Patterns of cerebral glucose utilization in Parkinson's disease and Huntington's disease.
Patterns of local cerebral glucose utilization were measured with positron emission tomography using the fluorine-18-labeled fluorodeoxyglucose (18FDG) method in 8 patients with Parkinson's disease, in 13 patients with Huntington's disease, in 15 subjects at risk for Huntington's disease, and in aged-matched normal control subjects. On the average, global cerebral metabolism in patients with Parkinson's disease was moderately reduced (20%), but the relative distribution of glucose utilization throughout the brain in these patients was normal. These results support the conclusion that alterations of the nigrostriatal pathway in Parkinson's disease have no major selective effect on the metabolism of particular cerebral regions. In Huntington's disease, however, there was a characteristic decrease in glucose utilization in the caudate nuclei and putamen, and this local hypometabolism appeared early and preceded bulk tissue loss. In patients with Huntington's disease, glucose utilization typically was normal throughout the rest of the brain, regardless of the severity of symptoms and despite the apparent shrinkage of brain tissue. The results also suggest the possibility that the caudate nuclei may be hypometabolic in some asymptomatic subjects who are potential carriers of the autosomal dominant gene for Huntington's disease.[1]References
- Patterns of cerebral glucose utilization in Parkinson's disease and Huntington's disease. Kuhl, D.E., Metter, E.J., Riege, W.H., Markham, C.H. Ann. Neurol. (1984) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
