In Reply: The Sagittal Angle of the Trigeminal Nerve at the Porus Trigeminus is a Radiologic Predictor of Surgical Outcome in Microvascular Decompression for Classical Trigeminal Neuralgia

To the Editor: We appreciate the attention and careful review1 that Drs Yang and Xiong have given our paper titled “The Sagittal Angle of the Trigeminal Nerve at the Porus Trigeminus is a Radiologic Predictor of Surgical Outcome in Microvascular Decompression for Classical Trigeminal Neuralgia.”2 They have raised several excellent points about this novel radiologic biomarker. We agree with Drs. Yang and Xiong that the sagittal angle of the trigeminal nerve at the porus trigeminus (SATNaPT) is only one feature among many that may contribute to the pathogenesis of trigeminal neuralgia (TN). But in patients with a hyperacute SATNaPT, our current surgical techniques are much less likely to be successful. Thus, novel surgical approaches are needed to address this variant of TN. The fact that some patients with a hyperacute SATNaPT do get relief from surgery reinforces the conclusion that there are many contributing factors, even in this subset of patients, and that SATNaPT is not the only biomarker of interest. We also agree with Drs Yang and Xiong that postoperative imaging to assess the state of the nerve, and to determine whether the SATNaPT was improved in patients who responded to surgery, would be a fascinating contribution to the discussion. Unfortunately, we do not have consistent postoperative imaging, as most of our patients recover completely and do not require further imaging. Thus, our results in the small group of patients with follow-up imaging would be biased toward those with recurrent symptoms and would have to be considered anecdotal. Clearly, more research into this question would be beneficial. This is particularly intriguing in light of our finding that patients who had both hyperacute SATNaPT and severe radiologic vascular compression of the trigeminal nerve responded well to surgery, whereas patients with hyperacute SATNaPT but no distortion responded poorly.2 Regarding the presence of minor vascular compression that might be exacerbated by a hyperacute SATNaPT, we find this a very difficult question to answer. There are almost always tiny vascular branches adjacent to the affected nerve. It is difficult to know whether these tiny vessels are in fact causative of TN, either with or without a hyperacute SATNaPT. However, we know that the radiologic degree of vascular compression is an independent biomarker of surgical outcome in patients with classical trigeminal neuralgia,3 and also that outcomes are predicted by a combination of SATNaPT and degree of vascular compression.2 In our experience, intraoperative findings are less compelling, likely because of cerebrospinal fluid drainage, than preoperative high-resolution MRI.4 In this subset of patients, the majority of patients underwent interpositional microvascular decompression (MVD), and although there is no compelling evidence to suggest that transpositional MVD is associated with improved outcomes as compared with interpositional MVD in a broad cohort of patients,5 it is possible that transpositional MVD may result in improved outcomes in patients with a hyperacute SATNaPT.