Surgical management of temporal meningoencephaloceles ......Thinning of the tegmen tympani and mastoideum components of the temporal bone may predispose to the development of meningoencephaloceles

Neurosurg Focus / Volume 32 / June 2012

Neurosurg Focus 32 (6):E6, 2012

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Several mechanisms have been proposed for thin-ning of the tegmen cortex of the temporal bone and the resultant CSF leaks. Potential causes include congenital defects, trauma, infection, and intracranial hypertension.6,7,10–12,15 As the middle fossa cranial base develops progressively enlarging defects, CSF pulsations contribute to dehiscence and can lead to meningoenceph-alocele development and eventual dural disruption.4,8,12,16 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 eusta-chian tube.1–3,5,11,12,15

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 indi-cations for VP shunt placement.

MethodsPatient Characteristics

We conducted a retrospective chart review of 23 con-secutive 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 (March 2006–September 2011). This review received approval from our local institutional review board.

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

Tyler J. Kenning, M.D.,1 ThoMas o. Willcox, M.D.,2 gregory J. arTz, M.D.,2 Paul schiffMacher, B.f.a.,3 chrisToPher J. farrell, M.D.,1 anD JaMes J. evans, M.D.1,2

Departments of 1Neurological Surgery and 2Otolaryngology, and 3Medical Media Services, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania

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 as-sociated 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/m2. Sixty-five percent of the patients (15 of 23) were obese (BMI > 30 kg/m2). Preoperative intracranial pressures (ICPs) averaged 21.8 ± 6.0 cm H2O, with 10 patients (43%) demonstrating an ICP > 20 cm H2O. 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 recur-rence. 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 H2O, BMI > 30 kg/m2, 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).(http://thejns.org/doi/abs/10.3171/2012.4.FOCUS1265)

Key WorDs • cerebrospinal fluid • otorrhea • otorhinorrhea • tegmen repair • temporal meningoencephalocele • mastoidectomy • intracranial hypertension

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Abbreviations used in this paper: BMI = body mass index; ICP = intracranial pressure; OP = opening pressure; VP = ventriculo-peritoneal.

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T. J. Kenning et al.

2 Neurosurg Focus / Volume 32 / June 2012

Surgical TechniqueAfter inducing general anesthesia, a lumbar puncture

is performed to determine OP and for placement of a lum-bar drainage catheter. The lumbar drain is used intraop-eratively and maintained for 48–72 hours postoperatively to aid with decompression of the dural repair. Patients are placed supine with the head turned to the contralateral side (Fig. 1). Lateral positioning is used for very obese patients or those with very limited cervical spine rotation. A Mayfield 3-pin head holder is used for head fixation. The postauricular and inferior temporal area are clipped, prepared, and draped in the usual fashion. A C-shaped retroauricular incision is marked starting 3–4 cm behind the ear, beginning at (or below) the mastoid tip, extend-ing superiorly over the ear, and curving down toward the root of the zygomatic process (Fig. 2). The scalp is incised down to and through the galea. A pedicle of pericranium is created from the superior portion of the incision poste-rior to the temporalis muscle and is used during closure and reconstruction. The temporalis muscle is elevated in the subperiosteal plane and reflected as one layer with the skin flap. A self-retaining retractor is placed, and a mas-toidectomy is performed.

The mastoidectomy allows for closure of the tegmen mastoideum as well as the tegmen tympani and aids in functional preservation of the incus and malleus. After the sigmoid sinus and tegmen are skeletonized, the aditus is identified and opened widely so that the incus and the head of the malleus can be skeletonized in the epitympa-num. Careful exploration along the tegmen, usually in the region of the epitympanum, will often allow for identifi-cation of the (meningo)encephalocele(s), which may be in contact with the ossicles. The encephaloceles can then be reduced toward the middle cranial fossa.

Aided by the judicious removal of CSF via lumbar drain, the temporal craniotomy is started. A bur hole is created in the temporal region above the tegmen tym-pani, and the dura mater is dissected away from the inner table of the skull. Because of chronic epidural inflam-mation, the dura can be extremely adherent, and multi-ple bur holes may be required to prevent dural violation and injury to the underlying brain during the exposure. A temporal craniotomy is made with a craniotome, and the inferior temporal dura is carefully dissected from the temporal floor. An extradural dissection is performed along the tegmen mastoideum and tegmen tympani, ex-posing the cranial base defect and any associated me-ningoencephaloceles. The bony defect is then dissected circumferentially, and when involved, the middle ear os-sicles are identified. This dissection allows full exposure of the dural defect(s) (Fig. 3).

The lateral temporal dura is incised and opened. Dural dissection allows for mobilization of the encephalocele, which can be cauterized. An appropriately sized sheet of synthetic collagen-based dural inlay substitute is placed along the intradural surface of the dural defect, and the dural incision is closed with a running 4-0 Nurolon suture (Ethicon, Inc.). Once the dura is reinforced, the osseous defect must be repaired. If the middle ear ossicles are vis-ible through the defect, they must be protected to prevent the dura from contacting them directly and restricting

their movement. In this case, a portion of the temporal craniotomy bone flap is cut and appropriately shaped for concave repair of the tegmen tympani. Autologous bone repair of the cranial base defect is also used when there is a large defect (> 1 cm in diameter). A sheet of pericra-nium (or temporalis fascia if pericranium is unavailable) is dissected free from the scalp flap, placed over the teg-men repair, and covered with a small amount of fibrin glue (Fig. 4). The temporal craniotomy defect is covered with heavyweight titanium mesh (Fig. 5).

For smaller cranial base defects, bone is not used for the repair. In these cases, only the inlay synthetic dural graft and extradural pericranium or temporalis fascia are used, and the temporal craniotomy bone is secured back in position using titanium microplates (Fig. 6). The tem-poralis fascia and galea are closed in separate layers with interrupted sutures, and the skin is closed with a running absorbable monofilament suture. A sterile mastoid dress-ing is then applied.

The lumbar drain is used to drain 5–10 ml/hour post-operatively and is usually removed on postoperative Day 3 after a 24-hour period of clamping to ensure there is no recurrent otorhinorrhea. Prior to the lumbar drain’s re-moval, a determination is made regarding the need for a VP shunt. This decision is based on an assessment of an individual patient’s risk factors for recurrence, including etiology, preoperative OP measurement, and body habi-tus.

Follow-Up EvaluationBoth radiological and clinical follow-up are required

to evaluate the efficacy of the repair and to allow for early recognition of any recurrence of CSF otorrhea. In the im-mediate postoperative period, a cranial noncontrast CT with fine-cut and reconstructed images of the temporal

Fig. 1. Illustration demonstrating lateral positioning and the incision used for tegmen repair (dotted line). Printed with the permission of Paul Schiffmacher, 2012.



Tegmen repair for temporal meningoencephalocele

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bones is obtained. Following discharge, the patient is seen in the outpatient clinic at 2 weeks and 3 months postop-eratively by both the neurosurgeon and the otolaryngolo-gist to evaluate wound healing and the patient’s clinical condition. At 1 year postoperatively, the patient is again seen with a new temporal bone CT to assess the tegmen repair, including osseous integration of any autologous bone graft that may have been used. It is also important to ensure that the middle ear ossicles are free and have not become impacted by the graft. A final CT is obtained and reviewed at the 2-year postoperative outpatient visit. Additional radiological studies are obtained for any new symptoms, including an MRI for the evaluation of any neurological concerns.

Clinical AnalysisPreoperative demographics reviewed for each patient

included age, sex, BMI, etiology, history of meningitis, presence of hearing loss, presenting symptoms, history of myringotomy tube placement, laterality of cranial base defect, and presence of an empty sella or contralateral cranial base defects on preoperative MRI. The intraop-erative parameters collected were preoperative OP, use of intraoperative lumbar drain, and type of intradural and extradural repair. The need for VP shunting was record-ed, as was the recurrence of a CSF leak and associated symptoms. All complications were reviewed.

Statistical AnalysisStandard descriptive methods were used to summa-

rize the data. Frequencies and percentages were used for nominal variables, and means and standard deviations or medians and ranges were used for continuous variables.

Fig. 2. Illustration showing indications (dotted lines) for a mastoidec-tomy, as well as a middle fossa craniotomy. Printed with the permission of Paul Schiffmacher, 2012.

Fig. 3. Illustration demonstrating thinning of the tegmen tympani cor-tex and associated meningoencephaloceles contacting the middle ear ossicles. Printed with the permission of Paul Schiffmacher, 2012.

Fig. 4. Illustration of the middle fossa repair of a large tegmen defect and exposed middle ear ossicles after meningoencephalocele reduc-tion/resection. An autologous bone graft from the temporal craniotomy is used to cover the tegmen defect. An epidural layer of local pericra-nium (pink layer) is placed, and an intradural collagen graft (gray layer) is used prior to closure of the dura. Printed with the permission of Paul Schiffmacher, 2012.




ResultsPatient Demographics

Twenty-three patients underwent surgical repair of tegmen defects during the study period. A summary of

the preoperative demographics is shown in Table 1. The average age of the patients was 55.1 ± 12.5 years. There was no sex predilection, with nearly equal distribution be-tween males (11) and females (12). The patients reviewed were generally overweight, with an average BMI of 33.2 ± 7.2 kg/m2. In fact, only 4 patients (17%) had a BMI < 25 kg/m2, and 65% (15 of 23) were obese (BMI > 30 kg/m2).

Five patients (22%) had a history of cranial trauma that was suspicious for an inciting event for the develop-ment of a tegmen defect and CSF fistula. In 4 patients (17%), there was a history of meningitis. All 23 patients presented with hearing loss in the ear ipsilateral to the tegmen defect to be repaired. The presenting symptom in 19 patients (83%) was CSF otorrhea. In all but 2 of these patients, the CSF otorrhea occurred after placement of the myringotomy tubes for middle ear fullness and fluid. Other presenting symptoms were temporal meningoen-cephalocele (discovered intraoperatively during a prior otological procedure, 2 patients), an episode of acute oti-tis media and mastoiditis (1 patient), and pulsatile tinni-tus (1 patient). The tegmen defect repairs occurred nearly equally in the right (10 patients) and left (13 patients) tem-poral bones. However, there were bilateral defects in 10 of the patients (43%). An empty sella was noted on preop-erative MRI in 4 patients (17%).

Operative DetailsThe intraoperative findings are summarized in Table

2. The average preoperative OP obtained during lumbar puncture under general anesthesia was 21.8 ± 6.0 cm H2O. A lumbar drain was placed preoperatively in every patient, with the exception of 2 in whom difficulty with passing the catheter prevented its use. Both of these pa-tients had had previous lumbar spinal fusion procedures. The lumbar drain was maintained throughout the surgi-cal procedure and was usually removed on postoperative Day 3. In 22 patients (96%), a synthetic dural inlay was used for intradural repair. The one exception was a pa-tient with significant intradural adhesions due to chronic inflammation and very prominent temporal veins. An in-tradural graft was not placed in this case given concerns that venous drainage might be disrupted. Extradurally, autologous tissue, either pericranium or temporalis fascia, was used to cover the osseous cranial base defect in 20 patients (87%). In 11 of them (48%), a portion of the tem-poral craniotomy bone was used to cover exposed middle ear ossicles prior to the placement of autologous graft. In 2 patients (9%), allograft was used both intradurally and extradurally. A single patient had only autologous bone used for extradural repair since a significant dural defect was not identified, and this patient only presented with pulsatile tinnitus and not otorrhea.

Intracranial Hypertension ManagementOur experience with intracranial hypertension man-

agement in this population is summarized in Table 3. Ten patients in the study had a preoperative OP ≥ 20 cm H2O, with 7 patients demonstrating an OP ≥ 25 cm H2O. Long-term CSF diversion in the form of VP shunting was suggested to 8 patients. Three of them refused shunts. A

Fig. 5. Postoperative coronal CT of the temporal bone demonstrat-ing the autologous bone graft spanning the tegmen defect and the tita-nium mesh used to repair the craniotomy site.

Fig. 6. Illustration of the middle fossa repair of a smaller tegmen de-fect when the middle ear ossicles are not exposed. An epidural layer of local pericranium (pink layer) is placed, and an intradural collagen graft (gray layer) is used prior to closure of the dura. Printed with the permis-sion of Paul Schiffmacher, 2012.




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recurrent leak developed in 1 patient within a week but was managed with aggressive lumbar drainage; despite the recurrence, the patient continues to refuse a VP shunt and remains under close observation. One of the patients who underwent shunting had an OP of 12 cm H2O, but because of the presence of a high-volume leak and a BMI of 40.4 kg/m2, a VP shunt was placed. In 3 others with an OP ≥ 20 cm H2O, VP shunt placement was deferred. This was the case in 2 patients with a history of cranial trauma that might have been the cause of the tegmen de-fect rather than intracranial hypertension. The third pa-tient under observation without a VP shunt had a normal BMI, a low-volume leak, and no other radiographic signs of intracranial hypertension (that is, bilateral tegmen de-fects or empty sella).

Patient OutcomesDuring an average follow-up of 10.4 ± 6.4 months

(range 3–26 months), operative repair prevented further CSF leaks or recurrent symptoms in 22 patients (96%). The 1 patient with transient residual postoperative CSF otorrhea was successfully treated with the replacement of a lumbar drain and aggressive drainage for 7 days. With 19 months of follow-up, that patient continues to be free of any further symptoms of CSF leakage. Unfortunately, he did require ossicular chain reconstruction 5 months postoperatively because the tegmen repair was contact-ing the middle ear structures despite being covered with a segment of the temporal craniotomy bone. In this case, the head of the incus became fused with the overlying bone graft. Additional complications (Table 4) included 1 case each of local wound infection, meningitis, deep vein thrombosis, and postoperative seizures. These last 3 complications all occurred in 1 patient who had a number of preoperative medical comorbidities, including a BMI of 40.4 kg/m2 and Type 2 diabetes mellitus.

DiscussionPatient Outcomes

The occurrence of temporal meningoceles and/or meningoencephaloceles in the middle ear or mastoid is often insidious in onset and usually only occurs with ipsi-lateral aural fullness or CSF egress from a disrupted tym-panic membrane or through the eustachian tube.3,6 Once this fluid is determined to be CSF, usually by testing for β-2 transferrin, and not a serous middle ear fluid collec-tion, the cranial base should be examined radiologically to identify a cortical dehiscence. Imaging should include both thin-cut CT scanning of the temporal bone and MRI to evaluate for the presence of meningoencephaloceles (Figs. 7 and 8). Any abnormalities should be surgically addressed to prevent persistent leakage and the associ-ated risk of meningitis, intracranial abscess, and seizures. With a combined mastoid/middle fossa approach, we were able to achieve a high success rate (96%) of CSF fis-tula closure, comparable to rates in previously published reports.2,5,8,13,14

Our surgical technique involves a robust dural clo-sure following extradural dissection and encephalocele reduction/resection. We use a multilayer closure for direct repair of the dural and cranial base defects. Using both a synthetic dural inlay and an epidural autologous graft along the tegmen helps to ensure that the areas of dural and osseous disruption are fully covered and reinforced. As mentioned above, when the middle ear ossicles are ex-posed, we use a concave calvarial bone graft cut from the temporal craniotomy flap to protect these structures prior to placing a piece of pericranium extradurally. Despite this precaution, we did have 1 patient who required an os-sicular chain reconstruction after suffering postoperative hearing loss when the head of the incus became fixed to the surgical repair. Following his revision procedure, his hearing improved dramatically but remained depressed as compared with the contralateral side. Subsequently, we now take care to ensure that the graft is shaped so that the concave side faces the tegmen defect and that there is sufficient space between the middle ear and bone graft to allow for normal mobility of the ossicles (Fig. 4).

Impact and Management of Intracranial HypertensionAlthough thinning of the tegmen cortex appears to

TABLE 1: Summary of demographics in 23 patients undergoing treatment for a tegmen defect*

Factor No. (%)

mean age (yrs) 55.1 ± 12.5M:F 11/12mean BMI (kg/m2) 33.2 ± 7.2history of trauma 5 of 23 (22) history of meningitis 4 of 23 (17)ispilat hearing loss 23 of 23 (100)presentation symptom CSF leak 19 of 23 (83) intraop encephalocele on prior surgery 2 of 23 (9) acute OM/mastoiditis 1 of 23 (4) pulsatile tinnitus 1 of 23 (4)leak after myringotomy tubes 17 of 23 (74)laterality of repair (rt:lt) 10/13bilat defects 10 of 23 (43) empty sella 4 of 23 (17)

* OM = otitis media.

TABLE 2: Intraoperative findings in 23 patients treated for bony defects

Finding No. (%)

mean preop OP (cm H2O) 21.8 ± 6.0intraop lumbar drain 21 of 23 (91)encephalocele 22 of 23 (96)dural inlay used for intradural repair 22 of 23 (96)extradural repair autologous 9 of 23 (39) autologous + bone 11 of 23 (48) allograft 2 of 23 (9) bone 1 of 23 (4)




be fairly common in autopsy studies, ranging from 15% to 34%, the occurrence of CSF otorrhea is fairly infre-quent.1,4,16 The predisposing factor to the formation of cra-nial base (meningo)encephaloceles is thought by many to be intracranial hypertension.2,7,11,15 It is believed that the pathogenesis of tegmen thinning shares many character-istics with benign intracranial hypertension, or pseudotu-mor cerebri.12 Although not our experience, a female pre-ponderance in middle fossa CSF leaks has been reported by many groups.2 Additionally, a patient’s body habitus appears to play a significant role, as these patients tend to be obese (BMI > 30 kg/m2).2,7 Other signs of intracranial hypertension may also be evident, such as the radiograph-ic finding of an empty sella, which was noted in 17% of the patients in our series, a higher rate than the 5%–6% seen in the normal population.7,10 Furthermore, it is likely that the rate of intracranial hypertension is underestimat-ed in this population if the ICP is measured while CSF is actively leaking or at least before the defect(s) is fully repaired. Unrecognized intracranial hypertension may be a reason for recurrent CSF leakage, either from the same site or from a remote cranial base defect, after surgical repair.

Thus, our treatment of this disorder involves not only repair of the disrupted dura and reinforcement of the middle fossa floor but also an assessment of intracranial hypertension and CSF diversion, if present. We use an intraoperative lumbar drain to aid temporal lobe relax-ation during evaluation of the tegmen cortex. The drain is then left in place for 3 days postoperatively to allow for

decompression of the dural closure during early healing of the repair. The drain is always placed immediately pre-operatively under general anesthesia to record the most accurate OP. In our review, the measured preoperative ICPs averaged 21.8 ± 6.0 cm H2O, with 10 patients (43%) demonstrating ICP > 20 cm H2O.

Although a CSF fistula develops through a single site in these patients, the disease process more likely repre-sents a global intracranial problem. We found that 43% of our patients had bilateral tegmen defects and thus were at risk for a recurrent CSF leak through the same site on the contralateral side. For this reason, we have selectively used long-term CSF diversion via VP shunting in patients with significant risk factors for recurrence. We propose that those risk factors include a spontaneous CSF leak not caused by a predisposing condition (that is, trauma, chronic infections, or prior surgery), high-volume leaks, CSF OP > 20 cm H2O, BMI > 30 kg/m2, preoperative imaging demonstrating multiple cranial base cortical de-fects and/or an empty sella turcica, and any history of an event that leads to inflammation of the arachnoid granu-lations and impairment of CSF absorption (that is, men-ingitis, intracranial hemorrhage, significant closed head injury, and so forth).

Utilizing these criteria, we suggested VP shunt place-ment to 8 of the 10 patients with an ICP > 20 cm H2O, 3 of whom refused this treatment. A recurrent leak de-veloped in 1 of these patients within 1 week of surgical repair. Another patient with a normal OP received a shunt given the presence of other risk factors for recurrence. In general, the decision for VP shunt placement is made on an individual basis. Although we are aggressive with long-term CSF diversion in this group of patients, we be-lieve that the prevention of recurrent or additional leaks and the associated risk of meningitis outweigh the risks related to VP shunts.

Critique of Current StudyThe limitations of this study include its retrospective

nature and limited size. The duration of postoperative follow-up was also variable, with 1 patient not returning

TABLE 4: Complications in patients treated for bony defects*

Complication No. (%)

wound infection 1 of 23 (4)meningitis 1 of 23 (4)DVT 1 of 23 (4)seizures 1 of 23 (4)

* DVT = deep vein thrombosis.

TABLE 3: Intracranial hypertension management

Case No.

OP (cm H2O) BMI

History of Trauma

Bilat Tegmen Defects

Empty Sella

VP Shunt Placed Comment/VP Shunt Reasoning

1 26 32 yes yes no no trauma suspected as cause of defect2 25 38.1 yes no no no trauma suspected as cause of defect3 23 43.6 no no no yes significantly elevated BMI4 25 34.1 no yes no no patient refused VP shunt5 25 37.8 no yes yes yes multiple risk factors6 31 29.2 yes no no yes high-volume leak7 33 49.9 no no no yes significantly elevated BMI8 25 42.5 no yes no no patient refused VP shunt, postop transient leak9 24 21 no no no no low BMI

10 24 31.1 no no no no patient refused VP shunt11 12 40.4 no no yes yes high-volume leak, high BMI




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at all postoperatively and 6 patients lost to follow-up after only 5 months of monitoring. This follow-up may be long enough, however, to identify most recurrent CSF leaks, despite their insidious nature. The 1 recurrence in our series occurred in a patient within a week of his initial tegmen repair, and other reports have indicated that re-lapses occur most often within a few months of surgery.9 Note, however, that rare cases of recurrent CSF leakage have been reported up to 2–4 years after surgery.2,9 The development of new CSF fistulas at remote sites of the cranial base likely occurs years, or even decades, after an initial leak, and further follow-up of this group of patients is needed.

Relying on an OP measurement at the time of an ac-tive CSF leak to determine intracranial hypertension may not always provide an accurate assessment. Some patients with a normal pressure may demonstrate recurrent CSF leakage at the repair site or elsewhere in the cranial base as a result of continued unrecognized intracranial hyper-tension. In those patients for whom this may be a concern, it may be prudent to perform a lumbar puncture for OP measurement at a later postoperative date.

ConclusionsThe occurrence of thinning or dehiscence of the teg-

men cortex is fairly common, and a portion of patients with this finding will demonstrate meningoencepha-loceles and CSF skull base fistulas. Surgical repair of these defects should address the osseous and dural de-fects as well as any underlying intracranial hypertension. Assessing the latter and determining which patients will require long-term CSF diversion are difficult in this set-ting. We have suggested some risk factors that should be considered in making these decisions.

Disclosure

The authors report no conflict of interest concerning the mate-rials or methods used in this study or the findings specified in this paper.

Author contributions to the study and manuscript preparation include the following. Conception and design: Kenning, Evans. Ac quisition of data: Kenning. Analysis and interpretation of data: Ken ning. Drafting the article: Kenning. Critically revising the ar ticle: Willcox, Artz, Farrell, Evans. Reviewed submitted version of manuscript: Evans. Approved the final version of the manuscript on behalf of all authors: Kenning. Statistical analysis: Kenning. Ad min-istrative/technical/material support: Kenning, Schiffmacher. Study supervision: Evans.

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Manuscript submitted February 15, 2012.Accepted April 5, 2012.Please include this information when citing this paper: DOI:

10.3171/2012.4.FOCUS1265.Address correspondence to: Tyler J. Kenning, M.D., Department

of Neurological Surgery, Thomas Jefferson University Hospital, 909 Walnut Street, 2nd Floor, Philadelphia, Pennsylvania 19107. email: [email protected].


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Surgical management of temporal meningoencephaloceles ......Thinning of the tegmen tympani and mastoideum components of the temporal bone may predispose to the development of meningoencephaloceles