Arachnoid cysts are congenital fluid-filled compartments within cerebrospinal fluid (CSF) cisterns and major cerebral fissures, intimately bordered by the arachnoid membrane. The cysts are filled with clear, colourless fluid nearly identical to CSF 5. They have been originally described on autopsy reports from the early 19th century6
True arachnoid cysts are congenital. They may develop when alterations of CSF flow during the early phase of subarachnoid space formation lead to rupture of the developing webbed arachnoid. An alternative theory involves splitting of the arachnoid membrane during delamination from the overlying dura. However, the exact mechanism remains speculative7.
The first description of an AC with intracystic bleeding or subdural haematoma was described in 19388. The coexistence of an intracranial cyst with intracystic bleeding and subdural haematoma is quite rare. To our knowledge, less than such 40 cases have been confirmed1.
Arachnoid cysts show a slight predilection for the male sex4. They can develop anywhere within the subarachnoid space, intimately related to the cisterns. In the general population, nearly half of cysts occur within the sylvian fissure. It is also known that the supratentorial cysts far outnumber the infratentorial ones9. Less common sites of appearance are the suprasellar region, the cerebellopontine angle, the cerebral convexity and the quadrigeminal plate10.
A majority of the arachnoid cysts are recognized during the first two decades of life. Their natural history and course are poorly understood. Most of them constitute dormant fluid compartments that remain silent for many years. In distinct cases they enlarge producing mass effect on brain structures5. Signs related to arachnoid cysts include cranial enlargement, seizures, hydrocephalus and mental retardation11. In middle cranial fossa cysts, headache is the most frequent presenting symptom12. In rare occasions they can resolve spontaneously13.
On Computed Tomography (CT) scan arachnoid cysts appear normally as extra-parenchymal hypo intense without any contrast-medium enhancement. In post traumatic cases however, the borders of isointense AC are not clearly demonstrated. In these patients, cyst location and relationship to adjacent structures is best visualized by T1 weighted sequences. Cyst fluid has normally low attenuation on T1 images and a high signal on T2 sequences which is nearly identical to CSF. However, previous intracystic haemorrhage may change the attenuation values in all image sequences14.
Intracystic haemorrhage and/or subdural haematoma as a complication of AC may occur spontaneously or after a minor head trauma. They may result from rupture of the intracystic or bridging vessels15. This could be presumably explained by the presence of unsupported veins that surround the cyst walls. Moreover, the fragile supporting stroma also predisposes to rupture even after a minor injury15. In some occasions, subsequent re-bleed or osmotic influx of fluid could explain the gradual increase in the subdural or intracystic fluid collection3.
Management decisions balance the imaging findings and the clinical symptoms. Many collections are asymptomatic and are managed conservatively with observation. However, symptomatic patients are candidates for surgery2. Sizeable subdural collections with mass effect should be evacuated with application of usual neurosurgical techniques. The optimal cyst manipulation is still under debate. The two most commonly used surgical procedures are cyst peritoneal shunting and cyst fenestration16. Endoscopic membrane excision has also been used with good outcomes17. Whatever the choice of the surgical procedure, membranectomy and cyst communication to the basal cisterns must be accomplished19.