What Causes Arachnoid Cysts
Arachnoid cysts are caused by herniation of arachnoid tissue through a defect in the diaphragma sellae (for sellar arachnoid cysts) or by developmental abnormalities involving splitting or duplication of the arachnoid membrane during embryonic development 1.
Primary Mechanisms of Formation
The pathophysiology of arachnoid cysts remains debated, but the most recent high-quality guideline evidence identifies the following mechanisms:
Congenital (Primary) Arachnoid Cysts
- Developmental malformation of the arachnoid membrane is the predominant cause, occurring during embryonic development 2
- For sellar arachnoid cysts specifically, herniation of arachnoid tissue through a defect in the diaphragma sellae creates the cyst, representing 1.4% of sellar lesions 1
- These are benign CSF-filled collections coated with a single layer of flattened arachnoid cells 3
Proposed Pathophysiological Theories
Four main theories explain cyst development and expansion 4:
- Ball-valve mechanism - one-way fluid flow into the cyst
- Osmotic gradient - between intra- and extracystic fluid
- Primary arachnoid membrane malformation - splitting or duplication during development (most supported)
- Fluid hypersecretion - by cyst wall lining cells
The latter two theories (primary malformation and fluid hypersecretion) have stronger evidence supporting them as the primary causes 4.
Secondary (Acquired) Causes
While less common, arachnoid cysts can develop secondary to:
- Head trauma - particularly in infancy, with a latent period of 10 months to 6.2 years before clinical manifestation 5
- Perinatal trauma 5
- Hemorrhage 3, 6
- Meningitis or infection 3, 6
Important caveat: Approximately 15.6% of arachnoid cysts may be related to head trauma in infancy, though this remains controversial 5. These traumatic cysts most commonly occur in the suprasellar area (6 of 7 cases) and have a mean latent period of 2.2 years before symptoms appear.
Clinical Context
The vast majority (92.5% of adults and 72.4% of children) remain asymptomatic 1. These cysts are isointense to cerebrospinal fluid on MRI with no contrast enhancement due to higher protein content than CSF 1. The benign natural history—with 95% showing unchanged volume over 31 months of follow-up and only 0.9% developing new symptoms 1—supports the predominantly congenital, non-progressive nature of these lesions.