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)

Local cerebral blood flow (CBF) in the steady state and after intravenous administration of levodopa (1 mg/kg) was measured by xenon-enhanced computed tomography in patients with Parkinson's disease (PD, n = 16), progressive supranuclear palsy (PSP, n = 6), olivopontocerebellar atrophy (OPCA, n = 5), and arteriosclerotic parkinsonism (AP, n = 7). Three patterns of local CBF changes following levodopa were observed: (1) diffuse CBF increases, especially in striatum and thalamus, as found in patients with PD; (2) no significant changes in CBF, as in patients with OPCA and AP; and (3) CBF reductions in basal ganglia and thalamus, as seen in patients with PSP. The CBF increases after levodopa in PD may be secondary to metabolic activation of the nigrostriatal dopaminergic system. The poor CBF responses in patients with OPCA, AP, and PSP appeared to reflect degeneration of the dopaminergic neurons and dopamine receptors to various degrees. The CBF increases, especially in striatum and thalamus, tended to be greater (not significant) among responders to oral levodopa therapy. Levodopa-induced CBF measurements may be useful for the differential diagnosis of parkinsonian syndromes of various etiologies, but are not necessarily sufficient for predicting outcomes of long-term levodopa therapy.
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PMID:Levodopa-induced local cerebral blood flow changes in Parkinson's disease and related disorders. 773 97

We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (> 60% of control) to moderately reduced (20-60% of control) to severely depleted (< 20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC-immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.
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PMID:Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy. 788 42

High field intensity MRI may demonstrate signal abnormalities consistent with deposits of iron or other paramagnetic substances in several extrapyramidal disorders. Hallervorden-Spatz disease was the only disorder widely known to have iron deposits in the pallidum, that are now easily demonstrated in vivo by MRI. However, lower field intensity MRI may also demonstrate characteristic findings. In progressive supranuclear palsy, definite atrophy of the midbrain and of the region around the third ventricle is seen in slightly more than half of the cases. Minimal signal abnormalities are sometimes seen in the periaqueductal region, but MRI studies remain of little help in establishing the diagnosis of the disease. Asymmetric atrophy in the parietal regions is seen in corticobasal degeneration, as expected from pathological studies. Minimal alterations may be seen in the substantia nigra in Parkinson's disease. The most interesting MRI findings are observed in multiple system atrophies. Variable abnormal signal intensities, depending on the field intensity, are visible in the putamen in striatonigral degeneration and in Shy-Drager syndrome; in this latter condition the abnormalities are due to its striatonigral degeneration component. Atrophy of the pons, middle cerebellar peduncles, and cerebellum, and signal abnormalities in a characteristic distribution are visible in olivopontocerebellar atrophy. A combination of these posterior fossa abnormalities and putaminal alterations may confirm the involvement of the cerebellar and extrapyramidal systems in multiple system atrophies.
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PMID:Magnetic resonance imaging in progressive supranuclear palsy and other parkinsonian disorders. 796

Clinical diagnoses of Parkinson's disease (PD) is highly inaccurate. Olivopontocerebellar atrophy (OPCA) is a major source of diagnostic confusion. We have studied the clinical characteristics of 50 patients with PD, 24 patients with OPCA judged by the presence of selective atrophy of the cerebellum and brainstem (diagnosed by CT brain scan) and 30 normal controls of similar age. The typical triad of PD, tremor, rigidity and akinesia, did not distinguish among patients from either group. The presence of severe postural imbalance and reflex myoclonus (in OPCA but not in PD) were the 2 most highly discriminative clinical features.
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PMID:[Olivopontocerebellar atrophy and Parkinson's disease: diagnostic problems]. 816 68

The blink reflex and its recovery curve were studied in 12 patients with neurologic and psychiatric disorders, i.e., juvenile Parkinson's disease (case 1), Gilles de la Tourette's syndrome (case 2), anorexia nervosa (case 3), mild developmental delay (cases 4 and 5), a meningomyelocele with winking spasms (case 6), Parkinson's disease (cases 7-10) and OPCA (cases 11 and 12). The cases were divided into 4 groups on the basis of the results, (1) hyperexcitability of facial motoneurons only (case 6), (2) hyperexcitability of facial motoneurons and brainstem interneurons (case 1 and 2), (3) hyperexcitability of brainstem interneurons only (cases 4, 5 and 7-12) and (4) hypoexcitability of both sides (case 3). Therefore, as to the excitability an abnormal pattern of blink reflexes could be a neurophysiologic marker of some neurologic and psychiatric disorders.
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PMID:The excitability of blink reflexes in patients with neurologic and psychiatric disorders. 818 76

Twenty-five patients with suspected Parkinson's disease were submitted to optoelectronic movement analysis with the Posturo-Locomotor-Manual (PLM) test before and 60 min after a single dose of L-Dopa. They were then examined clinically for diagnosis. Two patients were excluded due to L-Dopa intolerance. Seventeen of the remaining patients were classified as having Parkinson's disease. The movement time (MT) in the PLM test was increased for all these patients, and they improved their performance after L-Dopa. The degree of improvement was roughly proportional to the pretreatment augmentation of MT in comparison to healthy subjects of the same age. The PLM phase analysis showed a specific disability profile for each individual. Six patients were given diagnoses other than PD. Some improvement was found in one patient with suspected olivopontocerebellar atrophy and one patient with multiple brain injury. Two patients with progressive supranuclear palsy, one with suspected striatonigral degeneration, and one with functional disturbance deteriorated after L-Dopa. In conclusion, truly objective and fully reproducible evaluation of the motor performance before and after a single L-Dopa dose is easily accomplished with computer-assisted modern optoelectronic recording equipment. The technique is a valuable tool for the quantitative measurement of treatment effects and contributes to the differential diagnosis.
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PMID:Single-dose L-dopa response in early Parkinson's disease: measurements with optoelectronic recording technique. 841 8

Rapid eye movement (REM) sleep behavior disorder (RBD) involves complex behavior and a loss of muscle atonia occurring during REM sleep. Half of these patients with RBD have an underlying neurologic disorder including dementia, olivopontocerebellar atrophy, subarachnoid hemorrhage, and cerebrovascular disease. Clonazepam is the drug of choice for RBD. RBD has been rarely reported to precede the onset of Parkinson's disease (PD). Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment. It is postulated that levodopa ameliorates RBD by suppressing REM sleep, and it remains to be seen whether levodopa can be an alternative to clonazepam in idiopathic RBD without PD.
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PMID:Rapid eye movement sleep behavior disorder preceding Parkinson's disease with therapeutic response to levodopa. 868 94

Pain is a recognized feature of idiopathic Parkinson's disease (IPD) but has never been studied in multiple system atrophy (MSA), the commonest cause of atypical parkinsonism. We retrospectively analysed histories of pain in 100 consecutive cases of clinically probable MSA. Details were obtained from the medical records of 100 patients with MSA, comprising 82 with the striatonigral degeneration (SND) type and 18 with the olivopontocerebellar atrophy (OPCA) type of MSA. Pain was reported in 47% of the MSA patients. It was classified as rheumatic in 64% of MSA patients reporting pain, sensory in 28%, dystonic in 21%, and levodopa-related in 16%, mostly related to off-period or diphasic dystonias. There was a mixed pain syndrome in 19% of these patients. Pain was significantly more commonly reported by females (P = 0.02), and by patients with levodopa-induced dyskinesias (P = 0.02). No other clinical feature differentiated MSA patients who reported pain from those who did not. The mean delay between disease onset and onset of pain was 2.9 years, but pain was reported at the time of, or before, disease onset in about 30% of patients. The overall prevalence of pain in MSA was similar to that reported in IPD, but the distribution of pain categories was different.
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PMID:Pain in multiple system atrophy. 875 May 53

The brain glucose metabolism was studied by PET with 18F-FDG in 11 patients with multiple system atrophy (MSA) and 12 patients with idiopathic Parkinson's disease (PD). Seven of the 11 MSA patients were diagnosed as having olivopontocerebellar atrophy, two had striatonigral degeneration, while two demonstrated Shy-Drager syndrome. The glucose metabolic rates for each region in the PD patients showed no difference from the normal controls. The frontal, temporal and parietal cortical glucose metabolic rates and the caudate, the putaminal, the cerebellar and the brainstem glucose metabolic rates in the MSA patients decreased significantly from the controls. The atrophy of the cerebellum and the brainstem in the MSA patients were scored by MRI. The cerebellar and brainstem glucose metabolism in the MSA patients decreased as the atrophy score in such regions advanced in each group; however, some patients with no atrophy showed a decreased glucose metabolism. Although the cerebellar and the brainstem glucose metabolism decreased in all MSA patients, such a decrease was not observed in the SND patients. The decrease in the glucose metabolism for the non-cortical regions in the MSA patients seems to be due to a diffuse depletion of the neurons not restricted to the nigrostriatal neurons. Deafferentation to the cerebral cortices seems to result in a decreased cortical metabolism. The differences in the glucose metabolism between MSA and PD as assessed by PET may be caused by the pathophysiological differences between MSA and PD, and such differences therefore appear to be useful when making a differential diagnosis between MSA and PD. The relative sparing of the brainstem and cerebellar glucose metabolism is considered to be a feature of patients with SND.
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PMID:Glucose metabolism in the cortical and subcortical brain structures in multiple system atrophy and Parkinson's disease: a positron emission tomographic study. 899 7

"Parkinson plus" is a group of sporadic degenerative disorders associating Parkinsonism, poorly sensitive to L-dopa, to other neurological syndromes. Thus, progressive supranuclear palsy includes Parkinson's disease, vertical gaze paralysis, nuchal dystonia and dementia; multisystem atrophies associate to different degrees Parkinson's disease (striatonigral degeneration), a cerebellar syndrome (olivopontocerebellar atrophy), dysautonomia (Shy-Drager syndrome), pyramidal syndrome, etc. Other diseases (corticobasal degeneration, diffuse Lewy body disease) also belong to the Parkinson "plus" group. Clinical differentiation between Parkinson "plus" and idiopathic Parkinson's disease is difficult. Their prognosis and treatment are substantially different. Certain diagnosis is based solely upon anatomical observations.
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PMID:[Parkinson "plus"]. 920 70


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