Disease relevance of Movement Disorders

• The selective destruction by MPTP of nigrostriatal dopamine neurons that is responsible for the movement disorder also appears to result in an increase in central noradrenergic activity, which is not possible in Parkinson's disease [1].
• Early-onset torsion dystonia is a movement disorder, characterized by twisting muscle contractures, that begins in childhood [2].
• These results identify a gene that is mutated in generalized epilepsy and paroxysmal dyskinesia and have implications for the pathogenesis of human epilepsy, the neurophysiology of paroxysmal movement disorders and the role of BK channels in neurological disease [3].
• Rapid-onset dystonia-parkinsonism (RDP, DYT12) is a distinctive autosomal-dominant movement disorder with variable expressivity and reduced penetrance characterized by abrupt onset of dystonia, usually accompanied by signs of parkinsonism [4].
• Clinical evidence suggests that a similar agonist-induced hypersensitivity may play a role in the development of dyskinetic movement disorders and psychoses in humans following the chronic use of such dopamine agonists as amphetamine and levodopa [5].

Psychiatry related information on Movement Disorders

• The D2 dopamine receptor has been implicated in the pathophysiology and treatment of movement disorders, schizophrenia and drug addiction [6].
• A 65-year-old woman with bipolar disorder and complicated cardiovascular disease who was on maintenance lithium therapy developed a movement disorder following high doses of trazodone for treatment of an acute depression [7].
• We studied, in a "blind" and quantitative fashion, the density of cerebellar Purkinje cells in 17 adult cases of Huntington's disease (HD), 17 patients with other movement disorders, 17 with schizophrenia, and 23 normal controls [8].
• Gilles de la Tourette syndrome (GTS) is a movement disorder that involves disturbances in the structure and function of the striatum and related circuitry [9].
• Some recurrent nonepileptic events seen in children can be mistaken for seizures, including shuddering attacks, paroxysmal vertigo, breath-holding spells, cardiogenic syncope, night terrors, and movement disorders, such as paroxysmal kinesigenic choreoathetosis [10].

High impact information on Movement Disorders

• Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder [3].
• Essential tremor (ET), the most common movement disorder in humans, appears to be inherited as an autosomal dominant trait in many families [11].
• L-tryptophan in drug-induced movement disorders with insomnia [12].
• In two cebus (Cebus albifrons) monkeys given weekly oral doses of 0.25 milligram of haloperidol per kilogram, movement disorders appeared 1 to 8 hours after drug administration following the tenth weekly dose [13].
• Levodopa aids certain movement disorders [14].

Chemical compound and disease context of Movement Disorders

• Early-onset dystonia is an autosomal dominant movement disorder associated with deletion of a glutamic acid residue in torsinA [15].
• These findings suggest that movement disorders induced by chronic neuroleptic treatment may result, at least in part, from a hypersensitivity of presynaptic D2 dopamine receptors regulating the release of glutamate [16].
• Depletion of striatal dopamine (DA) has been hypothesized to explain some of the neurological and psychiatric complications of chronic use of cocaine, including increased risk for neuroleptic-precipitated movement disorders [17].
• Metoclopramide-induced movement disorders. Clinical findings with a review of the literature [18].
• This report supports the anticholinergic basis of the clinical manifestations of such overdosages, provides information on the role of acetylcholine and dopamine in psychiatric and movement disorders, and illustrates dramatically the need for accurate diagnosis and treatment [19].

Biological context of Movement Disorders

• Myoclonus-dystonia (M-D) is a movement disorder characterized by rapid muscle contractions and sustained twisting and repetitive movements and has recently been associated with mutations in the epsilon-sarcoglycan gene (SGCE) [20].
• No mutations were found in exons of GCH1 and SPG3A, two genes from the candidate region involved in movement disorders [21].
• CONCLUSIONS: The movement disorder in AADC deficiency, particularly the characteristic eye movement abnormalities, should facilitate the identification of patients with this rare but possibly underrecognized disorder [22].
• In addition to the potential clinical benefit of improving decarboxylation efficiency in Parkinson's disease, our approach may be relevant for the treatment of AADC deficiency, a rare, autosomal recessive disorder causing a severe movement disorder and progressive cognitive impairment [23].
• BACKGROUND: Paroxysmal dystonic choreoathetosis (PDC) is a rare familial movement disorder that has been mapped to chromosome 2q31-36 [24].

Anatomical context of Movement Disorders

• A unilateral microinjection of adrenocorticotropin 1-24 in the rat brainstem in the region of the locus ceruleus resulted in postural asymmetry and movement disorder that resembled human dystonia, the severity and duration (2 to 3 days) being dose-dependent [25].
• TorsinA is the causative protein in the human neurologic disease early onset torsin dystonia, a movement disorder involving dysfunction in the basal ganglia without apparent neurodegeneration [26].
• Mitochondria and dystonia: the movement disorder connection [27]?
• Moreover, in and of itself, nigral degeneration without Lewy bodies, such as that encountered in other (non-PD) movement disorders, apparently is not associated with CA2/3 neuritic change [28].
• Parkinson's disease (PD) is an age-associated and progressive movement disorder that is characterized by dopaminergic neuronal loss in the substantia nigra and, at autopsy, by fibrillar alpha-synuclein inclusions, or Lewy bodies [29].

Gene context of Movement Disorders

• The X chromosome-linked dystonia-parkinsonism syndrome (XDP) is a severe movement disorder, characterized by both dystonia and parkinsonism [30].
• Mice with different mutant alleles of Scn8a provide models of the movement disorders ataxia, dystonia, tremor and progressive paralysis [31].
• Early onset dystonia is a movement disorder caused by loss of a glutamic acid residue (Glu(302/303)) in the carboxyl-terminal portion of the AAA+ protein, torsinA [32].
• RESULTS: Of 15 patients, 7 received specific diagnoses or appear to be sporadic cases, 4 have a possible but uncertain relation to HD, and 4 have unknown familial progressive movement disorders [33].
• Screening of movement disorder patients with other clinical features of FXTAS (e.g., ataxia and parkinsonism) may be more likely to yield expanded FMR1 alleles [34].

Analytical, diagnostic and therapeutic context of Movement Disorders

• In addition to increasing our understanding of the pathophysiology of idiopathic dystonia, animal models may help to improve therapeutic strategies for this movement disorder [35].
• In addition to its low liability for movement disorders and its favorable tolerability record in short- and long-term clinical trials, ziprasidone is associated with a favorable metabolic safety profile (in terms of its effect on plasma lipid and glucose levels) and a negligible effect on weight [36].
• This new movement disorder disappeared after treatment with haloperidol was stopped [37].
• This study analyzed temporal changes of striatal dopamine-D2 receptor binding during the course of different extrapyramidal movement disorders using 123I-iodobenzamide (IBZM) SPECT [38].
• A potential role for the endogenous opiate peptides in neuroleptic-induced movement disorders is suggested by the immunocytochemical localization of met5-enkephalin (ME) in the striatopallidal projection pathway, and by the increased levels of ME measured by radioimmunoassay in the rat caudate-putamen nuclei (CPN) following haloperidol treatment [39].

References