Mechanism Of Trigeminal Neuralgia Research Articles

A comprehensive two-sample Mendelian randomization analysis of trigeminal neuralgia and modifiable risk factors

ObjectiveTo conduct a comprehensive search and causality study of potential modifiable risk factors for trigeminal neuralgia. To provide new ideas for subsequent treatment and management of patients with trigeminal neuralgia.MethodsData were obtained from large GWAS databases and then analyzed by Mendelian randomization analysis. The causal relationship between 36 potentially modifiable risk factors and trigeminal neuralgia was explored based on the results of the inverse variance weighting method(IVW). p < 0.05 was considered statistically significant.ResultsYears of schooling [OR (95%CI), 0.59(0.42–0.84), p = 0.003] to be a significant protective factor. Anxiety disorders [OR (95%CI), 1.62(1.05–2.48), p = 0.028], Depression [OR (95%CI), 1.53(1.03–2.28), p = 0.035] and Autoimmune [OR (95%CI), 1.16(1.01–1.32), p = 0.033] were significant risk factors. Sleep duration [OR (95%CI), 0.43(0.18–1.01), p = 0.051] was a close protective factor. Body mass index [OR (95%CI), 1.24(0.98–1.57), p = 0.077] was a close risk factor.ConclusionMendelian randomization analysis shows Years of schooling and Sleep duration as protective factors. Anxiety disorders, Depression, Autoimmune, and Body mass index are risk factors. This will help in the research of diagnosis, treatment, and mechanism of trigeminal neuralgia. And reduce the prevalence of trigeminal neuralgia through positive psychological and lifestyle interventions.

Fluorescence visualization of the neuropathic pain triad in trigeminal neuralgia.

Trigeminal neuralgia (TN), an exemplary condition of neuropathic facial pain, seriously affects the physical and mental health of patients, becoming a major medical and social problem. So far, the mechanism of TN and its relation to neuronal activity remain unclear, largely limited by the spatial resolution of visualization methods. In the meanwhile, current therapeutic strategies targeting neurons have not achieved satisfactory outcome. Here, we investigate the neuropathic pain triad in TN by establishing an animal model of TN by chronic constriction injury of the unilateral infraorbital nerve (ION-CCI) and leveraging the single-cell resolution of confocal microscopy, including neuronal hyperexcitability, glial activation, and macrophage polarization. These results can broaden the understanding of TN pathogenesis from neurons to the neuropathic pain triad, and suggest that optical microscopy can provide new opportunities for understanding the complex pathogenesis of TN at single-cell resolution, potentially contributing to the identification of more precise therapeutic targets and the development of more effective treatment modalities.

S65 Neurophysiological data favoring a central mechanism of trigeminal neuralgia

Current opinion is that TN is caused by a proximal compression of the trigeminal nerve root by a ectasic blood vessel leading to mechanical twist of nerve fibers and secondary demyelination. These changes lower the excitability threshold of affected fibers and promote inappropriate ephaptic propagation towards adjacent fibers. Not all patients have a nerve vessel conflict and 25% of people without any clinical signs of TN did show a nerve vessel contact. Possible involvement of central factors, suggesting a central facilitation and resulting hyperexcitability of the trigeminal system sustained by peripheral as well as central mechanisms were discussed. Sensitisation of second order wide dynamic range (WDR) neurons was discussed as additional pathophysiological mechanism. Since these WDR neurons receive convergent information from tactile (A-beta) and nociceptive (A-delta and C) fibers, their sensitisation could facilitate nociceptive input while promoting the perception of pain in response to tactile stimuli (i.e., allodynia). Central facilitation was demonstrated in TN patients with additional constant dull background pain besides their typical TN attacks using pain-related evoked potentials (PREP) and nociceptive blink reflex (nBR) [4]. Borsook et al. (2007) reported increased fMRI activation of a single TN patient in the primary somatosensory cortex, insula, anterior cingulate, and thalamus to further support cortical involvement [28]. Structural changes of the cortical grey matter was also reported to further support a central origin of the disease.

Underlying Mechanism of Trigeminal Neuralgia: Central? Peripheral? Or Both?

Underlying Mechanism of Trigeminal Neuralgia: Central? Peripheral? Or Both?

Reply to Underlying Mechanism of Trigeminal Neuralgia: Central, Peripheral, or Both?

Reply to Underlying Mechanism of Trigeminal Neuralgia: Central, Peripheral, or Both?

Pathogenesis of trigeminal neuralgia.

To the editor, I read with interest the article, “Differences in individual susceptibility affect the development of trigeminal neuralgia” by Duransoy et al. (2013). The authors have analyzed the possible pathogenesis of trigeminal neuralgia, with illustrative case examples. They have drawn very important conclusions, which may have implications in management of trigeminal neuralgia. The concept of microvascular compression at the root entry zone of trigeminal neuralgia as the pathogenetic mechanism of trigeminal neuralgia has been contested by various authors (Adams, 1989). This has been shown by the very high incidence of vascular compression at the root entry zone in asymptomatic population (Ramesh and Premkumar, 2009). Though the microvascular compression has been demonstrated in the majority of patients with trigeminal neuralgia and the microvascular decompression surgery results in pain relief, this alone does not explain the pathogenetic mechanism of trigeminal neuralgia. Focal demyelination has been observed in the area of vascular contact by some authors (Love and Coakham, 2001). But the demyelination does not occur in all individuals with the vascular contact. Hence, I also would agree with the authors’ view that there must be some individual susceptibility which predisposes to the development of focal demyelination at the root entry zone by vascular contact and causes trigeminal neuralgia and that mere vascular contact at the root entry zone need not result in trigeminal neuralgia. More studies and research are needed in this regard.

Mechanism of trigeminal neuralgia: an ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery.

Recent progress in the understanding of abnormal electrical behavior in injured sensory neurons motivated an examination, at the ultrastructural level, of trigeminal roots of patients with trigeminal neuralgia (TN). In 12 patients biopsy specimens of trigeminal root were obtained during surgery for microvascular decompression. Pathological changes in tissue included axonopathy and axonal loss, demyelination, a range of less severe myelin abnormalities (dysmyelination), residual myelin debris, and the presence of excess collagen, including condensed collagen masses in two cases. Within zones of demyelination, groups of axons were often closely apposed without an intervening glial process. Pathological characteristics of nerve fibers were clearly graded with the degrees of root compression noted at operation. Pain also occurred, however, in some patients who did not appear to have a severe compressive injury. Findings were consistent with the ignition hypothesis of TN. This model can be used to explain the major positive and negative symptoms of TN by axonopathy-induced changes in the electrical excitability of afferent axons in the trigeminal root and of neuronal somata in the trigeminal ganglion. The key pathophysiological changes include ectopic impulse discharge, spontaneous and triggered afterdischarge, and crossexcitation among neighboring afferents.

Middle fossa decompression of the trigeminal sensory root for trigeminal neuralgia--a re-appraisal and a modification of the technique.

Twenty-three patients with intractable trigeminal neuralgia were treated by a modified technique of middle fossa extradural decompression of the trigeminal sensory root at the petrous ridge. After exposing the ganglion and the root at the petrous ridge, by an extradural Frazier's approach a thin layer of autogenous fat was interposed between the dura propria and the middle fossa dura anteriorly, and between the petrous ridge and the root posteriorly. The fat layers were used to prevent dural adhesions and to maintain a space between the petrous ridge and the root. The dura propria was preserved intact. All patients obtained immediate relief of pain following surgery. Twenty patients continue to remain pain free. Two patients have mild occasional pains and one has a persistent pain of moderate intensity. One patient developed a dense sensory loss and two had delayed facial weakness which recovered completely within a month. The mechanism of trigeminal neuralgia is discussed on the basis of anatomical, histopathological and electrophysiological findings and the rationale of middle fossa decompression of the root is stressed. This method is short, simple and safe and may serve as an alternative to the more recent methods of treating trigeminal neuralgia.

Concerning the mechanism of trigeminal neuralgia and hemifacial spasm.

Concerning the mechanism of trigeminal neuralgia and hemifacial spasm.

Exposure of Meckel's cavity by extradural approach in the treatment of essential trigeminal neuralgia

Report of a new technique for the treatment of major trigeminal neuralgia, consisting of exposure (with no opening) of the cavum Meckelli following an extradural approach. Four patients were operated on, with the same encouraging results obtained by others (Taarnhoj, Love, Norlen) employing different procedures. Although the author does not intend to give any explanation on pathogenesis of trigeminalgia he feels that the compression of the trigeminal roots inside the cavum Meckelli invoked by Taarnhoj as the mechanism of trigeminal neuralgia has lost its support.