Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the clinical and laboratory findings in 2 siblings with a syndrome of pigmentary retinopathy, blepharospasm, and dystonia. This entity most resembles Hallervorden-Spatz disease, but appears to be a distinct disorder without identifiable neuroimaging or biochemical abnormalities.
Neurology 1990 Sep
PMID:A familial syndrome of dystonia, blepharospasm, and pigmentary retinopathy. 239 18

We report a case of a 55-year-old man in whom progressive extrapyramidal disease developed nearly 1 year after resuscitation from cardiopulmonary arrest. Parkinsonian features evolved within 3 months, and progressive generalized dystonia developed after 11 months. CT and MRI revealed bilateral basal ganglia infarction. Autopsy after 4 years of illness showed bilateral basal ganglia necrosis with preserved corticospinal tracts. These findings support earlier suggestions that postinfarction dystonia is mediated by a pyramidal system lacking normal striatal control.
Neurology 1990 Sep
PMID:Progressive dystonia following resuscitation from cardiac arrest. 239 36

The author evaluates the dynamics of immune reactivity of the body in patients with cerebral arachnoiditis with consideration of main clinical syndrome--hypertensive-hydrocephalic, epileptiform, autonomic-vascular dystonia syndromes in different variants of the course of the process. It is shown that regression of immune insufficiency did not depend on the leading clinical syndrome. The question of including immunomodulators for correction of immune insufficiency is discussed.
Vrach Delo 1989 Sep
PMID:[Changes in the immune reactivity of the body in cerebral arachnoiditis]. 260 35

Oral lisuride associated with the previous therapy (levodopa plus inhibitor) was given to 15 patients with complex fluctuations of mobility that were not controlled with usual therapy. In contrast with previous studies using this drug, in the present trial several lisuride doses (5-10 administrations) were distributed throughout the day. This therapeutic strategy permitted a greater control of the fluctuations, a significant reduction of the block hours and the disappearance or attenuation of biphasic dyskinesia and off dystonia. It is considered that the use of multiple doses of lisuride permits better therapeutic results than its usual administration schedule (3-4 times a day). Oral lisuride associated with levodopa may provide a definite improvement in motor function in patients with significant functional impairment. The general tolerance was very good using concomitant domperidone therapy.
Neurologia 1989 Sep
PMID:[Orally administered lisuride in the treatment of complex fluctuations of motion in Parkinson disease]. 263 88

Rapid, self paced and self terminated elbow flexion movements were studied in a group of 10 patients with dystonia affecting the arms. The movements were slower and for small amplitude movements, more variable than those recorded in normal subjects. The duration of the first agonist burst was prolonged, even when compared with normal subjects deliberately moving slowly. Cocontraction of agonist and antagonist muscles during ballistic movements was common and may contribute to the bradykinesia. These findings are compared with similar studies of other diseases of the motor system. Unlike many other conditions which also reduce the speed of ballistic voluntary movements, the patients with dystonia in the present study showed a normal symmetry of acceleration and deceleration times. One interpretation of this finding is that aspects of the basic motor programmes are relatively preserved in this condition and account for the surprising retention of motor skills shown by some patients with dystonia.
J Neurol Neurosurg Psychiatry 1989 Sep
PMID:Rapid elbow movements in patients with torsion dystonia. 279 73

The natural history of early-onset idiopathic dystonia was studied in 30 patients. Worsening of motor symptoms was observed in the early stages, followed by spontaneous stabilization. Most of the patients retained functional independence. None showed mental deterioration, mood alteration or personality disturbance.
J Neurol 1989 Sep
PMID:Idiopathic dystonia with onset in childhood. 279 98

The case of a female patient with infantile onset of progressive dystonia, disturbance of gait and dysarthria is presented. At age 7, the diagnosis of Hallervorden-Spatz disease was established by clinical findings including retinal pigment degeneration, basal ganglia hyperdensity on CT, and the rare association of acanthocytosis. The clinical course was followed over 15 years until the patient's death.
Monatsschr Kinderheilkd 1989 Sep
PMID:[Hallervorden-Spatz syndrome with acanthocytosis]. 281 85

A mutant mouse (wriggle mouse sagami, WMS) with neurological disorders was found in a colony of the BALB/c strain. The clinical signs included tremor, dystonia and involuntary movements. The concentrations of the neurotransmitter substances, noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT) and acetylcholine (ACh), were measured simultaneously with their metabolites in dissected brain regions by high-performance liquid chromatography with electrochemical detection. The turnover of 5-HT was significantly higher in the cerebral cortex, hippocampus, hypothalamus, midbrain and pons-medulla of WMS than of the genetic control, BALB/c. The intrastriatal DA and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid were increased. However, there was no evidence to suggest an increase in turnover rate of this neurotransmitter. An increase in concentration of and decrease in turnover rate of NA were observed in the cerebellum of this mutant. These findings suggest that multiple disturbance of the neurotransmitter system was largely responsible for the manifestation of the clinical signs of WMS.
Neurosci Lett 1989 Sep 11
PMID:Functional difference in monoamine transmitters in the behaviorally abnormal mouse mutant (wriggle mouse sagami). 281 21

(5-Amino-1,3-dimethyl-1H-pyrazol-4-yl)(2-fluorophenyl)methanone (1) was found to have an antipsychotic-like profile in behavioral tests predictive of antipsychotic efficacy but, unlike available antipsychotic agents, did not bind in vitro to dopamine receptors. Upon further evaluation, 1 was found to cause clonic seizures in aged rodents. An examination of related structures revealed that 5-(substituted aminoacetamide) analogues of 1 shared this novel pharmacology and did not cause seizures. The synthesis and pharmacological evaluation of this series of compounds are described. Two compounds, 2-(diethylamino)acetamide (25) and 2-[[3-(2-methyl-1-piperidinyl)propyl]-amino]acetamide (38), were selected for examination in secondary tests. Like known antipsychotics both compounds reduced spontaneous locomotion in mice at doses that did not cause ataxia and inhibited conditioned avoidance selectively in both rats and monkeys. Unlike known antipsychotics neither 25 nor 38 elicited dystonic movements in haloperidol-sensitized cebus monkeys, a primate model of antipsychotic-induced extrapyramidal side effects. Biochemical studies indicated that these compounds act via a nondopaminergic mechanism. Neither 25 nor 38 bound to dopamine receptors in vitro or caused changes in striatal dopamine metabolism in vivo. In addition, they did not raise serum prolactin levels as do known antipsychotics. Although adverse animal toxicological findings have precluded clinical evaluation of these agents, the present results indicate that it is possible to identify at the preclinical level nondopaminergic compounds with antipsychotic-like properties.
J Med Chem 1986 Sep
PMID:(5-Amino-1,3-dimethyl-1H-pyrazol-4-yl)(2-fluorophenyl)methanones . A series of novel potential antipsychotic agents. 287 84

"Extrapyramidal" reactions to antipsychotic drugs include acute dystonias, akathisia, Parkinson's syndrome, and tardive dyskinesia. Recent research suggests efficacy of prophylactic antiparkinson drugs in diminishing the incidence of acute dystonia in high-risk patients, although the use of lower neuroleptic doses also might lower the risk and cause fewer unwanted effects. New in the treatment of akathisia is the use of beta-blockers, specifically propranolol (Inderal and others). Many patients require maintenance antiparkinson drug therapy during prolonged antipsychotic drug treatment. There is no effective treatment for tardive dyskinesia, the prevalence of which may be growing, with an estimated annual incidence of new cases of 3%-4%; the elderly and patients with affective illness may be at greatest risk. Clinicians are also attending to the related syndrome of tardive dystonia.
J Clin Psychiatry 1987 Sep
PMID:Treating extrapyramidal reactions: some current issues. 288 54


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