— CNS TRAUMA Neuropathology Dr. Lilian Bosire — GENERAL PRINCIPLES The anatomic location of a lesion and the brain's limited capacity for functional repair
--- CNS TRAUMA Neuropathology Dr. Lilian Bosire --- GENERAL PRINCIPLES The anatomic location of a lesion and the brain's limited capacity for functional repair are the major determinants of outcome. The same volume of injury can be: Clinically silent → frontal lobe Severely disabling → spinal cord Fatal → brainstem Head injury produces three categories of damage that frequently coexist: 1. Skull fractures 2. Parenchymal injury 3. Vascular injury The nature and extent of injury depends on the shape of the object , force of impact , and whether the head was in motion at the time of injury. A blow may be penetrating or blunt, and cause open or closed injury. --- 1. SKULL FRACTURES A displaced skull fracture = bone displaced into the cranial cavity by a distance greater than the bone's own thickness . Resistance to fracture varies by location due to differing bone thickness. Pattern of falls influences which bones fracture: Awake fall (e.g., off a ladder) → occipital impact Fall after loss of consciousness (e.g., syncope) → frontal or occipital impact Basal Skull Fracture Typically follows impact to the occiput or sides of the head . Clinical clues: Lower cranial nerve deficits Cervico-medullary signs Orbital hematoma (periorbital ecchymosis — "raccoon eyes") Mastoid hematoma (Battle's sign) — hematoma distant from the point of impact CSF rhinorrhoea (nose) or CSF otorrhoea (ear) Risk of meningitis from CSF leakage --- 2. PARENCHYMAL INJURIES Parenchymal injuries range from mild to severe depending on the nature and force of trauma. They include: Concussion ← mild end Contusions and lacerations ← severe end Diffuse axonal injury ← deep white matter --- 2a. CONCUSSION A clinical syndrome of altered consciousness following head injury, typically caused by a change in momentum of the head . Clinical features: Sudden transient neurological dysfunction Loss of consciousness Temporary respiratory arrest Loss of reflexes Post-event amnesia (persists even after neurologic recovery) Pathogenesis: Likely involves dysregulation of the reticular activating system in the brainstem (exact mechanism unknown). Complications of repetitive concussions: Post-concussive neuropsychiatric syndromes Significant cognitive impairment Chronic Traumatic Encephalopathy (CTE) --- 2b. CONTUSIONS & LACERATIONS Contusion = bruise of brain tissue from blunt trauma (no breach of surface) Laceration = tearing of brain tissue from penetrating injury Kinetic energy is transmitted to the brain → rapid tissue displacement → disruption of vascular channels → hemorrhage, tissue injury, edema . Hemorrhage may extend into the subarachnoid space . Most susceptible sites: Crests of gyri (greatest direct force here) Most common locations: Frontal lobes along the orbital ridges Temporal lobes (overlie rough inner skull surface) Less common: occipital lobes, brainstem, cerebellum Fracture contusions can occur at adjacent skull fracture sites --- COUP vs. CONTRECOUP Feature Coup Contrecoup --- --- --- Location At point of impact Diametrically opposite to impact Head position Immobile head Mobile head Mechanism Direct force Brain strikes opposite inner skull after deceleration Appearance Identical microscopically Identical microscopically In a mobile head, contrecoup predominates . Both can coexist. Special scenario: Violent posterior/lateral hyperextension of the neck (e.g., pedestrian struck from behind) can avulse the pons from the medulla or medulla from the cervical cord → instant death. --- MORPHOLOGY OF CONTUSIONS Gross: Wedge-shaped on cross-section, broad base at the cortical surface Early: edema + pericapillary hemorrhage Hours later: extravasation extends across full cortical width into white matter and subarachnoid space Microscopic timeline: 12–24 hours: Morphologic neuronal injury appears — nuclear pyknosis, cytoplasmic eosinophilia, cell disintegration Axonal swellings develop along the full length of damaged neurons Inflammatory response: sparse neutrophils → abundant macrophages Old contusions (Plaque Jaune): Depressed, retracted, yellowish-brown patches on gyral crests Most common at contrecoup sites (inferior frontal cortex, temporal and occipital poles) Reflect hemosiderin accumulation Can become epileptic foci Larger hemorrhagic lesions → cavitated lesions resembling remote infarcts Histology: gliosis + residual hemosiderin-laden macrophages --- 2c. DIFFUSE AXONAL INJURY (DAI) Injury to deep white matter , cerebral peduncles, superior colliculi, and deep reticular formation of the brainstem. Key fact: Up to 50% of patients who develop coma after trauma (even without contusions) have DAI. Mechanism: Axons are injured directly by mechanical forces → alterations in axoplasmic flow . Can occur from marked angular acceleration (e.g., blast injuries) even without skull impact. Morphology: Widespread, often asymmetric axonal swellings within hours of injury (may persist much longer) Best demonstrated with silver impregnation or immunoperoxidase s