 Unilateral spasm of the masticatory andfacialmuscles in tetanyA 32-year-old woman presented with episodic spasm of thejaw, face, neck and limb muscles. She was not aware of anyprecipitating factors or warning symptoms. Each attacklasted between 2 and 5 minutes and was followed by com-plete recovery. There were no associated symptoms. Herpast and family history were unremarkable and she did nottake any medications. A typical attack was observed tobegin with hyperventilation and some 30 seconds later shewould develop spasm of the facial and masticatory musclesproducing a bizarre distortion of the face (fig 6). The neckmuscles would then contract particularly on the left side, sothat her head turned to the right. In addition she woulddevelop carpopedal spasm with inversion and internal rota-tion of the feet. The injection of 1 g of calcium gluconateintravenously produced total relief of the symptoms in lessthan 1 minute. The EEG did not change during attacks andserum calcium levels were normal both during attacks andwhen free of symptoms.

DiscussionThe differential diagnosis of causes of unilateral jawspasms with or without involvement of the facialmuscles is shown in the table. Of these conditions,mechanical and inflammatory disorders of the tempo-romandibular joint and oromandibular region will beevident on clinical examination. Tetanus may have tobe borne in mind as cephalic tetanus has beendescribed with unilateral facial weakness and trismusas presenting symptoms."4 Focal motor epilepsy willbe distinguished by the brevity of attacks, the repeti-tive clonic nature of the jaw (and facial) contractions,spread of movements elsewhere and other ictal events.The remaining causes of unilateral jaw spasm withjaw deviation are relatively uncommon. Amongthese, focal dystonia of the jaw, presenting as an iso-lated involuntary movement with sustained lateraldeviation of the jaw is the least well recognised causeofjaw spasms. In the cases of unilateral jaw dystoniadescribed in this report, deviation of the jaw wouldpersist for several days to weeks at a time beforeremitting, only to be followed by a further episodeafter a symptom free interval. In two patients (cases 3and 4) the presence ofmore familiar dystonic posturesat other sites (the neck and arm) confirmed that thejaw movements were part of a dystonic syndrome. Ina further patient (case 2), jaw spasm was preceded bytorticollis (which had resolved spontaneously) andwas followed by the evolution of typical oro-mandibular dystonia, with spasms of jaw openingreplacing the spasms of jaw deviation. Such changesin the nature of the involuntary jaw movements inoromandibular dystonia have previously been de-scribed2 and illustrate the variable natural history ofdystonia. In one other patient (case 1), jaw dystoniawas the only abnormality, but this was similar in allaspects to the jaw spasms seen in the other threepatients (cases 2, 3 and 4) who had evidence ofdystonia elsewhere.

Investigation of these patients with jaw dystoniafailed to reveal any underlying abnormality of thebrain. Accordingly, they must be described as havingidiopathic or primary dystonia. The morphology anddischarge pattern of motor units recorded from themasseter, facial and the lateral pterygoid muscles (inTable Differential diagnosis ofabnormal unilateralinvoluntary movement of thejaw andface1. local/mechanical disorders of the mandible or

temporo-mandibular joint2. tetanus and trismus3. focal motor epilepsy4. unilateral dystonia of the jaw5. tonic spasms of multiple sclerosis6. hemimasticatory spasm, with or without facial hemiatrophy7. tetany8. hemifacial spasm (face only)9. facial myokymia (face only)

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cases 1 and 3) were normal. In one patient (case 1) itwas possible to record the continuous lateral ptery-goid activity that was responsible for the jaw devi-ation in the "resting" position. When the patientattempted to straighten her jaw and clench her teeth,cocontraction of the masseter and pterygoid muscleswas present. This example of jaw dystonia is similarto a further case cited by Gowers in whom fixed lat-eral deviation of the jaw was thought to be ". ..due tospasm in the pterygoids of one side...".' In onepatient (case 3) detailed study of the blink and masse-ter reflexes disclosed an abnormality similar to thatdescribed in patients with oromandibular dystoniaand blepharospasm"3 further supporting the postu-late that the jaw movements in this case were part ofa restricted cranial dystonia. Treatment with anti-cholinergic drugs considerably improved the jaw dys-tonia in three of the four patients.The second group of patients with isolated jaw

spasms described in this report present a unique syn-drome with characteristic clinical and electro-myographic features. Hemimasticatory spasm withfacial hemiatrophy has been the subject of numerousreports.'0 11 The present report illustrates examplesof hemimasticatory spasm occurring both with andwithout facial hemiatrophy. Clinically the spasmswere similar in both. They were often painful, thetongue was frequently bitten by the forceful jaw clo-sure while the spasms were precipitated by voluntaryjaw closure and inhibited by jaw opening. Electro-myographically, spontaneous repetitive short burstsof motor unit discharges and longer spasms wererecorded from the masseter and the masseter reflexeswere abnormal in both cases. The similarity of thesefindings to hemifacial spasm and neuromyotonia haspreviously been noted.'0 12 These features suggestthat a peripheral trigeminal nerve lesion is responsiblefor the spasms in this condition although conclusiveproof of this is lacking.

In one patient (case 7) with paroxysmal episodes ofunilateral facial and masticatory spasm a diagnosis ofmultiple sclerosis was suspected. Although it was notpossible to establish a definite diagnosis, the stereo-typed nature of the attacks and the monocularadduction spasm (of case 2 of Matthews, ref 15)resembled the clinical features of paroxysmal eventsin multiple sclerosis described by previousauthors.'5 16 The complex facial spasms and abnor-mal foot posture when walking observed in this casewere also similar to the descriptions paroxysmal dys-tonia in multiple sclerosis.'7

Involvement of the cranial musculature in tetany isunusual, but is well illustrated by case 8. The presenceof spasms involving the limb musculature and theirprompt resolution after intravenous calcium dis-tinguishes this case from the other causes of jawspasms.

Thompson, Obeso, Delgado, Gallego, Marsden

The authors thank Dr NP Leigh, Consultant neu-rologist, Southampton General Hospital for referringcase 1 and Dr WM Carroll Consultant neurologist,Sir Charles Gairdner Hospital, Perth, WesternAustralia, for permission to report case 6.

Refereoces

IGowers WR. Manual of Diseases of the Nervous System.3rd ed, Vol 2. London: J and A Churchill, 1899:204-8.

2 Marsden CD. Blepharospasm-oromandibular dystoniasyndrome (Breughel's syndrome). J Neurol NeurosurgPsychiatry 1976;39:1204-9.

3Marsden CD, Tarsy D, Baldessarini RJ. Spontaneous anddrug-induced movement disorders in psychoticpatients. In: Benson DF, Blumer D, eds. PsychiatricAspects of Neurologic Disease. New York, Grune andStratton, 1975:219-66.

'Burke RE, Fahn S, Jankovic J, etal. Tardive dystonia:Late-onset and persistent dystonia caused by anti-psychotic drugs. Neurology (NY) 1982;32:1335-46.

Von Economo C. Encephalitis Lethargica. Its Sequelae andTreatment. London: Oxford University Press, 1931:50.

6Jelasic F, Freitag V. Inverse activity of the masticatorymuscles with and without trismus: a brainstem syn-drome. J Neurol Neurosurg Psychiatry 1978;61:798-804.

7Rugh JD, Solberg WK. Psychological implications in tem-poromandibular pain and dysfunction. Oral Sci Rev1976;1:3-30.

8Jenkyn LR, Walsh DB, Culver CM, et al. Clinical signs indiffuse cerebral dysfunction. J Neurol NeurosurgPsychiatry 1977;61:798-804.

9Satayoshi E. A syndrome of progressive muscle spasm,alopecia and diarrhoea. Neurology (Minneap) 1978;28:458-71.

Kaufman MD. Masticatory spasm in facial hemiatrophy.Ann Neurol 1980;7:585-7.

l Lapresle J, Desi M. Scleroderma with progressive crossedatrophy involving the left side of the body and the face.Rev Neurol (Paris) 1982;138:815-25.

'2Thompson PD, Carroll WM. Hemimasticatory spasm: aperipheral paroxysmal cranial neuropathy? J NeurolNeurosurg Psychiatry 1983;46:274-6.

13 Berardelli A, Rothwell JC, Day BL, Marsden CD. Patho-physiology of Blepharospasm and Oromandibular Dys-tonia. Brain 1985;108:593-608.

Mayo J, Berciano J. Cephalic tetanus presenting withBell's palsy. J Neurol Neurosurg Psychiatry 1985;48:290.

Matthews WB. Paroxysmal symptoms in multiple sclero-sis. J Neurol Neurosurg Psychiatry 1975;38:617-23.

16 Espir MLE, Millac P. Treatment of paroxysmal disordersin multiple sclerosis with carbamazepine. J Neurol Neu-rosurg Psychiatry 1970;33:528-31.

'7Berger JR, Sheremata WA, Melamed MD. Paroxysmaldystonia as the initial manifestation of multiple sclero-sis. Arch Neurol 1984;41:747-50.



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Focal dystonia diagnosis of unilateral jaw masticatory · J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.49.6.651 on 1 June 1986. Downloaded from Focaldystonia ofthejawandthe