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)

Because it is commonly believed that acetylcholine is a synaptic transmitter in the caudate nucleus and that the reduction of striatal biogenic amines in Parkinson's disease leads to acetylcholine supersensitivity in the caudate nucleus, we investigated the effects of the muscarinic blocking agent scopolamine on synaptic responses of neurons in the intact feline caudate nucleus and in the caudate nucleus depleted of dopamine by long-standing nigrostriatal lesions. In the intact caudate nucleus, micro-iontophoretic application of scopolamine selectively blocked the neuronal responses to stimulation of the caudate nucleus near the recording site without affecting the responses to stimulation of the sensorimotor cortex or the substantia nigra in the same fashion. This suggests that acetylcholine is a synaptic transmitter of caudate interneurons. Responses to thalamic stimuli were also blocked by scopolamine, suggesting that acetylcholine may be a transmitter of thalamic afferents although the course of these afferents is unclear. In the dopamine-depleted caudate nucleus scopolamine was more effective than in the intact caudate nucleus blocking the neuronal responses to stimulation of the caudate nucleus. This greater blocking effect by scopolamine suggests an increased effect of endogenous acetylcholine in this response and supports previous observations of an increased excitatory effect of iontophoretic acetylcholine in the dopamine-depleted caudate nucleus. These results suggest that the acetylcholine supersensitivity which follows nigrostriatal degeneration may be due to increased effectiveness of synaptic transmission by cholinergic interneurons in the caudate nucleus.
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PMID:Selective blockade by scopolamine of synaptic responses in cat's caudate nucleus and its modification by lesions of the substantia nigra. 21 58

Large numbers of Lewy bodies in the substantia nigra were found in a case of Alzheimer's disease. Parkinsonian symptoms were not recognized. The patient appears to be an example of an association recognized by Woodard but not yet understood. The case is discussed in the context of reported relationships between Parkinson's disease or "Lewy body disease" and dementia, on the one hand, and reports linking various forms of psychoses with an unusually high incidence of Lewy bodies, on the other.
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PMID:Lewy bodies in the presence of Alzheimer's disease. 21 17

Five cases of age range 62-72 years with progressive dementia and muscular rigidity are reported and discussed from the clinicopathologic point of view. The neuropathology of these cases was characterized by the widespread occurrence of Lewy bodies (LB) in the CNS as well as the presence of senile changes. The presence of numerous LB in the cerebral cortex and basal ganglia was especially characteristic, although their distribution pattern in the diencephalon and brain stem was identical to that found in paralysis agitans. On the other hand, the presence of senile changes in the cerebral cortex was almost identical to the neuropathology of senile dementia or Alzheimer's disease. Nosologically, the present cases may represent either a combination of atypical paralysis agitans with senile dementia and Alzheimer's disease, or a new disease.
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PMID:Dementia-Parkinsonism syndrome with numerous Lewy bodies and senile plaques in cerebral cortex. 22 31

Reassociation kinetics analyses with radioiodinated herpes simplex type 1 DNA and influenza A/NWS RNA were performed in the presence of tissue nucleic acids from defined loci of the brains of nine patients with idiopathic Parkinson's disease, one normal control brain, and the brains of uninfected mice or mice infected with either herpes simplex type 1 virus or influenza A/NWS virus. Herpes simplex type 1 DNA was detected by an increased reassociation rate in the herpes simplex type 1 virus-infected mouse brains. Influenza A/NWS RNA was detected by reassociation in the influenza A/NWS virus-infected mouse brains. Experimental limits for the detection of homologous nucleic acids are given for each separate experiment with human or mouse tissue. Within these detection limits, nucleic acids complementary to herpes simplex type 1 DNA or influenza A/NWS RNA were not detected in any of the brains of patients with idiopathic Parkinson's disease.
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PMID:Nucleic acid homology studies of viral nucleic acids in idiopathic Parkinson's disease. 22 43

Clinical data demonstrate that there is a significant difference between at least two types of idiopathic Parkinsonian patients; a benign type of Parkinson's disease and a malignant type. They can be distinguished by the time course of a disability-score, independent of the duration of the disease. The benign cases respond very well to L-Dopa (Madopar) treatment and show a long lasting (7 years) drop in the disability, whereas the improvement of disability in the malignant cases is much smaller and lasts for about one year, followed by an increase of disability. The duration of the disease is 12,5 +/- 0,4 years in the benign type but only 4,0 +/- 0,3 years in the malignant type. Akinetic crises, off-phases, hyperkinetic crises and toxic deliria after Madopar treatment can be observed later in the benign than in the malignant cases. These results suggest that the degeneration of the dopaminergic nigrostriatal system occurs much more rapidly in malignant cases than in benign cases of Parkinson's disease.
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PMID:Distinction between benign and malignant type of Parkinson's disease. 23 Sep 30

Sleep characteristics are studied in 7 patients with sequelae of manganese intoxication and in 8 controls. A reduction in the length of the REM stage was observed, which could be prolonged by L Dopa administration, but without achieving values comparable to the controls. No changes were noted in the non-REM stage of sleep. These results are similar to the ones obtained in Parkinson's disease, suggesting clinical and probably biochemical similarities between the 2 conditions. The blood concentrations of growth hormone during sleep in the manganic patients was lower than in the control group, and no significant variations were noted after L Dopa administration.
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PMID:[Sleep stages and growth hormone in manganese poisoning. Effects of L dopa]. 23 4

Thirty-five parkinsonian patients (five untreated, six with levodopa only, seven with levodopa plus Ro 4-4602, nine with anticholinergic and/or antihistaminic medication, and eight with the anticholinergic/antihistaminic medication plus amantadine) and 35 age-matched control subjects were studied. Platelets isolated from each individual plasma were incubated with 14C-dopamine. Uptake was found to be decreased to a significant degree in all treated or untreated parkinsonian patients when compared with control subjects. Anticholinergic and/or antihistaminic medication, with or without amantadine, further decreased the dopamine uptake into platelets, while levodopa alone or with Ro 4-4602 returned uptake values to near normal. Dopamine efflux paralleled exactly the uptake values. The fact that parkinsonian platelets exhibit impaired dopamine uptake, while age-matched control platelets do not, constitutes the first direct evidence in favor of a generalized dopamine defect in Parkinson's disease.
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PMID:Uptake and efflux of 14-C-dopamine in platelets: evidence for a generalized defect in Parkinson's disease. 23 81

The authors report experiments in rats with 6-hydroxydopamine (6-OHDA), a chemical agent used for creating lesions in catecholamine neurons. Stereotaxic injection of 6-OHDA into the compact zone of the substantia nigra induced degeneration of the nigrostriatal dopamine (DA) system, confirmed by histology and histochemistry of the substantia nigra and by dopamine determinations in the neostriatum. These observations closely mimic those found in Parkinson's disease. In the experimental model a rotatory behavior is induced by DA agonists; this response has been used to test drugs for potential therapeutic use and also in basic studies of the extrapyramidal system. This technique may be useful in developing other experimental models for neurosurgical problems involving catecholamine pathways.
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PMID:Use of 6-hydroxydopamine to create lesions in catecholamine neurons in rats. 23 24

The most prominent symptom of Shy-Drager syndrome is the asympathicotonic orthostatic (postural) hypotension, which is associated with a number of additional autonomic and neurological disturbances: disorders of micturition, sphincter disturbances, impotence, anhidrosis, hypokinesia, rigidity, pyramidal symptoms, cerebellar dysfunction and nuclear pareses due to anterior horn cell degeneration. The various disorders are not caused by ischemia or hypotension, but they represent parts of a multisystemic disease of still unknown etiology. According to different extension and neuropathological criteria it has been suggested to distinguish two types of neurogenic (idiopathic) orthostatic hypotension. Moreover, differential diagnosis of the Shy-Drager syndrome has to consider postural hypotension occuring as a symptom in some neuropathies and Parkinson's disease. Symptomatology, course, prognosis and treatment of Shy-Drager syndrome are described, as well as relevant findings of apparative investigations, pharmacological and hemodynamic tests and neuropathological findings in autopsied cases reported in the literature. This review was initiated by two clinically investigated cases of Shy-Drager syndrome.
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PMID:[The Shy-Drager syndrome (author's transl)]. 24 13

The diagnosis of Parkinson's disease is mostly likely to be made when it is kept in mind, when it is thought of in a broad context, when patients are seen while moving, and when the tests for the three disorders of movement are systematically performed.
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PMID:Parkinson's disease as a disorder of movement. 26 19


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