Materiały źródłowe

• #1 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that arise from the craniofacial area. […] One of the most common forms of craniofacial pain is trigeminal neuralgia. Trigeminal neuralgia is characterized by sudden, brief, and excruciating facial pain attacks in one or more of the V branches, leading to a severe reduction in the quality of life of affected patients. […] Classic trigeminal neuralgia is associated with neurovascular compression in the trigeminal root entry zone, which can lead to demyelination and a dysregulation of voltage-gated sodium channel expression in the membrane. These alterations may be responsible for pain attacks in trigeminal neuralgia patients. […] The etiology of TN and the underlying mechanisms of this condition are still poorly understood and based on the etiology, TN is classified into idiopathic TN, classic TN, and secondary TN.

• #2 The Molecular Basis and Pathophysiology of Trigeminal Neuralgia

  https://www.mdpi.com/1422-0067/23/7/3604

  Trigeminal neuralgia (TN) is a complex orofacial pain syndrome characterized by the paroxysmal onset of pain attacks in the trigeminal distribution. The underlying mechanism for this debilitating condition is still not clearly understood. Decades of basic and clinical evidence support the demyelination hypothesis, where demyelination along the trigeminal afferent pathway is a major driver for TN pathogenesis and pathophysiology. […] Compression of the trigeminal nerve is associated with a significant level of myelin erosion and disintegration from inflammation, particularly at the nerve indentation area. This structural abnormality is related to pathologic demyelination and remyelination of the injured nerve, a common feature in humans with peripheral nerve compression and animal models of chronic nerve compression.

• #3 The pathophysiology of trigeminal neuralgia: a molecular review in: Journal of Neurosurgery Volume 139 Issue 5 (2023) Journals

  https://thejns.org/view/journals/j-neurosurg/139/5/article-p1471.xml

  The goal of this study was to provide a comprehensive overview of the current understanding of molecular and genetic mechanisms underlying the pathophysiology of trigeminal neuralgia (TN). […] The current literature does not suggest a conclusive disease mechanism for TN in humans. In addition to neurovascular conflict/compression of the trigeminal nerve, recent studies have indicated that TN may be linked to inflammatory and reactive oxygen species signaling as well. Recent genetic studies in patients with TN have yet to be investigated further in animal models. […] TN traditionally has been attributed to physical compression of the trigeminal nerve from vascular compression or other underlying pathologies. However, recent evidence points to a role of intrinsic cellular pathways in potentially mediating TN.

• #4 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  Classic TN is associated with neurovascular compression (NVC) in the trigeminal root entry zone, which causes nerve root atrophy or displacement. […] According to the International Classification of Headache Disorder-3 Classical TN is caused by NVC, most frequently by the superior cerebellar artery of the trigeminal nerve roots into the pons. This compression usually results in the demyelination of nerve fibers, which then start firing ectopically. […] The ignition hypothesis, proposed by Devor et al., aims to correlate the structural changes with paroxysmal pain attacks, which are characteristic of the condition. It states that after trigeminal root damage, partially damaged neurons trigger a stimulus induced burst of activity, making them hyperexcitable and susceptible to cross excitation as a result from the physical proximity of the neurons to the root compression site.

• #5 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  Classic TN is associated with neurovascular compression (NVC) in the trigeminal root entry zone, which causes nerve root atrophy or displacement. […] According to the International Classification of Headache Disorder-3 Classical TN is caused by NVC, most frequently by the superior cerebellar artery of the trigeminal nerve roots into the pons. This compression usually results in the demyelination of nerve fibers, which then start firing ectopically. […] The ignition hypothesis, proposed by Devor et al., aims to correlate the structural changes with paroxysmal pain attacks, which are characteristic of the condition. It states that after trigeminal root damage, partially damaged neurons trigger a stimulus induced burst of activity, making them hyperexcitable and susceptible to cross excitation as a result from the physical proximity of the neurons to the root compression site.

• #6 Update on neuropathic pain treatment for trigeminal neuralgia | Neurosciences Journal

  https://nsj.org.sa/content/20/2/107

  Trigeminal neuralgia is a syndrome of unilateral, paroxysmal, stabbing facial pain, originating from the trigeminal nerve. […] Most cases are caused by vascular compression of the trigeminal root adjacent to the pons leading to focal demyelination and ephaptic axonal transmission. […] The cause of TN remains unclear. However, most cases are caused by compression of the trigeminal nerve root within a few millimeters of entry into the pons. The nerve impingement is often accompanied by a demyelination of sensory fibres within the nerve root or the root entry zone, or less commonly in the brainstem. Vascular compression by an aberrant loop of an artery or vein accounts for 80-90% of idiopathic TN. […] The IHS divides TN into classic and symptomatic categories based on presumed etiology. Trigeminal neuralgia is termed classic (or idiopathic) when investigation identifies no cause other than a neurovascular compression; and examination shows no clinical evidence of neurological deficit. […] Microvascular decompression (MVD), percutaneous trigeminal rhizotomies, and gamma knife radiosurgery (GKRS) are possibly effective in the treatment of TN.

• #7 Trigeminal neuralgia: pathology and pathogenesis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11701590/

  There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. […] In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. […] Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. […] Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation.

• #8 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  Trigeminal neuralgia (TN) is characterised by recurrent, unilateral, brief (1s2min), very painful, electric shock-like pain episodes in the trigeminal distribution that are abrupt in onset and termination. […] The current pathophysiological hypothesis for classical TN suggests that the pain mechanisms are precipitated by a proximal compression of the trigeminal sensory root near the brainstem (root entry zone) by a blood vessel (artery or vein). The root entry zone is considered a vulnerable area to demyelination, due to transition from the peripheral Schwann cell myelin sheath to central myelin generated by oligodendroglia. The vascular compression may start a process of focal demyelination and remyelination, probably mediated by microvascular ischaemic damages. These changes lower the excitability threshold of affected fibres and promote inappropriate ephaptic propagation towards adjacent fibres. Thus, tactile signals coming from the fast myelinated (A-) fibres can directly activate the slow nociceptive (A-) fibres, resulting in the high-frequency paroxysms that characterise TN.

• #9 Diagnosis and treatment of trigeminal neuralgia: Consensus statement from the Spanish Society of Neurology’s Headache Study Group | Neurología (English Edition)

  https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-diagnosis-treatment-trigeminal-neuralgia-consensus-S2173580823000275

  According to that theory, TN is caused by focal demyelination at the root entry zone (REZ) in the pons. The REZ includes the transition zone (or Obersteiner-Redlich zone), the site where central myelin (synthesised by oligodendrocytes) changes to peripheral myelin (synthesised by Schwann cells). […] Local nerve compression at the transition zone induces focal demyelination of proprioceptive fibres, which transmit tactile stimuli from the skin or mucosa of the face, promoting contact between exposed axons and the unmyelinated axons of the nociceptive fibres. […] This contact causes ephaptic transmission of action potentials between fibres. This cross-membrane transmission, with recruitment of proximal bundles of fibres (firing), between fibres carrying light touch information and those transmitting nociceptive information, may be the reason for which pain attacks are triggered after tactile stimulation of the face.

• #10 Trigeminal neuralgia: pathology and pathogenesis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11701590/

  There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. […] In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. […] Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. […] Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation.

• #11 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  Trigeminal neuralgia (TN) is characterised by recurrent, unilateral, brief (1s2min), very painful, electric shock-like pain episodes in the trigeminal distribution that are abrupt in onset and termination. […] The current pathophysiological hypothesis for classical TN suggests that the pain mechanisms are precipitated by a proximal compression of the trigeminal sensory root near the brainstem (root entry zone) by a blood vessel (artery or vein). The root entry zone is considered a vulnerable area to demyelination, due to transition from the peripheral Schwann cell myelin sheath to central myelin generated by oligodendroglia. The vascular compression may start a process of focal demyelination and remyelination, probably mediated by microvascular ischaemic damages. These changes lower the excitability threshold of affected fibres and promote inappropriate ephaptic propagation towards adjacent fibres. Thus, tactile signals coming from the fast myelinated (A-) fibres can directly activate the slow nociceptive (A-) fibres, resulting in the high-frequency paroxysms that characterise TN.

• #12 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  Trigeminal neuralgia (TN) is characterised by recurrent, unilateral, brief (1s2min), very painful, electric shock-like pain episodes in the trigeminal distribution that are abrupt in onset and termination. […] The current pathophysiological hypothesis for classical TN suggests that the pain mechanisms are precipitated by a proximal compression of the trigeminal sensory root near the brainstem (root entry zone) by a blood vessel (artery or vein). The root entry zone is considered a vulnerable area to demyelination, due to transition from the peripheral Schwann cell myelin sheath to central myelin generated by oligodendroglia. The vascular compression may start a process of focal demyelination and remyelination, probably mediated by microvascular ischaemic damages. These changes lower the excitability threshold of affected fibres and promote inappropriate ephaptic propagation towards adjacent fibres. Thus, tactile signals coming from the fast myelinated (A-) fibres can directly activate the slow nociceptive (A-) fibres, resulting in the high-frequency paroxysms that characterise TN.

• #13 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  Trigeminal neuralgia (TN) is characterised by recurrent, unilateral, brief (1s2min), very painful, electric shock-like pain episodes in the trigeminal distribution that are abrupt in onset and termination. […] The current pathophysiological hypothesis for classical TN suggests that the pain mechanisms are precipitated by a proximal compression of the trigeminal sensory root near the brainstem (root entry zone) by a blood vessel (artery or vein). The root entry zone is considered a vulnerable area to demyelination, due to transition from the peripheral Schwann cell myelin sheath to central myelin generated by oligodendroglia. The vascular compression may start a process of focal demyelination and remyelination, probably mediated by microvascular ischaemic damages. These changes lower the excitability threshold of affected fibres and promote inappropriate ephaptic propagation towards adjacent fibres. Thus, tactile signals coming from the fast myelinated (A-) fibres can directly activate the slow nociceptive (A-) fibres, resulting in the high-frequency paroxysms that characterise TN.

• #14 Diagnosis and treatment of trigeminal neuralgia: Consensus statement from the Spanish Society of Neurology’s Headache Study Group | Neurología (English Edition)

  https://www.elsevier.es/es-revista-neurologia-english-edition–495-articulo-diagnosis-treatment-trigeminal-neuralgia-consensus-S2173580823000275

  According to that theory, TN is caused by focal demyelination at the root entry zone (REZ) in the pons. The REZ includes the transition zone (or Obersteiner-Redlich zone), the site where central myelin (synthesised by oligodendrocytes) changes to peripheral myelin (synthesised by Schwann cells). […] Local nerve compression at the transition zone induces focal demyelination of proprioceptive fibres, which transmit tactile stimuli from the skin or mucosa of the face, promoting contact between exposed axons and the unmyelinated axons of the nociceptive fibres. […] This contact causes ephaptic transmission of action potentials between fibres. This cross-membrane transmission, with recruitment of proximal bundles of fibres (firing), between fibres carrying light touch information and those transmitting nociceptive information, may be the reason for which pain attacks are triggered after tactile stimulation of the face.

• #15 The pathophysiology of trigeminal neuralgia: a molecular review in: Journal of Neurosurgery Volume 139 Issue 5 (2023) Journals

  https://thejns.org/view/journals/j-neurosurg/139/5/article-p1471.xml

  Multiple studies in patients with TN have identified upregulated levels of inflammatory biomarkers in CSF and blood serum, including substance P (SP), calcitonin generelated peptide (CGRP), and vasoactive intestinal peptide (VIP), as well as endogenous regulators of inflammation like tumor necrosis factor (TNF) and inflammatory cytokine interleukin-6 (IL-6). […] Mechanistically, inflammatory mediators have also been shown to regulate expression of channels implicated in noxious signaling, with TNF contributing to an upregulation in noxious mechanosensitive receptors P2X purinoceptor 3 (P2X3) and P2X purinoceptor 4 (P2X4) in TG neurons, among others.

• #16 The pathophysiology of trigeminal neuralgia: a molecular review in: Journal of Neurosurgery Volume 139 Issue 5 (2023) Journals

  https://thejns.org/view/journals/j-neurosurg/139/5/article-p1471.xml

  Multiple studies in patients with TN have identified upregulated levels of inflammatory biomarkers in CSF and blood serum, including substance P (SP), calcitonin generelated peptide (CGRP), and vasoactive intestinal peptide (VIP), as well as endogenous regulators of inflammation like tumor necrosis factor (TNF) and inflammatory cytokine interleukin-6 (IL-6). […] Mechanistically, inflammatory mediators have also been shown to regulate expression of channels implicated in noxious signaling, with TNF contributing to an upregulation in noxious mechanosensitive receptors P2X purinoceptor 3 (P2X3) and P2X purinoceptor 4 (P2X4) in TG neurons, among others.

• #17 The pathophysiology of trigeminal neuralgia: a molecular review in: Journal of Neurosurgery Volume 139 Issue 5 (2023) Journals

  https://thejns.org/view/journals/j-neurosurg/139/5/article-p1471.xml

  Molecular investigations have identified potential abnormalities in the expressivity or function of cation channels as being associated with TN and other pain syndromes. […] A genetic study in patients with familial TN revealed mutations in ionotropic channels, including genes for transient receptor potential (TRP) channels, voltage-gated potassium channels, and voltage-gated calcium channels. […] Elevated ROS levels have been observed in chronic neuropathic pain syndromes such as diabetic neuropathy, chemotherapy-associated neuropathy, spinal cord injury, and, recently, TN. […] These studies indicate that TRPA1 may be a potential therapeutic agent for TN by targeting aberrant oxidative stress signaling. […] Orofacial pain in TN may also be affected by inflammatory signaling pathways.

• #18 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  There is accumulating evidence that voltage-gated sodium channels (VGSCs) play a crucial role in the generation of ectopic activity in trigeminal afferents. […] Several preclinical studies using a model of TN by constriction of the infraorbital nerve already demonstrated a dysregulation in VGSCs, which includes an upregulation of Nav1.3 and a downregulation of Nav1.7. […] These findings are in accordance with clinical studies which have shown that patients with TN present the same profile of dysregulation in VGSCs. […] Thus, VGSCs have been considered the main target for pain control in TN.

• #19 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  There is accumulating evidence that voltage-gated sodium channels (VGSCs) play a crucial role in the generation of ectopic activity in trigeminal afferents. […] Several preclinical studies using a model of TN by constriction of the infraorbital nerve already demonstrated a dysregulation in VGSCs, which includes an upregulation of Nav1.3 and a downregulation of Nav1.7. […] These findings are in accordance with clinical studies which have shown that patients with TN present the same profile of dysregulation in VGSCs. […] Thus, VGSCs have been considered the main target for pain control in TN.

• #20 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  There is accumulating evidence that voltage-gated sodium channels (VGSCs) play a crucial role in the generation of ectopic activity in trigeminal afferents. […] Several preclinical studies using a model of TN by constriction of the infraorbital nerve already demonstrated a dysregulation in VGSCs, which includes an upregulation of Nav1.3 and a downregulation of Nav1.7. […] These findings are in accordance with clinical studies which have shown that patients with TN present the same profile of dysregulation in VGSCs. […] Thus, VGSCs have been considered the main target for pain control in TN.

• #21 The pathophysiology of trigeminal neuralgia: a molecular review in: Journal of Neurosurgery Volume 139 Issue 5 (2023) Journals

  https://thejns.org/view/journals/j-neurosurg/139/5/article-p1471.xml

  Molecular investigations have identified potential abnormalities in the expressivity or function of cation channels as being associated with TN and other pain syndromes. […] A genetic study in patients with familial TN revealed mutations in ionotropic channels, including genes for transient receptor potential (TRP) channels, voltage-gated potassium channels, and voltage-gated calcium channels. […] Elevated ROS levels have been observed in chronic neuropathic pain syndromes such as diabetic neuropathy, chemotherapy-associated neuropathy, spinal cord injury, and, recently, TN. […] These studies indicate that TRPA1 may be a potential therapeutic agent for TN by targeting aberrant oxidative stress signaling. […] Orofacial pain in TN may also be affected by inflammatory signaling pathways.

• #22 A Novel Pathophysiological Mechanism Contributing to Trigeminal Neuralgia | Molecular Medicine | Full Text

  https://molmed.biomedcentral.com/articles/10.2119/molmed.2016.00172

  Trigeminal neuralgia (TN) is a form of neuropathic pain that affects the fifth cranial nerve, the most widely distributed nerve in the head. […] This compression causes progressive demyelination of the nerve and subsequent aberrant neural transmission. […] Very recently the substitution of methionine 136 by valine (MET126Val) in sodium channel Nav1.6 in a case study of typical TN has suggested a new possible mechanism for TN. […] Among several pathophysiological mechanisms, several lines of evidence have contributed to promoting the role of vascular compression in the posterior fossa as a causative factor of TN. […] Currently, we know that patients with trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia and other cranial nerve dysfunction syndromes may have blood vessels close to the respective cranial nerves, and that separating the blood vessel from the nerve by interposing a soft implant between them (microvascular decompression) may be curative.

• #23 Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6985973/

  Classic TN is associated with neurovascular compression (NVC) in the trigeminal root entry zone, which causes nerve root atrophy or displacement. […] According to the International Classification of Headache Disorder-3 Classical TN is caused by NVC, most frequently by the superior cerebellar artery of the trigeminal nerve roots into the pons. This compression usually results in the demyelination of nerve fibers, which then start firing ectopically. […] The ignition hypothesis, proposed by Devor et al., aims to correlate the structural changes with paroxysmal pain attacks, which are characteristic of the condition. It states that after trigeminal root damage, partially damaged neurons trigger a stimulus induced burst of activity, making them hyperexcitable and susceptible to cross excitation as a result from the physical proximity of the neurons to the root compression site.

• #24 Mechanism of trigeminal neuralgia: an ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery in: Journal of Neurosurgery Volume 96 Issue 3 (2002) Journals

  https://thejns.org/view/journals/j-neurosurg/96/3/article-p532.xml

  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). […] 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. […] 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.

• #25 Mechanism of trigeminal neuralgia: an ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery in: Journal of Neurosurgery Volume 96 Issue 3 (2002) Journals

  https://thejns.org/view/journals/j-neurosurg/96/3/article-p532.xml

  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). […] 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. […] 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.

• #26 Trigeminal neuralgia – Wikipedia

  https://en.wikipedia.org/wiki/Trigeminal_neuralgia

  The exact cause is unknown, but believed to involve loss of the myelin of the trigeminal nerve. […] This might occur due to nerve compression from a blood vessel as the nerve exits the brain stem, multiple sclerosis, stroke, or trauma. Less common causes include a tumor or arteriovenous malformation. […] It is, therefore widely accepted that trigeminal neuralgia is associated with demyelination of axons in the Gasserian ganglion, the dorsal root, or both. […] It has been suggested that this compression may be related to an aberrant branch of the superior cerebellar artery that lies on the trigeminal nerve. […] Further causes, besides an aneurysm, multiple sclerosis or cerebellopontine angle tumor, include: a posterior fossa tumor, any other expanding lesion or even brainstem diseases from strokes. […] Trigeminal neuralgia is found in 34% of people with multiple sclerosis, according to data from seven studies. […] It has been theorized that this is due to damage to the spinal trigeminal complex.

• #27 Trigeminal neuralgia secondary to multiple sclerosis: from the clinical picture to the treatment options | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-0969-0

  The role of the pontine demyelinating plaque is also supported by functional neuroimaging studies showing that tensor imaging abnormalities in patients with classical and idiopathic TN are located in the cisternal and REZ segments of the trigeminal nerve, whereas in patients with TN secondary to MS the abnormalities are located in the pontine tract of the trigeminal nerve. […] A prospective clinical and neuroimaging study in patients with MS revealed a significant association between neurovascular compression and TN secondary to MS, thus suggesting that a pontine plaque affecting the intra-axial primary afferents and neurovascular compression in concert might cause TN secondary to MS through a double-crush mechanism, involving inflammatory demyelination and mechanical demyelination, of the same first-order neurons.

• #28 Trigeminal neuralgia | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/trigeminal-neuralgia?lang=us

  Multiple sclerosis may also cause trigeminal neuralgia and, indeed, its incidence is much higher in multiple sclerosis patients than in the general population. It is thought that both pontine plaques and neurovascular compression in combination produce a „double-crush” mechanism whereby intra-pontine inflammatory demyelination and cisternal mechanical demyelination affect the same first-order neurons.

• #29 Trigeminal neuralgia secondary to multiple sclerosis: from the clinical picture to the treatment options | The Journal of Headache and Pain | Full Text

  https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-019-0969-0

  The role of the pontine demyelinating plaque is also supported by functional neuroimaging studies showing that tensor imaging abnormalities in patients with classical and idiopathic TN are located in the cisternal and REZ segments of the trigeminal nerve, whereas in patients with TN secondary to MS the abnormalities are located in the pontine tract of the trigeminal nerve. […] A prospective clinical and neuroimaging study in patients with MS revealed a significant association between neurovascular compression and TN secondary to MS, thus suggesting that a pontine plaque affecting the intra-axial primary afferents and neurovascular compression in concert might cause TN secondary to MS through a double-crush mechanism, involving inflammatory demyelination and mechanical demyelination, of the same first-order neurons.

• #30 The Molecular Basis and Pathophysiology of Trigeminal Neuralgia

  https://www.mdpi.com/1422-0067/23/7/3604

  Dysregulation of voltage-gated sodium (Nav) channels is functionally linked to TN. Both preclinical animal models of classical TN and biopsies from TN patients showed a significant upregulation of Nav1.3. […] The channelopathies and pathologic changes in the architectures of afferent neurons subsequently result in functional hyperexcitability of the trigeminal nerve observed in TN. Indeed, recording of trigeminal nerve roots in models of classical TN demonstrated ectopic generations of action potentials and prolonged after-discharges in demyelinated neurons. […] Although neurovascular compression accounts for most TN cases, primary demyelination disorders, such as multiple sclerosis, can also lead to TN symptoms. […] Central sensitization is a process through which the nociceptive system becomes hyperexcitable or a state of hyperexcitability, and it has been implicated in various chronic pain conditions.

• #31 The Molecular Basis and Pathophysiology of Trigeminal Neuralgia

  https://www.mdpi.com/1422-0067/23/7/3604

  Dysregulation of voltage-gated sodium (Nav) channels is functionally linked to TN. Both preclinical animal models of classical TN and biopsies from TN patients showed a significant upregulation of Nav1.3. […] The channelopathies and pathologic changes in the architectures of afferent neurons subsequently result in functional hyperexcitability of the trigeminal nerve observed in TN. Indeed, recording of trigeminal nerve roots in models of classical TN demonstrated ectopic generations of action potentials and prolonged after-discharges in demyelinated neurons. […] Although neurovascular compression accounts for most TN cases, primary demyelination disorders, such as multiple sclerosis, can also lead to TN symptoms. […] Central sensitization is a process through which the nociceptive system becomes hyperexcitable or a state of hyperexcitability, and it has been implicated in various chronic pain conditions.

• #32 SciELO Brazil – Trigeminal neuralgia: peripheral and central mechanisms Trigeminal neuralgia: peripheral and central mechanisms

  https://www.scielo.br/j/rdor/a/7jSLzbvTP77pTXXQrLKCPfR/?lang=en

  Central sensitization is the pathological and increased activation of central primary nociceptive neurons, anatomic reorganization (neuroplasticity), changes in electrophysiological properties with development of hyperexcitability and modifications in pain modulation controls. […] Neuronal hyperexcitability is a response to the remodeling of some transmembrane ion channels involved in the beginning of action potentials generation, such as sodium channels. […] Changes in channels density increase the period of neuronal depolarization and repetitive discharge and start central sensitization by several mechanisms, among them Nmethyl-D-Aspartate receptors (NMDA), c-fos expression and transcription of genes coding dynorphin and encephalin, with consequent functional cell changes. […] Different mechanisms are involved with neuropathic pain installation and maintenance, both at peripheral and central levels. Specific mechanisms underlying TN are not totally explained, in spite of simultaneously and interdependently acting in different types of neuropathic pain.

• #33 SciELO Brazil – Trigeminal neuralgia: peripheral and central mechanisms Trigeminal neuralgia: peripheral and central mechanisms

  https://www.scielo.br/j/rdor/a/7jSLzbvTP77pTXXQrLKCPfR/?lang=en

  Central sensitization is the pathological and increased activation of central primary nociceptive neurons, anatomic reorganization (neuroplasticity), changes in electrophysiological properties with development of hyperexcitability and modifications in pain modulation controls. […] Neuronal hyperexcitability is a response to the remodeling of some transmembrane ion channels involved in the beginning of action potentials generation, such as sodium channels. […] Changes in channels density increase the period of neuronal depolarization and repetitive discharge and start central sensitization by several mechanisms, among them Nmethyl-D-Aspartate receptors (NMDA), c-fos expression and transcription of genes coding dynorphin and encephalin, with consequent functional cell changes. […] Different mechanisms are involved with neuropathic pain installation and maintenance, both at peripheral and central levels. Specific mechanisms underlying TN are not totally explained, in spite of simultaneously and interdependently acting in different types of neuropathic pain.

• #34 SciELO Brazil – Trigeminal neuralgia: peripheral and central mechanisms Trigeminal neuralgia: peripheral and central mechanisms

  https://www.scielo.br/j/rdor/a/7jSLzbvTP77pTXXQrLKCPfR/

  Several factors contribute for the establishment of neuropathic pain without a specific etiology. TN pathophysiology involves different neurophysiologic mechanisms, both in peripheral and central nervous systems, such as activation of receptors, transmission and projection of nociceptive information and convergence of nociceptive afferents to central neurons, in addition to interactions between neurotransmitters and neuromodulators. […] Nervous and tissue injury caused by these processes leads to release of mediators which sensitize peripheral nervous terminations (peripheral sensitization), leading to neurochemical and phenotypic changes and increased excitability of trigeminal ganglion afferent neurons and trigeminal nuclei (central sensitization). […] Central sensitization is the pathological and increased activation of central primary nociceptive neurons, anatomic reorganization (neuroplasticity), changes in electrophysiological properties with development of hyperexcitability and modifications in pain modulation controls.

• #35 SciELO Brazil – Trigeminal neuralgia: peripheral and central mechanisms Trigeminal neuralgia: peripheral and central mechanisms

  https://www.scielo.br/j/rdor/a/7jSLzbvTP77pTXXQrLKCPfR/?lang=en

  Central sensitization is the pathological and increased activation of central primary nociceptive neurons, anatomic reorganization (neuroplasticity), changes in electrophysiological properties with development of hyperexcitability and modifications in pain modulation controls. […] Neuronal hyperexcitability is a response to the remodeling of some transmembrane ion channels involved in the beginning of action potentials generation, such as sodium channels. […] Changes in channels density increase the period of neuronal depolarization and repetitive discharge and start central sensitization by several mechanisms, among them Nmethyl-D-Aspartate receptors (NMDA), c-fos expression and transcription of genes coding dynorphin and encephalin, with consequent functional cell changes. […] Different mechanisms are involved with neuropathic pain installation and maintenance, both at peripheral and central levels. Specific mechanisms underlying TN are not totally explained, in spite of simultaneously and interdependently acting in different types of neuropathic pain.

• #36 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #37 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #38 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #39 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #40 Using gabapentin to treat trigeminal neuralgia | NDT

  https://www.dovepress.com/considerations-when-using-gabapentinoids-to-treat-trigeminal-neuralgia-peer-reviewed-fulltext-article-NDT

  Recent neurophysiological and neuroimaging studies supported the hypothesis that small fibre axonal loss, a direct consequence of neurovascular compression, may underly the pathophysiological mechanism of concomitant continuous pain. […] When the unmyelinated axonal loss reaches a threshold level, continuous pain can be triggered through a central mechanism of denervation supersensitivity. […] Concomitant continuous pain could therefore arise from an abnormal spontaneous activity of denervated second-order trigeminal neurons. […] Although first-line treatment with voltage-gated sodium channel blockers is highly effective in TN, some issues including the poor tolerability profile and the possible loss of efficacy in patients with concomitant continuous pain suggest the opportunity to test additional class of drugs. […] 2 ligands, despite the lower efficacy for treatment of paroxysmal pain in comparison with carbamazepine and oxcarbazepine, offers a favorable tolerability profile and may specifically act on continuous pain component.

• #41 Using gabapentin to treat trigeminal neuralgia | NDT

  https://www.dovepress.com/considerations-when-using-gabapentinoids-to-treat-trigeminal-neuralgia-peer-reviewed-fulltext-article-NDT

  Recent neurophysiological and neuroimaging studies supported the hypothesis that small fibre axonal loss, a direct consequence of neurovascular compression, may underly the pathophysiological mechanism of concomitant continuous pain. […] When the unmyelinated axonal loss reaches a threshold level, continuous pain can be triggered through a central mechanism of denervation supersensitivity. […] Concomitant continuous pain could therefore arise from an abnormal spontaneous activity of denervated second-order trigeminal neurons. […] Although first-line treatment with voltage-gated sodium channel blockers is highly effective in TN, some issues including the poor tolerability profile and the possible loss of efficacy in patients with concomitant continuous pain suggest the opportunity to test additional class of drugs. […] 2 ligands, despite the lower efficacy for treatment of paroxysmal pain in comparison with carbamazepine and oxcarbazepine, offers a favorable tolerability profile and may specifically act on continuous pain component.

• #42 Trigeminal neuralgia: pathology and pathogenesis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11701590/

  Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. […] The role of remyelination in initial symptomatic recovery after decompression is unclear. […] However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. […] Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.

• #43 Trigeminal neuralgia: pathology and pathogenesis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11701590/

  Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. […] The role of remyelination in initial symptomatic recovery after decompression is unclear. […] However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. […] Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.

• #44 Trigeminal neuralgia: pathology and pathogenesis – PubMed

  https://pubmed.ncbi.nlm.nih.gov/11701590/

  Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. […] The role of remyelination in initial symptomatic recovery after decompression is unclear. […] However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. […] Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.

• #45 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  A review of the literature on the symptomatology of TN, regardless of its etiology—be it classical, idiopathic, or secondary—highlights a convergence of evidence pointing to neural pathology at the root entry zone, primarily due to its compression by a blood vessel or a tumor. […] This region is anatomically distinct because of the transition from peripheral Schwann cell myelination to central oligodendroglia myelination, which is thought to make it particularly vulnerable to compression. […] Such demyelinated afferents are known to become hyperexcitable, a phenomenon that leads to the generation of ectopic impulses and manifests as spontaneous pain. […] Furthermore, it has been hypothesized that ephaptic connections between demyelinated Aβ and Aδ fibers may be responsible for touch-evoked pain, with the intense near-explosive characteristic pain possibly resulting from trigeminal ganglion cell somata developing touch-evoked prolonged discharges that propagate from cell to cell.

• #46 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  A review of the literature on the symptomatology of TN, regardless of its etiology—be it classical, idiopathic, or secondary—highlights a convergence of evidence pointing to neural pathology at the root entry zone, primarily due to its compression by a blood vessel or a tumor. […] This region is anatomically distinct because of the transition from peripheral Schwann cell myelination to central oligodendroglia myelination, which is thought to make it particularly vulnerable to compression. […] Such demyelinated afferents are known to become hyperexcitable, a phenomenon that leads to the generation of ectopic impulses and manifests as spontaneous pain. […] Furthermore, it has been hypothesized that ephaptic connections between demyelinated Aβ and Aδ fibers may be responsible for touch-evoked pain, with the intense near-explosive characteristic pain possibly resulting from trigeminal ganglion cell somata developing touch-evoked prolonged discharges that propagate from cell to cell.

• #47 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  A review of the literature on the symptomatology of TN, regardless of its etiology—be it classical, idiopathic, or secondary—highlights a convergence of evidence pointing to neural pathology at the root entry zone, primarily due to its compression by a blood vessel or a tumor. […] This region is anatomically distinct because of the transition from peripheral Schwann cell myelination to central oligodendroglia myelination, which is thought to make it particularly vulnerable to compression. […] Such demyelinated afferents are known to become hyperexcitable, a phenomenon that leads to the generation of ectopic impulses and manifests as spontaneous pain. […] Furthermore, it has been hypothesized that ephaptic connections between demyelinated Aβ and Aδ fibers may be responsible for touch-evoked pain, with the intense near-explosive characteristic pain possibly resulting from trigeminal ganglion cell somata developing touch-evoked prolonged discharges that propagate from cell to cell.

• #48 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  A review of the literature on the symptomatology of TN, regardless of its etiology—be it classical, idiopathic, or secondary—highlights a convergence of evidence pointing to neural pathology at the root entry zone, primarily due to its compression by a blood vessel or a tumor. […] This region is anatomically distinct because of the transition from peripheral Schwann cell myelination to central oligodendroglia myelination, which is thought to make it particularly vulnerable to compression. […] Such demyelinated afferents are known to become hyperexcitable, a phenomenon that leads to the generation of ectopic impulses and manifests as spontaneous pain. […] Furthermore, it has been hypothesized that ephaptic connections between demyelinated Aβ and Aδ fibers may be responsible for touch-evoked pain, with the intense near-explosive characteristic pain possibly resulting from trigeminal ganglion cell somata developing touch-evoked prolonged discharges that propagate from cell to cell.

• #49 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  Support for the causative role of neurovascular compression at the root entry zone in TN comes from neurophysiological studies using scalp far-field evoked potentials and quantitative sensory testing (QST), both of which have shown normalization after microvascular decompression. […] In idiopathic trigeminal neuralgia, suspected pathologies range from neuronal voltage-gated ion channel mutations leading to a gain of function to non-specific inflammation and non-multiple sclerosis brainstem lesions. […] Taken together, it is clear that the neuropathological features of TN, from the susceptibility of the root entry zone to neurovascular compression to genetic predisposition and central nervous system (CNS) involvement, paint a complex picture of this condition. […] The interplay of peripheral and central mechanisms, in addition to genetic factors, underscores the multifaceted nature of TN and requires a holistic approach to both research and treatment strategies to better understand and manage this debilitating condition.

• #50 Familial classic trigeminal neuralgia | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-avance-resumen-familial-classic-trigeminal-neuralgia-S2173580818301792

  Despite the limited understanding of familial classic trigeminal neuralgia (FCTN), it may account for 2% of cases; the literature includes reports of an autosomal dominant inheritance pattern. Aetiology includes various genetic factors, such as the inheritance of a disorder related to neuronal membrane instability, morphological anomalies of the base of the cranium, or a predisposition to developing premature atherosclerosis. […] Savica et al. proposed an inherited mutation affecting the calcium channels as a possible aetiology. Furthermore, anomalies of genetic origin at the base of the cranium have been described as a factor possibly favouring neurovascular compression. […] Familial arterial hypertension is another possible cause of the formation of tortuous vessels as the aetiology of FCTN; in fact, this possible association was observed in family 5 of our series. […] Whatever the cause of trigeminal compression, recurrence following transient improvement after decompression suggests that the vascular origin is only one of the factors involved.

• #51 Trigeminal Neuralgia | PM&R KnowledgeNow

  https://now.aapmr.org/trigeminal-neuralgia/

  Classical trigeminal neuralgia is typically caused by neurovascular compression near the brainstem, which leads to focal demyelination and ephaptic crosstalk between adjacent nerve fibers. Recent research also highlights the role of microvascular ischemic changes that further lower the excitatory threshold of affected fibers, contributing to the high-frequency discharges characteristic of TN. […] Additionally, Schwann cell activation has been identified as a key process in nerve repair, with two signaling pathways NGF-trkA and BDNF-trkB potentially playing a role in promoting myelin repair following nerve injury. […] Secondary trigeminal neuralgia (STN) is caused by a structural lesion other than vascular compression such as from tumors (either benign or malignant), multiple sclerosis, or arteriovenous malformations.

• #52 Neurofunction

  https://www.e-neurofunction.org/m/journal/view.php?number=322

  Multiple sclerosis (MS), arteriovenous malformation or saccular aneurysm, epidermoid cyst, acoustic neuroma and meningioma are some of the other reasons that can cause secondary TN. […] In TN, structural abnormalities are linked to pathologic demyelination and remyelination of the wounded nerve, which is a common feature in both humans and animal models of chronic nerve compression. […] With trigeminal nerve compression, there is evidence of axonal degeneration and Schwann cell injury. […] Schwann cells undergo significant apoptosis and persistent downregulation of myelin-associated glycoprotein resulting from chronic nerve compression injury, and given Schwann cells ability to inhibit axonal growth via myelin-associated glycoprotein expression, loss of this intrinsic growth regulation could result in the axonal sprouting seen in classic TN.

• #53 Neurofunction

  https://www.e-neurofunction.org/m/journal/view.php?number=322

  Although neurovascular compression is the most common cause of TN, it can also be caused by primary demyelination disorders. […] Lesions in second-order sensory neurons in the brainstem ipsilateral to the afflicted side were found in a group of individuals with comorbid TN and MS, which are hypothesized to be responsible for trigeminal pain and other orofacial sensory problems. […] Patients affected with MS or a brainstem infarction have been linked to intrapontine demyelination along the trigeminal afferent and trigeminal nucleus, which are associated with TN symptoms. […] The channelopathies and pathologic changes in the architectures of afferent neurons cause the trigeminal nerve to become functionally hyperexcitable, as seen in TN. […] In fact, recordings of trigeminal nerve roots in traditional TN models revealed ectopic action potential production and extended after-discharges in demyelinated neurons.

• #54 Neurofunction

  https://www.e-neurofunction.org/m/journal/view.php?number=322

  Although neurovascular compression is the most common cause of TN, it can also be caused by primary demyelination disorders. […] Lesions in second-order sensory neurons in the brainstem ipsilateral to the afflicted side were found in a group of individuals with comorbid TN and MS, which are hypothesized to be responsible for trigeminal pain and other orofacial sensory problems. […] Patients affected with MS or a brainstem infarction have been linked to intrapontine demyelination along the trigeminal afferent and trigeminal nucleus, which are associated with TN symptoms. […] The channelopathies and pathologic changes in the architectures of afferent neurons cause the trigeminal nerve to become functionally hyperexcitable, as seen in TN. […] In fact, recordings of trigeminal nerve roots in traditional TN models revealed ectopic action potential production and extended after-discharges in demyelinated neurons.

• #55 Pathogenesis, Diagnosis, and Management of Trigeminal Neuralgia: A Narrative Review

  https://www.mdpi.com/2077-0383/14/2/528

  Support for the causative role of neurovascular compression at the root entry zone in TN comes from neurophysiological studies using scalp far-field evoked potentials and quantitative sensory testing (QST), both of which have shown normalization after microvascular decompression. […] In idiopathic trigeminal neuralgia, suspected pathologies range from neuronal voltage-gated ion channel mutations leading to a gain of function to non-specific inflammation and non-multiple sclerosis brainstem lesions. […] Taken together, it is clear that the neuropathological features of TN, from the susceptibility of the root entry zone to neurovascular compression to genetic predisposition and central nervous system (CNS) involvement, paint a complex picture of this condition. […] The interplay of peripheral and central mechanisms, in addition to genetic factors, underscores the multifaceted nature of TN and requires a holistic approach to both research and treatment strategies to better understand and manage this debilitating condition.

• #56 Neurofunction

  https://www.e-neurofunction.org/m/journal/view.php?number=322

  TN is functionally connected to voltage-gated sodium (Nav) channel dysregulation. […] Nav1.3 was found to be significantly upregulated in both preclinical and clinical cases of TN, whereas, downregulation of Nav1.7 has also been reported. […] Upregulation of additional Nav channels, such as Nav1.1, has also been associated to excitation of the trigeminal nerve in a chronic constricted nerve injury model in rodents. […] In addition, in preclinical models of classical TN, hyperexcitability in trigeminal neurons has been discovered as a result of dysregulation of the resting potential mediated by the voltage-gated potassium channel. […] Along with the voltage-gated channels, painful attacks in TN patients increase activity in areas that are traditionally associated with pain-related sensory processing (trigeminal nuclei, thalamus, and somatosensory cortices). […] Neurovascular compression at the trigeminal nerve root entrance zone corresponds highly with TN symptoms and morphological nerve alterations, such as nerve atrophy, displacement, indentation, or flattening, according to high-resolution pictures.

• #57 Elucidating molecular lipid perturbations in trigeminal neuralgia using cerebrospinal fluid lipidomics | Scientific Reports

  https://www.nature.com/articles/s41598-025-89755-x

  Trigeminal neuralgia (TN) is a neuropathic facial pain disorder characterized by severe stabbing pain along the trigeminal nerve. While its pathogenesis remains unclear, nerve demyelination and inflammation are likely involved. […] These findings highlight considerable CSF lipidome alterations in TN, suggesting roles for nerve demyelination, neuroinflammation, and pain sensitization in its pathogenesis. […] Our lipidomic analysis of CSF in TN patients revealed elevated levels of Cer-NP, PC, LPC, TG, and OxTG, along with reduced stigmasterol hexoside. These findings suggest significant alterations in lipid metabolism associated with TN pathogenesis. […] The increased levels of PCs and LPCs observed in our study suggest alterations in cellular membrane composition and fluidity, potentially linked to nerve injury and inflammation. […] These lipidomic shifts offer insights into the molecular underpinnings of TN, highlighting a potential link between altered lipid metabolism and the disorder’s pathogenesis.

• #58 Elucidating molecular lipid perturbations in trigeminal neuralgia using cerebrospinal fluid lipidomics | Scientific Reports

  https://www.nature.com/articles/s41598-025-89755-x

  Trigeminal neuralgia (TN) is a neuropathic facial pain disorder characterized by severe stabbing pain along the trigeminal nerve. While its pathogenesis remains unclear, nerve demyelination and inflammation are likely involved. […] These findings highlight considerable CSF lipidome alterations in TN, suggesting roles for nerve demyelination, neuroinflammation, and pain sensitization in its pathogenesis. […] Our lipidomic analysis of CSF in TN patients revealed elevated levels of Cer-NP, PC, LPC, TG, and OxTG, along with reduced stigmasterol hexoside. These findings suggest significant alterations in lipid metabolism associated with TN pathogenesis. […] The increased levels of PCs and LPCs observed in our study suggest alterations in cellular membrane composition and fluidity, potentially linked to nerve injury and inflammation. […] These lipidomic shifts offer insights into the molecular underpinnings of TN, highlighting a potential link between altered lipid metabolism and the disorder’s pathogenesis.

• #59 Elucidating molecular lipid perturbations in trigeminal neuralgia using cerebrospinal fluid lipidomics | Scientific Reports

  https://www.nature.com/articles/s41598-025-89755-x

  Trigeminal neuralgia (TN) is a neuropathic facial pain disorder characterized by severe stabbing pain along the trigeminal nerve. While its pathogenesis remains unclear, nerve demyelination and inflammation are likely involved. […] These findings highlight considerable CSF lipidome alterations in TN, suggesting roles for nerve demyelination, neuroinflammation, and pain sensitization in its pathogenesis. […] Our lipidomic analysis of CSF in TN patients revealed elevated levels of Cer-NP, PC, LPC, TG, and OxTG, along with reduced stigmasterol hexoside. These findings suggest significant alterations in lipid metabolism associated with TN pathogenesis. […] The increased levels of PCs and LPCs observed in our study suggest alterations in cellular membrane composition and fluidity, potentially linked to nerve injury and inflammation. […] These lipidomic shifts offer insights into the molecular underpinnings of TN, highlighting a potential link between altered lipid metabolism and the disorder’s pathogenesis.

• #60 Familial classic trigeminal neuralgia | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-avance-resumen-familial-classic-trigeminal-neuralgia-S2173580818301792

  The classic form of trigeminal neuralgia is usually sporadic (no familial clustering). However, around 2% of all cases of trigeminal neuralgia may be familial. […] These family clusters support the hypothesis that classic trigeminal neuralgia may have a genetic origin. Several causes have been suggested, including inherited anatomical changes affecting the base of the skull which would promote compression of the trigeminal nerve by vascular structures, familial AHT (resulting in tortuous vessels that would compress the trigeminal nerve), and mutations in the gene coding for calcium channels leading to hyperexcitability. Classic trigeminal neuralgia may be an autosomal dominant disorder displaying genetic anticipation. […] In terms of pain physiopathology, compression of the trigeminal nerve causes focal demyelination of the nerve, which through axonal apposition generates spontaneous impulses with ephaptic conduction to adjacent fibres.

• #61 Familial classic trigeminal neuralgia | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-avance-resumen-familial-classic-trigeminal-neuralgia-S2173580818301792

  The classic form of trigeminal neuralgia is usually sporadic (no familial clustering). However, around 2% of all cases of trigeminal neuralgia may be familial. […] These family clusters support the hypothesis that classic trigeminal neuralgia may have a genetic origin. Several causes have been suggested, including inherited anatomical changes affecting the base of the skull which would promote compression of the trigeminal nerve by vascular structures, familial AHT (resulting in tortuous vessels that would compress the trigeminal nerve), and mutations in the gene coding for calcium channels leading to hyperexcitability. Classic trigeminal neuralgia may be an autosomal dominant disorder displaying genetic anticipation. […] In terms of pain physiopathology, compression of the trigeminal nerve causes focal demyelination of the nerve, which through axonal apposition generates spontaneous impulses with ephaptic conduction to adjacent fibres.

• #62 Familial classic trigeminal neuralgia | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-avance-resumen-familial-classic-trigeminal-neuralgia-S2173580818301792

  The classic form of trigeminal neuralgia is usually sporadic (no familial clustering). However, around 2% of all cases of trigeminal neuralgia may be familial. […] These family clusters support the hypothesis that classic trigeminal neuralgia may have a genetic origin. Several causes have been suggested, including inherited anatomical changes affecting the base of the skull which would promote compression of the trigeminal nerve by vascular structures, familial AHT (resulting in tortuous vessels that would compress the trigeminal nerve), and mutations in the gene coding for calcium channels leading to hyperexcitability. Classic trigeminal neuralgia may be an autosomal dominant disorder displaying genetic anticipation. […] In terms of pain physiopathology, compression of the trigeminal nerve causes focal demyelination of the nerve, which through axonal apposition generates spontaneous impulses with ephaptic conduction to adjacent fibres.

• #63 Familial classic trigeminal neuralgia | Neurología (English Edition)

  https://www.elsevier.es/en-revista-neurologia-english-edition–495-avance-resumen-familial-classic-trigeminal-neuralgia-S2173580818301792

  Despite the limited understanding of familial classic trigeminal neuralgia (FCTN), it may account for 2% of cases; the literature includes reports of an autosomal dominant inheritance pattern. Aetiology includes various genetic factors, such as the inheritance of a disorder related to neuronal membrane instability, morphological anomalies of the base of the cranium, or a predisposition to developing premature atherosclerosis. […] Savica et al. proposed an inherited mutation affecting the calcium channels as a possible aetiology. Furthermore, anomalies of genetic origin at the base of the cranium have been described as a factor possibly favouring neurovascular compression. […] Familial arterial hypertension is another possible cause of the formation of tortuous vessels as the aetiology of FCTN; in fact, this possible association was observed in family 5 of our series. […] Whatever the cause of trigeminal compression, recurrence following transient improvement after decompression suggests that the vascular origin is only one of the factors involved.

• #64 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #65 Trigeminal neuralgia: a practical guide | Practical Neurology

  https://pn.bmj.com/content/21/5/392

  The remarkable clinical effect of sodium channel blockers in TN has suggested that an abnormal expression of voltage-gated sodium channels could also constitute an important pathophysiological correlate for both classical and idiopathic TN, which might be sodium channelopathies. Nav1.7, Nav1.3 and Nav1.8 were found to be abnormally expressed in TN and possibly responsible for rapid activation and inactivation, as well as maintenance of the action potential. Over time hypersensitivity of tactile A- fibres may lead to sensitisation of second-order wide dynamic range neurones in lamina V of the dorsal horns and the trigeminal nerve nuclei. […] It was previously thought that TN with concomitant continuous pain occurred because of repetitive paroxysmal attacks. However, prospective cross-sectional studies show that the concomitant continuous pain often develops with or even before the onset of the paroxysmal pain. TN with concomitant persistent pain seems more prevalent in women and more often associated with sensory abnormalities than paroxysmal TN. Studies looking for impairment in trigeminal nociception have shown an abnormal nociceptive blink reflex and pain-related evoked potentials, indicating overactivation of central sensory transmission, as a potential mechanism to explain the constant facial pain of TN. Furthermore, an important recently published neuroimaging study using a 3T MR imaging of the trigeminal nerve roots in patients with TN purely paroxysmal and TN with concomitant continuous pain showed that the trigeminal nerve root was more severely atrophic in patients with concomitant continuous pain than in those with purely paroxysmal pain. The authors postulated that continuous pain most likely relates to axonal loss and abnormal activity in denervated trigeminal second-order neurones.

• #66 Using gabapentin to treat trigeminal neuralgia | NDT

  https://www.dovepress.com/considerations-when-using-gabapentinoids-to-treat-trigeminal-neuralgia-peer-reviewed-fulltext-article-NDT

  Recent neurophysiological and neuroimaging studies supported the hypothesis that small fibre axonal loss, a direct consequence of neurovascular compression, may underly the pathophysiological mechanism of concomitant continuous pain. […] When the unmyelinated axonal loss reaches a threshold level, continuous pain can be triggered through a central mechanism of denervation supersensitivity. […] Concomitant continuous pain could therefore arise from an abnormal spontaneous activity of denervated second-order trigeminal neurons. […] Although first-line treatment with voltage-gated sodium channel blockers is highly effective in TN, some issues including the poor tolerability profile and the possible loss of efficacy in patients with concomitant continuous pain suggest the opportunity to test additional class of drugs. […] 2 ligands, despite the lower efficacy for treatment of paroxysmal pain in comparison with carbamazepine and oxcarbazepine, offers a favorable tolerability profile and may specifically act on continuous pain component.

• #67 Using gabapentin to treat trigeminal neuralgia | NDT

  https://www.dovepress.com/considerations-when-using-gabapentinoids-to-treat-trigeminal-neuralgia-peer-reviewed-fulltext-article-NDT

  Recent neurophysiological and neuroimaging studies supported the hypothesis that small fibre axonal loss, a direct consequence of neurovascular compression, may underly the pathophysiological mechanism of concomitant continuous pain. […] When the unmyelinated axonal loss reaches a threshold level, continuous pain can be triggered through a central mechanism of denervation supersensitivity. […] Concomitant continuous pain could therefore arise from an abnormal spontaneous activity of denervated second-order trigeminal neurons. […] Although first-line treatment with voltage-gated sodium channel blockers is highly effective in TN, some issues including the poor tolerability profile and the possible loss of efficacy in patients with concomitant continuous pain suggest the opportunity to test additional class of drugs. […] 2 ligands, despite the lower efficacy for treatment of paroxysmal pain in comparison with carbamazepine and oxcarbazepine, offers a favorable tolerability profile and may specifically act on continuous pain component.

• #68 Percutaneous Procedures for Trigeminal Neuralgia

  https://www.jkns.or.kr/journal/view.php?number=7526

  Anatomical studies have found that the vulnerable area to the compression of vessels is the transition zone in the trigeminal nerve, where myelination changes from Schwann cell to oligodendroglial cell. […] Secondary TN is dependent on the etiology, such as multiple sclerosis plaques affecting the trigeminal root or space-occupying lesions, including tumors, arteriovenous malformations, or aneurysms. […] For surgical treatment microvascular decompression (MVD) is considered the gold standard in the treatment of TN. […] However, percutaneous procedures can be a promising alternative for patients who are unable to undergo a surgery. Various percutaneous treatment techniques for TN have been developed since 1911, when Harris successfully treated TN by percutaneous injection of alcohol into the trigeminal ganglion.

• #69 Percutaneous Procedures for Trigeminal Neuralgia

  https://www.jkns.or.kr/journal/view.php?number=7526

  Anatomical studies have found that the vulnerable area to the compression of vessels is the transition zone in the trigeminal nerve, where myelination changes from Schwann cell to oligodendroglial cell. […] Secondary TN is dependent on the etiology, such as multiple sclerosis plaques affecting the trigeminal root or space-occupying lesions, including tumors, arteriovenous malformations, or aneurysms. […] For surgical treatment microvascular decompression (MVD) is considered the gold standard in the treatment of TN. […] However, percutaneous procedures can be a promising alternative for patients who are unable to undergo a surgery. Various percutaneous treatment techniques for TN have been developed since 1911, when Harris successfully treated TN by percutaneous injection of alcohol into the trigeminal ganglion.

• #70 Percutaneous Procedures for Trigeminal Neuralgia

  https://www.jkns.or.kr/journal/view.php?number=7526

  Percutaneous procedures aim to selectively destroy the afferent A-delta and C pain nerve fibers chemically by glycerol injection, mechanically by balloon compression, or thermally by radiofrequency thermocoagulation, while preserving A-alpha and A-beta sensory nerve fibers. […] The results of percutaneous procedures are not inferior to MVD. In addition, patients preference for a less invasive method can influence the procedure they will undergo. […] RFT can offer immediate pain relief of 90% with a recurrence rate of up to 25%. […] Although the exact mechanism is unknown, it is thought that glycerol injection causes a rapid rate of change in intracellular osmolarity and results in axonal demyelination and fragmentation, which selectively injures large myelinated fibers. […] GR offers an initial pain relief of 90% and pain relief duration of 3 years in almost 50% of the cases.

• #71 Trigeminal Neuralgia | SpringerLink

  https://link.springer.com/chapter/10.1007/978-981-15-1346-6_26

  Compression on the REZ should cause a continuous pain, but TN patients suffer paroxysmal attacks, which are most likely to be caused by spontaneous discharges where the threshold for the repetitive firing has been altered. […] Rappaport and Devor explained that the development of atypical features of the TN may be due to central sensitization following a prolonged barrage of nerve impulses and also from progressive damage to trigeminal afferents, which become the source of continuous ectopic discharges. […] Interestingly, literature shows that different treatments of TN yield similar results in pain control however, the long-term results show that decompression provides prolonged pain relief compared to destructive peripheral procedures.

• #72 Trigeminal Neuralgia | PM&R KnowledgeNow

  https://now.aapmr.org/trigeminal-neuralgia/

  Idiopathic trigeminal neuralgia is when no pathology is identified. […] While known predictors of recurrence include female sex, symptoms lasting more than eight years, venous compression of the trigeminal-root entry zone, recent insights suggest that Schwann cell activation may also influence the long-term progression of TN. These cells play a crucial role in nerve repair, and their activation could help explain variations in disease recurrence and remission periods. […] Voltage gated potassium channel openers are being examined as potential therapeutic agents for TN pain. Preliminary data also suggests that selective sodium channel blockers targeting the Nav1.7 sodium receptor may offer improved efficacy compared to traditional treatments like carbamazepine or oxcarbazepine. Additionally, Schwann cell activation has emerged as a promising therapeutic target in TN. Research has identified two key signaling pathways, NGF-trkA and BDNF-trkB, which are crucial in promoting myelin repair following trigeminal nerve injury. These findings suggest that future therapies aimed at enhancing nerve regeneration through Schwann cell pathways could improve long-term outcomes for patients with TN.

• #73 Trigeminal Neuralgia | PM&R KnowledgeNow

  https://now.aapmr.org/trigeminal-neuralgia/

  Idiopathic trigeminal neuralgia is when no pathology is identified. […] While known predictors of recurrence include female sex, symptoms lasting more than eight years, venous compression of the trigeminal-root entry zone, recent insights suggest that Schwann cell activation may also influence the long-term progression of TN. These cells play a crucial role in nerve repair, and their activation could help explain variations in disease recurrence and remission periods. […] Voltage gated potassium channel openers are being examined as potential therapeutic agents for TN pain. Preliminary data also suggests that selective sodium channel blockers targeting the Nav1.7 sodium receptor may offer improved efficacy compared to traditional treatments like carbamazepine or oxcarbazepine. Additionally, Schwann cell activation has emerged as a promising therapeutic target in TN. Research has identified two key signaling pathways, NGF-trkA and BDNF-trkB, which are crucial in promoting myelin repair following trigeminal nerve injury. These findings suggest that future therapies aimed at enhancing nerve regeneration through Schwann cell pathways could improve long-term outcomes for patients with TN.

• #74 Trigeminal Neuralgia | PM&R KnowledgeNow

  https://now.aapmr.org/trigeminal-neuralgia/

  Idiopathic trigeminal neuralgia is when no pathology is identified. […] While known predictors of recurrence include female sex, symptoms lasting more than eight years, venous compression of the trigeminal-root entry zone, recent insights suggest that Schwann cell activation may also influence the long-term progression of TN. These cells play a crucial role in nerve repair, and their activation could help explain variations in disease recurrence and remission periods. […] Voltage gated potassium channel openers are being examined as potential therapeutic agents for TN pain. Preliminary data also suggests that selective sodium channel blockers targeting the Nav1.7 sodium receptor may offer improved efficacy compared to traditional treatments like carbamazepine or oxcarbazepine. Additionally, Schwann cell activation has emerged as a promising therapeutic target in TN. Research has identified two key signaling pathways, NGF-trkA and BDNF-trkB, which are crucial in promoting myelin repair following trigeminal nerve injury. These findings suggest that future therapies aimed at enhancing nerve regeneration through Schwann cell pathways could improve long-term outcomes for patients with TN.

• #75 Trigeminal neuralgia: approaches and interventions | JPR

  https://www.dovepress.com/trigeminal-neuralgia-current-approaches-and-emerging-interventions-peer-reviewed-fulltext-article-JPR

  Trigeminal neuralgia (TN) has been described in the literature as one of the most debilitating presentations of orofacial pain. […] What is increasingly clear is that there is no catch-all medical or surgical intervention that is effective for all patients with trigeminal neuralgia, likely reflective of the fact that TN is likely a heterogenous group of disorders that jointly manifests in facial pain. […] Ultimately, elucidation of the molecular mechanisms underlying trigeminal neuralgia will pave the way for novel, more effective and less invasive therapies. […] The authors proposed that neurovascular compression, along with a pontine demyelinating plaque in tandem, may play a two-hit mechanism underlying TN pathophysiology in MS patients. […] The fact that a subset of patients with multiple sclerosis uniformly derives less benefit from all medical and surgical interventions implies that neuroinflammation may play a role in disease pathogenesis and severity. […] Further studies will be needed to define the neuronal-glial interface in trigeminal neuralgia, and a more precise mechanistic understanding of TN will hopefully allow for the development of novel and more effective therapeutics.

• #76 Trigeminal neuralgia: approaches and interventions | JPR

  https://www.dovepress.com/trigeminal-neuralgia-current-approaches-and-emerging-interventions-peer-reviewed-fulltext-article-JPR

  Trigeminal neuralgia (TN) has been described in the literature as one of the most debilitating presentations of orofacial pain. […] What is increasingly clear is that there is no catch-all medical or surgical intervention that is effective for all patients with trigeminal neuralgia, likely reflective of the fact that TN is likely a heterogenous group of disorders that jointly manifests in facial pain. […] Ultimately, elucidation of the molecular mechanisms underlying trigeminal neuralgia will pave the way for novel, more effective and less invasive therapies. […] The authors proposed that neurovascular compression, along with a pontine demyelinating plaque in tandem, may play a two-hit mechanism underlying TN pathophysiology in MS patients. […] The fact that a subset of patients with multiple sclerosis uniformly derives less benefit from all medical and surgical interventions implies that neuroinflammation may play a role in disease pathogenesis and severity. […] Further studies will be needed to define the neuronal-glial interface in trigeminal neuralgia, and a more precise mechanistic understanding of TN will hopefully allow for the development of novel and more effective therapeutics.

• #77 Trigeminal neuralgia: approaches and interventions | JPR

  https://www.dovepress.com/trigeminal-neuralgia-current-approaches-and-emerging-interventions-peer-reviewed-fulltext-article-JPR

  Trigeminal neuralgia (TN) has been described in the literature as one of the most debilitating presentations of orofacial pain. […] What is increasingly clear is that there is no catch-all medical or surgical intervention that is effective for all patients with trigeminal neuralgia, likely reflective of the fact that TN is likely a heterogenous group of disorders that jointly manifests in facial pain. […] Ultimately, elucidation of the molecular mechanisms underlying trigeminal neuralgia will pave the way for novel, more effective and less invasive therapies. […] The authors proposed that neurovascular compression, along with a pontine demyelinating plaque in tandem, may play a two-hit mechanism underlying TN pathophysiology in MS patients. […] The fact that a subset of patients with multiple sclerosis uniformly derives less benefit from all medical and surgical interventions implies that neuroinflammation may play a role in disease pathogenesis and severity. […] Further studies will be needed to define the neuronal-glial interface in trigeminal neuralgia, and a more precise mechanistic understanding of TN will hopefully allow for the development of novel and more effective therapeutics.

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