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PubMed2003

New perspectives on dystonia.

Dystonia is a syndrome of sustained muscular contractions with numerous underlying etiologies. This review examines the varied phenomenology of dystonias, its evolving classification including recent genetic data as well as its clinical investigation and treatment. Although age of onset, anatomical distribution and family history are key elements of the investigation of dystonia, classification increasingly relies on etiologic and genetic criteria. Physiological abnormalities in striato-cortical circuits are common in dystonia but the pathophysiology is still unclear. In recent years, a great deal has been learned on the more common primary dystonias such as primary torsion dystonia and on dystonia-plus syndromes such as dopamine responsive dystonia. Treatment of dystonia has also evolved and there are now a number of therapeutic agents with clear beneficial effects including anticholinergics, benzodiazepines, and botulinum toxin and there is growing interest in neurofunctional surgery including deep brain stimulation.

Blepharospasm↗
PubMed2000

Elevated plasma levels of homocysteine in dystonia.

OBJECTIVE: Several case reports with dystonia and homocysteinuria suggest a putative pathogenetic importance of homocysteine for the development of dystonia. We investigated relations between plasma homocysteine, age, severity and duration of primary idiopathic torsion dystonia. SUBJECTS AND METHODS: We measured homocysteine levels in blood samples drawn from 24 subjects with dystonia and controls. RESULTS: Patients with dystonia (19.3 +/- 8.5, range 8.4-37 micromol/l) showed significantly (P= 0.008, t-test) increased levels of total homocysteine compared with age- and sex-matched controls (13.9 +/- 4.2, range 5.8-24.5 micromol/l). No significant influence of age and duration of dystonia appeared, but we found a significant trend for an association between severity of dystonia and homocysteine (P = 0.046, R = 0.41). CONCLUSIONS: Our study supports previous reports on subjects with dystonia with homocysteinuria. Neurotoxic effects and N-methyl-D-aspartate agonistic properties of homocysteine may hypothetically contribute to onset and severity of dystonia.

Adult↗
PubMed2001

Review of the functional surgical treatment of dystonia.

A review of functional surgery for dystonia is presented. Recently renewed interest in stereotaxy for dystonia has followed the resurgence of pallidotomy and the introduction of deep brain stimulation (DBS) in Parkinson's disease (PD) in the early 1990s. However, even since the 1950s, small series of patients treated with ablative surgery have been carefully studied, providing useful information, notably regarding the tolerability of surgery. In the setting of dystonia, thalamotomy was first performed with substantial benefits, but some authors outlined the great variability in outcome, and the high incidence of operative side-effects. In the 'modern' era of functional surgery for movement disorders, the globus pallidus internus (GPi) has emerged to be currently the best target for dystonia, based on small series of patients published in the last few years. Both bilateral posteroventral pallidotomy (PVP) and bilateral pallidal stimulation, performed by several teams, have benefited a variety of patients with severe dystonia, the most dramatic improvements being seen in primary dystonia with a mutation in the DYT1 gene. Whereas patients with secondary dystonia have often shown a lesser degree of improvement, some publications have nevertheless reported major benefit. There is today a strong need for carefully controlled studies comparing secondary and primary dystonia, DYT1 and non-DYT1 dystonia, ablative surgery and DBS, with additional assessment of neuropsychological changes, especially in children treated with bilateral pallidal procedures.

Dystonia↗
PubMed1999

Bruxism and cranial-cervical dystonia: is there a relationship?

To characterize the relationship between bruxism and dystonia, 79 patients (28 men and 51 women) with cranial-cervical dystonia were studied. Sixty-two patients (78.5%), 22 men and 40 women, had bruxism. The mean age at onset of dystonia in patients with bruxism was 52.4 +/- 12.6 years (range 14-80), similar to patients with cranial-cervical dystonia without bruxism. Involuntary oromandibular movements (46 patients) and blepharospasm (34 patients) were the most common initial symptoms among patients with dystonia. About one-fourth of bruxism patients had associated dental problems including TMD (21%) and tooth wear (5%). A majority (58%) of the bruxism patients had diurnal bruxism and 12% had nocturnal bruxism. The bruxism patients were compared to 100 patients with Parkinson's disease (PD), cervical dystonia, cranial dystonia, and normal controls, respectively. The prevalence of bruxism was much higher in the cranial-cervical dystonia patients when compared to normal controls (P < 0.001); however, this difference was not significant between other diseased groups and controls. Medications and botulinum toxin injections, used in the treatment of focal dystonia also provided effective relief of bruxism.

Adolescent↗
PubMed1998

The natural history of tardive dystonia. A long-term follow-up study of 107 cases.

The clinical picture, risk factors and natural history of tardive dystonia resulting from dopamine-receptor antagonist (DRA) treatment in 107 patients (57 male and 50 female), seen between 1972 and 1995, are described. The mean age at onset (+/- SD) was 38.3 +/- 13.7 years (range 13-68 years), and the age at last follow-up was 46.3 +/- 15.7 years (range 15-80 years). These patients had received DRAs for schizophrenia (39%), for other psychiatric conditions (51.5%) and for non-psychiatric disorders (9.5%). All classes of neuroleptics used were implicated in producing tardive dystonia, which was found to develop at any time, ranging from 4 days to 23 years after their introduction (median 5, mean 6.2 +/- 5.1 years); there was no 'safe' period. Men were significantly younger than women at onset of dystonia, which developed after shorter exposure in men. At onset, the dystonia was focal in 83% of cases, but progressed over months or years and remained focal in only 17% at the time of maximum severity. The craniocervical region was involved in 87% of cases, and was the most commonly affected site both at onset and at maximum severity. There was a correlation between the site and age of onset; the site of onset ascended from the lower limbs to the face as the mean age of onset increased. Overall, the phenomenology of tardive dystonia was indistinguishable from that of primary (idiopathic) dystonia, although retrocollis and anterocollis, as well as torticollis to the right, were significantly more common in tardive dystonia. It is a very persistent disorder; only 14% of our patients had a remission over a mean follow-up period of 8.5 years. Remission occurred after a mean of 5.2 years from onset (range 1-12 years) and 2.6 years after discontinuation of neuroleptics (range 1 month to 9 years). Discontinuation of neuroleptics increased the chances of remission fourfold. Patients with < or = 10 years on neuroleptics had a five times greater chance of remission than those with > 10 years exposure, suggesting that the pathogenetic changes in tardive dystonia may become irreversible after long-term use of these drugs. None of the numerous treatments tried in these patients, including clozapine and botulinum toxin injections, seemed to relate to overall outcome, but there was a significant negative association between the occurrence of remission and the use of benzodiazepines. Although there were hints of a possible genetic predisposition, the question as to whether patients with tardive dystonia have an underlying vulnerability remains unanswered.

Adolescent↗
PubMed2004

The syndrome of fixed dystonia: an evaluation of 103 patients.

We describe the clinical features of 103 patients presenting with fixed dystonia and report the prospective assessment and investigation of 41 of them. Most patients were female (84%) and had a young age of onset [mean 29.7 (SD 13.1) years]. A peripheral injury preceded onset in 63% and spread of dystonia to other body regions occurred in 56%. After an average follow-up of 3.3 years (overall disease duration 8.6 years), partial (19%) or complete (8%) remission had occurred in a minority of patients. The fixed postures affected predominantly the limbs (90%), and rarely the neck/shoulder region (6%) or jaw (4%). In the prospectively studied group, pain was present in most patients and was a major complaint in 41%. Twenty percent of patients fulfilled criteria for Complex Regional Pain Syndrome (CRPS). No consistent investigational abnormalities were found and no patient tested (n = 25) had a mutation in the DYT1 gene. Thirty-seven percent of patients fulfilled classification criteria for documented or clinically established psychogenic dystonia; 29% fulfilled DSM-IV (Diagnostic and statistical manual of mental disorders, 4th edition) criteria for somatization disorder, which was diagnosed only after examination of the primary care records in many cases; and 24% fulfilled both sets of criteria. Ten percent of the prospectively studied and 45% of the retrospectively studied patients did not have any evidence of psychogenic dystonia, and detailed investigation failed to reveal an alternative explanation for their clinical presentation. Detailed, semi-structured neuropsychiatric assessments in a subgroup of 26 patients with fixed dystonia and in a control group of 20 patients with classical dystonia revealed dissociative (42 versus 0%, P = 0.001) and affective disorders (85 versus 50%, P = 0.01) significantly more commonly in the fixed dystonia group. Medical and surgical treatment was largely unsuccessful. However, seven patients who underwent multidisciplinary treatment, including physiotherapy and psychotherapy, experienced partial or complete remission. We conclude that fixed dystonia usually, but not always, occurs after a peripheral injury and overlaps with CRPS. Investigations are typically normal, but many patients fulfil strict criteria for a somatoform disorder/psychogenic dystonia. In a proportion of patients, however, no conclusive features of somatoform disorder or psychogenic disorder can be found and, in these patients, whether this disorder is primarily neurological or psychiatric remains an open question. Whilst the prognosis is overall poor, remissions do occur, particularly in those patients who are willing and able to undergo multidisciplinary treatment including physiotherapy and psychotherapy, suggesting that this type of treatment should be recommended to these patients.

Adolescent↗
PubMed1984

The treatment of severe dystonia in children and adults.

Twenty-three children (aged less than 18 years) and 17 adults with severe widespread dystonia were treated with high doses of benzhexol (up to 130 mg daily introduced slowly over many weeks). Children tolerated higher doses (median 30 mg/day) than adults (median 20 mg/day). 52% of the children gained useful benefit, many (43%) without unwanted side effects. Such an approach was less successful in adults; 41% gained benefit, but only 35% had no side effects. Twelve adults with severe axial dystonia, and two children with life-threatening generalised dystonia were treated with a combination of a low constant dose of tetrabenazine to which were added pimozide and benzhexol as necessary. The dose of tetrabenazine was aimed at 75 mg daily; pimozide was increased (6 to 25 mg/day) until the dystonia was relieved or Parkinsonism and other side-effects prevented further increments; if necessary benzhexol (6 to 30 mg/day) then was added to control side-effects and to provide additional benefit. 75% of the adults with severe axial dystonia, and one of the two children with life threatening generalised dystonia gained useful benefit from this regime. It is concluded that high dose benzhexol is the present first treatment of choice for children with severe dystonia, and is worth a try in adults but with less expectation of success. When benzhexol treatment alone fails in adults with severe disabling axial dystonia, or in children with life-threatening generalised dystonia, combined therapy with tetrabenazine, pimozide and benzhexol may give valuable symptomatic relief.

Adolescent↗
PubMed1989

Clinical variants of idiopathic torsion dystonia.

Some patients with dystonic movements and postures not known to be caused by environmental or degenerative disorders can be segregated from classical-appearing idiopathic torsion dystonia on the basis of distinctive clinical and pharmacologic features. Many of them should be considered within the family of dystonia, as clinical variants of idiopathic torsion dystonia, while others are better classified as being part of other families of dyskinesias. In the former group are paradoxical dystonia, myoclonic dystonia, diurnal dystonia, and dopa-responsive dystonia. The latter group consists of dystonic tics and the various entities comprising paroxysmal dystonia, namely kinesigenic, nonkinesigenic and hypnogenic dystonia.

Diagnosis, Differential↗
PubMed1997

Clinical features and natural history of axial predominant adult onset primary dystonia.

The clinical features and natural history of 18 patients with adult onset axial predominant severe truncal primary dystonia are presented. The mean age of onset was 41 (42 for men, 39 for women) and there was a higher proportion of men (10:8). Analysis of their clinical features and follow up over three to five years or more showed that these patients generally conform to the characteristics of other types of adult onset primary dystonias. They tended to remain focal although there could be an initial contiguous spread, sometimes beginning in the craniocervical region and spreading axially or, rarely, vice versa. If spread occurred, involvement of the head, neck, and arms was mild in comparison with the severe dystonia of the trunk. However, in none of the patients with craniocervical or truncal onset did the dystonia spread to involve the legs. More than a third (seven of 18) of the patients had a prior history of injury at the site subsequently affected by dystonia. Treatment response to various drugs overall was poor but a third of the patients improved on treatment either with triple therapy (a combination of tetrabenazine, pimozide, and an anticholinergic drug) or high dose anticholinergic drugs alone. Severe depression occurred in 33% of patients, mainly due to the negative personal image arising from their disfiguring dystonia. None of the patients had a family history of dystonia and at the moment it is unclear whether these patients with sporadic axial dystonia are non-genetic phenocopies or are a manifestation of one or more of the genes that cause generalised dystonia or torticollis.

Adult↗
PubMed1999

Disturbances of dynamic balance in phasic cervical dystonia.

OBJECTIVE: To quantitatively assess control of balance under static and dynamic conditions in patients with tonic and phasic cervical dystonia. METHODS: Ten patients with purely tonic cervical dystonia with fixed postural deviation and 20 patients with cervical dystonia with phasic head movements were investigated at least 3 months after botulinum toxin injections. Seventeen age matched volunteers served as controls. Static posturography was performed on a force platform; dynamic equilibrium was studied on a stabilometer, which requires the subject to continuously adapt upright posture to an unstable tilting surface. Measurements of maximum amplitude and linear displacement of the pivot were taken with open and closed eyes. RESULTS: Sway path values in static posturography were not significantly different between patients with cervical dystonia and controls. On dynamic posturography, patients with phasic cervical dystonia showed significantly higher platform measures (maximum amplitude and linear displacement of the pivot) with eyes open and closed By contrast, none of the dynamic platform measures differed significantly between patients with tonic cervical dystonia and controls. CONCLUSIONS: Normal measures of dynamic equilibrium in tonic cervical dystonia argue against a primary abnormality of balance control in cervical dystonia. Impaired dynamic equilibrium in phasic cervical dystonia is likely to reflect a disruption of vestibular input due to repetitive, involuntary head oscillations.

Adult↗
PubMed2005

Reaching movements in childhood dystonia contain signal-dependent noise.

When reaching, children with dystonia exhibit movements that are slower and more variable than normal children. We hypothesize that in dystonia there is an increase in signal-dependent noise so that there is increased variability with increasing speed. This hypothesis predicts that slower movement in children with dystonia is at least partly due to a compensatory strategy to reduce variability by decreasing speed. To test this hypothesis, we measured the speed of arm movement while children attempted to contact buttons of different sizes. We tested 23 control children and 15 children between the ages of 4 and 16 years with dystonia owing to either cerebral palsy, idiopathic dystonia not due to the DYT1 (torsin A) mutation, or other identified causes. A consistent inverse relationship between movement time and button size was seen for both the control children and the children with dystonia. The variance of movement speed increased with the average speed for all subjects. Children with dystonia moved significantly more slowly at all button sizes, and their movement speed was more sensitive to changes in button size. Therefore, part of the reduction in speed in dystonia is due to relatively greater difficulty in contacting small targets. This finding is consistent with the hypothesis of increased signal-dependent noise in children with dystonia, and we present a simple computational model that provides a possible explanation for the origin of this noise.

Adolescent↗
PubMed1997

Secondary dystonia and the DYTI gene.

Early-onset (< 28 years) primary dystonia in most Ashkenazi Jews is due to a single founder mutation in the DYT1 gene on chromosome 9q34, as determined by very strong linkage disequilibrium with a haplotype of 9q34 alleles at surrounding marker loci. The role of this mutation in individuals with secondary causes for dystonia has never been tested, although environmental insults, such as neuroleptic exposure or perinatal asphyxia, are proposed to precipitate dystonia in genetically predisposed individuals. We assessed 9q34 haplotypes in 40 Ashkenazi patients with secondary dystonia; 25 had early onset of symptoms, including 15 with exposure to neuroleptic medication or perinatal asphyxia. Of the 25 patients with early onset, 9 were considered phenocopies of DYT1 having normal examinations except for dystonia, normal radiographic and other laboratory studies, and onset in a limb or the neck. Only one individual whose dystonia developed in the setting of a measles infection carried the associated haplotype. Our findings indicate that clinical diagnostic criteria that include historical information to detect tardive dystonia and perinatal asphyxia discriminate primary dystonia due to the DYT1 founder mutation. We found no evidence that the DYT1 founder mutation contributes to secondary dystonia.

Adolescent↗
PubMed2004

Pallidal stimulation for dystonia.

OBJECTIVE: High-frequency deep brain stimulation (DBS) of the globus pallidus internus (GPi) is a new and promising treatment option for severe dystonia. Yet only few studies have been published to date regarding this treatment. We present the results of DBS of the GPi in 17 patients with severe dystonia of different causes. METHODS: In our study, we included 10 patients with primary generalized dystonia, six patients with secondary generalized dystonia, and one patient with a severe dystonic cervical tremor. In all patients, DBS electrodes were implanted bilaterally within the GPi. Mean follow-up time was 36 months (range, 12-66 mo). Preoperative and postoperative evaluations (at least annually) were performed using the Burk-Fahn-Marsden scale. RESULTS: The best improvement was achieved in patients with DYT1-positive dystonia. Patients with DYT1-negative generalized dystonia showed inhomogeneous results. There was no significant change in patients with tardive dystonia. One case of Hallervorden-Spatz disease improved dramatically within the first 2 years. The improvement in the cervical dystonic tremor was disappointing, however. Three years after DBS implantation, we found a secondary worsening of symptoms in one patient with a DYT1-positive dystonia and in the patient with Hallervorden-Spatz disease. CONCLUSION: DBS of the GPi is a new and promising treatment option for dystonia. Secondary worsening may limit this therapy.

Adolescent↗
PubMed2006

Treatment of dystonia.

Dystonia may be a sign or symptom, that is comprised of complex abnormal and dynamic movements of different etiologies. A specific cause is identified in approximately 28% of patients, which only occasionally results in specific treatment. In most cases, treatment is symptomatic and designed to relieve involuntary movements, improve posture and function and reduce associated pain. Therapeutic options are dictated by clinical assessment of the topography of dystonia, severity of abnormal movements, functional impairment and progression of disease and consists of pharmacological, surgical and supportive approaches. Several advances have been made in treatment with newer medications, availability of different forms of botulinum toxin and globus pallidus deep brain stimulation (DBS). For patients with childhood-onset dystonia, the majority of whom later develop generalized dystonia, oral medication is the mainstay of therapy. Recently, DBS has emerged as an effective alternative therapy. Botulinum toxin is usually the treatment of choice for those with adult-onset primary dystonia in which dystonia usually remains focal. In patients with secondary dystonia, treatment is challenging and efficacy is typically incomplete and partially limited by side effects. Despite these treatment options, many patients with dystonia experience only partial benefit and continue to suffer significant disability. Therefore, more research is needed to better understand the underlying cause and pathophysiology of dystonia and to explore newer medications and surgical techniques for its treatment.

Botulinum Toxins↗
PubMed1994

[Postural tremor and dystonia. Clinical aspects and physiopathological considerations].

The coexistence of tremor and dystonia is usually seen but there is not a satisfactory explanation for it. Some consider that essential tremor (ET) and idiopathic dystonia (ID) may be genetically linked. To clarify this relationship we evaluated the frequency of postural hand tremor in ID and symptomatic dystonia (SD) patients. We studied the records of patients with dystonia seen in our Movement Disorders Unit. ID was considered when there was no other neurological abnormality in the examination aside from dystonia, normal laboratorial tests and neuroimaging related to dystonia, and a negative past history for any known cause for it, except for genetic predisposition. We analyzed the clinical characteristics of dystonia and the occurrence of postural tremor. We collected 185 patients, being 120 with ID and 65 with SD. Tremor was seen in 27 (22.5%) of ID and 14 (21.5%) of SD. Tremor was present in either focal, segmental or generalized dystonia in both ID and SD. Family history for ET was absent in all patients. The similar frequency of tremor in ID and SD patients suggests that the pathophysiologic derangement resulting in dystonia can favor the development of tremor.

Adult↗
PubMed2001

Bilateral pallidotomy for generalized dystonia.

OBJECTIVE: To evaluate the efficacy and safety of bilateral pallidotomies in five patients with generalized dystonia. BACKGROUND: Generalized dystonias are frequently a therapeutic challenge, with poor responses to pharmacological treatment. GPi (globus pallidus internus) pallidotomies for Parkinson's disease ameliorate all kinds of dyskinesias/dystonia, and recent studies reported a marked improvement of refractory dystonias with this procedure. METHODS: Five patients with generalized dystonias refractory to medical treatment were selected; one posttraumatic and four idiopathic. The decision to perform bilateral procedures was based on the predominant axial involvement in these patients. Dystonia severity was assessed with the Burke-Fahn-Marsden Dystonia Scale (BFM). Simultaneous procedures were performed in all but one patient, who had a staged procedure. They were reevaluated with the same scale (BFM) by an unblinded rater at 1, 2, 3, 30, 60, 90, 120 and 180 days post-operatively. RESULTS: The four patients with idiopathic dystonia showed a progressive improvement up to three months; the patient with posttraumatic dystonia relapsed at three months. One patient had a marked improvement, being able to discontinue all the medications. A mean decrease in the BFM scores of 52,58% was noted. One patient had a trans-operative motor seizure followed by a transient hemiparesis secondary to rack hemorrhage; other was lethargic up to three days after the procedure. CONCLUSIONS: Our results show that bilateral GPi pallidotomies may be a safe and effective approach to medically refractory generalized dystonias; it can also be speculated that the posttraumatic subgroup may not benefit with this procedure.

Adolescent↗
PubMed2003

[Botulinum toxin type B in the management of dystonia non-responsive to botulinum toxin type A].

BACKGROUND: Botulinum toxin (BTX) injection is the first choice treatment for focal dystonias. However 10% or more of patients who receive repetitive injections of BTX type A (BTX-A) lose response (secondary non-responders). One of the strategies to manage such patients is to treat them with another serotype. The aim of this article is to describe my experience with BTX type B (BTX-B) in the management of patients with focal dystonia who became secondary non-responders to BTX-A. METHOD: Open-label non-controlled use of BTX-B injections to treat dystonia patients who developed secondary nonresponse to BTX-A Response to treatment was rated on a 0-4 scale (Jankovic). RESULTS: Four patients entered the study. Pacient 1- At age 48 this man developed idiopathic cervical dystonia. Five years later he also presented with blepharospasm and idiopathic oromandibular dystonia. He was treated with 7604U of BTX-A along 23 sessions separated by a mean interval of 18.8 weeks (range 6-39). Loss of response was noticed after the seventh session. First treatment with BTX-B consisted of injection of 20000U with response rated 3 but duration of 3 weeks. Second session, 23500U, resulted in score 4 with response lasting 12 weeks. Patient 2- This man, with Tourette syndrome since age 8 years, developed tardive blepharospasm at age 51. On 8 sessions of BTX-A injections he received a cumulative dosage of 550U with a mean interval between sessions of 8.8 weeks (range 6-12). Decline of response was noticed after the fifth session. First treatment with BTX-B, 3000U, had a response rated 3 with duration of 12 weeks. Second session, 6000U, resulted in score 4. Patient 3- This woman noticed onset of blepharospasm at age 58 and developed oromandibular and laryngeal dystonia as well as cervical dystonia, respectively, at ages 59 and 65. In other institutions she received 6 sessions of BTX-A. In my service she received a dosage of 1404U along 8 sessions with a mean interval between sessions of 17.4 weeks (range 16-18). She became secondary non-responder after the ninth session. First treatment with BTX-B, 6000U, was rated 0. Second session, 12000U, was rated 4. Patient 4- At age 69 this man developed idiopathic cranial dystonia. Prior to follow up with me, he received 6 sessions of BTX-A in other services. In my institution he was treated with a cumulative dosage of 730U along 4 sessions with a mean interval between sessions of 16.3 weeks (range 15-18). He developed loss of response on the sixth session. Treatment with BTX-B, 12000U, was rated 4 and lasted 20 weeks. Side-effects: local pain (all patients) and dryness of mouth and ptosis (one patient each). CONCLUSION: My findings confirm that BTX-B injections are a safe and effective option for the management of dystonia patients who become secondary non-responders to BTX-A. The results also underscore the need of individualizing dosage regimens before optimum results are achieved.

Aged↗
PubMed1999

[Secondary dystonias. Clinical analysis and diagnostic approach].

DEFINITIONS: Dystonia is a muscle contraction disorder marked by sustained involuntary clonic contortions or abnormal posture. Primary dystonias can be divided into familial forms related to genetic anomalies and idiopathic forms. Secondary dystonias are related to an underlying neurological disease. METABOLIC DISEASES: Secondary dystonias related to metabolic diseases generally occur early before puberty although late onset forms have been described. Other signs, in association with the dystonia, include mental retardation, epilepsy, cerebellous or pyramidal signs, oculomotor disorders, or a neuropathy. Occasionally, extraneurological signs suggest the diagnosis. Biological markers are known for most of these dystonias. EVENT-RELATED DISEASES: In some cases, the dystonia is the only sign and develops as a sequela to an earlier neurological event such as neonatal anoxia, trauma, vascular event or adverse effect of neuroleptics. HEMI-DYSTONIAS: Dystonias limited to one side are generally secondary.

Dystonia↗