The Challenges in Clinical Diagnosis of Trigeminal Neuralgia: A Review.

The lack of established laboratory tests or biomarkers for trigeminal neuralgia (TN) makes diagnosing this relatively rare condition extremely challenging. Trigeminal nerve compression observable on magnetic resonance imaging may indicate TN, but many patients do not have visible lesions or compression. In particular, TN may be confused with migraine, cluster headache, temporomandibular disorder, and other types of headache. An accurate diagnosis is imperative for proper treatment since these conditions do not respond to the same treatment. Many symptoms of these headaches can be vague or overlap, and clinicians depend in large measure on the subjective reports of their patients. Nevertheless, it is imperative to diagnose TN better, which can cause excruciating pain, reduce the quality of life, and even result in disability. It is possible that TN is underestimated.

Herpes Zoster Ophthalmicus Initially Diagnosed As Cluster Headache, Complicated by Delayed Eruption.

Herpes zoster ophthalmicus (HZO) manifests as a consequence of the reactivation of the Varicella-zoster virus (VZV) and primarily affects the ophthalmic division of the trigeminal nerve. Identification of the vesicular eruption is central to the diagnostic process; however, the delayed manifestation of this cutaneous phenomenon poses a challenge to timely and accurate diagnosis. This report elucidates the case of a 61-year-old Japanese male with painful trigeminal neuropathy attributed to VZV that was initially diagnosed as cluster headache, mainly due to the delayed cutaneous eruption. Contrary to the expected pattern of cluster headache presentations, there was no discernible fluctuation in headache severity. The transient improvement of symptoms following interventions tailored for cluster headache management, including pure oxygen inhalation and subcutaneous sumatriptan injection, inadvertently contributed to a delay in accurate diagnosis. The importance of distinguishing HZO from cluster headache is emphasized, particularly in cases involving elderly patients or those with persistent cephalo-ophthalmalgia without the characteristic fluctuation of symptoms. In cases where clinical suspicion of HZO is raised, cerebrospinal fluid analysis should be performed. This approach is consistent with the overall goal of facilitating a prompt and accurate diagnosis.

[Investigation of Chronic Pain for the Development of Novel Analgesics Focusing on High Mobility Group Box-1].

Neuropathic pain is an infirm type of chronic pain, which results in functional and emotional impairment. There is an urgent need for novel therapeutic approaches because there is lack of effective treatment for neuropathic pain. Posttraumatic trigeminal neuropathy (PTTN), a chronic sensory disorder following trauma, for example, during dental implant surgery or third molar removal, can cause orofacial numbness, paresthesia and pain. Unlike other painful peripheral neuropathies, the chance of developing PTTN is predictable based on preoperative assessment such as X-ray of the trigeminal nerve tract and the surgery site. High mobility group box-1 (HMGB1) acts as damage associated molecular patterns (DAMPs) and contributes to the pathogenesis of neuropathic pain including diabetic and chemotherapy-induced peripheral neuropathy. Recently, we have demonstrated that HMGB1 around injured sciatic nerves is a key molecule triggering the onset of neuropathic pain. We therefore hypothesize that inhibition of HMGB1 could prevent the onset of PTTN. In a mouse PTTN model, pretreatment with anti-HMGB1 neutralizing antibody can attenuate PTTN-induced behavioral painful responses and suppress microglial activation in spinal trigeminal nucleus caudalis. In summary, perioperative inhibition of HMGB1 activity could be used to prevent the onset of PTTN. This review summarizes recent findings regarding the role of HMGB1 in the induction of neuropathic pain and may generate new translational opportunities for pain treatment.

Perineural Treatment with High Mobility Group Box-1 Monoclonal Antibody Prevents Initiation of Pain-Like Behaviors in Female Mice with Trigeminal Neuropathy.

Post-traumatic trigeminal neuropathy (PTTN) is a type of chronic pain caused by damage to the trigeminal nerve. A previous study reported that pretreatment with anti-high mobility group box-1 (HMGB1) neutralizing antibodies (nAb) prevented the onset of PTTN following distal infraorbital nerve chronic constriction injury (dIoN-CCI) in male mice. Clinical evidence indicates a high incidence of PTTN in females. Although our previous study found that perineural HMGB1 is crucial in initiation of PTTN in male mice, it is currently unknown whether HMGB1 is also involved in the pathogenesis of PTTN in female mice. Therefore, in the current study, we examined the effect of anti-HMGB1 nAb on pain-like behavior in female mice following dIoN-CCI surgery. We found that dIoN-CCI surgery enhanced reactivity to mechanical and cold stimuli in female mice, which was suppressed by treatment with anti-HMGB1 nAb. Moreover, the increase in macrophages after dIoN-CCI was significantly attenuated by pretreatment with anti-HMGB1 nAb. Furthermore, anti-HMGB1 nAb treatment inhibited microglial activation in the trigeminal spinal tract nucleus. These data suggest that HMGB1 also plays a crucial role in the onset of PTTN after nerve injury in female mice. Thus, anti-HMGB1 nAb could be a novel therapeutic agent for inhibiting the onset of PTTN in female and male mice.

Accuracy of MR neurography as a diagnostic tool in detecting injuries to the lingual and inferior alveolar nerve in patients with iatrogenic post-traumatic trigeminal neuropathy.

OBJECTIVES: MR neurography has the ability to detect and depict peripheral nerve injuries. This study evaluated the potential of MR neurography in the diagnosis of post-traumatic trigeminal neuropathy. METHODS: Forty-one participants prospectively underwent MR neurography of the lingual and inferior alveolar nerves using a 3D TSE STIR black-blood sequence. Two blinded and independent observers recorded the following information for each nerve of interest: presence of injury, nerve thickness, nerve signal intensity, MR neurography Sunderland class, and signal gap. Afterwards, the apparent nerve-muscle contrast-to-noise ratio and apparent signal-to-noise ratio were calculated. Clinical data (neurosensory testing score and clinical Sunderland class) was extracted retrospectively from the medical records of patients diagnosed with post-traumatic trigeminal neuropathy. RESULTS: Compared to neurosensory testing, MR neurography had a sensitivity of 38.2% and specificity of 93.5% detecting nerve injuries. When differentiated according to clinical Sunderland class, sensitivity was 19.1% in the presence of a low class injury (I to III) and improved to 83.3% in the presence of a high class (IV to V). Specificity remained unchanged. The area under the curve using the apparent nerve-muscle contrast-to-noise ratio, apparent signal-to-noise ratio, and nerve thickness to predict the presence of an injury was 0.78 (p < .05). Signal intensities and nerve diameter increased in injured nerves (p < .05). Clinical and MR neurography Sunderland scores positively correlated (correlation coefficient = 0.53; p = .005). CONCLUSIONS: This study shows that MR neurography can accurately differentiate between injured and healthy nerves, especially in the presence of a more severe nerve injury. CLINICAL RELEVANCE STATEMENT: MR neurography is not only able to detect trigeminal nerve injuries, but it can also provide information about the anatomical specifications of the injury, which is not possible with clinical neurosensory testing. This makes MR neurography an added value in the management of post-traumatic trigeminal neuropathy. KEY POINTS: • The current diagnosis of post-traumatic trigeminal neuropathy is mainly based on clinical examination. • MR neurography is able to visualize and stratify peripheral trigeminal nerve injuries. • MR neurography contributes to the diagnostic process as well as to further decision-making.

New-onset Immune-mediated Necrotizing Myopathy and Trigeminal Neuropathy after SARS-CoV-2 mRNA Vaccination in a Patient with Rheumatoid Arthritis and Sjögren's Syndrome.

We present the case of a 42-year-old woman with rheumatoid arthritis and Sjögren's syndrome treated with adalimumab who developed immune-mediated necrotizing myopathy (IMNM) and trigeminal neuropathy after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mRNA vaccination. Trigeminal neuralgia and elevated serum creatine kinase levels emerged 12 days post-vaccination, followed by myalgia in the femoral muscles. IMNM was histologically diagnosed. The pathogenesis may involve molecular mimicry between the SARS-CoV-2 spike glycoprotein and autologous tissues triggered by vaccination. This case emphasizes the association between SARS-CoV-2 vaccination, tumor necrosis factor inhibitor, IMNM, and trigeminal neuropathy, as well as the importance of monitoring immune-mediated adverse events following SARS-CoV-2 vaccination in patients with autoimmune disease.

Dosimetric investigation of radiation-induced trigeminal nerve toxicity in parotid tumor patients.

PURPOSE: We aimed to describe the association between trigeminal nerve (TN) dose and toxicity and determine a threshold value that leads to TN toxicity in patients with parotid tumors treated with adjuvant conventional fractionated radiation therapy. METHODS AND MATERIALS: Eighteen patients who underwent adjuvant radiotherapy (RT) between 2013 and 2018 were included in this retrospective study. TN and its branches were outlined subsequently on the planning CT scans. The doses received by TN were obtained based on the dose-volume histogram. The dose and toxicity relationship was investigated over the total prescribed dose. RT-related toxicity was graded according to Common Terminology Criteria for Adverse Events V4.0 (CTCAEv4.0). RESULTS: The median follow-up was 29.5 months. After RT, 61% of patients had Grade I-II late TN toxicity divided into Grade I in 4 (22%) and Grade II in 7 (39%) patients. TN injury symptoms were as follows: loss of sensation in the chin area in 3, difficulty in jaw movements in 3, and paresthesia in 5 patients. The total RT dose (p = 0.001), Dmax (p = 0.001), PTV-TN Dmax (p = 0.001), D1cc (p = 0.004), D0.5cc (p = 0.001), and D0.1cc (p = 0.01) had a significant effect on TN toxicity. Cut-off values leading to toxicity were determined as 66, 65.5, 65.25, 63.6, and 62.7 Gy for Dmax, PTV-TN Dmax, D0.1cc, D 0.5cc, and D1cc, respectively. CONCLUSIONS: Radiation-induced TN injury in head and neck cancer patients may further be investigated in clinically prospective trials by virtue of high toxicity rates with current RT doses in our retrospectively designed dosimetric study in parotid tumors.

Trigeminal Schwannoma: A Retrospective Analysis of Endoscopic Endonasal Management, Treatment Outcomes, and Neuropathic Sequelae.

Introduction Trigeminal schwannomas (TS) are rare skull base tumors that have been associated with significant neuropathic sequalae for patients. The authors aim to evaluate the clinical features, treatment outcomes, and neuropathic sequelae following endoscopic endonasal approach (EEA) for TS. Methods The study involves a retrospective review of patients who underwent EEA for resection of TS at a single academic institution between 2004 and 2020. Radiographic and clinical data were recorded and analyzed. Results A total of 16 patients were abstracted, with a mean age at the time of surgery of 44 years with a slight female (1.83:1) predominance. Primary preoperative symptomatology included facial pain/neuralgia ( n = 5, 31.3%), facial hypoesthesia ( n = 4, 25.0%), and headache ( n = 4, 25.0%). Following TS resection, patients were found to have facial hypoesthesia ( n = 11, 68.8%), neuropathic keratopathy ( n = 4, 25.0%), and mastication musculature atrophy ( n = 3, 18.8%). Patients with preoperative facial pain/neuralgia ( n = 5, 31.3%) were significantly more likely to try adjunctive pain therapies ( p = 0.018) as well as seek pain consultation ( p = 0.018). Patients with preoperative migraines ( n = 2, 12.5%) were significantly more likely to trial adjunctive pain therapies ( p = 0.025) and undergo evaluation with pain specialists ( p = 0.025). Finally, patients with preoperative pharmacologic agent utilization were significantly more likely to trial adjunctive pain therapies ( p = 0.036) and pursue pain consultation ( p = 0.036). Conclusion Some degree of trigeminal dysfunction may be more common than previously reported following EEA for TS resection. Factors that appear to play a role in the development of trigeminal dysfunction include pre-existing pain syndromes such as facial pain/neuralgia or headache and preoperative medication utilization.

Postoperative trigeminal neuropathy outcomes following surgery for tumors involving the trigeminal nerve.

OBJECTIVE: To observe the evolution and outcomes of postoperative trigeminal neuropathy following surgery of tumor involving the trigeminal nerve. METHODS: A prospective observational study was conducted between October 2018 and February 2019 involving 25 patients with tumors confirmed to involve the trigeminal nerve during surgery by senior author. Pre- and postoperative trigeminal nerve function status and clinical data were recorded. RESULTS: This study included 18 cases of meningioma and seven of trigeminal schwannoma. Among the meningioma cases, 55.6% of the patients reported facial sensory dysfunction before surgery, 33.3% presented ocular discomfort, and 5.6% had masticatory muscle atrophy. Postoperatively, all patients experienced facial paresthesia, 94.4% complained of eye dryness, and one (5.56%) exhibited keratitis. Additionally, one patient (5.56%) showed new-onset masticatory weakness. During follow-up, 50.0% of patients reported improvement in facial paresthesia, and one (5.56%) experienced deterioration. Eye dryness resolved in 35.3% of patients, and keratitis remission was observed in one patient. However, one patient (5.56%) developed neurotrophic keratitis. Overall, 55.6% of patients displayed mild masticatory weakness without muscle atrophy. In the cases of schwannoma, 28.6% of patients had facial paresthesia before surgery, 42.9% showed ocular discomfort, and one (14.3%) complained of masticatory dysfunction. Postoperatively, 85.7% of patients reported facial paresthesia and eye dryness, with one patient (16.7%) experiencing keratitis. During follow-up, 66.7% of patients demonstrated improvement in facial paresthesia, 28.6% showed eye dryness remission, and one patient (16.7%) recovered from keratitis. However, one patient (16.7%) developed new-onset neurotrophic keratitis. One patient (16.7%) experienced relief of masticatory dysfunction, but 42.9% reported mild deterioration. Another patient (14.3%) had facial anesthesia that had not improved. CONCLUSION: Postoperative trigeminal neuropathy is a common complication with a high incidence rate and poor recovery outcomes after surgery for tumors involving the trigeminal nerve. When trigeminal nerve damage is unavoidable, it is essential to provide a multidisciplinary and careful follow-up, along with active management strategy, to mitigate the more severe effects of postoperative trigeminal neuropathy.

A systematic review of the efficacy of ketamine for craniofacial pain.

Background: Craniofacial pain (CFP) poses a burden on patients and health care systems. It is hypothesized that ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can reverse central sensitization associated with causation and propagation of CFP. This systematic review aims to assess the role of ketamine for CFP. Methods: Databases were searched for studies published up to September 26, 2022, investigating the efficacy of ketamine for adults with CFP. Primary outcome was the change in pain intensity at 60 min postintervention. Two reviewers screened and extracted data. Registration with PROSPERO was performed (CRD42020178649). Results: Twenty papers (six randomized controlled trials [RCTs], 14 observational studies) including 670 patients were identified. Substantial heterogeneity in terms of study design, population, dose, route of administration, treatment duration, and follow-up was noted. Bolus dose ranged from 0.2-0.3 mg/kg (intravenous) to 0.4 mg/kg (intramuscular) to 0.25-0.75 mg/kg (intranasal). Ketamine infusions (0.1-1 mg/kg/h) were given over various durations. Follow-up was short in RCTs (from 60 min to 72 h) but longer in observational studies (up to 18 months). Ketamine by bolus treatment failed to reduce migraine intensity but had an effect by reducing intensity of aura, cluster headache (CH), and trigeminal neuralgia. Prolonged ketamine infusions showed sustainable reduction of migraine intensity and frequency of CH attacks, but the quality of the evidence is low. Conclusion: Current evidence remains conflicting on the efficacy of ketamine for CFP owing to low quality and heterogeneity across studies. Ketamine infusions are suggested to provide sustained improvement, possibly because of prolonged duration and higher dosage of administration. RCTs should focus on the dose-response relationship of prolonged ketamine infusions on CFP.

Contexte: La douleur crânio-faciale représente un fardeau pour les patients et les systèmes de soins de santé. L'hypothèse a été émise que la kétamine, un antagoniste du récepteur N-méthyl-D-aspartate (NMDA), peut inverser la sensibilisation centrale associée à la causalité et à la propagation de la douleur crânio-faciale. Cette revue systématique vise à évaluer le rôle de la kétamine dans la douleur crânio-faciale.Méthodes: Les bases de données ont été consultées pour y repérer les études publiées jusqu'au 26 septembre 2022 qui portaient sur l'efficacité de la kétamine chez les adultes atteints de douleur crânio-faciale. Le critère de jugement principal était le changement de l'intensité de la douleur 60 minutes après l'intervention. Deux évaluateurs ont examiné et extrait les données. L'inscription auprès de PROSPERO a été réalisée (CRD42020178649).Résultats: Vingt articles (six essais contrôlés randomisés, 14 études observationnelles) incluant 670 patients ont été répertoriées. Une hétérogénéité considérable en matière de devis d'étude, de population, de dose, de voie d'administration, de durée du traitement et de suivi a été notée. La dose bolus variait de 0,2 à 0,3 mg/kg (voie intraveineuse) à 0,4 mg/kg (voie intramusculaire) et à 0,25-0,75 mg/kg (voie intranasale). Les perfusions de kétamine (0,1-1 mg/kg/h) étaient administrées sur différentes durées. Le suivi était court dans les études contrôllées randomisées (de 60 min à 72 h) mais plus long dans les études observationnelles (jusqu'à 18 mois). La kétamine par traitement bolus n'a pas réussi à réduire l'intensité de la migraine mais a eu un effet en réduisant l'intensité de l'aura, la céphalée en grappe et la névralgie du trijumeau. Les perfusions de kétamine prolongées ont montré une réduction durable de l'intensité de la migraine et la fréquence des crises de CH, mais la qualité des données probantes est faible.Conclusions: Les données probantes actuelles demeurent contradictoires sur l'efficacité de la kétamine pour la douleur crânio-faciale en raison de la faible qualité et de l'hétérogénéité des études. Il est suggéré que les perfusions de kétamine procurent une amélioration soutenue, peut-être en raison de leur durée prolongée et de leur posologie d'administration plus élevée. Les essais contrôlés randomisés devraient se concentrer sur la relation dose-réponse des perfusions prolongées de kétamine sur la douleur crâno-faciale.

Postischemic Trigeminal Neuropathy Treated With Radiofrequency Ablation.

Trigeminal neuralgia is a pain syndrome that is defined by sharp electrical shock-like pain that radiates in the sensory distribution of the trigeminal nerve. The classical cause of this syndrome is vascular compression, but other causes, such as stroke, have also been described. Instances of post-ischemic trigeminal pain have been described as meeting the classic description, and are termed trigeminal neuropathy. The treatment paradigms for trigeminal neuralgia versus neuropathy differ significantly, especially with the consideration of surgical management.We present a case of a 78-year-old man with post-ischemic trigeminal neuropathy that was successfully treated with radiofrequency ablation after failure of conservative management.We also summarize three previous cases of post-ischemic trigeminal neuropathy that were also successfully treated with percutaneous surgical treatment, showing that percutaneous surgical management should be considered in patients with post-ischemic trigeminal neuropathy that fail conservative management.

Diagnosis and treatment of trigeminal neuralgia: Consensus statement from the Spanish Society of Neurology's Headache Study Group.

INTRODUCTION: Trigeminal neuralgia (TN) is a chronic neuropathic pain disorder affecting one or more branches of the trigeminal nerve. Despite its relatively low global prevalence, TN is an important healthcare problem both in neurology departments and in emergency departments due to the difficulty of diagnosing and treating the condition and its significant impact on patients' quality of life. For all these reasons, the Spanish Society of Neurology's Headache Study Group has developed a consensus statement on the management of TN. DEVELOPMENT: This document was drafted by a panel of neurologists specialising in headache, who used the terminology of the International Headache Society. We analysed the published scientific evidence on the diagnosis and treatment of TN and establish practical recommendations with levels of evidence. CONCLUSIONS: The diagnosis of TN is based on clinical criteria. Pain attributed to a lesion or disease of the trigeminal nerve is divided into TN and painful trigeminal neuropathy, according to the International Classification of Headache Disorders, third edition. TN is further subclassified into classical, secondary, or idiopathic, according to aetiology. Brain MRI is recommended in patients with clinical diagnosis of TN, in order to rule out secondary causes. In MRI studies to detect neurovascular compression, FIESTA, DRIVE, or CISS sequences are recommended. Pharmacological treatment is the initial choice in all patients. In selected cases with drug-resistant pain or poor tolerance, surgery should be considered.

Posttraumatic Trigeminal Neuropathic Pain in Association with Dental Implant Surgery.

Posttraumatic trigeminal neuropathy in association with dental implant surgery is preventable, and this should be the emphasis for all clinicians considering this treatment for a patient. Once the nerve injury and posttraumatic neuropathy with or without pain ensues, there is very little the clinician can do to reverse it and the high pain and permanency of the neuropathy will have a significant functional and psychological impact on the patient. Immediate implant removal is required, and home check should be routine for all cases. International diagnostic criteria are available and should be implemented in everyday practice.

Outcome of Surgical Treatments of Chronic Pain Caused by Trigeminal Neuropathy.

BACKGROUND: Trigeminal neuropathy represents a subset of several facial pain syndromes that are difficult to diagnose and treat. Although many surgical modalities are available, outcomes remain suboptimal. The aim of this study is to present our experience in management of trigeminal neuropathy with a focus on the effectiveness and long-term efficacy of the different surgical procedures. METHODS: A single-center retrospective cohort study was conducted from December 2012 until February 2020. RESULTS: Twenty-eight patients (19 females, 9 males) were included in this study. They had 40 surgical interventions. At last follow-up, 1 patient (33.3%) treated by spinal cord stimulation (SCS) had no pain recurrence and 2 patients (66.6%) had their devices removed because of therapeutic failure. Median time to pain recurrence after SCS was 19.5 months (interquartile range [IQR], 29.79 months). Six patients were treated with peripheral nerve stimulation (PNS). At last follow-up, 2 patients had satisfactory pain relief, whereas half of the patients had no improvement. For the 17 patients treated with computed tomography-guided trigeminal tractotomy/nucleotomy, true failure occurred 7 times in 6 patients. Median time to pain recurrence was 5.6 months (IQR, 6.2). Of the 6 patients treated with caudalis DREZ, 3 (50%) had satisfactory pain relief for >1 year and the median time to pain recurrence was 3.9 months (IQR, 29.53). CONCLUSIONS: Trigeminal neuropathy is a difficult to treat entity of facial pain syndromes. The long-term efficacy of available interventions does not meet patients' satisfaction. More organized prospective studies with longer follow-up are needed to define the patient population best served by each surgical modality.

Management of Trigeminal Neuralgia with Botulinum Toxin Type A: Report of Two Cases.

Trigeminal neuralgia is a chronic pain condition associated with sharp, shock-like pain in one or more divisions of the trigeminal nerve. For patients who do not respond well to pharmacotherapy, there is growing evidence that Botulinum toxin type A injections into the trigeminal ganglion provide pain relief for several weeks up to several months at a time. One option is to administer injections into the trigeminal ganglion in Meckel's cave by inserting a needle through the Pterygopalatine Fossa using fluoroscopy to guide and confirm the proper needle placement. However, there is evidence that Botulinum toxin travels across nerve synapses; thus, injecting directly into the trigeminal ganglion may not be necessary. We present two patients with a confirmed diagnosis of trigeminal neuralgia who were treated by injecting Botulinum toxin type A intraorally into the mental foramen which resulted in 6 months or longer of pain relief. Injections into the mental foramen are much easier to administer than those administered directly into the trigeminal ganglion, and both patients treated with this technique experienced comparable results to what can be expected from traditional fluoroscopy-guided botulinum toxin injections. Though more research is needed, these cases potentially imply that a less-invasive injection may be sufficient in managing trigeminal neuralgia-related pain.

Trigeminal neuropathy after tozinameran vaccination against COVID-19 in postmicrovascular decompression for trigeminal neuralgia: illustrative case.

BACKGROUND: Vaccines against coronavirus disease 2019 have a high level of efficacy and safety across all populations. However, numerous case series have been published on neurological disorders, including Bell's palsy, Guillain-Barre syndrome, transverse myelitis, and multiple sclerosis. The authors presented a case of trigeminal neuropathy after coronavirus vaccination in a patient who had undergone microvascular decompression (MVD) for trigeminal neuralgia (TN). OBSERVATIONS: A 77-year-old woman presented with acute trigeminal neuropathy after receiving a Pfizer-BioNtech vaccination (tozinameran) against severe acute respiratory syndrome coronavirus 2. The patient had undergone MVD for TN and the facial pain completely disappeared. One month later, she received the first injection of the tozinameran vaccine. Twelve hours after vaccination, she presented with numbness and pain induced by touching any place on the entire right face. No eruption was observed on her face. The serum herpes zoster virus antibodies were confirmed within the normal range. Magnetic resonance imaging revealed no abnormalities. The authors suspected a right trigeminal neuropathy after vaccination. Administration of carbamazepine and pregabalin improved TN but facial numbness persisted, especially in the mandibular division. LESSONS: The coronavirus is a possible etiology of secondary trigeminal neuropathy in the case of MVD for TN.

Botulinum toxin A for management of refractory concurrent buccal and inferior alveolar nerve post-traumatic neuropathies: a case report.

Painful post-traumatic trigeminal neuropathy (PPTTN) can result from iatrogenic injury to one or more branches of the trigeminal nerve during oral surgical procedures such as tooth extractions. Like other chronic neuropathic pain conditions, PPTTN can significantly alter the patient's quality of life, especially when pharmacological treatment is ineffective or not tolerated. As such, new treatment options have been investigated, including local injections of botulinum toxin type A (BTX-A). A 29-year-old woman presented to our tertiary orofacial pain clinic for evaluation of chronic electric shock-like pain attacks and severe allodynia in the territory of the right inferior alveolar nerve and buccal nerve following right mandibular third molar extraction 3 years prior. Following several failed attempts at classic pharmacological management (including carbamazepine, venlafaxine, duloxetine, pregabalin, clonazepam, and amitriptyline), BTX-A injections were administered in the vicinity of the right mental nerve. This treatment provided significant improvement in the patient's condition and overall quality of life with no significant adverse effects. Because both neuropathies were significantly improved by remote BTX-A injections, this case report provides preliminary clinical evidence supporting spinopetal transport of BTX-A, as shown in animal models, as an underlying pathophysiological mechanism of BTX-A-mediated analgesia.

Persistent Idiopathic Facial Pain (PIFP) in Patients Referred to a Multidisciplinary Centre in Italy: A Retrospective Observational Study.

BACKGROUND: Persistent Idiopathic Facial Pain (PIFP), previously named Atypical Facial Pain (AFP) is a poorly understood condition, often diagnosed after several inconclusive investigations. The aim of this retrospective study was to evaluate the demographic and clinical characteristics of patients with PIFP referred to a Facial Pain Center. METHODS: Between May 2011 and September 2014, data on 41 PIFP patients were analyzed regarding temporal, topographical and descriptive pain features, including onset, localization, pain descriptors and intensity. Pharmacological pain treatments were also registered. Finally, the presence and type of previous minor oro-surgery procedures in the painful area were investigated. RESULTS: Demographic and clinical characterization were similar to PIFP patients reported in literature. The presence of previous minor oro-surgery procedures in the painful area was reported in most of these patients, in particular endodontic treatments and tooth extractions. CONCLUSIONS: This retrospective analysis showed a high prevalence of minor oro-surgery procedures in our population, while its role in PIFP pathophysiology remains unknown. A new classification of PIFP built around the main discriminant factor of presence of these procedures in the painful area could be considered while available data were still insufficient to define specific diagnostic criteria.

Healthcare costs of post-traumatic trigeminal neuropathy in Belgium - A retrospective analysis.

The present aim was to estimate direct health care costs of patients suffering from post-traumatic trigeminal neuropathy (PTTN) and to compare the use of health care services, medications, and costs between temporary and persistent (>3 months) PTTN cohorts. A pre-existing clinical dataset of PTTN patients visiting a tertiary orofacial pain clinic in Belgium was utilized, including symptoms and quality of life measurements. Cost and resource utilization data were obtained by Belgium's largest health insurance provider for a period of 5 years after onset. Data from 158 patients was analyzed. The average cost per patient in the first year after injury was €2353 (IQR 1426-4499) with an out-of-pocket expense of 25% of the total cost. Hospitalization and technical interventions were the main drivers of cumulative costs, followed by consultation costs. For each cost category, expenditure was significantly higher in patients with persistent PTTN than in those with temporary PTTN (median 5-year total costs in persistent PTTN patients yielded €8866 (IQR 4368-18191) versus €4432 (IQR 2156-9032) in temporary PTTN, p <0.001) PTTN patients received repeated and frequent head and neck imaging (mean number of imaging investigations per patient was 10 ± 12). Medication consumption was high, with an unwarranted higher use of opioids and antibiotics in persistent PTTN patients. Within the limitations of this study, it seems there is a need for informing patients in detail on the inherent risks of nerve damage during dental and oromaxillofacial procedures. Every surgery should be preceded by a risk-benefit assessment in order to avoid unnecessary nerve damage.