Fig.23.7AandB ).Themicroscopicpictureandevolutionofhemorrhagicinfarctionparallelthoseofischemicinfarction,withtheadditionofbloodextravasationandresorption.Inindividualswithcoagulopathies,hemorrhagicinfarctsmaybeassociatedwithextensiveintracerebralhematomas.
Themacroscopicappearanceofanonhemorrhagic infarct evolvesovertime.Duringthefirst6hours,thetissueisunchangedinappearance,butby48hours,thetissuebecomespale,soft,andswollen.Fromdays2to10,theinjuredbrainturnsgelatinousandfriable,andtheboundarybetweennormalandabnormaltissuebecomesmoredistinctasedemaresolvesintheadjacentviabletissue.Fromday10toweek3,thetissueliquefies,eventuallyleavingafluid-filledcavity,whichgraduallyexpandsasdeadtissueisresorbed(see
Fig.23.7C
Microscopically,thetissuereactionfollowsacharacteristicsequence.Afterthefirst12hours,ischemicneuronalchange(redneurons)(see
Fig.23.1A )andcytotoxicandvasogenicedemaappear.Endothelialandglialcells,mainlyastrocytes,swell,andmyelinatedfibersbegintodisintegrate.Duringthefirstseveraldaysneutrophilsinfiltratetheareaofinjury,butthesearereplacedoverthenext2–3weeksbymacrophages.Macrophagescontainingmyelinorredbloodcellbreakdownproductsmaypersistinthelesionformonthstoyears.Astheprocessofphagocytosisandliquefactionproceeds,astrocytesattheedgesofthelesionprogressivelyenlarge,divide,anddevelopaprominentnetworkofcytoplasmicextensions.Afterseveralmonths,thestrikingastrocyticnuclearandcytoplasmicenlargementregresses.Inthewallofthecavity,astrocyteprocessesformadensefeltworkofglialfibersadmixedwithnewcapillariesandafewperivascularconnectivetissuefibers.
Hemorrhages within the brain are caused by (1) hypertension and other diseases leading to vascular wall injury, (2) structural lesions such as arteriovenous and cavernous malformations, and (3) tumors. Subarachnoid hemorrhages most commonly are the result of ruptured aneurysms but also occur with other vascular malformations. Subdural or epidural hemorrhages usually are associated with trauma.
Spontaneous (nontraumatic) intraparenchymal hemorrhages are most common in mid to late adult life, with a peak incidence at about 60 years of age. Most are due to the rupture of a small intraparenchymal vessel. Hypertension is the leading underlying cause, and brain hemorrhage accounts for roughly 15% of deaths among individuals with chronic hypertension. Intracerebral hemorrhage can be clinically devastating when it affects large portions of the brain or extends into the ventricular system; alternatively, it can affect small regions and be clinically silent. Hypertensive intraparenchymal hemorrhages typically occur in the basal ganglia, thalamus, pons, and cerebellum (
Fig. 23.8 ), with the location and the size of the bleed determining its clinical manifestations. If the individual survives the acute event, gradual resolution of the hematoma ensues, sometimes with considerable clinical improvement.