Surgical management of temporal meningoencephaloceles, cerebrospinal fluid leaks, and intracranial hypertension: treatment paradigm and outcomes
Neurosurg Focus 32 (6):E6, 2012 1 S everal mechanisms have been proposed for thinning of the tegmen cortex of the temporal bone and the resultant CSF leaks. Potential causes include congenital defects, trauma, infection, and intracranial hypertension. 6, 7,    15 As the middle fossa cranial base develops progressively enlarging defects, CSF pulsations contribute to dehiscence and can lead to meningoencephalocele development and eventual dural disruption. 4, 8, 12, 16 This sequence
... 16 This sequence of events results in effusions in the middle ear and mastoid air cells that can manifest as CSF fistulas, through a disrupted tympanic membrane or via the eustachian tube.    5, 11, 12, 15 Given that intracranial hypertension has been impli-cated as a significant factor in temporal encephalocele formation, 7,10-12,15 we hoped to clarify this correlation by reviewing a series of tegmen defects repaired surgically and the associated ICP measurements in these patients. Additionally, we aimed to determine the rate of and indications for VP shunt placement. Methods Patient Characteristics We conducted a retrospective chart review of 23 consecutive patients undergoing a combined mastoidectomy and middle cranial fossa craniotomy for the treatment of a tegmen defect. These patients were all treated at a single institution over a 66-month period (Object. 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. Methods. 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. Results. 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). Conclusions. 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). Key WorDs • cerebrospinal fluid • otorrhea • otorhinorrhea • tegmen repair • temporal meningoencephalocele • mastoidectomy • intracranial hypertension 1 Abbreviations used in this paper: BMI = body mass index; ICP = intracranial pressure; OP = opening pressure; VP = ventriculoperitoneal.