Huber M, Pawlik G, Bamborschke S, Fink G R, Karbe H, Schlenker M, Bewermeyer H, Heiss W D
Neurologische Universitätsklinik, Köln, Federal Republic of Germany.
J Neurol. 1992 Mar;239(3):157-61. doi: 10.1007/BF00833917.
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.
