Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diphenylhydantoin (DPH) diminished the therapeutic effects of levodopa both in patients with parkinsonism and in patients with chronic manganese poisoning, as well as the levodopa-dependent dyskinesia for which the former were selected. In patients with Huntington chorea, it enhanced chorea and mental agitation and, thus, failed to conform with the postulated pharmacological reciprocity between Parkinson disease and Huntington chorea. These findings are in agreement with experiments done in animals in which DPH blocked a neuronal response to dopamine.
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PMID:Diphenylhydantoin. Blocking of levodopa effects. 12 56

The therapeutic action of Tiapridal appeared to the authors particularly precious and constant in delirium tremens, senile agitation and turbulence, whatever the origin, and bucco-linguo-facial dyskinesia, whether the latter were linked to age or whether they formed part of a neuroleptic syndrome. Their experience does not permit them to have any opinion concerning the use of this drug in tremor and chorea, the patients seem to respond favourably to treatment but in an erratic manner. On the other hand the drug was totally inefficacious in patients suffering from spasmodic torticollis and writer's cramp. Finally, it seemed to them useful to emphasise the improvement in comfort in patients suffering from various pains when given Tiapridal. This justifies the place given to Tiapridal among drugs necessary for the daily practice of neurology.
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PMID:[A new therapeutical approach in neurology (author's transl)]. 21 5

P, an Indonesian boy, 5 years old, 15 kg of body weight and 110 cm of body length, was admitted to the PTP IX Hospital on March 30, 1987 with cerebral palsy. The patient had fever since 10 days before admission which lasted 7 days; he showed restlessness by involuntary movements when catching, thus when holding something in his hand, it fell off. He had difficulty in walking and talking. On physical examination, were hyperemic the tonsils and pharynx; there was muscular hypotonia, flexed arms and metacarpophalangeal extension. Laboratory findings showed leukocytosis, increased ASTO titer, positive CRP and normal cerebral spinal fluid. Head CT scan showed no abnormality. Electrocardiogram and EEG were in normal limits. Throat swab culture produced Group A Streptococcus beta hemolyticus. The diagnosis of sydenham's chorea was established. Procaine penicillin, phenobarbital and vitamins were administered to the patient. After 5 weeks in the ward the patient was doing well, and now he is working and speaking normally; he is on ambulatory treatment with 1.2 million units/month of long-acting benzathine penicillin, at the Department of Child Health, Tembakau Deli Hospital, Medan.
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PMID:Sydenham's chorea. 207 7

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in primates induced a parkinsonian syndrome that could be reversed by levodopa treatment. Animals quickly developed an apparent restlessness ("akathisia") of the lower limbs after as little as five doses. After 4-10 weeks of regular levodopa therapy, animals developed "peak dose" choreiform movements in the lower limbs that spread, with time, to involve the upper limbs and orofacial musculature. With further treatment (5-21 months), animals developed "peak dose" dystonia that variably involved the limbs and orofacial musculature. These conditions represent novel models of levodopa-induced chorea and dystonia in humans. They depend on the same underlying neuropathology and treatment regimen as their human counterparts. It is to be anticipated that these models of dyskinesia will be useful in determining the mechanisms underlying chorea and dystonia in humans and are ideally suited for experimental evaluation of new treatment strategies.
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PMID:Induction of chorea and dystonia in parkinsonian primates. 229 55

A 74-year-old man with a remote history of Sydenham's chorea but no personal or family history of mood disorder had simultaneous onset of severe, generalized chorea and a mild manic syndrome in clear consciousness. Both chorea and hypomania improved after treatment with sodium valproate and clonazepam. Agitated delirium or mood lability have been described in Sydenham's, but this case is the first report of criteria-based secondary mania with probable Sydenham's chorea, as well as the longest reported remission between symptomatic Sydenham's episodes. The parallel course of this patient's hypomania and chorea supports current pathophysiologic theories of idiopathic mania.
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PMID:Septuagenarian Sydenham's with secondary hypomania. 915 May 17

Huntington disease (HD) is an adult-onset, autosomal dominant inherited human neurodegenerative disorder characterized by hyperkinetic involuntary movements, including motor restlessness and chorea, slowing of voluntary movements and cognitive impairment. Selective regional neuron loss and gliosis in striatum, cerebral cortex, thalamus, subthalamus and hippocampus are well recognized as neuropathological correlates for the clinical manifestations of HD. The underlying genetic mutation is the expansion of CAG trinucleotide repeats (coding for polyglutamines) to 36-121 copies in exon 1 of the HD gene. The HD mRNA and protein product (huntingtin) show widespread distribution, and thus much remains to be understood about the selective and progressive neurodegeneration in HD. To create an experimental animal model for HD, transgenic mice were generated showing widespread expression of full-length human HD cDNA with either 16, 48 or 89 CAG repeats. Only mice with 48 or 89 CAG repeats manifested progressive behavioural and motor dysfunction with neuron loss and gliosis in striatum, cerebral cortex, thalamus and hippocampus. These animals represent clinically relevant models for HD pathogenesis, and may provide insights into the underlying pathophysiological mechanisms of other triplet repeat disorders.
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PMID:Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA. 977 16

Chorea (Greek for "dance") refers to irregular, rapid, flowing, non-stereotyped and random involuntary movements that often possess a writhing quality, referred to as choreoathetosis. When mild, it may be difficult to differentiate from restlessness. The movements can be strikingly asymmetric, as in hemichorea, or generalized. When chorea is proximal and of large amplitude, it is called ballism. Chorea is worsened by stress and anxiety and subsides during sleep. Movements can interfere with the completion of many daily activities, making fastening a button a substantial effort. Chorea often is incorporated into a purposeful activity in an attempt to disguise it. Motor impersistence is a common associated feature, demonstrated by varying intensity of grip strength (milkmaid's grasp) or by an inability to sustain eye closure or tongue protrusion.
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PMID:Chorea and its disorders. 1153 50

Among the movement disorders associated with acanthocytosis, McLeod syndrome (McKusick 314850) is the one that is best characterized on the molecular level. Its defining feature is low reactivity of Kell erythrocyte antigens. This is due to absence of membrane protein KX that forms a complex with the Kell protein. KX is coded for by the XK gene on the X-chromosome. We present six males (aged 29 to 60 years), with proven XK mutations, to discuss the chorea associated with McLeod syndrome. The movement disorder commonly develops in the fifth decade and is progressive. It affects the limbs, the trunk and the face. In addition to facial grimacing, involuntary vocalization can be present. In early stages there may only be some restlessness or slight involuntary distal movements of ankles and fingers. Lip-biting and facial tics seem more common in autosomal recessive choreoacanthocytosis linked to chromosome 9. This, together with the absence of dysphagia in McLeod syndrome, may help in differential diagnosis. Recent findings suggest a role for the endothelin system of the striatum in the pathogenesis of McLeod syndrome.
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PMID:The chorea of McLeod syndrome. 1174 18

An 11-year-old girl with Sydenham chorea presented with a rapid onset of serious restlessness of mainly the right side of the body. Additional laboratory investigations revealed no abnormalities, yet this is not unusual for such cases. Valproic acid and pimozide were then successively prescribed because of the chorea. For secondary prevention she received long-term oral penicillin. Sydenham chorea is a manifestation of rheumatic fever and occurs after a throat infection by group A streptococci. The disease is characteristic and consists of a combination of choreic movements, hypotonia and emotional lability. The clinical course is diverse. Improvement usually occurs over a period of several months, although a significant proportion of patients exhibit little recovery.
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PMID:[A child with peculiar movements: Sydenham chorea]. 1262 82

Group A beta-hemolytic streptococcal infections have been reported to cause neuropsychiatric symptoms, such as chorea, tics, and obsessive-compulsive disorder, presumably through autoimmune damage to basal ganglia. Mycoplasma pneumoniae infections have also been reported to cause damage to the basal ganglia. Restless legs syndrome is a movement disorder with focal restlessness, an irresistible desire to move, and exacerbation by long periods of sitting or lying. We present three children with transient restless legs syndrome-like symptoms possibly associated with group A beta-hemolytic streptococcal infection or Mycoplasma pneumoniae infection. One of three patients had persistently elevated enzyme-linked immunosorbent optical density values against human caudate and putamen.
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PMID:Restless legs syndrome: association with streptococcal or mycoplasma infection. 1530 31


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