外傷性遷延性昏睡における脳循環動態に関する一知見—131I-MAAを用いて

STUDY ON THE HEMODYNAMICS OF APALLIC SYNDROME USING 131I-MAA

Ｉ．はじめに

　我々は¹³¹I-MAA （¹³¹I標識大凝集アルブミン）を用いて脳動静脈奇型の脳短絡血流量を測定する方法を開発し，脳動静脈奇型の循環動態の解明，特に治療効果の判定に有用である事を報告した^7,13）。今回我々は同様の方法を外傷性遷延性昏睡症例を中心に，その他種々の原因による意識混濁患者に応用してみた。外傷性であれ，脳血管障害であれ，高度に脳が侵されている患者の脳循環動態にangioparalyticな要素が関与している事はすでに多く報告されている^{4,6,8,10,15,20）}。そしてangiopara—1ysisが存在するか否かの臨床的な示標の一つとして，脳血管撮影上のearly venous fillingがあげられる。

　このearly venous fillingの発現にはいろいろの機序があげられているが，形態学的には脳血管の拡張特に動静脈吻合の開大の関与が推測される。もしそれが事実であるならば，頸動脈に注入したMAA粒子の一部は脳の末梢循環を通過してしまうはずである。そのことを確かめるために我々は種々の原囚による意識混濁患者の頸動脈内に¹³¹I-MAAを注入し検索した。その結果興味ある知見を得たので報告し，あわせて若干の文献的考察を加えたい。

It is true that early venous filling is often visu-alized in the angiogram of a severely damaged brain, while the gas clearance analysis of the cerebral circulation sometimes show the third rapid phase which suggests existence of luxury perfusion or shunting of blood from arterial to venous channels.

From these facts it is assumed that pathological cerebral hemodynamics in the patients of severely disturbed consciousness might permit the particles larger in size than the caliber of capillaries to pass through the cerebral vascular net works.

For the purpose to confirm the assumption in-tracarotid injection of ¹³¹I-MAA were performed on eleven cases, which included, according to the severity of consciousness disturbance, three of apallic state, four of comatous state and four of comatous state and four of slightly demented mental state. The last four were selected as normal controls.

The ¹³¹I-MAA was especially prepared in its size ranging from 25 to 30 lung liver ratio, which is the conventional parameter representing the particle size distribution of ¹³¹I-MAA.

Linear scanning tests of the cases after intra-carotid injection of ¹³¹I-MAA revealed that in two traumatic apallic patients the ¹³¹I-MAA particlespassed through the brain and were captured by the capillary net works of the lungs. Such patho-logical findings were not recorded in other cases including normal controls.

Pathogenesis of the passing through phenomena was discussed and it was suggested that in someof the apallic syndromes the function of preca-pillary arteriovenous anastomoses was more en-hanced than normal ones, which made it possible for the larger MAA particle to pass through the cerebral vascular net works of the patients.