--- 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 stains for axonally transported proteins (amyloid precursor protein, α-synuclein) - Later: increased microglia in damaged cortex → degeneration of involved fiber tracts --- 3. TRAUMATIC VASCULAR INJURY Disruption of vessel walls leads to hemorrhage in various anatomic compartments, sometimes in combination. Patterns of CNS Hemorrhage (Summary Table) Location Etiology Key Features --- --- --- Epidural Trauma Associated with skull fracture; arterial blood; lucid interval → rapid deterioration Subdural Trauma Venous blood; slow evolution; may follow minor trauma; bilateral in 10% Subarachnoid Trauma / vascular anomaly Accompanies parenchymal trauma; spontaneous = ruptured aneurysm; thunderclap headache Intraparenchymal Trauma, HTN, amyloid angiopathy, tumors Location varies by cause --- 3a. EPIDURAL HEMATOMA Vessel involved: Dural arteries, most notably the middle meningeal artery Mechanism: Temporal skull fracture crosses the vessel → arterial laceration → blood accumulates under arterial pressure → dura strips from periosteum → expanding hematoma compresses brain In children , the skull is deformable, so temporary displacement without fracture can still lacerate the vessel. Clinical course: - Lucid interval may occur when blood accumulates slowly - Followed by rapid neurological deterioration - Neurosurgical emergency — without prompt drainage, fatal herniation occurs within hours --- 3b. SUBDURAL HEMATOMA Vessel involved: Bridging veins (cortical hemispheres → dural sinuses) Mechanism: Traumatic displacement of brain tears bridging veins at the dura → venous blood dissects between the two dural layers At-risk groups: - Elderly — brain atrophy stretches bridging veins - Infants — thin-walled bridging veins (also seen in non-accidental injury/shaken baby) - Patients with coagulopathy or significant cerebral atrophy (even minor trauma can cause it) Morphology timeline: Time Change --- --- Acute Fresh clotted blood along brain surface; subarachnoid space clear; brain flattened ~1 week Clot lysis ~2 weeks Fibroblast ingrowth from dural surface 1–3 months Hyalinized connective tissue; organized hematoma attached to inner dura Late Retraction → thin "subdural membrane" OR chronic rebleeding from thin-walled granulation vessels Clinical features: - Symptoms within 48 hours of injury - Most common over lateral cerebral hemispheres - Bilateral in ~10% - Symptoms: headache, confusion, focal deficits (often non-localizing) - Slowly progressive deterioration ± acute decompensation - Treatment: Surgical evacuation of blood and organizing tissue - Risk of rebleeding highest in the first few months --- 4. SEQUELAE OF BRAIN TRAUMA Sequela Notes --- --- Posttraumatic hydrocephalus Obstruction of CSF resorption from subarachnoid hemorrhage Chronic Traumatic Encephalopathy (CTE) After repeated head trauma; formerly "dementia pugilistica"; brain atrophy, enlarged ventricles, tau-containing