TRIGEMINAL AFFERENTS AND BRAIN-STEM CENTERS INVOLVED IN THE OCCURRENCE OF CEREBRAL VASOSPASM

Cisternal injections of blood in the rat and squirrel monkey produce a n angiographically demonstrable biphasic vasospasm with a maximal late spasm at two days in the rat and six days post-subarachnoid hemorrhag e (SAH) in the monkey. The SAH induces a decrease in cerebral blood fl ow of about 25% and a corresponding increase in glucose uptake of betw een 30% and 50%. In about half of the animals low-flow areas were note d in the cortex and the basal ganglia with a corresponding marked incr ease in glucose uptake. Lesioning of the A2-nucleus, its ascending pat hway or the median eminence prevents the occurrence of spasm. Similarl y, treatment with a substance P antagonist or gammaglobulin against su bstance P prevents or significantly reduces the degree of spasm. A uni lateral post-ganglionic trigeminal lesion causes an ipsilateral constr iction of the cerebral arteries of 27%, while a preganglionic lesion d oes not affect the baseline diameter. A pre- or post-ganglionic trigem inal lesion induces an increase in glucose uptake globally of about 50 % without influencing cerebral blood flow. Following SAH the decrease in blood flow in both groups of lesioned animals is similar to that se en in controls. After SAH there is no further change in glucose uptake in the animals with a preganglionic lesion, while in the post-ganglio nically lesioned animals there is an additional increase in glucose up take of about 50% as compared to controls or the animals with a pregan glionic lesion.