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Japanese

A Case of Organized Chronic Subdural Hematoma Presented with Transient Neurologic Deficits Seikou Kuwahara 1 , Hirohisa Miyake 1 , Yoko Koan 1 , Masaaki Fukuoka 1 , Yuko Ono 2 , Akihito Moriki 2 , Koreaki Mori 2 , Toshihiko Mokudai 3 , Yasufumi Uchida 3 1Department of Neurosurgery, Mominoki Hospital 2Department of Kochi Gamma Knife Center, Mominoki Hospital 3Department of Neurosurgery, Uchida Neurosurgical Clinic Keyword: organized chronic subdural hematoma , transient neurological deficit , transient ischemic attack(TIA) , CT perfusion pp.355-359
Published Date 2004/4/1
DOI https://doi.org/10.11477/mf.1406100275
  • Abstract
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 A 59-year-old diabetic male presented with transient motor aphasia and monoparesis of the right upper limb. Brain CT scan showed a low density area in the left subdural space with a mild midline shift. Magnetic resonance(MR) T2-weighted and fluid-attenuated inversion recovery(FLAIR) imagings revealed homogenous hyperintensity with a hypointense web-like structure in the subdural hematoma. Cervical MR angiography showed no abnormal lesion at the bifurcation of the bilateral common carotid arteries. Conventional cerebral angiography showed an avascular, crescent, space-occupying mass over the left hemisphere without an etiologic lesion of cerebral ischemia. CT perfusion imagings indicated reduced cerebral blood flow(CBF) and prolonged mean transit time(MTT) in the left middle cerebral artery territory underneath the subdural hematoma. No epileptic discharge was found in electroencephalogram. Operative findings indicated that the hematoma was encapsulated with thickened outer and inner membranes including paste-like materials, and the brain surface was intact. Postoperative CT perfusion imagings revealed normal CBF and MTT. The pathophysiological mechanism which the chronic subdural hematoma produces the transient neurological deficit is still uncertain. The mechanical pressure of the hematoma on the neighboring cerebral vessels may cause impairment of blood flow leading to cerebral ischemia and paralysis of function. Our case indicated the transient neurological deficits attributed to a decreased CBF around the subdural hematoma and a change in pressure exerted by the hematoma during changes of head position and increased blood viscosity.

(Received : February 13, 2004)


Copyright © 2004, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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