arachnoid villi

**Anatomy/Physiology** - Microscopic arachnoid villi are protrusions of arachnoid mater through the dura. They are larger and more numerous with age, and the grossly visible ones are called arachnoid (Pacchionian) granulations. They project into the dural venous sinuses, especially the superior sagittal sinus and its lateral lacunae. - Function: CSF reabsorption. CSF drains from the subarachnoid space into venous blood. Flow is one-way, passive, and pressure-dependent. It occurs when CSF pressure exceeds venous sinus pressure (about 5-7 mmHg), and the villi act as valves. - CSF circulation: choroid plexus (lateral ventricles) → interventricular foramen of Monro → third ventricle → cerebral aqueduct of Sylvius → fourth ventricle → foramina of Luschka (lateral) and Magendie (median) → subarachnoid space (cisterns) → arachnoid villi → superior sagittal sinus. - CSF is produced at about 500 mL/day by the choroid plexus (ependymal cells, via Na⁺/K⁺-ATPase and carbonic anhydrase). Total volume is about 150 mL, so it turns over about 3-4 times/day.

**Clinical significance** - *Communicating hydrocephalus:* the ventricular system is open but CSF reabsorption is impaired. All ventricles are dilated. Causes include: - Subarachnoid hemorrhage, where blood clogs the villi. This is a classic cause. - Meningitis, where inflammation and scarring obstruct the villi. - Dural venous sinus thrombosis, which raises venous pressure and reduces reabsorption. - Leptomeningeal carcinomatosis. - *Normal pressure hydrocephalus (NPH):* a chronic communicating hydrocephalus in older adults. The classic triad is "wet, wobbly, wacky" (urinary incontinence, gait apraxia/magnetic gait, dementia). Opening pressure is normal on LP. Treatment is a ventriculoperitoneal shunt. - *Idiopathic intracranial hypertension (pseudotumor cerebri):* associated with impaired CSF outflow or raised venous pressure. It occurs in obese women of childbearing age, and vitamin A, tetracyclines, and OCPs are risk factors. Features are headache, papilledema, and vision loss (enlarged blind spot, then peripheral loss), with CN VI palsy possible. Imaging is normal, and LP shows high opening pressure with normal CSF composition. Treat with acetazolamide, weight loss, and serial LP. Optic nerve sheath fenestration or a shunt can be used if vision is threatened. - *Hydrocephalus ex vacuo:* a compensatory increase in CSF volume after brain atrophy (Alzheimer disease, Pick disease). Pressure is normal and no villi pathology is involved. - *Obstructive (noncommunicating) hydrocephalus:* a blockage within the ventricular system (e.g., aqueductal stenosis, Dandy-Walker malformation, tumors). Villi function is normal, so it differs from communicating hydrocephalus. - *Imaging:* granulations appear as well-circumscribed, CSF-density filling defects in the venous sinuses on CT/MRV. They can mimic dural sinus thrombosis or a lytic skull lesion (foveolae granulares).

**High-yield pearls** - Villi/granulations are the site of CSF reabsorption. The choroid plexus is the site of production. - Subarachnoid hemorrhage and meningitis → villi dysfunction → communicating hydrocephalus. - Layers of the meninges: dura → arachnoid → subarachnoid space (CSF, vessels) → pia. The villi cross the dura to reach the sinus. - Acetazolamide reduces CSF production by inhibiting carbonic anhydrase.