Revision Microvascular Decompression for Trigeminal Neuralgia and Hemifacial Spasm: Risk Factors for Surgical Failure

Objective Trigeminal neuralgia (TN) and hemifacial spasm (HFS) result from cranial nerve compression by surrounding structures. Microvascular decompression (MVD) has proven to be an effective treatment strategy; however, decompression of the nerve does not always lead to symptom resolution. We aim to investigate the cause of symptoms returning in patients requiring a repeat MVD surgery.

Methods We retrospectively reviewed the medical records of all patients undergoing revision MVD surgeries by the senior author at our institution. Patient demographics, radiographic data, severity of symptoms, follow-up data, records of Gamma Knife radiosurgery (GKRS), and initial operative reports, were queried for analysis.

Results Seventeen patients were identified in our analysis, 8 cases of recurrent HFS and 9 cases of recurrent TN. Six of the cases had the same surgeon for the initial and revision surgeries. Timing between surgeries ranged considerably between 2 weeks and 12 years. The causes of surgical failure were slippage of the Teflon pledget (n = 6/17), inflammation leading to scarring and adhesions around the nerve (n = 5/17), new site of nerve compression (n = 5/17), and no obvious anatomic cause in the final patient (n = 1/17). Seven patients had preoperative magnetic resonance imaging (MRI) available, all of which demonstrated nerve compression. The TN cohort (n = 9) had recurrent symptoms from scarring and adhesions (n = 4/9) most commonly, followed by a new site of nerve compression (n = 3/9), slipped pledget (n = 1/9), and no obvious anatomic cause (n = 1/9). Three of the TN patients underwent GKRS prior to the revision MVD, two of which were found to have an inflammatory reaction, though it is unclear if the adhesions formed from the initial surgery or from GKRS. TN symptoms completely resolved in four patients, significantly improved though still required medications in four patients, and continued in the patient without identified anatomic nerve compression. The HFS cohort (n = 8) had recurrent symptoms from a slipped pledget (n = 5/8), new site of nerve compression (n = 2/8), and an inflammatory reaction with scarring in the final case (n = 1/8). Symptoms of HFS resolved immediately in all but one case, which had minor continued spasms, hypalgesia, and facial numbness. The case with continued symptoms was complicated by postoperative meningitis, though symptoms did significantly improve at the time of follow-up.

Conclusion Scarring and adhesion formation was the most common cause of recurrent TN. A slipped pledget was the most common cause of continuing symptoms of HFS, likely reflective of surgeon reluctance to apply Tisseel immediately adjacent to the cranial nerves. Scarring did not affect HSF as it did TN cases. None of the cases that developed scarring were performed by the same surgeon; therefore, it is unclear if the primary surgery or, in three cases, GKRS somehow lead to scar formation. Preoperative imaging identifying scarring as a cause of return of symptoms tend to have less of a response to revision surgery and should prompt the neurosurgeon to consider alternative treatments such as glycerol, radiofrequency ablation, balloon occlusion, or GKRS.