Cerebral Edema, Herniation & CNS Trauma

• Edema = an increase in brain water content.
• Brain swelling = edema + vascular congestion (more blood volume in the brain). In trauma it is mainly edema.
• Swelling is common in TBI and is the main driver of raised ICP → the most common cause of death in severe TBI.
• Swelling can be:
  • Focal → around a contusion or intracerebral hemorrhage; usually vasogenic (barrier breakdown).
  • Diffuse, one hemisphere → typically with an acute subdural hematoma; it persists even after the clot is removed.
  • Diffuse, both hemispheres → now less frequent because modern care aggressively prevents hypoxia and ischemia.

• Real lesions are often mixed: an infarct starts cytotoxic (minutes–hours), then adds vasogenic edema as the barrier breaks down (days).

• The skull is a solid box. Its contents (brain + blood + CSF) have a fixed total volume = Monro-Kellie doctrine.
• A growing mass (hematoma, tumor, abscess, diffuse swelling) must displace something:
  • First CSF (pushed into the spinal sac) and venous blood (squeezed out) → ICP barely changes = compensation.
  • Once these buffers are used up, each extra mL → a steep rise in ICP = decompensation.
• Pressure is then unequal between compartments → a pressure differential → tissue herniates into the neighboring compartment (LO 2).

• ICP thresholds (the dashed lines on the curve): normal 0–10 mmHg → prolonged >20 = abnormal → >40 = neurologic dysfunction + compromised cerebral circulation → >60 = fatal.
• Raised ICP from swelling = the most common cause of death in severe TBI.

• Cerebral perfusion pressure (CPP) = MAP − ICP. As ICP rises, CPP falls.
• Autoregulation normally keeps flow constant over a wide pressure range, but injured brain loses it.
• Low CPP → global ischemia → cytotoxic edema → even higher ICP → the vicious cycle.
• If ICP approaches MAP, CPP → 0 → no cerebral perfusion = brain death.

Two routes to diffuse ischemic injury after TBI

• Headache (worse lying down / on waking), vomiting (often without nausea), papilledema.
• ↓ Level of consciousness → confusion, drowsiness, then coma.
• CN VI (abducens) palsy → lateral gaze palsy, a false-localizing sign (the nerve is stretched against the petrous ligament).
• Late: Cushing triad = hypertension (widened pulse pressure) + bradycardia + irregular respirations.

The falx cerebri (between hemispheres) and the tentorium cerebelli (roof over the cerebellum) split the cranium into compartments. A pressure differential pushes tissue under the falx, through the tentorial notch, or down the foramen magnum; vessels and nerves at these edges get notched, kinked or stretched → secondary infarcts, more edema, more swelling.

• What gets compressed:
  • ACA against the falx → ACA infarct.
  • PCA against the free tentorial edge → PCA infarct.
  • Abducens (CN VI) against the petrous ligament → lateral gaze palsy.
  • Oculomotor (CN III) distortion → third-nerve palsy.
  • Opposite cerebral peduncle against the tentorium (Kernohan notch) → ipsilateral hemiparesis (same side as the mass; false-localizing). Direct uncal pressure on the same-side peduncle → contralateral hemiparesis.
• Tonsillar herniation: tonsils occlude the foramen magnum → block CSF → hemorrhagic tonsillar necrosis + medullary ischemia → cardiopulmonary arrest.
• Duret = caudal displacement → deformity and traction of basilar perforators.
• Late swelling after severe diffuse injury pushes the brain down into the foramen magnum → brainstem compression → respiratory failure.

• Tonsillar: tonsils plug the foramen magnum → blocks CSF (↑ICP), tonsils undergo hemorrhagic necrosis, the medulla (respiratory + cardiovascular centers) becomes ischemic → pressure + ischemia → cardiopulmonary arrest.
• Duret: brainstem is pushed down and elongated; the basilar artery is tethered to the circle of Willis, so its paramedian perforators are stretched and tear → midline hemorrhages in midbrain and pons. A secondary brainstem injury.

No single scheme captures everything, so three lenses are used together:

• Know both lists: 5 focal (scalp, skull fracture, contusion/laceration, intracranial hemorrhage, raised-ICP lesions) and 3 diffuse (ischemia, axonal/vascular injury, swelling).
• Epidemiology: TBI is the leading cause of death under 40 and accounts for 1–2% of all deaths; falls are the most common mechanism (~35%).

• Total 3–15; higher = better (milder injury). 13–15 mild · 9–12 moderate · ≤8 severe. The three components are eye, verbal, motor; a score <8 is worrisome for severe injury.
• Work-up: history of the mechanism (bystanders if needed) → exam (loss of consciousness, mental status, focal deficits, GCS) → imaging (CT first in the ER: fast, sensitive for blood; MRI for subtle injury).
• Admit if: neurologic deficit, seizures, nausea/vomiting, severe headache, fever (infection, especially open wounds), prolonged loss of consciousness, altered mental status, or an unexplained / inconsistent story (forgotten LOC or possible abuse). Brief LOC alone is less worrying.

• An immediate, usually reversible episode of cerebral dysfunction after TBI, typically (not always) with brief loss of consciousness and memory loss. The mildest form of TBI.
• Think TIA vs stroke: concussion is the transient, no-visible-lesion end; DAI is the devastating end of the same rotational spectrum.
• Sport guidance has moved away from grading systems. In rare autopsies of people who died of other causes 2–99 days after a concussion, sparse β-APP-positive axonal injury was found → "reversible" may not mean "no structural damage".

• Mental-status sequence after closed head injury: retrograde amnesia (events just before) → post-traumatic amnesia (coma/confusion afterward, cannot lay down new memories) → usually recovery of memory.

• Contusion = bruise of the brain surface: mechanical force damages small vessels → blood leaks into tissue. Worst at the crests of gyri (where the cortex hits bone).
• Pia intact = contusion; if the pia is torn → laceration.
• Caused by impact with acceleration/deceleration (e.g., a fall). Coup = under the impact; contrecoup = opposite side (LO 5).
• Most common sites: tips of the temporal lobes (temporal poles) and inferior frontal lobes (orbital gyri): the brain rubs across the rough bony floor of the anterior and middle cranial fossae.
• Contusions trigger focal vasogenic edema and can enlarge into intracerebral hematomas.
• Old contusion = "plaques jaunes": depressed, yellow-brown (hemosiderin) gliotic plaques in the cortex, on gyral crests, with shrinking of the surrounding gyri → a common epileptic focus.

• Cause: high-velocity rotational acceleration/deceleration of an unrestrained head (road traffic accidents, falls from a height). No skull impact needed.
• Mechanism: shear, tensile and compressive strain deforms long white-matter tracts → immediate breakage of microtubules → axonal transport stops → transported material piles up → axon swells and later disconnects (secondary, delayed axotomy).
• Sites: grey–white junction, corpus callosum (especially the splenium), white matter near the midline (internal capsule), dorsolateral rostral brainstem.
• Clinical: comatose immediately, no lucid interval, remains unconscious, vegetative or severely disabled. CT may look nearly normal; MRI (DWI, susceptibility/T2*) shows punctate lesions.
• Grades by coma length: mild = coma 6–24 h; moderate = >24 h without brainstem signs; severe = >24 h with brainstem signs (posturing).

• Time course, in order: β-APP → varicosities (H&E, 12–24 h) → swellings/spheroids + microglial nodules (24 h–2 mo) → Wallerian degeneration, atrophy.
• The β-APP window is quoted as within <2 hours with current techniques (older teaching: 4–5 hours). "Earliest finding" → β-APP either way.
• The H&E image is white matter: oligodendrocytes present, neurons absent.
• DAI is a severe injury; delayed swelling can push the brain into the foramen magnum → brainstem compression → respiratory failure.

• First recognized in boxers as dementia pugilistica; now described in football, hockey, soccer and military personnel.
• Cause not fully defined; probably repeated concussive or sub-concussive blows.
• Clinical: mood disturbance, depression, impulsivity, memory loss → dementia, or parkinsonism / ALS-like disease; suicide risk.
• Pathology: extensive hyperphosphorylated tau in neurons and glia (astrocytes), classically perivascular at the depths of sulci; sometimes TDP-43 inclusions (the protein is TDP-43).
  • Tau → also seen in Alzheimer disease.
  • TDP-43 → also seen in ALS and frontotemporal dementia.

Work from the outside in: skull → (epidural space) → dura → (subdural space) → arachnoid → (subarachnoid space, CSF + surface arteries) → pia → brain. The epidural and subdural spaces are potential spaces: they exist only when blood forces them open.

• Epidural = arterial, rapid; subdural = venous, slow.
• EDH: blood strips dura from the inner table and deforms the underlying brain; squamous temporal fracture tears a meningeal artery or vein.
• SDH: tearing of bridging veins that traverse the subdural space between cortex and dura; can also be non-traumatic.
• Traumatic SAH usually accompanies contusions; an isolated massive basal SAH = vertebral artery injury (blow to the neck).
• ICH does not extend through the cortex (frontal/temporal; striatum in road traffic accidents). Traumatic IVH: rarely alone, poor prognosis.

Most clinical injuries combine contact + inertial forces ("blunt force head injury"). Epidemiology: falls ~35%, motor vehicle ~17%, struck by/against an object ~17%, assaults ~10%. Road traffic injuries are falling in Western countries but rising in developing ones.

• Scalp laceration/bruise = proof of contact injury. Occipital bruise → backward fall → look for contrecoup frontal/temporal contusions.
• A scalp "goose egg" hematoma may crackle when pressed (fibrin), not because of broken bone.

• Coup = contusion under the point of impact. Contrecoup = contusion on the opposite side, as the brain rebounds and strikes the inside of the skull.
• Fall (moving head stops): brain keeps moving → contrecoup often worse than coup. Fall on the occiput → orbital frontal + temporal pole contusions.
• Blow to a still head (punch, pipe): mainly coup; with more force some contrecoup appears, but the coup side still dominates.
• Coup is essentially always present; contrecoup appears as severity rises.

• Spinal cord injury: common (≈12–58 per million); causes = road traffic accidents, falls, sports, assaults.
• Most are closed injuries with fracture or dislocation of the spine from hyperflexion / hyperextension.

• Head trauma is present in ≈60% of fatal child abuse; most abuse occurs under age 3.
• Red flags: age <3, presentation in coma / low GCS, inconsistent or absent history, parental risk factors (young age, low socioeconomic status, education, family history).
• Findings: subdural hematoma (bridging veins torn by acceleration–deceleration), retinal hemorrhages, DAI, contusion, cervical cord injury; skeletal survey may show posterior rib and metaphyseal ("corner") fractures.
• Shaking alone more often injures the cervical cord; fatal inflicted brain trauma usually shows evidence of impact too. A controversial forensic area: always document carefully.

• Carotid–cavernous fistula: basilar fracture tears the ICA inside the cavernous sinus → arterial blood floods the venous sinus → pulsatile exophthalmos, chemosis, orbital bruit, CN III/IV/VI palsies.
• Venous sinus injury/thrombosis: headache, papilledema, seizures, hemorrhagic venous infarcts.