Cerebrovascular Anatomy, Physiology, and Pathophysiology
Core concepts
Know the anterior and posterior circulations and the collateral routes that determine viability. The internal carotid gives ophthalmic, posterior communicating, anterior choroidal, and terminal anterior and middle cerebral arteries; the vertebrobasilar system supplies brainstem, cerebellum, and posterior cerebral territories. Circle of Willis completeness varies, so a normal variant can explain selective infarction. Leptomeningeal anastomoses between ACA, MCA, and PCA and external carotid collaterals matter in chronic steno-occlusive disease. Watershed infarcts occur at border zones and can be embolic or hemodynamic. Physiologically, cerebral blood flow is tightly coupled to metabolism. Autoregulation maintains flow across a mean arterial pressure range but is impaired in acute ischemia and chronic hypertension. CBF thresholds explain the core-penumbra model: below roughly 10-12 mL/100 g/min infarction occurs rapidly; 12-20 mL/100 g/min is ischemic but potentially salvageable. Excitotoxicity, calcium influx, oxidative stress, inflammation, and blood-brain barrier breakdown evolve over hours. Cytotoxic edema precedes vasogenic edema; malignant MCA infarction can cause herniation.
Traps
Do not equate a syndrome with one artery; aphasia with hemiparesis usually suggests left MCA but can occur with ICA occlusion. Thalamic infarcts can be PCA, basilar perforator, or artery of Percheron. Top of basilar is not simply PCA.
Rule of thumb
In acute MCA occlusion, robust leptomeningeal collaterals predict a larger penumbra and better reperfusion response. Example: sudden right hemiparesis and global aphasia with left MCA occlusion and a small core on perfusion imaging. Reperfusion should not be delayed merely because symptoms are severe; the penumbra is the target.