- Barrow Neurological Institute Pain Intensity Scale
- cross-sectional area
- Gamma Knife radiosurgery
- microvascular decompression
- neurovascular compression.
Since Dandy1 first described arterial contacts with the dorsal root of the trigeminal nerve, the association of neurovascular compression (NVC) with trigeminal neuralgia (TN) was recognized by demonstrating the beneficial effects of decompressing the trigeminal nerve.2,3 However, the presence of NVC does not always lead to TN because NVC is common on both the symptomatic and asymptomatic sides.4-6 Therefore, the severity of NVC has been taken into account in distinguishing symptomatic trigeminal nerve from asymptomatic trigeminal nerve. Nerve atrophy, defined as the reduced volume of the nerve at the site of NVC, and displacement were independently associated with the signs and symptoms of trigeminal neuralgia, and these patients tended to exhibit favorable outcomes after microvascular decompression (MVD).4,7-13 Moreover, TN can occur even in the absence of NVC.14 In this regard, the International Headache Society currently classifies TN based on the etiology of facial pain. Classical TN demonstrates vascular compression with morphological changes in the trigeminal nerve seen on preoperative MRI or during surgery.11,15
Morphological changes in the trigeminal nerve quantified either by the cross-sectional area (CSA) or the volume of the nerve in the cistern showed a significant decrease on the symptomatic side.16,17 However, there has been no study on the morphological changes in the trigeminal nerve using postoperative MRIs. If NVC results in morphological changes in the trigeminal nerve without inducing intrinsic damage to the nerve fibers, the successful elimination of NVC would recover trigeminal nerve CSA or volume on postoperative MRIs when the patients achieved favorable outcome. In the present study, we measured the trigeminal nerve CSAs in both the preoperative and postoperative periods to estimate whether the increase in trigeminal nerve CSA could be radiologically confirmed after MVD and whether this finding predicts favorable outcomes.
We retrospectively reviewed the medical records of 59 patients who received surgical treatment for TN fulfilling the diagnostic criteria of the International Classification of Headache Disorders-3 13.1.1 from January 2016 to September 2021.11 Nine patients were excluded from the study because 5 patients did not have postoperative MRIs, 1 patient was finally diagnosed with painful trigeminal neuropathy, and the remaining 3 patients had no offender identified despite thorough exploration during surgery. Finally, 50 patients diagnosed with classical TN were enrolled in the study. This study was approved by the local institutional review board, and the requirement for informed consent was waived because of the retrospective nature of the study.
Supplemental Digital Content, https://links.lww.com/NEU/D405 contains the detailed MRI protocols. The trigeminal nerve CSA was measured using 3-dimensional (3-D) Slicer imaging software (version 4.11.2; Surgical Planning Laboratory, Harvard University). Either 3D-TSE or 3D-PD images were transferred to a personal computer as Digital Imaging and Communications in Medicine files, and coronal/sagittal reformatted images were obtained using a multiplanar reconstruction algorithm. The coronal plane was aligned parallel to the line that crossed the entry points of each trigeminal nerve in the pons (Figure 1). Preoperative and postoperative MRIs were coregistered using the general registration module in 3D Slicer to ensure that the trigeminal nerve CSAs were measured at the same point between 2 images and adjust the anatomic distortion formed by the different angle between the trigeminal nerve root and coronal plane. The preoperative trigeminal nerve CSA was measured by manually delineating the trigeminal nerve 4 mm from the nerve entry into the pons in the coronal image supposing that this point was included in the transitional zone (Figure 1).18 Using the same method, the postoperative trigeminal nerve CSA was also measured. The CSA change rate was calculated as [(symptomatic trigeminal nerve CSA on postoperative MRI)/(symptomatic trigeminal nerve CSA on preoperative MRI) − 1] × 100. Two independent observers blinded to the patients' profiles and surgical outcomes independently analyzed the images.
One senior neurosurgeon conducted all surgeries and wrote the operative records. After identifying the trigeminal nerve root, circumferential dissection of the arachnoid membrane was performed to straighten the axis of the trigeminal nerve root in the cistern.19 When the offending vessel was isolated, transposition was primarily considered by attaching the vessel to the dura mater of the petrous bone using Tachosil soaked with fibrin glue.20 If transposition was not feasible, a piece of Teflon prosthesis was interposed between the offending vessel and the root entry point. In this case, we intended to avoid the Teflon prosthesis directly touching the nerve root to prevent secondary compression by the prosthesis.19 No intentional traumatic manipulation of the trigeminal nerve was performed. Using the operative records, the decompression method (transposition/interposition), type of offending vessel (artery or vein), location of the NVC categorized as either distal or proximal (proximal was defined as the half of the cisternal segment from the root entry point), and the severity of NVC (grade I, simple neurovascular contact without indentation; grade II, displacement or distortion of the root; grade III, marked indentation and displacement of the root) were collected.12
All patients' surgical outcomes were estimated using the Barrow Neurological Institute Pain Intensity Scale (BNI-PS) at every visit to the outpatient clinic.21 Surgical outcomes were categorized as favorable when the pain was well controlled without medication (BNI-PS I or II) 6 months after surgery and did not recur until the latest follow-up. Unfavorable outcome indicates the patients could not discontinue medication because of the remaining pain (BNI-PS ≥ IIIA) at any time point from 6 months after surgery to the latest follow-up.
The Mann–Whitney U test was used to compare the means of continuous variables. The Fisher exact test was used to assess the associations between categorical variables. Receiver operating characteristic curve analysis was used to obtain the cutoff value of the CSA change rate that best predicted surgical outcomes. Using the cutoff value, Kaplan–Meier survival analysis was performed, and the log-rank test was used to compare the survival curves. Correlations of surgical outcomes and CSA change rates with the CSA of the symptomatic nerve, proximal NVC, decompression method (transposition/interposition), duration of illness, and severity of NVC were calculated using the Spearman rho correlation coefficient. Interobserver variability was assessed using the Pearson correlation coefficient. All tests were two-tailed, and P < .05 was considered statistically significant. IBM SPSS Statistics 24 (IBM Corp.) was used for all statistical analyses.
Patient Characteristics and Surgical Outcomes
The mean follow-up period was 24.6 ± 11.7 months. At the latest follow-up, 41 patients (82.0%) showed favorable outcomes without medication, whereas 9 patients (18.0%) showed unfavorable outcomes. Table 1 shows the characteristics of the groups with respect to surgical outcomes. There were no significant differences in age, sex, operation side, duration of symptoms, previous interventions, rate of transposition, arterial NVC, and proximal NVC between the 2 groups. However, the severity of NVC showed a significant association with surgical outcomes (P = .03).
TABLE 1. -
Patient Characteristics With Respect to Surgical Outcomes
||Favorable (n = 41)
||Unfavorable (n = 9)
||61.1 ± 10.1
||55.7 ± 9.7
|Duration of symptoms (mo)
||71.4 ± 55.7
||61.9 ± 40.6
|Severity of NVC
NVC, neurovascular compression.
The changes in CSA with respect to surgical outcomes are described in Table 2. Pearson correlation coefficients for the CSA measurements were 0.93 and 0.91 (P < .01) for the preoperative and postoperative symptomatic trigeminal nerves, respectively. In the preoperative period, the symptomatic trigeminal nerve CSA was significantly smaller than that of the asymptomatic trigeminal nerve in the favorable outcome group (symptomatic: 4.37 ± 1.64 mm2 vs asymptomatic: 5.24 ± 1.71 mm2, P = .02). However, this change was not significant in the unfavorable outcome group (symptomatic: 4.20 ± 1.19 mm2 vs asymptomatic: 4.16 ± 0.93 mm2, P = .95).
TABLE 2. -
Changes in CSA With Respect to Surgical Outcomes
|Symptomatic trigeminal nerve CSA (mm2)
||4.37 ± 1.64
||6.26 ± 1.76
||4.20 ± 1.19
||4.43 ± 1.24
||4.34 ± 1.56
||5.93 ± 1.81
|Asymptomatic trigeminal nerve CSA (mm2)
||5.24 ± 1.71
||5.51 ± 1.63
||4.16 ± 0.93
||4.35 ± 1.08
||5.05 ± 1.65
||5.29 ± 1.60
CSA, cross-sectional area.
In the overall 50 patients, the symptomatic trigeminal nerve CSA was significantly increased in the postoperative period compared with that in the preoperative period (preoperative: 4.34 ± 1.56 mm2 vs postoperative: 5.93 ± 1.81 mm2, P < .01). This change in the symptomatic trigeminal nerve CSA occurred in the favorable outcome group (Figure 2, preoperative: 4.37 ± 1.64 mm2 vs postoperative: 6.26 ± 1.76 mm2, P < .01), whereas the change in the CSA was not significant in the unfavorable outcome group (preoperative: 4.20 ± 1.19 mm2 vs postoperative: 4.43 ± 1.24 mm2, P = .69). The CSA change rate was also significantly higher in the favorable outcome group (favorable: 55.74 ± 53.55% vs unfavorable: 5.95 ± 11.32%, P < .01).
Association of CSA Changes With Surgical Outcomes
Using receiver operating characteristic curve analysis, 20% of the CSA change rate was determined to be the most appropriate cutoff value to predict surgical outcomes. A CSA change rate of >20% predicted a favorable outcome with 73.2% sensitivity and 88.9% specificity (P < .01). Kaplan–Meier survival analysis showed that those with the CSA change rate of >20% were more likely to experience favorable outcomes (Figure 3; χ2 = 13.90, P < .01). The estimated 3-year probability of maintaining a favorable outcome was 92.3 ± 7.4% and 56.1 ± 11.9% for those with a CSA change rate of >20% and ≤20%, respectively. Figure 4 illustrates examples of trigeminal nerve CSA changes in patients with favorable (A, B) and unfavorable (C, D) outcomes.
Table 3 shows the correlation of surgical outcomes and CSA change rates with various parameters. Surgical outcome was correlated with the postoperative symptomatic trigeminal nerve CSA (r = 0.41, P < .01), CSA change rate (r = 0.44, P < .01), CSA change rate >20% (r = 0.49, P < .01), and severity of NVC (r = 0.36, P = .01). The CSA change rate was negatively correlated with the preoperative symptomatic trigeminal nerve CSA (r = −0.56, P < .01) and positively correlated with the postoperative symptomatic trigeminal nerve CSA (r = 0.36, P = .01) and severity of NVC (r = 0.39, P < .01).
TABLE 3. -
Correlation of Surgical Outcomes and CSA Change Rates With Various Parameters
||Correlation with surgical outcome
||Correlation with CSA change rate
|Preoperative symptomatic CSA
|Postoperative symptomatic CSA
|CSA change rate
|CSA change rate >20%
|Duration of symptoms
|Severity of NVC
CSA, cross-sectional area; NVC, neurovascular compression.
ap < .05.
bCSA change rate = [(postoperative symptomatic CSA)/(preoperative symptomatic CSA) − 1] × 100.
Prognostic Value of MRI
Various prognostic factors of MVD for TN have been reported.12,13,22-26 Although the preoperative MRI showed excellent capability of predicting the presence of NVC, it showed limited accuracy in prediction of the severity of NVC.27 However, the severity of NVC in both intraoperative finding and the preoperative MRI had significant association with favorable outcomes.5,10,12,25,26,28 Previous studies that quantitatively analyzed morphological changes in the trigeminal nerves represented by either CSA or volume and their associations with surgical outcomes are summarized in Table 4.7,10,29-32 All previous studies were based on preoperative MRIs. Except for 1 study by Danyluk et al,32 CSAs or volumes in the symptomatic trigeminal nerve were smaller than those in the asymptomatic trigeminal nerve.10,29 Leal et al7 and Cheng et al10 showed that preoperative symptomatic trigeminal nerves in cured patients had significantly smaller CSAs or volumes than those in patients with partial pain relief or treatment failure. The present study also showed that the symptomatic trigeminal nerve had a smaller CSA than the asymptomatic trigeminal nerve in the favorable outcome group. This finding supports previous reports that morphological changes in the symptomatic trigeminal nerve induced by NVC predict favorable outcomes.7,10,11
TABLE 4. -
Previous Studies of Quantitative Analysis of Trigeminal Nerve Atrophy and Association With Surgical Outcomes
||MRI scan timing
||No. of patients with TN
|Leal et al
||Volume and CSA at 5 mm from the pons
||Symptomatic trigeminal nerve showed a smaller volume than the asymptomatic side (60.35 ± 21.74 mm3 vs 78.62 ± 24.62 mm3, P < .05).
Symptomatic trigeminal nerve showed a smaller CSA than the asymptomatic side (4.17 ± 1.74 mm2 vs 5.41 ± 1.89 mm2, P < .05).
Symptomatic trigeminal nerve in cured patients' had a smaller CSA than that of the symptomatic trigeminal nerve of patients with partial pain relief or treatment failure (P < .05)
|Cheng et al
||Symptomatic trigeminal nerve showed a smaller volume than the asymptomatic side (65.8 ± 21.1 mm3 vs 77.9 ± 19.3 mm3, P < .01).
Smaller volume of symptomatic trigeminal nerve than that of the asymptomatic side was associated with long-term outcomes after MVD (OR = 1.18, P = .035)
|Wang et al
||Volume and CSA at 5 mm from the pons
||Symptomatic trigeminal nerve showed a smaller volume than the asymptomatic side (62.37 ± 8.92 mm3 vs 80.71 ± 10.17 mm3, P < .05).
Symptomatic trigeminal nerve showed a smaller CSA than the asymptomatic side (3.92 ± 0.57 mm2 vs 5.04 ± 0.63 mm2, P < .05).
The CSA of the symptomatic trigeminal nerve with partial relief or treatment failure did not significantly differ from that in the cured patients (P = .80).
|Duan et al
||Proximal CSA: at midpoint of the cistern
Distal CSA: at the porus trigeminus
||Symptomatic trigeminal nerve showed a smaller CSA than the asymptomatic side (P < .05).
Atrophy of the distal trigeminal nerve was significantly more pronounced in patients who had residual pain or required continued medical treatment (P < .05)
|Hu et al
||CSA at 5 mm from the pons
||The median CSA of the symptomatic nerves was significantly smaller than that of the asymptomatic nerves (4.95 mm2 vs 5.9 mm2, P < .01).
Larger nerve CSA was associated with lower initial pain relief (hazard ratio = 0.81, P = .03) and lower pain recurrence after initial response (hazard ratio = 0.58, P = .02)
|Danyluk et al
||The volume of the symptomatic trigeminal nerves was not significantly different with respect to surgical outcomes.
The patients with favorable outcomes showed significantly smaller asymptomatic trigeminal nerve volumes than those with unfavorable outcomes (31.3 ± 11.5 mm3 vs 53. 3 ± 19.5 mm3, P < .01)
|The present study
||Pre, post (4 days after)
||CSA at 4 mm from the pons
||In preoperative MRI, the symptomatic trigeminal nerve CSA was significantly smaller than the asymptomatic trigeminal nerve in the favorable outcome group (4.37 ± 1.64 mm2 vs 5.24 ± 1.71 mm2, P = .02).
Symptomatic trigeminal nerve CSA was increased in postoperative MRIs compared to that in preoperative MRIs. This change was exclusively observed in the favorable outcome group (4.37 ± 1.64 mm2 vs 6.26 ± 1.76 mm2, P < .01)
CSA, cross-sectional area; GKRS, Gamma Knife radiosurgery; MVD, microvascular decompression; post, postoperative; pre, preoperative; TN, trigeminal neuralgia.
Increase in CSA After MVD
Previous study examined the ultrastructure of the trigeminal nerve root found circumscribed zone of chronic demyelination in the region of indentation.33 It was believed that NVC could damage trigeminal nerve fibers and that the subsequent damage could induce atrophic changes in the trigeminal nerve.10 However, decreased trigeminal nerve CSAs in this study can be explained by extrinsic compression of viable tissue rather than degeneration of trigeminal nerve fibers because we showed an immediate increase in the CSA through postoperative MRI. Increase in the trigeminal nerve CSA may result from re-expansion of viable tissue. This finding may accord with the previous report by Leal et al34 with diffusion tensor imaging sequences used to explore structural changes in the trigeminal nerve. In postoperative MRI, they reported decreased apparent diffusion coefficient in the symptomatic trigeminal nerve, suggesting an improved conduction and reduced edema of the nerve root after surgery. Successful decompression may result in improved diffusion and re-expansion of the nerve root.
Whether the offending vessel was transposed or interposed was not significantly correlated with the increase in the CSA after MVD (Table 3). However, it is hard to conclude that the decompression method does not influence the symptomatic trigeminal nerve CSA because we took special care not to directly contact the Teflon prosthesis with the nerve root. The implanted Teflon prosthesis was made as small as possible to prevent adhesion and secondary compression to the nerve root (Figure 5).
In addition to the elimination of NVC, adhesiolysis of the arachnoid membrane may contribute to increases in the trigeminal nerve CSA when the nerve root was tethered by a thickened arachnoid membrane. Larger postoperative symptomatic trigeminal nerve CSA than that of the asymptomatic side might have resulted from the arachnoid membrane dissection other than swelling to the nerve root. However, whether the arachnoid membrane dissection can affect surgical outcomes was not addressed in the present study.
By contrast, an unchanged CSA in unfavorable outcome group may be explained by insufficient decompression or intrinsic atrophy in the nerve root. Moreover, increases in the CSA may be limited when initial morphological change in the trigeminal nerve was not severe since the preoperative trigeminal nerve CSA was negatively correlated with the CSA change rate (r = −0.56, P < .01). Reviewing the postoperative MRIs of 9 patients with unfavorable outcomes, 2 patients had insufficient decompression, but the NVC of the other 7 patients was successfully eliminated, as intended. In these cases, it is presumed that pathophysiology other than NVC was involved and the effect of MVD was limited.
This study had several limitations including its retrospective nature and heterogeneous follow-up period. The CSAs were measured with coronal reformatted images not perpendicular to the axis of the trigeminal nerve. Therefore, the CSA would have been overestimated if the angle between the trigeminal nerve and the sagittal plane was large. However, these errors could be compensated because we focused on the changes in the CSAs rather than absolute values assuming that the angle was consistent after coregistration of preoperative and postoperative MRIs. Because we consistently measured the CSA at 4 mm anterior to the nerve entry into the pons, the measurement result might not have reflected morphological changes when NVC occurred in the distal nerve root. Measuring the CSA at point of maximal compression or the trigeminal nerve volume in the cistern might have overcome this limitation, but we measured only the CSA at 4 mm anterior to the nerve entry into the pons to focus on the morphological changes in the proximal trigeminal nerve in the cistern, considered to be more relevant to the pathogenesis of classical TN.35 The postoperative CSA may be varied by the surgeon's preference such as size and position of Teflon prosthesis, circumferential dissection of the arachnoid membrane, and intentional traumatic injury to the nerve root. Therefore, although a 20% increase of the CSA in postoperative MRI was suggested as a cutoff value to determine the prognosis, this value can be changed by each surgeon's surgical technique. Last of all, a consecutive study is necessary to estimate whether the morphologic changes in the trigeminal nerve will be maintained in the long-term follow-up period when the surgical manipulation effects have subsided.
In this study, we compared the trigeminal nerve CSA between preoperative and postoperative periods for patients with classical TN who underwent MVD. We confirmed that morphological changes in the trigeminal nerve could be recovered by MVD and that increases in the symptomatic trigeminal nerve CSA could predict favorable outcomes.
This study did not receive any funding or financial support.
The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.
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Supplemental Digital Content
Supplemental Digital Content. Methods. Image Examinations
This original study evidences that patients in whom the root cross section area (CSA) increased after the Micro-Vascular Decompression (MVD) procedure, had a better relief at last follow-up than those without a marked effect on CSA.
From this finding, it can be extrapolated that cases with a (presumed) diminution in caliber at the site of the potential Neuro-Vascular Conflict (NVC) should benefit from a favorable effect of the procedure.
Some personal team's works were also a plea for that hypothesis. K.M. analysis demonstrated proportionality between the degree of compression by the vessel and probability of long-term relief.1a The degree the higher, the outcome the better.
It was also demonstrated that the CSA of the roots ipsilateral to the neuralgia was significantly reduced compared to contralateral side or both sides in control group,2a feature found correlated with the quality of outcome.
It was also shown—using Diffusion Tension Imaging methods—a decreased Fraction of Anisotropy and an increased Apparent Diffusion Coefficient on the neuralgic compared to contralateral side, and positive correlation with the efficacy of the MVD.3a,4a
Decrease in CSA as well as DTI abnormalities on the side of the neuralgia, should be taken into account—as marker of root structural alteration—for indication of MVD. This would be especially important in the patients in whom MRI does not allow to ascertain the responsibility of the suspected vessel, namely in those in whom estimation of the degree of compression at MRI corresponds to a mere contact (ie, grade I).5a
1a. Sindou M, Leston J, Decullier E, Chapuis F. Microvascular decompression for primary trigeminal neuralgia: long-term effectiveness and prognostic factors in a series of 362 consecutive patients with clear-cut neurovascular conflicts who underwent pure decompression. J Neurosurg. 2007; 107(6):1144-1153.
2a. Leal PR, Barbier C, Hermier M, Souza MA, Cristino-Filho G, Sindou M. Atrophic changes in the trigeminal nerves of patients with trigeminal neuralgia due to neurovascular compression and their association with the severity of compression and clinical outcomes. J Neurosurg. 2014;120(6):1484-1495.
3a. Leal PR, Roch JA, Hermier M, Sindou M. Structural abnormalities of the trigeminal root revealed by diffusion tensor imaging in patients with trigeminal neuralgia caused by neurovascular compression: a prospective, double-blind, controlled study. Pain
4a. Leal PRL, Roch J, Hermier M, Berthezene Y, Sindou M. Diffusion tensor imaging abnormalities of the trigeminal nerve root in patients with classical trigeminal neuralgia: a pre- and post-operative comparative study four years after microvascular decompression. Acta Neurochir (Wien). 2019;161(7):1415-1425.
5a. Brinzeu A, Drogba L, Sindou M. Reliability of MRI for predicting characteristics of neurovascular conflicts in trigeminal neuralgia: implications for surgical decision making. J Neurosurg. 2018:1-11.
This study examined the difference in the cross-sectional area (CSA) between preoperative and postoperative MRI in patients with classical TN (cTN) who underwent MVD. A majority of patients in the study underwent vascular decompression via transposition rather than placement of an interpositional graft. A significant increase in trigeminal nerve CSA was found in those patients who were pain free without medication or experiencing occasional pain not requiring medication. The authors conclude that an increase in trigeminal nerve CSA by postoperative MRI may predict a long-term favorable outcome. This study further supports the notion that severity of morphological changes of the trigeminal nerve (eg, from neurovascular compression) is a strong predictor of a favorable outcome following MVD.1bBased upon our own work,2b I do disagree with the authors' assertion (ie, based upon the work of Sindou et al3b), “Although the preoperative MRI showed excellent capability of predicting the presence of NVC, it showed limited accuracy in prediction of the severity of NVC.” My experience suggests that a loss of CSF during exploration of the trigeminal nerve likely overestimates rather than underestimates the degree of NVC as compared to preoperative MRI. In all, however, this is a terrific study, which provides novel and potentially important new information for clinicians caring for patients with TN.
Raymond F. Sekula, Jr.
New York, New York, USA