Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (768 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Intracranial or spinal cavities containing a cerebrospinal-like fluid, the wall of which is composed of arachnoidal cells. They are most often developmental or related to trauma. Intracranial arachnoid cysts usually occur adjacent to arachnoidal cistern and may present with hydrocephalus; headache; seizures; and focal neurologic signs. (From Joynt, Clinical Neurology, 1994, Ch44, pp105-115)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Cyst, Arachnoid; Cysts, Arachnoid; Arachnoid Diverticula; Arachnoid Diverticulas; Diverticula, Arachnoid; Diverticulas, Arachnoid; Leptomeningeal Cysts; Cyst, Leptomeningeal.
Where it fits in the MeSH classification
- Broader topics
- Cysts; Central Nervous System Cysts
Related concepts
- Hydrocephalus
- Headache
- Seizures
Research landscape
PubMed indexes 2,619 records tagged with the MeSH heading “Arachnoid Cysts” (counts retrieved 2026-10-29). 397 of them (15.2%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 841 records.
Reviews account for 396 records (15.1%) and meta-analyses for 10. Randomized controlled trials number 5 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 568 |
| 2000-2009 | 813 |
| 2010-2019 | 841 |
| 2020 onward | 397 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 396 | 15.1% |
| Meta-analyses | 10 | 0.4% |
| Randomized controlled trials | 5 | 0.2% |
Method: PubMed query "Arachnoid Cysts"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in rare and inherited diseases
Rare conditions are difficult to study: few patients means small studies, case reports and registries are common, and randomized trials are the exception. Small samples limit precision and can exaggerate effects, and cases reported in the literature may be the most severe or unusual. Evidence from many small studies is best read together. Check how patients were identified, how many were included and how long they were followed.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Magnetic resonance imaging provides evidence of glymphatic drainage from human brain to cervical lymph nodes | 2018 | Research article Design not recorded in structured metadata | 254 | cc by PMID 29740121 · DOI · PMC5940793 |
| Defective Gpsm2/Gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome | 2017 | Research article Design not recorded in structured metadata | 86 | cc by PMID 28387217 · DOI · PMC5385604 |
| FOXC2 mutations in familial and sporadic spinal extradural arachnoid cyst | 2013 | Research article Design not recorded in structured metadata | 23 | cc by PMID 24278289 · DOI · PMC3838418 |
| Spinal arachnoid diverticula in cats: Clinical presentation, diagnostic imaging findings, treatment, and outcome | 2025 | Research article Design not recorded in structured metadata | 3 | cc by PMID 39739353 · DOI · PMC11683399 |
Magnetic resonance imaging provides evidence of glymphatic drainage from human brain to cervical lymph nodes [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Pre-clinical research in rodents provides evidence that the central nervous system (CNS) has functional lymphatic vessels.
- Closing excerpt
- The time course of lymph node enhancement coincided with brain glymphatic enhancement rather than with CSF enhancement.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Pre-clinical research in rodents provides evidence that the central nervous system (CNS) has functional lymphatic vessels. In-vivo observations in humans, however, are not demonstrated. We here show data on CNS lymphatic drainage to cervical lymph nodes in-vivo by magnetic resonance imaging (MRI) enhanced with an intrathecal contrast agent as a cerebrospinal fluid (CSF) tracer. Standardized MRI of the intracranial compartment and the neck were acquired before and up to 24-48 hours following intrathecal contrast agent administration in 19 individuals. Contrast enhancement was radiologically confirmed by signal changes in CSF nearby inferior frontal gyrus, brain parenchyma of inferior frontal gyrus, parahippocampal gyrus, thalamus and pons, and parenchyma of cervical lymph node, and with sagittal sinus and neck muscle serving as reference tissue for cranial and neck MRI acquisitions, respectively. Time series of changes in signal intensity shows that contrast enhancement within CSF precedes glymphatic enhancement and peaks at 4-6 hours following intrathecal injection. Cervical lymph node enhancement coincides in time with peak glymphatic enhancement, with peak after 24 hours. Our findings provide in-vivo evidence of CSF tracer drainage to cervical lymph nodes in humans. The time course of lymph node enhancement coincided with brain glymphatic enhancement rather than with CSF enhancement.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29740121 · DOI · PMC5940793
Defective Gpsm2/Gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies.
- Closing excerpt
- Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Mutations in GPSM2 cause Chudley-McCullough syndrome (CMCS), an autosomal recessive neurological disorder characterized by early-onset sensorineural deafness and brain anomalies. Here, we show that mutation of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defects. The G-protein subunit Gαi3, a well-documented partner of Gpsm2, participates in the elongation process, and its absence also causes hearing deficits. We show that Gpsm2 defines an ∼200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Gαi3, myosin 15 and whirlin. Using single-molecule tracking, we report that loss of Gpsm2 leads to decreased outgrowth and a disruption of actin dynamics in neuronal growth cones. Our results elucidate the aetiology of CMCS and highlight a new molecular role for Gpsm2/Gαi3 in the regulation of actin dynamics in epithelial and neuronal tissues.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28387217 · DOI · PMC5385604
FOXC2 mutations in familial and sporadic spinal extradural arachnoid cyst [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Spinal extradural arachnoid cyst (SEDAC) is a cyst in the spinal canal that protrudes into the epidural space from a defect in the dura mater.
- Closing excerpt
- Seven sporadic SEDAC subjects had no FOXC2 mutations, no symptoms of LDS, and showed differing clinical characteristics from those who had FOXC2 mutations, suggesting that other gene(s) besides FOXC2 are likely to be involved in SEDAC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (189 words)
Spinal extradural arachnoid cyst (SEDAC) is a cyst in the spinal canal that protrudes into the epidural space from a defect in the dura mater. Most cases are sporadic; however, three familial SEDAC cases have been reported, suggesting genetic etiological factors. All familial cases are associated with lymphedema-distichiasis syndrome (LDS), whose causal gene is FOXC2. However, FOXC2 mutation analysis has been performed in only 1 family, and no mutation analysis has been performed on sporadic (non-familial) SEDACs. We recruited 17 SEDAC subjects consisting of 2 familial and 7 sporadic cases and examined FOXC2 mutations by Sanger sequencing and structural abnormalities by TaqMan copy number assay. We identified 2 novel FOXC2 mutations in 2 familial cases. Incomplete LDS penetrance was noted in both families. Four subjects presented with SEDACs only. Thus, SEDAC caused by the heterozygous FOXC2 loss-of-function mutation should be considered a feature of LDS, although it often manifests as the sole symptom. Seven sporadic SEDAC subjects had no FOXC2 mutations, no symptoms of LDS, and showed differing clinical characteristics from those who had FOXC2 mutations, suggesting that other gene(s) besides FOXC2 are likely to be involved in SEDAC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24278289 · DOI · PMC3838418
Spinal arachnoid diverticula in cats: Clinical presentation, diagnostic imaging findings, treatment, and outcome [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundSpinal arachnoid diverticulum (SAD) is considered a rare disease in cats.
- Closing excerpt
- Conclusions and clinical importanceSpinal arachnoid diverticulum should be considered for cats with chronic, progressive, symmetrical, nonpainful myelopathy, particularly if male and with a history of spinal disease or surgery.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (237 words)
BackgroundSpinal arachnoid diverticulum (SAD) is considered a rare disease in cats. Previous reports mainly classified SAD in cats as acquired.Hypothesis/objectivesThe aim of this study was to describe the signalment, clinical presentation, diagnostic imaging findings, and outcome in a group of cats with SAD.AnimalsTwenty-one client-owned cats.MethodsMulticenter observational retrospective review of the medical records of cats diagnosed with SAD by magnetic resonance imaging.ResultsMost cats were Domestic Short Hair (67%), male (63%), and had a wide range of ages (18 weeks to 13 years old). Neuroanatomical localization was consistent with a T3-L3 myelopathy in 18 cats (86%) and C1-C5 myelopathy in 3 cats (14%). One cat with a C1-C5 myelopathy demonstrated bilateral vestibular clinical signs. One cat (5%) had fecal incontinence. Most cats demonstrated a chronic, progressive, nonlateralized, nonpainful myelopathy. No underlying previous or concurrent spinal condition was found in 48% of the cats. No difference in age, body weight, breed, sex, treatment, or outcome was found between cats with or without a concurrent spinal disorder. One cat was euthanized after diagnosis. Six cats improved, 1 deteriorated and 1 remained static after surgery, whereas 3 cats improved, 5 deteriorated and 4 remained static after medical management on the short-term outcome. Overall, 73% (8/11) of the cats deteriorated on available long-term follow-up information.Conclusions and clinical importanceSpinal arachnoid diverticulum should be considered for cats with chronic, progressive, symmetrical, nonpainful myelopathy, particularly if male and with a history of spinal disease or surgery.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39739353 · DOI · PMC11683399
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Cerebrospinal fluid flow imaging by using phase-contrast MR technique [5]
- Research article Intracranial arachnoid cysts in children: a review of pathogenesis, clinical features, and management [6]
- Research article Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature [7]
- Research article Arachnoid cysts: case series and review of the literature [8]
- Research article Intracranial arachnoid cysts: current concepts and treatment alternatives [9]
- Research article Arachnoid cyst rupture producing subdural hygroma and intracranial hypertension: case reports [10]
References
- Eide PK, Vatnehol SAS, Emblem KE, Ringstad G. Magnetic resonance imaging provides evidence of glymphatic drainage from human brain to cervical lymph nodes. . 2018. PMID 29740121 · DOI · PMC5940793
- Mauriac SA, Hien YE, Bird JE, Carvalho SD, Peyroutou R, Lee SC, et al.. Defective Gpsm2/Gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome. . 2017. PMID 28387217 · DOI · PMC5385604
- Ogura Y, Yabuki S, Iida A, Kou I, Nakajima M, Kano H, et al.. FOXC2 mutations in familial and sporadic spinal extradural arachnoid cyst. . 2013. PMID 24278289 · DOI · PMC3838418
- De Frias JM, Bhatti SFM, Nye G, Gonçalves R, Harcourt-Brown T, Fadda A, et al.. Spinal arachnoid diverticula in cats: Clinical presentation, diagnostic imaging findings, treatment, and outcome. . 2025. PMID 39739353 · DOI · PMC11683399
- Battal B, Kocaoglu M, Bulakbasi N, Husmen G, Tuba Sanal H, Tayfun C. Cerebrospinal fluid flow imaging by using phase-contrast MR technique. Br J Radiol. 2011. PMID 21586507 · DOI · PMC3473435
- Gosalakkal JA. Intracranial arachnoid cysts in children: a review of pathogenesis, clinical features, and management. Pediatr Neurol. 2002. PMID 11897472 · DOI
- Parsch CS, Krauss J, Hofmann E, Meixensberger J, Roosen K. Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature. Neurosurgery. 1997. PMID 9055286 · DOI
- Pradilla G, Jallo G. Arachnoid cysts: case series and review of the literature. Neurosurg Focus. 2007. PMID 17608350 · DOI
- Cincu R, Agrawal A, Eiras J. Intracranial arachnoid cysts: current concepts and treatment alternatives. Clin Neurol Neurosurg. 2007. PMID 17764831 · DOI
- Albuquerque FC, Giannotta SL. Arachnoid cyst rupture producing subdural hygroma and intracranial hypertension: case reports. Neurosurgery. 1997. PMID 9316060 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.