Vascular compression of the trigeminal nerve root is the leading cause of classic TGN. Other causes include focal arachnoid thickening, adhesion, cerebello-pontine angle tumors, inflammation, multiple sclerosis, brainstem infarction, and arteriovenous malformations [7, 8]. In patients who did not respond to or could not tolerate pharmacological treatments, MVD is the first choice regardless of the presence or absence of NVC as determined by MRI due to the low sensitivity of MRI in detecting NVC [9]. In a small percentage of the patients, NVC could not be identified despite of complete dissection of entire length of the trigeminal nerve root. In addition, complete dissection of the trigeminal nerve in recurrent cases after previous MVD is often difficult, if not impossible, due to adhesion [10, 11].
Partial sensory rhizotomy (PSR) is one option in patients with no identifiable NVC. In a study of 83 cases, Young et al. reported 15% rate of severe complications (complete loss of sensory function and corneal ulcer) [12]. A literature review of 10,493 patients undergoing a variety of surgical treatments for trigeminal neuralgia also supported the high rate of severe complication with PSR [13]. As a result, PSR has been practically abandoned in clinical practice. Nerve combing is another option in TGN patients with no identifiable NVC, but is associated with relatively high rate of 5-year recurrence (approximately 40%) [14,15,16].
Percutaneous balloon compression (PBC) at the site of the trigeminal Gasserian ganglion is currently recommended as the first-choice extracranial treatment of TGN [17]. The physiological basis of PBC is the higher sensitivity of the larger pain fibers in the trigeminal nerve to physical damages compared to smaller fibers that transmit other sensory input and the afferent fibers [18]. Despite of the advantage of PBC, MVD is the treatment of choice in patients with TGN regardless of the presence or absence of NVC as determined by pre-operative MRI. In other words, PBC is typically used in patients who failed MVD treatment, and must be conducted separately [3, 4].
Cheng et al. used bipolar electrocoagulation tip to produce neurapraxia in 28 patients without OV. 20 patients (71.4%) achieved immediate complete pain relief. With a median follow-up of 46 months (range: 8–60 months), the recurrence rate was 38.4%, and only 13 patients (46.4%) remained pain-free without medication during the follow-up. Four patients (14.3%) developed permanent facial numbness [19]. Revuelta-Gutierrez et al. used bipolar electrocoagulation tips to produce neurapraxia to the trigeminal nerve root in 21 patients, and achieved immediate complete pain relief in all 21 patients. Recurrence rate was 14.8% at 12–36 months and 43.2% at 48 months. Permanent hypoesthesia was present in 6 patients (28.6%), whereas transient loss of corneal reflex was observed in 1 patient (4.8%). Motor function of the trigeminal nerve was intact in all patients [6].
In the current study, we achieved 100% immediate complete pain relief with acceptable complications in 26 patients with no identifiable NVC during MVD. Within a median of 3-year follow-up, the recurrence rate was 11.5%. In our opinion, these encouraging results reflect consistent degree of damage to the sensory fibres of the trigeminal nerve due to the use of consistent force (90 g) and 40-s clipping duration. Whether this method could be developed as a standardizable approach requires further study in different settings.
From a surgical viewpoint, the trigeminal nerve root must be completely exposed to reveal possible OVs. If possible, only the sensory root should be clipped. Also, duration of the clipping is essential. In a pilot series that consisted of 3 cases, we clipped the trigeminal nerve root for 2.5 min, and unfortunately, all 3 patients developed severe hemifacial numbness and masseter weakness. The protocol that we have been using since 2015 is clipping for 40 s if the procedure could be completely in a single attempt, and for a total of 60 s if the procedure must be suspended temporarily and repeated due to bradycardia or hypertension.
In addition to the retrospective nature, the current study is limited by the relatively small sample size and the relatively short follow-up (median at 3 years). Also, 3 patients who were lost to follow-up were not included in the analysis. It is likely that these 3 patients experienced relapse or complications but chose not coming back to us. This could produce some bias to our results. The follow-up was conducted via telephone in some patients, and not based on office visit, adding another layer of limitation to the current study. Having said that, we believe that the key results are solid since recurrence and majority of the complications are sensory abnormalities without standard objective examinations.