Fig.23.12A ).Withinafewhoursofinjury,bloodextravasatesthroughouttheinvolvedtissue,acrossthewidthofthecerebralcortex,andintothewhitematterandsubarachnoidspaces.Althoughfunctionaleffectsareseenearlier,morphologicevidenceofneruonalinjury(nuclearpyknosis,cytoplasmiceosinophilia,cellulardisintegration)takesabout24hourstoappear.Theinflammatoryresponsetotheinjuredtissuefollowsitsusualcourse,withneutrophilsprecedingtheappearanceofmacrophages.Incontrastwithischemiclesions,inwhichthesuperficiallayerofcortexmaybepreserved,traumaaffectsthesuperficiallayersmostseverely.
Oldtraumaticlesionscharacteristicallyappearasdepressed,retracted,yellowishbrownpatchesinvolvingthecrestsofgyri(see
Fig.23.12B ).Theselesionsshowgliosisandresidualhemosiderin-ladenmacrophages.
Althoughcontusionsaremoreeasilyseen,traumamayalsocausemoresubtlebutwidespreadinjurytoaxonswithinthebrain(calleddiffuse axonal injury),sometimeswithdevastatingconsequences.Themovementofoneregionofbrainrelativetoanotheristhoughttodisruptaxonalintegrityandfunction.Angularacceleration,evenintheabsenceofimpact,maycauseaxonalinjuryaswellashemorrhage.Asmanyas50%ofpatientswhodevelopcomashortlyaftertraumaarebelievedtohavewhitematterdamageanddiffuseaxonalinjury,usuallyintheformofaxonalswellingsthatappearwithinhoursoftheinjury.
Concussion describes reversible altered brain function, with or without loss of consciousness, from head injury. The characteristic transient neurologic dysfunction includes loss of consciousness, temporary respiratory arrest, and loss of reflexes. Neurologic recovery is the norm, although amnesia for the event persists. The pathogenesis of the sudden disruption of nervous activity is unknown. Repeated episodes of concussion can result in persistent and profound neurologic deficits including cognitive impairment, parkinsonism, and others, and later development of neurodegenerative processes. Initially described in boxers (dementia pugilistica), it is now recognized to occur in a wider range of settings, such as in athletes participating in contact sports. This syndrome is termed chronic traumatic encephalopathy and is characterized by accumulation of tangles in cerebral cortex and other brain regions (see the “ ” section later in the chapter).
CNS trauma often directly disrupts vessel walls, leading to hemorrhage (
Table 23.1 ). Depending on the affected vessel, the hemorrhage may be epidural, subdural, subarachnoid, or intraparenchymal (
Fig. 23.13A ), occurring alone or in combination. Subarachnoid and intraparenchymal hemorrhages most often occur at sites of contusions and lacerations.
Fig. 23.12 Cerebraltrauma.(A)Acutecontusionsarepresentinbothtemporallobes,withareasofhemorrhageandtissuedisruption.(B)Remotecontusions,seenasdiscoloredyellowareas,arepresentontheinferiorfrontalsurfaceofthisbrain.
Dural vessels—especially the middle meningeal artery— are vulnerable to traumatic injury. In infants, traumatic displacement of the easily deformable skull may tear a vessel, even in the absence of a skull fracture. In children and adults, by contrast, tears involving dural vessels almost always stem from skull fractures. Once a vessel tears, blood accumulates under arterial pressure and dissects the tightly applied dura away from the inner skull surface (see