Arachnoid cyst is a benign congenital extra-axial lesion formed by developmental duplication or splitting of the arachnoid membrane, containing clear CSF (cerebrospinal fluid). It is most commonly found in the middle cranial fossa (Sylvian fissure — 50%) and constitutes approximately 1% of all intracranial lesions. Following CSF signal on all sequences, complete suppression on FLAIR, no diffusion restriction on DWI, and no enhancement form the diagnostic quartet. Most are asymptomatic and incidentally detected; however, large cysts may cause mass effect and hydrocephalus.
Age Range
0-80
Peak Age
-
Gender
Male predominant
Prevalence
Common
Arachnoid cyst forms due to congenital duplication or splitting of the arachnoid membrane during embryogenesis. The cyst wall is lined by normal arachnoid membrane cells (meningothelial cells) and contains collagen and elastic fibers. The intracystic fluid is biochemically identical or very similar to CSF — this forms the basis for CSF signal on all MRI sequences. The cyst growth mechanism is debated: one explanation proposes a one-way valve mechanism (ball-valve effect) in the arachnoid membrane allowing CSF to enter but not exit; another proposes active fluid secretion by the cyst wall contributing to growth. Due to collagen and serous fluid composition of the cyst wall, osmotic gradient differences may develop, leading to passive fluid accumulation. Large cysts may cause compression of surrounding brain parenchyma and bone remodeling.
Pure CSF signal on all MRI sequences (T1 hypointense, T2 hyperintense), complete suppression on FLAIR, no diffusion restriction on DWI, and absence of enhancement form the pathognomonic quartet for arachnoid cyst. The presence of all four findings together provides definitive differentiation from all important differential diagnoses including epidermoid cyst (FLAIR not suppressed, DWI restriction present), cystic tumors (enhancement present, FLAIR not fully suppressed), dermoid cyst (T1 hyperintense), and neuroepithelial cyst (FLAIR may not fully suppress).
On non-contrast CT, a CSF-density (0-10 HU) extra-axial, well-circumscribed, homogeneously hypodense lesion is observed. No septation, calcification, or solid component in internal structure. Bone remodeling (thinning, expansion) may be seen in adjacent osseous structures with large cysts. Compression but no invasion of surrounding brain parenchyma. Temporal lobe hypoplasia may accompany cysts in the middle cranial fossa. Differentiation from epidermoid cyst on CT is difficult — both are at CSF density.
Report Sentence
On CT, an extra-axial, CSF-density, well-circumscribed homogeneously hypodense lesion is identified without calcification or solid component.
On T1-weighted images, arachnoid cyst shows hypointense signal identical to CSF. No internal heterogeneity, debris, or proteinaceous content — pure, clean CSF signal is observed. Cyst wall is very thin and generally not separately visible on T1. Surrounding brain parenchyma is compressed but not infiltrated. Pulsation artifacts may create areas of low signal in some cysts that could be confused with flow voids. Any deviation from CSF signal on T1 (hyperintensity) should raise consideration for epidermoid cyst, dermoid cyst, or hemorrhagic cyst.
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On T1-weighted sequence, the extra-axial lesion shows hypointense signal identical to CSF without internal heterogeneity or proteinaceous content.
On T2-weighted images, arachnoid cyst shows markedly hyperintense signal identical to CSF. Signal is homogeneous without 'dirty CSF' appearance (internal heterogeneity seen in epidermoid cyst). Cyst margins are smooth without uninterrupted communication with cisterns (does not show insinuative growth unlike epidermoid cyst). Compression of adjacent brain parenchyma and cyst size are best evaluated on T2. CSF flow artifacts may appear as low signal bands in some cysts.
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On T2-weighted sequence, the extra-axial lesion shows markedly hyperintense, homogeneous signal identical to CSF.
On FLAIR, arachnoid cyst signal is completely suppressed and shows low signal identical to CSF. This is the most important diagnostic finding of arachnoid cyst and provides definitive differentiation from epidermoid cyst (not suppressed on FLAIR — hyperintense), cystic tumors, and neuroepithelial cysts. Complete suppression confirms that cyst contents are pure CSF — no proteinaceous content, debris, or solid material. On FLAIR, incomplete suppression may be seen in some ventricle-adjacent cysts due to CSF flow artifacts; in this case, evaluation with phase contrast MRI should be performed.
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On FLAIR, the extra-axial lesion shows complete suppression identical to CSF, which is pathognomonic for arachnoid cyst and definitively differentiates from epidermoid cyst and cystic tumors.
On DWI, arachnoid cyst shows no diffusion restriction: low signal on DWI (or mild T2 shine-through) and high signal on ADC map (~3.0 × 10⁻³ mm²/s — pure CSF diffusion coefficient) are observed. This finding provides definitive differentiation from epidermoid cyst which shows marked restriction on DWI (ADC: 0.6-1.0 × 10⁻³ mm²/s) and is the most valuable differential sequence after FLAIR. Pure CSF diffusion is unimpeded and approaches the free water diffusion coefficient.
Report Sentence
On DWI, the extra-axial lesion shows no diffusion restriction with high signal on ADC map identical to CSF, definitively differentiating from epidermoid cyst.
On contrast-enhanced MRI, arachnoid cyst shows no enhancement — no gadolinium passage is observed in either cyst contents or cyst wall. No abnormal enhancement in surrounding brain parenchyma. If any enhancement is detected, alternative diagnoses (cystic tumor, malignant transformation of epidermoid cyst, infectious cyst) should be considered. This finding confirms the intact vascular barrier and avascular nature of the cyst wall.
Report Sentence
On post-contrast T1-weighted sequence, no enhancement is observed in the extra-axial lesion or surrounding tissues.
On SWI, arachnoid cyst shows no blooming artifact or susceptibility effect. No hemosiderin deposition, calcification, or blood products are present. This finding is valuable for differentiation from cavernous malformation (pathognomonic hemosiderin ring and blooming). Magnetic susceptibility of cyst contents is identical to CSF. Blooming may be seen on SWI if intracystic hemorrhage develops as a traumatic complication.
Report Sentence
On SWI, no blooming artifact, hemosiderin deposition, or blood products are identified within the lesion.
Criteria
Most common type (50%). Adjacent to Sylvian fissure and temporal pole. Galassi classification (I-III): I = small, within Sylvian fissure; II = medium, opens insular cortex; III = large, fills entire middle cranial fossa. Temporal lobe hypoplasia may accompany.
Distinct Features
Galassi III cysts may be symptomatic (headache, seizure). Temporal bone thinning and middle cranial fossa expansion visible on CT. Incidental detection is common — most do not require treatment.
Criteria
Cysts located in suprasellar cistern or interhemispheric fissure. Second most common location in children. May cause obstructive hydrocephalus by compressing the 3rd ventricle. May present with endocrine dysfunction (hypothalamic compression) and visual disturbances (optic chiasm compression).
Distinct Features
Differential diagnosis with craniopharyngioma and Rathke cleft cyst is required. Complete FLAIR suppression is determinative for differentiation from craniopharyngioma (craniopharyngioma cystic component does not suppress on FLAIR). Phase contrast MRI may show cyst-ventricle communication.
Criteria
Located in cerebellopontine angle (CPA), retrocerebellar region, or cisterna magna. CPA cysts are frequently confused with epidermoid cyst — FLAIR and DWI are differentiating. Retrocerebellar cysts may be confused with mega cisterna magna (vermis is intact in mega cisterna magna, no cyst). May cause hydrocephalus by compressing 4th ventricle.
Distinct Features
CPA arachnoid cyst: complete FLAIR suppression + no DWI restriction → arachnoid cyst. FLAIR non-suppression + DWI restriction → epidermoid cyst. Retrocerebellar cyst: differentiation from Dandy-Walker malformation (vermis agenesis) — in Dandy-Walker, vermis is absent or hypoplastic.
Distinguishing Feature
Epidermoid cyst does not suppress on FLAIR (hyperintense) and shows marked diffusion restriction on DWI (low ADC). Arachnoid cyst completely suppresses on FLAIR and shows no restriction on DWI (high ADC). These two sequences provide definitive differentiation.
Distinguishing Feature
Craniopharyngioma cystic component is generally T1 hyperintense (cholesterol content), does not fully suppress on FLAIR, contains calcification (90%), and shows enhancement (rim or solid component). None of these are present in arachnoid cyst.
Distinguishing Feature
Colloid cyst is hyperdense on CT, variable on T1 (usually hyperintense — proteinaceous content), does not suppress on FLAIR, and is located at the foramen of Monro. Arachnoid cyst follows CSF density/signal and completely suppresses on FLAIR.
Distinguishing Feature
Hemangioblastoma cystic component does not fully suppress on FLAIR (proteinaceous fluid) despite being CSF-like, contains enhancing mural nodule and flow voids. Arachnoid cyst has no enhancing component, mural nodule, or flow voids and completely suppresses on FLAIR.
Urgency
non-urgent — most are incidental findingsManagement
observation for asymptomatic; surgical (fenestration/shunt) for symptomaticBiopsy
Not NeededFollow-up
Follow-up MRI in 6-12 months for new findings, then only if symptomatic change occursThe vast majority of arachnoid cysts are asymptomatic and do not require treatment — when incidentally detected, the patient is informed and follow-up is sufficient unless symptoms develop. Surgical treatment is indicated for symptomatic cysts (hydrocephalus, seizures, progressive headache, developmental delay): endoscopic fenestration (creating cyst-ventricle or cyst-subarachnoid communication) is first-line surgery. Cystoperitoneal shunt may be applied as an alternative. Craniotomy with cyst wall excision may be preferred for large cysts. Post-traumatic intracystic hemorrhage may require emergency surgery. Growing cysts in children should be followed with serial imaging.
Most arachnoid cysts are asymptomatic and require no treatment. Surgical drainage or fenestration may be performed for symptomatic cysts (headache, seizures, focal neurological deficit, hydrocephalus). Size stability on follow-up is important.