Arachnoid Cyst (AC)
Last Updated: March 27, 2020
- Intracranial, extra-axial, CSF-containing cyst without communication to the ventricular system
- Accounts for 1% of all intracranial masses
- Originates from embryonic meninges that fail to fuse during Sylvian fissure development
- CSF contents may arise from unidirectional inflow (ball-valve mechanism) versus secretion by cells lining AC wall
- Wall may contain ciliated cells, arachnoid tissue, or fibrous connective tissue
- Usually sporadic
- Rare association with Aicardi and Pallister-Hall syndromes
- Associated with temporal lobe hypoplasia, subdural hematomas, foramen of Monro and/or aqueductal stenosis
- No inflammatory or neoplastic features
- Affects all ages
- Male gender predilection
- Common presenting signs/symptoms: range from asymptomatic/incidental finding to headache, sensorineural hearing loss, obstructive hydrocephalus
- Gradual enlargement is typical
- Most require no treatment
- Surgical resection, fenestration, and/or shunting for larger, symptomatic ACs
- Well-marginated extra-axial cyst which follows CSF density/signal intensity
- Mass effect and displacement of adjacent cortex
- Size variable
- Middle cranial fossa >> cerebellopontine angle cistern, suprasellar cisterns
- CSF-density, extra-axial mass
- ± Adjacent bony remodeling
- No enhancement on contrast-enhanced CT
- T1WI: isointense to CSF
- T2WI: isointense to CSF
- FLAIR: complete drop out of signal (just like CSF)
- DWI: no diffusion restriction
- T1WI+C: no enhancement
- MRI without and with IV contrast (to exclude other lesions) including FLAIR and DWI
For more information, please see the corresponding chapter in Radiopaedia.
Contributor: Rachel Seltman, MD
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