Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethylene oxide is a gas widely used in the production of industrial chemicals. It is also used to sterilize heat-sensitive medical supplies. Previous reports of acute and chronic exposure have described neurotoxic effects like peripheral neuropathy and cognitive impairment. We describe a pure parkinsonian syndrome following acute ethylene oxide intoxication. A 39-years-old male was referred to our Movement Disorders Clinic for evaluation of a parkinsonian syndrome. He was acutely exposed to ethylene oxide four years before and remained comatose for three days, and gradually regained consciousness. At that time he showed a global parkinsonian syndrome including bradykinesia, rigidity and rest tremor, with a severe motor disability; no other neurological disorders were found. The symptomatology was partially controlled with biperidene and levodopa plus carbidopa. Two years later he developed L-dopa induced dyskinesias. Four years after the intoxication he was evaluated at our clinic. General examination showed no abnormalities. Neurologic examination revealed a normal mental status. Motor evaluation disclosed moderate bradykinesia, rigidity and rest tremor, shuffling gait, poor facial mimic, stooped posture, and his speech was low and monotonous; deep tendon reflexes were brisk. The Hoehn-Yahr disability score was degree IV. Routine laboratory and radiological exams showed results within normal limits. The CSF examination was normal. Brain computed tomography and magnetic ressonance were normal. A trial with bromocriptine and levodopa plus carbidopa did not improve dyskinesia, and he was put on a schedule including amantadine and biperidene with improvement to grade III in Hoehn-Yahr scale. In the present case there was a clear relation between the acute exogenous intoxication and irreversible parkinsonism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parkinsonism secondary to ethylene oxide exposure: case report]. 130 62

A 29 year old student of chemistry took 50 ml of a 1% potassium cyanide solution (500 mg) in attempted suicide. He became comatose, mydriatic and was admitted to hospital in an apneic state. He woke up after seven hours and developed Parkinsonism in the following weeks. This regressed slowly in the second month after the poisoning apart from dysarthria, bradykinesia of the upper limbs and very brisk monosynaptic reflexes. Three weeks after the intoxication, CCT was largely normal, and there was CSF-dense hypodensity in both putamina after five months. Sharply delimited signal elevation in T2 corresponding to the two putamina was detected in the MRI eight weeks and five months after ingestion of the poison.
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PMID:Extrapyramidal disturbances after cyanide poisoning (first MRT-investigation of the brain). 175 44

A 26-year-old female developed mental deterioration, general convulsion, cataract and spastic gait in order since her entrance into elementary school. A diagnosis of cerebrotendinous xanthomatosis (CTX) was made because of hypercholestanolemia. At the time of admission, cataract, a mild thickening of Achilles tendons, mental deterioration, spastic paraparesis, truncal ataxia, and bradykinesia were noted. Bilateral slowing of 2 to 7 Hz was recorded in EEG, and brain CT and MRI revealed mild cerebellar atrophy. HVA and 5-HIAA levels in CSF were low. Oral administration of chenodeoxycholic acid, 300 mg per day, resulted in improvement of bradykinesia and EEG abnormality, increase of HVA and 5-HIAA levels in CSF, and decrease of serum cholesterol level in two weeks. Bradykinesia observed in the present case is a rare clinical finding of CTX, and the improvement of bradykinesia soon after the treatment with chenodeoxycholic acid has not been reported yet. This case is important for elucidating the mechanism of neurological disorders in CTX.
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PMID:[A case of cerebrotendinous xanthomatosis with spastic paraparesis, epilepsy, and bradykinesia]. 193 87

Bradyphrenia is considered the mental equivalent of bradykinesia in Parkinson's disease. Patients are described as inattentive and "slow thinking," but not demented. We compared the performance of three groups: parkinsonians age-matched controls, and mildly impaired patients with probable Alzheimer's disease in tests of general intellect, memory reaction time, and in a continuous performance task measuring attention and vigilance. Metabolites of the major biogenic amine in CSF were also measured. The parkinsonians formed two distinct groups. In one, intellectual function and CSF measures were similar to that of controls. The other group of parkinsonians had significantly more omission errors and fewer correct response on the continuous performance task than did controls or patients with Alzheimer's disease. We considered this second group to have bradyphrenia. Their performance on measures of general intellectual and memory function was similar to that of the patients with Alzheimer's disease. CSF-MHPG, the major metabolite of norepinephrine, correlated with the continuous performance task and reaction time in all parkinsonians, and those with bradyphrenia had the highest CSF-MHPG levels. Our data suggest that bradyphrenia is an impairment of attention and vigilance, unique to Parkinson's disease, that may be associated with dementia and with an alteration in norepinephrine metabolism.
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PMID:Clinical and biochemical correlates of bradyphrenia in Parkinson's disease. 243 47

A 29-year-old chemistry student took 50 ml of a 1% potassium cyanide solution (500 mg) in an attempted suicide. He became comatose, mydriatic, and was admitted to hospital in an apneic state. He woke up after 7 h and developed Parkinsonism in the following weeks. This regressed slowly during the 2 months after the poisoning apart from dysarthria, bradykinesia of the upper limbs, and very brisk monosynaptic reflexes. At 3 weeks after the intoxication, computerized tomography was largely normal, and there was CSF-dense hypodensity in both putamina after 5 months. Sharply delimited signal elevation in T2 corresponding to the two putamina was detected by magnetic resonance imaging 8 weeks and 5 months after ingestion of the poison.
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PMID:Computer tomography and magnetic resonance imaging in cyanide poisoning. 338 20

A Parkinson-like syndrome was produced in nonhuman primates and successfully reversed through transplantation of heterologous fetal mesencephalic brain tissue. Rigidity and bradykinesia were induced by the chronic administration of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Once the deficits were fixed, Macaca mulatta with well-developed Parkinson-like behavior received fetal mesencephalic cell preparations stereotactically implanted into multiple sites of the head of the caudate bilaterally. Both animals demonstrated a normalization of CSF L-dopa and significant improvement in observed activity. The neuropathological studies performed 2 months following transplantation demonstrated successful integration of fetal cells in the caudate.
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PMID:Preliminary report on the use of fetal tissue transplantation to correct MPTP-induced Parkinson-like syndrome in primates. 387 97

It is controversial if early onset Parkinson's disease (EOPD) (onset at < 41 years of age) is Parkinson's disease (PD) occurring at a younger age or a different disease. This controversy is due to some clinical and pathological differences between EOPD and PD. Within EOPD, there appear to be two groups namely: young onset Parkinson's disease (YOPD), with onset between 21 and 40 years, and juvenile parkinsonism (JP), with onset at < 20 years. The two major clinical differences between these groups are a higher familial occurrence of PD and dystonia in JP. In this study, we determine if the two groups have the classical features of PD, namely rest tremors, rigidity, bradykinesia, and postural instability, and have a meaningful response to levodopa. Furthermore, we compare their other clinical features, autonomic and cognitive functions, and levels of CSF monoamine metabolites to determine differences between these groups. We observe that all YOPD (100%) and JP (85%) patients had rest tremors. Most of these patients also had a meaningful response to levodopa (YOPD: 72%; JP: 100%). The prevalence of family history of PD was similar, whereas dystonia was more frequent in JP (43%) compared to YOPD (9%). Autonomic symptoms were twice as common in JP (42%) compared to YOPD (17%). However, bedside autonomic functions were abnormal in similar proportions and, like in PD, suggest involvement of parasympathetic nervous system. Cognitive dysfunction does occur but with no difference in severity between the two groups. The difference in number of patients between YOPD and JP groups makes statistical comparison of the occurrence of clinical features like dystonia and autonomic dysfunction difficult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early onset Parkinson's disease: are juvenile- and young-onset different? 752 83

In a prospective series of symptomatic adult hydrocephalus characterized by gait disturbance, cognitive impairment, and/or urinary incontinence, 88 of 118 patients (75%) had additional akinetic, tremulous, hypertonic, or hyperkinetic movement disorders. Their prevalence was highest in patients with idiopathic normal pressure hydrocephalus (NPH) of the elderly (56/65 patients, 86%), and they were less frequent in patients with secondary NPH (10/15, 66%), with nonhydrodynamic atrophic/other hydrocephalus (20/33, 61%), and with obstructive hydrocephalus/aqueductal stenosis (2/5, 40%). Akinetic symptoms were found in 73 of 118 patients (62%), and the most frequent movement disorder was upper extremity bradykinesia (55%). Akinetic, tremulous, hypertonic, and hyperkinetic movement disorders were exclusively secondary to causes not related to hydrocephalus in 24 of 118 patients (20%). The proportion of patients with movement disorders not attributable to only such causes was highest in the idiopathic NPH group (44/65, 68%). Thirteen of 118 patients (11%) presented with a parkinsonian syndrome. There was evidence for coexistent Parkinson's disease in four of these patients. Parkinsonism was found to be secondary to NPH in five patients and was found improved after shunting. Akinetic symptoms in patients with NPH generally responded favorably to CSF diversion, which was evident in 80% of a subset of this group. Various other movement disorders did not show definite improvement. The high prevalence of bradykinesia and other akinetic symptoms in NPH and the beneficial effect of shunting on such symptoms suggest that NPH may cause a more generalized disorder of motor function.
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PMID:Movement disorders in adult hydrocephalus. 899 54

We reported a 32-year-old man with general paresis. He showed slowly progressive bradykinesia and recent memory loss. Argyll Robertson pupils were not present. Muscle strength and sensations were normal except for slight vibratory disturbance. Tendon reflexes were slightly exaggerated. MMSE, HDS-R and WAIS-R scores showed the intellectual impairment. His laboratory investigations revealed elevated both TPHA and FTA-ABS titers in the serum and the CSF. The CSF contained leukocytosis (25/mm3) and protein 80 mg/dl. Cranial CT and MRI demonstrated diffuse cortical atrophy. SPECT revealed marked reduction of the blood flow in bilateral cerebral hemisphere. Cerebral angiography revealed moderate stenosis of the major vessels. The diagnosis of neurosyphilis (general paresis) was made and the treatment of intravenous benzyl penicillin potassium 24 million units per day was started. After 6 weeks of the treatment, the clinical signs (includes MMSE, HDS-R and WAIS-R scores) and the findings of SPECT and cerebral angiography showed improvement. Although the cell count and protein in the CSF became decreased, the titers of TPHA and FTA-ABS in the serum and the CSF were not decreased. Neurosyphilis should always be considered in a etiologically unknown case with bradykinesia and dementia.
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PMID:[Therapeutic case of general paresis manifested by bradykinesia and recent memory loss]. 1061 61

The authors report a kindred in which GTP-CH deficiency resulted in a myoclonus-dystonia syndrome. The proband, a 17-year-old boy, presented with early-onset myoclonus and later, dystonia and bradykinesia. Blood prolactin was increased and CSF homovanillic acid, 5-hydroxyindoleacetic acid, and biopterin were all reduced. L-Dopa/carbidopa administration resulted in clinical improvement. In the paternal branch, the grandfather and three relatives had myoclonus-dystonia and resting or postural tremor of limbs. The authors found a missense mutation in the exon 6 of GCH-1 gene (K224R).
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PMID:Autosomal dominant GTP-CH deficiency presenting as a dopa-responsive myoclonus-dystonia syndrome. 1239 38


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