The Coexistence of Tics and

Dystonia

Lael A. Stone, MD, Joseph Jankovic, MD

\s=b\ We studied nine patients with motor and phonic tics and other features of Tourette's syndrome, who developed persistent dystonia in addition to their tics. All, except one, were males (mean age, 35.8 years; range, 8 to 59 years), and had onset of tics prior to age 18 years (mean age, 9 years; range, 1.5 to 17 years). None of the patients were treated with neuroleptic drugs prior to the onset of dystonia. Torticollis and blepharospasm were the most common forms of dystonia. Seven patients had a history of tics in first degree relatives. While these patients were seen in a specialized movement disorder clinic and may, therefore, represent a population with atypical and more severe symptoms, the high prevalence rate of dystonia (5.0% of all patients with Tourette's syndrome seen in the clinic) suggests that some patients with tics may have an increased risk for dystonia. (Arch Neurol. 1991 ;48:862-865)

clinical hallmark of Tour"|\/ ette's syndrome (TS), may be cate¬ gorized phenomenologically as either clonic (brief, jerklike) or tonic (sus¬ tained, dystonic) movements.1 Clonic tics are more commonly recognized and otor tics,

a

rarely represent a diagnostic problem. However, patients with tonic tics are often misdiagnosed as having idiopathic torsion dystonia (ITD).2 Tonic tics, phe¬ nomenologically similar to dystonic movements in ITD, hence the term dys¬

tonic tics, are not often recognized as a part of the spectrum of motor manifes¬ tations of TS.3 While dystonic tics re¬ semble dystonic movements seen in pa¬ tients with ITD,4 they differ in that they are usually accompanied by other feaAccepted for publication January 31,1991. From the Department of Neurology, Baylor College of Medicine, Houston, Tex. Reprint requests to the Department of Neurology, Baylor College of Medicine, 6550 Fannin, Room 1801, Houston, TX 77030 (Dr Jankovic).

including clonic motor and phonic tics. Furthermore, in contrast to ITD, dystonic tics do not result in per¬ sistent abnormal postures, they are not continuously repetitive, usually are not aggravated by voluntary movement, and they are more suppressible than dystonia. Like clonic tics, dystonic tics occur out of a background of normal mo¬ tor activity. Although dystonic tics occur in a ma¬ jority of patients with TS,3 the coexis¬ tence of TS and persistent dystonia is uncommon. The association of dystonia with essential tremor, myoclonus, and parkinsonism is well recognized,4"'' but the association of dystonia with tics, while previously noted,7"11 has not been fully characterized. We therefore stud¬ ied nine patients with the combination of TS and persistent dystonia. Although tures of TS,

the coexistence of the two movement disorders may be simply coincidental, it is possible that the two disorders share common pathophysiologic mechanisms. PATIENTS AND METHODS

The nine

patients included in this series of

tics-dystonia syndrome, were selected from a database of 223 patients with motor and

vocal tics and 1126 with various forms of dystonia. Medical records and videotapes for these patients were reviewed, and the data were coded and entered into a relational da¬ tabase. Ofthe tic patients, 181 met the fol¬ lowing Diagnostic and Statistical Manual of Meritai Disorders, Third Edition, Revised, criteria for TS: (1) both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently; (2) the tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a pe¬ riod of more than 1 year; (3) the anatomic

location, number, frequency, complexity, and severity of the tics change over time;

(4) onset before age 21 years; and (5) the symptoms could not be explained by action of

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psychoactive substance or by known central nervous system disease.12 Four pa¬ tients with coexistent tics and dystonia were excluded because they were exposed to neu¬ roleptic medications before the development of their dystonia and three additional pa¬ tients with TS were excluded because their dystonia followed local trauma and, there¬ fore, they may have had a peripherally in¬ duced dystonia. Our patients were unique because, in addi¬ tion to clonic, dystonic, or both types of tics typically seen in TS, they have persistent dystonia typically seen in ITD (Table). All patients in this series were videotaped. some

REPORT OF CASES

CASE 1. —This 8-year-old boy was noted to have a wobbling, rubbery gait from age 17 months. He had dystonic inversion of the right foot and truncal posturing when walk¬ ing. At the same time, he developed blinking, rolling of his eyes, throat clearing, sniffing, and supinating-pronating "shaking" of his hands. Examination was notable for blink¬ ing, eye opening, throat clearing, sniffing, and shaking ofthe hands, as well as shoulder shrugging and truncal extension. While walking, he exhibited dystonic extension of the left hand at the wrist. His dystonic gait consisted of irregular steps interrupted by intermittent flexion and tilting of his trunk to the right. He had dystonic inversion of his right foot, and his right leg crossed over the left. Trihexyphenidyl therapy improved his tremors, but treatment with haloperidol, carbamazepine, and clonidine had no effect on either the dystonia or the tics. Adminis¬ tration of tetrabenazine improved his gait, but because of drowsiness he was switched to fluphenazine, which resulted in mild im¬ provement of his dystonia and tics. His fa¬ ther has motor and vocal tics and severe writer's cramp since high school. A paternal first cousin also has multifocal tics and a pa¬ ternal aunt and grandfather also have hand tremors.

CASE 2.—This

33-year-old

man

noted in¬

voluntary, intermittently repetitive opening and closing of the jaw at 4 years of age. At 9 years old, he began to produce throat clear-

Demographics, Type Age

at

Onset,

of Tic, and

Type

of

y

Patient/

Gender/Age, y

Tics

2/M/33

4

1.5

3/M/57 4/M/51 5/M/27 6/M/31

Dystonia 1.5

Latency, y_ Initial Tic 0 Body jerking, blinking

29

17_55 10_36 3 9

right with slight retrocollis, and shrugging of

Dystonia*

13 30

Type of Dystonie

25_Jaw opening-closing

38_Blinking 26_Blinking, 10

Blinking

21

_Blinking

B, OMD, SD, C sniffing

B, OMD, SD Blinking, grimacing H-A 20 9/F/36 8 Blinking, limb jerking 28 *B indicates blepharospasm; G, generalized dystonia; OMD, oromandibular dystonia; SD, spasmodic dysphonia; C, cervical dystonia (eg, torticollis); and -A, hand-arm. 7/M/59

16

47

ing, singing, humming, and other noises, as well as increased blinking and constant Ste¬ reotypie movements of his fingers, hands,

and feet. In addition to these tics, he has had a variety of compulsions such as checking and rechecking that appliances are off and watch¬ ing the gas gauge in the car. He has had no coprolalia or copropraxia. At age 29 years he noted jerking of his head to the left, which evolved into a sustained, painful torticollis to the left. He had received only clonazepam therapy with minimal improvement in tics. On examination he was anxious and exhib¬ ited prominent palilalia repeating "ok, ok," frequently clearing his throat and grunting. In addition to frequent blinking, he shrugged and anteriorly rotated his left shoulder and exhibited several complex tics, particularly tapping his left shoulder with the left hand. He had blepharospasm and persistent torti¬ collis to the left with contraction and hyper¬ trophy ofthe right sternocleidomastoid mus¬ cle. Even with effort he could not volitionally hold his head in primary position. A year later, his torticollis was more severe and it interfered with activities of daily living. Roentgenographic examination of the cervi¬ cal spine showed no evidence of subluxation. With 75 mg/d of tetrabenazine his tics moder¬ ately improved, but there was no improve¬ ment in dystonia. His father, 62 years old, was described as "nervous" with frequent throat clearing, cursing, and involuntary twitching movements. The patient's pater¬ nal grandmother had severe jerking of the head and facial muscles. A brother also has abnormal, jerklike head movements. CASE 3.—A 57-year-old man presented with involuntary eye closure for 15.5 years, and worsening jaw clenching. The patient noted periods of excessive blinking at age 17 years, with facial grimacing and throat clear¬ ing occurring soon thereafter. These motor and phonic tics have continued and, at age 40 years, he developed neck pain and difficulty turning his head. At age 55 years he first noted blepharospasm. Administration of hal¬ operidol increased the blepharospasm, and it was discontinued. Lorazepam and carbama¬ zepine therapy were tried without benefit. Botulinum toxin injections into his eyelids provided only a temporary relief. After two orbicularis oculi myectomies his blepharo¬ spasm improved, but the jaw clenching and

31

Neck jerk/stretch

in his throat, platysmal contrac¬ tions, and voice strain increased. On examination, the patient had evidence

tightness

of spasmodic dysphonia and dysarthria with gulping and throat-clearing sounds. He had rhythmic 1/second contractions of the soft palate, protrusion ofthe lower jaw with facial grimacing, and contraction of the platysmal muscles. He had torticollis to the right, and

anterocollis, with contractions ofthe left tra¬ pezius and left sternocleidomastoid muscles. There was a low-amplitude and rapid postur¬

al tremor in his hands. Administration of tetrabenazine failed to improve his involun¬ tary movements and he became increasingly disabled. He obtained only partial relief from receiving clonazepam. His brother, 45 years old, has excessive blinking and "ner¬ vousness." CASE 4.—This 51-year-old man has had frequent blinking, facial grimacing, sniffing, and other noises since early childhood. His mother was described as "very hyper" hav¬ ing many features of obsessive-compulsive behavior. The patient also describes himself as "hyper." At age 36 years he noted pain in the right posterior neck region and spasmod¬ ic involuntary turning ofthe head to the right and backward. Examination showed fre¬ quent bursts of blinking without blepharo¬ spasm, facial grimacing, and spasmodic torti¬ collis to the right and retrocollis associated with contractions ofthe right splenius capitis and trapezius muscles. The cervical dystonia improved after treatment with botulinum toxin. CASE 5.—This 27-year-old electronics technician began to have increased blinking at age 3 years. At age 10 years, he developed grunting, throat clearing, and left shoulder shrugging with involuntary pulling of the neck to the side. At age 13 years, he had dystonic turning ofthe head to the right and pain on the left side ofthe neck and shoulder. His scapula protruded and his shoulder shrugged almost continuously. The involun¬ tary movements improved with tetrabena¬ zine therapy, especially when trihexyphenidyl was added. His father has had lifelong blinking, neck pulling, and arm movements. His paternal grandmother also has blinking and neck pulling, and his paternal grandfa¬ ther had "St Vitus dance." An examination showed increased blinking, torticollis to the

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the left shoulder. CASE 6.—This 31-year-old man noted eye twitching at age 9 years, accompanied by facial grimacing. He later manifested other motor and vocal tics as well as sniffing. Torti¬ collis to the left appeared at age 30 years. Treatment with trihexyphenidyl caused re¬ markable improvement in his torticollis. On examination, in addition to the cervical dys¬ tonia manifested by marked torticollis to the left side and marked hypertrophy ofthe right sternocleidomastoid muscle, the patient had facial grimacing, sniffing, and contraction of paranasal muscles. His son, 13 years old, has facial grimacing and blinking, and the pa¬ tient's father made sucking sounds. A pater¬ nal grandmother licked her lips and made sucking and grunting sounds. Case 7.—A 59-year-old man presented with complaints of eye closure, facial grimac¬ ing, and voice change for over 6 years. At age 16 years the patient had involuntary stretch¬ ing of his neck with head turning and neck extension. He also developed severe throat clearing that worsened at age 21 years. At 47 years old he noted a drawing sensation in the left arm with an involuntary spasm ofthe left eyelids. The left eye winking progressed to bilateral blepharospasm. Treatment with benztropine and haloperidol were tried with¬ out relief, and treatment with baclofen and trihexyphenidyl produced only minimal im¬ provement. In addition to the blepharo¬ spasm, he had marked facial grimacing, lip pursing, and lip smacking. The tics were su¬ perimposed on oromandibular dystonia. His voice became increasingly strained and dur¬ ing conversations he had frequent voiceless pauses. He had bursts of sequential head turning to the left, shrugging of the left shoulder, and jerking ofthe right leg. Tetra¬ benazine improved the tics but caused unac¬ ceptable restlessness. Fluphenazine and pi¬ mozide were tried but the patient felt they worsened his difficulties. Examination re¬ vealed sustained blepharospasm, spasmodic dysphonia, facial grimacing, lip pursing, head jerking, and left shoulder shrugging. CASE 8.—This 20-year-old man had onset of facial grimacing and blinking at age 13 years. Additionally, he involuntarily extend¬ ed the fingers of his left hand and had contin¬ uously hummed and sang. At age 18 years, he had the onset of torticollis for which he was treated with haloperidol and trihexypheni¬ dyl for approximately 1 year. On physical examination, in addition to frequent blinking and intermittent head jerking, he had retro¬ collis with contraction of both splenius capitus muscles, left more than right, and hyper¬ trophy of the left sternocleidomastoid muscle. The retrocollis improved remark¬ ably with botulinum toxin injections into his splenius capitus muscles. His father, 44 years old, has head jerking, typing motions with his fingers, and sniffing. The paternal grandfather and grandmother had throat

clearing.

CASE 9.—When she

was

8 years old, this be "hyper¬

36-year-old woman was noted to

active" with a "short attention span." She also had a variety of involuntary movements such as blinking, facial grimacing, arm and leg jerking, and vocalizations, including coughing, throat clearing, and whistling (her

nickname was "whistler"). She also frequent¬ ly shouted obsenities. The "hyperactivity" was initially treated with methylphenidate, but her motor and other behavioral symp¬ toms have persisted. She also describes her¬ self as a worrier and a "workaholic," often staying at work until 3 AM. She has many other features of obsessive-compulsive be¬ havior and these symptoms improved re¬ cently with fluoxetine treatment. Her moth¬ er and brother were described as restless and very "hyper." At age 28 years, she began to notice painful cramping in her hand when writing, associ¬ ated with a very tight grip on the pen and involuntary flexion at the wrist. In addition to the mutifocal tics, frequent coughing, throat clearing, and coprolalia, the examina¬ tion showed dystonic posturing of the right hand. The dystonic flexion at the wrist was accompanied by very tight grip on the pen when writing and an elevation of the elbow. The hand dystonia initially benefited from treatment with benztropine and later from botulinum toxin injections into the forearm muscles. RESULTS

In this group of nine patients with coexistent TS and dystonia, with a mean age of 35.8 years (range, 8 to 59 years), there were eight males and one female (Table). The mean age at onset of tics was 9 years (range, 1.5 to 17 years). Eight patients had a mean latency of 22 years (range, 10 to 38 years) between onset of their tics and dystonia, while one patient had simultaneous appear¬ ance of dystonia and tics at age 17 months. Brain-imaging studies were

performed on seven patients (computed tomographic scan in four and magnetic resonance imaging in three); only one had an abnormal scan showing asymme¬ try with the left cerebral hemisphere slightly larger than the right. Multiple motor tics and at least two vocal tics were witnessed in all patients. The distribution of dystonias was as fol¬ lows: focal in six, segmental in two, and generalized in one. Torticollis was the most common form of dystonia, seen in six patients (Table). In three patients, the presenting tic and the dystonia were found in the same or in a closely related body part. The patient with generalized dystonia began with whole body jerks. Tics were present in first-degree rela¬ tives of seven patients, but dystonia (writer's cramp in the patient's father) and tics were present in only one pa¬ tient. Four patients had a history of tics in second- and third-degree relatives, all paternal. The tics and dystonia responded vari¬ ably to different therapies. Tetrabena¬ zine therapy improved tics in all six pa¬ tients in whom it was tried, but it had to be discontinued due to side effects in two. Treatment with trihexyphenidyl

benztropine improved dystonia in patients. Botulinum toxin injections were effective in relieving fo¬ cal dystonia at least temporarily in five patients. or

five of seven

COMMENT

This study draws attention to the pos¬ sible association between TS and dys¬ tonia. All nine patients described in this article have the unusual combination of tics and persistent dystonia. The dys¬ tonia in these patients is different from dystonic tics; it consists of continuously twisting (eg, torticollis) and spasmodic

(eg, blepharospasm) movements typi¬ cally seen in patients with ITD. All pa¬ tients fulfilled the diagnostic criteria for TS.12,13 The tics preceded the onset of dystonia by 0 to 31 years. Since tics are relatively common, it is possible that the coexistence of tics and dystonia in our patients is merely a chance occur¬ rence. Alternatively, it is possible that tics and dystonia share common patho¬ genic mechanisms and that their ex¬ pression is age-determined, tics usually preceding the onset of dystonia. The association of tics with other neu¬ and neurobehavioral disor¬ ders14,10 is well established. However, a possible link between TS and dystonia has not been previously explored. Our patients with coexistent TS and dys¬ tonia are similar to the four patients presented by Shale et al9 and the four described by Lees et al.8 Our nine pa¬ tients with TS and dystonia may pro¬ vide further support for the hypothesis that the two movement disorders are pathophysiologically related. Further evidence for the possible as¬ sociation of tics and dystonia is the oc¬ currence of both in different members of a family. Tolosa7 found a high preva¬ lence of facial tics among relatives of patients with cranial dystonia. Elston et al11 described a family in which three generations were affected with eye-

rologic4"6

winking tics, blepharospasm, or both, with two family members exhibiting other dystonias, torticollis, and oro¬ mandibular dystonia as well. They sug¬ gested that common pathophysiologic

mechanisms underlie the facial tics and the focal dystonia (blepharospasm). We previously encountered a family in which different members had varying combinations of increased blinking, ble¬ pharospasm, oromandibular dystonia, essential tremor, TS, obsessive-com¬ pulsive behavior, and sleep disorders.10 We studied two other families with one or more members having TS or dys¬ tonia. However, because none of the patients in these families had the simul¬ taneous occurrence of tics and dystonia, they were not included in this series.

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We also excluded seven TS patients with possibly secondary (drug induced and peripherally induced) dystonia. The prevalence of dystonia and of tics is unknown and the findings of pub¬ lished epidemiologie studies are difficult to interpret because of méthodologie problems.16'19 Furthermore, it would not be appropriate to apply epidemiologie data from the general population to a population of patients seen in a special¬ ized clinic. If the relatively high preva¬ lence of dystonia (nine [5.0%] of 181 patients with TS) found in our patients with TS, can be verified by a longitudi¬ nal, population-based study, it could in¬ dicate that the coexistence of the two hyperkinetic movement disorders is more than just a chance occurrence. Al¬ ternatively, our study suggests that the prevalence of TS in a population of dys¬ tonic patients is 0.8% (nine of 1126 pa¬ tients with dystonia), three times high¬ than found in the general er population.16 If there is an association between TS and dystonia, this could have diagnostic and therapeutic impli¬ cations. Because tics usually precede the onset of dystonia, the clinician should be alert to the possibility of un¬ derlying TS in patients with dystonia.

Furthermore, dopamine receptorblocking drugs, frequently used in the symptomatic treatment of TS, should be used cautiously in those patients who have associated dystonia. What clinical features

or

mecha¬

nisms, shared by both tics and dystonia,

might link the two hyperkinetic move¬ ment disorders? Dystonic movements are

due to excessive cocontraction of

antagonist muscles with overflow of contractions to adjacent or to remote muscles.3,20 Rapid dystonic movements, phenomenologically similar to dystonic tics, may be seen in patients with ITD. In contrast to dystonic tics, however, rapid dystonic movements associated with ITD are continuously repetitive and remain localized to the same group of muscles. Muscle contraction produc¬ ing typical clonic tic lasts 50 to 500 milli¬ seconds, whereas dystonic movement consists of a sustained contraction of agonist and antagonist muscles lasting at least 1 second.20 Electrophysiologic

recordings, however,

cannot

reliably

differentiate between dystonic move¬ ments, such as those seen in ITD, and dystonic tics. The accompanying fea¬ tures of torsion dystonia or TS should help to distinguish the two hyperkinetic disorders. Both tics and dystonia have been at¬ tributed to a dysfunction in the basal ganglia21 and brain stem.22 Evidence of brain-stem neuronal hyperexcitability, suggested by abnormal blink reflex re-

covery cycles, has been found in both dystonia and TS.20,23,24 Patient 2 had se¬ vere head jerking, which progressed to a sustained cervical dystonia suggest¬ ing the possibility that in this patient the tics might have contributed to a posttraumatic dystonia.2" Tardive dys¬ tonia due to antidopaminergic drugs is another mechanism by which patients with TS may develop dystonia.26 Our patients, however, exhibited their dys¬ tonias prior to prolonged neuroleptics. Differing effects of pharmacologie agents on tics and dystonia suggest that

the two movement disorders have dif¬ ferent neurotransmitter mechanisms. Improvement of tics with antidopamin¬ ergic agents suggests that the dopamin-

ergic system is important in the patho¬ physiology of TS. This is further supported by the patient with TS who was reported to have improvement of his tics after the onset of parkinsonism.27 Further, two brothers with tics due to

neuroacanthocytosis were previously described as having improved when parkinsonism developed.0 In contrast, dystonias often worsened in these pa¬ tients by the addition of antidopaminer¬ gic agents, but improved with anticho¬ linergic agents. These examples support the contention that the study of coexistent movement disorders may

provide insight into the pathogenesis of either or both hyperkinesias. Both tics and dystonia are genetically

determined, usually transmitted in

an

autosomal dominant pattern. While the coexistence of the two disorders may occur by chance alone, it is possible that the two disorders are linked by some common pathogenic mechanisms. If such a link can be confirmed, it could be partly explained by a variable expres¬ sion (tics, dystonia, or both) ofthe same genetic defect or by a close linkage be¬ tween the dystonia and the TS gene.28 These hypotheses could be tested by screening and segregation analyses of large families with TS for the dystonia marker, recently localized to chromo¬ some

9q32-q34.29

We thank K. Schwartz, assistance.

PA, for

his technical

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33:1237-1240. 23. Tolosa E, Monserrat L, Bayes A. Reduction of brainstem interneuron excitability during voluntary tic inhibition in Tourette's syndrome. Neurology. 1986;36(suppl 1):118-119. 24. Smith P, Lees A. Abnormalities in blink reflex in Gilles de la Tourette syndrome. J Neurol

Neurosurg Psychiatry. 1989;52:895-898. 25. Jankovic J, Van der Linden C. Dystonia and tremor induced by peripheral trauma: predisposing factors. J Neurol Neurosurg Psychiatry. 1988; 51:1512-1519. 26. Singh SK, Jankovic J. Tardive dystonia in patients with Tourette's syndrome. Mov Disord.

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The coexistence of tics and dystonia.

We studied nine patients with motor and phonic tics and other features of Tourette's syndrome, who developed persistent dystonia in addition to their ...
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