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Purpose of review 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. Recent findings 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. Summary 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.

ObjectiveTo assess the prevalence of facial pain (V2 and/or V3) presentations among nearly 3,000 patients with headache treated in a university tertiary care center.MethodsBetween 2010 and 2018, we routinely assessed the prevalence of facial pain presentations of all patients with primary headaches.ResultsOf 2,912 patient datasets, 291 patients reported facial pain either as an independent or as an additional symptom. Among patients with migraine, 2.3% (44 of 1,935) reported a facial involvement, most commonly in V2. Of these, 18 patients (40.9%) experienced the pain predominantly in the face. In patients with cluster headache, 14.8% (42 of 283) reported a facial involvement, of which 31.0% perceived the pain predominantly in the face. A facial involvement was seen in 45.0% of patients with paroxysmal hemicrania (9 of 20), 21.4% of patients with hemicrania continua (9 of 42), and 20.0% of patients with short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing/short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (3 of 15). In addition, we present 6 patients who reported a constant side-locked facial pain with superseded well-defined facial pain attacks of 10- to 30-minute duration that appeared several times per day.ConclusionOur data suggest that a facial involvement in primary headaches is infrequent but not uncommon. A sole facial presentation of primary headache symptomatology seems to be exceptionally rare. We describe 3 different types of facial pain involvement and, in this context, distinguish patients with paroxysmal orofacial pain syndromes that have not been previously described. These patients may represent a new entity that could tentatively be called constant unilateral facial pain with added attacks.

Trigeminal neuralgia is one of the most severe facial pain syndromes. The annual incidence varies between 4-13% and has a significant effect on patient quality of life. The initial treatment of trigeminal neuralgia is pharmacological, and although other drugs have demonstrated efficacy, albeit in more limited form, carbamazepine is the only drug with sufficient level of evidence. When medical treatment fails, surgery should be considered and can opt for open surgery or minimally invasive percutaneous techniques. This paper reviews the medical and surgical therapeutic options for the treatment of trigeminal neuralgia, based on current available evidence.

Facial pain is not only one of the most common and bothersome symptoms affecting patients with obstructive sialadenitis but also a prominent symptom of numerous non-salivary pathologies. In the evaluation of patients presenting with symptoms suggestive of salivary disorders, it is critical to rule out other etiologies which may result in similar symptoms. This chapter will review a range of common and less common facial pain syndromes, with a goal of helping the provider distinguish between salivary and non-salivary etiologies of facial pain and related symptoms.

Background: Based on a classification scheme for facial pain syndromes and a binomial (yes/no) facial pain questionnaire, we previously reported on the ability of an artificial neural network (ANN) to recognize and correctly diagnose patients with different facial pain syndromes. Objectives: We now report on an updated questionnaire, the development of a secure web-based neural network application and details of ANNs trained to diagnose patients with different facial pain syndromes. Methods: Online facial pain questionnaire responses collected from 607 facial pain patients (395 female, 65%, ratio F/M 1.86/1) over 5 years and 7 months were used for ANN training. Results: Sensitivity and specificity of the currently running ANN for trigeminal neuralgia type 1 and trigeminal neuralgia type 2 are 92.4 and 62.5% and 87.8 and 96.4%, respectively. Sensitivity and specificity are 86.7 and 95.2% for trigeminal neuropathic pain, 0 and 100% for trigeminal deafferentation pain and 100% for symptomatic trigeminal neuralgia and postherpetic neuralgia. Sensitivity is 50% for nervus intermedius neuralgia (NIN) and 0% for atypical facial pain (AFP), glossopharyngeal neuralgia (GPN) and temporomandibular joint disorder (TMJ). Specificity for AFP, NIN and TMJ is 99% and for GPN, 100%. Conclusions: We demonstrate the utilization of question-based historical self-assessment responses used as inputs to design an ANN for the purpose of diagnosing facial pain syndromes (outputs) with high accuracy.

Nine days after left ophthalmic-distribution zoster, a 47-year-old man developed SUNCT headaches (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing). In contrast to two prior cases of SUNCT that developed after varicella zoster virus (VZV) meningoencephalitis without rash, this case describes an association of SUNCT with overt zoster, thus adding to the spectrum of headache and facial pain syndromes caused by VZV reactivation.

A classification scheme for facial pain syndromes describing seven categories has previously been proposed. Based on this classification scheme and a binomial (yes/no) facial pain questionnaire, we have designed and trained an artificial neural network (ANN) and as an initial feasibility assessment of such an ANN system examined its ability to recognize and correctly diagnose patients with different facial pain syndromes. One hundred patients with facial pain were asked to respond to a facial pain questionnaire at the time of their initial visit. After interview, an independent diagnosis was assigned to each patient. The patients’ responses to the questionnaire and their diagnoses were input to an ANN. The ANN was able to retrospectively predict the correct diagnosis for 95 of 100 patients (95%), and prospectively determine a correct diagnosis of trigeminal neuralgia Type 1 with 84% sensitivity and 83% specificity in 43 new patients. The ability of the ANN to accurately predict a correct diagnosis for the remaining types of facial pain was limited by our clinic sample size and hence less exposure to those categories. This is the first demonstration of the utilization of an ANN to diagnose facial pain syndromes.

Trigeminal autonomic cephalgias (TACs) include a spectrum of primary headache syndromes associated with cranial autonomic dysfunction. Other types of headache and facial pain syndromes can be associated with marked localized facial or ear autonomic changes. We report on a group of patients suffering from episodic migraine with cranial autonomic features, patients with different presentations of the ‘red ear syndrome’ (RES), cluster headache with prominent lower facial involvement and crossover cases. In our experience crossover between TACs and migraine, RES and cluster headache is not uncommon. We propose that all these conditions belong to the same group and a unifying causative mechanism is proposed.

Orofacial pain syndromes have traditionally been divided into two groups: the typical neuralgias and atypical facial pain. While typical neuralgias are well characterised, the term atypical facial pain (now persistent idiopathic facial pain) covers a variety of poorly defined head and face pains whose aetiological mechanisms are poorly understood. This paper examines the characteristics and nosography of these conditions, and suggests they should not be considered as neuralgias (section 13 of the 2004 IHS classification) but as other primary headaches (section 4).

In 1908 Sluder described a symptom complex consisting of neuralgic, motor, sensory and gustatory manifestations that he attributed to the sphenopalatine ganglion. He stated that treatment directed at the ganglion successfully alleviated these symptoms. Over the last 90 years several reports have described patients as having sphenopalatine neuralgia and have directed treatment at the ganglion. The symptoms described and the criteria for patient selection in these studies has often been varied and deviated from Sluder’s description. In reports claiming cures with treatment directed at the ganglion the duration of post-treatment follow-up has been short. This article discusses Sluder’s description and attempts to analyse its features in the light of current understanding of the different mechanisms and categories of facial pain. It is proposed that the condition described by Sluder is a neurovascular headache that most closely resembles cluster headache in its aetiology and clinical manifestations. Wepropose that the term Sluder’s neuralgia should be discarded as there are serious flaws in its original description and many authors have misused the term leading to persistent confusion about it.

Chronic facial pain etiologies characterized by constant and unrelenting pain are often classified as trigeminal neuropathic pain or trigeminal deafferentation pain. These terms are frequently applied to a large number of facial pain syndromes that do not fall within the description of classic trigeminal neuralgia (TN). These “atypical” etiologies can be refractory to a number of pharmacological and surgical treatments. Intracranial neurostimulation therapies, such as deep brain stimulation (DBS) and motor cortex stimulation (MCS), can be utilized in an attempt to alleviate disabling pain conditions. This chapter provides a brief history of DBS and MCS for treating facial pain, along with a summary of surgical procedures, potential mechanisms of action, and clinical outcomes.

Craniofacial neuralgias and facial pain syndromes are not uncommon. According to the 2009 National Health Interview Survey, the prevalence of face pain in the US population was 3.3% in males and 6.6% in females. Although trigeminal neuralgia and temporomandibular joint dysfunction are most commonly encountered in clinical practice, the differential diagnosis list can be very exhaustive. Special emphasis should be placed on correct diagnosis and treatment rather than on symptomatic management.

This chapter will review different proposed algorithms to guide practitioners to make a precise diagnosis and hence better utilize interventional management for common headaches and facial pain syndromes. In intractable resistant headaches, patients usually benefit the most from a multidisciplinary approach incorporating physical therapy, pharmacotherapy, psychotherapy (biofeedback and relaxation therapy), and the judicious utilization of interventional pain management modalities.

Dr. Klausner reviews three common facial pain syndromes: temporomandibular pain and dysfunction syndrome, phantom tooth pain and burning mouth syndrome. Three chronic facial pain conditions—temporomandibular pain and dysfunction syndrome, phantom tooth pain and burning mouth syndrome—can puzzle dentists trying to provide diagnoses and treatment plans. Epidemiologic data and their usefulness in providing diagnostic criteria for these conditions are explored.

Atypical facial pain is a residual category for otherwise unclassifiable pain syndromes in the facial region. In 35 patients (31F, 4M) with a mean age of 53.2 ± 14.9 years and a chronic facial pain syndrome we tested the new diagnostic criteria of the International Headache Society (IHS). There was a marked female preponderance, vague description of symptoms and a long history of incorrect diagnoses. A high number of invasive procedures (3.5 ± 3.0 (1–13)) were performed in this group. In agreement with the IHS criteria, an operaiion or injury to the face was a suspected cause in 43%. In contrast to the IHS criteria, our patient sample had dysaesthesiae (63%), bilateral occurrence (37%), remission periods (57%), pain attacks (23%) and superficial as well as deep pain. The IHS classification is insufficient to separate atypical facial pain from other primary headache and facial pain syndromes. We suggest a modified version of the IHS criteria for atypical facial pain.

To preoperatively detect, by using diffusion-tensor imaging coregistered with anatomic magnetic resonance (MR) imaging, suspected microstructural tissue changes of the trigeminal nerves in patients with trigeminal neuralgia (TN) resulting from neurovascular compression.The study was approved by the institutional review board, and written informed consent was obtained from all patients. Twenty patients (mean age, 51.3 years) with TN and evidence of neurovascular contact were examined with use of a 3.0-T MR unit combined with an eight-channel head coil before undergoing surgical decompression. A single-shot diffusion-tensor echo-planar sequence was used along 15 different diffusion directions, with a b value of 1000 sec/mm(2) and a section thickness of 2 mm. For anatomic correlation, 0.6-mm isotropic three-dimensional fast imaging employing steady-state images were acquired for coregistration with the functional diffusion-tensor maps. After region of interest placement, mean fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were calculated for each nerve by using the paired-sample two-tailed t test (with P.005 indicating significance) and compared with surgical findings.FA was significantly lower (P = .004) on the trigeminal neuralgia-affected side (mean FA, 0.203) than on the contralateral side (mean FA, 0.239). ADCs were nearly identical between the normal and TN-affected nerve tissues.These findings suggest that diffusion-tensor imaging enables the identification and quantification of anisotropic changes between normal nerve tissue and TN-affected trigeminal nerves. Coregistration of anatomic three-dimensional fast imaging employing steady-state imaging and diffusion-tensor imaging facilitates excellent delineation of the cisternal segments of the trigeminal nerves.

In patients with facial pain, making the correct diagnosis is essential to avoid erroneous diagnostic and therapeutic measures. Most importantly, primary facial pain syndromes and symptomatic facial

Headaches are a significant component of many facial pain syndromes. These facial pain/headache syndromes often have various etiologies, including neurologic, vascular, musculoskeletal, or combinations of vascular/musculoskeletal origins. Referred rhinologic headache, however, can be overlooked as a cause of facial pain in the dental literature. We report a case of nasal mucosal headache that presented as facial pain and include a review of the literature.

This chapter will address a specific, and in many ways unique, pain problem: facial pain. The discussion will include, but will not be limited to a discussion of trigeminal neuralgia. Trigeminal neuralgia stands out from other facial pain syndromes in that it is relatively easily and reliably diagnosed with a brief history, and it has a number of highly effective nonsurgical and surgical treatments. Other facial pain syndromes are often not so easily diagnosed and treated, but will nevertheless appear in a clinical practice of neurosurgery from time to time.

A patient with typical trigeminal neuralgia involving the first branch of the nerve developed short-lasting unilateral attacks in the same area which were associated with severe vasomotor phenomena consistent with the recently described SUNCT syndrome. This evolution suggests that SUNCT might correspond, at least in this case, to a “transformed” trigeminal neuralgia and emphasizes the close relationship between these unilateral facial pain syndromes.

59. Burchiel KJ, Clarke H, Haglund M, et al: Long-term efficacy of microvascular decompression in trigeminal neuralgia. J Neurosurg 69:35, 1988 60. Hoffert MJ: The neurophysiology of pain. Neurol Clin 7:183, 1989 61. Kline DG, Hudson AR: Acute injuries to peripheral nerves, in Youmans JR (ed): Neurological Surgery (ed 3). Philadelphia, PA, Saunders, 1990, pp 2423-2510 62. Grey WH: Lancing the gums in stridulous convulsions. Am J Dent Sc 3:228, 1842 63. Shaber EP, Krol AJ: Trigeminal neuralgia: A new treatment concept. Oral Surg 49:286, 1980 64. Mathis B J, Oafis GW, Grisius R J: Jaw bone cavities associated with facial pain syndromes: Case reports. Milit Med 146:719, 1981 65. Wang M, Xiwei J, Qingrong I, et al: [A study of the relation between the various trigger zones of idiopathic trigeminal neuralgia and jaw bone cavities]. Acta Acad Med Sichuan 13:233, 1982 66. Demerath RR, Sist T: Treatment of osteocavitation lesions in facial pain patients: Preliminary results. J Dent Res 61:218, 1982 (abstr) 67. Grecko VE, Puzin MN: [Odontogenic trigeminal neuralgia]. Zh Nevropatol Psikhiatr 84:1655, 1984 68. McMahon RE, Griep J, Marfurt CP: Local anesthetic effects in the presence of chronic osteomyelitis of the mandible. Anesth Prog 38:189, 1991 (abstr) 69. Neville, Damm, Allen, et al: Oral and Maxillofacial Pathology. Philadelphia, PA, Saunders, 1995, pp 631-632

Effects of depression on dental care and treatment are examined, along with factors in the recognition and management of patients with depressive illness. Depressive illness may affect the patient’s response to dental care. It has been implicated both as a causal factor and a sequela in facial pain syndromes. Depression is treated with various medications that may influence function and health of the oral cavity and that may adversely interact with drugs used to control pain and anxiety.

Management of intractable facial pain is often referred to a specialised Pain Relieving Clinic, especially in light of the evidence that psychological factors play a part in the maintenance of the pain. A group of 60 patients so referred were divided into two groups according to diagnosis. The 32 diagnosed as suffering from trigeminal neuralgia were found to be more likely to deny non-pain problems, less irritable, but less convinced that there was a physical disease process responsible for their pain, than the 28 patients with non-neuralgic facial pain. Personality factors did not discriminate between the two groups. The relevance of the difference between these two groups to our understanding of pain is discussed, as is the special place of pain in the face.

Depression, anhedonia, state anxiety (A-state), trait anxiety (A-trait), and self-reported pain estimate were measured in almost 500 facial pain patients. These patients were divided into 3 diagnostic categories: myofascial pain dysfunction syndrome (MPD) [8], arthritis of the temporomandibular joints (TMJ arthritis), and trigeminal neuralgia. Three control groups were measured for comparison. They consisted of a normal, or non-patient group, a group of arthritis patients, and a group of movement disorder patients attending a neurology clinic. Among the facial pain patients and the normal controls few differences were found with regard to anhedonia and depression. The arthritis and neurology patients produced significantly higher depression and anhedonia scores than did several of the facial pain groups. Pain estimate ranged from 0 for the controls, to a mean of 67.6 ± 31.3 for the trigeminal neuralgia patients with the MPD ( x = 56.2 ± 32.5 ) and the TMJ arthritis patients ( x = 46.7 ± 30.8 ) somewhat lower. Clinical variables such as duration of pain, help seeking behavior and total number of symptoms were correlated with depression but not with anhedonia scores. It is hypothesized that anhedonia is a measure separate from depression and may be more closely linked to suffering behavior than to pain behavior. Psychological variables did not discriminate among facial pain patients and in particular did not distinguish between so-called functional and organic illness.

Claims for the first description of cluster headaches have been in dispute for years and we may never be certain who deserves the credit. Before one reviews the literature in search of the historical background of cluster headaches, it is necessary to establish acceptable clinical criteria I have undertaken to do this by relying on my own personal experience with cluster headache and on many of the criteria published in the literature.1–9

In Reply. —We agree with Dr Albert's position that TMJ syndrome and many other facial pain syndromes present numerous diagnostic and treatment problems for both the patient and clinician. Unfortunately, the treatment of TMJ syndromes takes almost as many forms as there are concerned medical specialties. Three problems contribute to this diversity: lack of a recognized cause of many of the disorders, lack of controlled and/or replicable studies of treatment outcomes, and lack of longterm follow-up examination. Moreover, the most widely used procedures do irreversible damage to teeth, nerve tissue, and the structure of the jaws. Indeed, we see many patients who are worse off than they were originally, prior to treatment. Given such considerations, Dr Albert's emphasis on invasive, irreversible modalities of treatment must be viewed with caution. He supports his views entirely with anecdotal and case history reports. We obviously need to reiterate the position taken in our original article.