{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T09:53:05Z","timestamp":1777801985701,"version":"3.51.4"},"reference-count":20,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[1996,5,1]],"date-time":"1996-05-01T00:00:00Z","timestamp":830908800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Child Neurol"],"published-print":{"date-parts":[[1996,5]]},"abstract":"<jats:p>In infants, extreme extension or rotation of the head can occlude one or both vertebral arteries. We sought to determine whether small communicating arteries or asymmetric vertebral arteries could predispose the brain stem to ischemia should such head movements occur. In 68 infants, the carotid, posterior communicating, precommunicator posterior cerebral, basilar and vertebral arteries were fixed in formalin, embedded in resin, the circumferences measured by image analysis, and the relative conductance of blood in each artery per gram of brain calculated. Conductance in the vertebrobasilar and carotid systems lagged behind increases in brain weight during the postnatal growth spurt. In 81% of infants, conductance through the communicating arteries was less than 25% of basilar artery conductance. Conductance in one vertebral artery was less than half that of the contralateral artery in 41% of infants. In conclusion, the lag in available blood flow and small communicating and asymmetric vertebral arteries may predispose the infant brain stem to ischemia if one or both vertebral arteries are occluded by head rotation or extension. Because these head movements are likely to be accentuated in the prone sleeping position (a risk factor for sudden infant death syndrome), we suggest that vertebral artery occlusion may underlie some cases of sudden unexpected infant death. (J Child Neurol 1996;11:181-184).<\/jats:p>","DOI":"10.1177\/088307389601100302","type":"journal-article","created":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T02:13:25Z","timestamp":1230084805000},"page":"181-184","source":"Crossref","is-referenced-by-count":15,"title":["Vulnerability of the Infant Brain Stem to Ischemia: A Possible Cause of Sudden Infant Death Syndrome"],"prefix":"10.1177","volume":"11","author":[{"given":"Roger","family":"Pamphlett","sequence":"first","affiliation":[{"name":"Department of Pathology (Neuropathology Division), University of Sydney, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nichole","family":"Murray","sequence":"additional","affiliation":[{"name":"Department of Pathology (Neuropathology Division), University of Sydney, Sydney, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1996,5,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.7.5.331"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196808082790609"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.26.6.547"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.28.2.185"},{"key":"atypb5","doi-asserted-by":"crossref","first-page":"335","DOI":"10.1542\/peds.72.3.335","volume":"72","author":"Hope EE","year":"1983","journal-title":"Pediatrics"},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1001\/archpedi.1979.02130010036005"},{"key":"atypb7","unstructured":"Aherne WA, Dunnil MS: Morphometry. 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