ABSTRACT
Stroke is the third leading cause of death in the United States. Intracranial atherosclerotic disease plays a role in cerebrovascular accidents, with well-characterized modifiable and nonmodifiable risk factors. Surgical bypass has so far not proved to be superior to medical therapy. Both medical and endovascular therapies for intracranial atherosclerosis have evolved since the initial off-label use of cardiac devices for its treatment. Initial reports on the results of stent placement for symptomatic high-grade intracranial atherosclerotic disease were initially encouraging. However, debate remains as to the optimal treatment of symptomatic intracranial atherosclerotic disease.
Subject(s)
Anticoagulants/therapeutic use , Atherosclerosis/therapy , Cerebral Revascularization/methods , Cerebrovascular Disorders/therapy , Endovascular Procedures/methods , Platelet Aggregation Inhibitors/therapeutic use , Stents , Atherosclerosis/diagnosis , Cerebral Revascularization/instrumentation , Cerebrovascular Disorders/diagnosis , Combined Modality Therapy , Endovascular Procedures/instrumentation , Humans , Neuroimaging/methods , Surgery, Computer-Assisted/methodsABSTRACT
OBJECTIVE: The adult brain is capable of neurogenesis after cerebral ischemia. We investigated the presence of new neural precursors after transient middle cerebral artery ischemia adult rats. METHODS: Transient middle cerebral artery ischemia was induced in adult Wistar rats (n=13) using the monofilament method. In the experimental group (n=8), animals were harvested at days 3, 7, 10, 17 and 21 after ischemia. Five animals served as controls. Sagittal sections through the ischemic cortex were double-stained for neural (nestin and beta-tubulin, nestin and PCNA), glial (nestin and GFAP) and oligodendroglial (nestin and O4, CNP and PCNA) precursors. Double-stained cells were also counted under high-power view and tabulated over time. RESULTS: In the subventricular zone (SVZ), there was positive double-staining starting at day 3 showing proliferating astrocytic precursors (nestin + GFAP, 5-20% of cells), neuronal stem cells (nestin + PCNA, 95% of cells) and neuronal precursors (nestin + beta-tubulin, 50% of cells). Within the penumbra, a more robust response showed more astrocytic precursors (50-80% of cells), premature and differentiated oligodendrocytes, neuronal stem cells (85% of cells) and neuronal precursors (15% of cells). In the area of the stroke, there was an intermediate response consisting of more astrocytic precursors (10-20% of cells), premature oligodendrocytes (45-100% of cells), neuronal stem cells (95% of cells) and neuronal precursors (25% of cells). Results were confirmed with cell counting analysis. DISCUSSION: Our results show that not only do neural precursors proliferate in the SVZ, there is definite and real response in the penumbra and ischemic cortex, suggesting the ability of repair in the central nervous system.
