Etiology Of Trigeminal Neuralgia Research Articles

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

Trigeminal neuralgia (TN) is an excruciating neurological disorder characterized by intense, stimulus-induced, and transient facial stabbing pain. The classification of TN has changed as a result of new discoveries in the last decade regarding its symptomatology, pathogenesis, and management. Because different types of facial pain have different clinical therapy and neuroimaging interpretations, a precise diagnosis is essential. Diagnosis should include magnetic resonance imaging with specific sequences to rule out secondary causes and to identify possible neurovascular contact. The purpose of demonstrating a neurovascular contact is to aid in surgical decision making, not to validate a diagnosis. Microvascular decompression is the first-line procedure for individuals who do not respond to medical management, whereas carbamazepine and oxcarbazepine are the preferred medications for long-term care. New developments in animal models and neuroimaging methods will shed more light on the biology and etiology of TN. This paper reviews the pathogenesis, the clinical features, the diagnosis, and the management of TN. Furthermore, the potential role of low-intensity pulsed ultrasound in neurological disorders is discussed.

Clinical Management and Outcomes of Primary Trigeminal Neuralgia in 75-year-old Male Patient: A Case Study

Abstract Trigeminal neuralgia (TN) is a rare neurological condition, with an annual incidence estimated at approximately 4–5 cases per 100,000 people. It predominantly affects individuals over the age of 50 years and is more common in women. The etiology of TN often involves compression of the trigeminal nerve by adjacent blood vessels, leading to demyelination and hyperactivity of nerve fibers. This vascular compression is associated with classical TN, which accounts for about 90% of cases. Secondary TN, on the other hand, is linked to identifiable conditions such as multiple sclerosis or tumors that impact the nerve, presenting more often in younger patients. This case report discusses a 75-year-old male patient who presented with episodic pain localized to the left maxillary branch (V2) of the trigeminal nerve. The pain was provoked by daily activities such as face washing and did not respond to nonspecific treatments. Following clinical evaluation and a brain magnetic resonance imaging that excluded secondary causes, a primary TN diagnosis was confirmed. The patient was treated with carbamazepine, starting at 200 mg BID, with titration leading to sustained relief of symptoms over subsequent months. This highlights the efficacy of appropriate pharmacological management.

Multimodality Treatment of Trigeminal Neuralgia: An Institutional Experience.

Object Trigeminal neuralgia (TN) consists of excruciating paroxysmal pain, which lasts for seconds to minutes, in the distribution of fifth cranial nerve. TN is not life-threatening, but life became miserable because of high intensity of pain. This study aimed to assess the overall success rates of different treatments, considering pain relief, recurrence rates, and potential side effects. Material and Methods A total of 203 patients of TN treated in the period of last 10 years, that is, 2013 to 2022, were included. Medial management was in 103, radiofrequency ablation in 17, neurectomy in 9, tumor excision in 6, and microvascular decompression (MVD) was done in 68 patients. Magnetic resonance imaging brain with fast imaging employing steady-state acquisition was the basic investigation to decide the etiology of disease. Results Preliminary findings from our institutional experience indicate that a multidisciplinary approach, combining medical, surgical, and noninvasive treatments, yielded the most favorable results in managing TN. The majority of patients achieved significant pain reduction and improved quality of life with these selected therapies. However, certain subgroups of patients exhibited a higher propensity for treatment resistance, necessitating further investigation into personalized treatment strategies. Conclusion Our study concludes that there is no definitive treatment modality (either medical or surgical) available for patients with TN. As the etiology of TN is varied, management of TN also varied, that is, multidisciplinary approach. Every type of treatment has pros and cons but when the cause of TN is vascular compression and patient's general condition permits for surgery, in such cases MVD should be preferred over the ablative procedures.

Peculiarities of diagnosis and treatment methods for tripendic neuralgia

The article describes the features of diagnosis and methods of treatment of trigeminal neuralgia. The etiology of trigeminal neuralgia has not yet been established. Currently, the point of view is generally accepted about the decisive role in the origin of TN, compression of the fifth nerve root at the site of its exit to the brain post by a pathologically

A study to evaluate neurovascular conflict of trigeminal nerve in trigeminal neuralgia patients with the help of 1.5\xa0T MR imaging

IntroductionTrigeminal neuralgia is a neuropathic pain that occurs in the sensory supply region of the trigeminal nerve (V cranial nerve). The common etiology of trigeminal neuralgia is said to be vascular compression on the trigeminal nerve root. In our day-to-day practice, we see many asymptomatic patients having vascular loops around the trigeminal nerve root. We undertook this study to see the significance of nerve root compression by the vascular loop as a cause for trigeminal neuralgia.Materials and methodsA total of 67 classical trigeminal neuralgia patients with NVC involving the trigeminal nerve as diagnosed on MRI brain sequences including FIESTA sequence were included in the study. NVC in all the patients were studied for the side, site of neurovascular contact of cisternal segment of the trigeminal nerve from the brainstem, deviation of nerve at NVC, atrophy of nerve, nature and origin of vascular loop causing NVC and correlated with TGN symptoms.ResultsOut of 67 patients studied, all of them (100%) had NVC on ipsilateral side and 26 patients (34%) had NVC at contralateral trigeminal nerve. Incidence of trigeminal neuralgia was most commonly seen between the 41 and 60 years age (64%) followed by 61–80 years with mean age of 55.6 years. Incidence in females (64%) was found to be more common than in males (35%). NVC was observed at the root entry zone (< 7 mm from brain stem) in 63 trigeminal nerves on symptomatic side and 5 trigeminal nerves on the asymptomatic side. NVC occurring at REZ on symptomatic side was found to be statistically significant with P < 0.001. Mean distance of NVC from brain stem at symptomatic side was 3.4 mm and was 8.4 mm in asymptomatic side NVCs. Atrophy was seen in 8 trigeminal nerves, all on symptomatic side and NVC occurring at root entry zone. No displacement of nerve root at the point of neurovascular contact was observed in our study. Most common vessel causing was found to be ipsilateral superior cerebellar artery followed by the ipsilateral anterior inferior cerebellar artery.ConclusionsNeurovascular contact of trigeminal nerve occurring at the nerve root entry zone has a strong association with ipsilateral trigeminal neuralgia symptoms. In addition, the presence of the trigeminal nerve thinning is also associated with ipsilateral trigeminal neuralgia. With the increase in age, there are higher chances of association of NVC with ipsilateral trigeminal neuralgia symptoms.

Relationship of Inflammation With Trigeminal Neuralgia.

Trigeminal neuralgia (TN) is a common cranial nerve disease. Inflammation is suggested in many recent studies to be involved in neuropathic pain, but its role in TN remains unclear so far. Therefore, the current study aimed to explore the relationship of inflammation with TN. The levels of inflammatory markers, such as white blood cell (WBC), neutrophil (NE), lymphocyte (LY), monocyte (MO), platelet (PLT), and albumin (ALB), as well as the neutrophil/lymphocyte ratio (NLR), derived NLR (dNLR), platelet/lymphocyte ratio (PLR), monocyte/lymphocyte ratio (MLR), and prognostic nutritional index (PNI) had been compared between TN patients and healthy controls using nonparametric tests. Moreover, multiple logistic regression models had been employed to assess the associations of inflammatory markers with TN. Besides, the receiver operating characteristic (ROC) curve was plotted to analyze the values of these inflammatory makers, as well as their matched combinations in diagnosing TN. The levels of WBC, NE, MO, NLR, dNLR, and MLR in TN patients were evidently increased combined with those in normal subjects. In addition, multivariate logistic regression models illustrated that inflammation had close correlation with TN. Meanwhile, the area under the curve (AUC) values for NE, NLR, and dNLR, as well as those for the matched combinations of NLR+PLR, NLR+PNI, dNLR+NLR, and dNLR+PLR in TN were >0.7, which might have predictive value for TN compared with those for normal subjects. Findings of this study reveal that inflammation could have played a close and important role in the progression and etiology of TN.

Successful combination therapy with radiofrequency ablation and phenol injection in a young patient with refractory trigeminal neuralgia

Trigeminal neuralgia (TN) is defined as sudden, usually unilateral, severe, brief, stabbing, and recurrent pain in the distribution of one or more branches of the fifth cranial nerve. The pain is generally abrupt, severe, and can pose a significant impact on the quality of life. The etiology of TN is not always clear, and therefore, treatment can be challenging and multimodal. Pharmacotherapy is generally the first-line treatment though unsuccessful in over a third of patients requiring minimally invasive modality. We report the case of a young patient with refractory and debilitating TN with failed four sessions of radiofrequency ablation (RFA) in addition to the regular use of oral medications. Our treatment included simultaneous RFA and phenol injection with complete symptomatic resolution within fortnight after intervention. In conclusion, the treatment of TN poses a clinical challenge. Although RFA or phenol injections are recognized invasive treatment modalities, we have proven that simultaneous use of both therapies at the same time is safe and effective treatment option for refractory TN with failed previous multi-modal therapy.

The expression of voltage-gated sodium channels in trigeminal nerve following chronic constriction injury in rats

Objectives: Despite the etiology of trigeminal neuralgia has been verified by microvascular decompression as vascular compression of the trigeminal root, very few researches concerning its underlying pathogenesis has been reported in the literature. The present study focused on those voltage-gated sodium channels, which are the structural basis for generation of ectopic action potentials. Methods: The trigeminal neuralgia modeling was obtained with infraorbital nerve chronic constriction injury (ION-CCI) in rats. Two weeks postoperatively, the infraorbital nerve (TN), the trigeminal ganglion (TG), and the brain stem (BS) were removed and analyzed with a series of molecular biological techniques. Results: Western blot depicted a significant up-regulation of Nav1.3 in TN and TG but not in BS, while none of the other isoforms (Nav1.6, Nav1.7, Nav1.8, or Nav1.9) presented a statistical change. The Nav1.3 from ION-CCI group was quantified as 2.5-fold and 1.7-fold than that from sham group in TN and TG, respectively (p < .05). Immunocytochemistry showed the Nav1.3-IR from ION-CCI group accounted for 21.2 ± 2.3% versus 6.1 ± 1.2% from sham group in TN, while the Nav1.3-positive neurons from ION-CCI group accounted for 34.1 ± 3.5% versus 11.2 ± 1.8% from sham group in TG. Immunohistochemical labeling showed the Nav1.3 was co-localized with CGRP and IB4 but not with GFAP or NF-200 in TG. Conclusion: ION-CCI may give rise to an up-regulation of Nav1.3 in trigeminal nerve as well as in C-type neurons at the trigeminal ganglion. It implied that the ectopic action potential may generate from both the compressed site of the trigeminal nerve and the ganglion rather than from the trigeminal nuclei.

Prognostic Impact and Post-operative Evaluation of Volumetric Measurement of the Cerebellopontine Cistern in Trigeminal Neuralgia Using 3 Tesla Magnetic Resonance Imaging.

The aim of this study was to evaluate the importance of pre- and post-operative volumetric measurement of the cerebellopontine angle (CPA) using 3 Tesla (3T) magnetic resonance imaging (MRI). Between April 2012 and December 2015, a total of 87 consecutive patients underwent microvascular decompression (MVD) for trigeminal neuralgia (TN), of whom 51 with primary TN caused by arterial compression were enrolled in this study. Bilateral CPA cistern volume was evaluated using 3T MRI before and after surgery; the Cistern Deviation Index was used to represent the degree of deviation of the CPA cistern. The relationships between CPA cistern volume and the etiology of TN were assessed, and post-operative changes in anatomical parameters were examined to determine differences between recurrent and non-recurrent patients with TN. The mean volume of the CPA cistern on the affected side was significantly smaller than the unaffected side (P < 0.001). Five of 51 (10%) patients experienced TN recurrence. The recurrent cases demonstrated significantly lower pre-operative Cistern Deviation Index scores than non-recurrent cases (P = 0.035). On the unaffected side—but not the affected side—post-operative volume reduction was significantly greater in the recurrence group than in the non-recurrence group (P = 0.004). The pre-operative Cistern Deviation Index was a useful parameter to predict the recurrence of TN. In recurrent patients, post-operative inflammatory reaction may extend to not only the operated side but also the healthy side and reduce the volume of the CPA cistern.

Narrow Foramen Ovale and Rotundum: A Role in the Etiology of Trigeminal Neuralgia.

Primary trigeminal neuralgia (TN) may occasionally occur in absence of neurovascular compression. A mechanism other than nerovascular compression may play a role in TN. High-resolution computed tomographies (CTs) of 21 consecutive TN patients without vascular compression during surgery and 30 healthy volunteers were retrospectively performed. Measuring parameters (length, width, and aspect ratio) were obtained in the axial plane for foramen ovale, and in the reconstructed coronal plane for foramen rotundum on both sides in each subject. The right-sided foramen ovale is slightly narrower than the left-sided, but no difference was observed between the sides. No correlation was found between the foramen size and the gender in both groups. The affected side with a narrower ovale foramen (>0.5 mm) and a significantly greater aspect ratio compared with the unaffected side may contribute to TN. Meanwhile, no significant correlation, but more likely a tendency, was found between the right and left sides in size of foramen rotundum (P = 0.09). This study has speculatively suggested that a narrow skull foramen may be etiologically important in a small percentage of TN patients. If recurrent or residual TN was encountered in cases of TN without vascular compression during surgery, high-resolution CT may help to evaluate the anatomical morphology of skull foramen in great detail.

P006 - Association between trigeminal neuralgia and multiple sclerosis: A population-based study

Background Multiple sclerosis (MS) is a chronic neuro-inflammatory disease of central nervous system (CNS) which is characterized by variable evolution and different clinical manifestations. Although pain is one of the most common problems of MS patients, the presence of trigeminal neuralgia (TN) in a patient's life-span is rare. Methods In a retrospective study, we investigated the presence of TN amongst MS patients inspecting total Isfahan multiple sclerosis (TIMs) records which were registered in Isfahan Multiple Sclerosis Society (IMMS) from April 2003 until July 2014. Results We could find 20 cases with diagnosis of both TN and MS, suggesting a significant higher prevalence of TN among MS patients (0.4%) in comparison with general population (0.04%) (P?0.05). Conclusions Our results showed a significant association between these two disorders supporting previous hypothesis based on the role of MS in etiology of TN. Multiple sclerosis (MS) is a chronic neuro-inflammatory disease of central nervous system (CNS) which is characterized by variable evolution and different clinical manifestations. Although pain is one of the most common problems of MS patients, the presence of trigeminal neuralgia (TN) in a patient's life-span is rare. In a retrospective study, we investigated the presence of TN amongst MS patients inspecting total Isfahan multiple sclerosis (TIMs) records which were registered in Isfahan Multiple Sclerosis Society (IMMS) from April 2003 until July 2014. We could find 20 cases with diagnosis of both TN and MS, suggesting a significant higher prevalence of TN among MS patients (0.4%) in comparison with general population (0.04%) (P?0.05). Our results showed a significant association between these two disorders supporting previous hypothesis based on the role of MS in etiology of TN.

Trigeminal neuralgia occurs and recurs in the absence of neurovascular compression

Vascular compression of the trigeminal nerve is the most common factor associated with the etiology of trigeminal neuralgia (TN). Microvascular decompression (MVD) has proven to be the most successful and durable surgical approach for this disorder. However, not all patients with TN manifest unequivocal neurovascular compression (NVC). Furthermore, over time patients with an initially successful MVD manifest a relentless rate of TN recurrence. The authors performed a retrospective review of cases of TN Type 1 (TN1) or Type 2 (TN2) involving patients 18 years or older who underwent evaluation (and surgery when indicated) at Oregon Health & Science University between July 2006 and February 2013. Surgical and imaging findings were correlated. The review identified a total of 257 patients with TN (219 with TN1 and 38 with TN2) who underwent high-resolution MRI and MR angiography with 3D reconstruction of combined images using OsiriX. Imaging data revealed that the occurrence of TN1 and TN2 without NVC was 28.8% and 18.4%, respectively. A subgroup of 184 patients underwent surgical exploration. Imaging findings were highly correlated with surgical findings, with a sensitivity of 96% for TN1 and TN2 and a specificity of 90% for TN1 and 66% for TN2. Magnetic resonance imaging detects NVC with a high degree of sensitivity. However, despite a diagnosis of TN1 or TN2, a significant number of patients have no NVC. Trigeminal neuralgia clearly occurs and recurs in the absence of NVC.

Magnetic resonance imaging criteria in vascular compression syndrome

EnAbstract Objectives The aim of this work is to show the imaging criteria of the offending vessel in neurovascular compression syndrome in the cerebellopontine angle using MRI. This will increase the acceptance of the concept of vascular compression syndrome of the cranial nerves as an etiology of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and some cases of disabling vertigo and tinnitus. Materials and methods Between 1994 and 2008, MRI radiographs of 782 cases of vasculoneural compression were reviewed to analyze the imaging criteria of the offending vascular loop and were correlated with intraoperative vascular decompression findings in various pathologies such as hemifacial spasm, trigeminal neuralgia, glossopharyngeal neuralgia, vertigo, and tinnitus. Results The specificity and high sensitivity of the T2 constructive interference in steady state or fast spin eco sequence MRI allowed us to precisely define the vasculoneural conflict in almost all cases and to highlight certain radiological criteria required for a vasculoneural conflict diagnosis in general. These criteria are mainly the presence of a vascular loop that is perpendicular to the course of the nerve and the presence of distortion of the neural structures. Conclusion MRI in the T2 sequence is the key assessment in neurovascular compression syndrome.

Esmail Jorjani (1042–1137) and His Descriptions of Trigeminal Neuralgia, Hemifacial Spasm, and Bell's Palsy

Esmail Jorjani was a prominent Persian physician of the 11th and 12th centuries. We present Jorjani's descriptions of probable trigeminal neuralgia, hemifacial spasm, and Bell's palsy. Additionally, on the basis of our translations of his original text, we believe that Jorjani may have been the first to implicate an artery-nerve conflict as an etiology of trigeminal neuralgia. This theory, documented in Jorjani's Treasure of the Khawarazm Shah and elaborated on by Dandy and Jannetta, constitutes the basis of a modern surgical approach to trigeminal neuralgia. The authors also describe the life and works of Esmail Jorjani and review his Treasure for its descriptions related to the aforementioned cranial nerve pathologies.

Cranial neuralgias: from physiopathology to pharmacological treatment

Cranial neuralgias are paroxysmal painful disorders of the head characterised by some shared features such as unilaterality of symptoms, transience and recurrence of attacks, superficial and "shock-like" quality of pain and the presence of triggering factors. Although rare, these disorders must be promptly recognised as they harbour a relatively high risk for underlying compressive or inflammatory disease. Nevertheless, misdiagnosis is frequent. Trigeminal and glossopharyngeal neuralgias are sustained in most cases by a neurovascular conflict in the posterior fossa resulting in a hyperexcitability state of the trigeminal circuitry. If the aetiology of trigeminal neuralgia (TN) and other typical neuralgias must be brought back to the peripheral injury, their pathogenesis could involve central allodynic mechanisms, which, in patients with inter-critical pain, also engage the nociceptive neurons at the thalamic-cortical level. Currently available medical treatments for TN and other cranial neuralgias are reviewed.

Neuro-ophthalmic considerations in trigeminal neuralgia and its surgical treatment

In this review, we will briefly discuss the clinical manifestations and etiology of trigeminal neuralgia, outline the neuro-ophthalmic features of trigeminal neuralgia, and detail the neuro-ophthalmic side effects and complications of the surgical treatment of trigeminal neuralgia. There is a variety of surgical treatment modalities available for patients with trigeminal neuralgia intolerable or resistant to medical therapy. Significant ocular and visual morbidity can result from the surgical treatment of trigeminal neuralgia. Percutaneous or open surgical procedures for trigeminal neuralgia can result in corneal anesthesia, neurotrophic keratitis, exposure keratitis, herpetic keratitis, ocular motor cranial neuropathies, and optic neuropathy. Ophthalmologists should be aware of these potential problems because they may need to evaluate and provide care to patients with ocular or visual complaints following surgery for trigeminal neuralgia.

A method for intraoperative microneurographic recording of unitary activity in the trigeminal ganglion of patients with trigeminal neuralgia

The etiology of trigeminal neuralgia appears to be vascular compression of the nerve at the root entry zone. However, the physiologic mechanism of trigeminal neuralgia remains uncertain. To gain insight into the pathophysiology of the disorder, we developed a method for intraoperative microneurographic recordings from the trigeminal ganglion of patients with trigeminal neuralgia. The recordings are performed immediately prior to standard percutaneous trigeminal gangliolysis for pain relief. Spontaneous or evoked single- and multi-unit action potential activity can be recorded and the location of receptive fields determined. The method should facilitate the testing of hypotheses concerning the origin of this unique pain disorder.

Substance P, somatostatin and monoaminergic transmitters in the cerebrospinal fluid of patients with chronic idiopathic trigeminal neuralgia

The etiology of trigeminal neuralgia is unknown, but both peripheral and central causes have been suggested. To investigate the role of central neurochemical mechanisms we measured epinephrine, norepinephrine and their breakdown product, vanilly mandelic acid (VMA), in the cerebrospinal fluid (CSF) of 16 patients (53.3 +/- 8.3 years) suffering from trigeminal neuralgia. As markers for the dopaminergic system, we determined CSF levels of dopamine and its metabolite homovanillic acid (HVA). As a marker for the serotonergic system, we measured CSF levels of serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). In addition, levels of the neuropeptides substance P and somatostatin were determined. The concentration of norepinephrine (P < 0.01), VMA (P < 0.05) and HVA (P < 0.05) were significantly decreased in patients with trigeminal neuralgia and correlated with the duration of the disease and depression scores. 5-HIAA was also significantly decreased (P < 0.05) compared to control patients. Whereas substance P was significantly elevated (P < 0.05), somatostatin was significantly decreased (P < 0.05). Various correlations between the classical neurotransmitters and the neuropeptides could be established. We hypothesize than the sum of complex neurochemical changes plays a role in the etiology of trigeminal neuralgia, which can be separated in local and more central proceedings. The increase in substance P, a major nociceptive neuromodulator, supports the concept of a local neurogenic inflammation, possibly located in the trigeminovascular system. Depending on the duration of the disease and depression, the loss of serotonergic, dopaminergic and noradrenergic innervation seems to reflect more central changes, possibly due to alterations in their antinociceptive descending pathways.

Twenty-five years experience in the treatment of trigeminal neuralgia. Comparison of three different operative procedures in forty-nine patients

A series of 49 patients with trigeminal neuralgia (TN) were treated by three different surgical procedures: (1) peripheral ablative procedures in 10 patients; (2) percutaneous rhizotomy in 17 patients and (3) intracranial rhizotomy (IR) in 22 patients. On the basis of surgical treatment, the concept that neurovascular compression is a mechanical factor in the aetiology of TN was supported in 14 to 18 patients who underwent posterior fossa exploration. The results support the conclusion that retromastoid craniectomy with IR is the procedure of choice for the majority of patients with TN.

Neurovascular compression and trigeminal neuralgia

N eurovascular compression (NVC) seems to play an important role in the genesis of trigeminal neuralgia. In fact, the theme of NVC is played out in a number of other cranial nerve syndromes, most notably hemifacial spasm s and glossopharyngeal neuralgia? That NVC is the cause of trigeminal neuralgia is supported by considerable circumstantial evidence as presented in the focus article. I happen to agree with Dr. Jannetta's hypothesis, and have stated so previously? However, this conclusion is not yet irrefutable. For one thing, weshould not make the mistake of confusing a strong pathologic association with an understanding of the etiology of trigeminal neuralgia. Available contemporary surgical observations certainly support the role for NVC in trigeminal neuralgia. It was, in fact, Gardner and Miklos 7 at the Cleveland Clinic who first conceived and described decompression of the trigeminal nerve for trigeminal neuralgia in 1959. Later, while a resident at UCLA, Dr. Jannetta worked with Rand 11 (personal communication, May 1993), with whom he performed the first microvascular decompression (MVD) for trigeminal neuralgia using a surgical microscope in 1966. A hypothetical mechanism for the pathophysiology of trigeminal neuralgia has recently been reiterated by Fromm. 6 However, until we have a better grasp of the neurophysiology of trigeminal neuralgia, ultimate conclusions regarding the origins of the disorder will remain elusive. Dr. Jannetta has made a major contribution to the management of trigeminal neuralgia and other cranial neuropathies. He was among the first neurosur-