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Periodic limb movements and other movement disorders in sleep: neuropsychiatric dimensions.

Movement disorders such as Parkinson's disease and Tourette's syndrome, primarily manifest during wakefulness, intrude into sleep. There are some disorders, however, such as periodic limb movements in sleep, restless legs syndrome, paroxysmal nocturnal dystonia, bruxism, and somnambulism, which occur primarily during sleep. The diagnosis and management of these disorders pose a challenge to neuropsychiatric practice, not only because they may be difficult to distinguish from other neuropsychiatric disorders, but also because psychiatric disorders are often co-morbid with them. Study of these disorders is necessary for an understanding of the interaction of sleep and movement, and how disturbance in one may affect the other.

Adult↗

Case vignettes of movement disorders.

This paper reports five movement disorders cases to serve as a basis for discussion of the problems encountered in the clinical management of these cases, and the pathophysiological mechanisms involved in these disorders as presented. Case 1 is a description of the subjective experience of a patient with acute orofacial dystonia from promethazine. Case 2 is the use of clonazepam is post-head injury tics. Case 3 is the complication from discontinuation of haloperidol and benztropine mesylate treatment. Case 4 is myoclonus in subacute sclerosing Panencephalitis, and Case 5 is rebound tremor from withdrawal of a beta-adrenergic blocker.

Adult↗

[Transcranial magnetic stimulation (TMS) in movement disorders].

Transcranial magnetic stimulation (TMS) has been used to study several aspects of movement disorders: central motor conduction time (CMCT), electromyographic (EMG) silence evoked by TMS, reset of tremor rhythm by TMS, GABAergic inhibitory interneuronal function of the motor cortex studied with paired-pulse TMS. In this communication, We briefly summarize results of paired-pulse TMS in movement disorders. NORMAL SUBJECTS: A subthreshold conditioning stimulus over the motor cortex reduced the size of EMG responses to a succeeding suprathreshold test stimulus given to the same motor cortex. This inhibition is considered to be an inhibitory effect on the motor cortex because the same conditioning stimulus has no influence on H-reflexes or electrical cortical responses. Pharmacological effects on this inhibition suggested that it is mediated by GABAergic inhibitory systems in the motor cortex. PATIENTS: The cortical inhibition was reduced in cortical myoclonus, which is consistent with the notion that the studied effect is mediated by GABAergic systems. The inhibition was disturbed in focal dystonia, whereas normal inhibition was elicited in Segawa's disease. Reduced inhibition was seen in Parkinson's disease (PD), whereas normal inhibition in essential tremor. Normal inhibition was evoked in all patients with chorea. Abnormal inhibition in basal ganglia disorders must reflect damaged movement selection in the motor cortex secondary to the primary lesion in the basal ganglia. This abnormality occurs in some movement disorders and does not occur in the others, which indicates different pathomechanisms for involuntary movements. It is conspicuous that normal inhibition was evoked in Segawa's disease even though the patients had dystonia.

Basal Ganglia↗

Selective serotonin-reuptake inhibitor-induced movement disorders.

OBJECTIVE: To compile and evaluate all available data suggesting an association between selective serotonin-reuptake inhibitor (SSRI) administration and the occurrence of movement disorders, and to characterize these reactions in terms of onset, duration, treatment and outcome, and potential predisposing factors. METHODOLOGY: Reports of movement disorders were identified by conducting a comprehensive literature search that included tertiary adverse drug reaction resources, MEDLINE, EmBASE, Biological Abstracts, Current Contents, Reactions, ClinAlert, and International Pharmaceutical Abstracts. In addition, reports were solicited from the Canadian proprietary manufacturers of SSRIs, and from the Therapeutic Products Program of Health Canada. Each case was then classified according to the description of the movement disorder, based on predefined diagnostic criteria. RESULTS: A total of 127 published reports of SSRI-induced movement disorders were identified involving akathisia (n = 30), dystonia (19), dyskinesia (12), tardive dyskinesia (6), parkinsonism (25), and 15 cases of mixed disorders. Ten isolated cases of bruxism were identified. Ten additional reports could not be classified. Manufacturers of SSRIs provided 49 reports of akathisia, 44 of dystonia, 208 of dyskinesia, 76 of tardive dyskinesia, 516 of parkinsonism, and 60 of bruxism. Treatment strategies included discontinuation of the SSRI; dosage reduction; or the addition of a benzodiazepine, beta-blocker, or anticholinergic agent. CONCLUSIONS: SSRI use appears to be associated with the development of movement disorders, as either a direct result of the drug or exacerbation of an underlying condition. Predisposing factors may include the use of neuroleptics, existing neurologic diagnoses, or preexisting movement disorders. Clinicians should be cognizant of the potential for these reactions, as prompt recognition and management is essential in preventing potentially significant patient morbidity.

Akathisia, Drug-Induced↗

Movement disorders as a complication of acute hemiplegia of childhood.

We evaluate three cases of acute hemiplegia in childhood complicated by tremor and/or choreoathetosis. Each patient experienced the abrupt onset of hemiplegia thought to be localized to an insult involving the middle cerebral distribution without associated seizure, trauma, loss of consciousness or demonstrable cardiac, hematological or neoplastic causes. All three patients recovered most, if not all, strength on the affected side, but each was left with a disorder of movement involving the previously hemiplegic upper extremity. These disorders included resting and intention tremors, as well as choreoathetosis. Anticholinergic drugs failed in treating two patients, but biofeedback techniques were quite successful in one of the two patients so treated.

Acute Disease↗

Quality of life in Parkinson's disease: movement disorders clinic vs general medical clinic--a comparative study.

OBJECTIVES: to determine the effect of attending a movement disorders (MD) clinic on quality of life (QOL) outcomes for patients with Parkinson's disease (PD). METHODS: Postal questionnaire study of forty-two patients with Parkinson's disease attending either a movement disorders clinic or more conventional general medical clinic were selected consecutively to complete the Parkinson's Disease Quality of Life Questionnaire (PDQL). All patients were diagnosed by a consultant physician with an interest in Parkinson's disease (S.B.R.) and had attended either the movement disorders clinic or the general medical clinic on at least three occasions. Questionnaires were completed independently of the examiners and returned by post. RESULTS: Mean PDQL score was 124.1 [5.16] in the movement disorders clinic and 95.9 [5.86] in the general medical clinic. Analysis of covariance revealed that those subjects attending the MD clinic reported a significantly higher QOL than those subjects in general medical care (F(1,39)= 161.98, P < 0.001). CONCLUSION: These data indicate that the quality of life of respondents attending the movement disorders clinic is significantly higher than those attending the general medical clinic.

Aged↗

Tetrabenazine for involuntary movement disorders.

The use of tetrabenazine to treat the movement disorder of Huntington's chorea and other dyskinesias is described. Tetrabenazine produced moderate to marked improvement in the movement disorder in 79% of a series of 40 Australian patients. The most commonly reported side effects were depression, drowsiness and Parkinsonism.

Humans↗

Tetrabenazine treatment in movement disorders.

Tetrabenazine (TBZ) is a catecholamine depletor used for the treatment of a variety of movement disorders. The purpose of this study was to assess the efficacy of TBZ in a retrospective chart review in 3 tertiary care movement disorders centers over long-term treatment. Of 150 patients to whom TBZ was prescribed, 118 were followed up and assessed using the Clinical Global Impression of Change (CGIC), (-3 to +3), a composite grade from a patient and caregiver scale over variable periods. The patients had a variety of hyperkinetic movement disorders including dystonia (generalized and focal: axial, Meige syndrome, torticollis, blepharospasm, bruxism), Huntington disease (HD) or other choreas, tardive dyskinesia (TD) or akathisia, and Tourette syndrome. Mean patient age was 48.8 +/- 18.7 years; 48 were men (40.7%) with a mean disease duration of 93 months. The mean follow-up time was 22 months and the mean TBZ dose was 76.2 +/- 22.5 mg/d (median 75 mg, range 25-175 mg/d). The mean CGIC score was +1 (mild improvement). The group of patients who scored +3 on the CGIC (very good improvement) represented 18.6% (n = 22) of all patients. They had HD or other types of chorea 7.6% (n = 9), facial dystonia/dyskinesia (n = 7, 5.9%), 1 with TD, 2 with trunk dystonia, 2 with Tourette syndrome, and 1 with tardive akathisia. This group had the longest treatment duration and received a mean TBZ dose of 70.5 mg/d (median 75 mg/d) for a mean of 25.4 +/- 21.3 months. The report concludes that TBZ is a moderately effective treatment of a large variety of hyperkinetic movement disorders, with excellent effects in a subgroup with chorea and facial dystonia/dyskinesias.

Adult↗

Chemical and structural changes in the brain in patients with movement disorder.

Neurochemical indices of dopaminergic function were assessed in basal ganglia of post-mortem brains of control subjects and schizophrenic patients who had been rated in life for the presence of movement disorder and neuroleptic intake. In schizophrenics who had been treated chronically with doses of neuroleptics, concentrations of dopamine D2 receptors were significantly increased above controls, whereas dopamine D1 receptors and dopamine metabolism were unchanged. Increased D2 receptors were also observed in basal ganglia of drug-free patients. Concentrations of dopamine D1 and D2 receptors in schizophrenics with movement disorder. Moreover, no relationship was found between dopamine receptor levels and the severity of movement disorder. Concentrations of the dopamine metabolite homovanillic acid were increased in the putamen and nucleus accumbens in a small number of patients with movement disorder compared with controls or patients without movement disorder. No changes were observed in markers of cholinergic and GABA-containing neurones. The present findings are not consistent with a "dopamine receptor hypersensitivity" concept of movement disorder in schizophrenia.

3,4-Dihydroxyphenylacetic Acid↗

Cerebrospinal fluid free choline in movement disorders of paediatric onset.

We measured free choline in cerebrospinal fluid (CSF) of 78 patients with movement disorders of paediatric onset and various controls as a putative index of central phospholipid metabolism. Most of the disorders studied were myoclonic disorders, such as progressive myoclonus epilepsy, the opsoclonus-myoclonus syndrome, and essential myoclonus, but other movement disorders, interictal seizure disorders, and different neurological and nonneurological disorders were also included. There were no significant differences in CSF choline concentrations in myoclonic disorders or other movement disorders compared with controls. The CSF choline levels were lowest in children with seizure disorders including progressive myoclonus epilepsy. In progressive myoclonus epilepsy, the CSF choline values resembled other epileptic disorders rather than other myoclonic disorders. When all the data were analysed collectively, no significant relation of CSF choline was found to patient age, gender, aliquot of CSF measured, or the length of time the sample was stored at -70 degrees C. Separate analyses of data from children and adults showed a trend toward a biphasic relation between patient age and CSF choline which could be pursued in developmental studies of normal subjects. Reduced CSF choline may indicate increased choline incorporation into brain phospholipids, disturbances of choline metabolism, decreased choline release, or non-neural factors.

Acetylcholine↗

[Drug-induced tremor and acute movement disorders].

The main clinical characteristics and aetiology of drug-induced tremor and acute movement disorders (myoclonus, chorea, athetosis, dyskinesia, dystonia, tics) are reviewed and discussed in this article. Tremor is the most frequent drug-induced acute movement disorder. Drug intake (and, initially, true or 'hidden' neuroleptic or psychoactive drugs) should be suspected as the cause of every abnormal movement. Drug-induced acute movement disorders usually disappear spontaneously after withdrawal of the suspected drug without any drug treatment. Drug-induced tremor and movement disorders are often poorly described in the Summary of Products Characteristics (SPC).

Dyskinesia, Drug-Induced↗

Iron status, movement disorders, and acute phase response in elderly psychiatric patients.

The previously reported relation between iron deficiency and movement disorders was studied in a population with a high prevalence of both problems. There was no evidence of a direct statistical relation between iron deficiency and movement disorders. Significant associations were, however, found between movement disorders and features of the acute phase response to physiological stress. Indices of iron status are known to be affected by the acute phase response and it is suggested that the previously reported abnormalities in iron status may be secondary to this.

Acute-Phase Reaction↗

Gamma knife radiosurgery as a lesioning technique in movement disorder surgery.

OBJECT: To increase knowledge of the safety and efficacy of the use of gamma knife radiosurgery in patients with movement disorders, the authors describe their own experience in this field and include blinded independent assessments of their results. METHODS: Fifty-five patients underwent radiosurgical placement of lesions either in the thalamus (27 patients) or globus pallidus (28 patients) for treatment of movement disorders. Patients were evaluated pre- and postoperatively by a team of observers skilled in the assessment of gait and movement disorders who were blinded to the procedure performed. The observers were not associated with the surgical team and concomitantly and blindly also assessed a group of 11 control patients with Parkinson's disease who did not undergo any surgical procedures. All stereotactic lesions were made with the Leksell gamma unit using the 4-mm secondary collimator helmet and a single isocenter with maximum doses from 120 to 160 Gy. Clinical follow-up evaluation indicated that 88% of patients who underwent thalamotomy became tremor free or nearly tremor free. Statistically significant improvements in performance were noted in the independent assessments of Unified Parkinson's Disease Rating Scale (UPDRS) scores in the patients undergoing thalamotomy. Of patients undergoing pallidotomy who had exhibited levodopainduced dyskinesias, 85.7% had total or near-total relief of that symptom. Clinical assessment indicated improvements in bradykinesia and rigidity in 64.3% of patients who underwent pallidotomy. Independent blinded assessments did not reveal statistically significant improvements in Hoehn and Yahr scores or UPDRS scores. On the other hand, 64.7% of patients showed improvements in subscores of the UPDRS, including activities of daily living (58%), total contralateral score (58%), and contralateral motor scores (47%). Total ipsilateral score and ipsilateral motor scores were both improved in 59% of patients. One (1.8%) of 55 patients experienced a homonymous hemianopsia 9 months after pallidotomy due to an unexpectedly large lesion. No other complications of any kind were seen. Neuropsychological test scores that were obtained for the combined pallidotomy and thalamotomy treatment groups preoperatively and at 6 months postoperatively demonstrated an absence of cognitive morbidity. Follow-up neuroimaging confirmed correct lesion location in all patients, with a mean maximum deviation from the planned target of 1 mm in the vertical axis. Measurements of lesions at regular intervals on postoperative magnetic resonance images demonstrated considerable variability in lesion volumes. The safety and efficacy of functional lesions made with the gamma knife appear to be similar to those made with the assistance of electrophysiological guidance with open functional stereotactic procedures. CONCLUSIONS: Functional lesions may be made safely and accurately using gamma knife radiosurgical techniques. The efficacy is equivalent to that reported for open techniques that use radiofrequency lesioning methods with electrophysiological guidance. Complications are very infrequent with the radiosurgical method. The use of functional radiosurgical lesioning to treat movement disorders is particularly attractive in older patients and in those with major systemic diseases or coagulopathies; its use in the general movement disorder population seems reasonable as well.

Activities of Daily Living↗

Sequential observation of movement disorders and brain images in the case of central pontine myelinolysis and extrapontine myelinolysis.

Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are well recognized syndromes related to rapid correction of hyponatremia and have been reported to show a variety of movement disorders. However, sequential observation of movement disorders as well as brain images has seldom been reported. We report a case of CPM and EPM presenting with various sequential changes in movement disorders including delayed choreic movement over 11 months; we present sequential brain magnetic resonance images showing increased T1 and decreased fat-suppression T1 signal intensity. We suggest that delayed low signal intensity, in the fat-suppression T1-weighted images, is a result of the destruction of myelin and by products. Damage to the myelin may cause various movement disorders in a delayed manner.

Adult↗

Severe and uncommon involuntary movement disorders due to psychotropic drugs.

Disorders of involuntary movement due to psychotropic drugs pose a major problem when treating mentally ill patients. These adverse drug reactions (ADR) frequently undermine the patients' compliance and may have serious consequences as well. The drug safety program in psychiatry AMSP (Arzneimittelsicherheit in der Psychiatrie) surveyed a population of 122,562 patients between 1993 and 2000, and documented 129 especially severe or uncommon involuntary movement disorders (IMD): 9 episodes of severe acute dyskinesia, 32 of severe Parkinsonism, 5 of especially severe akathisia, 16 of 'atypical dyskinesia', 38 of Pisa syndrome, 6 of catatonic neuroleptic syndrome, 15 of neuroleptic malignant syndrome, and 8 of tardive dyskinesia. The epidemiological data for this population were systematically analyzed as regards the patient's history of medication, comedication, and clinical course. In those cases, in which a certain drug was imputed to cause an ADR alone and the causal relationship was rated as definite or probable, typical neuroleptics with mainly antipsychotic effects showed a relatively high incidence of 0.1047 %, those with hypnotic-sedative effect a lower incidence of 0.0198 %, and the atypical neuroleptics an incidence of 0.0567 %. This difference was highly significant in an chi (2)-analysis (chi (2) = 18.81, df = 2, p < 0.0001). Our data provide important information on the frequency, severity, and the consequences of ARD for the patients' compliance, and thus are of clinical interest.

Adult↗

Pathophysiology of antipsychotic drug-induced movement disorders.

Explaining the underlying mechanisms of antipsychotic drug-induced movement disorders remains a substantial challenge. The association of atypical antipsychotic agents with fewer drug-induced movement disorders than conventional agents has engendered several pathophysiologic hypotheses: (1) the hypothesis that, unlike conventional antipsychotic agents, atypical antipsychotics have greater activity in blocking serotonin-2A (5-HT(2A)) receptors than dopamine-2 (D(2)) receptors, which mitigates extrapyramidal symptoms; (2) the hypothesis that atypical antipsychotics block D(2) receptors only long enough to cause an antipsychotic action, but not as long as conventional agents; (3) the hypothesis that, in tardive dyskinesia, the nigrostriatal dopamine receptor system might develop increased sensitivity to dopamine as a result of treatment with conventional antipsychotic drugs, but this may not occur with atypical antipsychotics; and (4) the hypothesis that there might be a genetic association in tardive dystonia relating to the dopamine D(3) allele. A number of factors contribute to the difficult task of gaining insight into the pathophysiologic processes of antipsychotic agents and why these agents may lead to drug-induced movement disorders.

Age Factors↗

[Choreatic movement disorders as a psychosomatic syndrome].

A psychogenic movement disorder can immitate sometimes a choreatic syndrom. In the present report a young lady with choreatic movement disorders is described, the causes of which were psychogenic. Of central importance in this case history is the repressed agression, which is experienced as "killing".

Adult↗

Persistent movement disorders following Japanese encephalitis.

The authors report on movement disorders that persist for a long duration following Japanese encephalitis (JE). Fifteen patients with diagnosed JE were followed up after an interval of 3 to 5 years. Of the four patients with a movement disorder, two were children with severe generalized dystonia in whom MRI revealed bilateral thalamic lesions. The two adult patients had parkinsonism. MRI in both adult patients showed lesions confined to the substantia nigra. Viral antibody and antigen were absent in the CSF of all patients.

Acute Disease↗