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

Until a few years ago, the anti-parkinsonian effect of amantadine hydrochloride (AHCl) and amantadine sulfate (AS) could not be explained. The beneficial effect of amantadine, which has been observed for a long time, may be connected with its site of action at the glutamatergic excitatory transmitter system, i.e. the N-methyl-D-aspartate receptor. A clear distinction can be made between AHCl and AS with regard to this pharmacokinetic profile. Therefore, AS can be administered in higher doses than AHCl and is thus more effective. A major advantage of AS is that it can also be given intravenously. Yet so far it is marketed only in twelve countries of the world. Intravenous infusions of AS permit the treatment of patients with aphagia during akinetic crises and when L-dopa and dopaminergic agonists are not tolerated in the akinetic terminal stage. Amantadine has the best ratio of therapeutic effects to side effects when compared with the other anti-parkinsonian drugs currently used. Long-term treatment with amantadine may have a considerable L-dopa saving effect. Given in higher doses, amantadine may permit a drastic reduction of L-dopa dosis and dopaminergic agonists so that the well known side effects of such drugs disappear. In addition, some authors assume a neuroprotective action of amantadine. Unlike L-dopa and dopaminergic agonists, AS does not produce hemiballism or dystonia.
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PMID:Twenty-five years of amantadine therapy in Parkinson's disease. 882 Oct 75

The use of neuroleptics in the acute management of traumatic brain injury (TBI) is controversial and may be detrimental to recovery. The following case report describes a patient developing neuroleptic malignant syndrome (NMS) secondary to the use of haloperidol given to control the patient's agitation. The patient began to exhibit symptoms consistent with NMS (high fever, dystonia, diaphoresis, tachycardia, and decerebrate posturing) shortly after administration of the haloperidol. Upon transfer to a rehabilitation hospital, the symptoms persisted. When NMS is suspected, the first intervention is to remove the offending agent; thus, the administration of haloperidol was suspended, and the patient was placed on Amantadine and propranolol. Amantadine was used to increase the availability of dopamine to the mid-brain region, and the propranolol was used to control the fever, which was believed to be central in origin. The patient was able to complete his rehabilitation with no further incidence of fever or agitation. The patient met or exceeded all short-term physical therapy goals and was able to complete most of the neuropsychological tasks presented. The patient returned home 38 days after admission to the rehabilitation hospital and was able to perform most activities of daily living. At the 6-months follow-up visit, the patient was considering entrance into an adult vocational school.
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PMID:Neuroleptic malignant syndrome induced by haloperidol following traumatic brain injury. 1062 7

Amantadine suppressed severe levodopa-induced choreic dyskinesia, which developed at initiation of levodopa therapy, in two siblings manifesting dystonia with motor delay phenotype of GTP cyclohydrolase I deficiency caused by compound heterozygous GCH1 mutations. Our finding suggests a beneficial effect of amantadine on this type of dyskinesia frequently observed in relatively severe dopamine-deficient metabolic disorders.
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PMID:Amantadine for levodopa-induced choreic dyskinesia in compound heterozygotes for GCH1 mutations. 1538 92

We evaluated the effects of amantadine on levodopa-induced dyskinesia (LID) in eighteen consecutive Parkinson's disease (PD) patients in a randomized, double-blind, placebo-controlled study. The primary outcomes were the Clinical Dyskinesia Rating Scale (CDRS) and the Unified Parkinson's Disease Rating Scale (UPDRS) part IVa score changes. The secondary outcomes were the UPDRS II and III score changes. Amantadine did not change the CDRS score for hyperkinesia or dystonia, but decreased the duration of LID and its influence on daily activities (p=0.04) and the UPDRS II score (p=0.01) more than placebo. These findings show that amantadine reduces the duration of LID and improves motor disability in PD.
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PMID:Amantadine reduces the duration of levodopa-induced dyskinesia: a randomized, double-blind, placebo-controlled study. 1615 88

Although levodopa is the gold standard for treating motor symptoms of Parkinson's disease (PD), long-term therapy leads to levodopa-induced dyskinesia (LID). Dyskinesia refers to involuntary movements other than tremor and most commonly consists of chorea that occurs when levodopa-derived dopamine is peaking in the brain ("peak-dose dyskinesia"). However, dyskinesia can also consist of dystonia or myoclonus and occur during other parts of the levodopa dosing cycle. New validated rating scales and home diaries can better help the health care provider assess the timing and severity of dyskinesia. The exact etiology of LID is unknown, but there is evidence that abnormal pulsatile stimulation of dopamine receptors may be contributory. Treatment of LID includes adjustment of PD medications to maximize "on" time without troublesome dyskinesia. Amantadine is the only medication available with demonstrated ability to reduce the expression of established LID without reducing antiparkinsonian benefit. Other medications that are currently being studied to treat established LID include antiepileptics and serotonergic medications. Deep brain stimulation of the subthalamic nucleus is now the most commonly used surgical procedure for PD patients, and it is very effective in treating LID.
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PMID:Levodopa-induced dyskinesia in Parkinson's disease: epidemiology, etiology, and treatment. 1761 36