subfalcine herniation

**Definition/Anatomy:** The falx cerebri is a dural fold in the longitudinal fissure that separates the two cerebral hemispheres. In subfalcine herniation, a supratentorial mass (tumor, hematoma, abscess, infarct with edema) pushes the cingulate gyrus of one hemisphere beneath the inferior free margin of the falx to the contralateral side. This is also called cingulate herniation or midline shift.

**Pathophysiology:** Mass effect raises intracranial pressure (Monro-Kellie doctrine: skull is a fixed volume containing brain, blood, and CSF). Unilateral expansion displaces tissue along the path of least resistance, under the falx. Consequences: - **ACA compression** against the falx: pericallosal and callosomarginal branches are squeezed, causing ischemia/infarction of the medial frontal and parietal lobes. This produces **contralateral leg > arm weakness and cortical sensory loss**, and possibly abulia, urinary incontinence, or akinetic mutism with bilateral involvement. - **Compression of the lateral ventricle/foramen of Monro:** can cause contralateral ventricular dilation (obstructive hydrocephalus). - **Midline shift** is seen on CT/MRI (septum pellucidum and third ventricle displaced from midline; the contralateral lateral ventricle may be compressed or trapped).

**Clinical significance:** Often asymptomatic or subtle by itself, and it is an early sign of rising ICP. It may progress to other herniation syndromes.

**Comparison with other herniations (high-yield):** - **Uncal (transtentorial):** medial temporal lobe (uncus) herniates over the tentorium. It compresses CN III ("blown pupil": ipsilateral dilated, "down and out" eye), the ipsilateral PCA (contralateral homonymous hemianopia with macular sparing), and the contralateral cerebral peduncle against the tentorial edge (**Kernohan notch phenomenon**: ipsilateral hemiparesis, a false localizing sign). Also causes ipsilateral hemiparesis in some cases. - **Central transtentorial:** downward displacement of the diencephalon/midbrain. It causes **Duret hemorrhages** (pontine/midbrain paramedian artery rupture), altered consciousness, and bilateral pupillary changes. - **Tonsillar:** cerebellar tonsils pass through the foramen magnum, compressing the medulla (respiratory/cardiac centers), causing Cushing triad (hypertension, bradycardia, irregular respirations), coma, and death. - **Upward (transtentorial) herniation:** posterior fossa mass pushes the cerebellum upward through the tentorial notch. - **Extracranial (transcalvarial):** brain herniates through a skull defect (e.g., after craniectomy or trauma).

**Diagnosis:** Noncontrast head CT is the first-line study (midline shift, effacement of sulci, ventricular asymmetry). MRI is better for detail and for ACA territory infarcts.

**Management:** Treat the underlying cause and lower ICP: - Elevate the head of the bed to 30°, keep the neck midline, and ensure adequate oxygenation/ventilation. - Hyperosmolar therapy (mannitol or hypertonic saline). - Brief controlled hyperventilation (target PaCO2 ~30 to 35 mmHg) as a temporizing bridge only, since it causes cerebral vasoconstriction. - Sedation, and CSF drainage via EVD if hydrocephalus is present. - Corticosteroids (dexamethasone) for vasogenic edema from tumors/abscesses (not for traumatic brain injury or stroke). - Neurosurgical intervention: hematoma evacuation or decompressive craniectomy.

**Board pearls:** Subfalcine = most common herniation; the key complication to know is **ACA compression with contralateral leg weakness**. Do not confuse it with uncal herniation, which causes CN III palsy and PCA infarct (visual field defect).