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Biomedical subjects

J M Fein

Publications and source records attributed to J M Fein.

At least 19 recordsLinked to original sources
PubMed1985

Bypass induced cerebral aneurysm.

The development of aneurysm after EC-IC bypass was studied in 6 cases by angiography. Increase in blood flow and alteration of slow pattern are contributing factors. It is suggested that the difference in structure between cortical arteries and scalp arteries enhances their sensitivity to transcranial pressure difference. High TCP gradients may induce post-operative aneurysm, and careful management of blood flow through the bypass is recommended.

Adult↗
PubMed1977

Brain death. I. A status report of medical and ethical considerations.

Use of neurologic criteria to pronounce death, although accepted by many, has caused controversy among physicians, lawyers, legislators, philosophers, and theologians. The present work attempts to resolve this by accomplishing four objectives. (1) It summarizes scientific information that establishes the ability to determine the state of brain death with certainty on the basis of presently available clinical and laboratory criteria. (2) It shows that the concept of brain death is in accord with secular philosophy and the three major Western religions. (3) It documents the need for legislative recognition that death may be pronounced on the basis of neurologic criteria. (4) It reviews the present status of judicial and statutory law relating to the determination of death in the United States.

Brain Death↗
PubMed1976

Brain energetics and circulatory control after subarachnoid hemorrhage.

Ischemia-provoking factors such as vasospasm, decreased cerebral perfusion pressure, and intravascular thrombosis may be present after subarchnoid hemorrhage (SAH). When these factors were not present during controlled SAH, a primary depression of cerebral glycolysis associated with normal stores of energy-rich phosphates was found. Although cerebral blood flow usually changes in response to changes in cerebral metabolic needs, this influence on the circulation was not evident in the early hours after SAH. After 3 to 4 hours an erratic decrease in blood flow occurred, probably related to vasospasm, and there were measurable decreases in energy-rich phosphates similar to those occurring after more severe and prolonged ischemias. These findings are indicative of abnormally erratic vascular responses to metabolic cues and may play a role in producing the encephalopathy of SAH.

Animals↗