Introduction

Trigeminal neuralgia (TN) is a chronic neuropathic pain condition resulting from neurovascular conflict, while neurogenic hypertension primarily arises from elevated blood pressure due to vessel compression in the medulla oblongata. The causal connection between hypertension and TN has been a subject of debate. Our study aimed to examine the onset of TN and hypertension by analyzing the association between conflicting blood vessels and hypertension.

Methods

To explore the relationship between hypertension and neurovascular conflict (NVC), we conducted a retrospective population-based study. We gathered data from 484 cases of TN patients admitted for neurosurgery at our hospital between October 2019 and November 2022. Ultimately, 457 patients were included in our final analysis. Based on MRI imaging, we categorized the conflicting vessels into several groups, including the superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA), posterior inferior cerebellar artery (PICA), vertebrobasilar artery (VBA), unidentified vessels (e.g., arteries like internal carotid artery branches, veins like petrosal vein), and cases without NVC. Additionally, we determined whether these conflicting vessels were located in the root exit zone (REZ) or not. We defined resistant hypertension as office BP≥140/90 mm Hg, even when managed with appropriate lifestyle modifications along with a diuretic and two other antihypertensive drugs.1 We employed Fisher's exact tests and a multivariate logistic regression model, building upon single-factor analysis, to identify independent risk factors. Statistical significance for the odds ratios tables was determined using a χ2 test.

Results

Hypertension occurred in 40% of the cases, with varying rates among different vessels: 36.4% (104/286) in cases with SCA involvement, 59.1% (13/22) in AICA cases, 55.2% (16/29) in VBA cases, 49.1% (28/57) in cases with unidentified vessels, and 20% (2/10) in PICA cases (Figure 1). Among the vascular conflicts leading to TN, SCA was responsible for 60% (286/471) of cases, while 15.5% (69/471) showed no evidence of NVC, and only 2.1% (10/471) were attributed to PICA. Notably, patients with AICA, VBA, and unidentified vessels who had hypertension exhibited the highest incidence of hypertension, collectively accounting for half of the hypertension cases (Figure 2). AICA, VBA, and unidentified vessels were associated with a higher likelihood of hypertension (OR 2.768, 2.360, and 1.848, respectively), while PICA was less likely to be linked to hypertension (OR 0.479, CI 0.252-0.909, p = 0.024). SCA in the REZ area was typically associated with hypertension, with an odds ratio of 2.857. Regarding onset timing, TN occurring before hypertension was the most prevalent scenario (106 cases), followed by TN onset after the onset of hypertension (60 cases), and simultaneous onset of TN and hypertension (16 cases) (Figure 3). The V2,3 distribution areas accounted for the highest proportion (29.7%) and were more likely to be associated with hypertension (OR 1.749, CI 1.147-2.667, p = 0.009).

Discussion

To the best of our knowledge, our study boasts the largest sample size among population studies focusing on TN patients with hypertension.2 Several studies suggest that elevated blood pressure can accelerate arteriosclerosis and vessel distortion, potentially leading to trigeminal nerve compression and TN.3-7 The origin and course of SCA make it prone to trigeminal nerve compression through arteriosclerosis. Trigeminal nerve fibers enter the pons via the REZ, influencing the cardiac sympathetic excitatory reflex in the medulla oblongata.8, 9 Our findings highlight SCA's presence in the REZ as an independent risk factor for TN with hypertension. Most studies emphasize neurogenic hypertension resulting from RVLM compression. RVLM vascular decompression can lower blood pressure. 10-14Neuronal aggregates near the human VLM's surface may affect cardiovascular function (Figure 4). Our study revealed that half of the medulla's compressing vessels were AICA, increasing the risk of CN III compression. VBA courses through the medulla oblongata, potentially compressing both it and the trigeminal nerve. 5 Thus, MVD is preferred for VBA cases due to the elevated risk of complex hypertension.4, 5, 15, 16 PICA is less likely to be the conflicting vessel in hypertension cases since it's farther from RVLM during CN III compression, reducing the hypertension risk.17 Furthermore, our study unveiled a stronger association between pain distribution in the V2,3 areas and hypertension. These two compressed regions are adjacent to the caudal pons, which has been identified as a potential target for neuromodulation in the treatment of hypertension.18

Conclusion

In this study, we conducted a comprehensive analysis of the relationship between hypertension and the location, type, and pain distribution associated with neurovascular conflict (NVC) in TN patients. Our findings aim to enhance the screening process for identifying TN patients with coexisting neurogenic hypertension.

Acknowledgements

No acknowledgement found.

References

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