Trigeminal facial pain: systematics of clinical forms, principles of diagnosis and treatment

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Tibetan medicine classifies inflammation of the trigeminal nerve as a disorder of the Rlung (Wind) system, which controls the functioning of nerve structures, as well as brain activity. Therefore, with this disease, sedatives, warming or anti-inflammatory drugs should be used.

Pepper patches are widely used as a warming agent in Eastern medicine. They should be applied to painful (trigger) areas.

Another popular remedy is balms based on essential oils. For example, Vietnamese balm “Golden Star”, which should be gently, effortlessly rubbed into painful points of the face with your fingertips. A reflexologist will draw up a regimen for you to use this balm, which you can use at home.

Causes of inflammatory damage to the trigeminal nerve

Factors contributing to inflammation of the trigeminal nerve are:

• surgical interventions on the jaw bones;
• fractures of the base of the skull, lower and upper jaws;
• tumors;
• complex tooth extraction;
• hypothermia;
• surgery on the maxillary sinus;
• improperly administered anesthesia;
• incorrectly performed dental prosthetics;
• metabolic disorders;
• the presence of foreign bodies that irritate the nerve trunk or injure nerve endings;
• bacterial or viral infection;
• various types of intoxication of the body;
• hypovitaminosis;
• weakening of the immune system.

Why is pulp needed?

Pulp is a soft connective tissue that fills the internal cavity of the tooth. It ensures the supply of essential nutrients. The pulp contains many nerve endings, as well as blood and lymphatic vessels. This is where the perception of various sensations occurs. And pain too.

The pulp performs a plastic function, participating in the formation of dentin. And also protective, which consists in the disposal of dead cells, the formation of tertiary dentin and the synthesis of immunoglobulins. We are interested in its sensory function, which can be carried out thanks to a fairly large number of nerve fibers.

Symptoms of trigeminal neuritis

The maxillary trigeminal nerve consists of three types of nerve fibers:

• vegetative;
• motor;
• sensitive.

The symptomatic picture of neuritis may vary depending on which fibers were affected by the inflammatory process.

Damage to sensory fibers

In particular, with inflammation of the sensory fibers, the patient may complain of a tingling sensation, numbness, and weakened sensitivity in the area innervated by the trigeminal nerve.

Damage to motor fibers

When motor fibers are damaged, there is a partial or complete decrease in strength in the innervated muscles, their atrophy and deterioration of tendon reflexes.

Damage to vegetative fibers

When the vegetative fibers are inflamed, the patient experiences cyanosis and swelling of the skin, dryness and thinning of the skin, and the potential risk of developing a trophic ulcer increases.

Treatment of neuritis of the nerve: ulnar, radial and median

The mobility of the hand is impaired. It is impossible or difficult to bend and straighten it. Moving your fingers hurts. There is a tingling or numbness sensation in the affected area.

Neuropathy occurs with fractures, dislocations of the bones of the shoulder, forearm, hand, or compression in the area of ​​fibrocystic canals. Compression is most often formed as a result of prolonged trauma. In the area of ​​the cubital canal, it is provoked by: systematically repeated flexion movements of the elbow, constant support when working with the elbow on a machine, table, workbench.

In the area of ​​Guyon's canal, compression occurs due to the use of a cane, frequent cycling, motorcycling, or regular work with the same tool: screwdriver, pliers, pliers, jackhammer. Neuralgia can also be caused by:

• tumor;
• enlarged lymph nodes;
• aneurysm of a nearby vessel;
• arthritis or arthrosis of the elbow joint.

When a nerve is damaged, the patient experiences pain, muscle strength decreases, and movement disorders occur. To diagnose, the doctor performs a physical examination, prescribes tests and an MRI.

Treatment for median nerve neuritis, like ulnar neuritis, depends on the cause of the problem. If compression occurs in the area of ​​the cubital canal or Guyon's canal, reduce the compression of the fibers during movement by applying fixing devices: bandages, splints, orthoses. Movements that cause compression should be avoided.

Non-steroidal anti-inflammatory drugs are prescribed to treat ulnar nerve neuritis and reduce symptoms in the form of swelling and pain. Massage and acupuncture have a positive effect on the nervous system. Physiotherapy helps with neuropathy and nerve compression due to fractures and injuries.

However, the disease must be treated after the first signs appear. As soon as one of the symptoms of hand neuritis appears, treatment begins. Otherwise, conservative methods will become ineffective.

Pain due to inflammation

In addition, a disease such as inflammation or neuritis of the facial trigeminal nerve makes itself felt with attacks of pain of a very diverse nature:

• cutting,
• burning,
• pricking,
• tearing
• shooting, etc.

In this case, the area of ​​pain does not always correspond to the area of ​​innervation and can spread to the lower jaw, cheeks and chin.

Pain may be accompanied by:

• muscle spasms (facial, chewing),
• the appearance of nasal discharge,
• development of hypersalivation,
• increased lacrimation.

Lack of sensation in the tongue, lips and chin

With inflammatory damage to the trigeminal nerve, not only the entire nerve can be damaged, but also its individual branches. This is why numbness and pain can occur in various areas of the face. For example, when the lingual branch of the nerve is inflamed, patients complain of pain and sensitivity disturbances in the anterior part of the tongue, and when the mental branch is damaged, in the area of ​​the lips and chin.

Pain when laughing, chewing, brushing teeth and shaving

Pain due to neuritis of the maxillary trigeminal nerve can intensify with touching, chewing, laughing and with changes in temperature. That is why patients, trying to prevent the recurrence of painful attacks, avoid excessive mobility and prolonged conversations, and refuse brushing their teeth and shaving.

Trigeminal facial pain: systematics of clinical forms, principles of diagnosis and treatment

Facial pain, which includes pain on the surface of the face and/or in the mouth (orofacial pain), is one of the most common types of pain. Most often, orofacial pain manifests itself as acute dental pain, which usually regresses after dental treatment. However, in a number of cases, facial pain itself (prosopalgia) is noted, manifested by chronic or recurrent pain, often resistant to various methods of conservative treatment. A kind of primacy in severity belongs to trigeminal facial pain, especially trigeminal neuralgia and deafferentation trigeminal neuropathy, during exacerbation of which the severity of pain is many times greater than the intensity of acute toothache familiar to most people.

Taxonomy of trigeminal prosopalgia

Trigeminal prosopalgia (Greek prosopon (face) + algos (pain)) includes facial pain caused by damage to the trigeminal nerve. From the point of view of topical diagnosis, the development of any form of trigeminal prosopalgia is associated with damage to the peripheral trigeminal neuron - the peripheral trigeminal branches, the sensory trigeminal ganglion (located at the base of the skull), the sensory root of the trigeminal nerve that follows it in the direction of the brain stem, as well as those entering the brain stem sensory trigeminal fibers and sensory nuclei of the trigeminal nerve (

).

Despite the difference in the symptomatology of the clinical forms of trigeminal prosopalgia, the features of facial pain are of primary importance for their differentiation, in some cases manifested by prolonged (constant) pain, and in others in the form of paroxysms of pain. Paroxysmal forms of trigeminal pain are traditionally referred to as neuralgia, and non-paroxysmal forms - trigeminal neuropathy. However, non-paroxysmal postherpetic facial pain is also called neuralgia. These forms of facial pain—neuralgia and trigeminal neuropathy—fundamentally differ in their approaches to treatment.

Paroxysmal trigeminal prosopalgia

Paroxysmal facial pain, lasting from several seconds to several minutes, is manifested by trigeminal neuralgia (typical trigeminal neuralgia), trigeminal neuralgia due to multiple sclerosis, and symptomatic trigeminal neuralgia arising from a tumor lesion of the trigeminal nerve.

Until recently, trigeminal neuralgia, not associated with multiple sclerosis and tumor lesions of the trigeminal nerve, was called idiopathic, i.e. occurring for no apparent reason. However, as it was established as a result of serial neurosurgical interventions, the main etiological factor of typical trigeminal neuralgia is compression of the sensory root of the trigeminal nerve by an atypically located arterial or venous vessel.

Trigeminal neuralgia

Trigeminal neuralgia is the most common form of paroxysmal (paroxysmal) facial pain. It is also considered the most excruciating type of facial pain. It manifests itself as attacks of sharp, high-intensity pain in the area of ​​innervation of the trigeminal nerve. The cessation of an attack of facial pain within a few tens of minutes after taking the anticonvulsant carbamazepine radically distinguishes trigeminal neuralgia from most other types of chronic pain. The symptoms of trigeminal neuralgia undergo significant changes as the pain syndrome increases and regresses, reaching its greatest severity at the height of the exacerbation period.

In secondary (symptomatic) forms of trigeminal neuralgia, which arise from tumor damage to the trigeminal nerve, already at the first stage of the disease symptoms may be observed that differ from the typical clinical picture.

Non-paroxysmal trigeminal prosopalgia

Non-paroxysmal trigeminal prosopalgia, manifested by prolonged facial pain, as well as sensitivity deficit (hypesthesia, anesthesia) in the facial area, includes various clinical forms of trigeminal neuropathy, including postherpetic neuralgia (). Most often, the development of trigeminal neuropathy is associated with obvious etiological factors - trigeminal herpes zoster and traumatic injury to the trigeminal nerve. In some cases, trigeminal neuropathy is one of the early manifestations of systemic diseases, in particular systemic scleroderma, systemic lupus erythematosus, sarcoidosis and Lyme disease.

Traumatic trigeminal neuropathy

It is the main form of trigeminal neuropathy, the clinical signs of which are non-paroxysmal facial pain, sensory impairment (numbness) and, very rarely, motor impairment. As a rule, the acute development of these symptoms has an obvious relationship with local pathological processes and iatrogenic effects in the maxillofacial area.

The first sign of traumatic trigeminal neuropathy is acutely developed sensory insufficiency - from mild hypoesthesia to anesthesia, limited to the innervation zone of the affected sensory branch. Subsequently, paresthesia (a feeling of “pins and needles”) and/or non-paroxysmal pain occurs in the same area of ​​the face. Symptoms of sensory loss that accompany facial pain may persist significantly longer than facial pain. In the affected area, hyperesthesia is often detected, as well as pain on palpation of limited areas of facial skin.

Postherpetic trigeminal neuralgia

Trigeminal postherpetic neuralgia is persistent facial pain and/or burning and itching that persists from the time herpetic lesions develop or occurs several weeks after the lesions resolve (delayed postherpetic neuralgia).

Trigeminal postherpetic neuralgia most often develops in patients over 60 years of age. Its occurrence is usually facilitated by:

• late seeking medical help during the period of acute herpes zoster;
• presence of concomitant pathology;
• complicated resolution of rashes - rashes with a hemorrhagic component and secondary pyoderma;
• pronounced residual sensory deficit (“numbness” of the skin after resolution of the rash).

Deafferentation trigeminal neuropathy (prosopalgia)

Deafferentation facial pain (prosopalgia) is the most severe form of trigeminal lesion, manifested by highly intense facial pain, often resistant to conservative therapy, and severe sensory impairment. Develops as a result of significant damage (destruction) of the peripheral or central structures of the trigeminal system.

The concept of “deafferentation trigeminal prosopalgia”, as a general syndromological definition, was proposed by Yu. V. Grachev and Yu. A. Grigoryan (1995) to designate a special form of facial pain that develops as a result of deafferentation in the sensory system of the trigeminal nerve. The pathophysiological term “deafferentation” (de- + lat. afferentis bringing), literally means the separation of the receptor zones of peripheral nerves from the central sensory structures, due to a violation of the integrity or conductivity of nerve fibers.

Typical peripheral forms of deafferentation trigeminal prosopalgia are postherpetic, tumor and iatrogenically caused facial pain (caused by destruction of the ganglion and trigeminal nerve root), and central are two quite rare forms caused by syringobulbia and medulla oblongata infarction.

Diagnosis of trigeminal prosopalgia

The examination of a patient experiencing facial pain should begin with a systematic medical interview, including clarification of the clinical characteristics of the pain and analysis of anamnestic data (

).

The presence of facial pain requires a detailed study of the function of the cranial nerves, and also makes certain additions to the traditional neurological examination. Objective signs of damage to the nervous system of the face are sensory disturbances in the orofacial region - trigger zones, areas of increased and/or decreased sensitivity (Fig. 2, 3), local autonomic disorders, as well as the presence of local palpation pain.

When conducting palpation examination of the facial area, it is necessary to distinguish between “neuralgic” and “myofascial trigger” (English trigger).

1. Neuralgic trigger points or zones (in patients with trigeminal neuralgia) are hyperexcitable areas of the skin and mucous membrane, with mechanical irritation, including light touch, causing a painful attack. At the same time, strong pressure, usually applied by the patient himself, not only does not cause pain, but in some cases leads to a decrease or disappearance of pain.
2. Myofascial trigger points (essentially pain points) are located in the soft tissues of the face in the projection of the masticatory muscles. “Pressing” on them is accompanied by localized or radiating pain.

Establishing a specific form of trigeminal facial pain, which usually requires an interdisciplinary clinical examination, involves excluding a number of forms of orofacial pain not associated with damage to the trigeminal nerve, in particular temporomandibular (arthrogenic and myofascial), symptomatic (ophthalmo-, rhino- and odontogenic) and psychogenic prosopalgia.

Treatment of trigeminal prosopalgia

The complexity of treating patients with trigeminal facial pain is due to the need to determine differentiated treatment approaches due to the ineffectiveness of the use of conventional analgesics for certain forms of trigeminal prosopalgia, the frequent need to change standard treatment regimens and, in some cases, the development of “pharmacoresistant” forms of facial pain that require surgical treatment.

The ineffectiveness of traditional analgesics (for example, NSAIDs) prescribed in connection with the development of trigeminal facial pain is an indication for the use of drugs from other groups, in particular carbamazepine, gabapentin or amitriptyline, which have analgesic activity in a number of forms of prosopalgia (scheme of differentiated therapeutic approaches for paroxysmal and non-paroxysmal trigeminal prosopalgia is presented in

).

Over the past few decades, carbamazepine has remained the most effective and affordable drug in the treatment of patients with trigeminal neuralgia. At the same time, the maximum effectiveness of carbamazepine (as a “monotherapy”) appears in the initial period of the disease. The main indication for the use of carbamazepine is paroxysmal pain, covering the area of ​​innervation of the trigeminal nerve. The daily dose of carbamazepine during an exacerbation of trigeminal neuralgia is usually 600–1200 mg (with a 3–4-time dose of the usual dosage form or 2 times of the retard form), but with uncontrolled use by a doctor it often exceeds 2000 mg/day. As neuralgia regresses, a transition is made to maintenance doses of carbamazepine and its gradual withdrawal when facial pain disappears. If there are contraindications for the prescription of carbamazepine or its forced withdrawal, gabapentin is used as an alternative remedy for the elimination of paroxysmal trigeminal pain.

Gabapentin (Gabagamma) is an anticonvulsant that has an analgesic (GABAergic-like) effect. Obviously, this explains its effectiveness in the treatment of patients with neuropathic pain, including paroxysmal and non-paroxysmal trigeminal prosopalgia. Indications for the use of gabapentin (Gabagamma) are paroxysmal facial pain in trigeminal neuralgia and trigeminal neuralgia caused by multiple sclerosis, as well as subacute and chronic non-paroxysmal pain (including deafferentation) in herpetic and traumatic trigeminal neuropathy. The daily dose of Gabagamma in patients with trigeminal prosopalgia can range from 300 to 1500 mg, with a dosage frequency of at least 3 times a day. Gabagamma is used for a long time and is gradually withdrawn. In general, the use of gabapentin (Gabagamma) is considered safer than carbamazepine and especially amitriptyline.

Amitriptyline is a tricyclic antidepressant that is a norepinephrine and serotonin reuptake inhibitor. This drug is widely used for the treatment of postherpetic neuralgia, especially accompanied by a burning sensation. The analgesic effect of amitriptyline usually develops within 1–2 weeks. To reduce the sedative and anticholinergic effects of amitriptyline, treatment begins with small doses of the drug - 10 mg 2-3 times a day (especially at night), gradually increasing the daily dose (due to evening administration) to 75-100 mg. If amitriptyline is insufficiently effective and facial pain persists, gabapentin (Gabagamma) is indicated.

Treatment of patients with damage to the trigeminal nerve also includes the use of high doses of B vitamins in the form of multicomponent preparations “Milgamma” and “Milgamma compositum”. The composition of the drug "Milgamma" (solution for intramuscular administration) includes 100 mg of thiamine and pyridoxine, 1000 mcg of cyanocobalamin and 20 mg of lidocaine. Milgamma compositum is available in the form of tablets containing 100 mg of benfotiamine and pyridoxine. The effectiveness of Milgamma in the treatment of patients with neuropathic pain is associated with inhibition (probably serotonergic) of nociceptive impulses, as well as acceleration of the regeneration of axons and the myelin sheath of peripheral nerves. The regimen for using Milgamma for trigeminal facial pain includes: prescribing Milgamma in the form of a solution for intramuscular administration - 2 ml daily, for 10 or 15 days, then Milgamma compositum - orally, 1 tablet 3 times a day, for 6 weeks.

Yu. V. Grachev , Doctor of Medical Sciences, V. I. Shmyrev, Doctor of Medical Sciences, Professor, Scientific Research Institute of Advanced Promotion of the Russian Academy of Medical Sciences, State Medical University of the Administration of the President of the Russian Federation, Moscow

Treatment of neuritis of the maxillary trigeminal nerve

Therapy

The treatment program for trigeminal neuritis is drawn up taking into account the causes of the disease and its clinical signs. The main goals of treatment are:

• achieving a sensitizing effect;
• fight against bacterial and viral infection;
• increasing the body's immune forces;
• elimination of swelling of the nerve trunk;
• restoration of natural adaptive and compensatory reactions;
• normalization of the patency of nerve impulses.

Healing procedures

The set of procedures aimed at blocking the inflammatory process and eliminating all manifestations of neuritis includes:

• antibacterial therapy;
• antiviral therapy;
• elimination of factors contributing to the occurrence of intoxication;
• removal of tumor-like neoplasms or dissection of adhesions compressing the nerve;
• prescribing vitamin and mineral complexes to the patient;
• stimulation of nerves and muscles;
• acupuncture;
• physiotherapy (electrophoresis, phonophoresis, UHF, ultrasound, paraffin therapy).

People suffering from trigeminal neuritis are advised to regularly visit dental clinics and have their oral cavity sanitized.

Possible complications

Almost all diseases of the trigeminal nerve are associated with either damage (pinching) or an inflammatory process. In both cases, high-quality treatment is necessary, since the consequences of trigeminal nerve disease can be serious. Disruption of the structure of nervous tissue not only causes severe and sudden pain, but also affects facial expressions, tissue sensitivity and even the psychological state of a person. The difficulty is that it is sometimes quite difficult to determine the cause of problems with the trigeminal nerve. Only high-quality diagnostics helps to create an optimal treatment plan.

Treatment methods

Inflammation of the trigeminal nerve and neuralgia are treated in a comprehensive manner and only under the guidance of specialists. This is taking antibiotics, NSAIDs, glucocorticoids, muscle relaxants and anticonvulsants, coupled with novocaine blockades. Additionally, a number of physiotherapeutic procedures are prescribed. If these measures do not bring the desired result, surgical intervention is required. Depending on the clinical case, radiofrequency destruction or microvascular decompression is prescribed.

You can read more about the treatment of neuritis and neuralgia in a separate article.

Types of diseases

All types of trigeminal nerve diseases can be divided into inflammatory and non-inflammatory.

Neuritis

An inflammatory disease of the trigeminal nerve that over time destroys the myelin sheath and nerve trunk. As a rule, inflammation of the trigeminal nerve is characterized by burning pain (sometimes accompanied by itching), impaired sensitivity and muscle atrophy.

Neuralgia

The disease trigeminal neuralgia is not inflammatory. It refers to any pain that occurs due to damage or pinching of the trigeminal nerve. Experts distinguish between primary (idiopathic) and secondary neuralgia. The causes of idiopathic neuralgia are usually difficult to determine, and secondary neuralgia is actually a manifestation of other pathologies. A characteristic feature of neuralgia is a sharp shooting pain, reminiscent of an electric shock and overtaking the patient suddenly.

Attention!!!

Gradenigo syndrome is also closely related to trigeminal neuralgia. It is characterized by abducens nerve palsy and can affect the functionality of the branches of the trigeminal nerve, pain and dysfunction of the eyeball. Some experts also distinguish damage to the nucleus of the trigeminal nerve and trismus - spasms of the masticatory muscles caused by pathologies of the trigeminal nerve.