Abstract |
18FDG-positron emission tomography performed at different stages in the course of subacute sclerosing panencephalitis revealed a changing pattern of metabolic disturbance. In clinical stage II patients the inflammation in the basal ganglia appeared to lead to neuronal excitation accompanied by hypermetabolism. Widespread cortical functional inhibition of metabolism followed. The striatal inflammation ended with necrosis and hypometabolism, with resulting functional cortical disinhibition; later, deep midbrain structures and brain stem became hypermetabolic. A patient clinically in remission showed no such changes in cerebral glucose metabolism.
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Authors | M Huber, G Pawlik, S Bamborschke, G R Fink, H Karbe, M Schlenker, H Bewermeyer, W D Heiss |
Journal | Journal of neurology
(J Neurol)
Vol. 239
Issue 3
Pg. 157-61
(Mar 1992)
ISSN: 0340-5354 [Print] Germany |
PMID | 1573420
(Publication Type: Journal Article)
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Chemical References |
- Antibodies, Viral
- Fluorodeoxyglucose F18
- Deoxyglucose
- Glucose
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Topics |
- Adolescent
- Antibodies, Viral
(immunology)
- Basal Ganglia
(diagnostic imaging, metabolism)
- Deoxyglucose
(analogs & derivatives)
- Electroencephalography
- Female
- Fluorodeoxyglucose F18
- Glucose
(metabolism)
- Humans
- Male
- Measles virus
(immunology)
- Subacute Sclerosing Panencephalitis
(diagnostic imaging, immunology, metabolism)
- Tomography, Emission-Computed
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