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PubMed2006

Movement disorders in patients taking anticonvulsants.

BACKGROUND: A wide variety of movement disorders may occur as a consequence of the administration of antiepileptic drugs (AEDs). Although it has been suggested that the risk of parkinsonism is 10-fold higher in those taking valproate as compared with other AEDs, there have been no large, systematic trials assessing this. AIM: To establish more precisely the prevalence of and risk factors for developing parkinsonism associated with valproate use,and to assess the occurrence of movement disorders with the newer AEDs. METHODS: Patients with epilepsy were recruited from the Toronto Western Hospital Epilepsy Clinic (University of Toronto, Toronto, Ontario, Canada). Each patient was examined by a movement disorder specialist who was blinded to the treatment status of the patient. RESULTS: 201 patients were included. Postural tremor was the most common movement disorder (45%), followed by parkinsonism (4.5%). The odds of having parkinsonism were 5 times higher with valproate than with other AEDs. No single factor predicted the presence of parkinsonism; however, many (5/9) of the patients concurrently used other drugs or had comorbidities that could have caused or exacerbated parkinsonism. None of the newer AEDs were clearly associated with the presence of movement disorders; however, the numbers were too small to make a formal analysis. CONCLUSION: Although the risk of parkinsonism with valproate is higher than with other AEDs, it is lower than originally reported. The cases available were not enough to accurately comment on the prevalence of movement disorders with the newer AEDs.

Adult↗

PubMed1993

[Genetics in movement disorders].

Genetic considerations in movement disorders are described. 1) Familial parkinsonisms are heterogeneous; genes for two of them, 'Lubag' and Waisman syndrome have been mapped to X chromosome, though genes for others do not have been mapped. 2) The responsible gene for Huntington's disease has been cloned recently and named huntingtin. A (CAG)n repeat longer than the normal range was observed in huntingtin gene. The (CAG)n repeat appears to be located within the coding sequence of a predicted approximately 348 kD protein that is widely expressed but unrelated to any known gene. The expansion of an unstable trinucleotide CAG repeat are also the causes of hereditary neurodegenerative diseases such as X-linked bular and spinal muscular atrophy and spinocerebellar ataxia type 1. 3) There are various forms in hereditary dystonia. Although the responsible gene for idiopathic torsion dystonia, inherited as an autosomal dominant pattern, has been mapped to 9q 32-34, genes for others do not have been mapped. 4) The Gilles des la Tourette syndrome (GTS) is a hereditary, neuropsychiatric-neurobehavioral disorder with childhood onset that is characterized by motor and vocal tics. About 80% of the human genome could be excluded as possible site for the GTS gene by studies with over 600 DNA markers in an international collaborative effort, but actual localization has not yet been accomplished.

Chromosome Mapping↗

PubMed1995

Movement disorders in multiple sclerosis.

Movement disorders (MD), other than tremor, associated with multiple sclerosis (MS) occur infrequently. We report 14 new cases of whom nine had dystonia, three parkinsonism, and two had myoclonus. We also reviewed 135 such cases from the literature. From an analysis of the individual MDs and the site of the lesions described, we conclude that paroxysmal dystonias (tonic spasms), ballism/chorea, and palatal myoclonus can be caused by demyelinating lesions. Parkinsonism, dystonia, and other types of myoclonus, however, often appear to be coincidental.

Adolescent↗

PubMed1998

Drug-induced movement disorders.

Drug-induced movement disorders are often unrecognized, especially when not due to dopamine receptor blockers. This review discusses acute, subacute, and chronic syndromes. Pathophysiology relates almost always to dopaminergic transmission. Patient-dependent vulnerability and drug-dependent sensitivity are contributing factors. Young patients are more prone to acute reactions, and tardive or chronic conditions are more frequent in the elderly. Subclinical Parkinsonism can be unmasked by medication exposure. Treatment of tardive dyskinesia remains a challenging task for the clinician, but novel antipsychotics and dopamine depleting agents can be beneficial.

Drug-Related Side Effects and Adverse Reactions↗

PubMedDate not supplied

Further observations showing the impact of the probenecid test in movement disorders.

Two patients with movement disorders are described and neurochemically studied. The first subject concerns a central anticholinergic syndrome in a 83 years old man treated with l-dopa and amantadine for red nucleus tremor. The second one is an association of parkinsonism and chorea in a 76 years old woman presenting with FAHR's syndrome. In both cases, CSF HVA levels were measured before and after oral probenecid load. The observations confirm the usefulness of this neurochemical strategy in order to classify aging patients with parkinsonism into dopasensitive and doparesistant groups.

Aged↗

PubMed1997

[Stereotactic treatment of movement disorders].

Stereotactic surgery for movement disorders is currently undergoing a re-evaluation. A new understanding of the pathophysiology makes the surgical lesion a logical step for the aleviation of both hyperkinetic symptoms such as tremor and hypokinetic symptoms like bradykinesia. Advances in imaging and electrophysiological control render these procedures more accurate and safer. Indications are medically refractory, Parkinsonean tremor, essential tremor, cerebellar tremor, bradykinesia and L-Dopa induced dyskinesis. The standard procedure is ablative surgery, i.e. thalamotomy for tremors and pallidotomy for bradykinesia, dystonia and L-Dopa induced dyskinesias. Deep brain stimulation is a novel alternative for selected patients which is currently evaluated. Neural transplantation of autologus, fetal or genetically manipulated cell suspensions into the striatum for the time being is experimental.

Brain Mapping↗

PubMed2006

Movement disorders after resuscitation from cardiac arrest.

It is difficult to predict precisely the final neurologic outcome from cardiac arrest and accompanying cerebral hypoxia. Although rare, several movement disorders may arise as a consequence of hypoxic injury, including myoclonus, dystonia, akinetic-rigid syndromes, tremor, and chorea. Dys-function of various portions of the central nervous system, including the basal ganglia, thalamus, midbrain, and cerebellum, is implicated in the pathogenesis of these posthypoxic movement disorders. The development of animal models of posthypoxic movement disorders and of newer imaging techniques applied to human patients who have movement disorders after hypoxic episodes has improved understanding of the pathophysiology of posthypoxic movement disorders and has suggested newer treatments. Many outstanding questions remain, however. What factors promote susceptibility to the development of posthypoxic movement disorders? Why do patients who have similar clinical hypoxic insults develop markedly dis-similar movement disorders? Why are the basal ganglia especially vulnerable to cerebral hypoxia? Why do some movement disorders occur in delayed fashion and progress for years after the hypoxic insult? Is the pathogenesis of progressive posthypoxic movement disorders related to that of neurodegenerative diseases? What are the most effective medications for the various posthypoxic movement disorders? Is there a role for deep brain stimulation in the treatment of posthypoxic movement disorders? We anticipate that current and future research in the area of posthypoxic movement disorders will reveal answers to some of these important questions.

Brain Ischemia↗

PubMed2005

Surgical treatment of cervical myeloradiculopathy associated with movement disorders: indications, technique, and clinical outcome.

OBJECTIVE: Movement disorders may be associated with advanced cervical myeloradiculopathy, which represents a major management challenge. We report on eight patients with movement disorders causing progressive cervical myeloradiculopathy who were treated successfully by cervical decompression and reconstruction. RESULTS: The mean age of our patients was 44 years with a male/female ratio of 3:1. The average duration of symptoms prior to presentation was 10 months. The most common levels decompressed and reconstructed were C3-C4 and C4-C5. Six cases showed improvement, and two cases showed stabilization of neurologic status at a mean follow-up of 21 months. Our management strategy and results are interpreted in the context of a systematic review of the literature in which 78 cases are reported. CONCLUSIONS: Movement disorders cause premature cervical spondylosis most commonly involving the C3-C4 and C4-C5 levels. Ventral pathology with kyphotic angulation requires corpectomy or discectomy with or without posterior decompression and reconstruction. Decompression should always be combined with segmental internal fixation. Perioperative use of botulinum toxin and halo vest immobilization can increase the rate of clinical success but requires vigilance to minimize complications. Laminectomy with lateral mass fixation may be used successfully in the absence of kyphotic deformity.

Adult↗

PubMed1997

Posttraumatic movement disorders after moderate or mild head injury.

We examined the occurrence of posttraumatic movement disorders after moderate or mild head injury with a three-level follow-up study including questionnaires, telephone interviews, and personal examinations 4-6 years after the trauma (mean 5.2 years). Sixteen of 158 patients (10.1%) for whom a detailed follow-up was available had developed movement disorders most probably related to craniocerebral trauma. The most frequent finding was a low-amplitude postural/intention tremor that appeared to resemble enhanced physiological or essential tremor. Twelve patients reported transient tremor, two patients had persistent tremor, one patient had transient tremor and persistent hyperekplexia, and another patient had mild persistent cervical myoclonic twitches. Overall, the movement disorder was transient in 12 patients (7.6%) and persisted in only 4 patients (2.6%). These movement disorders were not disabling and did not require medical therapy. Taking into account possible bias by selection of the sample group, the frequency of movement disorders secondary to moderate or mild head trauma might be lower than 10.1%. Posttraumatic movement disorders occurred significantly more often in the group of patients with Glasgow Coma Scores between 9 and 14 than in those with a score of 15. Severe movement disorders such as low-frequency kinetic tremor or hemidystonia were not identified in this survey.

Adolescent↗

PubMed1999

Cerebral arteriovenous malformations and movement disorders.

A series of six patients with movement disorders associated with cerebral arteriovenous malformations (AVM) is reported. The AVMs were classified according to the Spetzler-Martin classification as grade V (one patient), grade IV (four patients), and as grade III (one patient). One patient had action-induced hemidystonia caused by a contralateral frontoparietal AVM which compressed the putamen and was supplied partially by enlarged lenticulostriate arteries. Two patients presented with unilateral cortical tremor associated with contralateral high-frontal cortical/subcortical AVMs sparing the basal ganglia. Another patient developed hemidystonia and hemichorea-hemiballism after bleeding of a contralateral temporooccipital AVM and subsequent ischemia. Two patients had focal dystonia after thalamic and basal ganglia hemorrhage from AVMs. Five patients were operated on. The movement disorder was abolished in one patient postoperatively. Different mechanisms were identified that are relevant for the development of AVM-related movement disorders: mass effect, diaschisis, local parenchymal altered cerebral blood flow, and hemorrhagic or ischemic structural lesions.

Adult↗

PubMed2006

Psychogenic movement disorders.

Diagnosis and treatment of psychogenic movement disorders are challenging for both neurologists and psychiatrists. Symptoms can mimic the full range of organic abnormal involuntary movements, affect gait and speech, or present as unusual undifferentiated movements. Typical clinical characteristics of these disorders are acute onset, fast progression, movement patterns incongruent with organic movement disorders, distractibility, variability, and simultaneous occurrence of various abnormal movements and dysfunctions. Avoidance of iatrogenic damage by unnecessary invasive tests or inappropriate medication, as well as use of appropriate psychiatric treatments are pivotal steps in the management of these disorders. The few clinical trials specific to psychogenic movement disorders focus on antidepressants and psychotherapy. Presence of a comorbid psychiatric diagnosis of depression or an anxiety disorder is a positive prognostic factor, whereas long-standing symptoms, insidious onset of movements, and a psychiatric diagnosis of hypochondriasis, factitious disorder, or malingering are associated with poor outcome.

Humans↗

PubMed1989

Metoclopramide-induced movement disorders. Clinical findings with a review of the literature.

Metoclopramide, a dopamine-2 receptor antagonist used for various gastrointestinal disorders, may cause or exacerbate a variety of extrapyramidal movement disorders. To draw attention to the frequent occurrence of metoclopramide-induced movement disorders, we identified and studied 16 patients who had been exposed to this neuroleptic. The average age at onset was 63 years (range, 24 to 85 years), and women outnumbered men 3 to 1. Tardive dyskinesia was the most common movement disorder (n = 10 [63%]). Five patients had metoclopramide-induced parkinsonism, 1 patient had tardive dystonia, and 1 patient had akathisia. The average duration of exposure prior to onset of movement disorders was 12 months (range, 1 day to 4 years). Therapy was continued for an average of 6 months (range, 1 day to 2 years) after the onset of symptoms, reflecting clinical nonrecognition of the movement disorder and its relationship to metoclopramide. To prevent persistent and disabling movement disorders, long-term use of metoclopramide should be avoided, and patients should be carefully observed for potential neurologic reactions.

Adult↗

PubMed2006

Persistent hand spasm: movement disorder or seizure?

Dystonia is a movement disorder characterized by involuntary, sustained or repetitive, patterned muscle contractions or spasms, frequently causing squeezing and twisting movements or abnormal postures. Dystonic posturing could be one of the accompanying features of epilepsy. We report an elderly lady with intractable focal seizure who presented with more than a year of persistent hand spasms. The clinical importance of differentiating epilepsy from movement disorders is discussed.

Aged↗

PubMed1993

Antineuronal antibodies in movement disorders.

OBJECTIVE: To determine whether children with recent onset of movement disorders (Tourette syndrome, motor and/or vocal tics, chorea, choreiform movements) show evidence of serological antibodies directed against the human central nervous system as previously documented in research on Sydenham's chorea. METHODS: Serum antibodies against previously frozen human caudate nucleus sections were analyzed using a blinded design and immunofluorescent staining methods. The sera of one group of 50 children referred for evaluation of attention deficit hyperactivity disorder, behavior disorders, and learning disabilities (24 with an associated movement disorder) seen between June 1989 and June 1990 were analyzed. The study was replicated in 33 children (21 with an associated movement disorder) seen between June 1990 and November 1990. RESULTS: In the original sample of 50 children, those with movement disorders were significantly more likely to have evidence of antineuronal antibodies than were those without movement disorders (odds ratio [OR] 4.80, 95% confidence interval [CI] 2.58 to 8.93). Results of the replication were similar (OR 6.00, 95% CI 2.56 to 14.03). For the total group, the OR was 5.50, (95% CI 3.54 to 8.99), which is highly significant. The percentage of children with a movement disorder whose sera were strongly positive for antineuronal antibodies (44%) was very similar to that previously found in children with Sydenham's chorea (46%). Children with movement disorders were also more likely than children without movement disorders to have at least one antistreptococcal titer elevated. CONCLUSIONS: The data strongly suggest an association between antecedent group A beta-hemolytic streptococcal infection as inferred from elevated antistreptococcal titers and the presence of serum antineuronal antibodies, which may, in turn, be linked to childhood movement disorders.

Adolescent↗

PubMed2000

Spastic movement disorder.

This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of first, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the first symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap reflexes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the significance of, for example, impaired reflex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and significance of the mechanisms underlying the disorder of functional movement which impairs the patient.

Humans↗

PubMed1993

Evaluation of the effect of treatment on movement disorders in astrocytomas of the basal ganglia and the thalamus.

Twenty patients with movement disorders associated with astrocytomas (grade I-IV according to the WHO tumour classification) of the basal ganglia and the thalamus were evaluated for the effects of treatment. Five patients had more than one movement disorder when the histological diagnosis was verified by stereotactic biopsy. Twelve had tremors, eight hemidystonia, three hemichorea, and one hemichorea/ballismus, and myoclonus respectively. Ten patients died during the follow up period, and for the surviving patients follow up periods ranged from 6-21 years. The movement disorders changed over long periods of time related to therapeutic interventions. CSF shunt operations and percutaneous radiotherapy had no definite effect on the movement disorders. There was a moderate response to medical treatment in a few patients. Stereotactic aspiration of tumour cysts had a marked influence on the movement disorder in two patients, and functional stereotactic surgery abolished tumour induced tremor in one. Interstitial radiotherapy was performed in fifteen patients for treatment of the underlying neoplasm and resulted in different and variable alterations of the movement disorders. These differences may be explained by complex interactions involving structures affected primarily by the tumour, as well as by secondary functional lesions of adjacent structures.

Adolescent↗

PubMed1998

Post-traumatic movement disorders: effect of the legal system on outcome.

Since patients with post-traumatic, neurologic, movement disorders often seek legal counsel and become involved in litigation, we used this group of disorders as a model for testing the hypothesis that an interaction with the legal system may influence its outcome. We reviewed 100 consecutive medical records of patients with post-traumatic movement disorders from the Movement Disorders Clinic at the Baylor College of Medicine. Additionally, 40 patients completed a detailed questionnaire and a health survey. Nineteen of the 40 respondents had obtained legal representation in regards to compensation for their medical problems. The group of patients with attorneys differed from those without legal representation in that they were significantly younger and a significantly higher percentage of these patients were disabled as compared to the group without attorneys. While most were dissatisfied with the legal system, 68% were satisfied with services provided by their attorneys. Although the patients with legal aspects of their movement disorders seemed to have more severe and persistent disability, we could not definitely conclude that the legal system had adversely affected the outcome of the post-traumatic movement disorders.

Adolescent↗

PubMed2005

Movement disorders in the older patient: differential diagnosis and general management.

Movement disorders are especially prevalent in the elderly, and some are highly treatable. Because reduced agility and slowing of gait are associated with numerous movement disorders as well as with the normal aging process, the differential diagnosis of movement disorders in the elderly can be challenging. Many of these disorders share features of parkinsonism-hypokinesia, tremor, and muscular rigidity. This article reviews common and less common movement disorders in the elderly from a primary care perspective, with an emphasis on the presenting features and the differential diagnosis. It also provides general management recommendations with advice for tailoring treatment to elderly patients.

Aged↗