An arachnoid cyst can develop when cerebrospinal fluid (CSF) collects between layers of the arachnoid matter of the meninges. Most of these cysts are said to be primary and arise from abnormal development of the brain meninges in utero. However, some cysts are acquired and result from loculation of CSF within layers of arachnoid mater because of inflammatory adhesions.
Some cysts enlarge gradually over time; Dyck and Gruskin1
suggested that this enlargement might result from progressive secretion of CSF into the cysts by the lining cells, osmotic passage of CSF into the cyst, or entrapment of the CSF within the cyst by a ball-valve mechanism.
According to Pascual-Castroviejo et al
42% of arachnoid cysts are found in the supratentorial fossa; of these, 5% are located on the convexity of the brain (as in our patient). The cyst content never communicates with the lateral ventricles but may or may not communicate with the subarachnoid space. Meizner et al3
found that eight of their 32 cases of primary arachnoid cysts had additional central nervous system or other body anomalies, the commonest being cranial asymmetry.
Arachnoid cysts comprise approximately 1% of all intracranial space-occupying lesions. The widespread use of brain imaging has disclosed the presence of asymptomatic cysts. Most of these asymptomatic cysts were found in adults; in contrast, around 75% of cysts found in the paediatric age group were symptomatic. Persistent headache, epilepsy, focal deficits and cognitive impairment are the usual manifestations in symptomatic patients with supratentorial arachnoid cysts. However, in their study, Spansdahl and Solheim4
found that there was great variation in the presenting symptoms, apparently without any relation to cyst localisation. They also concluded that individuals with arachnoid cysts had low employment status, decreased quality of life scores and prevalent symptoms of anxiety. Therefore, such cysts might not be entirely asymptomatic.
Although our patient admitted to having had pancephalic headache occasionally over the past few years, she first noticed body aches and stiffness 1 year ago; this complaint was investigated three times with thyroid function tests (the patient came from an area with endemic hypothyroidism), which were normal. This stiffness was punctuated by episodic weakness. However, she denied any muscle weakness, stiffness, sensory loss or seizures in the preceding years. The patient lives in a mountainous area on the Iraqi–Iranian border, which lacks medical services; this explains her delayed visit to our department in spite of having had recurrent neurological complaints over the past year.
The patient had developed relapsing–remitting MS, which was unrelated to the primary frontal arachnoid cyst. The pertinent literature mentions that surgical intervention should be considered in symptomatic cysts only. Immune-modulating therapy in relapsing MS is only moderately effective and associated with side effects. The long-term effect of these therapies is unknown. The use of immune-modulating therapy should follow shared decision-making by the patient and their neurologist after discussion of expectations and side effects.
The medical literature does not mention that arachnoid cysts are risk factors for the future development of MS. The authors think that, in our patient, both diseases simply coexisted with each other without any direct association.
- Arachnoid cysts are often an incidental finding on cranial MRI.
- Arachnoid cysts are often asymptomatic and do not need neurosurgical intervention.
- Primary arachnoid cysts may be associated with central nervous system and other body malformations but they are not risk factors for multiple sclerosis.