There is no universally accepted definition of AFP, and it is defined less by what it is as what it is not. Various definitions of AFP include:

- "a nonmuscular or joint pain that has no a detectable neurologic cause."

- "a condition characterized by the absence of other diagnoses and causing continuous, variable-intensity, migrating, nagging, deep, and diffuse pain."

- "a continuous unilateral deep aching pain sometimes with a burning component."

- "facial pain not fulfilling other criteria" (previous IHS definition, which now uses the term "Persistent idiopathic facial pain", see below).

- "persistent pain in the maxillofacial region that does not fit the diagnostic criteria of any other orofacial pain and has no identifiable cause." (Neville "et al.")

Some sources list some non-specific signs that may be associated with AFP/AO. These include increased temperature and tenderness of the mucosa in the affected area, which is otherwise normal in every regard.

Patient often reports symptoms of paresthesia, pain, and throbbing. Physical examination may be normal, but hypoesthesia, hyperesthesia, and allodynia may be found.

The features of atypical facial pain can be considered according to the Socrates pain assessment method (see table).

ATN pain can be described as heavy, aching, stabbing, and burning. Some sufferers have a constant migraine-like headache. Others may experience intense pain in one or in all three trigeminal nerve branches, affecting teeth, ears, sinuses, cheeks, forehead, upper and lower jaws, behind the eyes, and scalp. In addition, those with ATN may also experience the shocks or stabs found in type 1 TN.

Many TN and ATN patients have pain that is "triggered" by light touch on shifting trigger zones. ATN pain tends to worsen with talking, smiling, chewing, or in response to sensations such as a cool breeze. The pain from ATN is often continuous, and periods of remission are rare. Both TN and ATN can be bilateral, though the character of pain is usually different on the two sides at any one time.

ATN is usually attributed to inflammation or demyelination, with increased sensitivity of the trigeminal nerve. These effects are believed to be caused by infection, demyelinating diseases, or compression of the trigeminal nerve (by an impinging vein or artery, a tumor, or arteriovenous malformation) and are often confused with dental problems. An interesting aspect is that this form affects both men and women equally and can occur at any age, unlike typical trigeminal neuralgia, which is seen most commonly in women. Though TN and ATN most often present in the fifth decade, cases have been documented as early as infancy.

Signs and symptoms of temporomandibular joint disorder vary in their presentation. The symptoms will usually involve more than one of the various components of the masticatory system, muscles, nerves, tendons, ligaments, bones, connective tissue, or the teeth.

The three classically described, cardinal signs and symptoms of TMD are:

- Pain and tenderness on palpation in the muscles of mastication, or of the joint itself (preauricular pain – pain felt just in front of the ear). Pain is the defining feature of TMD and is usually aggravated by manipulation or function, such as when chewing, clenching, or yawning, and is often worse upon waking. The character of the pain is usually dull or aching, poorly localized, and intermittent, although it can sometimes be constant. The pain is more usually unilateral (located on one side) rather than bilateral. It is rarely severe.

- Limited range of mandibular movement, which may cause difficulty eating or even talking. There may be locking of the jaw, or stiffness in the jaw muscles and the joints, especially present upon waking. There may also be incoordination, asymmetry or deviation of mandibular movement.

- Noises from the joint during mandibular movement, which may be intermittent. Joint noises may be described as clicking, popping, or crepitus (grating).

Other signs and symptoms have also been described, although these are less common and less significant than the cardinal signs and symptoms listed above. Examples include:

- Headache (possibly), e.g. pain in the occipital region (the back of the head), or the forehead; or other types of facial pain including migraine, tension headache. or myofascial pain.

- Pain elsewhere, such as the teeth or neck.

- Diminished auditory acuity (hearing loss).

- Tinnitus (occasionally).

- Dizziness.

- Sensation of malocclusion (feeling that the teeth do not meet together properly).

Sometimes distinction is made between acute TMD, where symptoms last for less than 3 months, and chronic TMD, where symptoms last for more than 3 months. Not much is known about acute TMD since these individuals do not typically attend in secondary care (hospital).

By definition, BMS has no signs. Sometimes affected persons will attribute the symptoms to sores in the mouth, but these are in fact normal anatomic structures (e.g. lingual papillae, varices). Symptoms of BMS are variable, but the typical clinical picture is given below, considered according to the Socrates pain assessment method (see table). If clinical signs are visible, then another explanation for the burning sensation may be present. Erythema (redness) and edema (swelling) of papillae on the tip of the tongue may be a sign that the tongue is being habitually pressed against the teeth. The number and size of filiform papillae may be reduced. If the tongue is very red and smooth, then there is likely a local or systemic cause (e.g. eythematous candidiasis, anemia).

This disorder is characterized by episodes of severe facial pain along the trigeminal nerve divisions. The trigeminal nerve is a paired cranial nerve that has three major branches: the ophthalmic nerve (V), the maxillary nerve (V), and the mandibular nerve (V). One, two, or all three branches of the nerve may be affected. Trigeminal neuralgia most commonly involves the middle branch (the maxillary nerve or V) and lower branch (mandibular nerve or V) of the trigeminal nerve.

An individual attack usually lasts from a few seconds to several minutes or hours, but these can repeat for hours with very short intervals between attacks. In other instances, only 4-10 attacks are experienced daily. The episodes of intense pain may occur paroxysmally. To describe the pain sensation, people often describe a trigger area on the face so sensitive that touching or even air currents can trigger an episode; however, in many people, the pain is generated spontaneously without any apparent stimulation. It affects lifestyle as it can be triggered by common activities such as eating, talking, shaving and brushing teeth. The wind, chewing, and talking can aggravate the condition in many patients. The attacks are said by those affected to feel like stabbing electric shocks, burning, sharp, pressing, crushing, exploding or shooting pain that becomes intractable.

The pain also tends to occur in cycles with remissions lasting months or even years. 1–6% of cases occur on both sides of the face but extremely rare for both to be affected at the same time. This normally indicates problems with both trigeminal nerves, since one serves strictly the left side of the face and the other serves the right side. Pain attacks are known to worsen in frequency or severity over time, in some people. Pain may migrate to other branches over time but in some people remains very stable.

Rapid spreading of the pain, bilateral involvement or simultaneous participation with other major nerve trunks (such as Painful Tic Convulsif of nerves V & VII or occurrence of symptoms in the V and IX nerves) may suggest a systemic cause. Systemic causes could include multiple sclerosis or expanding cranial tumors.

The severity of the pain makes it difficult to wash the face, shave, and perform good oral hygiene. The pain has a significant impact on activities of daily living especially as people live in fear of when they are going to get their next attack of pain and how severe it will be. It can lead to severe depression and anxiety.

However, not all people will have the symptoms described above and there are variants of TN. One of which is atypical trigeminal neuralgia ("trigeminal neuralgia, type 2" or trigeminal neuralgia with concomitant pain ), based on a recent classification of facial pain. In these instances there is also a more prolonged lower severity background pain that can be present for over 50% of the time and is described more as a burning or prickling, rather than a shock.

Trigeminal neuropathic pain is similar to TN2 but can have the electric pulses associated with classic TN. The pain is usually constant and can also give off a tingling, numbness sensation. This pain is due to unintentional damage to one or more of the trigeminal nerves from trauma, oral surgery, dentistry work, etc. It is difficult to treat but sufferers are usually given the same anticonvulsant and tricyclics antidepressant medicines as with the other types of neuralgias. Surgical options are DREZ (dorsal root entry zone) lesion and MCS or Motor Cortex Stimulation.

TN needs to be distinguished from other forms of unilateral pain which are related to damage to the trigeminal nerve by trauma to the face or dental treatments. This is often termed painful trigeminal neuropathy or post-traumatic neuropathy as some sensory changes can be noted e.g. decrease in pain sensation or temperature. This is important as different care pathways are used. Trigeminal pain can also occur after an attack of herpes zoster, and post-herpetic neuralgia has the same manifestations as in other parts of the body. Trigeminal deafferentation pain (TDP), also termed anesthesia dolorosa, is from intentional damage to a trigeminal nerve following attempts to surgically fix a nerve problem. This pain is usually constant with a burning sensation and numbness. TDP is very difficult to treat as further surgeries are usually ineffective and possibly detrimental to the person.

In about 50% of cases of burning mouth sensation no identifiable cause is apparent, these cases are termed (primary) BMS. Several theories of what causes BMS have been proposed, and these are supported by varying degrees of evidence, but none is proven.

As most people with BMS are postmenopausal women, one theory of the cause of BMS is of estrogen or progesterone deficit, but a strong statistical correlation has not been demonstrated. Another theory is that BMS is related to autoimmunity, as abnormal antinuclear antibody and rheumatoid factor can be found in the serum of more than 50% of persons with BMS, but these levels may also be seen in elderly people who do not have any of the symptoms of this condition. Whilst salivary flow rates are normal and there are no clinical signs of a dry mouth to explain a complaint of dry mouth, levels of salivary proteins and phosphate may be elevated and salivary pH or buffering capacity may be reduced.

Depression and anxiety are strongly associated with BMS. It is not known if depression is a cause or result of BMS, as depression may develop in any setting of constant unrelieved irritation, pain, and sleep disturbance. It is estimated that about 20% of BMS cases involve psychogenic factors, and some consider BMS a psychosomatic illness, caused by cancerophobia, concern about sexually transmitted infections, or hypochondriasis.

Chronic low-grade trauma due to parafunctional habits (e.g. rubbing the tongue against the teeth or pressing it against the palate), may be involved. BMS is more common in persons with Parkinson's disease, so it has been suggested that it is a disorder of reduced pain threshold and increased sensitivity. Often people with BMS have unusually raised taste sensitivity, termed hypergeusia ("super tasters"). Dysgeusia (usually a bitter or metallic taste) is present in about 60% of people with BMS, a factor which led to the concept of a defect in sensory peripheral neural mechanisms. Changes in the oral environment, such as changes in the composition of saliva, may induce neuropathy or interruption of nerve transduction. The onset of BMS is often spontaneous, although it may be gradual. There is sometimes a correlation with a major life event or stressful period in life. In women, the onset of BMS is most likely three to twelve years following menopause.

The reported symptoms are very variable, and frequently have been present for many months before the condition is diagnosed. Reported symptoms may include some of the following:

- Sharp pain when biting on a certain tooth, which may get worse if the applied biting force is increased. Sometimes the pain on biting occurs when the food being chewed is soft with harder elements, e.g. seeded bread.

- "Rebound pain" i.e. sharp, fleeting pain occurring when the biting force is released from the tooth, which may occur when eating fibrous foods.

- Pain when grinding the teeth backward and forward and side to side.

- Sharp pain when drinking cold beverages or eating cold foods, lack of pain with heat stimuli.

- Pain when eating or drinking sugary substances.

- Sometimes the pain is well localized, and the individual is able to determine the exact tooth from which the symptoms are originating, but not always.

If the crack propagates into the pulp, irreversible pulpitis, pulpal necrosis and periapical periodontitis may develop, with the respective associated symptoms.

Trigeminal neuralgia (TN or TGN) is a chronic pain disorder that affects the trigeminal nerve. There are two main types: typical and atypical trigeminal neuralgia. The typical form results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of these episodes can occur over a few hours. The atypical form results in a constant burning pain that is less severe. Episodes may be triggered by any touch to the face. Both forms may occur in the same person. It is one of the most painful conditions and can result in depression.

The exact cause is unclear but believed to involve loss of the myelin around the trigeminal nerve. This may occur due to compression from a blood vessel as the nerve exits the brain stem, multiple sclerosis, stroke, or trauma. Less common causes include a tumor or arteriovenous malformation. It is a type of nerve pain. Diagnosis is typically based on the symptoms after ruling out other possible causes such as postherpetic neuralgia.

Treatment includes medication or surgery. The anticonvulsant carbamazepine or oxcarbazepine is the usual initial treatment and is effective in about 80% of people. Other options include lamotrigine, baclofen, gabapentin, and pimozide. Amitriptyline may help with the pain but opioids are not usually effective in the typical form. In those who do not improve or become resistant to other measures, a number of types of surgery may be tried.

It is estimated that 1 in 8,000 people develop trigeminal neuralgia a year. It usually begins in people over 50 years old, but can occur at any age. Women are more commonly affected than men. The condition was first described in detail in 1773 by John Fothergill.

Cracked tooth syndrome (abbreviated to CTS, and also termed cracked cusp syndrome, split tooth syndrome, or incomplete fracture of posterior teeth), is where a tooth has incompletely cracked but no part of the tooth has yet broken off. Sometimes it is described as a greenstick fracture. The symptoms are very variable, making it a notoriously difficult condition to diagnose.

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

The pain of GN is sharp, shooting or burning and can last for hours. Painful attacks can be triggered by cold, noise, swallowing or touch, but triggers are usually unique to the sufferer. Other related symptoms that may be experienced include increased salivation, bitter taste, tinnitus and vertigo.

GN is rare, and only limited data is available regarding the incidence, prevalence, and risk factors associated with this condition. Middle-aged adults, however, seem to be predominantly affected, women more than men.

GN may be caused by compression of somatic sensory branch of cranial nerve VII which goes through the nervus intermedius. In sufferers of GN, signals sent along these nerves are altered and interpreted by the geniculate ganglion (a structure in the brain) as GN pain. GN may also develop following herpes zoster oticus (Ramsay Hunt syndrome), where cold sores occur on the ear drum or ear. This may also be associated with facial paresis (weakness), tinnitus, vertigo and deafness. Disorders of lacrimation, salivation and/or taste sometimes accompany the pain. There is a common association with herpes zoster.

Non-dental causes of toothache are much less common as compared with dental causes. In a toothache of neurovascular origin, pain is reported in the teeth in conjunction with a migraine. Local and distant structures (such as ear, brain, carotid artery, or heart) can also refer pain to the teeth. Other non-dental causes of toothache include myofascial pain (muscle pain) and angina pectoris (which classically refers pain to the lower jaw). Very rarely, toothache can be psychogenic in origin.

Disorders of the maxillary sinus can be referred to the upper back teeth. The posterior, middle and anterior superior alveolar nerves are all closely associated with the lining of the sinus. The bone between the floor of the maxillary sinus and the roots of the upper back teeth is very thin, and frequently the apices of these teeth disrupt the contour of the sinus floor. Consequently, acute or chronic maxillary sinusitis can be perceived as maxillary toothache, and neoplasms of the sinus (such as adenoid cystic carcinoma) can cause similarly perceived toothache if malignant invasion of the superior alveolar nerves occurs. Classically, sinusitis pain increases upon Valsalva maneuvers or tilting the head forward.

Painful conditions which do not originate from the teeth or their supporting structures may affect the oral mucosa of the gums and be interpreted by the individual as toothache. Examples include neoplasms of the gingival or alveolar mucosa (usually squamous cell carcinoma), conditions which cause gingivostomatitis and desquamative gingivitis. Various conditions may involve the alveolar bone, and cause non-odontogenic toothache, such as Burkitt's lymphoma, infarcts in the jaws caused by sickle cell disease, and osteomyelitis. Various conditions of the trigeminal nerve can masquerade as toothache, including trigeminal zoster (maxillary or mandibular division), trigeminal neuralgia, cluster headache, and trigeminal neuropathies. Very rarely, a brain tumor might cause toothache. Another chronic facial pain syndrome which can mimic toothache is temporomandibular disorder (temporomandibular joint pain-dysfunction syndrome), which is very common. Toothache which has no identifiable dental or medical cause is often termed atypical odontalgia, which, in turn, is usually considered a type of atypical facial pain (or persistent idiopathic facial pain). Atypical odontalgia may give very unusual symptoms, such as pain which migrates from one tooth to another and which crosses anatomical boundaries (such as from the left teeth to the right teeth).

Establishing a diagnosis of nondental toothache is initially done by careful questioning about the site, nature, aggravating and relieving factors, and referral of the pain, then ruling out any dental causes. There are no specific treatments for nondental pain (each treatment is directed at the cause of the pain, rather than the toothache itself), but a dentist can assist in offering potential sources of the pain and direct the patient to appropriate care. The most critical nondental source is the radiation of angina pectoris into the lower teeth and the potential need for urgent cardiac care.

Apical abscesses can spread to involve periodontal pockets around a tooth, and periodontal pockets cause eventual pulp necrosis via accessory canals or the apical foramen at the bottom of the tooth. Such lesions are termed periodontic-endodontic lesions, and they may be acutely painful, sharing similar signs and symptoms with a periodontal abscess, or they may cause mild pain or no pain at all if they are chronic and free-draining. Successful root canal therapy is required before periodonal treatment is attempted. Generally, the long-term prognosis of perio-endo lesions is poor.

According to the third edition of the International Classification of Headache Disorders (ICHD), which terms this condition "primary headache associated with sexual activity", it normally begins as a dull headache that increases with sexual excitement, and becomes intense at orgasm. For some patients, the headache begins suddenly, often at orgasm. In two thirds of cases, it is bilateral, and unilateral in the rest. The pain lasts from one minute to 24 hours with severe intensity, or as long as 72 hours with mild intensity. Its occurrence is unpredictable, and may not follow every sexual act.

Previous editions of the ICHD divided the condition into two subforms, "preorgasmic headache" and "orgasmic headache". These subforms were merged into one entity with varying presentation because clinical studies could not distinguish them. Post-orgasmic headaches associated with posture may be better attributed to a spontaneous cerebrospinal fluid leak. Sudden, severe headaches during sexual activity may also be caused by intracerebral hemorrhage, subarachnoid hemorrhage, or cerebral infarction, which require immediate medical attention.

A cold-stimulus headache, also known as brain freeze, ice-cream headache, trigeminal headache or its given scientific name sphenopalatine ganglioneuralgia (meaning "pain of the "sphenopalatine ganglion""), is a form of brief pain or headache commonly associated with consumption (particularly quick consumption) of cold beverages or foods such as ice cream and ice pops. It is caused by having something cold touch the roof of the mouth, and is believed to result from a nerve response causing rapid constriction and swelling of blood vessels or a "referring" of pain from the roof of the mouth to the head. The rate of intake for cold foods has been studied as a contributing factor. An cold-stimulus headache is distinct from dentin hypersensitivity, a type of pain that can occur under similar circumstances.

Cats and other animals have been observed experiencing a similar reaction when presented with a similar stimulus.

The term "ice-cream headache" has been in use since at least January 31, 1937, contained in a journal entry by Rebecca Timbres published in the 1939 book "We Didn't Ask Utopia: A Quaker Family in Soviet Russia".

Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience a learned hyperalgesia of the latter, diffuse form.

The focal form is typically associated with injury, and is divided into two subtypes:

- "Primary hyperalgesia" describes pain sensitivity that occurs directly in the damaged tissues.

- "Secondary hyperalgesia" describes pain sensitivity that occurs in surrounding undamaged tissues.

Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain. Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. This side effect can be severe enough to warrant discontinuation of opioid treatment.

Diagnostic criteria:

A. Pain paroxysms of intermittent occurrence, lasting for seconds or minutes, in the depth of the ear

B. Presence of a trigger area in the posterior wall of the auditory canal

C. Not attributed to another disorder

Signs and symptoms may include:

- Persistent or recurrent enlargement of the lips, causing them to protrude. If recurrent, the interval during which the lips are enlarged may be weeks or months. The enlargement can cause midline fissuring of the lip ("median cheilitis") or angular cheilitis (sores at the corner of the mouth). The swelling is non-pitting (c.f. pitting edema) and feels soft or rubbery on palpation. The mucous membrane of the lip may be erythemaous (red) and granular. One or both lips may be affected.

- Oral ulceration (mouth ulcers) which may be aphthous like, or be more chronic and deep with raised margins. Alternatively, lesions similar to pyostomatitis vegetans may occur in OFG, but this is uncommon.

- "Full width" gingivitis (compare with marginal gingivitis).

- Gingival enlargement (swelling of the gums).

- Fissured tongue (grooves in the tongue).

- Enlargement of the mucous membrane of the mouth, which may be associated with cobblestoning and mucosal tags (similar lesions often occur on the intestinal mucosa in Crohn's disease).

- Enlargement of the perioral and periorbital soft tissues (the tissues of the face around the mouth and the eyes). The facial skin may be dry, exfoliative (flaking) or erythematous.

- Cervical lymphadenopathy (enlarged lymph nodes in the neck).

- Facial palsy (weakness and altered sensation of the face).

The enlargement of the tissues of the mouth, lips and face seen in OFG is painless. Melkersson-Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve. The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression.

Hyperalgesia ( or ; 'hyper' from Greek ὑπέρ (huper, “over”), '-algesia' from Greek algos, ἄλγος (pain)) is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves. Prostaglandins E and F are largely responsible for sensitizing the nociceptors. Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.

A cold-stimulus headache is the direct result of the rapid cooling and rewarming of the capillaries in the sinuses leading to periods of vasoconstriction and vasodilation. A similar but painless blood vessel response causes the face to appear "flushed" after being outside on a cold day. In both instances, the cold temperature causes the capillaries in the sinuses to constrict and then experience extreme rebound dilation as they warm up again.

In the palate, this dilation is sensed by nearby pain receptors, which then send signals back to the brain via the trigeminal nerve, one of the major nerves of the facial area. This nerve also senses facial pain, so as the neural signals are conducted the brain interprets the pain as coming from the forehead—the same "referred pain" phenomenon seen in heart attacks. Brain-freeze pain may last from a few seconds to a few minutes. Research suggests that the same vascular mechanism and nerve implicated in "brain freeze" cause the aura (sensory disturbance) and pulsatile (throbbing pain) phases of migraines.

It is possible to suffer from a cold-stimulus headache in both hot and cold weather, because the effect relies upon the temperature of the food being consumed rather than that of the environment. Other causes that may mimic the sensation of cold-stimulus headache include that produced when high speed drilling is performed through the inner table of the skull in people undergoing such a procedure in an awake or sedated state.

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

Sexual headaches, also known as coital cephalalgia, are a rare type of headache that occur in the skull and neck during sexual activity, including masturbation or orgasm. These headaches are often benign, but should be evaluated by a clinician to rule out intracranial hemorrhage and cerebral infarction, especially if the pain is sudden and severe. They may be caused by general exertion, sexual excitement, or contraction of the neck and facial muscles. Most cases can be successfully treated with medication.

The symptoms and signs include acute facial nerve paralysis, pain in the ear, taste loss in the front two-thirds of the tongue, dry mouth and eyes, and an erythematous vesicular rash in the ear canal, the tongue, and/or hard palate.

Since the vestibulocochlear nerve is in proximity to the geniculate ganglion, it may also be affected, and patients may also suffer from tinnitus, hearing loss, and vertigo. Involvement of the trigeminal nerve can cause numbness of the face.