Reasons for development
Facial nerve neuropathy can develop for the following reasons:
- progression of herpes, polio, mumps, enterovirus;
- hormonal imbalances (the disease appears especially often in the first half of pregnancy);
- tooth infections;
- sudden and severe hypothermia;
- injuries of the skull and jaws;
- sinusitis, otitis;
- diabetes;
- poor circulation in the blood vessels of the face;
- multiple sclerosis.
Most often, the disease in question develops when the facial nerve is cold - a short stay in a draft is enough for the inflammatory process to begin its progression.
standard treatment
For the treatment of neuritis, drug therapy is mainly used: hormonal, diuretic and vasodilating drugs, B vitamins. For pain, analgesics are used. If the cause of neuritis is an infection, then antibiotics and immune drugs are used.
Physiotherapy is indicated from the first days of the disease. After the acute period, massage and physical therapy for the affected muscles, anti-inflammatory drugs, drugs that improve metabolic processes in the nerve and muscles, electrical neurostimulation and acupuncture are prescribed.
The presence of a tumor along the nerve requires surgical treatment.
Symptoms of facial neuritis
The development of the inflammatory process always begins acutely, but before the main clinical picture reveals itself, the patient may feel discomfort in the back of the head and pain symptoms in the eye. The main symptoms of trigeminal facial neuritis:
- the affected side of the face becomes immobilized and takes on the appearance of a mask;
- the eye on the affected side is wide open;
- the corner of the mouth is lowered;
- nasolabial folds are smoothed;
- speech becomes slurred;
- special sensitivity to sounds;
- increased dry mouth.
Over time, as the disease progresses and in the absence of treatment, paresis of the facial nerve develops - the face becomes asymmetrical, the patient cannot fully smile or control his own facial expressions.
Possible complications
If a person does not pay attention to the symptoms and simply takes analgesics to relieve attacks of pain, the condition may worsen.
Untreated inflammation can cause:
- loosening of teeth (molars and wisdom teeth);
- atrophy of the muscles with which chewing occurs;
- earlier appearance of wrinkles;
- inflammation of the mucous membrane of the organs of vision or cornea due to a failure in the production of moisturizing fluid;
- deterioration in the appearance of the skin due to lack of normal nutrition;
- madarosis, that is, loss of eyelashes and eyebrow hair.
In order not to encounter unpleasant complications, you need to take preventive measures, and if there are initial signs, do not postpone a visit to the doctor.
Diagnosis of inflammation of the facial nerve
If the doctor is properly qualified, then only based on the patient’s complaints will he be able to make a diagnosis and identify the severity of the pathological process. But even if the clinical picture is typical, the patient will have to undergo a series of diagnostic examinations:
- take blood and urine tests;
- undergo magnetic resonance imaging;
- do electroneurography.
The results obtained will help determine what treatment for inflammation of the facial nerve will be. In addition, such an examination will allow the doctor to identify the body’s perception of non-steroidal anti-inflammatory drugs - these are the drugs that will be used for therapy.
our treatment
Our center provides treatment for peripheral neuritis, which is caused by pinching of the facial nerve in the area where it exits the cranial cavity.
We resolve dense scars, eliminate tissue degeneration and relieve muscle spasm around the pinched facial nerve. This leads to its release and restoration of normal conduction of nerve impulses.
To treat neuritis of the facial nerve, we use a special technology using the method of muscle mesotherapy.
If necessary, a course of nutraceuticals and osteopathy sessions are prescribed.
The main condition for successful treatment is early seeking help.
Newspaper "News of Medicine and Pharmacy" Neurology (396) 2011 (thematic issue)
Paresis of facial muscles (prosoparesis) due to damage to the facial nerve in children ranks first in the structure of diseases of the peripheral nervous system. The incidence of facial nerve neuropathy (FN) in childhood averages 5–7 people per 10 thousand children, in equal proportions among boys and girls.
In ICD-10, damage to the facial nerve (FN) is represented by code G51. Currently, idiopathic lesions of the FN are interpreted as Bell's palsy, named after S. Bell, who in 1836 first described the clinic of lesions of the FN (ICD code - G51.0). Bell's palsy accounts for 50 to 75% of all NPLs. The term “neuropathy/neuritis of the facial nerve” is used to refer to other forms with a known or unspecified etiology (ICD code: G51.8 - Other lesions of the facial nerve and G51.9 - Lesions of the facial nerve, unspecified). NLN has its own code for inflammation of the knee joint (G51.1) and Melkersson-Rossolimo syndrome (G51.2). Thus, idiopathic Bell's palsy is a diagnosis of exclusion. All other etiological factors of prosoparesis, including traumatic, infectious, congenital, metabolic, immunological, autoimmune, neoplastic, must be excluded.
There are several anatomical features that contribute to damage to the FN: 1) phylogenetically, the nerve is one of the youngest and most vulnerable cranial nerves; 2) the nerve has a complex course in a narrow bone canal, occupying 70% of the diameter; 3) the main vessels in the conditions of a narrow bone bed behave like the terminal ones, which contributes to primary and secondary ischemia.
Recently, clinicians are inclined to believe that NLN is a polyetiological, but monopathogenetic disease. Despite many theories regarding the pathogenesis of NLN (ischemic, vascular, inflammatory, toxic, immune, viral), Bell's palsy is currently considered as a tunnel syndrome caused by compression of the ischemic and edematous nerve in the narrow fallopian canal. Conditions for compression of the facial nerve are most favorable in its lower part, where at the level of the stylomastoid foramen the epineural sheath is thickened and very elastic.
The immediate trigger for the development of vascular disorders and nerve ischemia can be: hypothermia, infections, autoimmune diseases, hormonal and metabolic disorders, and pain. In the emerging pathobiochemical complex, an important place is occupied by the disintegration of metabolism, activation of lipid peroxidation, increased membrane permeability for potassium ions, inhibition of antioxidant systems, development of myelino- and axonopathy of the LN and disruption of neuromuscular transmission.
Pathologically, nerve damage is classified according to Sunderland. There are five degrees of severity: from neuropraxia (loss of myelin) and axonothemesis to severe neurothemesis with Wallerian degeneration and loss of peri- and epineurium. The degree of damage to the FN correlates with the severity of the clinical picture and the unfavorable prognosis for functional recovery.
In children, NLN develops against the background of intense processes of growth and myelination of nerve fibers, which determines the course and prognosis. On the one hand, childhood is prognostically favorable in restoring FN function. On the other hand, in 10–20% of cases, the trigeminal and FN on the healthy side are involved in the process; in 60% of children, when studying visual evoked potentials, signs of bilateral conduction disorders along the optic nerve are revealed. These data predetermine the risk of developing recurrent NLN and sometimes allow us to consider this pathology a variant of cranial demyelinating polyneuropathy or a clinically isolated syndrome at the onset of multiple sclerosis.
Clinical symptoms of FN damage will consist of prosoparesis and associated accompanying symptoms, which are determined by the topical level of damage. The following levels of FN damage are distinguished:
— supranuclear damage (central palsy of the FN);
— damage at the core level (processes in the area of the pons);
— damage to the FN root in the posterior cranial fossa (cerebellopontine angle);
— damage to the FN root at the entrance to the temporal bone canal;
— damage to the FN in the fallopian canal proximal to the origin of n. petrosus superficialis major (to the lacrimal gland);
— damage to the FN in the fallopian canal proximal to the origin of the branch to m. stapedius;
- damage to the FN in the fallopian canal between n. stapedius and chorda tympani;
— damage to the FN in the fallopian canal distal to the origin of the chorda tympani;
— damage to the FN distal to the foramen stylomasto-ideum.
The diagram of the FN from the trunk through the internal auditory foramen and the fallopian canal (labyrinthine, tympanic and mastoid segments) to the stylomastoid foramen is shown in Fig. 1.
According to MR imaging with gadolinium, involvement of the FN was revealed at the level of the supragenicular segment - 47%, genicular segment - 25%, tympanic part - 2%, mastoid part - 15%. In 11% the level of the lesion could not be localized.
Clinical picture
The disease develops acutely, within a few hours (less commonly, 3–10 days). Slow progression of prosoparesis (over weeks or months) is unusual and in most cases has a neoplastic etiology. The development of the disease is often preceded by general or local hypothermia. In approximately 60% of cases, Bell's palsy begins with an aching or burning pain behind the ear, which can sometimes radiate to the face or back of the head. Typically, weakness of the facial muscles is detected in the morning upon awakening. General health remains normal.
At rest in the acute period of the disease, smoothing of the folds on the forehead, widening of the palpebral fissure, drooping of the eyebrow, lower eyelid, wing of the nose, and corner of the mouth are noted. As a result of paralysis of the ear muscles, the auricle is slightly turned anteriorly. The palpebral fissure does not close completely during sleep, the lower eyelid moves slightly away from the mucous membrane of the eyeball, blinking is absent or becomes rare. When trying to close the eyes, Bell's symptom is observed, which consists of a synergistic upward and slightly outward movement of the eyeball with closing the eyes. When looking up, Negro's symptom is observed: the eye on the diseased side seems to rise higher than on the healthy side, and a wider strip of sclera forms between the cornea and the lower eyelid. The consequence of damage to the orbicularis oculi muscle is not only lagophthalmos, but also lacrimation, which is explained by irritation of the constantly open eye, as well as the fact that tears do not enter the nasolacrimal canal. Lacrimation is present in 2/3 of patients, less often (17%) dry eye occurs due to damage to the fibers of the greater petrosal nerve. About 30% of patients note a distorted, unpleasantly enhanced perception of sounds (hyperacusis) on the affected side, associated with paresis of the stapedius muscle. In many cases, taste perception is impaired in the anterior 2/3 of the tongue (dysgeusia). Active movements on the affected side are absent or significantly limited. When checking them, it is necessary to pay attention to wrinkling of the forehead (function of the frontalis muscle), frowning of the eyebrows (the so-called proud muscle), closing and squinting of the eye (orbicularis oculi muscle), wrinkling of the back of the nose (nasal muscle), movements of the corner of the mouth with closed lips and baring of teeth (muscles that raise and lower the angle of the mouth), movement of the lips anteriorly (orbicularis oris muscle). When the cheeks are puffed out on the side of the paresis, the hypotonic buccal muscle parousitis, and if the lips are not closed sufficiently, puffing out the cheeks becomes impossible, and sometimes food falls out of the mouth. With minor paresis of the orbicularis oculi muscle, a symptom of eyelashes is observed, which consists in the fact that the patient can close his eyes, but when he tries to close them tightly, the tips of the eyelashes on the affected side are visible.
The following degrees of severity of NLN are distinguished:
1) mild - prosoparesis, lacrimation;
2) moderate - prosoparesis, dysgeusia, hyperacusis, dry eye, pain;
3) severe - prosoplegia and other accompanying symptoms.
Regression of symptoms, up to complete recovery, with favorable development occurs within 4–6 weeks. In other cases, improvement occurs after 3–6 months and is only partial. A favorable outcome is observed in approximately 80% of cases, significant residual effects are observed in 5–8% of cases. A recurrent course is observed in 7–9% of cases.
Unfavorable prognostic factors for NLN are:
- severe prosoparesis;
- facial pain;
- high level of damage (hyperacusis, impaired tear and salivation, dysgeusia);
- excessive facial dysmorphia;
— relapses of prosoparesis and family predisposition;
- late start of therapy (after 3 days);
- absence of acoustic stapedial reflex;
— electrophysiological signs of denervation.
The localization of facial nerve damage and accompanying symptoms of prosoparesis are presented in Table. 1.
One of the main prognostic criteria for complications in NLN is the severity and duration of paralysis of the facial muscles. If spontaneous or treatment-induced recovery does not begin within four weeks or more, or if it is extremely slight, then the probability of developing contractures or synkinesis is very high and amounts to 28–37%.
The severity of prosoparesis is determined by the House-Brackmann scale (Table 2).
Contracture of facial muscles in the initial period, in its clinical signs, differs only quantitatively from the trigger stage of NLN. The trigger, on the one hand, helps to increase the tone of paretic muscles, on the other hand, serves as a prerequisite for the formation of contractures. Their first symptom is the presence of mild spontaneous pain in the face. However, unlike the pain that is often observed in the first days of the disease, the muscles themselves also turn out to be painful on palpation. The patient notes pulsating twitching of individual muscle bundles, imperceptible to the eye, and a feeling of tightness on the affected half of the face. These pulsations are easily determined by applying a finger. More often, contracture occurs against the background of incomplete recovery of Bell's palsy. In advanced cases, when examining the patient, one gets the impression that it is not the sick side that is paralyzed, but the healthy side. The following signs of contracture are detected: the palpebral fissure becomes narrower; the nasolabial fold is more clearly expressed at rest; Spontaneous hyperkinesis is observed in the form of small fascicular twitching of the chin or eyelids. The mechanical excitability of facial muscles increases sharply. The feeling of tightness on the affected half of the face intensifies, especially with excitement, in the cold, during physical and mental stress. During the massage, it is clearly felt that the cheek is thicker than on the healthy side. When a contracture has formed, trigger points can be found in any facial muscle. They are felt in the form of compactions, painful when pressed and stretched.
During the process of muscle reinnervation, another extremely undesirable phenomenon may appear - pathological synkinesis :
- eyelid-labial (when the eye is closed, the corner of the mouth on the same side rises);
- eyelid-frontal (when closing the eye, the forehead wrinkles);
- eyelid-platysma (when you close your eyes, the subcutaneous muscle of the neck contracts);
- eyelid-auricular (when you close your eyes, the auricle involuntarily rises);
— Huye synkinesis (when you close your eyes, the wing of the nose rises upward and outward);
- labial-palpebral (narrowing of the palpebral fissure when the cheeks are puffed out, when the lips are pulled into a tube, while eating);
- frontolabial (involuntary raising of the corner of the mouth when the forehead is wrinkled);
- a symptom of crocodile tears (tearing from the eye on the affected side when chewing or even when moving the lower jaw). This phenomenon is an example of pathological motor-visceral synkinesis.
Diagnostics
Particular attention is paid to the history of the disease, the rate of increase in prosoparesis, clinical symptoms and identification of accompanying symptoms. Provoking factors, previous injuries, somatic and neurological diseases, and otological pathology are determined.
A reliable and significant method is electroneuromyography (ENMG) . Stimulation and needle ENMG allows one to assess the dynamics of the disease, determine the stage and degree of the denervation process in the facial muscles, and also assess the effectiveness of reinnervation. If the magnitude of the M-response on the diseased side is 30% or more of that on the healthy side, the probability of complete recovery is 84%; on the contrary, if it is less than 30%, then in 88% of cases the recovery will be incomplete. The most accurate method for studying taste is electrogustometry . If the subject does not feel a sour or metallic taste at 300 μA, then this indicates that he has a disorder of taste sensitivity.
The diagnostic algorithm includes the following laboratory and instrumental studies and consultations with specialists (Table 3).
Differential diagnosis of prosoparesis
Unilateral prosoparesis:
1. Idiopathic Bell's palsy.
2. Family forms of NLN.
3. Melkersson-Rossolimo-Rosenthal syndrome (SMRR): autosomal dominant type; 9p11 with incomplete penetrance of the gene. It is characterized by recurrent NLN, recurrent characteristic swelling of the face, lips and other parts of the body, cheilitis and folded tongue. Prosoplegia can be unilateral or bilateral; the affected side may alternate from relapse to relapse. There are patients with various variants of incomplete SMRR. To diagnose SMDD in children, it is proposed to use an algorithm that includes the components of the triad of the classic symptom complex, combined with facial dysmorphia, signs of neurological deficiency, autonomic and somatic disorders, autoallergic manifestations and hereditary predisposition.
4. Infectious lesions: Herpes simplex is the most common cause; borreliosis, HIV infection; polio; syphilis and tuberculosis; sarcoidosis and other granulomatous diseases; cat scratch disease, etc. Ramsay Hunt syndrome is a herpetic lesion of the ganglion of the intermediate nerve (pain and characteristic skin rashes in the ear area, oral mucosa, sometimes involving the VIII nerve).
5. Middle ear diseases: otitis media and (less commonly) middle ear tumors such as glomus tumor. NLN due to these diseases is always accompanied by hearing loss and corresponding radiological findings.
6. Multiple sclerosis, clinical isolated syndrome.
7. Dysmetabolic disorders are described in the form of mononeuropathy, or a picture of polyneuropathy, or multiple mononeuropathy in diabetes mellitus, hypothyroidism, uremia, porphyria, arterial hypertension.
8. Injuries: fracture and penetrating wounds of the pyramid of the temporal bone, iatrogenic injuries, birth injuries. TBI, especially with a fracture of the temporal bone, often leads to damage to the facial and vestibulocochlear nerves.
9. Neoplastic and space-occupying processes (benign and malignant): neuroma, hemangioma, cholesteatoma, meningioma, metastases, salivary gland tumor, arachnoid cyst.
10. Alternating syndromes (with vascular and tumor lesions of the brain stem).
11. Syringobulbia.
12. Diseases of the skull bones.
13. Congenital syndromes: Mobius syndrome, cardiofacial syndrome, motor neuron disease, osteopetrosis, oculoauriculovertebral syndrome, CHARGE syndrome (coloboma, heart disease, choanal atresia, genital hypoplasia, auricular anomaly), CULLP syndrome (congenital unilateral lower lip paresis).
c syndrome (SM) is caused by a congenital malformation of the rhombencephalon and occurs in three genetic variants. General characteristics of SM: prosoparesis can be unilateral or bilateral in 90%. In some cases, external ophthalmoplegia is possible, most often the abducens nerve is involved. In 9% there may be congenital fibrosis of the extraocular muscles. 34% have Duane retraction syndrome. 56% had pharyngeal dysfunction and hypoglossal nerve involvement. Respiratory disorders in 19%. From birth, muscle hypotonia is observed in 88% of cases and incoordination is observed in 83% of cases.
SM type 1, dominant, 13q12.2-q13. Clinical features: congenital asymmetrical diplegia of the facial muscles, ophthalmoplegia, orofacial anomalies, cognitive delay, peripheral neuropathy, arthrogryposis, rib defect, respiratory disorders, calcifications in the brainstem, hypogonadotropic hypogonadism. Aplasia of the trunk nuclei.
SM type 2, dominant, 3q21-q22. Asymmetric weakness of the facial muscles, uneven involvement of the branches of the FN, absence of ophthalmoplegia. The FN core is reduced, the facial nerve is reduced in size. The structures of the rhomboid fossa and the corticospinal tract are intact.
SM type 3, dominant, 10q21.3-q22. Unilateral or bilateral prosoparesis, ophthalmoplegia, congenital deafness or progressive hearing loss with age.
Cardiofacial syndrome (Cayler-Di George syndrome, 22q11.2 deletion, dominant or multifactorial). Congenital complete prosoparesis or paresis of the lower lip in a mild case, heart disease, muscle hypotonia, myopathy, facial dysmorphia, thymic hypoplasia, T-cell abnormalities, in 10% - microcephaly, cognitive impairment.
Carey-Fineman-Ziter syndrome , A-R. Clinically non-progressive myopathy, hypotension. Hypoplasia of the pectoral and shoulder muscles (Poland variant). Macrocephaly, ophthalmoplegia, ptosis, bilateral facial weakness, dysphagia, micrognathia, glossoptosis, cleft palate (50%), scoliosis (40%), flatfoot (40%), brachydactyly (70%), delayed motor development.
Bilateral weakness of the facial muscles in children, developing simultaneously or sequentially, occurring in 0.3–2% of all prosoparesis, always serves as a reason for the following diagnostic search:
1. Acute inflammatory demyelinating polyneuropathy (Guillain-Barré and Miller Fisher variants).
2. Idiopathic cranial polyneuropathy.
3. Chronic inflammatory demyelinating polyneuropathy.
4. Melkersson-Rossolimo-Rosenthal syndrome.
5. Multiple sclerosis.
6. Hyperostosis cranialis interna: an autosomal dominant hereditary disease that manifests itself as thickening of the internal bony plate of the skull with osteosclerosis and tunnel cranial neuropathies with variable disturbances of smell, taste, vision, and cochleovestibular dysfunction.
7. Sarcoidosis (Heerford syndrome) - infiltration of the parotid glands, iridocyclitis, damage to the lymph nodes, skin, respiratory organs, liver, spleen, bones, fever (uveoparotid syndrome), basal process (tuberculous, leukemic, cryptococcal, paraneoplastic, etc.), always involved other cranial nerves; paresis is often bilateral, characterized by rapid onset.
8. Infectious damage to the cranial nerves (mononucleosis, herpetic infection, borreliosis, HIV infection).
9. Systemic diseases (periarteritis nodosa, Wegener's granulomatosis, Kawasaki disease, etc.) lead to mononeuropathies and polyneuropathies, as well as damage to other cranial nerves.
10. Syringobulbia.
11. Cholesteatoma.
12. An-a-lipoproteinemia (Tangier disease 9q31) - in addition to diparesis of the facial muscles, weakness, decreased muscle strength and tendon reflexes, paresthesia, excessive sweating, oculomotor disorders and selective loss of pain and temperature sensitivity are observed. Deposits of cholesterol esters in the corneal membrane, tonsils, liver, spleen, rectal mucosa cause spleno- and hepatomegaly, lymphadenopathy, tonsils are enlarged, orange or yellow. High levels of triglycerides in the blood; hypocholesterolemia.
13. Motor neuron disease.
14. Myasthenia.
15. Myopathies.
Recurrent weakness of facial muscles
1. Idiopathic neuropathy of the facial nerve (including familial).
2. Melkersson-Rossolimo-Rosenthal syndrome.
3. Myasthenia gravis.
The therapeutic tactics of NLN depend on the etiology and period of the disease: 1) acute (up to 10 days, usually 3–72 hours); 2) early recovery (10–30 days); 3) late recovery (1 month); 4) period of residual effects (more than 6 months) - synkinesis, weakness of the facial muscles, contractures, blepharospasm, crocodile tears symptom (Frey's syndrome).
The main goal of therapeutic measures in the acute period is aimed at relieving edema, improving microcirculation, and remyelination.
To prevent the development of keratitis, it is necessary to instill moisturizing eye drops, wear protective glasses during the day, and apply an eye patch at night. These activities are carried out until voluntary closure of the eye becomes possible and the blink reflex is restored.
Treatment of idiopathic Bell's palsy. In the presence of one of the clinically unfavorable prognostic factors, glucocorticoid therapy is indicated (prednisolone 1 mg/kg/day for 7–10 days).
In other cases, non-steroidal PVA is used for 2 weeks.
Low-molecular dextrans and dehydrating drugs (Lasix, L-lysine escinate) in the acute period are administered parenterally and combined with vasoactive (Trental, Actovegin), neurometabolic drugs (alpha-lipoic acid (espalipon, berlition, thiogamma), nucleo-CMF and vitamins B1, B2, B12.
Antibiotic therapy is prescribed for otogenic lesions of FN, Lyme disease (cefuroxime or amoxicillin 50 mg/kg/day).
Acyclovir 80 mg/kg/day for 5 days is prescribed for diseases of herpetic etiology, Ramsay Hunt syndrome.
The effectiveness of physiotherapy treatments, electrical stimulation and reflexology has not been proven. Traditionally, from the first day of the disease, a UHF electric field is used, which has a pronounced anti-inflammatory, analgesic and dehydrating effect, a course of treatment of 8–10 procedures, or phonophoresis with hydrocortisone. The principles of kinesiotherapeutic rehabilitation for paresis of facial muscles include positional treatment, therapeutic exercises and massage. Massage is indicated from the 3rd day from the onset of prosoparesis. There is evidence that exercises using biofeedback lead to improved functional outcome and a decrease in the frequency of synkinesis.
The prescription of anticholinesterase drugs, including when using electrophoresis, leads in 60–75% of cases to the development of secondary contractures of facial muscles and spasmoparesis.
In the case of the formation of early or late secondary contracture of the facial muscles, the abolition of medicinal and physiotherapeutic stimulating techniques . Muscle relaxants (mydocalma or sirdaluda) are used in combination with tranquilizers or carbamazepine at a dose of 10 mg/kg/day, magnesium B6. Botulinum toxin preparations (Botox or Dysport) are used. Thermal procedures include mud or paraffin applications on the affected half of the face at a temperature of 38–40 °C, lasting 20 minutes.
The method of choice for kinesiological therapy is post-isometric muscle relaxation (PIRM) . The essence of this technique is to alternate short-term isometric work in the first 5–7 s and passive muscle stretching in the next 6–10 s.
Consultation with a pediatric neurosurgeon is indicated for the purpose of nerve decompression or traumatic injury. In cases where pronounced asymmetries and motor defects persist (lagophthalmos, drooping lower lip, etc.), it is recommended to refer the patient for a consultation with a neurosurgeon or plastic surgeon for the purpose of revision of the facial nerve or plastic surgery.