Cerebral Edema & Herniation Syndromes

2.3 Cerebral Edema & Herniation Syndromes

Cerebral edema is an abnormal accumulation of fluid within brain parenchyma resulting in volumetric expansion. When tissue expansion exceeds spatial compensatory reserve, pressure gradients develop across rigid dural partitions—the falx cerebri, tentorium cerebelli, and foramen magnum. The resulting mechanical displacement compresses vital neurovascular pathways, culminating in stereotypical herniation syndromes.

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Pathophysiologic Subtypes of Cerebral Edema

Cerebral edema is categorized into four distinct pathophysiologic classes:

1. Vasogenic Edema

Vasogenic edema stems from breakdown of blood-brain barrier (BBB) tight junctions (claudin-5, occludin, ZO-1) driven by VEGF and inflammatory cytokines. Plasma proteins and fluid extravasate into extracellular spaces, tracking through subcortical white matter along parallel axonal tracts that offer minimal mechanical resistance, sparing cortical gray matter. Neoplastic vasogenic edema responds dramatically to dexamethasone ($4\text{--}10\text{ mg}$ IV q6h), which stabilizes tight junctions and downregulates VEGF.

2. Cytotoxic (Cellular) Edema

Cytotoxic edema results from cellular energy failure. Depletion of ATP halts $\text{Na}^+/\text{K}^+$-ATPase pumps, causing intracellular $\text{Na}^+$ accumulation and osmotic swelling of neurons and astrocytes. Astrocytic water entry is mediated by aquaporin-4 (AQP4) channels. Involving both gray and white matter, it produces sulcal effacement and loss of gray-white differentiation on CT. It is unresponsive to corticosteroids, requiring osmotherapy (mannitol, hypertonic saline) and decompressive surgery.

3. Interstitial and Osmotic Edema

• Interstitial (Hydrocephalic) Edema: Elevated intraventricular pressure in acute hydrocephalus forces CSF across the ventricular ependymal lining into periventricular white matter (trans-ependymal transudation), seen as a periventricular halo on CT/FLAIR. Definitive therapy is CSF diversion via EVD.
• Osmotic Edema: Acute drops in serum osmolality create a trans-barrier gradient driving water into parenchymal cells. Etiologies include rapid correction of hypernatremia, acute hyponatremia, and water intoxication.

Mechanical Brain Herniation Syndromes

When localized edema or mass lesions generate compartmental pressure gradients, parenchyma shifts across internal dural folds or through the foramen magnum:

1. Uncal (Lateral Transtentorial) Herniation

Uncal herniation occurs when an expanding supratentorial mass forces the medial temporal uncus over the tentorium cerebelli into the posterior fossa:

• CN III Compression: Parasympathetic pupillomotor fibers travel on the superficial dorsomedial perimeter of CN III. Extrinsic compression produces ipsilateral pupillary sluggishness progressing rapidly to mydriasis and light unresponsiveness ("blown pupil"). Deeper somatic motor fibers fail later, causing ptosis and ophthalmoplegia.
• Cerebral Peduncle Compression: Compression of the ipsilateral cerebral peduncle produces contralateral hemiparesis.
• Kernohan's Notch Phenomenon (False-Localizing Sign): Severe lateral midbrain shift crushes the contralateral cerebral peduncle against the opposite tentorial edge (Kernohan's notch), causing motor weakness ipsilateral to the mass lesion. The ipsilateral dilated pupil correctly localizes the lesion side.
• Vascular Sequelae: PCA compression causes occipital infarction. Downward basilar artery traction tears paramedian perforators, causing fatal Duret hemorrhages in the midbrain and pons.

2. Central (Transtentorial) Herniation

Central herniation involves symmetric downward displacement of hemispheres and diencephalon through the incisura, manifesting as rostrocaudal deterioration:

• Diencephalic Stage: Stupor, small reactive pupils ("diencephalic pupils"), Cheyne-Stokes breathing, and decorticate (flexor) posturing.
• Midbrain-Upper Pons Stage: Deep coma, fixed mid-position pupils (3–5 mm), loss of oculocephalic reflexes, central neurogenic hyperventilation, and decerebrate (extensor) posturing.
• Medullary Stage: Flaccid quadriplegia, ataxic breathing, and terminal cardiopulmonary arrest.

3. Subfalcine, Tonsillar, and Other Syndromes

• Subfalcine Herniation: The cingulate gyrus shifts beneath the falx cerebri, compressing anterior cerebral artery (ACA) branches to cause contralateral leg-predominant weakness, abulia, and trapped hydrocephalus from foramen of Monro occlusion.
• Tonsillar Herniation: Cerebellar tonsils are forced through the foramen magnum, crushing the medulla. This triggers Cushing's triad (hypertension with widened pulse pressure, bradycardia, irregular breathing) followed by sudden apnea and arrest.
• Upward Transtentorial Herniation: Posterior fossa masses drive the vermis upward through the incisura, compressing the tectal plate to cause upward gaze impairment, fixed pupils, and hydrocephalus.
• Transcalvarial Herniation: Brain tissue extrudes through a craniectomy defect. Bone edge pressure strangulates cortical veins, causing hemorrhagic venous infarction.