Arachnoid cyst

An arachnoid cyst is a noncancerous, fluid-filled sac that forms within the arachnoid membrane, one of the three protective layers surrounding the brain and spinal cord, and is filled with cerebrospinal fluid (CSF), the clear liquid that cushions these structures.^[1] These cysts arise from a splitting or duplication of the arachnoid membrane and represent the most common type of intracranial cyst, often located in the middle cranial fossa near the temporal lobe of the brain or along the spinal cord.^[2] They are typically congenital, present at birth due to developmental abnormalities during early pregnancy, though secondary cysts can develop later in life from trauma, infection, tumors, or surgical complications.^[3] Most arachnoid cysts are asymptomatic and discovered incidentally during imaging for unrelated issues, with many individuals never experiencing problems throughout their lives.^[1] When symptoms do occur, they depend on the cyst's size and location and may include headaches, seizures, nausea, vision or hearing disturbances, dizziness, or developmental delays in children; spinal cysts can cause back pain, leg weakness, or tingling.^[3] Diagnosis is confirmed through neuroimaging, primarily magnetic resonance imaging (MRI) for detailed visualization or computed tomography (CT) scans for initial detection, as the cysts appear as well-defined, CSF-filled structures without enhancement.^[2] Treatment is generally unnecessary for small, asymptomatic cysts, which are monitored with periodic imaging to check for growth.^[1] For symptomatic or enlarging cysts, surgical interventions such as cyst fenestration (creating an opening to drain fluid into the subarachnoid space), cystoperitoneal shunting, or complete excision via microsurgery or endoscopy are employed to alleviate pressure and symptoms, though recurrence is possible in some cases.^[3] Arachnoid cysts occur more frequently in males than females, with a ratio of approximately 4:1, and are associated with certain genetic syndromes like Aicardi syndrome, though the exact etiology remains incompletely understood.^[1]

Anatomy and Pathophysiology

Arachnoid membrane structure

The arachnoid mater, the middle layer of the three meninges enveloping the brain and spinal cord, is a thin, transparent, and avascular membrane that derives its name from its delicate, web-like (arachnoidal) appearance.^[4] It lies immediately deep to the dura mater, to which it is loosely adherent without direct attachment, separated by the potential subdural space, and bridges the cortical sulci without conforming to their contours.^[4] This avascular structure consists primarily of a superficial mesothelial layer of flattened arachnoidal cells joined by tight junctions, a central layer of loosely arranged cells, and a deep layer containing collagen fibers and fibroblasts, lacking a true epithelial lining.^[4][5] The arachnoid mater forms the outer boundary of the subarachnoid space, a CSF-filled compartment between the arachnoid and the innermost pia mater, which contains major cerebral blood vessels and delicate connective tissue trabeculae spanning the space like a supporting web.^[4] In normal CSF circulation, fluid produced by the choroid plexus in the ventricles flows through the ventricular system and exits via the foramina of Luschka and Magendie into the subarachnoid space, where it circulates over the brain and spinal cord surfaces before absorption.^[6] This pathway ensures nutrient delivery, waste removal, and intracranial pressure regulation.^[6] Arachnoid villi and granulations, specialized protrusions of the arachnoid mater, extend through the dura mater into the dural venous sinuses, particularly the superior sagittal sinus, serving as one-way valves for CSF reabsorption into the systemic venous circulation.^[6] These microscopic to macroscopic structures, lined by arachnoidal cells, facilitate bulk flow of CSF driven by pressure gradients, with granulations becoming more prominent in adults.^[6][5]

Cyst formation mechanisms

Arachnoid cysts primarily form through the abnormal duplication or splitting of the arachnoid membrane layers during embryogenesis, which creates a cleft that traps cerebrospinal fluid (CSF) within the intra-arachnoid space, leading to the development of a fluid-filled cavity.^[2][7] This splitting results in a non-communicating or partially communicating sac bounded by the arachnoid layers, distinguishing it from other cystic lesions.^[2] The expansion of these cysts is often attributed to the "ball-valve" mechanism, where a one-way valve-like defect in the cyst wall allows unidirectional CSF flow into the cyst during arterial pulsations but prevents outflow, causing progressive accumulation and enlargement.^[7][8] This theory explains the gradual pressure buildup, though it is not universally observed and may apply more to certain dynamic cases.^[2] The cysts contain clear, acellular fluid that is chemically identical to CSF, with matching electrolyte concentrations, protein levels, and low cellularity, confirming its origin from trapped subarachnoid fluid.^[7][3] Histologically, the cyst wall consists of flattened arachnoidal cells supported by a thin layer of collagen, lacking an epithelial lining or secretory epithelium.^[2][7] Arachnoid cysts exhibit significant size variability, ranging from a few millimeters to several centimeters, occasionally compressing adjacent neural structures.^[2] Most cysts demonstrate slow or no growth, with 80-90% remaining stable over time, while 10-20% may enlarge due to osmotic gradients across the cyst membrane or external factors such as trauma.^[7][8]

Causes and Risk Factors

Congenital origins

Arachnoid cysts of congenital origin represent the majority of cases and are present from birth due to disruptions in early brain development.^[2] These primary cysts develop during fetal embryogenesis, typically without identifiable postnatal triggers, distinguishing them from secondary forms.^[9] The primary developmental mechanism involves errors in the formation of the arachnoid membrane, such as incomplete fusion of its layers during early embryogenesis around weeks 7 to 8 of gestation.^[9] This process leads to localized separations or duplications in the meninges, creating fluid-filled spaces that persist and expand with cerebrospinal fluid accumulation.^[7] While the exact triggers remain under investigation, these anomalies are thought to stem from subtle irregularities in meningeal cell migration and differentiation.^[10] Congenital arachnoid cysts are rarely associated with broader genetic syndromes, including neurofibromatosis type 1 and Aicardi syndrome, where they may appear as part of multisystem involvement.^[11] Recent genetic research highlights potential links to mutations affecting cerebrospinal fluid (CSF) regulation and extracellular matrix integrity, as identified in studies from 2025 analyzing high brain-expressed genes intolerant to loss-of-function variants.^[9] These findings suggest that disruptions in CSF dynamics could contribute to cyst persistence in syndromic contexts.^[12] The majority of congenital cases are idiopathic, lacking a specific identifiable genetic marker, though familial clustering has been observed, often through multiplex families or twin studies indicating heritability.^[10] This underscores the primarily sporadic nature, with genetic factors playing a minor role in most patients.^[13] Detection of congenital arachnoid cysts frequently occurs incidentally during pediatric neuroimaging, such as MRI scans for unrelated concerns, with a prevalence ranging from 1.4% to 2.6% in children under age 10.^[7] These findings are often asymptomatic at discovery, highlighting the cysts' benign course in early life.^[14]

Acquired etiologies

Acquired arachnoid cysts, in contrast to their congenital counterparts, develop postnatally as a result of environmental or pathological events that disrupt the arachnoid membrane, leading to cerebrospinal fluid (CSF) accumulation through adhesions or entrapment. These secondary cysts represent a minority of all arachnoid cysts, with most literature indicating they are rare compared to congenital forms, though precise incidence rates are not well-established due to challenges in distinguishing etiologies in retrospective studies.^[15] They are triggered primarily by trauma, infection, inflammation, or iatrogenic interventions, accounting for an estimated small fraction of cases overall.^[9] Trauma is a key precipitant of acquired arachnoid cysts, often involving head injury that causes hemorrhage into the subarachnoid space or formation of adhesions, which trap CSF and promote cyst development. For instance, post-traumatic adhesions can alter CSF flow dynamics, leading to localized collections within the arachnoid layers. Such cysts have been documented following severe traumatic brain injury (TBI), though they remain uncommon complications even in this population, with case reports highlighting their occurrence after minor or moderate head trauma as well.^[16][3] Infectious processes, particularly meningitis, contribute to acquired cysts by inducing arachnoiditis, where inflammation results in fibrous adhesions that compartmentalize CSF. Bacterial or viral meningitis can scar the arachnoid membrane, creating loculated cysts; notable examples include post-tuberculous arachnoiditis leading to spinal cysts and viral infections precipitating intracranial collections. These inflammatory sequelae are well-recognized in the literature, with adhesions forming as a direct response to meningeal irritation.^[17][18][19] Iatrogenic factors also play a significant role, with cysts arising after neurosurgical procedures such as tumor resection or aneurysm clipping, where manipulation of the arachnoid leads to adhesions or CSF leakage into potential spaces. Hemorrhagic events like subarachnoid hemorrhage can similarly promote cyst formation through blood-induced inflammation and clotting within the subarachnoid space. Additionally, less invasive interventions, including lumbar punctures or spinal anesthesia, have been implicated in rare cases of intradural cyst development due to localized trauma or irritation.^[20][21][22] Individuals with subtle pre-existing arachnoid weaknesses, such as minor developmental variants, may be predisposed to acquired cyst formation following these triggering events, as underlying membrane vulnerabilities can exacerbate adhesion development or CSF entrapment. This interplay suggests that while acquired cysts are primarily event-driven, congenital factors may amplify risk in susceptible populations.^[23]

Clinical Presentation

General symptoms

Most arachnoid cysts are asymptomatic, with estimates indicating that 80% to 95% of cases are discovered incidentally during neuroimaging for unrelated reasons and do not cause any clinical manifestations throughout life.^[24][25][18] Symptomatic cysts, which represent a minority of cases, typically present with nonspecific symptoms related to mass effect, compression of adjacent brain structures, or alterations in cerebrospinal fluid (CSF) dynamics. Headaches are the most common symptom among those with symptomatic arachnoid cysts, occurring in approximately 40% to 60% of such patients, often described as positional, intermittent, or exacerbated by Valsalva maneuvers due to cyst-induced mass effect or transient increases in intracranial pressure (ICP).^[18][26] These headaches may mimic primary headache disorders but are frequently the initial complaint prompting diagnostic imaging. Seizures affect 10% to 30% of individuals with symptomatic arachnoid cysts, manifesting as focal or generalized events resulting from cortical irritation or irritation of surrounding neural tissue, particularly in supratentorial locations.^[9] Cognitive and neurological deficits are also reported, typically mild and including attention deficits, executive dysfunction, or developmental delays in pediatric patients, arising from subtle compression of eloquent brain areas.^[9][27] A smaller subset of cases, around 5% to 20%, involves hydrocephalus due to cyst obstruction of CSF pathways, leading to symptoms such as nausea, vomiting, and papilledema from elevated ICP.^[26][18] While symptom severity varies, location can influence the predominant presentation, though general symptoms like headaches and seizures remain common across sites.^[2]

Location-specific manifestations

Arachnoid cysts in the Sylvian fissure, accounting for approximately 50-60% of cases, most commonly exert mass effect on the temporal lobe, leading to symptoms such as seizures, developmental delays in children, and focal neurological deficits including hemiparesis or language impairments, particularly with left-sided cysts.^[9] Auditory disturbances may also arise from compression of adjacent structures.^[28] Cysts in the posterior fossa, comprising 10-20% of occurrences, often involve the cerebellum or brainstem, resulting in ataxia, nystagmus, balance disturbances, and vertigo.^[9] Sensorineural hearing loss, tinnitus, and imbalance are frequent otologic manifestations due to involvement of the cerebellopontine angle or nearby cranial nerves.^[29][30] Suprasellar or infratentorial cysts, representing 5-10% of cases, can compress the optic chiasm, hypothalamus, or pituitary gland, causing visual field defects such as bitemporal hemianopsia, diplopia from cranial nerve involvement, and endocrine dysfunction including growth hormone deficiency or precocious puberty.^[9] Obstructive hydrocephalus may exacerbate these effects through increased intracranial pressure.^[31] Spinal arachnoid cysts, which occur in 1-5% of instances and are predominantly thoracic, lead to radiculopathy, myelopathy, or chronic pain from spinal cord compression, often presenting with backache, leg weakness, gait disturbances, sensory deficits, and sphincter dysfunction.^[9][1][32] In rare locations such as the interhemispheric fissure, cysts may induce behavioral changes, memory deficits, or frontal lobe syndromes through mass effect on midline structures, potentially manifesting as cognitive impairments or psychiatric symptoms.^[33][34]

Diagnosis

Imaging modalities

Magnetic resonance imaging (MRI) serves as the gold standard for diagnosing arachnoid cysts due to its superior soft tissue contrast and ability to delineate cyst anatomy relative to surrounding structures. On MRI, arachnoid cysts appear as well-circumscribed, extra-axial lesions with signal intensity identical to cerebrospinal fluid (CSF) on all sequences, exhibiting hypointensity on T1-weighted images and hyperintensity on T2-weighted images.^[2][35] There is no contrast enhancement following gadolinium administration, confirming the absence of solid or vascular components, while fluid-attenuated inversion recovery (FLAIR) sequences suppress the cyst signal similarly to CSF, further verifying its benign, fluid-filled nature without proteinaceous or hemorrhagic content.^[9][35] Computed tomography (CT) is a valuable initial imaging modality, particularly when MRI is contraindicated or unavailable, revealing arachnoid cysts as hypodense lesions with attenuation values matching CSF (0-10 Hounsfield units) and smooth, non-enhancing margins.^[9][35] Unlike other cystic lesions, arachnoid cysts typically lack calcifications or hyperdense components, though larger cysts may demonstrate adjacent bony remodeling or erosion, which CT excels at assessing due to its bone window capabilities.^[2] Advanced MRI techniques provide additional diagnostic insights into cyst dynamics and differentiation from mimics. Cine phase-contrast MRI evaluates CSF flow, revealing potential communication with the subarachnoid space through signal voids or flow-related enhancements, aiding in understanding cyst pathophysiology.^[35][2] Diffusion-weighted imaging (DWI) is particularly useful for distinguishing arachnoid cysts from epidermoid cysts, as arachnoid cysts show no diffusion restriction and high apparent diffusion coefficient (ADC) values akin to CSF, whereas epidermoids exhibit restricted diffusion.^[35] Ultrasound is primarily limited to pediatric and fetal imaging for initial screening of intracranial arachnoid cysts, appearing as anechoic, well-defined cystic structures without internal echoes or Doppler flow, allowing non-invasive detection in infants with open fontanelles.^[36] Intraoperative confirmation, though rare, involves aspiration and analysis of cyst fluid, which typically matches CSF in composition—clear, acellular, with low protein and glucose levels consistent with normal CSF—distinguishing it from more viscous or xanthochromic fluids in other pathologies.^[37]

Classification systems

Arachnoid cysts are classified using several standardized systems that primarily consider anatomical location, size, and morphological features to aid in diagnosis and management decisions. The most widely adopted scheme for intracranial arachnoid cysts, particularly those in the middle cranial fossa or sylvian fissure, is the Galassi classification, proposed in 1982. This system categorizes cysts into three types based on size, degree of communication with the subarachnoid space, and mass effect on surrounding structures: Type I cysts are small and spindle-shaped, limited to the anterior middle cranial fossa, with free communication to the subarachnoid space and minimal mass effect; Type II cysts are larger and quadrangular, extending along the Sylvian fissure, with partial communication and moderate displacement of adjacent structures; Type III cysts are large and oval or round, filling the entire middle cranial fossa, with minimal communication but significant compression of brain tissue including potential midline shift.^[38][2] Location-based classification further divides arachnoid cysts into intracranial and spinal categories, with intracranial subtypes including supratentorial (e.g., temporal, frontal, or interhemispheric) and infratentorial (e.g., posterior fossa or cerebellopontine angle) variants, while spinal cysts are often intradural and localized to the thoracic or lumbar regions. For spinal arachnoid cysts, the Nabors classification is commonly used, dividing them into extradural (types I-III based on location relative to dura) and intradural types.^[39] This topographic approach helps correlate cyst position with potential clinical implications, such as hydrocephalus in posterior fossa cases. Size and shape are quantified through imaging-derived metrics, where cyst volume is calculated using formulas like the ellipsoid method (length × width × height × 0.52) from MRI or CT scans; larger cysts (e.g., volumes greater than approximately 40-50 mL) are more frequently associated with symptoms due to mass effect.^[40] Shape descriptors distinguish between smooth, oval configurations typical of benign cysts and irregular or septated forms that may suggest complications. Classification also involves differential diagnosis to exclude mimics, achieved by confirming the cyst's benign nature through lack of contrast enhancement, absence of solid components, and CSF-like signal intensity on imaging, thereby ruling out neoplasms, porencephaly, or enlarged Virchow-Robin spaces. Challenges in classification include the poor correlation between cyst size or type and symptomatic presentation, as many large cysts remain asymptomatic incidentally, complicating prognostic assessments.

Management and Treatment

Conservative management

Conservative management of arachnoid cysts primarily involves watchful waiting for asymptomatic or low-risk cases, where intervention is unnecessary unless progression occurs. Observation is recommended for asymptomatic cysts, particularly those demonstrating stability on serial imaging studies. Longitudinal studies indicate that approximately 80-90% of such cysts remain unchanged over time, with growth or symptomatic enlargement occurring in only a small minority.^[9][41] Follow-up protocols typically include initial magnetic resonance imaging (MRI) at 6-12 months after diagnosis to assess for any changes in size or characteristics, followed by annual imaging if stability is confirmed. Clinical evaluations are conducted concurrently to monitor for the emergence of new symptoms such as headaches, seizures, or neurological deficits, prompting reevaluation if concerns arise.^[42][43] For mild symptoms attributable to the cyst without evidence of mass effect or progression, non-invasive palliation focuses on symptom control rather than cyst-directed therapy. Analgesics, such as nonsteroidal anti-inflammatory drugs, are used to manage headaches, while antiepileptic medications are prescribed for seizure control in cases where electroencephalography confirms epileptiform activity linked to the cyst. These approaches aim to alleviate discomfort without surgical risks.^[44][2] Lifestyle modifications play a key role in minimizing potential complications, especially for cysts in locations vulnerable to trauma. Patients are advised to avoid high-impact or contact sports, such as football or boxing, to reduce the risk of cyst rupture or hemorrhage following head injury. Low-risk activities like swimming or cycling are generally permissible, with individualized guidance from neurosurgeons based on cyst location and patient age.^[45][46]

Surgical interventions

Surgical interventions are indicated for arachnoid cysts that cause symptomatic compression of surrounding neural structures, such as headaches, seizures, or focal neurological deficits.^[47] Growth documented on serial imaging, particularly when associated with increasing mass effect, also warrants consideration for surgery to prevent progression of symptoms.^[18] Additionally, cysts leading to hydrocephalus through obstruction of cerebrospinal fluid (CSF) pathways require operative management to alleviate intracranial pressure.^[48] Endoscopic fenestration represents a minimally invasive technique that involves creating a communication between the cyst and the subarachnoid space to facilitate CSF drainage and cyst decompression. This approach is particularly effective for middle cranial fossa or sylvian fissure cysts, with clinical success rates ranging from 76% to 83% in resolving symptoms like headache and neurological impairment.^[49][50] The procedure utilizes a neuroendoscope inserted through a small burr hole, allowing visualization and precise fenestration of the cyst wall while minimizing brain retraction.^[47] Microsurgical cystocisternostomy employs an open craniotomy to access the cyst, followed by excision or fenestration of the cyst wall to establish a wide connection with adjacent cisterns, promoting long-term drainage. This method is favored for complex or posteriorly located cysts, such as those in the posterior fossa, where endoscopic access may be limited due to anatomical constraints.^[51][52] It offers durable outcomes in challenging cases but involves greater tissue disruption compared to endoscopic options.^[53] Cystoperitoneal shunting diverts cyst fluid to the peritoneal cavity via a catheter and valve system, serving as an alternative for multiloculated cysts or those that recur after fenestration. This technique is reserved for cases where direct communication with CSF spaces is not feasible, though it carries a complication rate of approximately 20-30%, including infections, obstructions, and the need for revisions.^[54][55] Particularly in children, there is limited high-level evidence (primarily case series and retrospective studies) guiding valve pressure selection for cystoperitoneal shunts in arachnoid cysts. Programmable or adjustable valves are commonly recommended and used to enable non-invasive postoperative adjustments, as optimal pressure is difficult to predict and risks overdrainage (e.g., subdural collections, headaches) or underdrainage exist. Low-pressure valves have been reported as effective in only a minority of cases (e.g., 13% in one series), often requiring switch to medium or higher pressures. In overdrainage cases, increasing pressure (e.g., to 90 mm H₂O) has resolved symptoms. Gradual pressure increases are used after cyst resolution to assess for shunt removal. No standardized initial pressure exists; selection is individualized based on clinical and radiological response.^[56][57][58] Emerging techniques include robotic-assisted fenestration, which enhances precision in cyst navigation and reduces operative risks through stereotactic guidance, showing promise in optimizing outcomes for pediatric and adult patients.^[9] Laser-assisted endoscopic fenestration, utilizing tools like the GOLD laser for controlled tissue ablation, is under evaluation in recent trials for suprasellar and intraventricular cysts, aiming to improve safety in delicate regions.^[59] For recurrent cysts, reoperation rates range from 10% to 30%, often involving repeat fenestration or shunting to address incomplete decompression.^[60]

Prognosis and Complications

Long-term outcomes

Arachnoid cysts generally carry a favorable long-term prognosis, particularly following surgical intervention for symptomatic cases. Studies indicate that 73-82% of patients experience significant symptom resolution or improvement after decompression procedures, such as fenestration or shunting, with many achieving complete relief from headaches, neurological deficits, or hydrocephalus.^[9] For untreated asymptomatic cysts, progression is rare, as most remain stable over time, with only 10-20% showing enlargement that could lead to complications.^[9] In pediatric patients, early intervention yields high recovery rates, with over 90% demonstrating sustained clinical improvement and stable cognitive function when treated promptly. Microneurosurgical fenestration has been shown to enhance general intelligence, verbal abilities, and processing speed, with these gains persisting without significant decline over five-year follow-ups.^[61] Addressing cysts before age 5 minimizes potential cognitive impacts, as younger children exhibit minimal long-term deficits when managed proactively.^[62] Recurrence rates for arachnoid cysts post-surgery range from 10-30%, influenced by the technique employed; microsurgical fenestration typically results in lower recurrence compared to shunting, though endoscopic approaches may carry a slightly higher risk.^[9] Long-term monitoring with annual MRI is recommended to detect any reaccumulation early, ensuring timely re-intervention if needed.^[9] Most patients regain normal activities and report enhanced quality of life following treatment, with 66-83% noting better overall function and reduced symptoms at extended follow-ups averaging 8 years. Persistent deficits occur in only 5-10% of cases, often limited to challenges like epilepsy management, but severe impairments are uncommon.^[63] Recent 2025 analyses of longitudinal data confirm high stability, with 80-90% of cysts showing no progression over 10 years under proper follow-up protocols, though gaps persist in understanding lifelong cognitive impacts on asymptomatic individuals.^[9]

Associated risks

Arachnoid cysts carry a low but notable overall risk of rupture, with an annual incidence estimated at less than 0.04% and overall rates reported between 2.3% and 4.6% depending on cyst size and location, with post-traumatic rupture often leading to subdural hematoma formation, particularly in middle cranial fossa cysts following minor head injury.^[64][65] Hemorrhage within the cyst is rare, occurring in less than 1% of cases, and is typically associated with trauma or spontaneous events that can exacerbate mass effect on surrounding brain tissue.^[2] Surgical management of arachnoid cysts introduces specific complications, including postoperative complications in approximately 5% of cases, often linked to fenestration procedures.^[54] Cerebrospinal fluid (CSF) leaks occur in 3% to 10% of interventions, potentially requiring additional repair and increasing infection risk if persistent.^[66] In patients treated with cystoperitoneal shunting, malfunction rates are high, often requiring revisions due to obstruction or overdrainage, with event rates up to 60% reported in some series.^[54] Neurological risks from arachnoid cysts include hydrocephalus, which develops in over 30% of cases due to CSF flow obstruction, particularly in symptomatic patients with enlarging cysts.^[18] Chronic seizures are associated with 10% to 30% of arachnoid cysts, particularly those in the temporal or sylvian regions, where mass effect may contribute to epileptogenesis.^[7] Suprasellar arachnoid cysts pose additional risks of endocrine dysfunction, such as growth hormone deficiency or precocious puberty, due to compression of the hypothalamic-pituitary axis.^[67] Long-term risks in untreated large arachnoid cysts include cognitive decline in about 5% of cases, manifesting as impairments in memory, executive function, and visuospatial abilities from chronic compression.^[68] Cyst growth may accelerate during adolescence, potentially linked to hormonal changes, leading to increased mass effect or new symptoms in previously stable cases.^[69] Recent reviews highlight gaps in understanding the lifelong cognitive impact of arachnoid cysts, with limited longitudinal data on subtle neurodevelopmental effects in asymptomatic or mildly affected individuals.^[70]

Epidemiology

Prevalence and incidence

Arachnoid cysts are relatively common benign intracranial lesions, with an overall prevalence estimated at 1-2% in the general population based on autopsy and magnetic resonance imaging (MRI) studies.^[9] In adult populations specifically, incidental MRI findings report a prevalence ranging from 0.3% to 3.1%.^[71] These rates reflect primarily congenital origins, as arachnoid cysts are developmental anomalies rather than frequently acquired postnatally.^[2] The incidence of new arachnoid cyst diagnoses in postnatal life is rare, accounting for approximately 1% of all intracranial lesions in newborns and even fewer cases annually thereafter, with most emerging as incidental discoveries rather than symptomatic presentations.^[72] Detection of these cysts has increased due to the expanded use of advanced neuroimaging, such as high-resolution MRI, leading to more frequent incidental identifications in both clinical and research settings since the early 2010s.^[73] In terms of anatomical distribution, arachnoid cysts most commonly occur in the Sylvian fissure, comprising 50-60% of cases, followed by the posterior fossa at 10-20%, and spinal locations representing 1-5% of all instances.^[9] Prevalence appears higher in pediatric populations, ranging from 1.4% to 2.6% in children under 10 years, compared to 0.2-1.7% in adults, where cysts are often stable and less likely to be newly detected unless associated with trauma or other factors.^[9][23]

Demographic patterns

Arachnoid cysts demonstrate a marked male predominance, with reported male-to-female ratios ranging from 2:1 to 4:1 across multiple studies.^[9] This disparity is particularly evident in cases involving the middle cranial fossa, where unilateral cysts occur more frequently in males.^[74] Detection of arachnoid cysts peaks during the first decade of life, with approximately 60% to 80% of cases identified in pediatric populations.^[75] While most cysts are congenital and present early, de novo development in the elderly is rare, though incidental findings increase with age-related neuroimaging.^[9] No strong geographic or ethnic variations in arachnoid cyst occurrence have been consistently reported, though prevalence estimates are higher in developed countries owing to routine use of MRI and CT imaging.^[76] Arachnoid cysts appear more frequently in cohorts with neurodevelopmental disorders, potentially linked to shared genetic factors affecting brain development.^[77] Familial cases constitute less than 5% of all instances, often suggesting polygenic or syndromic traits involving extracellular matrix genes.^[10] Recent 2025 analyses reaffirm the overall prevalence patterns but highlight increased incidental detection in aging populations through expanded neuroimaging, without altering the fundamental sex or age distributions.^[9]