Brain herniation syndromes

Background

• Brain herniation occurs when increased intracranial pressure causes brain tissue to shift across rigid dural structures (falx, tentorium) or through the foramen magnum
• Represents a life-threatening neurological emergency requiring immediate recognition and intervention
• Most commonly caused by mass lesions (intracranial hemorrhage, tumor, abscess) or diffuse cerebral edema

Types

Type of brain herniation

Uncal (Lateral Transtentorial)

• Most common clinically significant herniation pattern
• Medial temporal lobe (uncus) herniates over the tentorial edge
• Classic triad: ipsilateral blown pupil (third nerve palsy), contralateral hemiparesis, decreased consciousness
  • Contralateral hemiparesis occurs ~75% of the time (ipsilateral Kernohan notch phenomenon in ~25%)
• May progress to bilateral fixed dilated pupils and posturing if untreated

Central Transtentorial

• Both cerebral hemispheres herniate downward through the tentorium
• Progressive rostral-to-caudal deterioration:
  • Early: small reactive pupils, Cheyne-Stokes respiration, increased tone
  • Late: midpoint fixed pupils, extensor posturing, loss of brainstem reflexes

Cerebellotonsillar (Tonsillar)

• Cerebellar tonsils herniate through foramen magnum → brainstem compression
• Pinpoint pupils
• Sudden respiratory and cardiovascular collapse
• Flaccid quadriplegia
• Most rapidly fatal herniation pattern

Upward (Ascending) Transtentorial

• Posterior fossa mass pushes cerebellum upward through tentorial notch
• Pinpoint pupils, downward conjugate gaze
• Obstructive hydrocephalus may occur

Subfalcine

• Cingulate gyrus herniates under the falx cerebri
• May compress anterior cerebral artery → contralateral leg weakness
• Often clinically silent early but may progress to other herniation patterns

Clinical Features

• Decreasing GCS
• Unilateral or bilateral pupil dilation and fixation
• Abnormal posturing (decorticate → decerebrate)
• Cushing reflex: hypertension, bradycardia, irregular respirations (late finding)
• Loss of brainstem reflexes (corneal, gag, oculocephalic)
• Respiratory pattern changes (Cheyne-Stokes → central neurogenic hyperventilation → ataxic → apnea)

Management

• ABCs — secure airway early; avoid hypoxia and hypotension
• Elevate head of bed 30 degrees, keep head midline
• Hyperosmolar therapy:
  • Mannitol 1-1.5 g/kg IV bolus
  • Hypertonic saline (23.4%) 30 mL IV over 10-20 min via central line (or 3% saline 250-500 mL via peripheral line)
• Hyperventilation to PaCO2 30-35 mmHg (temporary bridge — effect lasts 15-20 min)
• Emergent neurosurgery consult for surgical decompression or EVD placement
• Treat underlying cause (evacuate hematoma, treat cerebral edema)
• Avoid hyperthermia, hyperglycemia, seizures

Disposition

• All patients with brain herniation require emergent ICU admission
• Neurosurgical consultation is mandatory
• Consider emergent operative intervention for:
  • Epidural hematoma with herniation signs
  • Large subdural hematoma with midline shift
  • Obstructive hydrocephalus
• Transfer to neurosurgical center if unavailable on site
• Goals of care discussion appropriate for devastating injuries

See Also

• Elevated intracranial pressure
• Head trauma (main)
• Intracranial hemorrhage (main)
• Glasgow Coma Scale (GCS)