A mask-like face (hypomimia) is observed in a number of neurological and mental diseases: Parkinson's disease, myopathies, paresis of the facial nerve, catatonia, depressive, generalized anxiety, hysterical and bipolar affective disorders. Detected in hypothyroidism and scleroderma. The reason for the development of a mask-like face is established on the basis of a survey, anamnestic data, the results of a neurological examination and additional studies. Treatment - dopaminergic drugs, psychotropic drugs, physiotherapy, surgery.
Why does a masked face occur?
Parkinson's disease and syndrome
Hypomimia is one of the manifestations of hypokinesia characteristic of Parkinson's disease. Occurs in the advanced phase of the disease. It is associated with trembling, rigidity, postural dysregulation. A distinctive feature of the pathology is the unilateral nature of disorders at the onset stage, the subsequent asymmetry of symptoms, tremor at rest, and the high effectiveness of treatment with levodopa.
In patients with secondary parkinsonism, the same signs are revealed with a symmetrical nature of the lesions and more rapid progression. The mask-like face is complemented by slow movements, constant muscle tension, and difficulties in maintaining a pose. Other neurological disorders are often found. Secondary parkinsonism can develop with the following pathologies:
- severe traumatic brain injury;
- cerebral infections: viral encephalitis;
- common infections: shingles, measles, mumps;
- toxic effects: some poisoning, heroin addiction, ecstasy addiction;
- vascular diseases: ischemic stroke, cerebral atherosclerosis;
- degenerative diseases of the central nervous system: dementia with Lewy bodies, multiple sclerosis;
- medication: neuroleptic syndrome, disorders due to the use of anticonvulsants, antidepressants, antispasmodics;
- other causes: intracerebral neoplasms, hydrocephalus, posthypoxic syndrome, frequent hypoglycemia.
Myopathies are characterized by a gradual onset with progressive muscle weakness. With the involvement of facial muscles, the face takes on a mask-like appearance, the patient cannot smile, frown his forehead, or stretch his lips with a tube. Dysarthria develops. The muscles of the trunk and limbs are affected symmetrically, atrophic changes develop, and there are difficulties in walking and standing up independently. Hypomimia may accompany the following myopathies:
- Metabolic: with Tarui disease, Pompe disease, some endocrine diseases.
- Secondary inflammatory: against the background of parasitosis (trichinosis, toxoplasmosis, cysticercosis), bacterial and viral infections (influenza, enterovirus, rubella, streptococcal infection).
- Idiopathic inflammatory: with rheumatoid arthritis, Sjögren's syndrome, SLE, scleroderma, systemic vasculitis.
- Mitochondrial: in Kearns-Sayre syndrome, MERRF, MELAS.
- Myofibrillar: desmin-dependent, alpha-B-crystallin-dependent, myotilin-dependent and others.
- Exogenous: alcoholic, steroid.
The mask-like face is formed as a result of the apathico-abulic syndrome. In mild cases, the patient is inattentive, inactive, has difficulty performing complex multicomponent actions. In severe lesions, astasia-abasia, inability to voluntary motor activity, is observed. Criticism is reduced or absent, mental disinhibition is revealed. The cause of frontal syndrome with hypomimia is extensive bilateral lesions in the following conditions:
- TBI: brain contusion, intracerebral, subdural and epidural hematomas.
- Vascular damage: ischemic and hemorrhagic stroke, arteriovenous malformations.
- Large volumetric formations: benign and malignant neoplasia.
- Degenerative pathologies: corticobasal degeneration, frontotemporal dementia, Pick's disease.
Damage to the facial nerve
Neuritis of the facial nerve is characterized by unilateral hypomimia in combination with facial asymmetry: drooping of the corner of the mouth, smoothing of the nasolabial fold, inability to close the eyelid and lagophthalmos on the affected side. Taste disorders, salivation, hyperacusis are observed. Bilateral neuritis is very rare. Clinical manifestations vary depending on the location of the lesion:
- the nucleus of the facial nerve (poliomyelitis) - isolated hypomimia;
- bridge (stem stroke) - a combination of a mask-like face and convergent strabismus;
- exit zone from the brain stem (neurinoma) - signs of neuritis and hearing impairment;
- pyramid of the temporal bone - hyperacusis, salivation disorders, dry eyes.
With Hunt syndrome, herpetic eruptions are detected, with neuritis against the background of chronic otitis media - shooting pains in the ear, hearing loss, with Melkerson-Rosenthal syndrome - swelling of the face, wrinkled tongue.
A mask-like face with a frozen expression of hopelessness, anguish and despair is typical of major depression. There is a slowdown in thinking, a steady decrease in mood and motor activity. Patients are passive, do not even find the strength to take care of themselves, lie in bed all day. Reluctant to make contact. Speech is slow and stingy. Painful insensitivity, suicidal tendencies are possible.
A similar picture is found in the depressive phase of BAD. Hypomimia is also sometimes identified in moderate or severe manic phases. In such cases, the facial expression, on the contrary, can be happy, blissful, in the presence of dysthymia - irritated, aggressive. The patient does not sleep, constantly moves, is distracted in conversation. Ideas of grandeur are observed, sometimes - psychomotor agitation, delirium and hallucinations.
Patients with catatonia repeatedly repeat the same movements or stay in the same position for a long time, sometimes extremely uncomfortable. The mask-like face is especially pronounced in the phase of catatonic stupor. Movements slow down sharply or completely disappear, muscle tone increases. Causes of catatonia are:
- condition after TBI;
- brain tumors;
- severe cerebral infections;
- thrombocytopenic purpura;
- postpartum psychosis.
Sometimes catatonia with hypomimia is observed in autism, cocaine addiction, some other drug addictions, and taking a number of medications.
With GAD, a mask-like face develops episodically, indicating a sharp increase in the level of anxiety. Accompanied by fussiness or, on the contrary, "fading". Short-term hypomimia can also be due to the development of a panic attack or getting into a frightening situation in a patient with a phobia. In hysterical neurosis, the symptom may be due to pseudoparesis.
With scleroderma, the mask-like face is due to thickening and tension of the skin. Raynaud's syndrome, trophic disorders (hair loss, brittle nails, ulceration, osteolysis of the nail phalanges of the fingers) are observed. There are cephalgia, dysfunctions of internal organs, polyarthralgia, myositis. With hypothyroidism, the face is edematous, yellowish. Hypomimia is complemented by lethargy, apathy, chilliness, and an increase in body weight.
Patients with hypomimia due to neurological diseases are examined by a neurologist. In case of mental disorders, an examination by a psychiatrist or psychotherapist is necessary. Taking into account the genesis of the pathology, accompanied by a mask-like face, patients are referred for a consultation with a rheumatologist, endocrinologist, narcologist, and other specialists. During the survey, the doctor determines the time and circumstances of the appearance of hypomia, reveals other complaints, ascertains the anamnesis of life and disease. The examination plan includes the following diagnostic methods:
- Neurological examination. With parkinsonism, bradykinesia, muscle rigidity, tremor, characteristic gait disturbances, and postural disorders are found. With myopathy, muscle weakness, decreased reflexes are detected. With frontal syndrome, the patient cannot consistently perform a series of movements in accordance with the instructions. The grasping reflex, signs of oral automatism are determined. Possible problems with speech, astasia.
- Tomographic neuroimaging. Informative in establishing the causes of parkinsonism, frontal syndrome. It is prescribed to exclude the secondary nature of facial paralysis. On CT scan of the brain, hematomas are clearly visible, signs of an injury. MRI of the brain is the method of choice for detecting neoplasms, post-stroke foci, and degenerative diseases.
- Other imaging techniques. Patients with impaired cerebral hemodynamics undergo duplex scanning or dopplerography of cerebral vessels. In scleroderma, x-rays of the hands and feet, CT or MRI of the liver, kidneys, and lungs are indicated to detect calcifications and signs of fibrosis. Thyroid ultrasound is recommended for patients with suspected hypothyroidism.
- Functional research. Electromyography, electroneurography and the study of evoked potentials help to establish the localization of the pathological process and the severity of nerve damage, are used to clarify the etiology of neuritis, differentiation of myopathy with myelitis, cerebrovascular accident, infectious myelopathy.
- Biopsy and morphological analysis. Patients with hypothyroidism may have a fine-needle biopsy of the thyroid gland to determine the nature of the lesion. In patients with scleroderma, skin biopsies are examined for differential diagnosis, with myopathies - to verify the form of the disease.
- Laboratory tests. In hypothyroidism, tests are carried out to determine the level of thyroid hormones, autoantibodies to thyroid tissues. With scleroderma, antibodies to topoisomerase and anticentromeric antibodies are detected in the blood, the functions of the kidneys and liver are evaluated according to the results of a biochemical blood test. With myopathies in the biochemical analysis of urine, an increase in the concentration of creatinine is detected, in the blood test - an increase in the level of LDH, AST, ALT, and other enzymes.
Therapeutic tactics is determined taking into account the causes of the appearance of a mask-like face:
- Disease, Parkinson's syndrome. Dopamine receptor agonists are used. At the initial stage monotherapy is recommended. With the progression of the disease, the lack of effectiveness of the drug, combined regimens are prescribed. Patients with secondary parkinsonism are treated for the underlying disease. Depending on the etiology, detoxifying and vascular agents, neurometabolites, etc. are used.
- Myopathies. In congenital forms, medications are indicated to stimulate metabolic processes in muscle tissue: amino acids, vitamin complexes, anabolic steroids, anticholinesterase drugs. With acquired forms, correction of the causative pathology is necessary: elimination of infections and intoxications, restoration of hormonal balance, etc. As part of non-drug therapy, exercise therapy, massage, ultrasound, iontophoresis, and electrophoresis are effective.
- Frontal Syndrome. Etiopathogenetic therapy may include thrombolytics, vascular and psychotropic drugs, neurometabolites, neuroprotectors, nootropics. Some patients with intracranial tumors are treated with chemotherapy. Comprehensive rehabilitation measures are required.
- Neuritis. At the initial stage, vasodilators and decongestants, glucocorticoids, B vitamins are used. In case of intense pain, therapeutic blockades are performed. UHF, ozokerite and paraffin treatment are carried out. Subsequently, anticholinesterase agents, phonophoresis, ultrasound, and sometimes electrical nerve stimulation are used. With insufficient efficiency, biostimulants are indicated.
- Mental disorders. With neurosis, psychotherapy comes to the fore. The method is selected individually, taking into account the problems and characteristics of the patient's personality. Cognitive-behavioral, emotional-figurative, psychoanalytic, body therapy, gestalt therapy, art techniques are practiced. In severe disorders, drug treatment is required using antidepressants, mood stabilizers, antipsychotics.
- Scleroderma. Pharmacological support includes antifibrotic and anti-inflammatory drugs, antiplatelet agents, vasodilators. With widespread induration of soft tissues, enzymes are administered by injection, application, or drug electrophoresis.
- Hypothyroidism. Recommended synthetic analogues of thyroid hormones. The dose and duration of treatment are determined individually. Patients who have undergone radiation therapy or surgical removal of the thyroid gland, suffering from autoimmune thyroiditis, require lifelong hormone therapy. With secondary hypothyroidism, treatment of the underlying pathology is necessary; with a lack of iodine in food, iodine-containing agents are indicated.
Surgical interventions are required for hypomia against the background of intracranial hematomas, intracranial tumors, and vascular anomalies. In TBI, transcranial removal, stereotaxic aspiration, or endoscopic hematoma evacuation are possible. Neoplasms are excised by an open method (by craniotomy) or stereotaxic surgery is used. For vascular anomalies, excision, embolization, or endovascular occlusion is performed.
Patients with hypomimia due to traumatic neuritis require nerve suturing or neurolysis. In some cases, plastic surgery of the facial nerve is indicated. Operations are carried out within a year after the manifestation of the disease, further correction of the mask-like face becomes impossible due to atrophy of the mimic muscles. In scleroderma, hypomimia, asymmetry, and cosmetic imperfections are sometimes eliminated by excision of the affected lesions and plastic replacement of defects with displaced skin flaps.