Painful Trigeminal Neuropathy Research Articles

Gasserian ganglion stimulation for refractory trigeminal neuropathic pain

Background and objectivePainful trigeminal neuropathy is a complex clinical entity due to its severity and refractoriness to pharmacological and interventional management. We describe our experience in treating refractory painful trigeminal neuropathy (RPTN) with gasserian ganglion stimulation (GGS). Materials and MethodsSix patients with RPTN were treated with GGS in our Unit between 2019 and 2022. The following data were collected: socio-demographic characteristics, triggering event, duration of the disease and treatment received prior to surgery, pre- and post-intervention visual analogue scale (VAS) score, follow-up time, and pre- and post-intervention functionality and quality of life. ResultsAll patients were women who had received aggressive first-, second-, and third-line pharmacological, non-pharmacological, and interventional management before being referred for GGS. Patients reported a 50%-72% decrease in pain on VAS and improved functionality during follow-up. ConclusionsGGS is a promising therapeutic alternative for patients with RPTN. Although the initial outcomes and experience are encouraging, RPTN is recommended on the basis of safety, reproducibility, and trends observed in clinical practice.

357 Postoperative Outcomes and Decreases in Pain Medication Utilization Following Nucleus Caudalis DREZ Lesioning for Painful Trigeminal Neuropathy: A Case Series

INTRODUCTION: Painful trigeminal neuropathy is characterized by treatment-resistant trigeminal pain. Nucleus Caudalis Dorsal Root Entry Zone lesioning (NC-DREZ) has been utilized to treat this condition, but changes in medication utilization has not been studied in this population. METHODS: We retrospectively reviewed patients who underwent NC-DREZ at an academic medical center for the treatment of painful trigeminal neuropathy between March 2014 and December 2022, with a minimum 30-day follow-up. Postoperative complications, emergency department visits, readmissions, reoperations, changes in patients' subjective pain, and the longitudinal dosage of pain medications were collected as outcomes. The Fisher's exact and Kruskal-Wallis tests, with alpha set at 0.05, were used to compare the proportion and doses of medications used at each timepoint. RESULTS: Thirty-nine patients were included (mean age 55.7 years, 66.7% female) Prior interventions included trigeminal ablation (35.9%), microvascular decompression (59.0%), and stereotactic radiosurgery (41.0%).Twelve patients (30.8%) had postoperative complications, including five with transient ataxia and two with pseudomeningocele. Nine patients (23.1%) visited the ED after surgery, and 7 (17.9%) were readmitted. The rate of opioid use decreased from 56.4% at baseline to 32.3% six months following surgery (p = 0.03). Additionally, the use of carbamazepine, gabapentin, pregabalin, duloxetine, and amitriptyline decreased. One year after surgery, 11/26 patients (42.3%) reported sustained pain relief. CONCLUSIONS: In this case series of NC-DREZ patients, we demonstrated that postoperative complications and subjective pain outcomes were comparable to those previously reported in the literature. Importantly, we demonstrated a reduction in the use of opioids six months after surgery. This study's findings support the use of NC-DREZ as an alternative treatment for painful trigeminal neuropathy. Large scale prospective studies are needed to confirm these results.

Estimulación del ganglio de Gasser para dolor neuropático del trigémino refractario

Background and objectivePainful trigeminal neuropathy is a complex clinical entity due to its severity and refractoriness to pharmacological and interventional management. We describe our experience in treating refractory painful trigeminal neuropathy (RPTN) with Gasserian ganglion stimulation (GGS). Materials and methodsSix patients with RPTN were treated with GGS in our unit between 2019 and 2022. The following data were collected: socio-demographic characteristics, triggering event, duration of the disease and treatment received prior to surgery, pre- and post-intervention visual analogue scale score, follow-up time, and pre- and post-intervention functionality and quality of life. ResultsAll patients were women who had received aggressive first-, second-, and third-line pharmacological, non-pharmacological, and interventional management before being referred for GGS. Patients reported a 50-72% decrease in pain on visual analogue scale and improved functionality during follow-up. ConclusionsGGS is a promising therapeutic alternative for patients with RPTN. Although the initial outcomes and experience are encouraging, RPTN is recommended on the basis of safety, reproducibility, and trends observed in clinical practice.

The use of Pulsed Radiofrequency in the treatment oftrigeminal neuralgia and painful trigeminal neuropathy –two clinical cases

Trigeminal neuralgia, one of the pain conditions with severe pain, can be effectively treated with pharmacotherapyand invasive methods of pain treatment (at the level of the peripheral nerve, Gasser's ganglion, or nerve root). Painfultrigeminal neuropathy is defined as facial pain in one or more branches of the trigeminal nerve caused by otherconditions or damage to the nerve. This condition can be effectively treated with individual pharmacotherapy andnon-pharmacological methods, and in some cases, invasive methods. In both diseases, many treatment methodscan be proposed, including the minimally invasive procedure of pulsed radiofrequency (PRF). The following studypresents two cases of successful therapy using pulsed radiofrequency of the peripheral branches of the trigeminalnerve in patients with trigeminal neuralgia and painful trigeminal neuropathy. Prior to the procedure, pain relief wasobtained in the painful branches of the trigeminal nerve after a diagnostic block. pulsed radiofrequency is a minimallyinvasive, safe for the patient treatment method.

Long-Term Results of Cortical Motor Stimulation for Neuropathic Peripheral and Central Pain: Real-World Evidence From Two Independent Centers.

Cortical motor stimulation (CMS) is used to modulate neuropathic pain. The literature supports its use; however, short follow-up studies might overestimate its real effect. This study brings real-world evidence from two independent centers about CMS methodology and its long-term outcomes. Patients with chronic refractory neuropathic pain were implanted with CMS. The International Classification of Headache Disorders 3rd Edition was used to classify craniofacial pain and the Douleur Neuropathique en 4 Questions Scale score to explore its neuropathic nature. Demographics and clinical and surgical data were collected. Pain intensity at 6, 12, and 24 months and last follow-up was registered. Numeric rating scale reduction of ≥50% was considered a good response. The Clinical Global Impression of Change scale was used to report patient satisfaction. Twelve males (38.7%) and 19 females (61.3%) with a mean age of 55.8 years (±11.9) were analyzed. Nineteen (61.5%) were diagnosed from painful trigeminal neuropathy (PTN), and seven (22.5%) from central poststroke pain. The mean follow-up was 51 months (±23). At 6 months, 42% (13/31) of the patients were responders, all of them being PTN (13/19; 68.4%). At last follow-up, only 35% (11/31) remained responders (11/19 PTN; 58%). At last follow-up, the global Numeric rating scale reduction was 34% ( P = .0001). The Clinical Global Impression of Change scale punctuated 2.39 (±0.94) after 3 months from the surgery and 2.95 (±1.32) at last follow-up ( P = .0079). Signs of suspicious placebo effect were appreciated in around 40% of the nonresponders. CMS might show long-term efficacy for neuropathic pain syndromes, with the effect on PTN being more robust in the long term. Multicentric clinical trials are needed to confirm the efficacy of this therapy for this and other conditions.

Occipital Nerve Stimulation for Recurrent Trigeminal Neuralgia Without Occipital Pain

ObjectivesTrigeminal neuralgia (TN) is a severe, debilitating pain condition causing physical and emotional distress. Although the management of TN is well codified with medical and then surgical treatments, 15% to 30% of patients will experience intractable pain. Neuromodulation techniques have been scarcely used for refractory TN, with only small case series and short-term follow-up. Materials and MethodsWe conducted a retrospective study of patients treated with occipital nerve stimulation (ONS) for medically and surgically resistant TN without painful trigeminal neuropathy. The effectiveness of the ONS was evaluated using the Barrow Neurological Institute (BNI) pain score and the pain relief (0%–100%) at best and at last follow-up. ResultsSeven patients who have refractory TN were included. The mean age at ONS was 49 years. The mean pain duration was 8.6 years. The mean number of medical and surgical treatments before ONS was six and five, respectively. A percutaneous trial was performed in five of seven patients; all responded (pain relief > 40%), and four of five patients experienced pain recurrence after explantation. Eventually, six patients had a permanent ONS implantation. The average BNI pain score before implantation was V. The mean follow-up after implantation was 59 months. All patients reported an improvement after implantation. The average BNI score and mean pain relief at best were IIIa and 86.7%, respectively. At last follow-up, the average BNI score and mean pain relief were IIIa and 58.0%, respectively, with three patients experiencing pain recurrence. Adverse events were reported for four patients who required surgical revision for lead breakage (1), erosion (1), migration (1), or hardware-related discomfort (1). One patient finally underwent explantation because of infection. ConclusionsAlthough ONS is not validated in this indication, these results suggest that it can induce an improvement in TN recurring after several surgical treatments, and the benefit of the stimulation can be sustained in the long term. Clinical Trial RegistrationThe Clinicaltrials.gov registration number for the study is NCT01842763.

Neuromodulation for Trigeminal Neuralgia.

Clinical studies on neuromodulation intervention for trigeminal neuralgia have not yet shown promising results. This might be due to the fact that the pathophysiology of chronic trigeminal neuropathy is not yet fully understood. Chronic trigeminal neuropathy includes trigeminal autonomic neuropathy, painful trigeminal neuropathy, and persistent idiopathic facial pain. This disorder is caused by complex abnormalities in the pain processing system, which is comprised of the affective, emotional, and sensory components, rather than mere abnormal sensation. Therefore, integrative understanding of the pain system is necessary for appropriate neuromodulation of chronic trigeminal neuropathy. The possible neuromodulation targets that participate in complex pain processing are as follows : the ventral posterior medial nucleus, periaqueductal gray, motor cortex, nucleus accumbens, subthalamic nucleus, globus pallidus internus, anterior cingulate cortex, hypothalamus, sphenopalatine ganglion, and occipital nerve. In conclusion, neuromodulation interventions for trigeminal neuralgia is yet to be elucidated; future advancements in this area are required

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.

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.

Painful Trigeminal Neuropathy and Horner's Syndrome as Manifestations of Cervical Myelopathy.

Painful Trigeminal Neuropathy and Horner's Syndrome as Manifestations of Cervical Myelopathy.

Prevention and diagnosis of neuropathy during dental treatment

Peripheral nerves are often subjected to various forces such as surgical invasion, trauma, disease infiltration, and drug action. These attacks cause the peripheral nerve fibers to be pulled, pressed, damaged, or ruptured, resulting in a decline in peripheral function or loss of function. This symptom is often expressed in various ways such as numbness, palsy, paralysis, neuropathy, and nerve abnormality. Paralysis in the oral and facial areas includes motor palsy associated with efferent peripheral neuropathy such as the facial and hypoglossal nerves and sensory palsy associated with afferent peripheral neuropathy such as the inferior alveolar nerve and the lingual nerve. In addition, dysgeusia, taste disorders, dysfunction of autonomic nerves, and autonomic neuropathy may occur in the oral cavity and the facial region as one of paralysis. If these symptoms or disorders recover within days to weeks, it is temporary loss of motor and sensory function due to blockage of nerve conduction, and the diagnosis is neurapraxia. On the other hand, if the symptoms of paralysis persist and the aftereffects remain, or if the function does not recover at all, it can be diagnosed as axonotmesis or neurotmesis. Paralysis is exceedingly difficult to diagnose the prognosis and degree of disability only by the initial symptoms. In particular, the sensory function is more difficult to evaluate than the motor function because the sensory cannot be visualized, and therefore the diagnostic criteria cannot be determined, and inaccurate diagnosis causes confusion in the course of treatment. As a result, despite the definitive diagnosis being Neurapraxia, there is the possibility of giving unnecessary medication, surgical treatment, or wrong physical therapy. Not only that, but for axonotmesis and neurotmesis, which must be treated early, there is a possibility that the start of treatment will be delayed. A quantitative and objective, reproducible and accurate diagnosis is needed to determine the prognosis of paralysis and to make treatment decisions. Accurately grasping the cause of external force applied to the peripheral nerves and the timing of damage, it is possible to cure peripheral functions if the amount and duration of drug therapy and physical therapy and the timing of surgical treatment can be correctly determined. The purpose of this review is to explore preventive and diagnostic methods for peripheral neuropathy during dental treatment. Therefore, we considered the need for a Precision tactile function test for painful trigeminal neuropathy and neuropathic pain, considering the time to fix the symptoms of neuropathy. In addition, we discussed the treatment experience of hyperalgesia and allodynia caused by disorders of the somatosensory nervous system.

Altered Brainstem Pain-Modulation Circuitry Connectivity During Spontaneous Pain Intensity Fluctuations.

BackgroundChronic pain, particularly that following nerve injury, can occur in the absence of external stimuli. Although the ongoing pain is sometimes continuous, in many individuals the intensity of their pain fluctuates. Experimental animal studies have shown that the brainstem contains circuits that modulate nociceptive information at the primary afferent synapse and these circuits are involved in maintaining ongoing continuous neuropathic pain. However, it remains unknown if these circuits are involved in regulating fluctuations of ongoing neuropathic pain in humans.MethodsWe used functional magnetic resonance imaging to determine whether in 19 subjects with painful trigeminal neuropathy, brainstem pain-modulation circuitry function changes according to moment-to-moment fluctuations in spontaneous pain intensity as rated online over a 12-minute period.ResultsWe found that when pain intensity was spontaneously high, connectivity strengths between regions of the brainstem endogenous pain-modulating circuitry—the midbrain periaqueductal gray, rostral ventromedial medulla (RVM), and the spinal trigeminal nucleus (SpV)—were high, and vice-versa (when pain was low, connectivity was low). Additionally, sliding-window connectivity analysis using 50-second windows revealed a significant positive relationship between ongoing pain intensity and RVM-SpV connectivity over the duration of the 12-minute scan.ConclusionThese data reveal that moment-to-moment changes in brainstem pain-modulation circuitry functioning likely contribute to fluctuations in spontaneous pain intensity in individuals with chronic neuropathic pain.

Painful trigeminal neuropathy associated with anti-Plexin D1 antibody.

ObjectiveTo determine whether anti-Plexin D1 antibody (Plexin D1-immunoglobulin G [IgG]), which is associated with limb and trunk neuropathic pain (NP) and binds to pain-conducting small unmyelinated dorsal root ganglion (DRG) neurons, exists in patients with idiopathic painful trigeminal neuropathy (IPTN) and whether Plexin D1-IgG binds to trigeminal ganglion (TG) neurons.MethodsWe enrolled 21 consecutive patients with IPTN and 35 age- and sex-matched controls without NP (25 healthy persons and 10 with neurodegenerative diseases). We measured serum Plexin D1-IgG using a mouse DRG tissue–based indirect immunofluorescence assay (IFA) and by Western blotting (WB) using a recombinant human Plexin D1 (rhPlexin D1) accompanied by immunoadsorption tests with rhPlexin D1. The reactivity of Plexin D1-IgG toward mouse TG, brain, heart, and kidney was assessed by tissue-based IFAs.ResultsSerum Plexin D1-IgG was detected more frequently in IPTN than in controls by both IFA and WB (14.3% vs 0%, p = 0.048). Three Plexin D1-IgG–positive patients also had limb or trunk NP and commonly showed tongue pain. In tissue-based IFAs, IgG from 2 Plexin D1-IgG–positive patients immunostained small TG neurons, which was prevented by preincubation with rhPlexin D1. Moreover, Plexin D1-IgG immunostaining mostly colocalized with isolectin B4-positive pain-conducting unmyelinated TG neurons. IFAs of other tissues with the same IgG revealed weak immunoreactivity only in endothelial cells, which was prevented by preincubation with rhPlexin D1.ConclusionsPlexin D1-IgG, which binds to pain-conducting small TG neurons in addition to DRG neurons, can be present in IPTN as well as limb and trunk NP.

Exploring the time course of painful post-traumatic trigeminal neuropathy: a pilot study

Patients suffering from painful post-traumatic trigeminal neuropathy (PTTN) often report circadian variations in pain. This pilot study aimed to assess the daily evolution of pain in patients fulfilling the following criteria: PTTN diagnosed based on ICHD-3 criteria; >18 years of age; no impairment in communication and signed informed consent. Primary study outcome was a self-declared quantitative assessment of pain intensity using an 11-point numerical scale (0–10) for 8 consecutive days. Impact on oral function and quality of life was also assessed, using psychometric questionnaires GOHAI and HADS. Eleven patients with PTTN were recruited (mean age: 66.1 ± 6.8 years old). Mean pain intensity was 3.6 ± 0.99. Mean pain intensity increased progressively and significantly during the day, from 1.8 ± 1.3 to 4.6 ± 2.3 (p < 0.0001). Mean HADS score was 7.8 ± 2.7. Mean GOHAI score was weak (35/60). In conclusion, PTTN seems to follow a circadian rhythm.

Хроническая нейропатическая лицевая боль при поражении черепных нервов: клиника, диагностика, лечение

The purpose — to study of the features of chronic neuropathic facial pain associated with cranial nerve damage. Material and methods. We studied the modern works on the features of the clinic, diagnosis and treatment of chronic orofacial pain caused the cranial nerves damage. Special attention was paid to the methods of diagnosing neuropathic facial pain of various etiologies, and identifying clinical variants of their course. Results. The best known and most common variant of neuropathic orofacial pain is trigeminal neuralgia. There are classic trigeminal neuralgia that occurs as a result of vaso-neural conflict, secondary trigeminal neuralgia (in multiple sclerosis, voluminous brain neoplasm, etc.), and idiopathic trigeminal neuralgia. Patients have short-term (from fractions of a second to 2 minutes) unilateral paroxysmal facial pain in classic trigeminal neuralgia. In case of secondary trigeminal neuralgia, mainly bilateral neuropathic pain is detected. Painful trigeminal neuropathy (trigeminal neuropathic pain other than trigeminal neuralgia) is caused by trauma and herpes zoster with acute neuropathic pain. After 3 months, painful manifestations after the herpes zoster are qualified as trigeminal postherpetic neuralgia. Post-traumatic neuropathic trigeminal pain is the result of external trauma or iatrogenic damage resulting from dental treatment or neuroablation procedures. Both classical and secondary, idiopathic neuralgia of the glossopharyngeal nerve is characterized by unilateral short-term stabbing pain in the ear, base of the tongue, tonsil region, posterior part of the pharynx; it is less common, in contrast to trigeminal neuralgia. Intermediate nerve neuralgia was first described in 1907 by Hunt; it is rare, manifests itself as unilateral, shooting, paroxysmal pain in the ear canal and temporal areas. Painful neuropathy of the intermediate nerve (Ramsey — Hunt syndrome) with herpes zoster is characterized by dull, persistent pain that occurs inside the ear canal, auricle or mastoid. Rarely, tumors of the face can be the cause of Ramsey — Hunt syndrome. Conclusion. Thus, chronic neuropathic facial pain associated with facial nerves damage has a varied etiology, which requires careful differential diagnosis and selection of adequate treatment tactics.

Pulsed radiofrequency of superior cervical ganglion for treatment of painful post-traumatic trigeminal neuropathy (PTTN): A case series report

ABSTRACT Objective: Painful post-traumatic trigeminal neuropathy (PTTN) is a clinical pain syndrome that occurs due to injuries to the peripheral branches of the trigeminal nerve and is characterized by a deep burning pain and accompanied by positive and negative neurological signs. In patients with recalcitrant PTTN, the sympathetic nervous system is a potential therapeutic target. The aim of this study was to investigate the therapeutic response of PTTN patients to pulsed radiofrequency treatment (PRF) of the superior cervical sympathetic ganglion (SCG). Methods: Thirty-five patients with PTTN who had a history of severe disabling facial neuropathic pain underwent PRF of the SCG under a new lateral fluoroscopic approach. Results: The patients’ pain intensity post-PRF was 3.94 (± 3.11), compared with 8.82 (± 1.27) pre-PRF (p < 0.001). Conclusion: PRF of the SCG could be an effective method to treat chronic PTTN.

Sleep Disorders and Chronic Orofacial Pain

Sleep disturbances have been linked to chronic pain disorders and it has been suggested that they affect each other in a circular fashion. However, with the exception of sleep bruxism and temporomandibular disorders, very little is known about the interaction between sleep and specific orofacial pain disorders. We aimed to review and evaluate the existing knowledge about the relationship between orofacial pain and sleep disorders. Furthermore, to elaborate on management options for patients with orofacial pain and sleep disorders. Orofacial pain disorders such as temporomandibular disorders, burning mouth syndrome, and painful post-traumatic trigeminal neuropathy are reciprocally related to disturbances in sleep quality. Furthermore, in the case of temporomandibular disorders, it has been shown that sleep quality disturbances occur before pain onset. Regarding sleep bruxism, the recent literature seems to indicate that when sleep bruxism is assessed objectively (i.e., polysomnography), most sleep bruxism parameters do not seem to be able to explain temporomandibular disorder occurrence. Finally, very few studies have assessed the effect sleep quality improvement has on chronic orofacial pain parameters such as intensity and frequency. In general, there is a lack of studies assessing the relationship between sleep disturbances and orofacial pain disorders, the exception being the relationship between sleep bruxism and TMD. The few studies that exist suggest an association between orofacial pain disorders and decreased sleep quality. As such, it is important that the orofacial pain clinician be aware of comorbid sleep disorders and a multidisciplinary and integrative approach should be used to manage these patients.

Role of Advanced Imaging in Gasserian Neurolysis in Head and Neck Cancer with Skull Base Invasion

Introduction A 46-year-old female with a postoperated case of carcinoma left upper alveolus diagnosed in March 2018, with recurrence, was presented to the hospital. She had lancinating pain around left facial pain, which gradually increased over 10 months. On numerical rating scale, her pain was 9 on 10. Her chief complaint was continuous dull pain above and below the left eye, with sudden, brief, paroxysmal episodes of intolerable burning and stabbing type of pain. This episodic pain lasted for 30 to 40 seconds. On examination, she had left III, V, and VI nerve palsy with ptosis. Magnetic resonance imaging of face and brain revealed an enhancing infiltrative mass in left maxillary sinus extending to base of skull. Clinical diagnosis of left-sided painful trigeminal neuropathy in ophthalmic and maxillary (V1 and V2) division was made. Aim This study was aimed to relieve patient’s pain and improve her quality of life. Materials and Methods Gasserian neurolysis was successfully completed under computed tomography (CT) guidance because of the distortion of skull base anatomy using a 22-G, 10-cm long spinal needle directed towards foramen ovale (FO) from a lateral approach. Conclusion CT-guided identification of foramen ovale can be labeled as a novel method of locating FO for precise percutaneous techniques to the trigeminal ganglion in advanced head and neck cancers.

Trigeminal autonomic cephalalgias presenting in a multidisciplinary tertiary orofacial pain clinic

Orofacial pain may have a variety of causes and offers a significant clinical challenge for its diagnosis and management.ObjectiveTo assess the headache disorders presenting in a tertiary multidisciplinary orofacial pain clinic, after dental causes have been excluded.MethodsClinic letters from the initial consultation and subsequent follow up reviews of the 142 patients, who were seen in the tertiary Multidisciplinary Orofacial Pain clinic between January 2015 until January 2018 were reviewed as a clinical audit.ResultsThe most common diagnoses were possible trigeminal autonomic cephalalgia (n = 62, 44%), migraine (n = 38, 27%) and painful post-traumatic trigeminal neuropathy (n = 17, 12%). The most common trigeminal autonomic cephalalgia diagnosis was hemicrania continua (n = 13, 9%), which is higher than the reported prevalence in neurology and headache clinics.ConclusionThis study demonstrates the importance of a multidisciplinary approach to diagnosing complex orofacial pain patients and the importance of awareness of primary headache disorders, in particular trigeminal autonomic cephalalgias, thereby reducing unnecessary diagnostic delays or procedures.

Injection of ropivacaine combined with pregabalin in a patient with post-traumatic trigeminal neuropathic pain

Introduction: Post-traumatic painful trigeminal neuropathy is a chronic facial pain secondary to trigeminal nerve injury. The treatment of this pain is a therapeutic issue due to the alteration of quality of life that it generates. Observation: A 58-year-old man whose main history of facial trauma has been consulted in the Odontology Department for bilateral trigeminal neuropathic pain that has been evolving for several months. The interrogation revealed continuous pain like electric shocks in the canine areas and daily painful exacerbations. Hyperesthesia and allodynia were found on clinical examination. The patient had received several treatments, oral and local, without significant improvement. As a last resort, injections of ropivacaine every 2 weeks associated with pregabalin (200 mg/day) were performed. At 6 months, there was a clear decrease in the burning sensation and a complete disappearance of painful exacerbations. Discussion: Two studies have recently shown the benefit of the combination of an antiepileptic and a local analgesic in the treatment of classical trigeminal neuralgia, justifying their use in a context of post-traumatic neuropathic pain. Conclusion: Further studies with higher levels of evidence are needed to confirm these preliminary results.