A 30-year-old woman presents with persistent headache, papilloedema, and elevated CSF opening pressure of 28 cm H2O on lumbar puncture; CSF composition is normal. She has no intracranial mass. The diagnosis of idiopathic intracranial hypertension (pseudotumour cerebri) is suspected. Which is the primary mechanism for CSF pressure elevation in this condition?

• A Increased CSF secretion by choroid plexus, reduced CSF absorption at the arachnoid granulations, or both, leading to CSF volume accumulation and raised ICP ✓
• B Cerebral vasodilation increases cerebral blood volume, transiently raising ICP by the Monro-Kellie doctrine
• C Increased plasma osmolality drives water across the blood-brain barrier into the CSF compartment
• D Hydrocephalus from blockage of the cerebral aqueduct obstructs CSF flow between lateral and third ventricles

Explanation

In idiopathic intracranial hypertension (IIH), the prevailing evidence points to impaired CSF absorption at the arachnoid granulations (dural venous sinus stenosis reduces the pressure gradient driving CSF absorption) and possibly increased choroid plexus secretion (influenced by acetazolamide-responsive carbonic anhydrase activity). Normal CSF composition and the absence of obstructive hydrocephalus exclude aqueduct blockage. The Monro-Kellie doctrine (option B) explains ICP dynamics in general but not the sustained elevation in IIH. Decreased plasma osmolality (not increased) would drive water into the CNS, but this is not the mechanism in IIH.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.