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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1979

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↗
PubMedDate not supplied

[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↗
PubMed1979

The trial use of clozapine for abnormal involuntary movement disorders.

Twelve patients with abnormal involuntary movement disorders were treated with clozapine in a double-blind, placebo-controlled trial. The cohort consisted of individuals with Gilles de la Tourette's syndrome, Huntington's disease, and atypical persistent dyskinesia that was drug induced. Two subjects were dropped from the protocol due to complications. Two patients with Huntington's disease showed a marked decrease in movements; other individuals obtained no significant therapeutic benefits. Seven of the 10 patients completing the trial experienced moderate or marked side effects.

Adolescent↗
PubMed1977

Subclinical eye movement disorders in patients with multiple sclerosis.

Eye movements were quantitatively evaluated in 16 patients with well-documented multiple sclerosis who had minimal or no clinically apparent eye movement disorder. Induced saccade and pursuit eye movements were recorded with electro-oculography and analyzed with newly developed programs on a laboratory digital computer. Thirteen of the 16 patients had significant (p less than 0.05) impairment of saccades and/or smooth pursuit when compared with 25 normal subjects tested in our laboratory. The type and frequency of abnormalities were as follows: saccade dysmetria, eight; delayed saccade reaction time, five; bilateral saccade slowing, four; slowing of adducting saccades only (medial longitudinal fasciculus syndrome), one; and impaired smooth pursuit, both directions, three, and one direction only, three. In addition, four patients had vestibular nystagmus with eyes closed, and one patient had typical rebound nystagmus. These data suggest that quantitative assessment of eye movements in patients with suspected multiple sclerosis can help in identifying the important "second lesion."

Adult↗
PubMed2025

Levodopa-induced dyskinesia is still a major clinical problem in Brazilian movement disorder clinics.

Levodopa-induced dyskinesia (LID) remains a significant motor complication in Parkinson's disease (PD), although opinions differ on its clinical relevance.To explore the current prevalence and impact of LID, we analyzed two cohorts from the Latin American Research Consortium on the Genetics of Parkinson's Disease from movement disorder clinics in the city of São Paulo, Brazil, recruited 10 years apart.The cohorts included 187 individuals diagnosed with PD in phase 1 (2007-2014) and 224 in phase 2 (2021-2022). The presence and functional impact of LID were measured using part IV (items 4.1 and 4.2 respectively) of the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS).The analysis revealed that LID frequency increased from 34.7 in phase 1 to 54.9% in phase 2 (more recent), with functional impact rising from 25.1 to 38.8%.The findings suggest that LID remains a relevant clinical issue in clinics specialized in movement disorders in Brazil, with no reduction in prevalence throughout the last decade. Further studies from other regions and less specialized neurology centers may help understand this motor complication in Brazil and in other developing countries.

Humans↗
PubMed1975

[Cerebellar movement disorders in monkeys. Comparison of rapidly alternating and slower target movements during cooling of the dentate nucleus (author's transl)].

The effects of short reversible cooling of the dentate nucleus in two groups of 3 and 4 cebus monkeys, with two different types of ipsilateral elbow movements, have been studied. One group was trained to turn a moving handle back and forth rapidly between two mechanical stops, while the second group was trained to move the handle between two target zones. Brief blocking of the dentate nucleus caused a delayed termination of contraction of the agonistic muscles (hypermetria) near the mechanical stop for very rapid, ballistic, alternating arm movements and, consequently, delayed initiation of the antagonistic return movement. The resulting increase of the duration of a single movement was not caused by a reduction of the peak acceleration of the movement. For the slower target movements, dentate nucleus cooling caused shortening of agonistic muscular contraction (hypometria) with corresponding, saccadic movement corrections. The frequency of the "movement tremor" lay between 3 and 5 Hz. The average velocity maxima during dentate cooling did not change. The findings indicate that different types of movements exhibit different disturbances of the movement pattern during the period of functional elimination of the same anatomical structure. The results indicate that the dentate nucleus and cerebellar hemispheres take part in preprogramming movement duration (Kornhuber) for rapid ballistic movements. In slower target movements, the dentate nucleus may be involved in sectional preprogramming of step movements.

Animals↗
PubMed1977

Movement disorders induced in monkeys by chronic haloperidol treatment.

After several months of treatment, Cebus apella, Cebus albifrons, and Saimiri sciurea monkeys maintained on haloperidol, in doses of 0.5 or 1.0 mg/kg orally 5 days per week, began to display severe movement disorders, typically 1-6 h post-drug. Cebus monkeys exhibited violent, uncontrolled movements that flung the animals about the cage. Such episodes usually lasted only a few minutes, recurring several times during the period following drug ingestion. Writhing and bizarre postures dominated the response in S. sciurea. Cessation of drug treatment produced no distinctive after-effects. When tested as long as 508 days after the last administration, however, Cebus monkeys responded to haloperidol with several episodes of hyperkinesis, even at challenge doses considerably lower than those in the original treatment.

Animals↗
PubMed1978

Pharmacological investigations of the cholinergic imbalance hypotheses of movement disorders and psychosis.

The hypotheses of relative cholinergic underactivity in Huntington's disease, tardive dyskinesia, mania, and schizophrenia were pharmacologically investigated, using physostigmine and choline chloride. Intravenous physostigmine improved the involuntary movements of all of four patients with tardive dyskinesia and three of six patients with Huntington's disease. Physostigmine infusion also decreased manic symptoms in six of nine patients with mania, but had no beneficial effects in three patients with schizophrenia. Precursorloading with choline chloride may increase brain acetylcholine levels and central cholinergic activity. In patients with movement disorders a transient improvement during physostigmine infusion predicted a positive response to a trial of oral choline chloride. One manic patient may have been improved by choline chloride, however choline chloride did not improve symptoms in four of six schizophrenix patients. Chronic treatment with oral choline chloride increases plasma levels of choline during administration and for approximately 48 hr after discontinuation of treatment. A single 5-g dose of choline chloride also transiently raises plasma choline levels. These results with physostigmine support the hypotheses of cholinergic underactivity in Huntington's disease, tardive dyskinesia, and mania. Agents which might chronically increase cholinergic activity such as choline chloride should be further tested in these disorders.

Acetylcholine↗
PubMed1978

Ventricular fluid homovanillic acid and 5-hydroxyindoleacetic acid concentrations in patients with movement disorders.

Ventricular fluid concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), the respective metabolites of dopamine and serotonin, were measured in 57 patients undergoing thalamotomy for relief of movement disorders. The diseases included were Parkinson disease, dystonia, cerebral palsy, multiple sclerosis, and posttraumatic or posthypoxic encephalopathy. Untreated parkinsonian patients had the lowest mean HVA level (119 ng per milliliter). Patients with multiple sclerosis or with posttraumatic or posthypoxic encephalopathy with both intellectual impairment and bilateral motor involvement had lower mean HVA levels (197 and 177 ng per milliliter, respectively) than cerebral palsy patients with bilateral motor disease (233 ng per milliliter), dystonia patients (246 ng per milliliter), or multiple sclerosis patients with normal intellect (376 ng per milliliter). The data suggest that diffuse cerebral disease may lead to diminished dopaminergic activity. Ventricular fluid 5-HIAA levels were similar in all groups of patients. Chronic cerebellar stimulation markedly increased ventricular fluid HVA and 5-HIAA levels, indicating that cerebellar stimulation affected cerebral dopaminergic and serotonergic systems.

Adult↗
PubMed1977

CSF studies on the relationship between dopamine and 5-hydroxytryptamine in Parkinsonism and other movement disorders.

In Parkinson's disease, the concentration of homovanillic acid (HVA) was reduced in lumbar CSF from patients with idiopathic Parkinsonism (n = 54, P less than 0.05) and post-encephalitic Parkinsonism (n = 19, P less than 0.01). The reduction in the concentrations of 5-hydroxyindolylacetic acid (5-HIAA) was not significant, and there was no alteration in the levels of 4-hydroxy-3-methoxyphenylethylene glycol (MHPG). Treatment with L-dopa increased the concentration of HVA in the CSF (P less than 0.05) but had no effect on the levels of 5-HIAA and MHPG. Carbidopa given in combinations with L-dopa produced similar CSF concentrations of dopa as did L-dopa alone but caused less than half the rise in HVA. Fourteen patients who became functionally independent on treatment with L-dopa had higher 5-HIAA levels than 23 patients who showed no such improvement (P less than 0.001), suggesting that intact 5-hydroxyltryptamine neurones may be important in the therapeutic response to L-dopa. In a variety of movement disorders, the levels of HVA, 5-HIAA, and MHPG were not significantly different from age-matched controls. Treatment with tetrabenazine did not significantly alter the metabolite levels in patients in whom it produced either improvement, or side effects.

Aged↗
PubMed1975

Cholinergic imbalance hypotheses of psychoses and movement disorders: strategies for evaluation.

It has been proposed that the etiologies of tardive dyskinesia and Huntington's chorea and of some forms of schizophrenia and the affective disorders involve a cholinergic imbalance with respect to a second neurotransmitter. This relative over- or underactivity of the cholinergic system could result from altered synthesis, storage, release, degradation, or reuptake or from a variety of receptor interactions. Under these hypotheses, clinical symptoms would reflect both the brain region in which the imbalance occurs and the neurotransmitter with which acetylcholine is interacting. Effective treatments could involve the correction of this hypothetical imbalance by changing the relative availability of either one or both of the neurotransmitters. Both precursor loading with choline or dimethylaminoethanol and cholinesterase inhibition may be useful in evaluating the effects of increased cholinergic activity in these disease states; the relative merits of these strategies are discussed.

Biogenic Amines↗