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)

A progressive parkinsonian disorder predicts pathology in the substantia nigra and possibly elsewhere in the basal ganglia. Parkinson's disease is a manifestation of Lewy body disease, which is characterized by the association between Lewy bodies and cell degeneration in specific neuronal populations. Striatonigral degeneration is part of multiple system atrophy and is characterized by striatal and nigral degeneration without neuronal inclusion bodies, but glial inclusions have been described. Steele-Richardson-Olszewski disease is characterized by the globose neurofibrillary tangle and predominant brain stem pathology. Corticobasal degeneration shows similar midbrain pathology and a round, filamentous inclusion in the substantia nigra, not unlike the globose tangle, but there is also focal frontoparietal cortical atrophy. The combination of the distribution of degeneration and nerve cell morphology identify apparently distinct disorders, but most of the neuronal inclusions are not disease specific.
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PMID:Neuropathology of Parkinson's disease and related syndromes. 158 79

Striatonigral degeneration (SND) is difficult to diagnose in vivo. The purpose of this study was to detect the best indicators for an early and reliable diagnosis of the disease. Eighteen patients clinically diagnosed as having SND were selected with rigorous inclusion criteria and compared to 18 patients with Parkinson's disease (PD) matched for age and disease duration. Apart from dysautonomia, the principal discriminant clinical features that distinguished SND from PD were the early appearance of the following symptoms and signs: (a) severe and atypical progressive parkinsonism characterized by bilateral bradykinesia and rigidity, slowness of gait, postural instability, and falls, and poor or absent response to adequate levodopa treatment; (b) increased tendon reflexes associated or not with frank pyramidal signs, severe dysarthria, and less consistently, dysphagia, stridor, antecollis, and stimulus-sensitive myoclonus, which, when present, are highly suggestive of the disease.
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PMID:"Pure" striatonigral degeneration and Parkinson's disease: a comparative clinical study. 765 45

Striatonigral degeneration (SND) is sporadic, middle-aged on set degenerative disease of the nervous system which etiology is unknown. SND is considered one of multiple system atrophy (MSA). Clinically parkinsonian symptom is dominant and then it is difficult to distinguish from idiopathic Parkinson's disease (PD). Pathologically neuron cell loss and gliosis are recognized principally striatum (mainly putamen) and substantia nigra. Putaminal hypointensity and slit-hyper intensity in the outer margin of putamen are often seen on T2-weighted 1.5 Tesla MRI. PET with [18 F] fluorodeoxyglucose indicates a considerably decreased glucose utilisation in the striatum of SND, whereas glucose utilisation are normal in PD. Striatal dopamine D1, D2 receptors are reduced. Response to Levodopa is poor or absent.
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PMID:[Striatonigral degeneration]. 901 34

Multiple System Atrophy (MSA) and idiopathic Parkinson's disease (PD) can be difficult to distinguish. There is an ongoing debate about the diagnostic value of the growth-hormone response to clonidine (CGH-test) in PD and MSA. We investigated whether the CGH-test can identify individual patients in the early stages of PD (n = 21) and Striatonigral Degeneration (SND, n = 11), a particular variety of MSA. Patients were diagnosed on the basis of clinical criteria and IBZM-SPECT. Clonidine induced a greater total serum growth-hormone production in PD than in SND (p = 0.01). However, taking the difference in prevalence of PD and SND into account, and because of the low likelihood ratios of the test, an increase of GH after clonidine increases the pre-test probability for PD by about only 5 %, while an absent response of GH also increases the pre-test probability for SND by about 5 %. We conclude that the CGH-test discriminates between groups of patients with PD and SND, but has little practical diagnostic value for identifying individual patients.
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PMID:Stimulation of growth-hormone release with clonidine does not distinguish individual cases of idiopathic Parkinson's disease from those with striatonigral degeneration. 1224 40