The facial nerve is responsible for the activity of all facial muscles. This nerve provides the ability to express emotions, squint, smile, etc. A person with facial paralysis does not have this option.
The Neurology Clinic of the Yusupov Hospital in Moscow offers services for high-quality diagnostics, effective treatment of facial paralysis, as well as successful rehabilitation of patients after an illness.
Facial nerve paralysis: causes of development
The exact cause of this disease has not been determined to date. However, it is known that the trigger for the development of facial paralysis can be damage to the following infectious viral pathologies:
- herpes infection;
- chickenpox and herpes zoster;
- adenoviral infections, acute respiratory viral infections, influenza;
- mononucleosis (Epstein-Barr virus);
- cytomegalovirus;
- Coxsackie virus;
- rubella.
In addition, paralysis of the facial nerve can occur with hypothermia, alcohol abuse, cancer in the brain, severe stressful situations, hypertension, head injuries (ears, face), atherosclerotic changes in blood vessels, dental diseases, diabetes, otitis media and sinusitis.
The risk group for the development of facial nerve paresis includes women during pregnancy and after childbirth, elderly people, especially those with weakened immune systems. The incidence of the disease increases during viral epidemics.
Among experts there is also an opinion about hereditary factors of the disease.
Why does it occur
The causes of facial neuritis are unknown. Numerous studies have not allowed scientists to determine the exact sources of damage to nerve fibers. It is assumed that the pathology may be a complication of existing neurological and infectious diseases. There is also an idiopathic form of neuritis, in which paralysis can appear against the background of complete clinical well-being. Previously, facial hypothermia was considered the main cause of the disease, but modern data refute the significance of this etiological factor.
Possible reasons:
- Herpes is a viral infection characterized by damage to the skin and mucous membranes. Most often, the disease affects the external genitalia, facial skin and mucous membrane of the eye. Viruses are transmitted primarily through sexual contact. According to research results, during herpes infection of the surface of the lips, viruses penetrate the long processes (axons) of sensory neurons. Pathogens can destroy the myelin sheath.
- Other infectious diseases: rubella, Lyme disease, influenza, Coxsackievirus, cytomegalovirus infections and herpes zoster. The likelihood of disease occurring in the presence of chronic infection depends on the state of the immune system.
- Autoimmune disorders are pathologies in which the immune system begins to attack healthy tissue. Multiple sclerosis and other diseases are characterized by destruction of the myelin sheaths of nerve fibers and severe neurological complications.
- Malignant or benign brain tumor. The pathological formation can compress the nuclei of the facial nerve.
- Ischemic or hemorrhagic stroke is an acute disorder of cerebral circulation in which brain tissue is destroyed.
With secondary Bell's palsy, addressing the underlying cause of the disorder is key to treatment. Chronic neuritis of the facial nerve is usually infectious in nature.
Facial nerve paralysis: symptoms
The development of facial paralysis is characterized by an acute onset: the condition of patients worsens quite sharply.
However, initial symptoms can be detected at an early stage of the disease, one to two days before visual manifestations appear.
Facial nerve palsy may present with the following symptoms:
- soreness in the area of the auricle, extending to the back of the head or face;
- pain in the eye from the affected area.
The appearance of the first signs is associated with an increase in swelling of the nerve column and its gradual compression.
Then more pronounced signs of facial paresis appear:
- violation of facial symmetry;
- lack of facial expressions and emotionality on the affected side of the face;
- drooping of the corner of the mouth, smoothing of the nasolabial fold, frontal folds on the affected side of the face;
- increased facial symmetry when trying to smile, speak, or cry;
- inability to completely close the upper eyelid;
- difficulty keeping liquid food and drinks in the mouth, pouring them from the affected side of the mouth - while the patient can chew and swallow normally;
- chewing food may be accompanied by biting the inside of the cheeks, which is associated with a lack of sensitivity in one’s own cheek;
- drying of the mucous membrane, decreased salivation (in some cases, on the contrary, its increase);
- impaired speech function associated with inactivity of certain parts of the mouth and lips;
- impaired blinking function, half-opening of the eye on the affected side, drying of the eye mucosa or, conversely, the appearance of excessive tearing;
- increased hearing on the affected side, changes in the perception of sounds (they seem louder to patients than usual);
- Patients have impaired taste sensations on the affected side of the tongue.
Facial paralysis: forms
There are several types of facial paralysis:
- Congenital facial paralysis occurs when the process of brain formation is disrupted in the prenatal period. In patients with this form of paralysis, there is a drooping of the corner of the mouth, a mask-like facial expression on the affected side, opening and moistening of the palpebral fissure. The skin on the cheek is smooth; during exhalation, the cheek on the affected side swells. The most severe form of congenital paralysis is Mobius syndrome;
- peripheral paralysis of the facial nerve - occurs if the patient has impaired motor function of the nerve trunk. With this type of paralysis, asymmetry occurs, complete immobility of the muscles of the affected part of the face;
- central paralysis of the facial nerve is caused by pathological changes in the cerebral cortex. The disease is most often localized in the lower part of the face. The main symptoms of central facial paralysis are: seizures, as well as involuntary muscle movements (a kind of tic).
Degrees
Doctors divide the severity of trigeminal nerve paresis into three degrees:
- light. In this case, the symptoms are mild. A slight distortion of the mouth may occur on the side where the lesion is localized. A sick person must make an effort to frown or close his eyes;
- average. A characteristic symptom is lagophthalmos. A person can practically not move the muscles in the upper part of the face. If you ask him to move his lips or puff out his cheeks, he will not be able to do this;
- heavy. The asymmetry of the face is very pronounced. Characteristic symptoms are that the mouth is severely distorted, the eye on the affected side practically cannot close.
Facial nerve paralysis: complications and consequences
In the absence of competent therapy, which requires a considerable amount of time and patience, facial paralysis can be aggravated by the development of the following complications:
- muscle atrophy (thinning and weakening of muscles), caused by prolonged dysfunction and impaired tissue trophism. This process is irreversible: restoration of atrophied muscles is impossible;
- facial contractures (muscle elasticity is lost on the affected side), spastic shortening of muscle fibers, muscle spasms. Visually, tension on the affected side and squinting of the eye are noted;
- facial muscle tics, spastic twitching (hemispasms, blepharospasms);
- associated movements (syncinesia) - characterized by the release of tears during chewing food, raising the edges of the lips when squinting the eyes;
- inflammatory processes in the conjunctiva or cornea of the eye, the development of which is associated with drying out of the eye mucosa as a result of its prolonged stay in an incompletely closed state.
Facial nerve paralysis: diagnosis
An experienced neurologist at the Yusupov Hospital can diagnose facial paralysis after the first examination of the patient. However, to determine the cause of the development of this disease, a general blood test may be prescribed to identify the inflammatory process and additional instrumental studies:
- magnetic resonance imaging for the possible detection of tumor processes, vascular disorders, inflammatory changes in the membranes of the brain, cerebral infarction;
- computed tomography - x-ray examination to identify the probable causes of the disease: post-stroke conditions, tumors, consequences of mechanical damage to the brain, disturbances of perinuclear blood flow;
- electroneurography - to determine the speed of passage of nerve impulses, which makes it possible to establish muscle atrophy, damage to the nerve branch, and the inflammatory process;
- electromyography with neurography - to identify the quality of intramuscular impulses for the diagnosis of muscle atrophy and contractures.
During the diagnostic process, facial nerve paresis must be differentiated from such pathologies as: stroke, Ramsay-Hunt syndrome, inflammatory processes in the mastoid process and middle ear, Lyme disease, temporal bone fractures, carcinomatosis or leukemia affecting the nerve trunk, chronic meningitis, tumor processes , multiple sclerosis, Guillain-Barre syndrome.
General information
Facial nerve neuropathy (synonym: facial nerve neuritis, Bell's palsy) is paralysis/paresis of the facial nerve, accompanied by sensory, motor and autonomic disturbances in the area of innervation of the facial muscles and facial asymmetry.
Facial nerve neuropathy (FN) is one of the most common and pressing problems in neurology. Specific lesions of the facial nerve, according to various authors, range from 9.3 to 12.8% of all diseases of the peripheral nervous system. Facial nerve neuritis code according to ICD-10: G51.0 - Bell's palsy. In modern terminology, the term “Bell's palsy” is usually used only to refer to damage to the facial nerve of unknown etiology (idiopathic origin), while neuropathy of the facial nerve is a broader concept that includes a whole variety of forms.
First of all, it should be noted that NLN always develops only when the nerve fiber is damaged from the motor nucleus of the facial nerve to its exit from the stylomastoid foramen (peripheral paresis) and always on the same side, in contrast to central paresis, which occurs mainly during a stroke and is often combined with paresis of the limbs developing on the side opposite to the lesion (Fig. below).
The facial nerve (FN) refers primarily to the motor nerves that provide facial expressions, the processes of blinking, chewing, swallowing, and frowning. However, the trunk of the facial nerve also contains components of the intermediate nerve - parasympathetic (secretory) and sensory (taste) fibers innervating the salivary glands, as well as the taste sensitivity of the tongue.
The relatively high incidence of damage to the facial nerve is largely due to its inherent anatomical and topographical features - the nerve has a complex and long course in the narrow bony canal of the temporal bone. The most vulnerable segment of the FN (in which it is pinched/compressed) is the segment located in a narrow convoluted canal where, in cases of edema development due to various reasons (for example, inflammation), it is compressed.
Among different localizations of damage to the peripheral part of the FN, Bell's palsy is the most common pathology (16-25 cases / 100,000 population) and is caused by the development of edema and its subsequent compression in the bone canal (tunnel syndrome). The high vulnerability of the FN in the fallopian canal is explained by its prevalence in the cross section of the canal, where it occupies 40%-70% of the total area. Moreover, despite the fact that the canal narrows in some places, the thickness of the nerve trunk itself remains unchanged.
In the vast majority of cases, peripheral paresis of the facial nerve is manifested by unilateral damage to the facial nerve. The right/left facial side is affected with equal frequency. Bilateral neuropathy of the FN accounts for only 6.2% of all its lesions. The average age of onset is about 40 years, but can occur at any age. The lowest incidence rate is observed in children under 10 years of age, increases in persons in the age group 10–29 years, stable rates are typical for persons 30–69 years of age, and reaches maximum rates in the population of patients after 70 years of age.
The disease is characterized by a high frequency of complications (7–18% of cases); recurrent FN neuropathies are observed in 24.5% of cases. Recurrent neuropathies, compared to primary ones, are more severe, more difficult to treat, and extremely rarely result in complete recovery. Neuropathy of the facial nerve, as many patients who visit a special forum write, is an extremely psychotraumatic situation for patients and has an extremely negative impact on the psycho-emotional sphere and physical condition of patients, up to the development of neurosis. FN palsy is a common cause of long-term disability and significantly reduces quality of life.
Facial nerve paralysis: treatment
The main method of treating facial paresis in the neurology clinic of the Yusupov Hospital is complex drug therapy using modern drugs of various effects:
- diuretics;
- anti-inflammatory drugs;
- glucocorticoids;
- antiviral drugs;
- antispasmodics;
- neurotropic drugs;
- vitamin preparations;
- agents for inhibiting cholinesterase.
Drug treatment of facial paralysis in the Yusupov Hospital in-patient department is carried out under the strict supervision of a neurologist, who can promptly adjust the dosage or replace the drug.
