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Background and Purpose: Radiation exposure from neurointerventional procedures and diagnostic neuroimaging can be substantial, with many recommendations offered to guide the interventionalist in the conscientious use of ionizing radiation. Patients presenting with an aneurysmal subarachnoid hemorrhage can undergo multiple imaging procedures during a prolonged hospital course. Therefore, we reviewed a cohort of such patients to identify the sources and quantify the cumulative radiation exposure seen during their hospitalization., Materials and Methods: We retrospectively reviewed a single-center experience with these patients to define the potential for short-term skin injury and long-term oncologic risk due to absorbed radiation dose and sources of ionizing radiation and their contribution to the cumulative absorbed dose to the cranial tissues., Results: We demonstrated that substantial cumulative doses can be seen, with 87% of the cumulative absorbed dose occurring during neurointerventional procedures and 7% from CT. Mathematic modeling was performed identifying potential techniques to further reduce the cumulative radiation absorbed dose to these patients., Conclusions: We conclude that repetitive irradiation during the care of patients with aneurysmal subarachnoid hemorrhage can result in significant cumulative doses and a variety of techniques can be applied to reduce this absorbed dose. Use of radiation for diagnostic and therapeutic purposes during prolonged procedures of patients with subarachnoid hemorrhage demands diligence throughout the hospitalization.

A 43-year-old patient with a basilar apex aneurysm had a 4.5-mm x 14-mm Enterprise stent placed from the midbasilar artery to the left P1 segment of the posterior cerebral artery. The patient experienced vertigo 4 months after stent placement and 1 week after stopping clopidogrel. At 5 months postembolization, angiography showed stent migration into the proximal basilar artery. This is the first described case of the spontaneous delayed migration of a self-expanding intracranial microstent.

Acidosis, hypoxia, and hypoglycemia rapidly and transiently appear after reduction of cerebral blood flow. Acidosis also accompanies head trauma and subarachnoid hemorrhage. These insults result in necrotic and apoptotic loss of neurons. We previously demonstrated that transient acidification of intracellular pH from 7.3 to 6.5 induces delayed neuronal loss in cultured hippocampal slices (49). We now report that acidosis induced both necrotic and apoptotic loss of neurons. Necrosis and apoptosis were distinguished temporally and pharmacologically. Necrosis appeared rapidly and was dose dependent with the duration of the acidosis treatment. Apoptosis was delayed with maximal number of apoptotic cells seen with a 30-min acidosis treatment. Apoptotic neuronal loss was accompanied by DNA fragmentation and was blocked by inhibitors of protein and RNA synthesis, ectopic expression of the anti-apoptotic gene bcl-2, or an inhibitor of caspases, proteases known to be activated during apoptosis. Necrotic neuronal loss was unaffected by these treatments. Hypothermia, a treatment known to attenuate neuronal loss following a variety of insults, blocked both acidosis-induced necrosis and apoptosis. These results indicate that acidosis is neurotoxic in vitro and suggest that acidosis contributes to both necrotic and apoptotic neuronal loss in vivo., (Copyright 2000 Academic Press.)