Microvascular Decompression for Treatment of Trigeminal Neuralgia in a patient with a Facial Nerve Schwannoma

Background Cerebellopontine angle tumors comprise up to 12% of secondary trigeminal neuralgia (TN).¹ The rarity of tumor-related etiologies of TN lends itself to overlooking coexistent causes during initial diagnosis, especially when existing mass effect is evident. This report illustrates the importance of considering concurrent actionable causes of TN in this setting.

Case Report A 51-year-old woman presented with abrupt onset left hemifacial TN and hypesthesia in a V2 and V2 nerve distribution. She denied changes in hearing, balance, or facial nerve dysfunction. MRI revealed a 1.6-cm contrast-enhancing cerebellopontine angle tumor that effaced the trigeminal nerve, consistent with a vestibular schwannoma. In addition, a branch of the superior cerebellar artery (SCA) abutted the cisternal segment of the trigeminal nerve on heavily T2-weighted thin slice MRI. A retrosigmoid craniotomy with tumor resection was planned ([Fig. 1]). Intraoperative mapping of the tumor capsule with the facial stimulating probe elicited facial nerve stimulation at low threshold over the entire accessible tumor surface, indicating that the tumor was instead a facial nerve schwannoma. Considering that the patient had no preexisting facial nerve deficit and the tumor exhibited no safe entry point for intracapsular debulking, tumor resection was not performed. Working between the superior pole of the tumor and tentorium, a culprit branch of the SCA was identified and decompressed with a Teflon pad ([Fig. 2]). Further, the petrous apex above the internal auditory canal was drilled to allow more room for the tumor and thus decompress the brain stem and cisternal root of the fifth nerve. Postoperatively, the patient exhibited complete resolution of her TN both immediately and at her last follow-up 3 months later. She reported no change in hearing and demonstrated normal facial nerve function. The patient subsequently elected to pursue Gamma Knife radiosurgery, which consisted of 10 isocenters of radiation covering a tumor volume of 3,760 mm³. Radiation was successfully delivered with a 12.5 Gy dose to the margin and a maximum dose of 25 Gy ([Fig. 3]).

Discussion Large vestibular schwannomas commonly induce trigeminal neuropathy; however, TN from a small- or medium-sized schwannoma is rare.² This report describes a unique situation where tumor resection was not ultimately advisable. However, MVD and anterior petrosectomy provided complete resolution of the patient’s TN, despite unrelieved mass effect by the tumor. Therefore, even in the setting of a known space-occupying lesion, classic and secondary TN may be concomitant yet treatable. The persistence of the patient’s hypesthesia postoperatively highlights the differing pathophysiology of classic and tumor-induced TN.^3–5 In this way, MVD alleviated the unpredictable lancinating facial pain, but hypesthesia secondary to direct tumor compression and irreversible nerve damage remained.

Conclusion Despite obstruction from a medium-sized tumor, it is still possible to achieve MVD of the fifth cranial nerve. This emphasizes the importance of considering other actionable pathology during surgical management of presumed tumor-induced TN. Further, TN is relatively uncommon with medium-sized vestibular schwannomas and coexistent causes should be considered.

Fig. 1 Preoperative imaging of facial nerve schwannoma, (a) Contrast enhanced T1-weighted axial MRI demonstrating 1.6 cm cerebellopontine angle mass with extension into the internal auditor canal with no enhancement of the labyrinthine segment of the facial nerve. (b) Axial CT of temporal bone demonstrating no apparent bony widening of labyrinthine or geniculate segments of the facial nerve. (c) Heavily T2-weighted thinly sliced axial MRI revealing compression of trigeminal nerve by a branch of the superior cerebellar artery (arrow).

Fig. 2 Postoperative imaging of (a) axial contrast enhanced T1-weighted MRI following partial decompression of internal auditory canal and microvascular decompression (arrow, indentation from Teflon pad). (b) Heavily T2-weighted thin sliced axial MRI following microvascular decompression (arrow, Teflon pad adjacent cisternal segment of trigeminal nerve).

Fig. 3 Axial contrast enhanced T1-weighted MRI following gamma knife radiosurgery showing loss or central enhancement consistent with treatment effect.