Primary trigeminal neuralgia (PTN) is a common chronic facial pain disorder [3] characterized by sudden and intense pain attacks along the branches of the trigeminal nerve [2]. The main cause of PTN is neurovascular conflict (classic TN), but in some cases, there are no registered underlying structural changes in the nerve root, branches, or nuclei (idiopathic TN). Surgical treatment is believed to be effective in patients with PTN when pharmacological pain control fails [3]. However, even after surgery, some patients do not improve or even deteriorate their clinical condition and require additional treatment options, especially in cases of idiopathic TN [2], [7].

Brain magnetic resonance imaging (MRI) is an essential diagnostic tool for patients with TN [11]. It provides detailed information about posterior fossa anatomy and allows the determination of the cause of TN and the development of a treatment algorithm ([2], [8], [12]). Advanced neuroimaging methods, such as diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI), can provide quantitative output, providing us with quantitative data regarding microstructural changes in the nerve root [24]. A number of studies have been published dedicated to the use of these techniques in patients with PTN to assess trigeminal nerve microstructural impairment or to evaluate surgical decompression outcomes [13], [14], [16], [33], [36].

The impact of chronic paroxysmal pain in patients with PTN is thought to extend beyond the confines of the trigeminal system. Prior studies in this field were generally devoted to morphometry and have shown that PTN results in different structural changes in the brain ([5]; H. [18]). DTI research in patients with PTN has primarily been focused on the microstructural changes in the cisternal part of the trigeminal nerve root [13], [15], [32], [36]; thus, brain white matter reorganization seems to be understudied in this group of patients. Previous published articles dedicated to hemispheric white matter plasticity in PTN have shown the presence of microstructural impairment in a number of regions involved in pain processing, such as the corticospinal tract, the cingulate gyrus, the corpus callosum, the internal capsule, and the corona radiata ([4]; J. [19], [30]). However, these studies were limited by small sample sizes.

It is considered that chronic pain leads to diffuse and focal hemispheric white matter changes, which has been demonstrated for patients with headache [21], low back pain [20], complex regional pain syndrome [9], and other pain disorders [31]. Furthermore, brainstem tractography also showed revealed white matter microstructural alterations within posterior cranial fossa structures in patients with different chronic pain syndromes [35]. However, it should be noted that there is no consensus on brain DTI changes in chronic pain syndromes due to existing data heterogeneity [6].

To date, there are few published data on the changes in DTI metrics within white matter tracts in patients with PTN. Therefore, our objective was to assess the differences in microstructural parameters of white matter (such as FA, MD, RD, and AD) between patients with PTN and controls in a relatively large sample size. We hypothesized that patients with PTN would show white matter microstructural damage, similar to patients with other chronic pain syndromes. Furthermore, we assumed that microstructural parameter changes would correlate with both nerve root compression grade and disease severity.