Cause Of Facial Pain Research Articles

“Burning mouth syndrome in Parkinson’s disease: dopamine as cure or cause?” Letter to the Editor Reply

We appreciate Drs. Fortuna and Pollio’s interest in our case report describing a woman with Parkinson’s disease who developed burning mouth syndrome (BMS) with carbidopa/levodopa therapy that resolved after its discontinuation and initiation of a dopamine agonist. The authors bring up an excellent and also contentious point regarding the semantics of burning mouth syndrome [1, 2]. We utilize the current diagnostic criteria from the International Headache Society which classifies primary BMS under “Central causes of facial pain” [3]. The intent of reporting our case was not to define the syndrome, but instead to contribute anecdotal evidence to the hypothesis that the pathophysiology of BMS is related to dopamine dysregulation. We believe our case supports this notion given our patient’s diagnosis of Parkinson’s disease and apparent accentuation of BMS symptoms with administration of carbidopa/levodopa [4–6]. Our speculation is that carbidopa/levodopa’s central action led to the neurophysiological manifestations of BMS. Beyond superficially dismissing our patient’s symptoms as drug induced, the value in our case is related to deeper consideration of the underlying pathogenesis of BMS. Although we agree with the authors that it is quite difficult to delineate the role of depression and anxiety in cases of burning mouth syndrome [7], we did not think these psychiatric factors were of primary relevance in our case as there was no history of such. As outlined in our report, her BMS symptoms precisely correlated to carbidopa/levodopa administration. We appreciate the input of Drs. Fortuna and Pollio and come to the agreement that it is helpful to look at BMS from a multidisciplinary perspective. This approach will only advance our understanding of a disease plaguing patients who seek care from a variety of specialists.

Die neurochirurgische Therapie der Trigeminusneuralgie

The Trigeminal Neuralgie (TN) is he most common cause of facial pain with an incidence of 27 per 100'000 patients per year. The symptoms are paroxysmal stabbing, tearing, and burning pain usually in the area of the second and third trigeminal nerve, that can be provoked by drinking, shaving, chewing or talking. If the classical drug therapy with anticonvulsants is not sufficient or must be discontinued due to side effects, then the retrosigmoidal craniotomy and micro-vascular decompression in vascular-nerve-contact ot partial rhizotomy are good pain-free procedures. Such operations are of low risk in the hands of experienced neurosurgeons and possible to be carried out even in elderly patients. A high percentage of free of complaints postoperative and low recurrence rate legitimate this method.

How to Investigate and Treat: Migraine in Patients with Temporomandibular Disorders

Migraine and temporomandibular disorders (TMD) are highly prevalent conditions that frequently coexist in the same patient. The relationship between migraine and TMD is complex. Migraineurs often have pain in the TMD area; TMD sufferers, in turn, often experience headaches in addition to the pain in the jaw. Finally, migraine and TMD are comorbid, and the final phenotype of patients with the comorbidity may represent the aggregated contribution of both. Herein we briefly discuss the clinical commonalities of migraine and TMD, and the differential diagnosis of these conditions with other causes of facial pain. We close by presenting our experience in the treatment of patients with the comorbidity.

Differential diagnosis for orofacial pain, including sinusitis, tmd, trigeminal neuralgia

Correct diagnosis is the key to managing facial pain of non-dental origin. Acute and chronic facial pain must be differentiated and it is widely accepted that chronic pain refers to pain of 3 months or greater duration. Differentiating the many causes of facial pain can be difficult for busy practitioners, but a logical approach can be beneficial and lead to more rapid diagnoses with effective management. Confirming a diagnosis involves a process of history-taking, clinical examination, appropriate investigations and, at times, response to various therapies. Although primary care clinicians would not be expected to diagnose rare pain conditions, such as trigeminal autonomic cephalalgias, they should be able to assess the presenting pain complaint to such an extent that, if required, an appropriate referral to secondary or tertiary care can be expedited. The underlying causes of pain of non-dental origin can be complex and management of pain often requires a multidisciplinary approach.

Nose and headache: what have we learned?

Sinonasal involvement in secondary headache has long been interpreted as sinusitis and overestimation has been a problem in the past. In the last 20years, the innovative interpretation of contact points between the lateral nasal wall and the septum as triggering cause of facial pain via the trigeminovascular system has gained importance in nasal secondary headaches. Also in this case, the prevalence and relevance has been misinterpreted in the beginning, undermining the success rate of pain improvement after surgical removal of these contact points. Therefore, studies have started to concentrate on the need of suitable preoperative evaluation to define the ideal, responsive candidate for surgical management of this form of headache. This article analyzes the outcome of these studies and tries to highlight the need for long-term follow-up to finally determine the relevance of surgical treatment for this particular headache form.

Venous haemangioma of the mandibular division of the trigeminal nerve

To present a rare cause of facial pain, and the differential diagnosis of a lesion of the mandibular division of the trigeminal nerve. A 19-year-old woman presented to a tertiary referral skull base centre with right periorbital pain and a progressive, right-sided deficit of the mandibular division of the trigeminal nerve. Clinical examination revealed right-sided hypoaesthesia in the mandibular division of the trigeminal nerve dermatome, mild trismus and some wasting of the right masseter muscle. Computed tomography and magnetic resonance imaging scans revealed a small area of mildly enhancing soft tissue centred within the foramen ovale, with concentric enlargement. Surgery was undertaken via an infratemporal fossa (Fisch) type D approach. A vascular lesion was found filling the foramen ovale, with no obvious nerve separate from the lesion. The lesion was removed en bloc. Histopathological analysis demonstrated a venous haemangioma within the nerve. Facial pain is common, and may be wrongly attributed to trigeminal neuralgia. A thorough clinical examination must be performed to identify subtle neurological abnormalities, and appropriate imaging undertaken to exclude rare causes, such as this venous haemangioma of the mandibular division of the trigeminal nerve.

Guidelines on the diagnosis and the current management of headache and related disorders.

There are at present no existing guidelines on “headache” that pertain to the Indian setting. With a view to standardizing headache diagnosis across the country and keeping in mind treatment issues peculiar to our setting, these Guidelines have been evolved to help primary care physician's deal with headache patients. These Guidelines have been drawn up by neurologists with a special interest in headache. With limited evidence in literature regarding headache practice and treatment in India, these guidelines are more experience based than evidence based. All contributors have adhered to the second edition of the International Classification of Headache Disorders (ICHD2-2004). In ICHD2, the first four categories deal with the primary headaches.[1–5] The next eight categories deal with headaches due to identifiable secondary causes.[6–13] The last two categories deal with cranial neuralgias and other causes of facial pain.[14–17] It is well accepted that no practice guidelines can cover all situations. Some headaches need to be handled by a neurologist but for the most part, primary care physicians are the ones who should be ideally handling headaches and these guidelines are targeted toward that end. These guidelines reflect current clinical practice trends in India. Every chapter has a brief introduction, followed by the salient diagnostic features, the way to investigate and treatment options. A summary of important practice points regarding when to refer to a specialist has also been included. Common entities have been described in greater detail while rare conditions that are seen less often are only mentioned in passing. The following is a brief listing of the headache conditions that are included in the second edition of The Classification of Headache Disorders of the International Headache society- ICHD2 (2004). The rubrics employed in all the chapters will be the same that is used in ICHD2.

Trigeminal Neuralgia: Role and Neurosurgical Indications of Peripheral Alcohol Injections, Controlled Radiofrequency Thermocoagulation, Gasserian Ganglion Compression with Balloon and Microvascular Decompression in Posterior Cranial Fossa. Experience in 437 Patients

Introduction: Trigeminal neuralgia is a common cause of facial pain. Many therapies are accomplishable; purpose of the study is to evaluate the role and the indications, in our experience, of peripheral alcohol injections, controlled radiofrequency thermocoagulation, gasserian ganglion compression with balloon and microvascular decompression in posterior cranial fossa. Methods: A series of 437 patients treated with various surgical methods for idiopathic trigeminal neuralgia refractory to medical therapy is presented. The treatments were performed according to the interested trigeminal division, the gravity of the neuralgia, the age and the general conditions of the patients. Moreover, the role of radiosurgery is underlined. Results: Peripheral alcohol injections resulted very effective for temporary control of dolorific attacks. Thermocoagulation resulted a very effective and stable method for isolated III division trigeminal neuralgia; balloon compression was very effective for pain control but entire hemifacial anesthesia was necessary to obtain a good outcome; microvascular decompression resulted affective but was reserved for young healthy patients (trigeminal neuralgia is predominant in advanced age). Conclusions: In our opinion, each treatment should be indicated according to neuralgia (interested trigeminal division, gravity) and patient (age, general conditions) characteristics, to perform the best treatment for each patient.

3. Persistent Idiopathic Facial Pain

Persistent idiopathic facial pain, previously known as atypical facial pain, is described as a persistent facial pain that does not have the classical characteristics of cranial neuralgias and for which there is no obvious cause (International Classification of Headache Disorders in 2004). According to these criteria, the diagnosis is possible if the facial pain is localized, present daily, and throughout all or most of the day. By definition, neurological and physical examination findings in persistent idiopathic facial pain should be normal. Forming a diagnosis is not simple and follows a process of elimination of other causes of facial pain. The precise incidence is unknown. The affliction is seen primarily in older adults and rarely in children. The pathophysiology is unknown. In persistent idiopathic facial pain, there is no abnormal processing of somatosensory stimuli in the pain area or facial area of the primary somatosensory cortex of the brain. The treatment is difficult and often requires a multidisciplinary approach. The most important part of the treatment is psychological counseling and pharmacological therapy. Pharmacological treatment with tricyclic antidepressants and anti-epileptic drugs can be tried. The conservative, pharmacological treatment with amitryptiline is the primary choice. Venlafaxine and fluoxetine treatment can also be considered. When the pharmacological treatment fails, pulsed radiofrequency treatment of the ganglion pterygopalatinum (sphenopalatinum) can be considered (2 C+).

1. Trigeminal Neuralgia

Trigeminal neuralgia is a common cause of facial pain. It has a significant impact on the quality of life and the socioeconomic functioning of the patient. The aim of this review is to provide recommendations for medical management of trigeminal neuralgia based on current evidence. Based upon the analyses of the literature combined with experience in pain management, symptoms, assessment, differential diagnosis, and treatment possibilities of trigeminal neuralgia are described and discussed. Recommendations for pain management are given and are displayed in a clinical practice algorithm. Treatment should be multidisciplinary. Various treatment options and their risks should be discussed with the patient. The first treatment of choice is carbamazepine or oxcarbazepine. In younger patients, the first choice of invasive treatment is probably microvascular decompression. For elderly patients, radiofrequency treatment of Gasserian ganglion is recommended and the technique is described in detail.

Practice Parameter: The diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review)

Trigeminal neuralgia (TN) is a common cause of facial pain. To answer the following questions: 1) In patients with TN, how often does routine neuroimaging (CT, MRI) identify a cause? 2) Which features identify patients at increased risk for symptomatic TN (STN; i.e., a structural cause such as a tumor)? 3) Does high-resolution MRI accurately identify patients with neurovascular compression? 4) Which drugs effectively treat classic and symptomatic trigeminal neuralgia? 5) When should surgery be offered? 6) Which surgical technique gives the longest pain-free period with the fewest complications and good quality of life? Systematic review of the literature by a panel of experts. In patients with trigeminal neuralgia (TN), routine head imaging identifies structural causes in up to 15% of patients and may be considered useful (Level C). Trigeminal sensory deficits, bilateral involvement of the trigeminal nerve, and abnormal trigeminal reflexes are associated with an increased risk of symptomatic TN (STN) and should be considered useful in distinguishing STN from classic trigeminal neuralgia (Level B). There is insufficient evidence to support or refute the usefulness of MRI to identify neurovascular compression of the trigeminal nerve (Level U). Carbamazepine (Level A) or oxcarbazepine (Level B) should be offered for pain control while baclofen and lamotrigine (Level C) may be considered useful. For patients with TN refractory to medical therapy, Gasserian ganglion percutaneous techniques, gamma knife, and microvascular decompression may be considered (Level C). The role of surgery vs pharmacotherapy in the management of TN in patients with MS remains uncertain.

Poster 238: RAGE, Inflammation, and Temporomandibular Joint Disorders

Temporomandibular Joint Disorders (TMDs) are a common cause of facial pain. Although the etiology of TMDs is yet to be fully elucidated, histologic and arthroscopic studies strongly suggest that the inflammatory process is similar to that seen in osteoarthritis of other synovial joints. The Receptor for Advanced Glycation Endproducts (RAGE) is a multiligand receptor that is present on cells of the monocyte/macrophage lineage, vascular cells, and many tumor cells. RAGE is expressed at low levels in most normal tissues and is upregulated where its ligands are present. This receptor binds multiple ligands including a number of Advanced Glycation Endproducts (AGEs), S100/calgranulins, proinflammatory cytokines, MAC-1, a leukocyte beta-2 integrin receptor, and amphoterin, also known as HMGB1, a DNA binding protein released during cell necrosis, resulting in activation of a number of critical cell signaling pathways as well as the generation of reactive oxygen species. It appears that RAGE is emerging as a key inflammatory mediator. In order to investigate the role that RAGE and its ligands play in TMD inflammation we have utilized a transgenic murine model that overexpressses human Tumor Necrosis Factor-alpha (tg hTNF-alpha), resulting in progressive inflammation and destruction of the synovial joints. Furthermore, to test the impact of genetic deletion of RAGE these transgenic animals were breed into the RAGE null background. Animals were sacrificed at 3, 5, and 11 months of age. The temporomandibular joints (TMJ) and knee joints were examined by H & E staining, immunocytochemistry, western blot analysis for RAGE and S100b protein, and ELISA for Interleukin-1 beta (IL-1 bet&cjs0744;a and AGEs). Age and sex-matched C57BL animals and RAGE null animals served as controls. Analysis was by ANOVA and the Tukey-Kramer poc-hoc test was performed for all pair-wise comparisons. Significance was set at p < 0.05. Transgenic animals showed progressive inflammation and joint destruction with increased age, although there were significant differences between the TMJ and knee joints. At 11 months knee joints showed a large amount of destruction and synovitis. While the TMJ had some synovitis, there was only minimal articular destruction. Histological examination showed a more aggressive disease pattern in affected females compared to males in both TMJ and knee joints. RAGE staining correlated with disease progression although there was greater intensity in the knee joints. This was confirmed by western blot analysis. A significant increase in S100b levels was found in tg hTNF-alpha mice compared to control C57B6 mice. Transgenic hTNF-alpha/RAGE null mice had baseline levels of both RAGE and S100b. TNF-alpha mice expressed significantly higher levels of AGEs than control mice. Interestingly, AGE levels were significantly increased in many of the tg hTNF-alpha/RAGE null samples compared with TNF-alpha mice. IL-1 beta ELISA results demonstrated that TNF-alpha affected samples had greater levels of IL-1 beta compared with control mice. However, TNF-alpha/RAGE null samples were comparable to controls. The tg hTNF-alpha mouse is a useful model of TMD inflammation. Affected animals showed significant inflammatory changes with more severe disease observed in the knee joints when compared to the TMJs. Furthermore, RAGE upregulation is critical in the arthritic progression as insertion of the RAGE null background into the TNF mouse decreases a number of inflammatory mediators to baseline levels. RAGE blockage may have therapeutic value in the treatment of TMDs and inflammatory arthridities.

Temporomandibular disorders and other causes of facial pain

Temporomandibular disorders and facial pain cause significant discomfort and disability for affected patients. Understanding the clinical presentation, pathogenesis, and therapy is essential in helping patients who have these problems. This article critically reviews these aspects, with an emphasis on their relationship to headache.

A model for foramen ovale puncture training: Technical note

Trigeminal neuralgia is a common cause of facial pain, characterized by shock-like pain affecting one or more branches of the trigeminal nerve. When conservative treatment fails and microdecompression is not indicated, percutaneous procedures are helpful. This percutaneous approach is done by a puncture up to the Gasserian ganglion, through the foramen ovale. Although simple and safe, this puncture demands some expertise from neurosurgeons. For that, a partnership between neurosurgeons and bio-engineers has developed a model for foramen ovale puncture, allowing practice for residents and young neurosurgeons. A model for foramen ovale puncture has been created by interposition of synthetic materials over a skull, simulating the human face. This model has shown great similarity with that found in conventional surgeries, even upon repeated testing by experienced functional neurosurgeons and young residents. This model for foramen ovale puncture training has demonstrated valuable help for initial practicing of this common neurosurgical procedure, particularly in centers where there are not many cadavers available for training.

Trigeminal Neuralgia

Trigeminal neuralgia (TN) is the most common facial neuralgia, and is considered to be one of the most painful conditions to affect patients. The rate of occurrence of TN in men and women is 2.5 and 5.7 per 100,000 per year respectively. TN is generally characterized by lancinating, unilateral, paroxysmal pain occurring in the distribution of the fifth cranial nerve. The diagnosis of TN is made clinically by excluding other possible causes of facial pain and is based on signs and symptoms from the patient history such as a trigger zone, typical unilateral lancinating paroxysms following neural disturbance, and a refractory period. Generally, TN can be diagnosed by the typical patient history, a negative neurologic exam, and response to a trial of carbamazepine. Imaging studies should be considered if the diagnosis is uncertain or neurologic abnormalities are noted. Most cases are caused by compression of the trigeminal nerve root, usually within a few millimeters of entry into the pons. In a few cases, TN is caused by a primary demyelinating disorder. The treatment modalities for the management of TN may be divided into medical, surgical, and gamma-knife radiosurgery. Generally, response to drug therapy is good, with over 80% of patients responding to some of the anticonvulsants. Percutaneous approaches to trigeminal gangliolysis are considered to have less associated risk and less cost than open surgical procedures. Three different techniques may be used to perform percutaneous destruction of the ganglion: percutaneous radiofrequency trigeminal gangliolysis (PRTG), percutaneous balloon microcompression (PBM), and percutaneous retrogasserian glycerol rhizotomy (PRGR). Open surgical procedures used in the treatment of TN include microvascular decompression of the trigeminal root and retrogasserian rhizotomy. Additionally, because both of these procedures have greater associated risks, morbidity, and mortality, they are customarily applied only to younger patients in good health. Stereotactic radiosurgery has been established as an alternative treatment for patients who do not respond to optimal medical management.

Epidemiology of typical and atypical craniofacial neuralgias

Trigeminal neuralgia (TN) has a prevalence of 0.1-0.2 per thousand and an incidence ranging from about 4-5/100,000/year up to 20/100,000/year after age 60. The female-to-male ratio is about 3:2. A review of several case series shows that pain is more predominant on the right side, but the difference is not statistically significant. TN is significantly associated with arterial hypertension, Charcot-Marie-Tooth neuropathy, glossopharyngeal neuralgia (GN) and multiple sclerosis. GN has an incidence of 0.7/100,000/year and epidemiological studies have shown it to be less severe than previously thought. Post-herpetic neuralgia has a comparable incidence to idiopathic TN. The epidemiology of the central causes of facial pain is still unclear, but it is known that persistent idiopathic facial pain is a widespread, not easily manageable problem.

Algies faciales typiques et atypiques : du diagnostic au traitement

Facial pain is a frequently encountered symptom in general medical practice and encompass a wide group of facial problems. As correct diagnosis can usually be reached by history and physical examination for well defined typical clinical entities (trigeminal neuralgia, cluster headache) atypical facial pain may have many other potential causes (sinuses infection, temporomandibular joint syndrome, dental disorders...) so that diagnosis not appear an easy task. Anatomical and physiological organization of facial nociceptive system, particularly trigeminal system, may explain the variability of facial pain. Although symptoms have been clearly identified mechanism of pain production remains controversial. Several factors (psychological, neurological, endocrine...) and mechanisms (neuropathic, vascular, myoarticular) may coexist and explain trouble in diagnosing and treating facial pain. Better knowledge in identifying the cause of facial pain may lead to improve patient care and avoid patient frustration, medical nomadism, repetitive dental and otolaryngologic procedures, and finally non-compliance with treatment.

A new guidance device facilitates percutaneous puncture of the foramen ovale in human cadavers

Trigeminal neuralgia is the most common neurological cause for facial pain. Contemporary interventional treatment relies on surgical microvascular decompression or, alternatively, percutaneous interventions targeting the semilunar ganglion via the foramen ovale. For the latter approach, only free-hand punctures using fluoroscopy devices have been reported. Therefore, the present study aimed to evaluate a new fluoroscopy-based guidance device for transforaminal puncture. Two experienced examiners punctured the foramen ovale bilaterally free-hand, and using a guidance device in human cadavers (n = 9). The number of attempts for puncture was recorded. A new attempt was counted each time the needle had to be retracted for redirection. As compared to the free-hand puncture of the foramen ovale (4.44 +/- 2.79), the new guidance device significantly reduced the number of trials needed (1.37 +/- 0.69). The employment of a guidance device facilitated percutaneous transforaminal puncture and resulted in a significantly decreased number of puncture attempts as compared to free-hand techniques in human cadavers.

Botulinum toxin treatment of temporomandibular disorders, masseteric hypertrophy, and cosmetic masseter reduction

Temporomandibular disorders (TMD) are a diverse group of disorders that are characterized by pain specific to the jaws. These disorders may be divided into the following primary groups: those related to the muscles acting on the joint (myofascial) and those related to the joint itself (arthrogenic). TMD may be associated with headache, periauricular pain, neck pain, decreased jaw excursion, locking episodes, and noisy joint movement (“clicking” or “popping” sounds). The pain of TMD may be unilateral or bilateral. Epidemiologic data on TMD is difficult to accurately measure because its symptoms are variable and there are no universally accepted specific diagnostic criteria. TMD is believed to be the most common cause of facial pain after toothache. It may be present in 10% of the population at any given point in time, and 25% to 30% of the population will seek medical care for TMD during their lifetimes. 1 TMD afflicts young adults between the ages of 20 and 40 years and females more frequently than males. 2

Poster 4: RAGE, inflamation, and the temporomandibular joint

Background: Temporomandibular joint disorders (TMDs) represent a common cause of facial pain. Although the etiology of TMD is not fully elucidated, histologic and arthroscopic studies suggest that inflammation is evident and similar to osteoarthritis of other synovial joints. Evidence suggests that chronic mechanical trauma to the temporomandibular joint (TMJ) triggers generation of reactive oxidant species, resulting in the formation of advanced glycation end products (AGEs). Engagement of AGEs by their signal transduction receptor, RAGE (receptor for AGE), initiates specific signaling pathways. AGE-RAGE interaction activates a range of inflammatory cells and generates cytokines at immune/inflammatory foci. Transgenic mice overexpressing human TNF-alpha (tghTNF-alpha) display sustained inflammation in synovial joints, including the TMJ, leading to synovitis and degeneration of the joint, consequent to upregulation of multiple cytokines and key MMPs. In this model, multiple pathologic and molecular properties are shared with those observed in human TMDs. We hypothesize the tghTNF-alpha mouse is appropriate to study the biochemical cascade in TMDs. We examined the presence of RAGE in human synovial biopsy samples and in a transgenic mouse overexpressing human TNF-alpha, where progressive inflammation and destruction of the TMJ occurs.