RESUMO
Atraumatic Non-aneurysmal sulcal subarachnoid hemorrhage is very rare. Sulcal subarachnoid hemorrhage (sSAH) is characterized by isolated bleeding in one or a few adjacent sulci. Central sulcus hemorrhage is a rare imaging finding. There are many causes for sSAH. In older patients, sSAH is due to Cerebral Amyloid Angiopathy (CAA), while in younger patients, reversible cerebral vasoconstriction syndrome (RCVS) is the most frequent etiology. Imaging studies help in the evaluation of sSAH. We report a rare case of an isolated central sulcus hemorrhage on computed tomography. sSAH usually occur on the side with acute ischemic stroke, and it is unusual for sSAH to occur on the opposite side of the infarct territory, but in our case sSAH occurred on opposite side, but after a gap of 3 years.
RESUMO
Cerebral amyloid angiopathy (CAA) is common in patients with Alzheimer's disease (AD) and may contribute to cerebral hemorrhage. We previously demonstrated that tissue plasminogen activator (tPA) and plasminogen (PLG) accumulated at the periphery of compact amyloid-cored plaques and in the walls of CAA-containing blood vessels in the brains of Tg2576 mice, a widely used AD mouse model. We had also observed that zinc-triggered tPA and PLG induction were observed in mouse cortical cultures. Because zinc also accumulates in amyloid plaques and blood vessel walls in AD brains, we examined whether zinc increases mRNA and protein levels of tPA and PLG in brain endothelial cells and pericytes. Four hours after the exposure of brain endothelial cells (bEnd.3) to 40 microM zinc, the mRNA and protein expressions of tPA and its substrate PLG were significantly increased. In the case of brain pericyte cultures, increases in tPA and PLG expression were also detected 2 hr after treatment. However, amyloid-beta (Abeta)1-42 oligomers did not augment tPA and PLG expression in bEnd.3 cells and pericytes, suggesting that zinc but not Abeta induces tPA and PLG accumulation in CAA found in the AD brain.