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At least 19 recordsLinked to original sources
PubMed1992

Trauma and movement disorders.

Movement disorders have been linked to trauma; however, these cases are uncommon and best substantiated if the movement disorder occurs in close temporal association with the trauma, occurs in context of other clinical signs of neurologic damage, and if evidence of CNS lesions on neuroimaging scans is evident. The pathophysiology of movement disorders relates to basal ganglia dysfunction, and traumatic lesions of peripheral nervous system structures or cortical regions could theoretically alter basal ganglia function indirectly and influence movement disorders. Parkinson's disease, the prototype of movement disorders, does not appear to be caused by trauma.

Brain↗
PubMed1990

Treatment of hyperkinetic movement disorders.

Movement disorders are subdivided based on a variety of criteria. One useful and popular approach to movement disorders, based on clinical phenomenology, categorizes these disorders into two groups, those displaying a poverty of movement (akinesia) and those displaying excessive movement (hyperkinesia). This article discusses diagnosis and treatment of the latter. By necessity, certain hyperkinesias such as hyperexplexia, akathisia, and restless leg syndrome are omitted or only briefly discussed. The major hyperkinesias, dystonia, tremor, tics, chorea (including tardive dyskinesia and ballism), and myoclonus are reviewed and a guide to practical management emphasizing symptomatic treatment is presented.

Benzodiazepines↗
PubMed1991

Movement disorders--limb movement and the basal ganglia.

The primary concern of this article is to review experimental methods that may lead to a better understanding of the functional role of the basal ganglia in the control of movement. Two models of basal ganglia impairment are considered: Parkinson's disease and Huntington's disease. The review focuses primarily on akinesia and bradykinesia because they are key abnormalities of basal ganglia dysfunction. In general, through electromyography and kinematic analysis of movement, it may be possible to characterize specific movement disorders. Specifically, if damage sustained by the central nervous system is traced to a certain structure, it may provide insight on the extent of involvement and functional role of that structure in the control of movement. Much of the data reviewed suggests that the basal ganglia may play a specific role in the initiation and regulation of force control.

Basal Ganglia↗
PubMed1977

Therapeutics of disordered movement.

Human motor behavior is organized around two major neurotransmitter systems in the basal ganglia--dopaminergic and cholinergic. Hypokinetic disease may result from hypofunction of the dopaminergic system or cholinergic hyperfunction. The reverse seems true for many hyperkinetic movement disorders. Drugs which facilitate dopaminergic neurotransmission or which block cholinergic transmission relieve many hypokinetic disorders; the opposite approach is useful in treating many hyperkinetic disorders.

Carbidopa↗
PubMed1992

Quantitative light microscopic demonstration of increased pallidal and striatal met5-enkephalin-like immunoreactivity in rats following chronic treatment with haloperidol but not with clozapine: implications for the pathogenesis of neuroleptic-induced movement disorders.

Acute and late onset movement disorders frequently complicate the treatment of psychosis with typical neuroleptic drugs like haloperidol, but not with atypical neuroleptic drugs like clozapine. Although the neural mechanisms underlying neuroleptic-induced movement disorders remain unknown, alterations in basal ganglia function are likely involved. A potential role for the endogenous opiate peptides in neuroleptic-induced movement disorders is suggested by the immunocytochemical localization of met5-enkephalin (ME) in the striatopallidal projection pathway, and by the increased levels of ME measured by radioimmunoassay in the rat caudate-putamen nuclei (CPN) following haloperidol treatment. We sought to determine whether met5-enkephalin-like immunoreactivity (MELI) in terminal fields within globus pallidus and in perikarya in CPN was differentially altered in rats chronically treated with haloperidol or clozapine. Acrolein-fixed forebrain sections were collected from cohorts of adult rats receiving 21-day oral administration of haloperidol, clozapine, or water. Sections from the three treatment groups were collectively processed for immunocytochemical labeling using varying dilutions of ME antiserum and the avidin-biotin peroxidase method. In globus pallidus, densitometry measures revealed significantly increased levels of immunoperoxidase labeling for ME in haloperidol-treated, but not in clozapine-treated animals. In CPN, optical densitometry as well as cell counting measurements also showed a significant increase in MELI only in the haloperidol-treated group. These results support the concept that alterations in endogenous opiate peptides in basal ganglia may contribute to movement disorders seen in patients receiving typical neuroleptic drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Movement disorders as a manifestation of nonketotic hyperglycemia.

Movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.

Adult↗
PubMed1990

Primate models of movement disorders of basal ganglia origin.

Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorders (of which Parkinson's disease is the best-known example) at one extreme to the hyperkinetic disorders (exemplified by Huntington's disease and hemiballismus) at the other. Both extremes of this movement disorder spectrum can be accounted for by postulating specific disturbances within the basal ganglia-thalamocortical 'motor' circuit. In this paper, Mahlon DeLong describes the changes in neuronal activity in the motor circuit in animal models of hypo- and hyperkinetic disorders.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2026

Prominent Movement Disorders in RNU2-2-Related Spliceosomopathy.

Pediatric movement disorders often overlap with neurodevelopmental diseases, suggesting shared molecular mechanisms. Variants in small nuclear RNA (snRNA) genes encoding spliceosome components have recently been associated with neurodevelopmental disorders, termed "RNUopathies." We analyzed genome sequencing data from 14 patients with undiagnosed pediatric movement disorders for pathogenic variants in snRNA genes. We identified recurrent de novo RNU2-2 variants (n.35A > G and n.4G > A) in two patients with intellectual disability, epilepsy, and hyperkinetic movement disorders. RNA sequencing of fibroblasts in one patient showed no characteristic transcriptomic signature. Spliceosomopathies should be considered in neurodevelopmental disorders and developmental and epileptic encephalopathies with hyperkinetic features.

Humans↗
PubMed1990

Movement disorders in alcoholism: a review.

A wide variety of movement disorders are associated with alcohol abuse. Some idiopathic movement disorders are markedly improved by small amounts of alcohol and this response occasionally may lead to alcoholism. Alcohol abuse alone or combined with hepatic encephalopathy can cause various types of tremor, asterixis, and cerebellar dysfunction. Alcohol withdrawal is occasionally complicated by transient basal ganglia dysfunction manifested by parkinsonism or chorea. These syndromes are distinct from the movement disorders complicating acquired hepatolenticular degeneration occurring in some chronic alcoholics. This review discusses the clinical and pathophysiologic aspects of the movement disorder syndromes that complicate alcohol abuse.

Alcoholism↗
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↗
PubMed1992

Unexpected movement disorders in neurosurgical practice: report of three cases.

Hyperkinetic movement disorders may develop as a complication of stereotactic thalamotomy or pallidotomy. However, such movement disorders are uncommon after nonsterotactic intracranial operations. The authors report three cases of involuntary movement disorders unexpectedly developing after intracranial operations. The patients had undergone clipping of an internal carotid aneurysm, removal of an intracerebral hematoma, and resection of a tentorial meningioma. Two patients developed choreic movements and a dystonic posture of the unilateral upper extremity. One patient showed a tremor that had features of both parkinsonism and essential tremor. The symptoms of these patients were medically uncontrollable, and they were successfully treated with stereotactic ventrolateral thalamotomy.

Aged↗
PubMed1991

Drug-induced and tardive movement disorders.

Drug-induced and tardive movement disorders represent a large number of extrapyramidal disorders seen in neurologic practice. Iatrogenically induced, most commonly by neuroleptics, these disorders can be characterized by any abnormal body movement including tremor, chorea, athetosis, dyskinesias, dystonia, myoclonus, tics, ballismus or akathisia. Parkinsonism, dyskinesias and dystonia tend to be the most common. Management of patients with drug-induced or tardive syndromes is complex. Prognosis is frequently poor as patients usually need the offending agent to manage their underlying psychiatric or medical problem. Neuroleptics and other drugs known commonly to cause movement disorders should be used cautiously and significant consideration of all risks and benefits measured before initiating therapy.

Dyskinesia, Drug-Induced↗
PubMed1990

Neurologic approach to drug-induced movement disorders: a study of 125 patients.

Of 125 patients with neuroleptic (dopamine blocking) drug-induced movement disorders who had been referred to a specialized clinic to differentiate the predominant movement disorder, 63% had tardive dyskinesia, 30% had parkinsonism, 24% had dystonia, 7% had akathisia, and 2% had isolated tremor. Two or more movement disorders coexisted in 31 patients (25%). Functional disability was more severe in patients with akathisia than in other patients. Women outnumbered men at a ratio of 4:1, except for tardive dystonia which affected both sexes equally. The average at onset was 56 years (range, 13 to 87); 69 patients (55%) had onset of movement disorder in the sixth decade. While tardive dystonia was distributed relatively evenly in all age groups, almost a third of patients with parkinsonism had it in the eighth decade. Haloperidol was implicated in 47 patients (37%), followed by amitriptyline/perphenazine in 30%, thioridazine in 27%, and chlorpromazine in 20%. Metoclopramide-induced movement disorders were found in 10 (8%). Most patients (101 or 81%) had history of psychiatric illnesses, but of these only 44 had psychosis. Neuroleptic drugs had been prescribed for 33 patients (26%) who had gastrointestinal problems. It is important to recognize and differentiate various drug-induced movement disorders because such differentiation has pathophysiologic and therapeutic implications. Many patients could have been treated with less potent drugs.

Adolescent↗
PubMed1991

Risk factors for neuroleptic-induced movement disorders.

Chronic neuroleptic therapy may be associated with the development of diverse movement disorders including Tardive dyskinesia (TD), Parkinsonism, dystonia, and akathisia in a subset of schizophrenic patients. It is presently unknown why only a proportion of neuroleptic-treated patients develop these movement disorders. In the following communication, we present a series of studies which demonstrate that the development of these movement disorders may be facilitated by certain risk factors including disturbances in pineal melatonin functions, diabetes mellitus, cognitive deficits, suicidal behavior, and disturbances in the functions of the choroid plexus. Recognition of these biological factors may prove useful in: (a) further understanding of the pathophysiology of these disorders, and (b) identifying patients at risk for these movement disorders.

Antipsychotic Agents↗
PubMed1977

New approaches in the management of hyperkinetic movement disorders.

This review covers recent advances in a variety of dyskinesias. Introduction of new drugs for the treatment of myoclonus and sensory biofeedback therapy for focal dystonia are expanding our concepts of these types of movement disorders. Progress in the treatment of action myoclonus is especially noteworthy and has led to the implication of serotonin deficit in the pathophysiology of this syndrome. Knowledge of the biochemical pathology of Huntington's chorea has outpaced therapy for this disorder, but new forms of therapy have been proposed based on the chemical findings. Basic pharmacologic studies suggest pathophysiologic mechanisms for the syndrome known as tardive dyskinesia, but treatment is still far from ideal for this disorder. Other movement disorders with recent therapeutic advances include essential tremor and hemiballism. This review will cover only those dyskinesias in which new therapies have been advanced in the last few years. Aside from parkinsonism, which will not be discussed here, progress in the treatment of movement disorders has been slow, but steady. New drugs are being tested constantly, and the purpose of this review is to call attention to the ongoing evaluation in this field. Descriptions and etiologies for these dyskinesias are covered elsewhere (Fahn, 1976a) and therefore are not repeated here.

5-Hydroxytryptophan↗
PubMed1991

Profile of patients enrolled in a new movement disorder clinic.

To assess the need for a regional expertise in movement disorders, the numbers of patients, clinic visits, and medication changes for a new movement disorder clinic were recorded. During 3 1/2 years, 355 patients were seen, with 1,329 clinic visits. Idiopathic Parkinson's disease was the most common diagnosis, comprising 36% of the population, followed by dystonia (17%), tremor (12%), parkinsonism (i.e., Parkinson's plus syndromes, drug-induced parkinsonism, etc.) (10%), chorea (10%), Tourette's syndrome (6.5%), and tardive dyskinesia (3.4%). Distribution of follow-up visits was similar, with Parkinson's disease (52%) being most frequent and Tourette's syndrome (3.1%) least frequent. The relative utilization of medical care by each patient group was assessed by determining the number of medication changes and the number of clinic visits per follow-up year. No differences in these measures were found using a one-way analysis of variance. Of the Parkinson's disease patients, 67% had Hoehn and Yahr stages III-IV and 77% of the clinic visits were made by this subgroup. When considered in light of the prevalence of each of the diseases, these data show a need for an expertise in movement disorders for a population base of the size we have served.

Cross-Sectional Studies↗
PubMed1977

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↗