Hypomimia

Hypomimia is observed in a number of neurological and mental diseases: Parkinson’s disease, myopathy, facial nerve paresis, catatonia, depressive, generalized anxiety, hysterical and bipolar affective disorders. It is detected in hypothyroidism and scleroderma. The cause of the development of a masked 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, surgical interventions.

Causes of hypomimia

Parkinson’s disease and syndrome

Hypomimia is one of the manifestations of hypokinesia characteristic of Parkinson’s disease. Occurs in the expanded phase of the disease. It is combined with trembling, rigidity, violations of postural regulation. A distinctive feature of pathology is the unilateral nature of disorders at the stage of debut, the subsequent asymmetry of symptoms, tremor at rest, and the high effectiveness of levodopa treatment.

In patients with secondary parkinsonism, the same signs are revealed with a symmetrical nature of lesions and faster progression. The masked face is complemented by slowness of movements, constant muscle tension, difficulties in holding a pose. Other neurological disorders are often found. Secondary parkinsonism can develop in the following pathologies:

• severe traumatic brain injuries;
• 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;
• taking medications: neuroleptic syndrome, disorders against the background of the use of anticonvulsants, antidepressants, antispasmodics;
• other causes: intracerebral neoplasms, hydrocephalus, posthypoxic syndrome, frequent hypoglycemia.

Myopathies

Myopathies are characterized by a gradual onset with progressive muscle weakness. When the facial muscles are involved, the face becomes masklike, the patient cannot smile, frown, or stretch his lips with a tube. Dysarthria is formed. The muscles of the trunk and limbs are affected symmetrically, atrophic changes develop, difficulties are observed when walking, getting up independently. Hypomimia may accompany the following myopathies:

• Metabolic: in 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: rheumatoid arthritis, Sjogren’s syndrome, SLE, scleroderma, systemic vasculitis.
• Mitochondrial: with Kerns-Sayre syndrome, MERRF, MELAS.
• Myofibrillar: desmin-dependent, alpha-B-crystallin-dependent, myotylin-dependent and others.
• Exogenous: alcoholic, steroid.
• Non-metallic.

Frontal syndrome

A masked face is formed as a result of apathetic-abusive syndrome. In mild cases, the patient is inattentive, inactive, has difficulty performing complex multicomponent actions. With a severe lesion, astasia-abasia is observed, an inability to voluntary motor activity. Criticism is reduced or absent, mental disinhibition is revealed. The cause of the frontal syndrome with hypomemia is extensive bilateral lesions in the following conditions:

• TBI: brain contusion, intracerebral, subdural and epidural hematomas.
• Vascular damage: ischemic and hemorrhagic stroke, arterio-venous malformations.
• Large volume formations: benign and malignant neoplasia.
• Degenerative pathologies: corticobasal degeneration, frontotemporal dementia, Peak disease.

Defeat of the facial nerve

Neuritis of the facial nerve is characterized by unilateral hypomimia in combination with facial asymmetry: lowering of the corner of the mouth, smoothing of the nasolabial fold, inability to close the eyelid and lagophthalmos on the diseased side. There are violations of taste, salivation, hyperacusis. Bilateral neuritis is very rare. Clinical manifestations vary depending on the location of the lesion:

• the nucleus of the facial nerve (polio) – isolated hypomimia;
• bridge (stem stroke) – a combination of a masked face and converging strabismus;
• the area of exit 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 rashes are detected, with neuritis against the background of chronic otitis – shooting pains in the ear, hearing loss, with Melkerson-Rosenthal syndrome – facial edema, a folded tongue.

Affective disorders

A masked face with a frozen expression of hopelessness, longing and despair is typical of a major depression. There is a slowdown in thinking, a steady decrease in mood and motor activity. Patients are passive, do not find the strength even to take care of themselves, they lie in bed all day. They are reluctant to make contact. Speech is slow, stingy. Painful insensibility, suicidal tendencies are possible.

A similar pattern is found in the depressive phase of the BAD. Hypomimia is also sometimes determined in the moderate or severe course of the manic phase. 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. There are ideas of greatness, sometimes psychomotor agitation, delirium and hallucinations.

Catatonia

Patients with catatonia repeatedly repeat the same movements or stay in the same position for a long time, sometimes extremely uncomfortable. The masked face is especially pronounced in the phase of catatonic stupor. Movements slow down sharply or disappear completely, muscle tone increases. The cause of catatonia are:

• schizophrenia;
• condition after TBI;
• brain tumors;
• epilepsy;
• severe cerebral infections;
• thrombocytopenic purpura;
• postpartum psychosis.

Sometimes catatonia with hypomimia is observed in autism, cocaine addiction, some other drug addictions, taking a number of medications.

Neurotic disorders

With GAD, a masked 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 caused by 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 a consequence of pseudoparesis.

Other reasons

In scleroderma, the masked face is caused by the compaction and tension of the skin. There are Raynaud’s syndrome, trophic disorders (hair loss, brittle nails, ulceration, osteolysis of the nail phalanges of the fingers). There are cephalgias, disorders of the functions of internal organs, polyarthralgia, myositis. With hypothyroidism, the face is swollen, yellowish. Hypomimia is complemented by lethargy, apathy, chilliness, and an increase in body weight.

Diagnostics

Patients with hypomimia due to neurological diseases are examined by a neurologist. In case of mental disorders, an examination by a psychiatrist or a psychotherapist is necessary. Taking into account the genesis of pathology accompanied by a masked face, patients are referred for consultation to a rheumatologist, endocrinologist, narcologist, and other specialists. During the survey, the doctor determines the time and circumstances of the appearance of hypomimia, identifies other complaints, finds out the anamnesis of life and disease. The examination plan includes the following diagnostic techniques:

• Neurological examination. With Parkinsonism, bradykinesia, muscle rigidity, tremor, characteristic gait disorders, postural disorders are detected. With myopathy, muscle weakness and decreased reflexes are revealed. 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. There may be problems with speech, astasia.
• Tomographic neuroimaging. It is informative in determining the causes of parkinsonism, frontal syndrome. It is prescribed to exclude the secondary nature of facial nerve paralysis. On the CT scan of the brain, hematomas and signs of trauma are clearly visible. MRI of the brain is the method of choice for detecting neoplasms, post-stroke foci, and degenerative diseases.
• Other visualization techniques. Duplex scanning or Dopplerography of cerebral vessels is performed in patients with impaired cerebral hemodynamics. With scleroderma, radiography of the hands and feet, CT or MRI of the liver, kidneys and lungs are shown to detect calcifications and signs of fibrosis. Thyroid ultrasound is recommended for patients with suspected hypothyroidism.
• Functional studies. 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, cerebrospinal circulation disorders, infectious myelopathy.
• Biopsy and morphological analysis. Patients with hypothyroidism may undergo a fine-needle thyroid biopsy 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 performed to determine the level of thyroid hormones, autoantibodies to thyroid tissues. In scleroderma, antibodies to topoisomerase and anticentromeric antibodies are detected in the blood, kidney and liver functions are evaluated based on the results of a biochemical blood test. With myopathies, an increase in the concentration of creatinine is detected in the biochemical analysis of urine, and an increase in the level of LDH, AST, ALT, and other enzymes is detected in the study of blood.

Treatment

Conservative therapy

Therapeutic tactics are determined taking into account the causes of the masked face:

• Disease, Parkinson’s syndrome. Dopamine receptor agonists are used. Monotherapy is recommended at the initial stage. With the progression of the disease, insufficient effectiveness of the drug, combined regimens are prescribed. Patients with secondary parkinsonism are treated for the underlying disease. Depending on the etiology, detoxification and vascular agents, neurometabolites, etc. are used.
• Myopathy. 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 causal pathology is necessary: elimination of infections and intoxications, restoration of hormonal balance, etc. Within the framework of non-drug therapy, therapeutic physical culture, massage, ultrasound, ionophoresis, electrophoresis are effective.
• Frontal syndrome. Etiopathogenetic therapy may include thrombolytics, vascular and psychotropic drugs, neurometabolites, neuroprotectors, nootropics. Some patients with intracranial tumors are indicated for chemotherapy. Comprehensive rehabilitation measures are required.
• Neuritis. At the initial stage, vasodilators and decongestants, glucocorticoids, group B vitamins are used. With intense pain, therapeutic blockades are performed. UHF, ozokerite and paraffin treatment are carried out. Subsequently, anticholinesterase agents, phonophoresis, ultrasound, and sometimes electroneurostimulation are used. With insufficient effectiveness, biostimulants are indicated.
• Mental disorders. With neuroses, 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-imaginative, psychoanalytic, body therapy, gestalt therapy, art techniques are practiced. In severe disorders, medication with the use of antidepressants, normotimics, and neuroleptics is required.
• Scleroderma. Pharmacological support includes antifibrotic and anti-inflammatory drugs, disaggregants, vasodilators. With widespread soft tissue induration, enzymes are administered by injection, application, or drug electrophoresis.
• Hypothyroidism. Synthetic analogues of thyroid hormones are recommended. 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 treatment

Surgical interventions are required for hypomimia on the background of intracranial hematomas, intracranial tumors, vascular anomalies. With TBI, transcranial removal, stereotactic aspiration or endoscopic evacuation of the hematoma are possible. Neoplasms are excised by an open method (by craniotomy) or stereotactic surgery is used. In case of vascular anomalies, removal, embolization or endovascular occlusion is performed.

Patients with hypomimia due to traumatic neuritis need nerve stitching or neurolysis. In some cases, facial nerve plastic surgery is indicated. Operations are carried out within a year after the manifestation of the disease, in the future, correction of the masked face becomes impossible due to atrophy of facial muscles. In scleroderma, hypomimia, asymmetry and cosmetic defects are sometimes eliminated by excision of the affected foci and plastic replacement of defects with displaced skin flaps.