Surgical management of temporal meningoencephaloceles, cerebrospinal fluid leaks, and intracranial hypertension: treatment paradigm and outcomes

Abstract

Thinning of the tegmen tympani and mastoideum components of the temporal bone may predispose to the development of meningoencephaloceles and spontaneous CSF leaks. Surgical repair of these bony defects and associated meningoencephaloceles aids in the prevention of progression and meningitis. Intracranial hypertension may be a contributing factor to this disorder and must be fully evaluated and treated when present. The purpose of this study was to establish a treatment paradigm for tegmen defects and elucidate causative factors. The authors conducted a retrospective review of 23 patients undergoing a combined mastoidectomy and middle cranial fossa craniotomy for the treatment of a tegmen defect. The average body mass index (BMI) among all patients was 33.2 ± 7.2 kg/m(2). Sixty-five percent of the patients (15 of 23) were obese (BMI > 30 kg/m(2)). Preoperative intracranial pressures (ICPs) averaged 21.8 ± 6.0 cm H(2)O, with 10 patients (43%) demonstrating an ICP > 20 cm H(2)O. Twenty-two patients (96%) had associated encephaloceles. Five patients underwent postoperative ventriculoperitoneal shunting. Twenty-two CSF leaks (96%) were successfully repaired at the first attempt (average follow-up 10.4 months). Among all etiologies for CSF leaks, those occurring spontaneously have the highest rate of recurrence. The surgical treatment of temporal bone defects, as well as the recognition and treatment of accompanying intracranial hypertension, provides the greatest success rate in preventing recurrence. After tegmen dehiscence repair, ventriculoperitoneal shunting should be considered for patients with any combination of the following high-risk factors for recurrence: spontaneous CSF leak not caused by another predisposing condition (that is, trauma, chronic infections, or prior surgery), high-volume leaks, CSF opening pressure > 20 cm H(2)O, BMI > 30 kg/m(2), preoperative imaging demonstrating additional cranial base cortical defects (that is, contralateral tegmen or anterior cranial base) and/or an empty sella turcica, and any history of an event that leads to inflammation of the arachnoid granulations and impairment of CSF absorption (that is, meningitis, intracranial hemorrhage, significant closed head injury, and so forth).