Surgical Treatment of Trigeminal Neuralgia Combined with Tumors of the Cerebellopontine Angle

Abstract

Introduction . Trigeminal neuralgia (TN) develops because of demyelination in the entry zone of the trigeminal nerve root (TNR) into the brainstem, which is accompanied by ectopic and cross-excitation of the nerve impulses with paroxysms of facial pain. One of the causes of TN are tumors of the cerebellopontine angle (CPA), which have a direct or indirect effect on the TNR. The optimal surgical approach in such cases depends on the anatomical relationship between the TNR and the tumor and vascular structures. The aim of the study was to evaluate the relationship between the anatomical variants of the TNR and the outcomes of using various surgical methods to treat TN in CPA tumors. Materials and methods. We performed a retrospective analysis of 52 patients (38 women and 14 men aged 22–82 years) with TN and ipsilateral tumors of the CPA: 29 with apical petrous meningiomas, 11 with epidermoid tumors, 10 with vestibular schwannomas, 1 with haemangioma, and 1 with cavernoma. Results. Six variants of the anatomical relationships of the TNR to CPA tumors and the adjacent vascular structures were identified: where the TNR is completely surrounded by the tumor; where the tumor compresses and displaces the TNR; where the tumor is located inside the TNR; where the tumor, together with the blood vessel, compresses the TNR; where the tumor displaces the TNR towards the vessel; and where the tumor is not in contact with the TNR, but the TNR is compressed by the blood vessel. Displacement and deformation of the TNR by CPA tumors was found in 50 patients, and no direct contact between the TNR nerve fibers and the neoplasm was observed in 2 cases. The neurovascular conflict caused by arterial and venous vessels was identified in 16 subjects. The type of a vascular decompression technique depended on the degree of stretching and deformation of the TNR. Postoperative MRI confirmed the complete removal of CPA tumors in 51 patients, while minor epidermoid residue in the contralateral cerebellopontine angle cistern was found in only one subject. There were no fatalities after surgical interventions, and the postsurgical cranial nerve neuropathies were transient and regressed within 2–3 months. In 15 cases, hypoesthesia developed or worsened in the trigeminal nerve innervation zone, then disappeared within several weeks, and was not accompanied by a recurrence of TN. Facial sensitivity improved in 6 cases, who had not previously undergone any surgical manipulations of the TNR and its peripheral branches. Complete regression of TN in the immediate postoperative period was observed in 51 patients. A percutaneous radiofrequency trigeminal rhizotomy was performed in 1 subject with an epidermoid tumor, to eliminate the intense pain paroxysms that persisted for a week. No recurrent growth of CPA tumors or relapses of TN were observed during the subsequent follow-up period of 2–10 years. Conclusion. TN can be caused by direct compression and deformation of the TNR and brainstem by CPA tumors and vascular structures. A detailed examination of the entire length of the TNR after tumor removal is necessary to evaluate the neurovascular relationships. In cases of vascular compression of the TNR, various methods of microvascular decompression can be used to treat TN.