Fig.23.6A ).Subacute changes, occurringat24hoursto2weeks,includenecrosisoftissue,influxofmacrophages,vascularproliferation,andreactivegliosis(see
Fig.23.6B ).Repair, seenafter2weeks,ischaracterizedbyremovalofnecrotictissueandgliosis(see
Fig.23.6C
Border zone (“watershed”) infarcts occurinregionsofthebrainandspinalcordthatlieatthemostdistalportionsofarterialterritories.Theyareusuallyseenafterhypotensiveepisodes.Inthecerebralhemispheres,theborderzonebetweentheanteriorandthemiddlecerebralarterydistributionsisatgreatestrisk.Damagetothisregionproducesawedge-shapedbandofnecrosisoverthecerebralconvexityafewcentimeterslateraltotheinterhemisphericfissure.
Cerebral arterial occlusion leads first to focal ischemia and then to infarction in the distribution of the compromised vessel. The size, location, and shape of the infarct and the extent of tissue damage that results may be modified by collateral blood flow. Specifically, collateral flow through the circle of Willis or cortical-leptomeningeal anastomoses can limit damage in some regions. By contrast, there is little if any collateral blood flow to structures such as the thalamus, basal ganglia, and deep white matter, which are supplied by deep penetrating vessels.
Embolic infarctions are more common than infarctions due to thrombosis. Cardiac mural thrombi are a frequent source of emboli; myocardial dysfunction, valvular disease, and atrial fibrillation are important predisposing factors. Thromboemboli also arise in arteries, most often from atheromatous plaques in the carotid arteries or aortic arch. Emboli of venous origin may cross over to the arterial circulation through a patent foramen ovale and lodge in the brain (paradoxical embolism; see Chapter 4); these include thromboemboli from deep leg veins and fat emboli, usually following bone trauma. The territory of the middle cerebral artery, a direct extension of the internal carotid artery, is most frequently affected by embolic infarction. Emboli tend to lodge where vessels branch or in areas of stenosis, usually caused by atherosclerosis.
Thrombotic occlusions causing cerebral infarctions usually are superimposed on atherosclerotic plaques; common sites are the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery. These occlusions may be accompanied by anterograde extension, as well as thrombus fragmentation and distal embolization. Thrombotic occlusions causing small infarcts of only a few millimeters in diameter, so-called “lacunar infarcts,” occur when small penetrating arteries occlude due to chronic damage, usually from long-standing hypertension (discussed later).
Fig.
23.7 ). Nonhemorrhagic infarcts result from acute vascular occlusions and may evolve into hemorrhagic infarcts when there is reperfusion of ischemic tissue, either through collaterals or after dissolution of emboli.
Fig. 23.6 Cerebralinfarction.(A)Infiltrationofacerebralinfarctionbyneutrophilsbeginsattheedgesofthelesion,wherethevascularsupplyisintact.(B)Byday10,anareaofinfarctionshowsthepresenceofmacrophagesandsurroundingreactivegliosis.(C)Oldintracorticalinfarctsareseenasareasoftissuelossandresidualgliosis.
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MORPHOLOGYHemorrhagic infarcts usuallymanifestasmultiple,sometimesconfluent,petechialhemorrhages(