Traumatic Brain Injury & Herniation Syndromes
How force, swelling, and a rigid skull injure the brain
Primary Brain Injury
Contusions. A contusion is a bruise of the crests of gyri. A coup lesion forms under the point of impact and a contrecoup lesion on the opposite side as the brain rebounds against the skull. Whatever the direction of the blow, the orbitofrontal cortex and anterior temporal poles are hit hardest because they scrape across the rough floors of the anterior and middle cranial fossae, producing disinhibition, personality change, and memory problems. Healed contusions leave depressed, yellow-brown, hemosiderin-stained scars (plaques jaunes).
Diffuse axonal injury. Rotational acceleration and deceleration, as in high-speed crashes, shear axons where tissues of different density meet: the gray-white junction, the corpus callosum, and the dorsolateral rostral brainstem. Patients are comatose from impact, yet CT is often nearly normal apart from small petechial hemorrhages; MRI is more sensitive. Microscopy shows axonal swellings (spheroids) that stain for β-amyloid precursor protein. Severe injury can leave a persistent vegetative state.
Concussion. A transient, trauma-induced disturbance of brain function (confusion, amnesia, headache, sometimes brief loss of consciousness) without a structural lesion on imaging.
Chronic traumatic encephalopathy. Repetitive head impacts in contact sports or military blast exposure lead to hyperphosphorylated tau in neurons and astrocytes clustered around small vessels at the depths of cortical sulci. Patients develop depression, impulsivity, and aggression, then progressive cognitive decline and dementia. CTE is confirmed only at autopsy.
Secondary Injury and Intracranial Pressure
Secondary injury is damage that develops after the impact from edema, hypoxia, hypotension, hypercapnia, fever, seizures, and rising intracranial pressure (ICP); preventing it is the goal of acute care.
| Feature | Vasogenic | Cytotoxic |
|---|---|---|
| Mechanism | Blood-brain barrier disruption | Na+/K+-ATPase failure from ATP depletion |
| Fluid location | Extracellular, spreading through white matter | Intracellular, gray and white matter |
| Settings | Contusion, tumor, abscess | Hypoxia, ischemia, cardiac arrest |
| Corticosteroids | Dexamethasone reduces tumor edema | Not helpful |
Monro-Kellie doctrine. The skull holds a fixed volume of brain, blood, and CSF, so an expanding hematoma or edema raises ICP (normal about 5–15 mmHg) once compensation is exhausted. Cerebral perfusion pressure equals mean arterial pressure minus ICP (CPP = MAP − ICP), so a falling blood pressure or rising ICP starves the brain. Elevating the head, osmotherapy with mannitol or hypertonic saline, and brief hyperventilation (hypocapnia constricts cerebral vessels) lower ICP; hyperventilation is only a temporizing bridge because excessive vasoconstriction causes ischemia.
Cushing reflex. When rising ICP makes the brainstem ischemic, the vasomotor center triggers a sympathetic surge that raises arterial pressure to restore perfusion. Baroreceptors respond with vagal bradycardia, and medullary compression makes breathing irregular. This Cushing triad is a late sign of impending herniation.
Herniation Syndromes
| Type | What moves | What is compressed | Key signs |
|---|---|---|---|
| Subfalcine (most common) | Cingulate gyrus under the falx | Anterior cerebral artery | Midline shift; contralateral leg weakness and numbness |
| Uncal (transtentorial) | Medial temporal uncus over the tentorium | Ipsilateral CN III, cerebral peduncle, PCA | Ipsilateral blown pupil, then down-and-out eye; contralateral hemiparesis; contralateral homonymous hemianopia (often macular-sparing) |
| Central (downward) | Diencephalon and midbrain through the tentorial notch | Paramedian basilar branches | Duret hemorrhages in midbrain and pons; posturing, coma |
| Tonsillar | Cerebellar tonsils through the foramen magnum | Medulla | Respiratory arrest, cardiovascular collapse |
Why the pupil blows first. Parasympathetic pupilloconstrictor fibers run on the outer surface of CN III, so compression by the uncus dilates the pupil before ptosis and eye deviation appear. An expanding epidural or subdural hematoma is the classic cause.
Kernohan notch: when the midbrain is pushed sideways, the opposite cerebral peduncle hits the far tentorial edge, producing hemiparesis on the same side as the mass. The blown pupil is the more reliable guide to the side of the lesion.
Lumbar puncture in a patient with a large or posterior fossa mass can precipitate tonsillar herniation; image first when there are focal deficits, papilledema, or depressed consciousness.
Posturing and Disorders of Consciousness
Posturing. Decorticate posturing (flexed arms, extended legs) indicates a lesion above the red nucleus, in the cortex, internal capsule, or thalamus; the intact rubrospinal tract facilitates upper-limb flexors. Decerebrate posturing (extended, internally rotated arms and extended legs) indicates a lesion below the red nucleus, in the midbrain or upper pons, where vestibulospinal and pontine reticulospinal extensor drive is unopposed; it carries a worse prognosis.
Glasgow Coma Scale. Eye opening (1–4), verbal response (1–5), and best motor response (1–6) sum to 3–15. A score of 8 or less is severe injury and calls for airway protection; 9–12 is moderate and 13–15 mild.
- Coma: eyes closed, unarousable, no sleep-wake cycles.
- Vegetative state: eyes open with sleep-wake cycles but no awareness of self or environment.
- Locked-in syndrome: ventral pontine lesion (often basilar artery occlusion) with quadriplegia and anarthria but preserved awareness; communication by vertical eye movements and blinking.
- Brain death: irreversible loss of all brain function, including brainstem reflexes and respiratory drive (no spontaneous breathing on apnea testing).