{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T11:19:23Z","timestamp":1761823163055},"reference-count":160,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1991,12]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides.<\/jats:p>","DOI":"10.3171\/jns.1991.75.6.0845","type":"journal-article","created":{"date-parts":[[2009,5,19]],"date-time":"2009-05-19T16:25:34Z","timestamp":1242750334000},"page":"845-855","source":"Crossref","is-referenced-by-count":119,"title":["The role of neuroeffector mechanisms in cerebral hyperperfusion syndromes"],"prefix":"10.3171","volume":"75","author":[{"given":"Robert","family":"Macfarlane","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael A.","family":"Moskowitz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Danos E.","family":"Sakas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erol","family":"Tasdemiroglu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Enoch P.","family":"Wei","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hermes A.","family":"Kontos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1754","reference":[{"key":"b1","series-title":"Brain Res","first-page":"247","article-title":"The calcium channel antagonist, \u03c9-conotoxin, and electric organ nerve terminals: binding and inhibition of transmitter release and calcium influx.","volume":"453","author":"Ahmad","year":"1988"},{"key":"b2","series-title":"Am J Physiol","first-page":"F89","article-title":"Failure to abolish reactive hyperemia by indomethacin in denervated kidneys of rabbits.","volume":"233","author":"Aizawa","year":"1977"},{"key":"b3","series-title":"Am J Pathol","first-page":"437","article-title":"Cerebral ischemia. 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