Trigeminal Neuropathy Research Articles

Prolonged blockade of the cervical sympathetic nerve by stellate ganglion block accelerates therapeutic efficacy in trigeminal neuropathy

Stellate ganglion block (SGB) is effective in treating head and neck pain and neuropathic diseases by increasing tissue blood flow through its sympatholytic effect. This study aimed to investigate the relationship between duration of cervical sympathetic nerve block by SGB and its therapeutic efficacy against trigeminal neuropathy after orthognathic surgery. Twenty-eight patients with trigeminal neuropathy were randomly assigned to two groups (mepivacaine and levobupivacaine) according to the drug used for SGB. Increased blood flow, which is a symptom of sympathetic blockade, was recorded for 180 min after SGB. Current perception threshold, warm or cool detection threshold, and tactile detection threshold were measured preoperatively, postoperatively, on day 10 after initiation of SGB, and 3 months postoperatively to compare therapeutic efficacy between the groups. The levobupivacaine group had a significantly longer duration of increased blood flow compared with the mepivacaine group. Values of current perception threshold, warm and cool detection threshold, and tactile detection threshold significantly improved in the levobupivacaine group on day 10 after initiation of SGB and 3 months postoperatively. A prolonged increase in blood flow due to long-term sympatholytic effects accelerates the therapeutic efficacy of SGB in trigeminal neuropathy.

Persistent, neuropathic-like trigeminal pain after dental implant loading.

BackgroundPainful post-traumatic trigeminal neuropathy (PTTN) is a known complication of dental implant therapy. Besides cases resulting of nerve damage during surgery or implant placement, some patients report delayed neuropathic-like symptoms only after implant loading i.e. crown placement. The present retrospective study aimed at describing the clinical features of pain experienced by these patients. Material and MethodsThe cohort of patients consulting for chronic orofacial pain at the Groupe Hospitalier Pitié-Salpêtrière (Paris, France) between 2015 and 2020 (ABCD study, IRB # TPS 1106180), was screened for patients with history of dental implant placement and persistent pain. Patients with no pain after surgery for 6 months and pain resulting from the loading of the implant, were included. ResultsAmong 675 files of patients screened, 5 fulfilled inclusion criteria. All patients were women, mean age 62.4 ± 9.8 y.o, and reported trigeminal neuropathic-like persistent pain. Intensity of pain was described as moderate to severe, with pin and needles, burning and tingling, and electric shocks as main symptoms. ConclusionsThese results suggest that implant loading can trigger trigeminal neuropathy, in a previously sensitized nerve. Putative neurophysiological basis of the phenomenon is discussed. Key words:Neuropathic pain, trigeminal nerve, lesion, dental implant, implant loading, allodynia.

Chemogenetic inhibition of trigeminal ganglion neurons attenuates behavioural and neural pain responses in a model of trigeminal neuropathic pain.

Nerve injury can lead to ectopic activation of injured nociceptorsand central sensitization characterized by allodynia and hyperalgesia. Reduction in the activity of primary afferent neurons has been shown to be sufficient in alleviating peripherally generated pain. The cell bodies of such trigeminal nociceptors are located in the trigeminal ganglia (TG) with central processes that terminate in the brainstem trigeminal nucleus caudalis (TNC). The TG is therefore a strategic locus where afferent input can be manipulated. We hypothesized that chemogenetic inhibition of TG would suppress TNC neuronal activity and attenuate pain behaviour in a rat model of painful traumatic trigeminal neuropathy (PTTN). Trigeminal neuropathic pain was induced in adult male Sprague-Dawley rats (n=24) via chronic constriction injury to the infraorbital nerve (ION-CCI). Naïve and sham rats were used as controls (n=20/group). Rats within each group received TG-directed microinjections of AAV virus containing either the inhibitory hM4Di-DREADD construct or EGFP. In the ION-CCI group, systemic administration of the DREADD agonist clozapine N-oxide (CNO) reversed the hypersensitivity phenotype in animals expressing hM4Di but not EGFP. CNO-mediated activation of hM4Di DREADD in ION-CCI animals was also associated with reduced Fos expression in the TNC elicited by repeated mechanical stimulation of the dermatome ipsilateral to the injury. There was no effect of CNO on pain behaviour or TNC Fos expression in eGFP animals. Our results indicate that DREADDs may offer an effective therapeutic approach for treatment of trigeminal neuropathic pain. Trigeminal neuropathic pain is highly resistant to therapy and we are in dire need of novel approaches. This study provides further evidence for the successful application of DREADDs as an effective tool for modulating central nervous system function. CNO mediated activation of hM4Di-DREADDs in the trigeminal ganglion (TG) attenuates nerve injury induced neuropathic pain by acting on hyperactive TG cells. It also establishes the TG as an effective target to manage pain in the face and head. Accessing the TG in clinical populations is a relatively simple and safe procedure, making this approach highly significant. Moreover, the methodology described here has applications in trigeminal neuropathic pain from traumatic other etiologies and in spinal neuropathic pain. Chronic pain syndromes are characterized by a progressive failure of brain centers to adequately inhibit pain and as these are identified, we may be able to target them for therapy. Therefore, our findings might have wide application in chronic pain syndromes.

Facial Paresthesia, a Rare Manifestation of Hereditary Neuropathy With Liability to Pressure Palsies: A Case Report

Trigeminal sensory neuropathy can be caused by a variety of conditions, including local, traumatic, iatrogenic, or systemic causes. Diagnosis and management remain a challenge for maxillofacial surgeons and neurologists. Therefore, a good clinical examination and objective tests and imaging are needed when diagnosing patients who present with facial numbness. We present a case with spontaneous episodes of facial paresthesia. He was diagnosed with hereditary neuropathy with liability to pressure palsies (HNPP), a rare condition that affects the peripheral nerves. Only a few case reports that describe involvement of the cranial nerves in patients with HNPP were found in the literature, and facial paresthesia has not been previously reported.

Evaluation of the response to electric pulp testing in multiple sclerosis patients without a history of trigeminal neuralgia: a case-control study

BackgroundThe importance of evaluating the pulpal threshold to electrical stimulation, as a side effect of probable neuropathy in Multiple Sclerosis (MS) patients is a novel issue. This study aimed to investigate electrical pulp test thresholds in MS patients without a history of trigeminal neuralgia compared to healthy individuals.MethodsSixty-nine maxillary central incisors, belonging to 34 relapsing-remitting MS patients, and 35 healthy individuals were included in this survey. The MS patients matched for intended variables, were 22–50 years old, had a more than 1-year history of MS, no history of trigeminal neuralgia and/or other neuropathy. The electric pulp sensibility test was performed on all samples. Electric pulp testing (EPT) results were recorded based on the pulp tester’s grade that evoked a response. Data were analyzed with paired T-test, Mann-Whitney test, and Spearman correlation (P < 0.05).ResultsAccording to the results of this study, the mean values of response to EPT were 1.2 ± 0.5 and 1.8 ± 0.5 in MS patients and healthy individuals, respectively. The pulpal response to EPT between the two groups was significantly different (P < 0.0001).ConclusionsMS patients showed a significantly reduced response to the electric pulp test in their maxillary central incisors in comparison to matched healthy persons.

Prediction of post-traumatic neuropathy following impacted mandibular third molar removal

ObjectivesThe extraction of impacted mandibular third molars is a common surgical procedure often associated with complications including post-traumatic neuropathy. Previous work has focused on identifying confounding factors, but a robust preoperative risk prediction model remains elusive. MethodsUsing a dataset of 648 patients and 812 impacted mandibular third molars, we used least absolute shrinkage and selection operator (LASSO) to fit prediction models based on risk factors assessed at both the tooth and patient levels. In addition, we fitted multivariable logistic regression models with the Firth correction for generalized estimating equations (GEE). ResultsThe LASSO model for post-traumatic neuropathy identified distoangular impaction of ≥ 45° (odds ratio [OR] = 2.9), proximity to the inferior alveolar nerve of ≤ 3 mm (OR = 1.9), disadvantageous curving (OR = 1.4), and psychiatric conditions (OR = 2.1) as predictors [area under the receiving operator characteristic curve (AUC) = 0.75]. Among other complications analyzed, the LASSO model for bleeding identified deep embedding or full impaction (OR = 1.8), psychiatric conditions (OR = 1.3), and age (OR = 0.9) as predictors (AUC = 0.64). These associations between predictors and postoperative complications were fundamentally reinforced by the corresponding GEE models. ConclusionsOur findings point to the predictability of post-traumatic neuropathy and bleeding based on tooth anatomy and patient characteristics, overall suggesting that preoperatively identifiable factors can predict the risk of adverse outcomes in the extraction of impacted mandibular third molars. Clinical significanceMandibular third molar extraction is both a routine procedure and a leading cause of trigeminal neuropathy. Prevention of post-traumatic neuropathy, aided by individualized preoperative risk prediction, is of high clinical relevance.

Stereotactic radiosurgery as the primary management for patients with Koos grade IV vestibular schwannomas.

While extensive long-term outcome studies support the role of stereotactic radiosurgery (SRS) for smaller-volume vestibular schwannomas (VSs), its role in the management for larger-volume tumors remains controversial. Between 1987 and 2017, the authors performed single-session SRS on 170 patients with previously untreated Koos grade IV VSs (volumes ranged from 5 to 20 cm3). The median tumor volume was 7.4 cm3. The median maximum extracanalicular tumor diameter was 27.5 mm. All tumors compressed the middle cerebellar peduncle and distorted the fourth ventricle. Ninety-three patients were male, 77 were female, and the median age was 61 years. Sixty-two patients had serviceable hearing (Gardner-Robertson [GR] grades I and II). The median margin dose was 12.5 Gy. At a median follow-up of 5.1 years, the progression-free survival rates of VSs treated with a margin dose ≥ 12.0 Gy were 98.4% at 3 years, 95.3% at 5 years, and 90.7% at 10 years. In contrast, the tumor control rate after delivery of a margin dose < 12.0 Gy was 76.9% at 3, 5, and 10 years. The hearing preservation rates in patients with serviceable hearing at the time of SRS were 58.1% at 3 years, 50.3% at 5 years, and 35.9% at 7 years. Younger age (< 60 years, p = 0.036) and initial GR grade I (p = 0.006) were associated with improved serviceable hearing preservation rate. Seven patients (4%) developed facial neuropathy during the follow-up interval. A smaller tumor volume (< 10 cm3, p = 0.002) and a lower margin dose (≤ 13.0 Gy, p < 0.001) were associated with preservation of facial nerve function. The probability of delayed facial neuropathy when the margin dose was ≤ 13.0 Gy was 1.1% at 10 years. Nine patients (5%) required a ventriculoperitoneal shunt because of delayed symptomatic hydrocephalus. Fifteen patients (9%) developed detectable trigeminal neuropathy. Delayed resection was performed in 4% of patients. Even for larger-volume VSs, single-session SRS prevented the need for delayed resection in almost 90% at 10 years. For patients with minimal symptoms of tumor mass effect, SRS should be considered an effective alternative to surgery in most patients, especially those with advanced age or medical comorbidities.

Surgical treatment for pain attributed to a lesion or disease of the trigeminal nerve – A single-center experience

According to ICHD-3, “Pain attributed to a lesion or disease of the trigeminal nerve” (PLDTN) includes both trigeminal neuralgia (TN) and painful trigeminal neuropathy. Despite initial preference for medical management, patients with refractory pain or intolerant to drug therapy side effects are candidates for surgical therapy. We aimed to characterize a single-center population of patients selected for surgical management of PLDTN, accessing surgery effectiveness and patient satisfaction.

Occurrence of Pure Sensory Neuropathy in a 45-Year-Old Female with Primary Sjögren’s Syndrome: A Case Report Study

: Complications of Sjögren’s syndrome (SS) and neuropathies may occur in some cases. Almost this complication occurs with peripheral neuropathy. Different forms of sensory neuropathy, multiple mononeuropathy, trigeminal neuropathy, multiple cranial neuropathy, radiculoneuropathy, and autonomic neuropathy can occur in SS. In this novel case presentation, polyneuropathy in a 45-year-old female patient with SS is reported with a complaint of ataxia, vertigo, dysarthria, abnormal gait, foreign body sensation, and deterioration of quadriparesis from six months ago. Fluorescent antinuclear antibody (FANA), anti-RO, anti-RO-52, and RF were strongly detected positive in her rheumatologic examination. Pure sensory polyneuropathy (ganglionopathy) was also reported in electromyography and nerve conduction velocity (EMG-NCV). Although peripheral neuropathy is the major and most common neurological aspect of neuron involvement in patients with SS, here, pure sensory polyneuropathy is reported in a 45-year-old female patient with SS. In conclusion, in this novel case presentation, a novel case of polyneuropathy concurrent with SS is demonstrated in a 45-year-old female patient.

Trigeminal neuropathy causes hypomyelination in the anterior cingulate cortex, disrupts the synchrony of neural circuitry, and impairs decision‐making in male rats

Infraorbital nerve‐chronic constriction injury (ION‐CCI) has become the most popular chronic trigeminal neuropathic pain (TNP) injury animal model which causes prolonged mechanical allodynia. Accumulative evidence suggests that TNP interferes with cognitive functions, however the underlying mechanisms are not known. The aim of this study was to investigate decision‐making performance as well as synaptic and large‐scale neural synchronized alterations in the spinal trigeminal nucleus (SpV) circuitry and anterior cingulate cortex (ACC) neural circuitry in male rats with TNP. Rat gambling task showed that ION‐CCI led to decrease the proportion of good decision makers and increase the proportion of poor decision makers. Electrophysiological recordings showed long‐lasting synaptic potentiation of local field potential in the trigeminal ganglia‐SpV caudalis (SpVc) synapses in TNP rats. In this study, TNP led to disruption of ACC spike timing and basolateral amygdala (BLA) theta oscillation associated with suppressed synchronization of theta oscillation between the BLA and ACC, indicating reduced neuronal communications. Myelination is critical for information flow between brain regions, and myelin plasticity is an important feature for learning. Neural activity in the cortical regions impacts myelination by regulating oligodendrocyte (OL) proliferation, differentiation, and myelin formation. We characterized newly formed oligodendrocyte progenitor cells, and mature OLs are reduced in TNP and are associated with reduced myelin strength in the ACC region. The functional disturbances in the BLA‐ACC neural circuitry is pathologically associated with the myelin defects in the ACC region which may be relevant causes for the deficits in decision‐making in chronic TNP state.

Prognostic factors, symptom evolution, and quality of life of posttraumatic trigeminal neuropathy.

Neurosensory disturbances (NSDs) caused by injury to the trigeminal nerve can affect many aspects of daily life. However, factors affecting the persistence of NSDs in patients with posttraumatic trigeminal neuropathies (PTTNs) remain largely unknown. The identification of such risk factors will allow for the phenotyping of patients with PTTNs, which is crucial for improving treatment strategies. We therefore aimed to identify the prognostic factors of NSD persistence, pain intensity, and quality of life (QoL) in patients with PTTNs and to use these factors to create a prognostic prediction model. We first performed a bivariate analysis using retrospective longitudinal data from 384 patients with NSDs related to posttraumatic injury of the trigeminal nerve (mean follow-up time: 322 ± 302 weeks). Bivariate and multivariate analyses were performed. The multivariable prediction model to predict persistent NSDs was able to identify 76.9% of patients with persistent NSDs, with an excellent level of discrimination (area under the receiver operating characteristic curve: 0.84; sensitivity: 81.8%; specificity: 70.0%). Furthermore, neurosensory recovery was significantly associated with sex; injury caused by local anesthesia, extraction, third molar surgery, or endodontic treatment; and the presence of thermal hyperesthesia. Pain intensity and QoL analysis revealed several factors associated with higher pain levels and poorer QoL. Together, our findings may aid in predicting patient prognosis after dental, oral, and maxillofacial surgery and might lead to personalized treatment options and improved patient outcomes.

Acute and Chronic Pain from Facial Skin and Oral Mucosa: Unique Neurobiology and Challenging Treatment.

The oral cavity is a portal into the digestive system, which exhibits unique sensory properties. Like facial skin, the oral mucosa needs to be exquisitely sensitive and selective, in order to detect harmful toxins versus edible food. Chemosensation and somatosensation by multiple receptors, including transient receptor potential channels, are well-developed to meet these needs. In contrast to facial skin, however, the oral mucosa rarely exhibits itch responses. Like the gut, the oral cavity performs mechanical and chemical digestion. Therefore, the oral mucosa needs to be insensitive, to some degree, in order to endure noxious irritation. Persistent pain from the oral mucosa is often due to ulcers, involving both tissue injury and infection. Trigeminal nerve injury and trigeminal neuralgia produce intractable pain in the orofacial skin and the oral mucosa, through mechanisms distinct from those seen in the spinal area, which is particularly difficult to predict or treat. The diagnosis and treatment of idiopathic chronic pain, such as atypical odontalgia (idiopathic painful trigeminal neuropathy or post-traumatic trigeminal neuropathy) and burning mouth syndrome, remain especially challenging. The central integration of gustatory inputs might modulate chronic oral and facial pain. A lack of pain in chronic inflammation inside the oral cavity, such as chronic periodontitis, involves the specialized functioning of oral bacteria. A more detailed understanding of the unique neurobiology of pain from the orofacial skin and the oral mucosa should help us develop novel methods for better treating persistent orofacial pain.

Post-traumatic trigeminal neuropathy: correlation between objective and subjective assessments and a prediction model for neurosensory recovery

BackgroundPost-traumatic trigeminal neuropathy (PTN) can have a substantial effect on patient well-being. However, the relation between the neuropathic symptoms and their effect on psychosocial functioning remains a matter of debate. The purpose of this study was to evaluate the association between objective and subjective assessments of neurosensory function in PTN and predict neurosensory outcome using baseline measurements.MethodsThis prospective observational cohort study included patients diagnosed with PTN at the Department of Oral and Maxillofacial Surgery, University Hospital Leuven, Belgium, between April 2018 and May 2020. Standardized objective and subjective neurosensory examinations were recorded simultaneously on multiple occasions during the follow-up period. Correlation analyses and principal component analysis were conducted, and a prediction model of neurosensory recovery was developed.ResultsQuality of life correlated significantly (P < 0.05) with percentage of affected dermatome (ρ = − 0.35), the presence of brush stroke allodynia (ρ = − 0.24), gain-of-function sensory phenotype (ρ = − 0.41), Medical Research Council Scale (ρ = 0.36), and Sunderland classification (ρ = − 0.21). Quality of life was not significantly correlated (P > 0.05) with directional discrimination, stimulus localization, two-point discrimination, or sensory loss-of-function. The prediction model showed a negative predictive value for neurosensory recovery after 6 months of 87%.ConclusionsWe found a strong correlation of subjective well-being with the presence of brush stroke allodynia, thermal and/or mechanical hyperesthesia, and the size of the neuropathic area. These results suggest that positive symptoms dominate the effect on affect. In patients reporting poor subjective well-being in the absence of positive symptoms or a large neuropathic area, additional attention towards psychosocial triggers might enhance treatment outcome. The prediction model could contribute to establishing realistic expectations about the likelihood of neurosensory recovery but remains to be validated in future studies.

Capsaicin-induced depolymerization of axonal microtubules mediates analgesia for trigeminal neuropathic pain

Pain management in craniofacial neuropathy is a major clinical challenge. Trigeminal neuralgia and painful post-traumatic trigeminal neuropathy are two major trigeminal neuropathic pain that need to be addressed. Capsaicin a specific agonist of transient receptor potential vanilloid 1 (TRPV1), a Ca2+-permeable ion channel, that is enriched in nociceptors. The capacity of capsaicin to ablate TRPV1-expressing nociceptive terminals has led to an FDA-approved therapy treat neuropathic pain conditions. We showed that capsaicin induces ablation of nociceptive nerve terminals through TRPV1/Ca2+/calpain-mediated mechanisms, which is necessary for long-lasting analgesia for neuropathic pain. However, the mechanisms underlying capsaicin-induced ablation and analgesia to achieve pain control are not fully understood. In this study, we hypothesize that capsaicin increases depolymerization of microtubules, which induces axonal ablation and analgesia for trigeminal neuropathic pain. To test the hypothesis, we determined the effects of microtubule stabilizer; paclitaxel, which binds to microtubules and stabilizes microtubules against depolymerization, on capsaicin-induced axonal ablation and analgesia for trigeminal neuropathic pain in mice. Paclitaxel decreased capsaicin-induced ablation of axonal terminals in-vitro in time-lapse imaging of axonal terminals from microfluidic chamber. Capsaicin increases the proportion of free tubulin in dissociated sensory neurons, which was inhibited by paclitaxel treatment, suggesting capsaicin increases depolymerization of microtubules. Subcutaneous injection of capsaicin to facial skin attenuated mechanical allodynia in mice with chronic constriction injury of the infraorbital nerve (ION-CCI). In contrast, co-administration of paclitaxel and capsaicin did not produce analgesic effects. Results from the present study supports that TRPV1-microtubule interactions can determine capsaicin-induced ablation of nociceptive terminals and the extent of capsaicin-induced analgesia, which further supports that capsaicin-induced ablation of nociceptive terminals is necessary for analgesia. Further understanding of TRPV1/Ca2+-dependent mechanisms of capsaicin-induced ablation and analgesia may help to improve the efficacy of this treatment. Support/grant information: NIH R01 DE027731 and R35 DE030045 Support/grant information: NIH R01 DE027731 and R35 DE030045.

A Value Assessment of Diagnostic Modalities for Trigeminal Sensory Neuropathy (1456)

A Value Assessment of Diagnostic Modalities for Trigeminal Sensory Neuropathy (1456)

Pretreatment with High Mobility Group Box-1 Monoclonal Antibody Prevents the Onset of Trigeminal Neuropathy in Mice with a Distal Infraorbital Nerve Chronic Constriction Injury

Persistent pain following orofacial surgery is not uncommon. High mobility group box 1 (HMGB1), an alarmin, is released by peripheral immune cells following nerve injury and could be related to pain associated with trigeminal nerve injury. Distal infraorbital nerve chronic constriction injury (dIoN-CCI) evokes pain-related behaviors including increased facial grooming and hyper-responsiveness to acetone (cutaneous cooling) after dIoN-CCI surgery in mice. In addition, dIoN-CCI mice developed conditioned place preference to mirogabalin, suggesting increased neuropathic pain-related aversion. Treatment of the infraorbital nerve with neutralizing antibody HMGB1 (anti-HMGB1 nAb) before dIoN-CCI prevented both facial grooming and hyper-responsiveness to cooling. Pretreatment with anti-HMGB1 nAb also blocked immune cell activation associated with trigeminal nerve injury including the accumulation of macrophage around the injured IoN and increased microglia activation in the ipsilateral spinal trigeminal nucleus caudalis. The current findings demonstrated that blocking of HMGB1 prior to nerve injury prevents the onset of pain-related behaviors, possibly through blocking the activation of immune cells associated with the nerve injury, both within the CNS and on peripheral nerves. The current findings further suggest that blocking HMGB1 before tissue injury could be a novel strategy to prevent the induction of chronic pain following orofacial surgeries.

Commentary: Anterior Petrosal Approach for Enlarging Previously Radiated Recurrent Trigeminal Schwannoma: 2-Dimensional Operative Video.

Trigeminal nerve schwannomas (TNSs) are rare lesions that typically present with symptoms of trigeminal neuropathy or other cranial nerve palsies. These lesions classically have a dumbbell shape, with an anterior component within Meckel's cave and posterior component extending into the posterior fossa through the porus trigeminus. Surgical resection of TNSs can often be achieved via an extradural subtemporal approach to Meckel's cave without an anterior petrousectomy, even for tumors with a significant posterior fossa component, as the tumor often erodes a portion of the petrous apex.1 We present the case of a 53-yr-old female presenting to our institution with complete trigeminal neuropathy secondary to a right-sided, previously resected and radiated TNS. Serial imaging demonstrated an interval growth of significant residual tumor despite multiple adjuvant therapies, and, thus, the patient was recommended to undergo additional surgical resection. The lesion was approached through a right-sided subtemporal approach to Meckel's cave,2 with a plan to utilize an anterior petrousectomy only if difficulty resecting the posterior fossa component of the tumor was encountered. Intraoperatively, the posterior fossa component was found to be densely adherent to the adjacent brainstem, likely secondary to prior surgery and radiation therapy, and, thus, an anterior petrousectomy was performed. Postoperatively, the patient had stable trigeminal neuropathy without any new neurological deficits and a magnetic resonance imaging (MRI) confirmed a gross total resection. In the accompanying video, we hope to demonstrate the steps and nuances of both the subtemporal approach to accessing Meckel's cave and anterior petrousectomy when employed for the resection of TNSs. The patient in question provided formal consent for the making of this video.

Anterior Petrosal Approach for Enlarging Previously Radiated Recurrent Trigeminal Schwannoma: 2-Dimensional Operative Video

Trigeminal nerve schwannomas (TNSs) are rare lesions that typically present with symptoms of trigeminal neuropathy or other cranial nerve palsies. These lesions classically have a dumbbell shape, with an anterior component within Meckel's cave and posterior component extending into the posterior fossa through the porus trigeminus. Surgical resection of TNSs can often be achieved via an extradural subtemporal approach to Meckel's cave without an anterior petrousectomy, even for tumors with a significant posterior fossa component, as the tumor often erodes a portion of the petrous apex.1 We present the case of a 53-yr-old female presenting to our institution with complete trigeminal neuropathy secondary to a right-sided, previously resected and radiated TNS. Serial imaging demonstrated an interval growth of significant residual tumor despite multiple adjuvant therapies, and, thus, the patient was recommended to undergo additional surgical resection. The lesion was approached through a right-sided subtemporal approach to Meckel's cave,2 with a plan to utilize an anterior petrousectomy only if difficulty resecting the posterior fossa component of the tumor was encountered. Intraoperatively, the posterior fossa component was found to be densely adherent to the adjacent brainstem, likely secondary to prior surgery and radiation therapy, and, thus, an anterior petrousectomy was performed. Postoperatively, the patient had stable trigeminal neuropathy without any new neurological deficits and a magnetic resonance imaging (MRI) confirmed a gross total resection. In the accompanying video, we hope to demonstrate the steps and nuances of both the subtemporal approach to accessing Meckel's cave and anterior petrousectomy when employed for the resection of TNSs. The patient in question provided formal consent for the making of this video.

Oral appliances in the management of neuropathic orofacial pain: A retrospective case series.

Neuropathic orofacial pain disorders are frequently managed with topical or systemic medications that carry a risk of dangerous side effects such as drowsiness, disorientation, and/or physical addiction. The aim of this paper is to report the use of neurosensory oral appliances as a safe means of providing symptomatic relief for neuropathic orofacial pain. This is a retrospective chart review of patients with diagnoses of persistent idiopathic facial pain (PIFP), painful post-traumatic trigeminal neuropathy (PTTN), or an oral dysesthesia, who utilized neurosensory appliances with or without the use of topical anesthetic gel. Eleven patients were identified. Eight patients (62.5%) found benefit with the neurosensory appliance alone, and three patients (37.5%) found relief with the addition of lidocaine 2% gel. All patients reported >50% resolution of their symptoms, with three (37.5%) reporting complete resolution. Seven patients maintained follow-up ≥3months, with efficacy lasting for a range of at least 3-8months. Oral neurosensory appliances, whether used alone as a physical barrier or as a vehicle to deliver topical anesthetic, represent a safe and effective modality for the management of neuropathic orofacial pain disorders. Additional studies are needed to assess long-term efficacy.

Facial pain beyond trigeminal neuralgia.

Trigeminal neuralgia is a well-known facial pain syndrome with several treatment options. In contrast, non-neuralgiform idiopathic facial pain syndromes are relatively rare, reflected by the fact that, until 2020, no internationally accepted diagnostic classification existed. Like trigeminal neuralgia, these non-dental facial pain syndromes need to be managed by neurologists and pain specialists, but the lack of pathophysiological understanding has resulted in an underrepresented and undertreated patient group. This work provides a brief overview of the most common primary facial pain syndromes, namely, the facial attack-like facial pain, which corresponds to attack-like headache, the persistent idiopathic facial pain (formerly 'atypical facial pain'), and trigeminal neuropathy. What these disorders have in common is that they should all be treated conservatively. On the basis of pragmatic classifications, permanent and attack-like primary facial pain can be relatively easily differentiated from one another. The introduction of the new International Classification of Orofacial Pain offers the opportunity to better coordinate and concentrate scientific efforts, so that in the future the therapy strategies that are still inadequate, can be optimized.