Launes J, Hokkanen L, Nikkinen P, Liewendahl K, Salonen O, Sirén J, Iivanainen M
Department of Neurology, University Central Hospital, Helsinki, Finland.
Neuroreport. 1995 May 30;6(8):1203-6. doi: 10.1097/00001756-199505300-00032.
We studied two patients with herpes encephalitis (HSE) by [99mTc]HMPAO and [123I]iomazenil single photon emission computed tomography. Increased uptake of HMPAO was seen for up to 63 days in the HSE affected brain area. Iomazenil binds to benzodiazepine receptors and can measure neurone loss. Decreased iomazenil uptake was observed a few days after onset, at a time when hyperfixation of HMPAO occurred. Because in HSE neurone loss occurs simultaneously with hyperfixation of HMPAO, it is unlikely that this hyperfixation is caused by increased neuronal activity, as in epilepsy. This suggests that the hyperfixation of HMPAO in HSE occurs in glia and is sustained by inflammation-related hypermetabolism and acidity. The early neurone loss in HSE stresses the importance of immediate antiviral treatment.
我们通过[99mTc]HMPAO和[123I]碘美普尔单光子发射计算机断层扫描研究了两名疱疹性脑炎（HSE）患者。在HSE受累脑区，HMPAO摄取增加可持续63天。碘美普尔与苯二氮䓬受体结合，可测量神经元损失。发病几天后观察到碘美普尔摄取减少，此时出现HMPAO摄取亢进。由于在HSE中神经元损失与HMPAO摄取亢进同时发生，因此这种摄取亢进不太可能像在癫痫中那样由神经元活动增加引起。这表明HSE中HMPAO摄取亢进发生在胶质细胞中，并由炎症相关的高代谢和酸性环境维持。HSE早期的神经元损失强调了立即进行抗病毒治疗的重要性。
