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)

The CSF proteins have previously been very little investigated in the cerebellar syndrome of chronic alcoholism and in essential tremor. Such studies have been carried out more thoroughly by electrophoretic methods in Parkinson's disease but generally with normal results. In the present investigation the CSF proteins were examined by isoelectric focusing and quantitative paper electrophoresis in 10 patients with the cerebellar syndrome of chronic alcoholsm, 12 patients with Parkinson's disease and 16 subjects with essential tremor. Abnormal CSF proteins of very similar appearance were found on isoelectric focusing in the acidic pH interval 5.6-5.8 in 80% of the patients with the cerebellar syndrome of chronic alcoholism. In Parkinson's disease the most common aberration was evidence of nonspecific blood-CSF-barrier damage which occurred in half of the patients. In only 17% of these cases did other alterations appear, situated in the pH range alkaline to pH 5.8. Abnormal CSF proteins were found in 94% of the patients with essential tremor. The aberrant proteins appeared in both the acidic and alkaline pH regions, most frequently with anisoelectric point at pH 5.9, 7.2 and 9.3. There was a considerably higher frequency of CSF protein abnormalities in different pH ranges in patients with tremor of more pronounced degree as compared to those with only mild symptoms. The electrophoretic examinations failed to show any conclusive alterations. Barrier-damage patterns of mild or moderate degree or slightly increased levels of CSF beta1-globulin were occasionally found in all 3 diseases. The results indicate that isoelectric focusing of the CSF proteins may be of diagnostic value in the cerebellar syndrome of chronic alcoholism and in essential tremor but does not reveal any characteristic abnormalities in Parkinson's disease.
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PMID:Isoelectric focusing and electrophoresis of the CSF proteins in tremor of different origins. 6 43

Although CSF HVA is derived from brain DA metabolism the value of its determination as an index of brain DA turnover and dopaminergic activity is limited, as other factors can affect CSF concentrations. These include the partitioning of HVA between different routes of elimination from the brain, the rates of transport from CSF to blood and from the lateral ventricle to the lumbar sac, CSF space volumes, and methodologic problems. The uses and limitations of CSF HVA determination is illustrated by findings in Parkinson's disease, Huntington's chorea, motor neuron disease, disseminated sclerosis, and hepatic coma. Finally, preliminary results on the effect on CSF HVA of the DA agonist CB 154 are described.
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PMID:CSF homovanillic acid: an index of dopaminergic activity. 12 31

Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.
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PMID:Cerebrospinal fluid gamma-aminobutyric acid in neurologic disease. 13 99

Huntington's chorea is a dominantly inherited disorder that usually leads to involuntary movements in the third or fourth decade. On gross pathological examination of the post-mortem brain there is a marked atrophy of the caudate nucleus and putamen. Histological examination reveals cell loss in most regions of the brain, although the hippocampus is usually remarkably free of any abnormalities. Studies to detect a biochemical defect in patients with chorea have been largely unrewarding. Since chorea appears to be the clinical counterpart of Parkinson's disease a number of investigations on dopamine metabolism have been carried out by measuring dopamine in the post-mortem choreic brain, and HVA, a metabolite of dopamine, in the CSF of patients. Most studies have found the dopamine concentrations to be normal or sometimes decreased and the activity of the biosynthetic enzyme for dopamine, tyrosine hydroxylase, is normal. The discovery that the inhibitory neurotransmitter, GABA, and the biosynthetic enzyme GAD are greatly decreased in the post-mortem choreic brain provides some rational explanation for the uncontrolled movements in this disorder. The other significant abnormality found in many, but not all, choreic post-mortem brains has been a decrease in the biosynthetic enzyme for acetylcholine, choline acetyl transferase. The evidence that GABA receptors are intact in choreic brain provides an added stimulus for the development of useful GABA-mimetic drugs. For the ultimate eradication of this distressing disorder, however, a search must continue for the primary defect in order that this can be detected before the onset of symptoms, or hopefully in amniotic fluid.
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PMID:Neurochemical findings in Huntington's chorea. 15 97

Because there is biochemical evidence of decreased GABAergic function in Parkinson's disease, sodium valproate, an inhibitor of GABA catabolism, was administered to eight Parkinsonian patients. Valproate treatment did not significantly alter any Parkinsonian feature, but tended to increase the dyskinesia in the "on-off" patients. The increased dyskinesias were not a result of altered peripheral metabolism of L-dopa. Despite obtaining high plasma levels of valproate, no consistent alteration of CSF GABA levels could be demonstrated. Thus, in these patients, an effect of valproate on GABA metabolism is unproven, and in turn, the role of GABA in Parkinsonism and dyskinesia uncertain.
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PMID:Treatment of Parkinson's disease with sodium valproate: clinical, pharmacological, and biochemical observations. 38 31

Two recent sporadic cases of progressive Parkinsonism after encephalitis are described. Both patients had two oligoclonal protein bands in their CSF. These bands were not present in patients with idiopathic Parkinson's disease and might, therefore, be useful for diagnostic purposes, particularly when the history of encephalitis is uncertain.
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PMID:Oligoclonal banding in the cerebrospinal fluid of patients with postencephalitic Parkinsonism. 50 78

In Parkinson's disease, the concentration of homovanillic acid (HVA) was reduced in lumbar CSF from patients with idiopathic Parkinsonism (n = 54, P less than 0.05) and post-encephalitic Parkinsonism (n = 19, P less than 0.01). The reduction in the concentrations of 5-hydroxyindolylacetic acid (5-HIAA) was not significant, and there was no alteration in the levels of 4-hydroxy-3-methoxyphenylethylene glycol (MHPG). Treatment with L-dopa increased the concentration of HVA in the CSF (P less than 0.05) but had no effect on the levels of 5-HIAA and MHPG. Carbidopa given in combinations with L-dopa produced similar CSF concentrations of dopa as did L-dopa alone but caused less than half the rise in HVA. Fourteen patients who became functionally independent on treatment with L-dopa had higher 5-HIAA levels than 23 patients who showed no such improvement (P less than 0.001), suggesting that intact 5-hydroxyltryptamine neurones may be important in the therapeutic response to L-dopa. In a variety of movement disorders, the levels of HVA, 5-HIAA, and MHPG were not significantly different from age-matched controls. Treatment with tetrabenazine did not significantly alter the metabolite levels in patients in whom it produced either improvement, or side effects.
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PMID:CSF studies on the relationship between dopamine and 5-hydroxytryptamine in Parkinsonism and other movement disorders. 59 81

Serum and CSF from patients with classic von Economo's postencephalitic Parkinson's disease, idiopathic Parkinson's disease and non-Parkinsonian neurological controls were tested for hemagglutination-inhibition antibodies to 17 arboviruses. All 35 CSF specimens from patients with idiopathic Parkinson's disease and controls were negative (ie, no inhibition of hemagglutination) with all the antigens. Of the total of 124 serums from the three study groups, 105 were also negative with all antigens tested. The only positive results were given by 19 serum specimens against one or more of group B arbovirus antigens, and/or against Batai and western equine encephalomyelitis antigens. There were no definitive differences in the distribution of these positive serum titers among controls, idiopathic Parkinson's, and postencephalitic Parkinson's cases. A causal relationship of the arboviruses tested with either the classical postencephalitic or idiopathic Parkinson's disease is not supported by the results of this study.
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PMID:Antibodies against arboviruses in postencephalitic and idiopathic Parkinson's disease. 64 78

The relationship between dopamine receptor activation and the relief of parkinsonian clinical features was studied in 40 patients with Parkinson's disease. Treatment with dopamine receptor agonists, piribedil or bromocriptine, decreased significantly both the basal level and probenecid-induced accumulations of homovanillic acid (HVA) in the CSF. But there were no changes in the concentrations of 5-hydroxyindole acetic acid (5-HIAA). Correlation analyses showed that patients who improved with both the dopamine agonists used had significantly lower probenecid response of HVA in the CSF and a less severe disease condition than those without beneficial effect. This relationship between dopamine receptor activation and improvement of parkinsonian disability suggests that the therapeutic efficacy of dopamine receptor agonists depends on the functional capacity of brain dopaminergic mechanisms.
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PMID:Brain dopamine turnover and the relief of parkinsonism. 90 36

Six patients with Parkinson's disease and five controls were premedicated with probenecid and the peripheral decarboxylase inhibitor alpha-methyldopathydrazine (Carbidopa) before intravenous administration of 50 muc of 14C-L-dopa in tracer quantity. Seven-and-one-half hours later lumbar CSF was obtained. 14C-homovanillic acid (HVA), a major metabolite of brain dopamine, was isolated by thin-layer chromatography and measured. The statistically significant positive correlation between endogenous HVA and 14C-HVA in the entire patient group and the slightly lower values of endogenous HVA and 14C-HVA in the CSF of the parkinsonians support the assumption that the concentration of HVA in the CSF after probenecid treatment reflects brain dopamine turnover. Measurement of labeled HVA here seems to have little advantage over measurement of endogenous HVA alone.
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PMID:14C-homovanillic acid in the cerebrospinal fluid of parkinsonian patients after intravenous 14C-L-dopa. 97 47


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