OBJECTIVE: To describe three cases of delayed development of intracranial hypertension (IH) after surgical treatment of intracranial arachnoid cyst, including the pathogenesis of IH and a review of the literature. METHODS: A retrospective and prospective analysis of three male patients (two 18 years old and one 45 years old) was performed. All patients underwent surgical intervention for symptomatic intracranial arachnoid cyst in the form of fenestration of the cyst and a cystoperitoneal shunt. RESULTS: All three patients presented at a later stage with new-onset headaches after the initial management of arachnoid cyst. Magnetic resonance imaging and magnetic resonance venography ruled out any intracranial vascular pathology. Lumbar puncture and intracranial pressure monitoring showed increased intracranial pressure suggestive of idiopathic IH. To manage IH, intracranial pressure monitoring, cystoperitoneal shunt, ventriculoperitoneal shunt, and lumboperitoneal shunt were performed. CONCLUSIONS: The pathogenesis of delayed development of IH in this clinical setting is not clearly elucidated. When intracranial arachnoid cysts are treated, the possibility of future development of IH should be borne in mind. Delayed presentation with headaches in patients after treatment of intracranial arachnoid cysts should raise the possibility of IH.
OBJECTIVE: To describe three cases of delayed development of intracranial hypertension (IH) after surgical treatment of intracranial arachnoid cyst, including the pathogenesis of IH and a review of the literature. METHODS: A retrospective and prospective analysis of three male patients (two 18 years old and one 45 years old) was performed. All patients underwent surgical intervention for symptomatic intracranial arachnoid cyst in the form of fenestration of the cyst and a cystoperitoneal shunt. RESULTS: All three patients presented at a later stage with new-onset headaches after the initial management of arachnoid cyst. Magnetic resonance imaging and magnetic resonance venography ruled out any intracranial vascular pathology. Lumbar puncture and intracranial pressure monitoring showed increased intracranial pressure suggestive of idiopathic IH. To manage IH, intracranial pressure monitoring, cystoperitoneal shunt, ventriculoperitoneal shunt, and lumboperitoneal shunt were performed. CONCLUSIONS: The pathogenesis of delayed development of IH in this clinical setting is not clearly elucidated. When intracranial arachnoid cysts are treated, the possibility of future development of IH should be borne in mind. Delayed presentation with headaches in patients after treatment of intracranial arachnoid cysts should raise the possibility of IH.