Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 13 patients with Friedreich's ataxia (Type Ia) and 17 with type IIa recessive ataxias, all were found to have levels of "free erythrocyte protoporphyrin" (FEP) above the normal range. The rise in FEP in Friedreich's ataxia correlated well with the age of the individual and thus appears to be related to the course of the disease. Subjects with olivo-ponto-cerebellar atrophy, Charlevoix syndrome, Duchenne muscular dystrophy, and Parkinson's disease were also found to have significantly elevated FEP, although the distribution overlapped with the normal range. The finding of elevated FEP may indicate a relative heme deficiency in ataxia due to inhibition of ferrochelatase leading to a state of ineffective, persistent erythropoiesis. The possibility of a prostaglandin abnormality being related to this defect and to the pathogenesis of ataxia is considered.
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PMID:Erythrocyte protoporphyrin levels in patients with Friedreich's and other ataxias. 48 15

We studied a family of Portuguese ancestry from the Azores who suffered a progressive neurologic disease characterized by gait ataxia, features similar to Parkinson's disease in some patients, limitation of eye movements, widespread fasciculations of muscles, loss of reflexes in the lower limbs, followed by nystagmus, mild cerebellar tremor and extensor plantar responses. Two post-mortem examinations revealed loss of neurons and gliosis in the substantia nigra, nuclei pontis (and in the putamen in one case) as well as in the nuclei of the vestibular and other cranial nerves, columns of Clarke and anterior horns, in the spinal cord there were also loss of fibers in the fasciculi gracilis and mild changes in the pyramidal tracts. Comparison of the disease in this family with the findings reported in three families of similar ancestry, previously thought to have different disorders, suggests that they may all represent a single genetic entity with variable expression.
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PMID:Azorean disease of the nervous system. 86 31

We examined whether the N-methyl-D-aspartate antagonist MK-801 (dizocilpine) would reverse parkinsonism or potentiate the effects of L-dopa in primates treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In contrast to its effect in rodent models, treatment with MK-801 (0.1 mg/kg) caused bradykinesia and ataxia in parkinsonian primates, but no locomotor stimulation. Coadministration of MK-801 (0.1 mg/kg) with L-dopa (20 mg/kg) induced marked dystonia accompanied by bradykinesia and ataxia. Dystonia was not induced by either treatment given alone. These findings indicate that MK-801 should not be advocated as an adjunct to dopamine agonist therapy in Parkinson's disease.
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PMID:Dystonia induced by combined treatment with L-dopa and MK-801 in parkinsonian monkeys. 164 62

Between 1986 and 1988 a door-to-door survey was conducted on a stable rural population of 60,820 in central Ethiopia. Trained lay health workers made a complete census and identified cases with symptoms and signs of neurological disorders, using specially designed questionnaires which, in a previous pilot study, were found to have a sensitivity of 91% and specificity of 85%. Neurological disorders in the rural population were epilepsy, postpoliomyelitis paralysis, mental retardation, peripheral neuropathy (mainly due to leprosy), and deaf-mutism with prevalence rates (cases/100,000 population) of 520, 240, 170, 150 and 130, respectively. The prevalence rates of the other less common neurological disorders were 62 for hemiparesis (15 of which were for cerebrovascular accidents), 20 for cerebral palsy, 16 for optic atrophy, 12 for perceptive deafness, 10 for tropical spastic paraparesis, 7 for Parkinson's disease and 5 for motor neuron disease, ataxia and chorea/athetosis. Among related non-neurological conditions, blindness, locomotor disability and deafness were predominant. The significance and role of such a neuroepidemiological study in laying the strategies for the prevention of neurological disorders and rehabilitation of patients are discussed in the context of a developing country.
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PMID:Community-based study of neurological disorders in rural central Ethiopia. 208 51

We studied the clinical features of 47 patients with a non-hereditary degenerative disease and with atrophy of brainstem or cerebellum or both in CT scanning. There was no relation between the CT findings and duration or severity of the disease, nor with the kind of the neurological signs which comprised ataxia, a hypokinetic rigid syndrome, oculomotor abnormalities, upper and lower motor neuron signs, orthostatic hypotension and dementia. The 2 main diagnoses were olivopontocerebellar atrophy (OPCA), or a combination of OPCA and striatonigral degeneration (SND). The differential diagnosis with Parkinson's disease and progressive supranuclear palsy was discussed. We concluded, that a CT scan is warranted in all cases of suspected Parkinson's disease, especially in those without tremor, and in cases of motoneuron disease with broad-based gait. In our patients with mainly hypokinesia and rigidity, levodopa treatment had no or brief beneficial effects. If ataxia predominated, OPCA appeared the most sensible diagnosis; if a hypokinetic-rigid syndrome predominated, the diagnoses SND plus OPCA appeared the most suitable. We assessed the degree of atrophy on CT subjectively, because an interobserver study of 60 normal CT scans, did not produce reliable measurements.
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PMID:Non-familial degenerative disease and atrophy of brainstem and cerebellum. Clinical and CT data in 47 patients. 235 20

In middle of Kii peninsula, one of the biggest mercury mine in Japan had been present until about 10 years ago. The mercury contents in water and fish are reported to be higher in this district. So we investigated the mercury in hair of patients and normal controls. In this study the subjects are 23 cases of ALS including 15 cases in Nara and Mie and 8 cases in other prefectures except in Kii peninsula, 14 cases with ataxia, 11 cases with other degenerative diseases like Parkinson's disease and Alzheimer's disease, 25 cases of cerebrovascular disease as compared to 26 normal controls. The hair are taken from 3 areas on head of patients and normal controls. They are washed in 2% sodium lauryl sulfate and stirred in distilled water several times, and they are soaked in acetone and dried in filter paper. They are inserted in fire and vaporized mercury are measured (Zeeman Effect Mercury Analyzer) in ppm. The hair mercury concentration is 2.81 ppm in ALS in total, 3.62 ppm in ALS in Nara and Mie and 1.39 ppm in outside of Kii Peninsula, 2.34 ppm in ataxia, 1.83 ppm in other degenerative diseases, 1.66 ppm in cerebrovascular disease and 1.44 ppm in normal controls. Statistically it is significant (p less than 0.05) between that in ALS in Nara and Mie and that in normal controls. 6 cases (40%) with ALS in Nara and Mie have the value above the mean +2 standard deviation of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mercury in hair of patients with ALS]. 280 5

Cerebrospinal fluid (CSF) levels of the anxiogenic neuropeptide diazepam binding inhibitor (DBI) were determined by radioimmunoassay in 281 patients who underwent evaluation for neurological problems. Serial dilution curves and reverse-phase high pressure liquid chromatography showed that the immunoreactive material in CSF behaved just as authentic DBI extracted from human brain. Furthermore in the assay there was no evidence of interference from CSF samples deprived of DBI by immunoaffinity. In 82 patients with no evidence of major lesions in the central nervous system, who acted as controls, the CSF DBI content was shown to be age- and sex-related. No correlation was observed with the CSF protein concentration. In patients with different types of dementia, the levels of CSF DBI were significantly increased in a group with normal pressure hydrocephalus. No significant differences were found between Alzheimer's disease, multi-infarct dementia, or dementia with Parkinson's disease and controls. In non-demented patients with Parkinson's disease the levels of DBI were increased in a subgroup with depressive disturbances whereas no differences was observed in the non-depressed cases. The content of DBI was markedly reduced in 5 cases with olivopontocerebellar atrophy and in 4 with spinocerebellar ataxia. In all the other disorders studied the levels of DBI were similar to or slightly lower (multiple sclerosis) than those of the controls. The origin of DBI in cerebrospinal fluid is uncertain; a number of various possibilities are discussed concerning the proposed role of DBI as modulator of brain GABAergic transmission.
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PMID:Diazepam binding inhibitor-like immunoreactivity (DBI-LI) in human CSF. Correlations with neurological disorders. 321 41

N-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a potent dopaminergic neurotoxin, was administered to cats systemically for 5 to 7 days. This treatment produced a behavioral syndrome characterized by akinesia, ataxia, bradykinesia, and feeding difficulties, lasting for several weeks. During this period of severe behavioral impairment, caudate and nucleus accumbens dopamine and norepinephrine concentrations were quite depleted. Behavioral recovery ensued over the next several weeks as did some recovery of striatal catecholamines. MPTP destroyed the majority of substantia nigra pars compacta neurons while affecting a much lesser number of locus ceruleus and ventral tegmental neurons. These results demonstrated for the first time that MPTP can cause long-lasting deficits in nigrostriatal functioning in the cat and may provide a means for studying the apparently selective neurotoxic effects of MPTP as well as for understanding the pathophysiology of Parkinson's disease.
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PMID:Production of a Parkinson-like syndrome in the cat with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP): behavior, histology, and biochemistry. 348 7

Most disorders of motor activity including disturbances of muscle tone and of locomotor activity observed in patients with neurological disorders have been reproduced experimentally in animals. Most motor disorders of the extrapyramidal type including those associated with Parkinson's disease and choreiform and athetoid involuntary movements, have been reproduced exclusively in primates. This is most likely related to the highly complex organization of the extrapyramidal and related nervous mechanisms subserving the corresponding peculiar type of motor control in the primate brain. Other types of motor disturbances including cervical and trunkal dystonias, ataxia, hypotonicity, spasticity and intention tremor, however, have been successfully induced in various mammalian species. The latter types of motor disorders are related to disturbances of central nervous mechanisms which show similar patterns in the brains of different animal species. Histopathological and neurochemical changes associated with extrapyramidal disorders have been discovered and more precisely determined as a consequence of the development of new technical approaches. Therefore numerous morphological, physiological and neurochemical data concerning the extrapyramidal system are now available but a better knowledge of their precise and subtle interrelationship is greatly needed in order to develop more efficient therapeutic procedures.
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PMID:Behaviour correlates of neurotransmitter activity. 614 9

We have examined anticipatory postural responses in calf muscles (triceps surae) in response to a small pull to the arm in standing subjects. This stimulus normally evokes a brisk automatic compensatory contraction of the calf muscles. This is not due to calf muscle stretch, for leg movement occurs after the response has appeared. It appears to be driven centrally by input produced by the pull to the arm. Such anticipatory postural responses were present in every one of the 50 normal subjects studied, but were absent or greatly reduced in many patients with Parkinson's disease when compared to age-matched normal subjects, particularly in those exhibiting postural instability. However, a normal anticipatory postural response was elicited in four patients with progressive supranuclear palsy and in a single patient with an akinetic rigid syndrome due to cerebrovascular disease. Cerebellar truncal ataxia only depressed the response in severe cases. We conclude that although these responses may not be necessary to maintain balance, they may be employed in fine adjustment of posture.
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PMID:Anticipatory postural reflexes in Parkinson's disease and other akinetic-rigid syndromes and in cerebellar ataxia. 739 84


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