Chronic facial pain that isn't caused by dental problems is a highly disabling but often underdiagnosed condition that affects thousands of patients. This comprehensive review, published in the journal Cephalalgia, explains that orofacial pain syndromes fall into three main categories: attack-like conditions (including neuralgias and facial variants of headaches), persistent pain disorders (including neuropathic pain and persistent idiopathic facial pain), and other conditions like temporomandibular disorders that can overlap with headaches. The authors emphasize that many of these syndromes can be effectively treated with medications that neurologists already commonly use for other pain conditions, and that proper diagnosis requires close collaboration between dental and neurological specialists.
Clinicians would never accept a vague diagnosis of "just headache" because treatment depends critically on identifying the specific type of headache syndrome. The International Classification of Headache Disorders (ICHD-3) has been remarkably successful in providing robust clinical criteria that define headache syndromes, leading to scientific and treatment advances.
Neurologists are rightly the primary specialists that patients consult for headache—pain in the first division of the trigeminal nerve—since the neurological examination is essential for distinguishing primary from secondary headaches. However, pain conditions affecting the second and/or third branches of the trigeminal nerve pose significant diagnostic and management difficulties for neurologists due to their heterogeneous nature.
Chronic orofacial pain that has no dental cause is certainly underdiagnosed and definitely undertreated. One reason why we don't recognize chronic orofacial pain as a neurological disease—with the possible exception of trigeminal neuralgia—is that we know so little about its mechanisms and have as yet no specific treatment to offer. The consequence is often a life-long odyssey for affected patients without a correct diagnosis.
As a result, management of orofacial pain conditions is frequently unsuccessful and risks irreversible harm to the patient. Indeed, orofacial pain and its many facets cannot be reduced to trigeminal neuralgia or persistent idiopathic (formerly called atypical) facial pain. We need to see orofacial pain syndromes as independent and distinct trigeminal disorders that deserve recognition in the headache field.
Orofacial pain (OFP) syndromes are diagnosed based on the criteria outlined in the International Classification of Orofacial Pain (ICOP), which was developed to work in harmony with the current headache classification, ICHD-3. Due to the interdisciplinary nature of orofacial pain disorders, the ICOP has been developed collaboratively by dentists, pain specialists, and neurologists to seek consensus among specialties, and it has been endorsed by the International Headache Society.
For example, the recent definitions of trigeminal neuralgia and temporomandibular disorder (TMD) are identical in both classifications, avoiding different definitions for the same disease. ICHD-3 and ICOP can therefore be cited equally, but given that ICOP is more specific for orofacial pain, it should be favored.
A close interaction between dental and neurological specialists is necessary for diagnosing such diseases. Dentists primarily exclude dental and other oral causes, while neurologists or orofacial pain specialists, on the basis of this exclusion, diagnose the specific facial pain and treat the patient. Trigeminal neurophysiology (somatosensory evoked potentials or SEP) and neuroimaging of the head (CT and MRI scans) may be needed based on the same principles as in headache diagnosis.
Just like in the diagnostic workup of headache disorders, diligent history taking and neurological examination are key to finding the right diagnosis—and therefore the right treatment—in non-dental facial pain.
If pain in the orofacial area occurs in clearly described attacks, there may still be a dental cause such as a "cracked tooth" or pulpitis. However, a non-dental pain condition is also possible, and neurologists should be aware of the relevant conditions. Broadly speaking, attack-like facial pains are subdivided into neuralgias and orofacial variants of headache syndromes.
Neuralgias can affect most cranial nerves, with the trigeminal, occipital, and glossopharyngeal nerve being the most common. The clinical characteristics of these conditions vary significantly, and proper diagnosis is essential for effective treatment.
In contrast to most other orofacial pain syndromes, cranial neuralgias are well-defined clinical syndromes with broad consensus among clinicians. As a result, diagnostic criteria have been harmonized in both ICHD-3 and ICOP, and clear guidelines for clinical management have been developed.
Due to some similarities in presentation, the most common cranial neuralgia—trigeminal neuralgia—is often misdiagnosed as dental pulpitis. It is not uncommon for patients with trigeminal neuralgia to have received invasive but ineffective dental treatment before the correct diagnosis is identified. The authors of this review refer readers to an excellent and exhaustive review on trigeminal neuralgia that has recently been published, as their focus is on the lesser-known orofacial pain syndromes.
The clinical borders between headache and orofacial pain are often blurred. Migraine and other primary headaches may extend to the maxillary dermatome (V2), sometimes even to the mandibular dermatome (V3) of the trigeminal nerve. Some patients experience an isolated facial migraine—defined as attacks fulfilling the criteria for migraine located exclusively in the V2/V3 dermatomes.
The signs and symptoms follow the diagnostic criteria of the eponymous headache syndromes. Facial manifestations of a primary headache present as three distinct types:
The prevalence of each subtype remains unclear and is probably frequently misdiagnosed and underreported. Isolated orofacial pain replicating headache (type 3) seems rarer, and in this specific and complex presentation, underreporting due to misdiagnosis is even more likely.
Migraine is probably the first primary headache that ignited interest in the relationship between head pain and facial pain. The fact that migraine involves orofacial structures was already noted by Harold Wolff in 1963. Without clear diagnostic criteria, various terms were assigned over the years, such as orofacial migraine, lower-half migraine, or migraine with isolated facial pain.
Applying the ICOP criteria, series of patients presenting with migraine as isolated facial pain have recently been published. Although the spread of headache to the face is certainly not rare, isolated migraine in the face is rather uncommon.
The presentation of isolated V2 migraine, often throbbing, accompanied by mild rhinorrhea (runny nose), and pain on head movement, may additionally lead to misdiagnosis as sinusitis. As a general rule, facial presentations of migraine are associated with later age at onset, and aura is absent or at least less common. The authors note that neither chronic facial migraine nor facial medication-overuse headache (MOH) has been described as yet.
TACs can present in the orofacial region (V2 and/or V3). These findings align with reports of "lower face cluster" headache, and short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) presenting equally in all trigeminal dermatomes. Even the facial variant of paroxysmal hemicrania has been reported.
Autonomic symptoms may vary in facial TAC, which raises the question of how specific symptoms such as conjunctival injection (redness of the eye) and tearing are for the diagnosis of TAC, or whether these autonomic signs are more specific for involvement of the ophthalmic division of the trigeminal nerve.
Reports of orofacial variants of primary headache types other than migraine and cluster headache occur with an unclear prevalence. An orofacial variant of idiopathic stabbing headache has been reported.
A very peculiar new entity is constant unilateral facial pain with additional attacks (CUFPA). In this condition, the constant dull pain is intercepted with distinct non-neuralgic pain attacks of a completely different pain character and without any accompanying symptoms. These attacks last 10–30 minutes and occur between two and 20 times per day.
These attacks distinguish this type of side-locked facial pain from persistent idiopathic facial pain (PIFP), which is defined as constant orofacial pain without any other positive or negative features and without attacks.
The treatment of a primary headache manifested as orofacial pain is similar to the corresponding primary headache. For example, an orofacial migraine is treated like a migraine, and an orofacial cluster headache is treated like a cluster headache.
While there may be subtle differences between a primary headache and its orofacial counterpart—such as the prevalence of aura or associated symptoms—no data exist on whether medications are more or less effective in orofacial variants of primary headaches. The publication of ICOP with its clear criteria will facilitate standardized trials to compare these types.
First bite syndrome (FBS) is an unusual but very memorable orofacial pain syndrome characterized by severe and piercing pain in the parotid region (the area around the salivary gland in front of the ear) that eponymously occurs with the first bite of each meal and improves with subsequent bites.
The pathophysiology has been attributed to an unbalanced sympathetic/parasympathetic innervation of the parotid gland. The syndrome is mostly seen following surgery of the parotid or parapharyngeal region. The pain lasts seconds to a few minutes.
This syndrome is sometimes misdiagnosed as atypical trigeminal neuralgia, but sodium channel blockers are largely ineffective. In contrast, botulinum toxin injections and medications used for the treatment of neuropathic pain are generally useful. However, since the syndrome is rather rare, there is no consensus regarding treatment of FBS, as evidence is limited to case reports and case series.
A typical differential diagnosis is salivary gland pain due to sialadenitis (inflammation of the salivary gland). Although a rare disorder, patients with first bite syndrome are likely to consult a neurologist or general practitioner rather than a dentist, making it important for these clinicians to recognize the condition.
Eagle syndrome is a rare disease characterized by unilateral neuralgiform pain usually in the pharynx, tongue, and jaw, triggered by jaw opening, swallowing, and neck rotation. Eagle himself described two types of this syndrome:
Repeated compression of the carotid artery may result in cerebrovascular complications. Neurological complications encompass aneurysm, dissection, occlusion of the internal and more rarely the external carotid arteries, transient ischemic attack, cerebral infarction, and sudden death due to mechanical irritation of the carotid sinus.
When a patient complains of oropharyngeal pain in association with neck and jaw movement, digital palpation of the tonsillar fossa is recommended. If there is an elongated styloid process, a bony structure may be palpable that triggers the pain and discomfort. Diagnosis of Eagle syndrome should be established with imaging modalities.
Differential diagnoses include idiopathic cranial neuralgias, migraine and TACs, temporomandibular disorders, ear, nose, and throat (ENT) diseases, and space-occupying lesions.
There is no established strong evidence for treatment of Eagle syndrome, and the treatment strategy should be discussed based on the seriousness of the patient's symptoms. Styloidectomy (surgical removal of the styloid process) is probably the method of choice, and if necessary, carotid stenting should be considered in patients with neurological signs.
However, surgical procedures are not always efficient, and first-line drugs including pregabalin, gabapentin, and duloxetine are recommended for the pain.
When non-dental orofacial pain is persistent and not attack-like, in principle two types exist: the pain is either accompanied with somatosensory changes (for example, post-traumatic trigeminal neuropathic pain, PTNP) or not accompanied by such changes (persistent idiopathic facial pain, PIFP).
If somatosensory changes occur, these characteristically appear directly in the painful area and can be either negative (hypesthesia, or reduced sensation, and hypoalgesia, or reduced pain perception) or positive (allodynia, where normally non-painful stimuli cause pain, and hyperalgesia, where painful stimuli cause exaggerated pain) or both.
Hence the old name "anaesthesia dolorosa" describing persistent pain following surgical nerve damage. Trigeminal neuropathic pain is persistent and dull/pressing in quality. Superimposed neuralgic pain paroxysms may occur, but these are not the predominant pain type.
Probably the best-known sub-form of trigeminal neuropathic pain is postherpetic neuralgia, which is usually easy to diagnose due to the pathognomonic efflorescence (characteristic skin rash) in the distribution of one or more branches of the trigeminal nerve, and consequently treated by neurologists or pain therapists.
The clinical picture of neuropathic pain and PIFP is nearly identical, although the pain character in neuropathic pain is more often described as "burning." It seems that in most cases PIFP ceases at night, and this may be an additional discrepancy between these two conditions.
Additionally, the pain location of PIFP may shift over the years and even cross to the other side, which is per definition not seen in neuropathic pain since the latter is elicited by damage to the affected peripheral nerve.
Persistent idiopathic facial pain, formerly called atypical facial pain, is defined as a constant facial pain with a dull, aching, or nagging quality, poorly localized and not following the distribution of a specific branch of the trigeminal nerve. Patients do not describe a neuralgiform, sharp-shooting pain component.
Maximum pain intensity is described mostly over the cheekbone and the upper jaw. Most PIFP patients describe a subjective swelling over the affected region, attributed to central mismatch or perceptual distortion. While initially the pain is unilateral, with increasing duration it may cross the midline.
Clinical and radiographic examinations in PIFP patients are normal and do not show local causes. If the pain is localized exclusively to a dentoalveolar site such as teeth and dentoalveolar bone, it is classified as persistent idiopathic dentoalveolar pain (PIDAP), formerly called atypical odontalgia.
It can be difficult to distinguish PIFP from painful post-traumatic trigeminal neuropathy. Many patients with persistent orofacial pain report a dental intervention or trauma around the time of pain onset. The key question is whether the orofacial pain is the result of dental pathosis or not.
Unfortunately, patients frequently have difficulties in reconstructing the sequence of events. The resulting difficulty in disentangling the causality of the orofacial pain, and the fact that these patients primarily consult dentists, lead to root-canal treatment or extraction of healthy teeth—even though tooth extractions (which effectively denervate the dental nerve fibers) carry a high risk of aggravating the situation further.
The combination of constant pain without objective findings frequently leads to the incorrect suggestion that the condition is the mere expression of a psychosomatic disorder, which adds weight to the psychological burden. This situation is reminiscent of that of a migraine patient 30 years ago. As a result, patients frequently move from specialist to specialist without receiving adequate diagnosis or treatment.
The underlying cause of PIFP remains unclear. Considering that the pain does not follow the action of a peripheral nerve, a central nervous system origin has been suggested. The clinical characteristics of PIFP and PIDAP are consistent with the recently introduced pain category: nociplastic pain, for which the underlying mechanisms are not completely understood but include an augmented pain response characterized by centrally altered sensory processing and pain modulation.
This can appear either in solitude or as a mixed-pain state also involving components of nociceptive and neuropathic pain. Part of the clinical picture is multifocal pain; co-morbidity between chronic pains is frequent. In line with this, PIDAP was recently proposed to be a chronic overlapping pain condition (COPC), although this attribution needs more clinical data.
PIDAP is characterized by constant pain localized to one tooth or a dentoalveolar site, without any spread even after tooth removal. The pain characteristics are similar to PIFP but limited to a single tooth location. Like PIFP, the clinical and radiographic examinations are normal and do not show local causes.
Treatment approaches for PIDAP mirror those for PIFP, including medications such as amitriptyline, gabapentin, pregabalin, carbamazepine, and duloxetine. Non-steroidal anti-inflammatory drugs (NSAIDs) may be used for acute pain, though their effectiveness is limited for this condition.
Burning mouth syndrome is a persistent orofacial pain condition characterized by a burning sensation in the tongue, lower lip, and hard palate mucosa. Patients often experience xerostomia (dry mouth) and dysgeusia (altered taste), as well as exaggerated responses to hot and spicy foods and drinks.
Treatment options include topical clonazepam and capsaicin, though evidence is limited to case reports and series. Cognitive behavioral therapy may also be helpful for some patients.
Painful temporomandibular disorders (TMD) and bruxism (teeth grinding) are important differential diagnoses in orofacial pain. These conditions may interfere with, trigger, or overlap with headache disorders. The definitions of TMD are now identical in both ICHD-3 and ICOP classifications, reflecting the collaborative effort between dental and neurological specialties.
TMD pain is typically located in the muscles of mastication, the temporomandibular joint, or both, and is often aggravated by jaw function such as chewing or yawning. Bruxism, which involves clenching or grinding of teeth, can contribute to muscle pain and headache.
Sinus pain is a common misdiagnosis for facial presentations of migraine. The presentation of isolated V2 migraine, often throbbing, accompanied by mild rhinorrhea, and pain on head movement, may lead to misdiagnosis as sinusitis. Patients may undergo unnecessary sinus treatments or surgeries before the correct diagnosis of migraine is established.
Dental pain, including pulpitis and cracked tooth syndrome, must always be excluded by dental examination before a diagnosis of non-dental orofacial pain is made. However, unnecessary dental interventions on healthy teeth are a significant problem in patients with neuropathic or idiopathic orofacial pain.
This review has several important implications for patients suffering from chronic facial pain:
The authors acknowledge several limitations in the current understanding of orofacial pain syndromes:
If you are experiencing chronic facial pain, here are important steps to consider:
Remember that chronic orofacial pain is a recognized medical condition with effective treatment options. You are not alone, and help is available from specialists who understand these complex pain syndromes.
PIFP is constant facial pain that is dull, aching, or nagging, poorly localized, and not following a specific nerve branch. It is not accompanied by sensory changes. The cause is unclear, but it may involve central nervous system changes. It is a recognized neurological condition, not psychological.
Diagnosis starts with a dental exam to exclude dental causes. Then a neurologist or orofacial pain specialist uses the International Classification of Orofacial Pain (ICOP) criteria. History, neurological exam, and sometimes imaging or nerve tests help identify the specific syndrome. Collaboration between dental and neurological specialists is essential.
Many orofacial pain syndromes respond to medications neurologists commonly use for other pain conditions, such as amitriptyline, gabapentin, pregabalin, carbamazepine, and duloxetine. For first bite syndrome, botulinum toxin injections and neuropathic pain medications may help. Treatment is tailored to the specific diagnosis.
Yes, migraine can spread to the face, and some patients have isolated facial migraine, with attacks fulfilling migraine criteria but located only in the cheek or jaw area. This is often misdiagnosed as sinusitis. Treatment is the same as for migraine.
Trigeminal neuralgia is a well-defined cranial neuralgia causing severe, sharp facial pain. It is often misdiagnosed as dental pulpitis, leading to unnecessary dental procedures. Unlike dental pain, it is a neurological condition. Diagnosis is based on clinical criteria, and treatment follows established guidelines.
If dental causes are excluded and pain persists, consult a neurologist or orofacial pain specialist familiar with ICOP. Keep a pain diary describing pain quality, triggers, and accompanying symptoms. Be cautious about further invasive dental procedures. A second opinion may be helpful if you've been told your pain is psychological.
Eagle syndrome is a rare condition with unilateral neuralgiform pain in the pharynx, tongue, or jaw, triggered by jaw opening, swallowing, or neck rotation. It is caused by an elongated styloid process. Diagnosis is by imaging. Treatment may include surgical removal of the styloid process, or medications like pregabalin, gabapentin, or duloxetine.
Original Article: "Orofacial pain for clinicians: A review of constant and attack-like facial pain syndromes"
Authors: Arne May, Rafael Benoliel, Yoshiki Imamura, Maria Pigg, Lene Baad-Hansen, Peter Svensson, and Jan Hoffmann
Journal: Cephalalgia, 2023, Vol. 43(8), pages 1–12
DOI: 10.1177/03331024231187160
Publication Date: Received April 4, 2023; revised May 23, 2023; accepted June 22, 2023
Affiliations: Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Germany; Rutgers School of Dentistry, New Jersey, USA; Department of Oral Medicine, School of Dentistry, Nihon University Tokyo, Japan; Faculty of Odontology, Malmö University, Sweden; Department of Dentistry and Oral Health, Aarhus University, Denmark; Wolfson Centre for Age-Related Diseases, King's College London, UK; Department of Neurology, King's College London, UK
This patient-friendly article is based on peer-reviewed research published in Cephalalgia, the official journal of the International Headache Society. The original article is available under the Creative Commons Attribution-NonCommercial 4.0 License.
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