抄録
Although the occurrence of so-called late cerebral vasospasm after subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysm is well-known, its etiology still remains obscure. The authors previously reported that C1q (q-subfraction of the first complement component) binding substance, formed in blood-stained cerebrospinal fluid, might trigger the activation of the complement system in the subarachnoid space and develop cerebral vasospasm. This time, the authors investigated constricted cerebral arterial walls after SAH by immunofluorescent technique to see what immunological changes they were subject to, following the activation of the complement system and in the course of the possible production of chemical mediators (anaphylatoxin, etc.). One hundred and thirty-eight major intracranial arterial specimens obtained from patients with and without central nervous system disorders at autopsy were examined for deposits of immunoglobulin G (IgG), immunoglobulin A (IgA), immunoglobulin M (IgM), the third complement component (C3) or fibrinogen in the arterial walls. In cases of SAH with definite or probable vasospasm, deposits of both IgG and C3 in the arterial media were observed in 74% of the arterial specimens examined. However, these deposits could not be found at all in the patients who died within 48 hours after aneurysmal rupture. The frequency of the deposits of both IgG and C3 was 42% in hypertensive intracerebral hematoma, 44% in cerebral infarction, 42% in brain tumor, 75% in meningoencephalitis. Deposits of IgA, IgM or fibrinogen were also observed in the media, but with much less frequency than those of IgG or C3 in all cases. The significance of deposits of IgG and C3 in the media found in cases with late vasospasm after SAH is unclear at present, but it is thought that they represent an antibody to degenerated arterial smooth muscles due to constriction and complement bound to the antibody. In other words, it is highly likely that those deposits indicate arteritis or an inflammatory process in the arterial wall.
