Patterns of cerebral glucose utilization in Parkinson's disease and Huntington's disease
- PMID: 6234856
- DOI: 10.1002/ana.410150723
Patterns of cerebral glucose utilization in Parkinson's disease and Huntington's disease
Abstract
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.
Similar articles
-
Local cerebral glucose utilization in symptomatic and presymptomatic Huntington's disease.Res Publ Assoc Res Nerv Ment Dis. 1985;63:199-209. Res Publ Assoc Res Nerv Ment Dis. 1985. PMID: 3161165
-
Cerebral metabolism and atrophy in Huntington's disease determined by 18FDG and computed tomographic scan.Ann Neurol. 1982 Nov;12(5):425-34. doi: 10.1002/ana.410120504. Ann Neurol. 1982. PMID: 6217782
-
Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease.Brain. 1996 Dec;119 ( Pt 6):2085-95. doi: 10.1093/brain/119.6.2085. Brain. 1996. PMID: 9010012
-
Positron emission tomography imaging of regional cerebral glucose metabolism.Semin Nucl Med. 1986 Jan;16(1):2-34. doi: 10.1016/s0001-2998(86)80002-2. Semin Nucl Med. 1986. PMID: 2935938 Review.
-
Cerebral glucose and dopa metabolism in movement disorders.Can J Neurol Sci. 1987 Aug;14(3 Suppl):448-51. doi: 10.1017/s0317167100037896. Can J Neurol Sci. 1987. PMID: 2960430 Review.
Cited by
-
Comparative Analysis of Mutant Huntingtin Binding Partners in Yeast Species.Sci Rep. 2018 Jun 22;8(1):9554. doi: 10.1038/s41598-018-27900-5. Sci Rep. 2018. PMID: 29934597 Free PMC article.
-
Transitions in metabolic and immune systems from pre-menopause to post-menopause: implications for age-associated neurodegenerative diseases.F1000Res. 2020 Jan 30;9:F1000 Faculty Rev-68. doi: 10.12688/f1000research.21599.1. eCollection 2020. F1000Res. 2020. PMID: 32047612 Free PMC article. Review.
-
Factor analysis of regional cerebral glucose metabolic rates in healthy men.Eur J Nucl Med. 1992;19(7):469-75. doi: 10.1007/BF00185851. Eur J Nucl Med. 1992. PMID: 1644103
-
[18F]FDG PET in conditions associated with hyperkinetic movement disorders and ataxia: a systematic review.Eur J Nucl Med Mol Imaging. 2023 Jun;50(7):1954-1973. doi: 10.1007/s00259-023-06110-w. Epub 2023 Jan 27. Eur J Nucl Med Mol Imaging. 2023. PMID: 36702928 Free PMC article. Review.
-
Are cognitive changes the first symptoms of Huntington's disease? A study of gene carriers.J Neurol Neurosurg Psychiatry. 1998 Feb;64(2):172-7. doi: 10.1136/jnnp.64.2.172. J Neurol Neurosurg Psychiatry. 1998. PMID: 9489526 Free PMC article. Clinical Trial.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
