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)

This article focuses on the current knowledge about movement disorders associated with alcohol and drug abuse. Chronic alcohol use can produce a wide spectrum of movement disorders including tremor, withdrawal parkinsonism and dyskinesias, cerebellar ataxia, and asterixis. MPTP, a neurotoxin first reported to cause parkinsonism in a group of drug abusers, has provided important insights into the pathogenesis of Parkinson's disease. There is a growing body of literature providing evidence that dyskinesias such as tics and dystonia may be precipitated or exacerbated by cocaine. Amphetamines have been implicated in the production of stereotypies and exacerbation of tics.
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PMID:Movement disorders. 837 47

The clinical features, outcomes, differential diagnoses, epidemiology, risk factors, and treatment approaches to tardive drug-induced extrapyramidal syndromes (EPS) are reviewed. Tardive forms of dyskinesia (TD), dystonia (TDt), akathisia (TA), Gilles de la Tourette syndrome (TGTS), myoclonus (TM), and parkinsonism (TP) are described. Moreover, pharmacological and topographical subtypes of TD are discussed. While TD, TDt, and TA are clearly delineated syndromes, there are limited data on TGTS, TM, and the questionable TP. TDt is distinguished from TD by clinical and treatment-related variables. Epidemiological studies provide evidence of better prognosis for TD compared with both TDt and TA. Two distinct groups of variables were found to be associated with a higher risk for TD: an exogenous factor (neuroleptic treatment variables and alcohol or drug abuse) and a factor of predisposition (elderly, female, affective disorder diagnosis, presence of EPS, diabetes mellitus type II, and signs of central vulnerability). In contrast, being younger and male was associated with TDt. A significant relationship between the hyperkinetic forms of tardive EPS was confirmed. Therapeutic strategy differs for the mild, moderate, and severe forms of tardive EPS. Using low doses of antipsychotics is a good preventive approach. Reducing the dose or switching to an atypical antipsychotic is the usual, but not yet fully explored, first therapeutic step. Clozapine, an antipsychotic with antidyskinetic and antidystonic effectiveness, is the second treatment step. Various suppressors of tardive movements were tested in controlled trials, mainly in TD. GABAergic benzodiazepines (clonazepam), adrenergic antagonists (propranolol, clonidine), antioxidants (alpha-tocopherol), and calcium channel blockers (nifedipine) are useful in the third step of treatment of more severe tardive EPS. Unlike TD, TDt and (partially) TA improve on higher doses of anticholinergic medication. Local injection of botulinum A toxin markedly ameliorates focal tardive dystonia over several months. Less verified therapeutic interventions are discussed.
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PMID:Tardive drug-induced extrapyramidal syndromes. 1107 62

The results of clinical, neuropsychological and MRI study of 21 patients with "ephedron" encephalopathy caused by intake of methcatinon ("ephedron"), a surrogate drug obtained from phenylpropanolamine-containing compounds by adding potassium permanganate, are presented. Signs of brain lesions emerged 3-14 (mean 6.8 +/- 4.9) months after the beginning of the regular drug intake. Neurological disturbances were measured using the Scale of clinical assessment of ephedron encephalopathy. In the acute stage of the disease, most patients had the combination of extrapyramidal disorders (parkinsonism, muscular dystonia, tremor, myoclonia) with pronounced postural instability, pseudobulbar syndrome, autonomic, cognitive and affective personality abnormalities of subcortical and frontal types. In 18 (86%) patients, MRI revealed a bilateral symmetric elevation of the signal from the basal ganglia on T1-weighted images, mostly from the medial segment of globus pallidus and the reticular part of substantia nigra that reflected magnesium accumulation. The spread of hyperintensive MRI changes negatively correlated with the disease duration (r = -0.6; p < 0.01), but did not depend on the drug abuse duration or its approximate total dosage, and also did not correspond to the disease severity. In follow-up, a tendency to spontaneous regress of symptoms was observed in 29% of the cases, and in 33% patients symptoms have been regressing even 4 years after stopping of methcatinon intake. The main mechanisms of "ephedron" encephalopathy development are probably related to the manganese accumulation in the brain that might trigger secondary pathogenetic mechanisms, such as mitochondrial dysfunction, oxidative stress, etc. The induction courses of calcium and sodium EDTA that accelerates manganese excretion decrease a probability of the further disease progress, though do not contribute significantly to symptoms regress. The data on possibilities of symptomatic therapy of movement and affective disturbances is presented.
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PMID:["Ephedron" encephalopathy]. 1611 41

The complex relation between movement disorders and substance abuse is reviewed. First, we discuss the wide variety of movement disorders that occur as a direct consequence of acute use or withdrawal of drugs of abuse, such as alcohol, cocaine, heroin, amphetamine and methcathinone. Second, we describe the recent advances in the comorbid relationship between alcoholism and two movement disorders: essential tremor and myoclonus-dystonia. Lastly, we discuss the abuse potential of the dopaminergic agents, apomorphine and levodopa, in patients with Parkinson's disease.
Curr Drug Abuse Rev 2009 Sep
PMID:Substance abuse and movement disorders. 2044 74

The relationship between movement disorders and substance abuse, which we previously reviewed, is updated. We examine these relationships bidirectionally with focus on drugs of abuse that are known to cause movement disorders, as well as primary movement disorders that are associated with use and abuse of alcohol and dopaminergic medications. First, we review the movement disorders that may develop from the acute use or withdrawal of frequent drugs of abuse, including alcohol, cocaine, heroin, amphetamine and methcathinone. We then comment on the interaction between alcoholism and alcohol-responsive movement disorders, such as essential tremor and myoclonus-dystonia. Lastly, we discuss the potential for abuse of antiparkinsonian dopaminergic agents in patients with Parkinson's disease (PD).
Curr Drug Abuse Rev 2012 Sep
PMID:Substance of abuse and movement disorders: complex interactions and comorbidities. 2303 Mar 52