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Transient Symptomatic Downregulation of Cortical Neurotransmitter Receptor Function Due to Cerebral Hyperperfusion after Arterial Bypass Surgery for a Patient with Ischemic Moyamoya Disease

Cerebral hyperperfusion syndrome following arterial bypass surgery is known as a surgical complication of moyamoya disease (MMD). How cerebral hyperperfusion affects neural function and causes neurological deficits remains unknown. We report here a case with cerebral hyperperfusion syndrome after ar...

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Detalles Bibliográficos
Autores principales: SHIMADA, Yasuyoshi, KOJIMA, Daigo, YOSHIDA, Jun, KOBAYASHI, Masakazu, YOSHIDA, Kenji, FUJIWARA, Shunrou, OGASAWARA, Kuniaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japan Neurosurgical Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236211/
https://www.ncbi.nlm.nih.gov/pubmed/30369534
http://dx.doi.org/10.2176/nmc.cr.2018-0143
Descripción
Sumario:Cerebral hyperperfusion syndrome following arterial bypass surgery is known as a surgical complication of moyamoya disease (MMD). How cerebral hyperperfusion affects neural function and causes neurological deficits remains unknown. We report here a case with cerebral hyperperfusion syndrome after arterial bypass surgery for ischemic MMD. Chronological changes of brain perfusion and central benzodiazepine receptor biding potential were observed using single-photon emission computed tomography. A 20-year-old woman with ischemic MMD underwent arterial bypass surgery. Six days later, cerebral hyperperfusion syndrome developed. During this syndrome, contralateral-to-ipsilateral cerebellar asymmetry of blood flow and a decrease in central benzodiazepine receptor binding potential in the area with hyperperfusion were observed. Four months later, these two findings resolved and a neurological examination revealed no abnormal signs. Cerebral hyperperfusion after arterial bypass surgery for ischemic MMD may lead to transient, reversible reduction of cerebral metabolism and downregulation of cortical neurotransmitter receptor function, resulting in transient neurological deficits.