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)

Echocardiography was used to study the cardio- and hemodynamic effects of corinfar in 22 patients with neurocirculatory dystonia and 24 with hypertensive disease. The agent showed a pronounced hyperdynamic effect in patients with neurocirculatory dystonia, whereas it significantly lowered systolic, diastolic, mean blood pressures in those with hypertensive disease, by facilitating left ventricular performance without hyperkinemia. It is concluded that neurocirculatory dystonia and hypertensive disease are different diseases, by judging from the cardio- and hemodynamic effects of the calcium antagonist in these patients.
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PMID:[Comparison of the hemodynamic effects of Corinfar in patients with neurocirculatory dystonia and hypertensive disease]. 152 32

We described a 41-year-old woman with idiopathic, symmetrical, non-arteriosclerotic, intracerebral calcification (Fahr's disease), associated with multiple myeloma. CT scans revealed severe calcification in the basal ganglia, floors of cortices, subcortical white matter, brainstem and cerebellum without calcification in the spinal cord. Cerebral angiography showed no evidence of arteriosclerosis. The cerebral blood flow measured by SPECT, parathyroid function and calcium metabolism were within normal range. The initial symptom was dystonia and spasticity in the left leg, when she was 30 years old, followed by gait disturbance, speech impairment, micrographia and dementia. M-proteinemia was pointed out when she 32 years old. M-proteinemia, which was due to primary benign monoclonal immunoglobulinemia (PBMI), made progress slowly, followed by multiple myeloma when she was 40 years old. Periodical CT scans revealed that the intracerebral calcification had worsened gradually through 8 years. Neurological abnormality had also progressed slowly. In literature, there has not been any report about Fahr's disease associated with PBMI and multiple myeloma. Our present study is the first to radiologically prove that the intracerebral calcification in Fahr's disease progresses gradually through its course.
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PMID:[A case of idiopathic, symmetrical non-arteriosclerotic, intracerebral calcification (Fahr's disease) associated with M-proteinemia, followed by multiple myeloma]. 178 68

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Experimental and clinical data clearly demonstrate that calcium antagonists (CA) may have an action on the central nervous system (CNS). The cerebrovascular action of CA justifies their use in cerebral ischaemia, vasospasm and hypoxia. Several clinical trials have demonstrated such beneficial effects. On the other hand a number of reports indicate that CA may have a direct neuronal effect, although most of such trials have not been verified or are mere case reports. In addition, the large number of conditions susceptible to being corrected by CA is impressive: epilepsy, pain, dystonia, dyskinesia, psychiatric conditions, etc. Other papers are disconcerting that report extrapyramidal disorders induced by flunarizine and cinnarizine in the elderly, whereas nicardipine does not produce such side effects and may even alleviate some parkinsonian symptoms. In various experimental models (e.g. stroke, oedema), pharmacological effects have been shown to vary from one compound to the other. Two main questions are yet to be answered: 1) has the direct neuronal effect of CA been clearly established? 2) are the multiple clinical effects on the CNS really linked to calcium antagonism?
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PMID:Clinical neuropharmacology of calcium antagonists. 269 95

The relationship between acute dystonic reactions and serum calcium levels in 17 acutely psychotic patients was studied. Previous studies have implicated an association between a lowered serum calcium value and acute dystonia. This study failed to note a significant incidence of hypocalcemia in a group of psychotic patients. It is not known whether other factors related to calcium-magnesium balance may be related to dystonia.
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PMID:Relationship between dystonia and serum calcium levels. 287 30

A comparative analysis of thyroid and calcium regulating functions in the diffuse toxic goiter was performed. At the initial stage TSH reaction to TRH was on a decrease in parallel with a sharp increase in the content of T4 T3. Two-third of the patients revealed an increase in the level of calcitonin resulting in an increase in the ratio of calcitropic hormones. In that case the content of ionized calcium was not increased. In one-third of the patients the level of calcitonin showed a tendency to a decrease in the normal ratio of calcitropic hormones not accompanied by change in the level of ionized calcium. In neurocirculatory dystonia polymorphism of clinical manifestation was accompanied by great variations (both rising and lowering tendencies) of all indices.
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PMID:[Interrelation of the thyroid and calcium-regulating functions in patients with diffuse toxic goiter]. 342 31

A dramatic improvement in a patient with tardive dystonia was obtained with verapamil after the failure of other medicines. The use of verapamil or other calcium-channel blockers should be considered when treating drug-induced movement disorders.
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PMID:Treatment of persistent myoclonic tardive dystonia with verapamil. 809 57

The effects of selective L-type Ca2+ channel antagonists on severity of dystonia were investigated in a mutant hamster model of idiopathic generalized dystonia. Nimodipine and diltiazem significantly decreased the severity of dystonia. Nimodipine was more potent in this respect and did not cause any behavioral side effects. The present data therefore suggest that Ca2+ channel antagonists could be useful in the treatment of idiopathic dystonia. The antidystonic effect of diltiazem and nimodipine may be based on their antidopaminergic action. However, the lack of significant effects of the L-type channel agonist (+/-)-BAY k-8644 (1-5 mg/kg; methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoro-methylphenyl) -pyridine-5-carboxylate)) on severity of dystonia may indicate that voltage-gated Ca2+ channels are not critically involved in the pathophysiology of dystonia in mutant hamsters.
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PMID:Antidystonic effects of L-type Ca2+ channel antagonists in a hamster model of idiopathic dystonia. 873 8

The case of a 52-year-old man with an ataxicspastic syndrome associated with dystonia, faciobuccolingual dyskinesias and partial epileptic seizures is reported. Neurological imaging showed aspecific brain stem parenchymal alterations. Cerebellar biopsy revealed calcifications and the accumulation of perivascular acid mucopolysaccharides compatible with a diagnosis of "Calcinosis Nucleorum Cerebri", with the absence of any Ca/P metabolism disturbances or other diseases predisposing to calcium deposits showing it to be sporadic and idiopathic. We fell that this case description is interesting because of some of its particular aspects and that it may help in providing a better nosographic classification of these diseases.
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PMID:Striopallidodentate calcifications: nosographic, neuropathological and clinical proposal. Case report. 879 74

We report a 55-year-old woman who developed symptoms resembling parkinsonism. Her psychiatric symptoms in the early stage, cervical dystonia and tremor increasing on movement were consistent with manganese poisoning. Manganese levels were elevated to 1.5 micrograms/l in the serum (normal; 0.3-1.1 micrograms/l) and to 1.4 micrograms/l in the urine (normal; less than 1.2 micrograms/l). Intravenous infusion of calcium disodium editate (CaEDTA; chelating agent) was followed by the marked excretion of manganese (27.3 micrograms/l) in the urine. These findings support manganese poisoning. Manganese poisoning is a disease which results from chronic exposure to manganese, but the source of manganese exposure remained obscure in this patient. T1-weighted MRI of the brain showed symmetric high signal intensity in the globus pallidus without any abnormality on T2-weighted images. There is a report that manganese induced brain lesions in Macaca fascicularis as revealed by MRI and the fascicularis developed signs of unsteady gait and hypoactivity. The patient responded to treatment with CaEDTA and the second MRI demonstrated regression of abnormal signal intensity. This may be due to enhanced manganese excretion. To our knowledge, this is the first case of probable manganese-induced human parkinsonism whom changes in MRI were noted after treatment with CaEDTA.
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PMID:[A patient with parkinsonism presenting hyperintensity in the globus pallidus on T1-weighted MR images: the correlation with manganese poisoning]. 893 1


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