Trigeminal neuralgia is a recurrent lesion of the trigeminal cranial nerve characterized by shooting paroxysmal prosopalgia. The clinical picture consists of repeated paroxysms of unilateral intense facial pain. Alternation of phases of exacerbation and remission is typical. Diagnosis is based on clinical data, the results of neurological examination, additional studies (CT, MRI). The basis of conservative therapy is anticonvulsant pharmaceuticals. According to the indications, surgical treatment is carried out: decompression of the root, destruction of the trunk and individual branches.
ICD 10
G50.0 Trigeminal neuralgia
General information
The first description of trigeminal neuralgia dates back to 1671. In 1756, the disease was isolated into a separate nosology. In 1773, the British physician J. Fothergill made a detailed report on the pain syndrome characteristic of the disease. In honor of the author of the report, neuralgia was named Fothergill’s disease. In modern neurology, the term “trigeminal (trigeminal) neuralgia” is more often used. According to the World Health Organization, the incidence is 2-4 people per 10 thousand population. Pathology is more susceptible to persons over 50 years of age. Women get sick more often than men.
Causes
During the entire period of research on the etiology of this disease, about 50 causal factors were mentioned by various authors. It was found that in 95% of cases the etiofactor is compression of the trunk and branches of the trigeminal nerve. Among the main causes of compression are the following:
- Pathology of blood vessels. The expansion, tortuosity, aneurysm of the vessel lying next to the nerve trunk leads to irritation and compression of the latter. The result is a pain syndrome. Predisposing factors are cerebral atherosclerosis, arterial hypertension.
- Volumetric formations. Cerebral tumors, neoplasms of the bones of the skull, localized in the area of the exit of the trigeminal nerve from the cerebral trunk or along its branches, begin to squeeze nerve fibers as they grow. Compression provokes the development of neuralgia.
- Changes in the structures of the skull. Etiological significance is the narrowing of the bone channels and openings resulting from head injuries, chronic sinusitis, otitis media. A change in the relative position of cranial structures is possible with malocclusion, deformation of the dentition.
In some cases, the lesion of the nervous membrane and fibers is caused by a herpetic infection, a chronic infectious process of the dental system (periodontitis, stomatitis, gingivitis). In some patients, trigeminal neuralgia is formed against the background of a demyelinating disease. Factors provoking the occurrence of pathology include hypothermia, dental manipulations, increased chewing load, in the case of infectious genesis — decreased immunity.
Pathogenesis
The above-mentioned etiofactors potentiate morphological changes in the trigeminal nerve sheath. Studies have shown that structural changes in the myelin sheath and axial cylinders develop 3-6 months after the onset of the disease. Local microstructural disturbances provoke the formation of a peripheral generator of pathologically enhanced excitation. Excessive impulses, constantly coming from the periphery, causes the formation of a central focus of hyperexcitation. There are several theories explaining the connection between local demyelination and the occurrence of hyperexcitation focus. Some authors point to the possibility of transverse interaxonal transmission of impulses. According to another theory, pathological afferent impulses cause damage to the trigeminal nuclei of the cerebral trunk. According to the third theory, at the site of the lesion, axon regeneration goes in the opposite direction.
Classification
The systematization of the disease in accordance with the etiology is of practical importance. This principle underlies the determination of the most appropriate therapeutic tactics (conservative or surgical). According to the etiological aspect , trigeminal neuralgia is divided into two main forms:
- Idiopathic (primary). It is caused by vascular compression of the trigeminal root, more often in the area of the brainstem. Due to the difficulties in diagnosing pathological vessel-nerve relationships, idiopathic neuralgia is assumed after excluding other causes of trigeminal pain syndrome.
- Secondary (symptomatic). It becomes the result of neoplasms, infections, demyelinating pathology, bone changes. It is diagnosed according to neuroimaging, tomography of the skull.
Trigeminal neuralgia symptoms
The clinical picture consists of paroxysms of prosopalgia (facial pain), characterized by a series of intense pain impulses coming from the side of the face to the center. Patients describe the pain syndrome as an “electric shock”, “lumbago”, “electric discharge”. The attack lasts up to two minutes, repeated many times. The localization of pain depends on the location of the lesion. In the pathology of individual branches, pain impulses occur in the supraorbital region, along the zygomatic arch, lower jaw. The defeat of the trunk leads to the spread of pain to the entire half of the face. Characteristic is the behavior of patients at the time of paroxysm: they freeze in place, afraid to move, afraid to speak. Despite the high intensity of pain, patients do not scream.
Trigeminal paroxysm is potentiated by various external influences: wind, cold air and water, shaving. Since the provoking factor can be the load on the facial and masticatory muscles, patients avoid opening their mouths wide, talking, laughing, taking hard food. Trigeminal neuralgia is characterized by a recurrent course. There are no paroxysms during remission. Subsequently, symptoms of loss of trigeminal nerve function appear – a decrease in the sensitivity of the facial skin. The symptomatic form proceeds with a combination of typical pain attacks and other neurological symptoms. Possible nystagmus, symptoms of damage to other cranial nerves, vestibular syndrome, cerebellar ataxia.
Complications
The fear of provoking a neuralgic paroxysm forces patients to chew only the healthy half of the mouth, which leads to the formation of seals in the muscles of the contralateral part of the face. Frequent paroxysms reduce the quality of life of patients, negatively affect their emotional background, worsen their performance. Intense excruciating pain, constant fear of another paroxysm can cause the development of neurotic disorders: neurosis, depression, hypochondria. Progressive morphological changes (demyelination, degenerative processes) cause deterioration of nerve functioning, which is clinically manifested by sensory deficiency, some atrophy of the masticatory muscles.
Diagnostics
In typical cases, trigeminal neuralgia is easily diagnosed by a neurologist. The diagnosis is established on the basis of clinical data and the results of a neurological examination. The main diagnostic criterion is the presence of trigger points corresponding to the exit of nerve branches into the facial region. The presence of neurological deficiency indicates in favor of the symptomatic nature of the pathology. To clarify the etiology of the lesion , the following instrumental studies are used:
- CT scan of the skull. Allows you to identify changes in the size and relative location of bone structures. It helps to diagnose the narrowing of the holes and channels through which the trigeminal nerve passes.
- MRI of the brain. It is produced to exclude volumetric formation as a cause of compression of the nerve trunk. Visualizes tumors, brain cysts, foci of demyelination.
- MR angiography. It is used for targeted verification of the vascular genesis of compression. It is informative if the vascular loop or aneurysm is large enough.
Trigeminal neuralgia differentiates with vascular, myogenic, and psychogenic prosopalgia. The presence of a pronounced vegetative component (lacrimation, swelling, redness) indicates the vascular nature of paroxysm, typical for bundle headache, paroxysmal hemicrania. Psychogenic facial pain is characterized by variability in the duration and pattern of pain paroxysm. To exclude ophthalmogenic, odontogenic and rhinogenic pain syndromes, consultation of an ophthalmologist, dentist, otorhinolaryngologist is required.
Trigeminal neuralgia treatment
Basic therapy is aimed at relieving peripheral and central focal hyperexcitation. The first-line remedies are anticonvulsants (carbamazepine). Treatment begins with a gradual increase in the dose until an optimal clinical effect is achieved. Maintenance therapy is carried out for a long time for several months, followed by a gradual reduction in dosages. In the absence of paroxysms, it is possible to cancel the pharmaceutical. To increase the effectiveness of anticonvulsant treatment, additional medications are used. Auxiliary methods of therapy include:
- Means that potentiate the effect of anticonvulsants. Antihistamines can reduce swelling. Antispasmodics contribute to the relief of pain paroxysm. Microcirculation correctors (nicotinic acid, pentoxifylline) provide increased oxygenation and nutrition of the nerve trunk.
- Therapeutic blockades. The introduction of local anesthetics, glucocorticoid hormones is carried out at trigger points. The therapeutic procedure gives a good analgesic effect.
- Physical therapy. Effective use of electroplating with novocaine, ultraphonophoresis with hydrocortisone, diadynamic currents. The procedures provide a reduction in the severity of inflammation, have an analgesic effect.
The presence of intracranial formation, insufficient effectiveness of pharmacotherapy are indications for surgical intervention. The feasibility of the operation is determined by the neurosurgeon. The basic techniques of neurosurgical treatment are:
- Microsurgical decompression. It is carried out in the area of nerve exit from the brain stem. It is necessary to remember about the high risk of using the technique in elderly patients, patients with a burdened premorbid background.
- Percutaneous radiofrequency destruction. A modern alternative to open interventions with the intersection of trigeminal branches. A significant disadvantage of the method is a relatively high percentage of relapses.
- Stereotactic radiosurgery. The operation consists in the destruction of the sensory root by directed local gamma radiation. Side effects include loss of sensitivity in the innervation zone of the destroyed root.
Prognosis and prevention
Trigeminal neuralgia is not life-threatening, but the attacks of the disease are excruciatingly exhausting. The outcome is determined by the etiology, premorbid background, and duration of the disease. For the first time, trigeminal neuralgia in young patients with adequate treatment has a favorable prognosis. Relapses after surgery are 3-15%. Primary prevention consists in timely treatment of inflammatory pathologies of the dental system, ear, paranasal sinuses. Measures of secondary prevention are regular observation by a neurologist, exclusion of the effects of trigger factors, preventive intake of anticonvulsants for colds.
