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Arachnoid cyst …
- Updated 02.10.2025
- Released 09.13.1995
- Expires For CME 02.10.2028
Arachnoid cyst
Introduction
Overview
Arachnoid cysts are sacs filled with cerebrospinal fluid that develop between the brain or spinal cord and the surrounding arachnoid membrane. They are the most common type of brain cysts and are common incidental findings on MRI. Primary arachnoid cysts are present at birth due to developmental abnormalities, whereas secondary cysts can develop after trauma, surgery, meningitis, and tumor progression. Most cysts are solitary, and multiple cysts may indicate evaluations for glutaric aciduria type 1, which is present in 25% of bitemporal cases.
Cysts may be asymptomatic and not require treatment; however, large cysts can cause symptoms via mass effect. Symptomatic arachnoid cysts may present with headache, nausea, seizures, sensory or motor deficiencies, and other neurologic symptoms based on location. Treatment options for symptomatic cysts are drainage, excisions, or fenestration. Asymptomatic arachnoid cysts can be monitored without surgical or medical intervention.
Key points
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• Be certain that the cyst is responsible for symptoms before considering intervention. Over 70% of pediatric and 90% of adult cases have no attributable symptoms. | |
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• Arachnoid cysts in children are more likely to present with hydrocephalus. Cyst resolution or shrinkage is more common than growth after the first year of life. | |
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• For suprasellar arachnoid cysts, endocrinopathies, such as precocious puberty and growth hormone deficiency, are common manifestations in children. | |
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• There may be a rupture of bridging veins or vessels in the cyst’s wall, which can result in a subdural hematoma or bleeding into the cyst. | |
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• Endoscopic procedures for temporobasal arachnoid cysts have the highest failure rate (81%), highest recurrence (19%), and highest complication rate (24%). | |
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• Cysts larger than 5 cm have a higher risk of rupture; however, a systematic review of published literature did not find evidence to support recommending against participation in sports for patients with arachnoid cysts. | |
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• Secondary arachnoid cysts are more likely to result in recurrence. |
Historical note and terminology
Cysts along the neuraxis have been discovered on autopsies for centuries (12; 42); however, the first description of an arachnoid cyst was in 1831 (12). Since this time, arachnoid cysts have been referred to as "meningitis serosa circumscripta," “chronic cystic arachnoiditis," "cerebral pseudotumor," or "leptomeningeal cyst” (71).
Historically, it was debated whether arachnoid cysts developed from agenesis of the underlying brain tissue (67) or from primary malformations of the arachnoid layer (71). This was settled, in favor of the latter, when radiological images demonstrated incidental arachnoid cysts without cortical hypoplasia (59; 26).
The first surgical treatment of an arachnoid cyst was completed in 1907 and resulted in clinical improvement. However, resection of the cyst wall was often complicated by recurrence or damage to nearby cortical structures (50). In the 1980s, shunting became a primary treatment for arachnoid cysts (72). By 2005, endoscopic cyst fenestration became a popular technique for treating arachnoid cysts in the middle cranial fossa, septal region, or suprasellar region (27; 15).
Arachnoid cysts are commonly differentiated by primary or secondary development, embryologic origin, location, and communication with the cerebrospinal fluid. Primary arachnoid cysts are congenital cysts present at birth (43). Arachnoid cysts can also develop following surgery, traumatic brain injury, or subarachnoid hemorrhage (58; 75).
Table 1. Classification of Intracranial Arachnoid Cysts
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Classification |
Types |
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Location | |
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Supratentorial |
• Sylvian |
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Infratentorial |
• Cerebellopontine angle |
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Supratentorial or infratentorial |
• Quadrigeminal |
|
Galassi classification | |
|
Type I cysts |
• Small |
|
Type II cysts |
• Located superiorly along the Sylvian fissure |
|
Type III cysts |
• Large |
|
| |
Clinical manifestations
Presentation and course
Arachnoid cysts can cause nonspecific clinical manifestations that are based largely on the location, the size of the cyst, and the age of the patient. The majority of arachnoid cysts are intracranial and are often found in the middle cranial fossa (34%), retrocerebellar region (33%), and cerebral convexity (14%) (03). Most arachnoid cysts are asymptomatic; however, midline cysts may present earlier in life due to hydrocephalus (04).
Spinal arachnoid cysts are rare and also present with nonspecific symptoms that depend on the location and size of the cyst. The most common symptom is progressive paraparesis, but they may also present with back pain or sensory changes (45). Spinal arachnoid cysts can develop in the cervical (11.5%), thoracic (80%), or lumbar (8.5%) regions (37).
Table 2. Summary of Intracranial Arachnoid Cyst Detection and Treatment
|
Fetal |
Children |
Adults | |||
|
Incidental |
Incidental (72%) |
Symptomatic (28%) |
Incidental (92%) |
Symptomatic (8%) | |
|
Age |
N/A |
7.5 years |
6 years |
54 years |
51 years |
|
Sex |
54.5% male |
80% male |
63% male |
56% male |
39% male |
|
Symptoms or imaging indications |
N/A |
Headaches (26%) |
Headaches (44%) |
Headaches (25%) |
Headaches (61%) |
|
Hydrocephalus |
47%* |
2.5% |
44% |
0.5% |
14% |
|
Incidence |
0.2-1.1 |
2.6% |
1.4% | ||
|
Location |
suprasellar (n = 44) |
Middle fossa 47% |
Middle fossa 36% |
Middle fossa 44% |
Middle fossa 29% |
|
(60; 29; 09; 28; 38; 30) | |||||
Prognosis and complications
There is significant variation in the prognosis of arachnoid cyst between fetuses, children (0–17 years old), and adults (18+). There is no known reason for the variation, though it is likely due to a complex interplay between genetics, brain growth, cyst location, and comorbidities.
Research on fetal arachnoid cysts is limited, though in general, isolated fetal arachnoid cysts are associated with favorable neurodevelopmental outcomes (30). Studies have shown that the majority (75%) of identified cysts do not change in size during pregnancy after identification, whereas 20% increase in size and 5% regress (61; 80). Of the cases that increase in size, the majority are skull base cysts. Prognostically, fetal mortality is 2.6%, but nearly every one of these cases is associated with comorbid malformations or genetic conditions (07; 13; 09). One study looking at 4-year outcomes in 45 patients showed normal behavior, intelligence, and neurodevelopment in 91% of cases (09). Common postpartum complications of symptomatic cases include seizures (5%), and neurodevelopmental limitations include developmental delay, abnormal weight gain, autism, visual impairment, and growth hormone deficiency. Additionally, although 87% of cases require surgical intervention after birth, surgical intervention has not been shown to be associated with overall prognosis.
Similarly, pediatric cysts are generally associated with favorable clinical outcomes. Previous studies have shown that the majority of expanding cyst cases occur in the first year of life (82%); this decreases to 10% and a higher likelihood of cyst stability or regression when analyzing all children (04; 47). In fact, age is the only significant predictor of cyst enlargement. The majority of identified cases (86%) are asymptomatic, whereas symptomatic patients generally present with headache, seizure, developmental delay, macrocephaly, or head deformity (47). One study also reports a high prevalence of comorbid mild intellectual disability and psychiatric disorders in these patients (21). Symptomatic cysts, enlarging cysts, and worsening of serial neuropsychological tests in middle fossa cysts are all indications for surgery, which is the case for 35% of pediatric cysts (47).
Like older children, asymptomatic cysts identified in adults are unlikely to enlarge or become symptomatic notwithstanding a secondary event like trauma or surgery. As estimated by longitudinal studies lasting up to 4 years, cyst stability is observed in 95% to 97% of cases, enlargement is seen in 2.3% of cases, and regression in 1% to 5% (03; 29). These same studies reveal that 5% of cases are symptomatic, and less than 1% of patients develop new or worsening symptoms. The most common symptoms include headache (60.7%), cranial nerve dysfunction (39.3%), and nausea or vomiting (25%). More urgent risks include subdural hematomas (4.6%) and bleeding from cyst rupture, which can occur even in previously asymptomatic cysts (68; 69; 76). Risks for cyst rupture or hemorrhage include trauma and size greater than 5 cm (16). Like the pediatric group, symptomatic cysts often indicate a need for surgical intervention (89.3%), compared to the 6.8% of all adult cyst patients who require surgery (29). Overall, with the surgical intervention options available for indicated cases, there are very few documented cases of isolated cyst-related mortality (64).
Clinical vignette
Vignette 1: Intracranial. A 26-year-old male presented to the emergency department with a 2-month history of recurrent neck pain that intermittently radiated to the head. In addition, he was experiencing nausea and a sense of tingling in his left foot prior to presentation. He denied any traumatic injury before the onset of this pain; however, he reported multiple concussions during high school due to playing football. A presentation, he had no focal neurologic deficits.
Investigations. A head CT without contrast was originally ordered and showed a 4x4 cm cystic mass in the posterior fossa. A follow-up MRA, MRV, cerebral angiogram, and MRI with and without contrast were completed to rule out arterial vascular malformation, venous sinus thrombosis, and hemangioblastoma. At this point, a diagnosis of an intracranial arachnoid cyst was made.
Outcome. The patient was discharged with close follow-up to monitor the intracranial arachnoid cyst with possible surgical resection. Approximately 1 month after discharge, he presented to the emergency department with worsening refractory headaches, vomiting, and disorientation. A new CT and MRI demonstrated partial effacement of the further ventricle, cerebellar tonsil herniation, and enlargement of the temporal horns, suggesting hydrocephalus. An emergent suboccipital craniectomy with cyst fenestration was completed. Postoperatively, the symptoms resolved.
Vignette 2: Spinal. A 17-year-old female presented with worsening lower back pain for the past year that intermittently radiated to her legs bilaterally. She also experienced intermittent bowel and bladder incontinence but denied saddle anesthesia. Pain was aggravated by ambulation, coughing, or sneezing. It improved when the patient was laying down.
Investigations. A lumbar MRI with and without contrast was completed, which demonstrated a large epidural CSF cyst in the lumbosacral region causing distortion of the transversing sacral nerve roots.
Outcome. The patient underwent a surgical exploration with cyst repair. Postoperatively, the patient’s pain improved.
Biological basis
Etiology and pathogenesis
The basis of primary arachnoid cyst development and growth is not completely understood. However, one widely accepted theory is that they are caused by a developmental defect in the arachnoid layer leading to membrane duplication (23). This is supported by the similar incidence of fetal cysts and nonfetal cysts. However, in the case of fetal cysts, 75% do not expand throughout the fetal period and commonly only expand after birth (30). Cyst location is also associated with growth, as interhemispheric fissure and skull base cysts are more likely to progress after birth than other locations (61).
Light and electron microscopic studies of cyst microstructure reveal variations in cyst wall structure, with some displaying normal arachnoid cell structure, others displaying fibrous tissue without elongated epithelial involvement, and some revealing nonarachnoid luminal epithelium suggestive of congenital teratoma formation (52; 65). Inner sheath structure includes layers of arachnoid cells with flattened cytoplasm, as well as plentiful desmosomes and tight junctions filled with collagen fibers and microfibrils.
The exact cause of CSF buildup is unknown, though it is postulated to be due to (1) anatomical shunting of CSF from the arachnoid space into the cyst, (2) an osmotic gradient between intra- and extra-cystic fluid, (3) arachnoid membrane malformation or cerebral agenesis, or (4) CSF secretion from cells composing the cyst wall (65).
Secondary cysts can form from several sources, including trauma (08), surgery or epidural anesthesia (34; 55), infections like meningitis, excess loss of CSF from a ventriculoperitoneal shunt (53), hemorrhage, oil-based contrast media (70), and tumor progression (08). It is believed that these factors can produce adhesions in the arachnoid membrane, which form into cysts when filled with CSF. Note that trauma may elicit symptoms due to cyst rupture rather than contributing to cyst growth. Similarly, excessive CSF loss can lead to decreased protection and, thus, decompression of the spinal cord when a cyst is present.
Symptoms of arachnoid cysts, including headache, nausea, sensory or motor deficiencies, and other neurologic symptoms, are dependent on mass effect, though the cause of epileptogenesis is debated (06). Cyst resection has been shown to resolve seizures in some cases, though the reason for inconsistent colocalization of epileptic foci with arachnoid cyst location and seizure improvement post-cyst treatment is unknown.
Epidemiology
Arachnoid cysts can be found in fetal, pediatric, adult, and elderly populations, though the majority are found in children (77). There is an estimated prevalence of 2.6% in the pediatric population (04) and 1.4% in adults (03), whereas fetal incidence estimations are between 0.2% and 1.1% (78; 28). Males are nearly twice as likely to be diagnosed compared to females in both pediatric and adult populations – possibly due to the increased incidence of males presenting with head trauma – though there is no difference in the elderly population. Arachnoid cysts are most often intracranial and most often located in the middle cranial fossa. Among spinal cases, most are located in the mid- to lower thoracic area (45).
A few genetic conditions are associated with arachnoid cysts. A greater incidence of intracranial cysts has been reported in patients with Down syndrome, mucopolysaccharidosis, schizencephaly, neurofibromatosis, autosomal dominant polycystic kidney disease, acrocallosal syndrome, Aicardi syndrome, and tuberous sclerosis (11; 02). Nontraumatic spinal, extradural meningeal cysts are often congenital and have associations with FOXC2 mutations and lymphedema-distichiasis syndrome (45). Similarly, intraspinal cases are associated with neural tube defects. Additionally, one study reports that gamma knife radiosurgery may elicit extratumoral cyst formation due to the osmotic gradient caused by tumor degeneration following radiosurgery (53).
Prevention
There remains no known prophylactic measure for primary or secondary arachnoid cysts.
Differential diagnosis
Confusing conditions
Intracranial. The differential diagnosis for intracranial arachnoid cysts includes conditions that elicit sensorimotor decline, increased intracranial pressure, headaches, or cranial nerve palsy. The most acutely dangerous of the differentials include epidural or subdural hematomas, acute obstructive hydrocephalus, bacterial meningitis, and intracerebral hemorrhage, all of which require ruling out if suspected. Other conditions to consider include tumors like glioma or meningioma, other cystic lesions, brain abscesses, expanded Virchow-Robin spaces, and infections like neurocysticercosis. With radiographic analysis, differentials should include other causes of hypoechoic lesions, including porencephalic cysts, glioependymal cysts, cystic neoplasms, schizencephaly, and intracranial hemorrhage, or aneurysms of the vein of Galen in neonates (62).
Spine. Differentials for spinal arachnoid cysts include other causes of spinal cord compression, which often manifest clinically as back pain, muscle weakness, or urinary incontinence. Similar to intracranial arachnoid cysts, options include hematoma, tumors like ependymomas or hemangioblastomas, other spinal cysts (epidermoid, dermoid, endodermal, hydatid), neural tube defects like meningocele, and infection.
Associated or underlying disorders
Children undergoing evaluation for epilepsy are commonly diagnosed with intracranial arachnoid cysts. However, there is no current evidence suggesting a causal relationship between arachnoid cysts and epilepsy (57).
Bilateral temporal arachnoid cysts are a presentation of glutaric aciduria type 1 (77). However, spinal extradural arachnoid cysts can be associated with lymphedema-distichiasis syndrome and FOXC2 mutations.
Diagnostic workup
Most cases of incidental arachnoid cysts are diagnosed on exploratory imaging for vague symptoms, including headache (25.4%), suspected stroke (12%), seizures (9.6%), and ear, nose, and throat symptoms (8.9%). Intracranial and spinal arachnoid cyst diagnosis is most often identified by CT or MRI imaging (29).
The gold standard technique is T1- and T2-weighted flair MRI combined with diffusion-weighted MRI (31). On MRI, arachnoid cysts are nonenhancing, well-demarcated, simple, and homogeneous. Alternative patterns indicate a possible different diagnosis. The cysts also have a similar enhancement to CSF on imaging. The level of communication between the arachnoid cysts and the subarachnoid space can be assessed by Cine-balanced steady-state free precession MRI (48). Spinal arachnoid cysts are identified via MRI (66). In addition, intrathecal gadolinium-enhanced MR can assist in differentiating between surgical and nonsurgical patients (73). In addition to CT or MRI, PET scans can indicate increased metabolism or blood flow to the area of the cyst (32).
There are certain imaging signs that are associated with the size or location of arachnoid cysts. The “Mickey Mouse” sign appears in suprasellar cysts that develop near the frontal horns of the lateral ventricles (74). Middle cranial fossa cysts are categorized based on size (22). Type 3 cysts occupy the temporal fossa, leading to severe compression of the frontal and parietal lobes.
Evaluation of specific labs is essential to understand the mass effects of the disease and possible associated diagnoses. Growth hormone and thyrotropin should be measured in suprasellar cysts due to the risk of disrupting the hypothalamic-pituitary axis (01). Urine labs can detect glutaric acid to diagnose glutaric aciduria type 1, which presents with bilateral temporal arachnoid cysts in 25% of cases (49). Neurophysiological testing is able to detect cognitive deficiencies that can present with arachnoid cysts (49; 81).
Management
In asymptomatic patients with an incidental finding of an arachnoid cyst, the management is predominately nonsurgical (35). Medical management of arachnoid cysts involves intracranial pressure monitoring and trialing acetazolamide to predict response to surgery (19; 39). Although cognitive ability may be impacted by an arachnoid cyst, this is not commonly an indication for surgery (40; 35). Signs that may warrant surgical treatment for an arachnoid cyst include papilledema, growth of the cyst on radiologic imaging, or focal neurologic deficits (56).
Patients with arachnoid cysts are at risk for increased intracranial pressure due to obstruction of the CSF, leading to hydrocephalus, or due to a leaking cyst (18). Increased intracranial pressure may also develop postoperatively for arachnoid cyst treatment, indicating a need for continued monitoring (36). Papilledema is a potential indication for surgical treatment of arachnoid cysts due to increased intracranial pressure (18).
A review and analysis comparing outcomes of the different surgical interventions for arachnoid cysts (excision, fenestration, or shunting) demonstrated similar success rates. However, individual differences may have led to certain approaches over others. Personalized treatment plans for each patient are a requirement for surgical management of these cysts (05).
Surgical excision. Spinal arachnoid cysts that require surgical management are commonly treated by total resection of the cyst and closure of the dural defect (44; 24). Surgical excision of spinal arachnoid cysts often results in improvement of symptoms, predominantly back pain (17). Excision may be a more complicated surgery if the cyst is closely adhered to nearby structures, and fenestration may be a better option in such cases (10).
Venticulo-cysto-peritoneal shunt. Shunting of arachnoid cysts is another common surgical intervention. One of the significant downsides of shunting an arachnoid cyst is shunt dependency and increased risk for complications from a craniotomy (54). However, this strategy may be beneficial in elderly patients and in large cysts (25; 51).
Cyst fenestration. Cyst fenestration has become the preferred method of surgical treatment for arachnoid cysts (63). This procedure involves creating an entrance and exit site around the thickened arachnoid region (33). This procedure is completed through a burr hole and allows patients to avoid a dependency on a shunt. However, there are still possible complications of intracranial hemorrhage or hydrocephalus (20).
Special considerations
Fetal
In cases of fetal arachnoid cysts, serial ultrasonography should be used to monitor for cyst growth and ventriculomegaly, followed by MRI to detect associated anomalies (30). If severe hydrocephalus is observed, preterm delivery is recommended. After birth, ultrasonography or MRI should be used to confirm cyst presence, followed by surgical resection, if indicated.
Pediatric
There remain no contradictions against pediatric patients with arachnoid cysts from participating in sports. Multiple studies have demonstrated that there is a low risk of concussion and cyst rupture in those participating in contact or noncontact sports, and there is no evidence recommending against participation in sports (82; 46). However, one study recommends testing for intellectual disability and psychiatric disorder in pediatric patients due to a high prevalence of comorbid mild intellectual disability and psychiatric disorders (21).
Elderly
There remains no evidence that elderly age affects arachnoid cyst development, diagnostic recommendations, or treatment recommendations (79). Some studies report a decline in symptomatic arachnoid cysts with increasing age, though this observation may be due to this population’s limited size (79).
Non-neurosurgical considerations
For unrelated procedures, neurologic clearance is not required for patients with an arachnoid cyst. There are no additional anesthetic considerations or changes when a patient has an arachnoid cyst.
Pregnancy
There remains no evidence that pregnancy affects arachnoid cyst development. In addition, it is generally deemed safe for pregnant patients with an isolated arachnoid cyst to undergo labor (14). However, intracranial pressure should be confirmed prior to an epidural because neuraxial techniques are not advised in patients with elevated intracranial pressure.
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Authors
-
Alexa Lauinger
Ms. Lauinger of Carle Illinois College of Medicine has no relevant financial relationships to disclose.
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Logan Burrington
Dr. Burrington of Carle Illinois College of Medicine has no relevant financial relationships to disclose.
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Anvita Mishra MD
Dr. Mishra of Carle Illinois College of Medicine has no relevant financial relationships to disclose.
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Wael Mostafa MD PhD FAANS
Dr. Mostafa of Carle Foundation Hospital has no relevant financial relationships to disclose.
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Editor
-
Rimas V Lukas MD
Dr. Lukas of Northwestern University Feinberg School of Medicine received honorariums from Jazz Therapeutics, Novocure, and Servier for speaking engagements, honorariums from Cardinal Health, Catalyx, Merck, and Novocure for advisory board membership, research support from BMS as principal investigator, and an honorarium from GT Medical Technologies for DSMB membership.
See Profile
Former Authors
- Robert Grant MD
- Jacob Young MD
- Nicholas Butowski MD
- Sushant Puri MBBS
- David Olayinka Kamson MD PhD
Patient Profile
- Age range of presentation
-
- 0 month to 65+ years
- Sex preponderance
-
- male>female, >2-4:1
- Heredity
-
- heredity may be a factor
- Population groups selectively affected
-
- none
- Occupation groups selectively affected
-
- none
ICD & OMIM codes
- ICD-10
-
- Cerebral cysts: G93.0
- Arachnoid cyst of spine: G96.19
- ICD-11
-
- Intracranial arachnoid cyst: 8D67
- OMIM
-
- Intracranial arachnoid cysts: 207790
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