雑誌文献を検索します。書籍を検索する際には「書籍検索」を選択してください。

Brain and Nerve No to Shinkei Volume 30, Issue 10 （October 1978）

Brain and Nerve 脳と神経 30巻10号（1978年10月発行）

Japanese English

原著

脳梗塞におけるCT contrast enhancement陽性像の出現機序—局所脳循環，脳血管螢光撮影および病理学的検討 MECHANISM OF CONTRAST ENHANCEMENT ON COMPUTED TOMOGRAPHY IN CEREBRAL INFARCTION : REGIONAL CEREBRAL BLOOD FLOW, FLUORESCEIN ANGIOGRAPHY, AND PATHOLOGlCAL STUDY 河瀬斌 ¹ , 水上公宏 ¹ , 金弘 ¹ , 竹前紀樹 ¹ , 荒木五郎 ² Takeshi Kawase ¹ , Masahiro Mizukami ¹ , Hiroshi Kin ¹ , Toshiki Takemae ¹ , Gorō Araki ² ¹脳血管研究所美原記念病院脳神経外科 ²脳血管研究所美原記念病院内科 ¹Department of Neurosurgery, Institute of Brain and Blood Vessels, Mikara Memorial Hospital ²Department of Internal medcine, Institute of Brain and Blood Vessels, Mikara Memorial Hospital pp.1121-1129

発行日 1978年10月1日 Published Date 1978/10/1

DOI https://doi.org/10.11477/mf.1406204322

PDF(11683KB)

有料閲覧

Abstract 文献概要
1ページ目 Look Inside

I．はじめに

　CTにおける造影剤増強法は疾患の診断精度の向上に重要となりつつある。脳梗塞においても造影剤注入後のCTにしばしば著しいhigh density （以下CE陽性像と略す）が出現することが知られている。しかしその発現機序については血管内の造影剤濃度を反映するという説，すなわちluxury perfusion,hyperemia，^10）新生血管内の血液のpoolingによるものであるとする説^19）と，血液脳関門破綻による造影剤の血管外漏出であるとする説^5,22），とに大別される。しかも前者の説に基づいて，contrast enhancement前後のX線吸収係数の変化から局所脳血液量（rCBV）を算出しようとする報告もみられる^15,21）。

　本報告の目的は脳梗塞におけるCE陽性像の発現機序を知ることにある。そのためにまず，CTの追跡から脳梗塞におけるCE陽性像の出現頻度，出現時期，および出現部位を検討した。さらにCE陽性部の増強値（value　of enhancement），局所脳循環量（rCBF），脳血管螢光撮影fluorescein angiography，（以下FCAと略す）および病理学的所見を検討することにより，CE陽性像の出現機序について考察を加えた。

Thirty-five patients with cerebral infarction were studied with serial computed tomography (CT). The patients with a small infarction located in the basal ganglia or the brain stem were excluded. Regional cerebral blood flow (rCBF) was also inves-tigated in 24 patients by the ¹³³Xe intracarotid injection method, and thirteen of them had rCBF study when CT showed positive contrast enhance-ment (CE). Additional three patients, who had shown positive CE, underwent surgery, and fluorescein cortical angiography (FCA) was per-formed at operation in two patients, and patho-logical specimen was obtained in one patient.

More than 90 percent of the patients with infarction showed positive CE, mostly 10 days to one month of stroke. The quantitative value of enhancement in the lesion was 5 to 22 times (average 9 times) higher than that of the opposite normal hemisphere. rCBF values of enhanced area were significantly higher (49.7±12.7m//100 g/min.) than that of the area where showed no enhance-ment on CT (29.0±9.3ml/100 g/min.). However, hyperemic regions were seen only in four patients, and two of them showed no enhancement on CT. This fact does not agree with the hypothesis that positive CE indicates a manifestation of the focal hyperemia. FCA showed extravasation of fluores-cein dye in the perivascular spaces. Microscopic examination of specimen revealed numerous lipid-laden microglias and capillaries in the infarcted area, particularly at the edges of the infarct.

These findings suggest that the positive CE in cerebral infarction may be caused by extravasation of contrast material by opening the blood brain barrier of newly formed or dilated vessels in the infarcted area.