Transient and permanent focal cerebral ischemia results in a series of typical pathophysiologic events. These consequences evolve in time and space and are not limited to the lesion itself, but they can be observed in perilesional (penumbra) and widespread ipsi- and sometimes contralateral remote areas (diaschisis). The extent of these areas is variable depending on factors such as the type of ...

BACKGROUND AND PURPOSE Increased intracellular calcium accumulation is known to potentiate ischemic injury. Whether endogenous calcium-binding proteins can attenuate this injury has not been clearly established, and existing data are conflicting. Calbindin D28K (CaBP) is one such intracellular calcium buffer. We investigated whether CaBP overexpression is neuroprotective against transient focal...

BACKGROUND AND PURPOSE Patients with ischemic stroke, cerebral transient ischemic attacks (TIAs), retinal artery occlusion (RAO), and amaurosis fugax are thought to have similar risk factors and underlying vascular disease. However, if risk factors are different in patients with eye compared with brain symptoms and in those whose symptoms last <24 hours (transient) compared with those lasting >...

BACKGROUND AND PURPOSE Excessive release of nitric oxide (NO) has been implicated in the pathophysiology of neurodegeneration in ischemic stroke. We compared intracerebral release of indicators of NO generation at the acute and subacute stages of transient focal cerebral ischemia. METHODS In vivo microdialysis in the rat striatum was performed at the acute (first hours) and subacute (after 24...

BACKGROUND Experimental studies have shown that gabapentin can reduce neuronal injury in the setting of cerebral ischemia, but the mechanisms have not yet been clearly determined. This study was conducted to determine whether gabapentin pretreatment altered expression levels of heat shock protein 70 and reduced acute phase neuronal injury in rats subjected to transient focal cerebral ischemia/r...