The etiology of trigeminal neuralgia (TN), particularly how neurovascular conflict or trigeminal nerve distortion induces pain, remains incompletely understood. This study aimed to investigate whether the anatomical configuration of the trigeminal nerve and its adjacent structures could serve as a predisposing factor for clinically significant neurovascular conflict in TN.

We conducted a retrospective analysis involving 70 patients with idiopathic TN and 70 healthy participants, utilizing Constructive Interference in Steady State (CISS) magnetic resonance imaging. Measurements included the length of both trigeminal nerves from the nerve root entry zone to the entrance into Meckel"s cave, intertrigeminal distance, prepontine distance, and sagittal angle on each nerve at the level of the porus trigeminus. Correlations were made between the length and sagittal angle of the nerve on the painful and non-painful sides. Intraoperative findings, such as arterial compression, venous compression, and arachnoid membranes distorting the nerve, were recorded along with side and distribution of pain.

The mean age at surgery was 56 years (19 to 91 years). Arterial compression was the most common intraoperative finding (88.8%), followed by arachnoid adhesions distorting the nerve (73.8%), and venous compression (50%). A statistically significant difference was found in the mean length of the trigeminal nerve on the pain side compared to the non-pain side (10.6 vs. 10.3). Patients with TN had shorter trigeminal nerves compared to the control group on the left (11.3 vs. 11.9 mm) and right side (9.9 vs. 10.4 mm). However, no statistically significant difference was observed in the intertrigeminal distance, sagittal angle, and prepontine distance between the two groups. Additionally, a shorter trigeminal nerve correlated with a higher number of intraoperative findings, particularly venous compression and arachnoid adhesions.

Our findings support the hypothesis that a shorter trigeminal nerve may render individuals more susceptible to clinically significant neurovascular conflict in trigeminal neuralgia.