Causes of facial pain

The most common cause of facial pain is trigeminal neuralgia (trigeminy). The prevalence of trigeminal neuralgia is quite high and amounts to 30-50 patients per 100,000 population, and the incidence according to WHO is within 2-4 people per 100,000 population. Trigeminal neuralgia most often occurs in women aged 50-69 and has right-sided lateralization. The development of the disease is facilitated by various vascular, endocrine, allergic disorders, as well as psychogenic factors. Trigeminal neuralgia is considered to be an idiopathic disease. However, there are several theories explaining the pathogenesis of the disease. The most likely cause of trigeminal neuralgia is compression of the trigeminal nerve at the intra- or extracranial level, therefore, a distinction is made between neuralgia of central and peripheral genesis.

Intracranial causes of compression may be a volumetric process in the posterior cranial fossa (tumors: acoustic neuroma, meningioma, pontine glioma), dislocation and expansion of tortuous cerebellar arteries, veins, basilar artery aneurysm, meningitis, adhesions after injuries, infections. Among the extracranial factors are: the formation of tunnel syndrome (compression of the II and III branches in the bone canals - infraorbital and mandible with their congenital narrowness and the addition of vascular diseases in old age), local odonto- or rhinogenic inflammatory process.

The role of trigeminal nerve compression became clearer with the advent of the "gate theory of pain". Compression disrupts axotok, leads to activation of autoimmune processes and causes focal demyelination. Under the influence of prolonged pathological impulses from the periphery, a "focus" similar to an epileptic one is formed in the spinal nucleus of the trigeminal nerve, a generator of pathologically enhanced excitation (GPE), the existence of which no longer depends on afferent impulses. Impulses from trigger points arrive at the leading neurons of the generator and cause its facilitated activation. GPE activates reticular, mesencephalic formations, thalamic nuclei, the cerebral cortex, involves the limbic system, thus forming a pathological algogenic system.

The disease may develop after tooth extraction (the alveolar nerve is affected) - odontogenic neuralgia; as a result of circulatory disorders in the brainstem, herpes infection; rarely - due to demyelination of the trigeminal nerve root in multiple sclerosis. Provoking factors may include infection (flu, malaria, syphilis, etc.), hypothermia, intoxication (lead, alcohol, nicotine), metabolic disorders (diabetes).

Other Causes of Facial Pain

Less common, but with a pronounced pain syndrome, are neuralgias of individual zones of the trigeminal nerve - Charlin's syndrome, Frey's syndrome, lingual nerve. Damage to the facial, intermediate nerve, glossopharyngeal and vagus nerves, vegetative ganglia of the face are accompanied by no less pronounced facial pain with their characteristic clinical features and also require urgent adequate therapy in the early stages.

Nasociliary neuralgia (Charlin syndrome). Accompanied by severe pain in the medial angle of the eye radiating to the bridge of the nose, sometimes orbital and periorbital pain. The attack lasts from several hours to a day. Facial pain is accompanied by lacrimation, photophobia, hyperemia of the sclera and nasal mucosa, swelling, hyperesthesia on the affected side and unilateral hypersecretion of the nasal mucosa. Treatment: non-narcotic analgesics and NSAIDs; 0.25% dicaine solution is instilled into the eye and nose 1-2 drops, to enhance the effect - 0.1% adrenaline solution (3-5 drops per 10 ml of dicaine).

Auriculotemporal neuralgia (Frey's syndrome). Characterized by the occurrence of paroxysmal pain on the affected side deep in the ear, in the area of the anterior wall, external auditory canal and temple, especially in the area of the temporomandibular joint, often radiating to the lower jaw. Accompanied by reddening of the skin, increased sweating in this area, salivation, change in pupil size on the affected side. Attacks are provoked by the intake of certain foods and even by their presentation, as well as by external irritants. Treatment: analgesics in combination with antihistamines, tranquilizers, neuroleptics; NSAIDs, vegetotropic (belloid, bellaspon).

Neuralgia of the lingual nerve. Diagnosis is based on clinical data: attacks of burning pain in the face, anterior 2/3 of the tongue, which appear spontaneously or are provoked by the intake of coarse, spicy food, tongue movements, infections (tonsillitis, sore throat, flu), intoxications, etc. On the corresponding half of the tongue, sensitivity disorders often appear, more often by the type of hyperesthesia, with a long course - loss of pain and taste sensitivity. Treatment: analgesics - analgin, sigan, on the tongue - 1% lidocaine solution, anticonvulsants, B vitamins.

Neuralgia of the facial nerve. In the picture of facial nerve neuropathy, the pain syndrome is manifested by shooting or aching pain in the area of the external auditory canal, with irradiation to the homolateral half of the head, migration to the area of the eyebrows, cheeks, inner corner of the eye, wing of the nose, chin, which intensifies with emotional stress in the cold and is relieved by heat. Pain in the face is accompanied by facial asymmetry along with a peculiar defect of facial expressions, pathological synkinesis and hyperkinesis, the development of paresis and secondary contracture of the facial muscles, occurs after hypothermia, less often against the background of an acute respiratory viral infection. Complex treatment includes "medicinal decompression" of the nerve in the facial canal (prescription of prednisolone, diuretics), vasoactive therapy (euphyllin, nicotinic acid), B vitamins, physiotherapy, therapeutic exercises, massage.

Neuralgia of the glossopharyngeal nerve. Paroxysmal pain in the face, always starting from the root of the tongue or from the tonsil and spreading to the soft palate, pharynx, radiating to the ear, sometimes to the eye, the angle of the lower jaw to the cheek. Accompanied by hypersalivation, redness of half of the face, dry cough. Pain attacks last from 1 to 3 minutes. During the attack, dry cough, taste disorder, unilateral increase in sensitivity in the posterior third of the tongue, rarely a decrease in blood pressure and loss of consciousness are noted. Usually, the attack is provoked by talking, eating, coughing, yawning.

Neuralgia of the superior laryngeal nerve (branch of the vagus nerve). Characterized by one-sided paroxysmal facial pain in the larynx area, which radiates to the ear area and along the lower jaw, occurs during eating or swallowing. Sometimes laryngospasm develops; cough and general weakness appear during an attack of pain.

Pterygopalatine ganglion syndrome (Sluder syndrome). Attacks of acute pain in the eye, nose, and upper jaw. The pain may spread to the temple, ear, back of the head, neck, shoulder blade, shoulder, forearm, and hand. Paroxysms are accompanied by pronounced vegetative symptoms: redness of half the face, swelling of facial tissues, lacrimation, and copious discharge of secretions from one half of the nose (vegetative storm). The duration of an attack ranges from several minutes to a day.

Myofascial facial syndrome. The main clinical manifestation is a combination of neuralgia of one of the cranial nerves (pain in the face, tongue, oral cavity, pharynx, larynx), motor disorders of the masticatory muscles, taste disturbances, dysfunction of the temporomandibular joint. Facial pain has no clear boundaries, its duration and intensity varies (from a state of discomfort to sharp excruciating pain). Facial pain is increased by emotional stress, clenching of the jaws, overload of the masticatory muscles, fatigue. Pain depends on the state of activity and localization of trigger points. Vegetative symptoms may occur: sweating, vascular spasm, runny nose, lacrimation and salivation, dizziness, tinnitus, burning sensation in the tongue, etc.

Treatment of these syndromes is carried out in conjunction with a neurologist.

Facial pain and trigeminal neuralgia

Trigeminal neuralgia (synonyms: trigeminal neuralgia, pain tic, Fothergill's disease) is a chronic disease that occurs with remissions and exacerbations, characterized by attacks of extremely intense, shooting pain in the innervation zones of the II, III or, extremely rarely, I branch of the trigeminal nerve.

Terminology

Traditionally, primary (idiopathic) and secondary (symptomatic) trigeminal neuralgia are distinguished. Symptomatic neuralgia develops as one of the manifestations of other CNS diseases (multiple sclerosis, brainstem glioma, tumors of the pontocerebellar region, brainstem stroke, etc.).

It has now been established that primary trigeminal neuralgia is in the vast majority of cases associated with compression of the trigeminal nerve root in the area of its entry into the brainstem. Compression is usually caused by a pathologically tortuous loop of the superior cerebellar artery (over 80% of cases). Therefore, if a patient has undergone neurosurgery, during which compression of the nerve root by a pathologically tortuous blood vessel is detected, secondary neuralgia should be diagnosed. However, the vast majority of patients do not undergo surgery. In such cases, although compression etiology of trigeminal neuralgia is assumed, the term “primary” (classical, idiopathic) is still used to describe it, and the term “secondary trigeminal neuralgia” is used in patients with pathological processes other than vascular compression (tumors, demyelination, etc.) identified during neuroimaging (or neurosurgery).

Pathogenesis

The mechanism of development of trigeminal neuralgia (as well as glossopharyngeal neuralgia) is explained from the standpoint of the "gate control of pain" theory of Melzack and Wall (1965). The "gate control of pain" theory suggests that fast-conducting (antinociceptive), well-myelinated type A fibers and unmyelinated (nociceptive) C fibers are in a competitive relationship, and normally the flow of impulses along the fibers of proprioceptive sensitivity predominates. In neuralgia of the V and IX pairs of cranial nerves, caused by compression of their roots at the entrance to the brainstem, demyelination of A fibers occurs with the appearance of many additional voltage-dependent sodium channels in the demyelinated areas, as well as the formation of contacts of these areas with type C fibers. All this leads to the formation of prolonged and high-amplitude activity of pathologically altered A fibers, which is manifested by painful paroxysms in the face and oral cavity.

Epidemiology

Typical trigeminal neuralgia debuts in the 5th decade of life. Women are more often affected (5 per 100,000 population; in men - 2.7 per 100,000). Trigeminal neuralgia most often occurs on the right (70%), on the left - (28%), in rare cases it can be bilateral (2%).

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Clinical picture and diagnostics

A full-blown attack of classical trigeminal neuralgia is characterized by a typical clinical picture and usually does not present difficulties for diagnosis. The most characteristic features of the pain syndrome are the following.

• The pain is paroxysmal, extremely severe, shooting in the face, compared by patients to electric shocks.
• The duration of a painful paroxysm never exceeds 2 minutes (usually 10-15 seconds).
• Between 2 separate attacks there is a “light” interval (refractory period), the duration of which depends on the severity of the exacerbation.
• During an exacerbation, pain has a specific localization within the innervation zones of the trigeminal nerve, which does not change significantly over many years of the disease.
• An attack of pain always has a certain direction - the pain comes from one part of the face and reaches another.
• The presence of trigger zones, i.e. areas on the skin of the face and in the oral cavity, the slight irritation of which causes a typical paroxysm. The most common location of trigger zones is the nasolabial triangle and the alveolar process.
• The presence of trigger factors - actions or conditions that cause typical pain attacks. Most often, such factors are washing, brushing teeth, chewing, talking.
• Typical behavior during an attack. As a rule, patients do not cry, scream, or move, but freeze in the position in which the attack caught them. Sometimes patients rub the painful area or make smacking movements.
• At the height of a pain attack, twitching of the facial or chewing muscles sometimes occurs (currently, due to the use of anticonvulsants for the treatment of trigeminal neuralgia, this symptom is rarely observed).
• Absence of sensory defect (loss of superficial sensitivity) in the area of pain attacks. This sign is not obligatory, since after nerve ectomy, retrogasseral thermorhizotomy or ethanol blocks, hypoesthesia remains for a long time in the places where the nerve exits on the face.

In some patients, secondary myofascial prosopalgic syndrome develops over time. All patients with trigeminal neuralgia, both during exacerbation and remission, use the healthy half of the mouth for chewing. Therefore, degenerative changes occur in the muscles of the homolateral side of the face with the development of typical muscle compactions (with the internal pterygoid muscles and the posterior belly of the digastric muscle being the most vulnerable). When auscultating the temporomandibular joint, a typical crunch is sometimes heard.

With a long-term course of the disease, the development of a neuralgoneuritic stage (dystrophic) is possible, in which moderate atrophy of the masticatory muscles and decreased sensitivity on the affected half of the face appear.

Symptomatic trigeminal neuralgia does not differ in clinical manifestations from classical idiopathic neuralgia, the symptomatic nature of which may be indicated by a gradually increasing sensory deficit in the innervation zone of the corresponding branch, the absence of a refractory period after a painful paroxysm at the onset of the disease, as well as the appearance of other focal symptoms of damage to the brainstem or adjacent cranial nerves (nystagmus, ataxia, hearing loss). One of the most common causes of symptomatic trigeminal neuralgia is multiple sclerosis. The occurrence of trigeminal neuralgia in a young patient, as well as changes in the side of neuralgia, are especially suspicious of multiple sclerosis.

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Neuralgia of individual branches of the trigeminal nerve

Nasociliary neuralgia

Nasociliary neuralgia (Charlin's neuralgia) is observed relatively rarely. It manifests itself as a stabbing pain radiating to the central region of the forehead when touching the outer surface of the nostril.

Supraorbital neuralgia

The disease is observed as rarely as nasociliary neuralgia. It is characterized by paroxysmal or constant pain in the supraorbital notch and medial part of the forehead, i.e. in the innervation zone of the supraorbital nerve. Palpation reveals pain in the supraorbital notch.

Neuralgia of other branches of the trigeminal nerve

Damage or compression of the branches of the trigeminal nerve can cause pain in the area of their innervation.

• Neuralgia (neuropathy) of the infraorbital nerve is usually symptomatic and is caused by inflammatory processes in the maxillary sinus or nerve damage during complex dental procedures. The pain is usually of low intensity, the predominant feeling is numbness of the mucous membrane of the upper jaw and infraorbital region.
• Causes of neuralgia of the lingual nerve may be prolonged irritation of the tongue by a prosthesis, a sharp edge of a tooth, etc. Moderate pain in half of the tongue is constant and sometimes intensifies when eating, talking, or making sharp facial movements.
• Neuralgia (neuropathy) of the lower alveolar nerve occurs with injuries and inflammatory diseases of the lower jaw, with the filling material extending beyond the apex of the tooth, with the simultaneous extraction of several teeth. It is characterized by moderate constant pain in the teeth of the lower jaw, in the area of the chin and lower lip. In some cases, neuropathy of the terminal branch of the lower alveolar nerve - the mental nerve - is observed. It manifests itself as hypoesthesia or paresthesia in the area of the chin and lower lip.
• Neuropathy of the buccal nerve is usually combined with neuropathy of the inferior alveolar nerve. There is no pain syndrome, hypoesthesia of the mucous membrane of the cheek, as well as the skin of the corresponding corner of the mouth, is typical.
• The term "tic neuralgia" refers to a combination of periodic migraine neuralgia and neuralgia of the first branch of the trigeminal nerve.

Postherpetic trigeminal neuralgia

Postherpetic trigeminal neuralgia (postherpetic trigeminal neuropathy) is a persistent or intermittent facial pain for at least 3 months after the onset of Herpes zoster infection. Postherpetic trigeminal neuralgia is observed significantly more often than classic trigeminal neuralgia (2 per 1000, and in people over 75 years old - one in 1000 of the population). Trigeminal nerve damage is noted in 15% of people with herpes zoster, and in 80% of cases the optic nerve is involved in the process (which is associated with its least myelination compared to the II and III branches of the V pair of cranial nerves). The onset of the disease is predisposed by a decrease in immunity in old age, which contributes to the activation of the Varicella-zoster virus, which persists in the body for a long time. The disease development goes through several stages: prodromal, preceding the rash (acute pain, itching); unilateral rash (vesicles, pustules, crusts); skin healing (2-4 weeks); postherpetic neuralgia. For a neurologist, it is important to diagnose the prodromal phase, when there are no rashes yet, but the pain syndrome has already appeared. Shingles can be suspected by identifying pink spots on the skin, in the area of which there is itching, burning, pain. After 3-5 days, the erythematous background disappears and blisters appear on healthy skin. After the appearance of the rash, diagnosis is not difficult. In the case of postherpetic neuralgia of the trigeminal nerve, after the crusts fall off and the skin heals with elements of scarring, the leading complaint of patients is constant pain, which appears within 1 month in 15% of cases, and within a year - in 25%. Risk factors for the development of postherpetic neuralgia include advanced age, female gender, the presence of severe pain in the prodromal and acute stages, as well as the presence of severe skin rashes and subsequent cicatricial changes in the skin. Clinical manifestations in the advanced stage of postherpetic neuralgia are quite typical.

• Scars on the skin (against the background of its hyper- and hypopigmentation) in the forehead and scalp area.
• Presence of trigger areas on the scalp (combing symptom), forehead, eyelids.
• Combination of permanent and paroxysmal pain syndromes.
• The presence of allodynia, hypesthesia, dysesthesia, hyperalgesia, hyperpathy.

Hunt syndrome

In case of herpes infection, in addition to the trigeminal nerve, the III, IV and/or VI pairs of cranial nerves may also be affected, and in case of infectious damage to the geniculate ganglion, dysfunction of the facial and/or vestibulocochlear nerve is possible.

• Hunt syndrome 1 (geniculate ganglion neuralgia, geniculate ganglion syndrome, Herpes zoster oticus, Zoster oticus), described by the American neurologist J. Hunt in 1907, is one of the forms of herpes zoster, occurring with damage to the geniculate ganglion. In the acute period, the rash is localized in the external auditory canal, on the auricle, soft palate, and palatine tonsils. The clinical picture of postherpetic neuralgia of the geniculate ganglion consists of unilateral constant or periodic pain in the ear, in the ipsilateral half of the face, external auditory canal, taste disturbance in the anterior 2/3 of the tongue, moderate peripheral paresis of the facial muscles.
• Hunt syndrome-2 is caused by damage to the sensory nodes of several cranial nerves - vestibulocochlear, glossopharyngeal, vagus, as well as the second and third cervical spinal nerves. Herpetic eruptions appear in the external auditory canal, the anterior 2/3 of the tongue, on the scalp. Pain in the back of the mouth radiates to the ear, back of the head, neck and is accompanied by salivation disorder, horizontal nystagmus, dizziness.

Tolosa-Hunt syndrome

Tolosa-Hunt syndrome occurs suddenly and is characterized by periodic pain in the orbit, swelling, and damage to one or more cranial nerves (III, IV, and/or VI), which usually resolve on their own. In some cases, the disease occurs with alternating remissions and exacerbations. Some patients experience a disturbance in the sympathetic innervation of the pupil.

Cranial nerve involvement coincides with the onset of pain or occurs within 2 weeks of pain. Tolosa-Hunt syndrome is caused by granulomatous tissue growth in the cavernous sinus, superior orbital fissure, or orbital cavity. Painful ophthalmoplegia may also occur with tumor lesions in the superior orbital fissure.

Glossopharyngeal neuralgia

Classical glossopharyngeal neuralgia is similar in clinical manifestations to trigeminal neuralgia (which often causes diagnostic errors), but develops significantly less frequently than the latter (0.5 per 100,000 population).

The disease occurs in the form of painful paroxysms, starting in the area of the tongue root or tonsil and spreading to the soft palate, pharynx, ear. Pain sometimes radiates to the angle of the lower jaw, eye, neck. Attacks are usually short-lived (1-3 minutes), provoked by tongue movements, especially during loud talking, eating hot or cold food, irritation of the tongue root or tonsil (trigger zones). The pain is always one-sided. During an attack, patients complain of dryness in the throat, and after the attack, hypersalivation appears. The amount of saliva on the side of pain is always reduced, even during the period of salivation (compared to the healthy side). Saliva on the side of pain is more viscous, its specific gravity increases due to the increase in mucus content.

In some cases, during an attack, patients develop presyncopal or syncopal states (short-term nausea, dizziness, drop in blood pressure, loss of consciousness). Probably, the development of these states is associated with irritation of the n. depressor (branch of the IX pair of cranial nerves), as a result of which the vasomotor center is suppressed and blood pressure drops.

During an objective examination of patients with neuralgia of the glossopharyngeal nerve, no changes are usually detected. Only in a small proportion of cases is there pain upon palpation of the angle of the lower jaw and individual sections of the external auditory canal (mainly during an attack), a decrease in the pharyngeal reflex, a decrease in the mobility of the soft palate, and a perversion of taste sensitivity in the posterior third of the tongue (all taste stimuli are perceived as bitter).

The disease, like trigeminal neuralgia, occurs with exacerbations and remissions. After several attacks, remissions of varying duration are noted, sometimes up to 1 year. However, as a rule, attacks gradually become more frequent, and the intensity of the pain syndrome increases. In the future, constant pain may appear, increasing under the influence of various factors (for example, when swallowing). Some patients may experience symptoms of loss corresponding to the innervation of the glossopharyngeal nerve (neuritic stage of glossopharyngeal neuralgia) - hypoesthesia in the posterior third of the tongue, the tonsil area, the soft palate and the upper part of the pharynx, taste disturbance at the root of the tongue, decreased salivation (due to the parotid salivary gland).

Classical glossopharyngeal neuralgia, like trigeminal neuralgia, is most often caused by compression of the nerve by a branch of a vessel in the medulla oblongata.

Symptomatic neuralgia of the glossopharyngeal nerve differs from the classical one by the frequent presence of constant aching pain in the interictal period, as well as progressive sensory impairment in the innervation zone of the glossopharyngeal nerve. The most common causes of symptomatic neuralgia of the glossopharyngeal nerve are intracranial tumors, vascular malformations, and volumetric processes in the area of the styloid process.

Neuralgia of the tympanic plexus

Neuralgia of the tympanic plexus (Reichert's syndrome) manifests itself with a symptom complex similar to damage to the geniculate ganglion (although the tympanic nerve is a branch of the glossopharyngeal nerve). This is a rare form of facial pain, the etiology and pathogenesis of which remain unclear to this day. There are suggestions about the role of infection and vascular factors.

Typical are sharp shooting pains in the area of the external auditory canal, appearing in attacks and gradually subsiding. The pains arise without any visible external causes. At the beginning of the disease, the frequency of attacks does not exceed 5-6 times a day. The disease proceeds with exacerbations that last for several months, and then are replaced by remissions (also lasting several months).

In some patients, the development of the disease may be preceded by unpleasant sensations in the area of the external auditory canal, which sometimes spread to the entire face. During examination, objective signs are usually not detected, only in some cases is pain noted during palpation of the auditory canal.

Neuralgia of the intermediate nerve

Intermediate nerve neuralgia is a rare disorder characterized by short paroxysms of pain deep in the ear canal. The main diagnostic criteria are periodically occurring paroxysms of pain deep in the ear canal lasting from a few seconds to several minutes, predominantly on the back wall of the ear canal, where there is a trigger zone. Sometimes the pain may be accompanied by lacrimation, salivation and/or taste disturbances, and a connection with Herpes zoster is often found.

Neuralgia of the superior laryngeal nerve

Superior laryngeal neuralgia is a rare disorder characterized by intense pain (paroxysms of pain lasting from a few seconds to a few minutes) in the lateral wall of the pharynx, submandibular region and below the ear, provoked by swallowing movements, loud talking or turning the head. The trigger zone is located on the lateral wall of the pharynx above the thyroid membrane. In the idiopathic form, the pain is not associated with other causes.

Frey's syndrome

Frey's syndrome (auriculotemporal nerve neuropathy, auriculotemporal hyperhidrosis) is a rare disease that manifests itself as minor, intermittent pain in the parotid region, as well as hyperhidrosis and hyperemia of the skin in the parotid region when eating. The disease is usually caused by trauma or surgery in this area.

Musculoskeletal prosocranialgias

Musculoskeletal prosocranialgias are most often associated with temporomandibular joint dysfunction and myofascial pain syndrome.

The term "pain dysfunction syndrome of the temporomandibular joint" was first introduced by Schwartz (1955), who described its main manifestations - impaired coordination of the masticatory muscles, painful spasm of the masticatory muscles, and limited movement of the lower jaw. Subsequently, Laskin (1969) proposed another term - "myofascial pain dysfunction syndrome of the face" with four main symptoms: facial pain, soreness during examination of the masticatory muscles, limited mouth opening, and clicking sounds during movements in the temporomandibular joint. There are two periods in the development of the syndrome - the period of dysfunction and the period of painful spasm of the masticatory muscles. The onset of one or another period depends on various factors affecting the masticatory muscles, the main ones being psychoemotional disorders leading to reflex spasm of the masticatory muscles. When muscles spasm, painful areas arise - trigger zones, from which pain radiates to neighboring areas of the face and neck.

The characteristic diagnostic signs of myofascial pain syndrome of the face are currently considered to be pain in the masticatory muscles, increasing with movements of the lower jaw, limitation of its mobility (mouth opening to 15-25 mm between the incisors instead of 46-56 mm in the norm), clicks and crepitus in the joint, S-shaped deviation of the lower jaw to the side or forward when opening the mouth, pain when palpating the muscles that lift the lower jaw. When palpating the masticatory muscles, painful seals (muscle trigger points) are detected. Stretching or squeezing these areas causes pain that spreads to adjacent areas of the face, head, neck (the so-called muscle pain pattern). The pain pattern does not correspond to neural innervation, but to a certain part of the sclerotome.

The development of myofascial pain dysfunction syndrome is associated with prolonged tension of the masticatory muscles without their subsequent relaxation. Initially, residual tension occurs in the muscle, then local compactions form in the intercellular space due to the transformation of the intercellular fluid into myogeloid nodules. These nodules serve as a source of pathological impulses. Most often, muscle trigger points are formed in the pterygoid muscles.

It has been found that musculoskeletal prosopalgias occur more often in middle-aged individuals with asymmetric adentia, as well as with certain behavioral habits (clenching the jaws in stressful situations, supporting the chin with the hand, pushing the lower jaw to the side or forward). Radiographic changes may be absent. In many cases, psychological causes (depression, hypochondria, neuroses) play a leading role in the development of the disease.

Cervicoprosocranialgia

Cervicoglossal syndrome is manifested by pain in the occipital or upper cervical region, which occurs when the head is turned sharply and is accompanied by unpleasant sensations in half of the tongue (dysesthesia, a feeling of numbness and pain).

Pain in the tongue is of a reflected nature and is caused by pathology of the cervical spine, most often by subluxation of the atlanto-occipital joint. The development of this syndrome is associated with the fact that proprioceptive fibers from the tongue enter the spinal cord as part of the second dorsal cervical root and are connected to the lingual and hypoglossal nerves. This fact explains the appearance of unpleasant sensations in the tongue with compression of C2 ₍ which is often observed with subluxation of the atlantoaxial joint).

Styloid process syndrome is characterized by pain of mild or moderate intensity in the back of the oral cavity, which occurs when swallowing, lowering the lower jaw, turning the head to the side, and palpating the projection of the stylohyoid ligament. The syndrome is caused by calcification of the stylohyoid ligament, but can also develop with trauma to the neck or lower jaw. To prevent attacks, patients try to keep their head straight, with a slightly raised chin (hence one of the names of the disease - "eagle syndrome").

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Central facial pain

Central facial pain includes painful anesthesia (anaesthesia dolorosa) and central pain after stroke.

• Painful anesthesia of the face is manifested by burning, permanent pain, hyperpathy in the innervation zone of the trigeminal nerve, usually occurring after nerve exeresis of the peripheral branches of the 5th pair of cranial nerves or thermocoagulation of the semilunar ganglion.
• Central facial pain after stroke is most often combined with hemidysesthesia on the opposite side of the body.

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Glossalgia

The incidence of the disease in the population is 0.7-2.6%, and in 85% of cases it develops in women in menopause. It is often combined with gastrointestinal pathology. Unpleasant sensations may be limited to only the anterior 2/3 of the tongue or spread to the anterior sections of the hard palate, the mucous membrane of the lower lip. Symptoms of the "mirror" (daily looking at the tongue in a mirror to detect any changes), "food dominant" (pain decreases or stops during meals), impaired salivation (usually xerostomia), taste changes (bitterness or metallic taste), psychological problems (irritability, fear, depression) are characteristic. The disease is characterized by a long course.

Psychogenic facial pain

Psychogenic facial pain is observed quite often in the practice of a neurologist, usually within the framework of depressive syndrome or neuroses (hysteria).

• Hallucinogenic pains accompany mental illnesses such as schizophrenia and manic-depressive psychosis. They are characterized by the complexity and difficulty of understanding verbal characteristics and a pronounced senestopathic component ("snakes are eating the brain", "worms are moving along the jaw", etc.).
• Hysterical facial pains are usually symmetrical, often combined with headaches, their intensity varies throughout the day. Patients describe them as "terrible, unbearable", but at the same time they have little effect on daily activities.
• Facial pains in depressions are often bilateral, usually combined with headaches, sensoropathy is often noted, expressed by simple verbal characteristics. Combined with the main symptoms of depression (motor retardation, bradyphrenia, facial markers of depression, such as drooping corners of the mouth, Verhaut's fold, etc.).

Atypical facial pain

Pains that do not fit into the description of neurogenic, vegetative, skeletal-muscular prosopalgia are classified as atypical facial pains. As a rule, their atypicality is associated with the simultaneous presence of signs characteristic of several types of pain syndromes, but in this case the psychopathological component usually dominates.

One of the variants of atypical facial pain is persistent idiopathic facial pain. The pain may be provoked by surgical intervention on the face, trauma to the face, teeth or gums, but its constancy cannot be explained by any local cause. The pain does not meet the diagnostic criteria of any of the described forms of cranial neuralgia and is not associated with any other pathology. Initially, the pain occurs in a limited area on one half of the face, for example, in the nasolabial fold or one side of the chin. In some cases, patients cannot accurately localize their sensations at all. No sensitivity disorders or other organic disorders are detected in the pain zone. Additional research methods do not reveal any clinically significant pathology.

Another form of atypical facial pain is atypical odontalgia. This term is used to describe prolonged pain in the teeth or their bed after tooth extraction in the absence of any objective pathology. This syndrome is similar to the so-called "dental plexalgia". Women of menopausal age predominate among patients (9:1). Constant burning pain in the area of the teeth and gums is typical, often with repercussion to the opposite side. Objective signs of dental or neurological disorders are usually absent, although in some patients the syndrome develops after dental procedures (simultaneous extraction of several teeth or filling material extending beyond the apex of the tooth). In some cases, pain decreases during meals and increases under the influence of emotions, adverse meteorological factors and hypothermia.

When the superior dental plexus is affected, pain may radiate along the second branch of the trigeminal nerve and be accompanied by autonomic symptoms, probably arising as a result of the plexus's connections with the autonomic ganglia (the pterygopalatine ganglion and the superior cervical sympathetic ganglion). As a rule, there is no pain at the exit points of the trigeminal nerve branches and no pronounced sensitivity disorders in the innervation zones of its second and third branches.

Bilateral dental plexalgia develops almost exclusively in women over 40 years of age and is characterized by a long course. Burning pain usually appears on one side, but soon appears on the opposite side. Almost all patients experience pain on both sides within 1 year. Simultaneous development of bilateral pain is also possible. As with unilateral dental plexalgia, the upper dental plexus is affected 2 times more often than the lower one.

Possible etiological factors of bilateral dental plexalgia include complex extractions of wisdom teeth, premolars and molars, conduction anesthesia, osteomyelitis of the sockets, surgical interventions on the jaws, the entry of filling material into the mandibular canal through the root canals of the teeth, the extraction of a large number of teeth in a short period of time during preparation of the oral cavity for prosthetics, infections, intoxication, mental trauma, etc.

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