実験・脳血管れん縮—脳かん流障害と血管撮影の比較

EXPERIMENTAL CEREBRAL VASOSPASM: COMPARISON OF PERFUSION DEFICITS WITH ANGIOGRAPHY

I．はじめに

　脳動脈瘤破裂後に発生する血管れん縮が，脳虚血更には脳梗塞を起し得ることは，一般に信じられているが，血管撮影上れん縮の見られる脳動脈瘤の患者の手術適応時期については，種々の意見に分れる。現在多くの脳外科医は血管れん縮の見られる患者では，れん縮が消退するまで手術を延期する策をとる^1）が，一部の脳外科医は，患者の神経症候が悪くなければ，れん縮の有無にかかわらず手術する^9）。この混乱は，血管れん縮の見られる患者のうち，どの患者で，れん縮が脳虚血を起したか，又は起す準備状態にあるのか，言い換えれば，どの患者で手術危険率が高いか判断できないことに起因する。今までの臨床的及び実験的血流量の測定に於ても，血管撮影上明らかなれん縮が見られるにもかかわらず，呼応した領域の血流量は低下するとは限らない^4,14）。又，血管撮影でれん縮の見られる動脈のかん流領域に剖検時，脳梗塞の見つからないこともしばしばである^13）。報告する予備実験は，クモ膜下出血後の血管撮影に見られるれん縮と，カーボンブラックでみた脳のかん流障害の関係を見る目的で行つた。

Current clinical management of patients withvasospasm is confused. Prior clinical and ex-perimental cerebral blood flow studies of vasospasmhave not revealed consistent blood flow changesdespite vasospasm demonstrated by angiography.As part of an investigation we have attempted toconfirm or deny a perfusion deficit in experimentalcerebral vasospasm seen on an angiogram, andfurther, to correlate this data with the degree ofspasm and its location.

The final data were collected from 22 Rhesusmonkeys, which underwent bi-axillal angiographybefore and after subarachnoid hemorrhage. Animalswere rearteriogramed intermittently, until sacrificedat varying intervals after the initial hemorrhage(immediate to 12 days). Each animal was perfusedwith a mixture of carbon black and formalin atarterial pressures. The brains were placed then informalin. Each brain was later coronally sectionedand non-carbon black perfused area was examinedmacroscopically.

No consistent correlation was found between thepresence of spasm measured by angiograms and theexistence of non-carbon black perfused areas ofthe brain. Although severe angiographic vasospasmwas often associated with perfusion deficits, thelatter were seen in 3 animals with subarachnoidhemorrhage but no angiographic spasm. The mosttypical perfusion deficit resembled "border zone"ischemia in both animals with minor and severeangiographic spasm. Conversely severe spasm wasoccasionally associated with normal perfusion.

These data suggest the following:

1) Angiography is an inadequate means ofevaluating the phenomenon of cerebral vasospasm.

2) Angiographic vasospasm does not always causea decrease in perfusion.

3) Angiographic vasospasm is sometimes inno-cent, and may not be an absolute contra-indicationto aneurysm surgery by itself alone.