Pathology of increased intracranial pressure (edema, herniation and hydrocephalus)

1. Overview

• Brain + spinal cord have rigid coverage (skull + spinal canal).
• Advantage: protection.
• Disadvantage: inability to expand during ↑ intracranial pressure (ICP).

Compensatory Mechanisms

• Venous plexus drains the brain.
• Elasticity of dura + spinal cord allows some compliance.
• Only small amount of CSF/blood can be displaced.

Critical Pressures

• Slow-onset swelling → compensated.
• Acute swelling → herniation develops.
• ICP > 30 mmHg → clinical symptoms appear.
• ICP > 60 mmHg → brain death.

2. Cerebral Edema

Definition

• Accumulation of excess fluid within brain parenchyma.

Types

A) Vasogenic Edema

• Damage to blood-brain barrier (inflammation, abscess, neoplasm).
• → ↑ vascular permeability → fluid accumulation in interstitial space.
• Usually localized (e.g., around tumor).

B) Cytotoxic Edema

• Ischemia, hypoxia, toxins → damage to neuronal/glial/endothelial cells.
• → Failure of Na/K-ATPase (transport mechanisms) → intracellular fluid accumulation.
• Generalized.

C) Osmotic Edema

• ↓ Extracellular osmotic pressure.
• Example: SIADH (syndrome of inappropriate ADH secretion), hyponatremia, dialysis.

D) Hydrostatic Edema

• E.g., hypertensive crisis.

Morphology

• Brain softer.
• Flattened gyri.
• Narrowed sulci.
• Compressed ventricular cavities.

3. Herniation

Mechanism

• ↑ Brain volume → ↑ ICP → brain tissue forced through anatomic openings.
• Compromise of blood supply to herniated tissue → infarction → further swelling → more herniation (vicious cycle).

Types

A) Subfalcine (Cingulate) Herniation

• Expansion of cerebral hemisphere → cingulate gyrus displaced under edge of falx cerebri.
• May compress branches of anterior cerebral artery → ischemia.
• Impaired sensory + motor functions (mainly the legs).

B) Transtentorial (Uncal) Herniation

• Uncus of temporal lobe compressed against the tentorium cerebelli.
• Duret hemorrhages: hemorrhagic lesions in midbrain + pons (bad prognostic sign).
• CN III compression → pupillary dilation (“blown pupil”) + impaired ocular movements ipsilateral to lesion.
• Posterior cerebral artery compression → ischemia of primary visual cortex.

C) Tonsillar Herniation

• Displacement of cerebellar tonsils through foramen magnum.
• Life-threatening: brain stem compression → respiratory + cardiac centers → death.

4. Hydrocephalus

Definition

• Accumulation of excessive CSF in the ventricular system.

Physiology of CSF

• Produced by choroid plexus → ventricular system → exits through foramina of Luschka + Magendie → subarachnoid space → reabsorbed by arachnoid granulations.
• Balance between production + reabsorption.

Pathophysiology

• Impaired flow or reabsorption (most common).
• Rarely: overproduction of CSF (choroid plexus tumor).

Types

Type	Mechanism
Communicating	↑ Production or ↓ absorption → enlargement of entire ventricular system; e.g., meningitis → arachnoid granulations fibrosed
Non-communicating (obstructive)	Localized obstruction of CSF flow within ventricles → enlargement only of segment upstream of block; e.g., aqueductal stenosis
Hydrocephalus ex vacuo	Not true hydrocephalus; brain atrophy (infarcts, degenerative) → compensatory ventricular dilation

Clinical

• Infants (sutures open): ↑ head circumference, bulging fontanelles, “sunset eyes” (downward gaze).
• Adults: headache, vomiting, papilledema, Cushing triad (HTN + bradycardia + irregular respiration).
• Normal pressure hydrocephalus (NPH): triad of wet, wobbly, wacky (urinary incontinence + ataxia + dementia) in elderly; LP-responsive.

5. Summary Table

Process	Mechanism	Key features
Vasogenic edema	BBB disruption	Tumor, abscess; interstitial fluid
Cytotoxic edema	Cell pump failure	Ischemia, hypoxia; intracellular fluid
Subfalcine herniation	Under falx	ACA compression, leg deficits
Uncal/transtentorial	Through tentorium	CN III → blown pupil, Duret hemorrhages, PCA ischemia
Tonsillar herniation	Through foramen magnum	Brain stem compression → death
Communicating hydroceph.	Post-hemorrhagic/meningitic absorption defect	All ventricles enlarged
Non-communicating hydroceph.	Aqueductal stenosis, tumor	Selective dilation
Hydrocephalus ex vacuo	Brain atrophy	Not true; passive ventricular dilation
NPH	Idiopathic	Wet + wobbly + wacky; LP-responsive

💡 High-yield: ICP > 30 mmHg = symptoms; > 60 mmHg = brain death. Cerebral edema: vasogenic (BBB → interstitial; tumors); cytotoxic (pump failure → intracellular; ischemia); osmotic (SIADH); hydrostatic (HTN). Herniation: subfalcine (under falx → ACA → leg deficits); uncal/transtentorial (uncus through tentorium → CN III → blown pupil, Duret hemorrhages in midbrain/pons, PCA ischemia); tonsillar (foramen magnum → brain stem → death). Hydrocephalus: communicating (↓ absorption; entire system), non-communicating (obstruction; selective), ex vacuo (brain atrophy, not true); NPH = wet/wobbly/wacky in elderly.