Facial hyperkinesis. Hyperkinesis, what is it? Involuntary neck movements are a symptom of what disease?
Hyperkinesis is unconscious, spontaneous muscle movements. The pathology has different localization and occurs as a result of disturbances in the functioning of the central and somatic nervous system. The disease has no clear restrictions regarding age and gender. Hyperkinesis is diagnosed even in children.
Etiology
The main reason for the development of this anomaly is dysfunction of the cerebral motor system. In addition, the following provoking factors for the development of hyperkinesis can be identified:
- damage to cerebral vessels;
- vascular compression of nerves;
- diseases of the endocrine system;
- congenital pathologies;
- severe brain injuries;
- toxic effects on the brain.
It is also worth noting that hyperkinesia can develop due to severe emotional shock, prolonged exposure to stressful situations and nervous tension. The development of an abnormal process as a result of other ailments - chronic - is no exception. In this case, the abnormal process is diagnosed in the area of the gallbladder or left ventricle of the heart.
Pathogenesis
Hyperkinesia has a rather complex development mechanism. It is based on damage to the central or somatic nervous system due to certain etiological factors. As a consequence of this, a malfunction occurs in the operation of the extrapyramidal system.
The extrapyramidal system is responsible for muscle contraction, facial expressions, and controls the position of the body in space. In other words, it controls all automatically occurring movements in the human body.
Disruption of the motor centers in the cerebral cortex leads to distortion of the impulses of motor neurons, which are responsible for muscle contraction. This is what leads to abnormal movements, that is, hyperkinesis. Damage to internal organs is also possible - the left ventricle of the heart, the gallbladder.
General symptoms
General symptoms of hyperkinesis can be identified:
- convulsive muscle contractions;
- localization of abnormal movements in one place;
- no symptoms during sleep;
- or (if the left ventricle of the heart is damaged);
- pain on the right or lower abdomen, for no apparent reason (with hyperkinesis of the gallbladder).
Such symptoms in adults and children do not yet indicate that this is hyperkinesis. Such a clinical picture may indicate obsessive movement neurosis. Therefore, for an accurate diagnosis, you should seek competent medical help and undergo a full examination.
Types of hyperkinesis
Today, the following types of hyperkinesis have been officially established in medicine:
- choreic hyperkinesis (generalized);
- hemifacial;
- athetoid;
- trembling (tremor);
- tic anomaly;
- slow;
- myoclonic hyperkinesis.
Each of these subtypes has its own clinical picture and possible complications.
Choreic hyperkinesis
Choreic hyperkinesis manifests itself in the form of abnormal movements of the limbs and muscles of the face.
Choreic hyperkinesis can appear as a consequence after a difficult pregnancy or degenerative diseases. Also, this subtype of pathology can be congenital.
However, choreic hyperkinesis can also develop as a result of severe brain injury or the development of a malignant tumor. If a person makes strong swings of his arms from side to side, then such a symptom may indicate the development of a brain tumor.
Facial hyperkinesis
Hemifacial hyperkinesis is usually diagnosed on only one side of the face. It can manifest itself in a variety of ways - a person often spontaneously closes his eyes, can stick his tongue out, or makes strange movements with his mouth. In some clinical cases, the development of a pathological process over the entire face is possible. In this case, paraspasm is diagnosed.
Athetoid hyperkinesis
Athetoid hyperkinesis has a well-defined clinical picture:
- involuntary flexion of fingers and toes;
- muscle spasms on the face;
- trunk cramps.
The main danger of this subtype of hyperkinesis is that if the anomaly is not treated, joint contracture (severe stiffness or immobility) may develop.
Trembling subtype
This subtype of hyperkinesis (tremor) manifests itself in the form of rhythmic, systematically repeated movements up and down with the head, limbs, and sometimes the entire body. In some cases, such a symptom may be especially severe when trying to perform some action or at rest. It is noteworthy that trembling hyperkinesis is the first sign of Parkinson's disease.
Tic subtype
Tic hyperkinesis is most often diagnosed. It manifests itself in the form of rhythmic vibrations of the head, frequent blinking or squinting. Symptoms are especially strong when a person is in strong emotional arousal. In addition, the tic subtype of anomaly may be some kind of reflex reaction to sudden loud sounds or a flash of bright light. Tic hyperkinesis occurs as a result of damage to the central nervous system.
Slow hyperkinesis
As for slow-type hyperkinesis, it is characterized as a simultaneous spasmodic contraction of some muscles and low tone of others. In view of this, a person can take the most unexpected poses. The more developed this syndrome is, the greater the threat to the entire musculoskeletal system. Such sudden changes in position against a person’s will and prolonged stay in them can lead to joint contracture.
Myoclonic subtype
Myoclonic hyperkinesis has the following clinical picture:
- synchronous, shock-point contractions of the muscles of the face and lower extremities;
- After an attack, tremors of the limbs are possible.
As medical practice shows, myoclonic hyperkinesis often implies a congenital form.
Hyperkinesis in children most often affects only the muscles of the face and torso. They manifest themselves in the form of involuntary contractions of individual muscle groups. Under certain factors, such symptoms can intensify significantly. As a result, another, underlying disease may develop.
The etiological picture is very similar to the pathology in adults. But still there are some differences:
- damage to the subcortex of the brain;
- cerebellar atrophy;
- imbalance of substances responsible for communication between nerve cells;
- damage to the sheath of neuronal fibers.
Such etiological factors can be either acquired (as a result of severe brain injury, incorrectly performed surgery, or underlying disease) or congenital.
If you suspect hyperkinesis in children, you should immediately contact a neurologist. If the pathological process affects internal organs (most often the left ventricle of the heart or the gall bladder), then the pathological process can lead to myocardial infarction and chronic cholecystitis. It is worth noting that such complications are especially likely for older people.
Possible complications
Hyperkinesis often causes the development of joint contracture or complete immobility of a person. But, in addition, the disease can become a kind of “indicator” of other, underlying diseases.
The pathological process in the gallbladder area is a subform of chronic cholecystitis. Such damage to the gallbladder significantly reduces the quality of human life. Chronic cholecystitis itself can develop due to infection, poor diet, or impaired metabolism.
If hyperkinesis occurs in the area of the gallbladder, then we can talk about the chronic stage of the disease. Therefore, if a person experiences pain or discomfort in the gallbladder area, he should immediately seek medical help.
Left ventricular hyperkinesia should not be considered as a separate diagnosis. But such disorders in the left ventricle of the heart often lead to serious diseases, including myocardial infarction.
If a person experiences pain in the left ventricle, he should immediately consult a cardiologist for qualified medical help to prevent myocardial infarction.
Most often, complications in the area of the gallbladder and left ventricle of the heart are diagnosed in elderly people and those who have previously suffered severe injuries, operations, and infectious diseases.
Diagnostics
Diagnosis for suspected hyperkinesis consists of a personal examination and collection of tests. The patient's family history must be taken into account. After a personal examination, laboratory and instrumental tests are performed.
The standard laboratory testing program includes only a general and biochemical blood test. As for instrumental studies, this includes the following:
- (if there is a suspicion of damage to the gallbladder);
- electrocardiogram (if symptoms indicate damage to the left ventricle of the heart, myocardial damage);
- cerebral angiography;
- electromyogram (study of the speed of nerve impulses).
Diagnosis of this kind of pathological processes is the most difficult. Therefore, at the first symptoms, you should contact a neurologist.
Treatment
It is impossible to completely cure this pathology. This is due to the fact that it is impossible to restore the damaged cerebral cortex. Therefore, drug therapy is aimed at reducing symptoms and improving the patient’s functioning.
If hyperkinesis is detected as part of the clinical picture of another disease - cholecystitis, suspicion of myocardial infarction, then hyperkinesis of the left ventricle and gallbladder is first eliminated. Since damage to the left ventricle manifests itself in the form of tachycardia or arrhythmia, unstable pressure, medications are first taken to eliminate these symptoms.
Drug therapy involves taking the following drugs:
- adrenergic blocking;
- anticholinergics;
- sedatives;
- neuroleptic;
- anticonvulsants.
If there is a risk of myocardial damage, then drugs are prescribed to stabilize the heart and general strengthening.
In addition to drug therapy, the patient is prescribed physiotherapeutic procedures:
- water procedures;
- massage.
Physiotherapy can significantly alleviate the patient’s condition and reduce symptoms. If there is even the slightest suspicion of myocardial damage, then exercise therapy is not used.
Treatment of hyperkinesis is carried out only comprehensively and under the supervision of a competent specialist. Taking medications without permission, without a doctor’s prescription, is a risk not only to health, but also to human life. Most often, follow-up with a doctor is lifelong.
Prevention
The main prevention is to maintain a healthy lifestyle. Therefore, you should adhere to a proper diet and be physically active.
Forecast
Unfortunately, it is impossible to completely cure this pathological process. Since the main etiological factors cause disturbances in the functioning of the brain and central nervous system, the prognosis cannot be positive by definition. But the correct drug therapy and regimen make it possible to significantly improve a person’s functioning.
Is everything in the article correct from a medical point of view?
Answer only if you have proven medical knowledge
Hyperkinesis is the general name for various syndromes characterized by involuntary movements, from trembling to convulsions. The term literally means "excessive movement." The common causes of these disorders lie in damage to the human nervous system.
Causes of hyperkinesis
Damaged areas of the brain (disturbances may affect the nervous tissue itself or the metabolism in it) generate “wrong” impulses that are transmitted along peripheral nerves to the muscles. Having received such a signal, the muscle involuntarily contracts or relaxes. Lesions in different parts of the brain (cortex, brainstem, and so on) cause different types of hyperkinesis, a review of which is given below.
Pathologies of the nervous system can be caused by:
- genetic disorders (hereditary diseases);
- lack of blood circulation (respiration and nutrition), for example, with fetal hypoxia, etc.;
- damage by toxins due to poisoning, infections, taking certain medications (for example, antipsychotics);
- injuries;
- demyelinating diseases (destroying myelin sheaths), such as multiple sclerosis.
Types of hyperkinesis
Every person, even an absolutely healthy person, sometimes experiences involuntary movements. For example, when we hiccup or we suddenly “shudder.” Of course, such one-off events are not associated with brain diseases, but simply reflect the complexity of the nervous regulation system. But if such episodes occur periodically, you should consult a doctor to find out the reasons.
Hyperkinesis can be classified according to the affected area of the nervous system - but such a division will be understandable only to specialists well versed in the anatomy and physiology of the brain. For a clearer perception, we present a classification according to the clinical manifestations of hyperkinesis:
- Tremor- trembling. May be a physiological reaction (eg to cold). But we find no obvious reasons for pathological tremors. The patient may tremble throughout the body or experience tremor of only the limbs and head.
- Myoclonus- single contractions of large muscles or their groups. Normally, a person may startle when falling asleep, out of surprise. Myoclonic convulsions resemble a sudden electric shock and can vary in nature - from mild spasms to severe epileptic seizures.
- - rhythmic, repetitive involuntary movements. Normally they shouldn't be there. However, tics can also develop in a relatively healthy person with a lack of microelements (calcium, magnesium). Tics can manifest themselves in more than just “eyelid twitching” or blinking. For example, with Tourette's syndrome, vocal tics are observed - involuntary exclamations.
- Athetoses- slow, smooth muscle contractions. Usually affects the fingers and hands, but athetoses of the facial muscles also occur.
- Dystonia- affect groups of opposing muscles, for example, “flexor-extensor”. As a result, the patient involuntarily rotates his limbs, takes strange poses, and flaps his limbs.
- Chorea- better known to the public under the name “St. Vitus’s dance.” The patient makes erratic movements with a large amplitude. To the uninitiated observer it may seem that he is moving consciously - but this is an illusion.
- Akathisia- painful internal tension, pathological need to move. Even if the patient is able to resist fuss, he feels increasing anxiety and fear. Typically a side effect of antipsychotic medications.
Often, in the manifestations of one disease, different types of hyperkinesis can be distinguished.
Hyperkinesis in children
This topic is especially important, since in young patients hyperkinesis, on the one hand, occurs more often than in mature people, and on the other hand, it does not always indicate severe brain pathology.
A child’s nervous system can “fail” under stress or overwork . It is interesting that parents do not always regard life situations as traumatic. For example, it seems to them that the child successfully fit into the new group in kindergarten, had a great rest during the family trip, and enjoyed going to first grade.
But the result may be a tick. This disorder affects up to 10% of children. Tics most often develop between the ages of 2 and 15 years, and boys suffer from them 3 times more often than girls. With local manifestations (affecting one muscle group), this condition goes away without a trace (subject to seeing a doctor and undergoing one or another therapy) in 90% of children. Common tics (affecting different muscle groups) are cured completely in half of the cases.
You should pay attention not only to stereotypical facial movements, for example, closing your eyes, blinking, sniffling, biting your lip. Tic can affect the limbs and torso: stereotypical movements of the fingers, retraction of the abdomen, shrugging of shoulders, jumping, and so on. Vocal phenomena are also possible - sniffing, snorting, gasping, coughing, and so on.
The most important thing is to show the child to a good doctor. In many cases, treatment consists of psychological and pedagogical assistance, supported by physiotherapy and vitamin preparations. Sometimes it is necessary to support metabolic processes in the brain with nootropic drugs. In the presence of severe lesions, anticonvulsants and antipsychotics are prescribed.
Of course, serious pathologies of the nervous system are possible in children, accompanied by hyperkinesis: Tourette's syndrome, cerebral palsy, epilepsy, and so on. Alas, these diseases cannot be “missed” or “not noticed” and such patients cannot live without specific treatment.
Treatment of hyperkinesis
In all cases of the appearance of regular (albeit very rare) involuntary movements in a person at any age, it is imperative and as soon as possible to consult a doctor. The stage at which treatment for hyperkinesis is started sometimes determines the ability to completely restore health or achieve stable remission (recession of symptoms).
Diagnostics
Naturally, the process begins with diagnostics. Modern research methods, for example, can reveal microscopic areas of damage to nervous tissue. The doctor receives important information when interviewing the patient or his relatives. There are also special methods for provoking hyperkinesis, which make it possible to identify the disease, even if there are no symptoms at the moment.
A difficult task, the solution of which is available only to specialists, is differential diagnosis. That is, distinguishing between types of hyperkinesis and accurately determining the pathology that is present in this particular patient. This is important because it can indicate different causes of the disease, damage to different parts of the nervous system and, ultimately, leads to different prescriptions.
Medications
Today there are a lot of drugs and groups of drugs that correct the state of the nervous system: the generation and conduction of nerve impulses, nutrition and respiration of tissue. Also, for hyperkinesis, medications that affect muscle tone can be prescribed. To restore the functions of the body as a whole, the doctor prescribes vitamin-mineral complexes and adaptogens.
Herbal medicines, herbal mixtures, tinctures and decoctions play a supporting role in such treatment. If you want to use them, discuss your chosen prescriptions with your doctor. But never neglect classical treatment in favor of “traditional medicine” , since in its arsenal there are no means of real correction of such severe pathologies as tics.
General restorative therapy
An integrated approach can achieve good results. In addition to taking medications, the patient should (together with the doctor) reconsider his lifestyle. A harmonious diet, rest and exercise, and psychological comfort will help you overcome hyperkinesis faster, or at least make it easier to endure its attacks.
Surgical methods
In the most extreme and severe cases, they resort to surgical methods of correction. Such interventions can be carried out with the aim of destroying the area of nervous tissue that provokes hyperkinesis, excision of peripheral nerves. Electrodes can also be implanted that will send the “correct” impulses, reservoirs that dose the medicine directly to the affected tissues (for example, a “baclofen pump”).
Any meaningful motor activity is controlled by the cerebral cortex. It is here that the impulse to action arises, which travels along nerve fibers to the spinal cord, from where impulses are sent to the muscles. We are able to maintain the center of gravity of the body and coordinate movements without much thinking thanks to the cerebellum. And the subcortical nuclei of the brain are responsible for muscle tone, rhythm and smoothness of movements. Thanks to them, we are capable of many different actions: running, jumping, dancing steps. The wealth of emotional reactions (crying, laughter, facial expressions) is also the sphere of activity of the subcortical nuclei.
Disturbances in the functioning of this complex system are manifested by all kinds of involuntary movements. This excessive activity is called in medicine hyperkinesis. Such conditions are characterized by a weakening of muscle tone combined with involuntary, meaningless movements and muscle spasms.
What are the manifestations of obsessive motor activity?
Tremor
Think about the nervous tremors that occur during fatigue, stress, anxiety, and excitement. This tremor. This reaction is typical for most healthy people. There is also tremor caused by lesions of the cerebellum. It is characterized by trembling in the arm or leg when they approach the intended target. Sometimes trembling begins when maintaining a certain posture or holding a heavy object. For example, strong trembling of the head and torso appears in a standing position and disappears if you lie down. With the “tremor of beating wings,” a person becomes like a bird trying to fly.
Myoclonus
Another type of involuntary motor activity familiar to most of us is myoclo** nia**. This is an instant contraction of one muscle or group of muscles. Night shudders when falling asleep, ordinary hiccups are also manifestations of myoclonus. By the way, the latter occurs when the muscles of the diaphragm involuntarily contract.
Teak
Another common type of uncontrolled activity is teak. These are short, sharp, repeated shudders of the head, torso, facial muscles, arms or legs. Simple teak(for example, involuntary blinking), often appears in childhood and is sometimes perceived by others as nervousness and mannerisms. It usually goes away on its own when the child becomes a teenager. However, it happens that movement disorders worsen with age. This happens when Tourette's syndrome when the tic begins to imitate more complex movements and is accompanied by obsessive pronunciation of the same sounds or words ( logorrhea). Vocal tic may manifest as barking or grunting sounds. Uncontrolled foul language is also common ( coprolalia).
Chorea
Chorea- These are fast chaotic movements. Sometimes they are quietly integrated into meaningful actions. Huntington's chorea, which is hereditary in nature, is manifested by jerking movements of the arms and legs, a comical dancing gait, and involuntary grimaces. It happens that a person loses the ability to maintain a particular position, for example, sitting with his knees together. With rheumatic lesions of the central nervous system (most often found in adolescence), chorea, which used to be called the dance of St. Vitus (outwardly it resembles grimacing and dancing). It also occurs chorea of pregnancy, developing in the first half of pregnancy.
Athetosis
Worm-like writhing movements of the hands and feet with changes in posture are characteristic of athetosis. At hemiballisma a person makes involuntary throwing or rotating lunges with one hand, or less often with a foot. Sometimes all this is accompanied by movements of the mouth.
Muscular dystonia
There are also disorders of muscle tone that force a person to take some unnatural posture that interferes with normal motor activity - muscular dystonia. They can spread throughout the body or be based in individual muscle groups. For example, torsion dystonia manifests itself in slow, corkscrew-like movements of the body. A spastic torticollis accompanied by tilting or turning the head to one side. And finally professional dystonia arise on the basis of any monotonous labor movements.
Causes of obsessive motor activity
Many of the described motor activity disorders indicate diseases of the nervous system. Their causes can be very diverse: neurotic disorders; toxic brain damage (for example, alcohol or copper compounds); hereditary or congenital diseases; taking certain medications; brain injuries, including birth injuries; use of certain drugs; brain tumors; cerebrovascular disorders (atherosclerosis, stroke and its consequences).
To get rid of obsessive movements, it is necessary to identify their root cause, to which treatment should be directed. Often it is impossible to do without long-term use of drugs that affect the activity of the motor systems of the brain. In difficult cases, neurosurgical treatment methods are used.
Hyperkinesis often occurs with encephalitis: epidemic (parkinsonism, torsion dystonia, athetosis and others), tick-borne (Kozhevnikov epilepsy), rheumatic (chorea minor), leukoencephalitis and other forms of encephalitis. Etiological factors for hyperkinesis are also vascular lesions of the brain, traumatic brain injury, brain tumors, intoxication, hereditary diseases (shaking paralysis, myoclonus epilepsy, Huntington's chorea and others).
Pathogenesis
Hyperkinesis occurs more often with damage to the extrapyramidal system: the striatum (striatum), the globus pallidus (pallidum) usually in combination with the substantia nigra of the midbrain (pallido-nigral system), the thalamus and its connections, the subthalamic nucleus, the dentate nucleus of the cerebellum, the red nucleus and their connections (olivo-dentato-rubral system). What matters is the dysfunction of the feedback system between the cortex and subcortex.
The importance of the cerebral cortex in the origin of hyperkinesis is revealed by local convulsive twitching that occurs when the motor zone (field 4) is irritated by a tumor, post-traumatic cyst, etc., and by the occurrence of local cortical convulsions in Kozhevnikov epilepsy. When the afferent cortical innervation of one hemisphere is disrupted (damage to thalamo-cortical connections), hemichorea occurs. In the pathogenesis of hyperkinesis, it is necessary to take into account the formation of a dominant in the subcortical parts of the brain, which are influenced by incoming afferent impulses, as well as the shutdown of the regulatory role of the cortex. Hyperkinesis is inhibited by sleep and rest; emotions enhance Hyperkinesis. The thalamus plays a large role, along with cortical and subcortical mechanisms, in the appearance and intensification of Hyperkinesis during excitement, emotions, and stress. The reticular formation of the brain stem can contribute to the development and intensification of hyperkinesis (tremorogenic effect), as well as their inhibition.
Extrapyramidal hyperkinesis is combined with changes in muscle tone and autonomic dysfunction. The localization of the pathological process is not unconditional for the manifestation of Hyperkinesis: with the same localization (thalamus, striatum) there may be different manifestations of excessive movements. Extrapyramidal hyperkinesis can be complex and sometimes include components of several forms, for example, choreoathetosis can be combined with elements of torsion spasm. Not only the location of the lesion is important, but also the degree of the lesion, the number of cells involved and their connections. In the pathogenesis of hyperkinesis, biochemical factors are important: disruption of catecholamine metabolism, especially changes in the content of dopamine in the striatum and acetylcholine, which interacts with it.
Clinical picture
Hyperkinesis of extrapyramidal origin is distinguished by a variety of clinical manifestations, often pretentious, unnatural, and combined with changes in muscle tone (decrease or increase of the plastic type).
Myoclonus is scattered, erratic, fast and irregular clonic muscle contractions, sometimes single, but constantly renewed.
Tics - myoclonic type Hyperkinesis (symptomatic myoclonus), manifested in various ways: twitching of facial muscles (Figure 1), gesticulation or rapid winces and other stereotypical motor acts (smacking, squinting of eyes, and so on).
Myoclonus usually causes a motor effect, but can be observed as contraction of isolated, non-synergic muscles or separate muscle bundles without movement of the limb. This type of myoclonus is called paramyoclonus, or Friedreich-Unferricht type myoclonus. Myoclonus epilepsy (Unferricht-Lundborg) is characterized by a combination of generalized myoclonus with epileptic seizures. It occurs when there is damage to the thalamus and its connections, the substantia nigra, the dentate nuclei of the cerebellum and the rubro-thalamic connections. Myoclonus occurs with epidemic and tick-borne encephalitis, vascular lesions of the cerebellum, brain stem, and others
Cerebellar myoclonic dyssynergia, or Hunt's myoclonia, is common, characterized by a combination of myoclonus in several muscles of the limbs, intensified by voluntary movements and emotions, combined with ataxia as a result of damage to the dentate nuclei of the cerebellum, in which there is a regular effect on the red nucleus and olive. Myoclonus in the form of widespread fibrillary twitches is observed in Morvan myoclonus.
A special form is infantile myoclonic encephalopathy, or West syndrome. Myoclonus with cerebellar dyssynergia is common and intensifies with voluntary movements and emotions. In the pathogenesis of these myoclonus, importance is attached to damage to the dentate nuclei of the cerebellum, affecting the red nucleus and olive. Myoclonic hyperkinesis is observed in encephalitis (epidemic, tick-borne), Van Bogart leukoencephalitis, Creutzfeldt-Jakob disease, Krabbe leukodystrophy.
Myorhythmias (rhythmic myoclonus) are twitches localized in certain muscles, which are wave-like (undulating) in nature with a constant rhythm (from 6-10 to 80-100 contractions per minute).
Localized myoclonus is observed in the muscles of the face, tongue, soft palate, pharynx, abdominal wall and others. Localized myoclonus is associated with damage to the olive medulla oblongata, the dentate nucleus of the cerebellum and the red nucleus and their connections. Myorhythm is associated mainly with damage to the inferior olive.
Spasmodic torticollis is a local torsion-dystonic syndrome, which is manifested by tonic contraction of the cervical muscles, causing the head to turn to the side (Figure 2). Spasmodic torticollis differs from reflex torticollis, which occurs in response to painful stimulation of the mastoid process, parotid gland, cervical roots, and others. Spasmodic torticollis occurs as a result of damage to the strio-pallidal system.
Choreic hyperkinesis manifests itself differently depending on the form of the disease; it consists of fast, scattered, irregular, varied movements of muscle groups of the limbs and face. Hyperkinesis increases with excitement, decreases at rest and stops during sleep. Chorea may affect standing, walking, speaking, and phonation. Choreic hyperkinesis is accompanied by severe muscle hypotonia.
The etiology of choreic hyperkinesis can be different: Sydenham's minor chorea with rheumatism, chorea of pregnant women, chorea with encephalitis, chronic progressive Huntington's chorea (see Huntington's chorea), senile atherosclerotic chorea, Henoch-Bergeron electric chorea (see Chorea), which occurs after brain injury and tick-borne encephalitis.
Polycythemic chorea in combination with gangrene of the fingers has been described (N.K. Bogolepov). Choreic hyperkinesis often occurs when there is a violation of cerebral circulation (with lesions in the midbrain and subcortical nodes), and hemichorea is often observed (Figure 3 and 4). In children, hemichorea is observed with cerebral hemiplegia. Intensifies with painful irritations and emotions.
Athetosis is manifested by slow, worm-like, continuously continuing tonic movements (spasms) of the fingers, hand, foot, and facial muscles, causing pretentious positions of the limbs. Athetosis (see) can be unilateral or bilateral.
Choreoathetosis occurs with damage to the thalamo-striatal system, with Schilder's periaxial encephalitis, with subacute leukoencephalitis of Van Bogart and Uzunov-Bozhinov hyperkinetic encephalitis, Govers' "tetanoid chorea" with cerebrovascular accidents. Clinically characterized by a combination of athetoid and choreic movements.
Hemiballismus consists of fast “throwing” rotational sweeping movements of the arm and leg on the side opposite to the lesion. Usually combined with hemihypotonia, changes in body position and gait disturbance. Hyperkinesis intensifies under the influence of emotions. Occurs when the subthalamic nucleus is damaged (cerebrovascular accident). With hemiballismus, muscle tone is impaired. Hyperkinesis occurs in the proximal parts of the upper and lower limbs.
Paraballism - throwing movements in both upper limbs with bilateral vascular lesions of the thalamo-subthalamic system.
Torsion dystonia (lordotic dysbasia) is manifested by tonic muscle spasm, unnatural posture of the body, which leads to an unnatural pretentious position of the body (rotation around the longitudinal axis), limbs, and head. Torsion or deforming dystonia is associated with improper distribution of muscle tone, especially in the trunk and neck, which causes curvature of the spine and torticollis. Hyperkinesis intensifies when walking, and can stop when running and developing compensatory techniques. Tonic convulsions are joined by clonic ones, and the position of the body with torsion dystonia (see) changes.
Hyperalgic clonic hyperkinesis occurs when the thalamus and its connections are damaged during cerebral circulatory disorders, and occurs paroxysmally when nociceptive stimulation is applied. Hyperkinesis that occurs in the irritated limbs manifests itself in the form of a cycle of successive movements (contralateral hyperalgic hyperkinesis). Hyperkinesis in the extremities opposite to the pathological focus is observed in the early period of circulatory disorders in the thalamo-striatal system.
Hyperkinesis of cortical origin. Cortical (Jacksonian) epilepsy is paroxysmal clonic muscle twitching on the side of the body opposite to the focus of irritation of the motor area cortex (anterior central gyrus, area 4 according to Brodmann). At the beginning of an attack, twitching is noted in certain parts of the face or one limb; subsequently, they usually take on a generalized character (see Jacksonian epilepsy).
Kozhevnikov epilepsy, or prolonged local cortical convulsions (epilepsia partialis continua), is manifested by clonic twitching of muscle groups in the limbs opposite to the lesion, which at times develop into a generalized epileptic seizure (see Kozhevnikov epilepsy).
Hemitonia (V.M. Bekhterev) is manifested by clonic contractions of paretic limbs during the period of restoration of motor functions after apoplexy and is apparently associated with irritation of the pyramidal tract (see also table).
Cramps and muscle spasms can be observed as components of hyperkinesis or sporadically. They differ in prevalence (in a limited group of synergistically acting muscles and widespread), persistence (manifest continuously or occur with extero-, intero- or proprioceptive stimulation, excitement and physical stress).
Seizures vary in pathogenesis and localization of the pathological process (in the cortex, subcortical formations, diencephalon) and manifestations. The dependence on disturbances in biochemical constants and hormonal balance (convulsions in swimmers as a result of hypercapnia, alkalosis, tetanic convulsions) is also important.
Rülf's intention spasm occurs suddenly in the muscles of the limb with which the patient intends to perform an unprepared movement. Starting in a limited muscle group, the spasm then spreads to other limbs and can develop into an epileptic seizure, but without loss of consciousness. The etiology of Rülf's cramp is not precisely established; it was observed in neuroinfections or as a family disease (see Rülf's intentional spasm).
A tonic gaze convulsion, in which the eyes periodically move upward and the head is thrown back, is observed in parkinsonism. In the genesis of seizures, importance is attached to damage to the striatal system, but observations show that a significant role is played by the reticular formation of the brain stem and especially its mesencephalic section (see Gaze paralysis, seizure).
Blepharospasm is a paroxysmal involuntary contraction of the circular muscles of both eyes (Figure 5), then supplemented by turning the head to the sides and sometimes convergence of the eyes (see Blepharospasm). May be the initial manifestation of paraspasm. It is observed in patients with encephalitis.
A spasm of the diaphragm is manifested by hiccups (episodic hiccups) in patients with encephalitis as a result of dysfunction of the reticular formation of the brain stem.
Facial paraspasm is observed in patients with atherosclerosis and consists of bilateral tonic-clonic spasms of the facial muscles (Figure 6). It is also observed in encephalitic processes in the area of the subcortical nodes. Facial muscle spasms are combined with neck muscle spasms.
Facial hemispasm - paroxysmal spasms of the muscles of half the face on the affected side (see Hemispasm). Occurs when the facial nerve is compressed in the fallopian canal, arachnoiditis of the posterior cranial fossa.
Painful spasm of the facial muscles occurs during an attack of trigeminal neuralgia.
Professional cramps occur when performing professional movements: writer's cramp in pianists, scribes, violinists, cramps of the thumb and index finger in tailors, typists, milkmaids, hairdressers, spasms of the orbicularis oculi muscle in watchmakers, leg spasms in ballerinas and others. In some cases, compensatory techniques are used to reduce writer's cramp (Figure 7).
Episodic hyperkinesis includes epileptic convulsions (cortical, diencephalic, mesencephalic), involuntary grasping of objects placed in the hand (a symptom of involuntary grasping), closing or opening of the mouth and eyes during distant impulses.
Treatment
Prescribed drugs affecting extrapyramidal formations (cyclodol, artane, parkopan, romparkin, ridinol, norakin, tropacin, bellazone, dynesin, 1-dopa), sedatives (bromides, valerian root and others), antihistamines (diphenhydramine, suprastin, tavegil, pipolfen and others), drugs affecting metabolism (glutamic acid, gammalon and others), multivitamins, sleeping pills (for insomnia). In some cases, psychotherapy is indicated. Etiological treatment and rehabilitation measures are mandatory. According to indications, neurosurgical (stereotactic) operations are performed on the thalamus, globus pallidus, intermediate nucleus of Cajal and superior longitudinal fasciculus (for torticollis), cordotomy and others
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Hyperkinetic syndrome (HS) combines all types of violent, involuntary, excessive movements and is found in the clinic of many neurological diseases. The pathogenesis of this pathology is not fully understood. It has been established that during HS, neurotransmitter metabolism is disrupted mainly in the structures of the extrapyramidal system. Dysfunction of specific dopaminergic, GABAergic neurons causes disruption of the cortico-nigro-strio-pallidal system. As a result, there is a relative excess of dopamine and catecholamines in the brain, as well as a lack of acetylcholine, serotonin, and glycine.
HS is characterized by significant clinical polymorphism and varies significantly in prevalence, symmetry, tempo, rhythm, localization and severity. In some cases, HS is the leading manifestation of independent, predominantly congenital neurological diseases. However, more often HS is symptomatic due to the impact on the brain of infectious, vascular, toxic, hypoxic, metabolic and other pathogenic factors.
There is no unified classification of HS. The proposed classifications take into account only one clinical sign. The proposed systematization of GS according to the level of motor integration is of significant importance.
Depending on the level of brain damage, three groups of hyperkinesis are distinguished:
I. Hyperkinesis predominantly at the stem level: tremor, myoclonus, myorhythmias, myokymia, tics, spastic torticollis, facial hemispasm, paraspasm of the facial muscles. Their characteristic features are stereotypicality, rhythm and relative simplicity of violent movements.
II. Hyperkinesis, predominantly at the subcortical level: athetosis, chorea, torsion dystonia, ballism, Rülf's intentional spasm. Their common features are polymorphism, arrhythmia, complexity of violent movements, and the presence of a dystonic component.
III. Subcortical-cortical hyperkinesis: myoclonus epilepsy, Hunt's myoclonic dyssynergia, Kozhevnikov epilepsy, the common features of which are frequent generalization of the process and epileptic seizures.
Diagnosis of hyperkinetic syndrome
Hyperkinesis predominantly at the stem level
Tremor is a rhythmic trembling of a body part and is manifested by fast, stereotypical fluctuations of small amplitude. Occurs at any age. In clinical practice, tremors of the hands, head, and lower jaw predominate; tremors of the legs are less common. Hyperkinesis is more pronounced during periods of muscle fatigue and anxiety. The amplitude of the jitter depends on the ambient temperature and visual control. Tremor can be physiological (with fatigue, emotional stress), neurotic, or occur as a result of a number of somatic and neurological diseases, as well as when taking certain medications (insulin, adrenaline, amphetamine, caffeine).
The following types of tremor are distinguished:
A. Rest tremor (static) - rhythmic, constant hyperkinesis of small amplitude, which is observed at rest, and weakens or disappears with movements. The most typical location is the distal extremities. Initially, tremor occurs only with excitement or minor physical activity (holding a cup, spoon). In the advanced stage of the disease, trembling of the hands appears, such as “rolling pills” or “counting coins”. Asymmetrical rest tremor is characteristic of Parkinson's disease, bilateral - for secondary (vascular, post-encephalitic, post-traumatic) parkinsonism.
B. Dynamic (kinetic) tremor has an average amplitude. There are several varieties of it:
o postural tremor - when changing body position (stretching arms forward);
o isometric tremor - with voluntary muscle contraction (clenching the hand into a fist);
o intention (terminal) tremor appears or sharply increases in amplitude at the end of a directed movement when approaching a target (when performing a finger-nose test) or holding a limb in a fixed position;
o “task specific” tremor occurs only when performing high-precision movements (writing, playing musical instruments, fastening jewelry).
Dynamic tremor is characteristic of Minor's essential tremor, multiple sclerosis, olivopontocerebellar atrophy, various polyneuropathies, and old age.
C. Statodynamic tremor has signs of static and dynamic tremor, is distinguished by greater amplitude (“flapping wings of a bird”), lower frequency and is observed with hepatocerebral degeneration or at the late stage of parkinsonism.
Myoclonus are sudden, short-term, erratic, irregular contractions of individual muscle bundles or muscle groups that do not lead to movement in the corresponding joint. There are positive (due to active muscle contraction) and negative (due to a decrease in muscle tone) myoclonus. According to distribution, generalized, multifocal, segmental and focal myoclonus are distinguished, in which individual muscle groups are involved in the process (face, tongue, eyes, soft palate). According to the mechanism of occurrence they distinguish:
o spontaneous myoclonus;
o reflex myoclonus that occurs with a sudden sound, flash of light, touch;
o kinetic myoclonus (actional, intentional, postural).
Myoclonus can be caused by physiological causes (fear, intense physical activity) and various pathological conditions: storage diseases (lipidoses, Tay-Sachs syndrome, Krabbe disease), viral encephalitis, metabolic, toxic, drug encephalopathies, degenerative diseases, slow infections (Creutzfeldt disease - Jacob), stereotactic operations.
Myorhythmias- a variant of myoclonus, localized in a specific muscle or muscle group, which is characterized by a constant rhythm. Myorhythmias of the soft palate and larynx (Foy-Hilleman syndrome), pharynx, tongue, vocal folds, and diaphragm occur in Economo encephalitis, multiple sclerosis, and brainstem stroke.
Myokymia characterized by constant or periodic contractions of individual muscle fibers without movement of a limb segment. The occurrence of myokymia is caused by an increase in the excitability of motor neurons in the anterior horns of the spinal cord. This type of hyperkinesis is observed in thyrotoxicosis, anemia, vertebrogenic radiculopathies or neurosis, manifested by selective contraction of the eyelids.
Tiki - These are sudden jerky, repetitive movements, reminiscent of certain cartoonish voluntary movements, which are characterized by an irresistible character. A tic is based on a short-term contraction of the muscle that causes the movement. Hyperkinesis most often occurs in childhood or adolescence. Tics can be simple (stereotypical) or complex (multivariate). According to their course, tics are divided into acute (after traumatic situations), persistent (persist for several years), and chronic (throughout life). Hyperkinesis can periodically migrate and change in intensity. According to localization, the frequency of tics decreases from the upper part of the face to the lower extremities. The most common tics are blinking, tics of the lower face, neck, shoulders, trunk and limbs. The causes of tics may be postencephalic parkinsonism, posthypoxic encephalopathy (carbon monoxide poisoning), minor chorea, overdose of certain medications (DOPA drugs, psychostimulants, antipsychotics). An independent nosological form is a generalized tic (Gilles de la Tourette's disease), which is based on complex hyperkinesis and local tics.
Spasmodic torticollis (cervical dystonia) is a localized hyperkinesis, in which tension in the neck muscles leads to a forced turn of the head. Men aged 25-35 years are most often affected. The onset of the disease is possible in three variants: gradual, acute development and with a preceding pain syndrome in the posterior cervical muscles. Depending on the direction of head movement, there are antecollis (tilting or moving the head forward), retrocollis (deviation of the head back) and laterocollis (turning the head to the side). Based on the nature of hyperkinesis, there are tonic, clonic and mixed forms of the disease. As a rule, all muscles of the neck are involved in the process, but most often the sternocleidomastoid, trapezius, and splenius muscles. At the initial stage, returning the head to the middle position is possible independently; hyperkinesis intensifies only when walking, and is absent during sleep. As the disease progresses, removal of the head becomes possible only with the help of hands. This stage is characterized by corrective gestures (a noticeable decrease in hyperkinesis when lightly touching certain areas of the face). Further progression leads to the inability to independently turn the head, hypertrophy of the affected muscles and vertebral radicular compression syndromes. Spasmodic torticollis is congenital, occurs in hepatocerebral degeneration, Hallervorden-Spatz disease, or can be an independent nosological form. In some patients, spastic torticollis transforms into torsion dystonia.
Facial hemispasm (Brissot's disease) characterized by paroxysmal and stereotypical contractions of facial muscles in the area of innervation of the facial nerve. In the initial stages of the disease, hyperkinesis is limited to the orbicularis oculi muscle, which is manifested by tonic-clonic closure of the eyelids (blepharospasm). Subsequently, hyperkinesis can spread to other facial muscles and the subcutaneous muscle of the neck. Attacks of facial hemispasm are provoked by conversation, food, emotions or appear spontaneously, often accompanied by synkinesis of muscles on the opposite side of the face. Double hemispasm of the face is possible, characterized by non-synchronous contraction of both halves. Facial hemispasm can be an independent nosological form. Its development is also caused by tumors, aneurysms of the cerebellopontine angle, or irritation of the facial nerve root by the branches of the basilar artery.
Paraspasm of facial muscles (Bruegel's syndrome, Meige's syndrome) most often occurs at the age of 50-60 years and is manifested by frequent involuntary blinking, then tonic or tonic-clonic hyperkinesis of the muscles of the orbital region with persistent closure of the eyelids joins. Subsequently, other muscles of the face, pharynx, tongue, and lower jaw are involved in the process (oromandibular dystonia). In later stages, there may be a disturbance in voice sonority, fluency of speech, and dysarthria. Hyperkinesis occurs spontaneously, sometimes provoked by smiling, eating, talking, or emotional stress. Paraspasm can be observed in postencephalitic parkinsonism, cerebral palsy, hepatocerebral degeneration, Steele-Richardson-Olszewski syndrome, or can be an independent nosological form.
Hyperkinesis, predominantly at the subcortical level
Athetosis characterized by slow, unsynchronized, elaborate movements mainly in the distal parts of the limbs (“movements of Javanese dancers”). Depending on the prevalence, monotype, hemitype, and double athetosis are distinguished. The spread of hyperkinesis to the facial muscles is manifested by violent curvature of the lips and mouth. Damage to the tongue muscles can cause changes in phonation and articulation (athetotic dysarthria). Emotional stimuli enhance hyperkinesis, and it disappears during sleep. Athetosis as a symptom occurs in cerebral palsy, hepatocerebral dystrophy, hypoxic encephalopathy, and in the post-stroke period. Double athetosis (Gammond's disease) is an independent hereditary disease.
Chorea manifests itself by rapid arrhythmic movements of the muscles of the tongue, face, torso, and limbs, increasing with excitement or an attempt to make a purposeful movement. Children and teenagers get sick more often. Hyperkinesis is accompanied by grimacing, unexpected sharp, sweeping flexion-extension and rotational movements of the limbs, head, and torso. The amplitude of hyperkinesis is aggravated by low muscle tone in the limbs. When walking, chorea intensifies, steps become uneven, and the gait becomes dancing. Due to the continuous nature of hyperkinesis, the patient cannot speak, eat, sit, or walk. Attempts at arbitrary delay only lead to increased hyperkinesis. A combination of chorea and athetosis is possible. Such hemichoreoathetosis of one half of the body occurs when there is a violation of blood circulation in the pool a. talama perforata profunda. Choreaic hyperkinesis is characteristic of minor chorea (Sydenham's disease), Huntington's chorea, senile chorea and chorea of pregnant women.
Torsion dystonia manifests itself by alternating muscle hypotonia and extrapyramidal rigidity, which leads to slow, uniform rotational (dystonic) movements in one or another part of the body. A characteristic feature of this hyperkinesis is the dystonic posture in which the patient remains if the muscle contraction lasts more than 1 minute. According to the distribution features, there are five possible variants of torsion dystonia: focal, segmental, multifocal, generalized and hemidystonia. Focal dystonia affects one part of the body and may involve dystonic movements of the hand (writer's cramp) or foot (foot dystonia). Segmental dystonia affects two or more parts of the body that merge into each other (neck, shoulder girdle, arm). Generalized dystonia is manifested by dystonic movements in the entire body or parts of the body that do not pass into each other (left arm and right leg), and the spine. Torsion dystonia can be a syndrome of hepatocerebral degeneration, postencephalitic parkinsonism, degenerative diseases, posthypoxic and dismetabolic (hepatic) encephalopathy. Torsion dystonia (Tiehn-Oppenheim disease) is also an independent hereditary disease.
Ballism characterized by fast sweeping, throwing, rotational movements in the torso and limbs. Hyperkinesis increases with emotional stress, voluntary movements, persists at rest and disappears during sleep. Muscle tone is reduced. There are possible variants of hemiballismus, in which hyperkinesis is more pronounced in the hand. The etiological cause of ballism is most often vascular disorders in the basin of the thalamo-perforating artery (vertebrobasilar system), as well as stereotactic operations in patients with parkinsonism.
Rülf's intention spasm is an independent hereditary disease that manifests itself as a tonic or tonic-clonic spasm in a muscle during its unexpected contraction. In some cases, muscle cramps can spread to other muscles of the same half of the body. The duration of the attack is on average 10-15 s, consciousness is preserved at the time of the attack. Between attacks the patient feels healthy.
Subcortical-cortical hyperkinesis.
Myoclonus-epilepsy manifests itself as sudden, periodic, irregular contractions, often of the muscles of the limbs, sometimes turning into a convulsive attack with a short-term loss of consciousness. Hyperkinesis is characterized by low amplitude, increases significantly with sudden movements and disappears during sleep. Myoclonus epilepsy can be a syndrome of tick-borne encephalitis, rheumatism, lead poisoning, or be an independent hereditary disease (Unferricht-Lundborg disease).
Hunt's myoclonic cerebellar dyssynergia - an independent hereditary disease that manifests itself at the age of 10-20 years. The disease begins with myoclonus and intention tremor in the hands, which are later joined by ataxia, dyssynergia, nystagmus, scanned speech, and decreased muscle tone. The course of the disease is progressive.
Kozhevnikovskaya epilepsy manifests itself as myoclonic hyperkinesis most often in the hand and facial muscles. Hyperkinesis is characterized by constancy, stereotypy, strict localization, large amplitude, continuity, frequent occurrence in sleep and intensification when performing precise movements. On the side of hyperkinesis, hypotrophy of the affected muscles, their weakness and the development of myogenic contractures are possible. In the classical version, Kozhevnikov epilepsy is described as a form of chronic tick-borne encephalitis.
Differential diagnosis of hyperkinetic syndrome
HS often requires differentiation with manifestations of various forms (hysterical, obsessive-compulsive) neurosis. The task is complicated by the fact that patients with HS always experience neurotic symptoms during the course of the disease. The distinctive features of neurotic hyperkinesis are the following:
o development of hyperkinesis (or its aggravation) following a traumatic situation;
o dependence of the severity of hyperkinesis on the presence of “spectators”;
o mannerism, exaggerated nature of poses and movements;
o variability and change of hyperkinesis in a short time in one patient;
o pronounced vegetative reactions and other neurotic symptoms;
o no changes in muscle tone.
Treatment of hyperkinetic syndrome
HS therapy is a complex and not yet fully resolved problem. Treatment of HS can be pathogenetic (correction of neurotransmitter disorders in the extrapyramidal system) and symptomatic. There are conservative and surgical treatment. The basis of conservative therapy for HS is drug treatment. Its most important principles are individuality in the selection of the dose, the frequency of administration of the drug and the duration of its administration. The optimal dose is selected gradually and is carried out within the “pharmacotherapeutic window”, i.e., achieving a clinical effect without its side effects. In some cases, a positive result of treatment is not the complete elimination of hyperkinesis, but the emergence in the patient of the ability to voluntarily control its occurrence. The maintenance dose should be kept to a minimum and re-evaluated periodically. The choice of a group of antihyperkinetic drugs largely depends on the type and form of hyperkinesis, but in most cases it is carried out ex juvantibus.
Main groups of antihyperkinetic drugs
Antiacetylcholinergics (cholinergics). The mechanism of their action is associated with a decrease in the functional activity of cholinergic systems. Their moderate positive effect was noted for rest tremor, myoclonus, and some focal forms of torsion dystonia (writer's cramp). The most commonly used is cyclodol (Parcopan) 1-2 mg three times a day. Side effects of the drugs include dry mouth, constipation, urinary retention, deterioration of accommodation, and the development of psychomotor disorders. Anticholinergics should be used with caution in men with prostate adenoma, in persons with glaucoma and in the elderly.
Dopamine receptor agonists directly stimulate specific dopamine receptors and ensure uniform synthesis and release of dopamine. One of the drugs in this group that has a moderate effect on static tremor is mirapex. It is advisable to prescribe treatment from small doses with a gradual increase to 1.5 g/day in three doses. Side effects of the drug include orthostatic hypotension, nausea, and sleep disturbances.
DOPA-containing drugs are metabolic precursors of dopamine. Their effectiveness in HS is not as great as in parkinsonism. Nakom (madopar, sinimet) is used for spastic torticollis and torsion dystonia, starting with a small dose of 62.5 mg, twice a day. If the results are positive, the dose is gradually increased to 500-750 mg, divided into three doses. Side effects of the drugs include nausea, orthostatic hypotension, psychotic disorders, dyskinesia and motor fluctuations.
Dopamine receptor antagonists (neuroleptics) influence excessive dopaminergic activity by blocking postsynaptic dopamine receptors. The drugs are widely used to treat various manifestations of HS: blepharospasm, paraspasm, ballism, athetosis, tics, chorea, torsion dystonia and spasmodic torticollis. The most commonly prescribed is haloperidol (Orap, Leponex, Sulpiride), starting with a dose of 0.25 mg twice a day, gradually increasing the dose to 1.5 mg, divided into three doses. Side effects of the drugs include signs of parkinsonism syndrome (bradykinesia, muscle rigidity), acute dystonic reactions, and autonomic disorders. In severe cases, neuroleptic malignant syndrome is possible.
Valproic acid preparations have an effect on GS by affecting the metabolism of the inhibitory mediator gamma-aminobutyric acid. Of the drugs in this group, derivatives of sodium and calcium salts of valproic acid (orphyril, convulex, convulsofin) are used. The most modern derivative of valproic acid is depakine, which is available in doses of 300 and 500 (chrono) mg. The daily dose of the drug is usually 300-1000 mg. Depakine has a positive effect on myoclonus, myorhythmias, tics, facial hemispasm, paraspasm, myoclonus epilepsy and Kozhevnikov epilepsy. Rare side effects of the drug include nausea, diarrhea, and possible thrombocytopenia.
Benzodiazepines have anticonvulsant, muscle relaxant and anxiolytic activity. These include phenozepam (diazepam, nozepam) and derivatives, in particular clonazepam (antelepsin, rivotril). Indications for their use are tics, myoclonus, chorea, dynamic tremor, paraspasm, spastic torticollis. The dosage is selected individually and is a maximum of 4-6 mg/day. In cases of insufficient effect, it is possible to combine benzodiazepines with anaprilin (40 mg/day), baclofen (50 mg/day) or antipsychotics. Side effects of benzodiazepines include dizziness, drowsiness, slower reactions, and possible addiction.
It is advisable to include psychotherapy, acupuncture, ozokerite applications, and training in post-isometric relaxation techniques in the complex of treatment of patients with HS. One of the modern methods of treatment is the use of botulinum toxin derivatives (Botox, Dysport), which cause local chemical denervation. Drugs are injected into the affected muscles for blepharospasm, facial hemispasm, spastic torticollis.
Surgical treatment (stereotactic thalamo- and pallidotomy) is carried out in drug-resistant cases of tremor, torsion dystonia and generalized tics. For facial hemispasm, neurosurgical separation of the facial nerve root from the branches of the basilar artery is performed.
Despite the fact that diagnosis and treatment of HS is a difficult task, its timely solution improves the quality of life in patients with this pathology.
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