Epidemiology

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Etiology

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• Idiopathic intracranial hypertension
• Space-occupying lesions
  • Intracranial hemorrhage or hematoma
  • Aneurysm
  • Intracranial tumors
• Increased CSF (hydrocephalus)
• Metabolic disturbances (e.g., hyponatremia, hepatic encephalopathy)
• Epilepsy and seizures

Pathophysiology

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• Cushing’s reflex
  • ↑ ICP → ↓ CPP → compensatory activation of the sympathetic nervous system → ↑ systolic blood pressure → stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia
  • ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing

Clinical features

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• Global
  • Cushing triad: irregular breathing, widening pulse pressure, and bradycardia
    • Increase in systolic, decrease in diastolic blood pressure
  • Reduced levels of consciousness
  • Headache
  • Vomiting
  • Papilledema
  • Psychiatric changes
  • In infants: macrocephaly, bulging fontanel, sunset sign

Subtypes

• Subfalcine
  • Herniation of cingulate gyrus underneath falx cerebri
  • No pupillary involvement, consciousness often preserved
  • Contralateral leg weakness (ipsilateral ACA compression)
• Uncal
  • Herniation of uncus (medial temporal lobe) under tentorium cerebelli
  • Ipsilateral dilated & fixed pupil (ipsilateral oculomotor nerve (CN III) compression)
  • Early: contralateral hemiparesis (ipsilateral cerebral peduncle compression)
  • Late: ipsilateral hemiparesis (contralateral cerebral peduncle compression)
• Central
  • Caudal displacement of diencephalon & brainstem
  • Rupture of paramedian basilar artery branches
  • Bilateral midposition & fixed pupils (loss of sympathetic & parasympathetic innervation)
  • Decorticate (flexor) → decerebrate (extensor) posturing
• Tonsillar
  • Herniation of cerebellar tonsils through foramen magnum
  • Coma, loss of CN reflexes, flaccid paralysis, respiratory arrest (brainstem compression)

Diagnostics

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Treatment

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