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 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

Deep-brain stimulation (DBS) of the subthalamic nucleus (STN) is an established treatment for motor complications in Parkinson's disease. 20 years of experience with this procedure have contributed to improved understanding of the role of the STN in motor, cognitive, and emotional control. In Parkinson's disease, the pathological STN neuronal activity leads to motor, cognitive, and emotional inhibition. Deafferentation of the STN by DBS can reverse such behavioural inhibition. The release of this brake allows both motor and non-motor improvement, but can also be associated with excessive motor, cognitive, and emotional behavioural disinhibition. Conversely, the notable reduction in anti-parkinsonian drug dose allowed by motor improvement can unveil mesolimbic hypodopaminergic behaviours such as apathy, anxiety, or depression. Fine-tuning of stimulation parameters with dopaminergic drugs is necessary to prevent or improve pathological behaviours.
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PMID:Mood and behavioural effects of subthalamic stimulation in Parkinson's disease. 2455 7