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)

In three cebus monkeys the chronic daily administration of haloperidol (0.5 mg/kg/day orally) created sedation and parkinsonism during the first 5-7 weeks. Later the animals developed signs reminiscent of acute dystonia, as seen in the clinic during treatment with neuroleptics. These signs were dose-dependent and in extreme cases included widespread tonic and clonic seizures. After 3 and 12 months, respectively, two of the cebus monkeys developed buccolingual signs (grimacing and tongue protrusion), similar to tardive dyskinesia in the clinic. The tardive dyskinesia symptoms were reduced in a dose-dependent manner after each haloperidol administration, being most pronounced in the morning before haloperidol was given. Biperiden reduced acute dystonia but reinstated signs of tardive dyskinesia, which had been abolished by haloperidol. It is suggested that cebus monkeys may provide a useful animal model for the study of neurologic long-term complications from neuroleptic drugs.
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PMID:Haloperidol-induced tardive dyskinesia in monkeys. 82 68

We studied the effect of biperiden in the treatment of dystonia in six patients aged 15-30 years. Five patients had generalized and one patient had segmental dystonia. Biperiden was started at a dose of 2 mg/day and was gradually increased to 40 mg/day in a few weeks. All patients had clinically significant response in varying degrees after a mean follow up of 1.9 years. Three patients showed considerable or dramatic benefit. The 40 mg/day was generally well tolerated. High dose anticholinergic therapy is effective in the management of torsion dystonia.
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PMID:High dose anticholinergic therapy (biperiden) in dystonia. 165 Nov 89

Selective D1 and D2 dopamine (DA) antagonists and agonists were given to 4 Cebus monkeys who had previously received haloperidol treatment for 4 years. SCH 23390 (a selective D1 antagonist) and raclopride (a selective D2 antagonist) induced identical syndromes consisting of dystonia and oral dyskinesia. Biperiden (an anticholinergic drug) and LY 171555 (a selective D2 agonist) completely antagonized the dystonia and dyskinesia induced by SCH 23390 as well as raclopride. The combined treatment with LY 171555 and SCH 23390 (but not LY 171555 and raclopride) caused pronounced sedation. LY 171555 induced repetitive movements of head, legs and trunk, but no oral dyskinesia. SKF 38393 (a partial D1 agonist) caused slight sedation, minimal oral dyskinesia and a significant reduction in D2 agonist-induced repetitive movements.
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PMID:Selective D1 and D2 receptor manipulation in Cebus monkeys: relevance for dystonia and dyskinesia in humans. 289 Nov 33

Sixty-two first-episode psychotic patients who were neuroleptic-naive were studied to examine predictors of acute dystonia after treatment with haloperidol. Twenty-three patients developed dystonia, two of them despite being treated with biperiden. Biperiden significantly prevented dystonic reactions. Dystonia development was significantly related to younger age, severity of illness, and negative symptoms at baseline and showed a trend to be related to positive symptoms as well. No significant effect of gender or diagnosis was found. The authors suggest that young, severely ill patients in their first psychotic episode who have never been treated with neuroleptics might be at higher risk to develop dystonia.
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PMID:Predictors of acute dystonia in first-episode psychotic patients. 797 94

A 33 year-old male presented with right upper limb rest tremor that disappeared on action, posture associated with bradykinesia, and rigidity of right upper and lower limbs (Video S1). Patient also presented right-sided pyramidal weakness (grade 4), hyperreflexia, extensor plantar response, and hemihypesthesia. Skull X-ray and computed tomography (CT) of the brain showed several metal pellets producing multiple artifacts (Fig. 1A,B). Only one pellet settled in brain parenchyma (left midbrain), while other pellets settled in the skull bone (Fig. 1A). Transcranial sonography (TCS) was performed, confirming that the midbrain pellet was placed within the left substantia nigra (Fig. 1C). Levodopa challenge test was conducted, showing no improvement (pre- and post-l-dopa motor UPDRS were 21 and 20, respectively). A further chronic trial of l-dopa (for 3 months) also proved negative. Biperiden and propranolol were also tried with negative results. Figure 1Computed tomography (CT) of the brain and X-ray skull showed several pellets that produced multiple streak artifacts (Fig. 1A,B). Only one pellet rested in the brain parenchyma, the left (contralateral) midbrain as detected by CT (Fig. 1A), and transcranial sonography (Esaote MyLab Five, Providian, Italy) via temporal window (Fig. 1C). Abbreviations: SN, substantia nigra.Hemiparkinsonism has been previously reported secondary to midbrain lesions.1, 2 To the best of our knowledge, movement disorders (secondary to brain injuries) related to bullet fragments have been scantly reported. In one reported case, hemiparkinsonism and dystonia were the result of a bullet in midbrain,2 and in another, dystonia was caused by a bullet in internal capsule.3.
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PMID:Patient with Hemiparkinsonism Secondary to a Gun Pellet in the Contralateral Substantia Nigra. 3086