Hyperkinesias

Unconsciously produced and physiologically inappropriate active movements - hyperkinesis - are related to pathologies of nervous regulation of muscles of various localizations and arise as a result of damage to the central and somatic nervous system.

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Causes hyperkinesias

The causes of hyperkinesis, like many other motor anomalies, are associated with partial dysfunction of the cerebral motor apparatus, motor neurons and inhibitory neurons of the motor area of the cerebral cortex, brainstem or spinal cord, motor nerve fibers, neuromuscular synapses, etc.

The key to the etiology of hyperkinesis is the "malfunction" of the extrapyramidal system of the central nervous system. The functional task of this extremely complex neurotransmitter system is to regulate muscle tension and relaxation, control the position of the body in space and control facial expressions, as well as all automatically occurring motor reactions of the body. Incoordination of the work of the motor centers of the cerebral cortex, the nuclei of the motor analyzer (located in the subcortex), the dentate nuclei of the cerebellum and the conduction pathways distorts the impulses of motor neurons that go to the muscles. Due to these disorders, a person's involuntary motor skills acquire an abnormal character, and then extrapyramidal hyperkinesis is diagnosed.

If organic or functional pathology affects the motor centers of the reticular zone of the brainstem, then brainstem dystonic hyperkinesis occurs, and damage to the subcortical motor structures produces subcortical hyperkinesis: choreic, athetoid, myoclonic.

The biochemical mechanism of unconscious human movements plays a key role, which is based on such basic neurotransmitters as dopamine, acetylcholine and gamma-aminobutyric acid (GABA). Dopamine, synthesized by the axons of the brain's nerve cells, is a stimulant of motor activity, and its effect is balanced by antagonist neurotransmitters - acetylcholine and GABA. If gamma-aminobutyric acid is the main inhibitory neurotransmitter of the central nervous system, then acetylcholine excites the neurons of the autonomic nervous system and ensures the transmission of nerve impulses from the motor nerves to the receptors of the postsynaptic membranes of the peripheral nerve endings of the muscles. In addition, other "chemical messengers" are also involved in the transmission of motor nerve impulses: adrenaline, noradrenaline, serotonin, glycine, glutamic and aspartic acids.

Neurophysiologists have established that an imbalance in the body's production of these neurotransmitter substances and, accordingly, a change in the response of their receptors can be the cause of movement disorders. Also, problems with the functioning of the basal ganglia - the structures of the forebrain subcortex that regulate movement functions - are directly related to the occurrence of extrapyramidal hyperkinesis. Damage to these neural nodes and disruption of their connections with the spinal cord causes uncontrolled hyperactivity of various muscle groups.

All this can occur as a result of damage to the brain vessels (chronic cerebral ischemia); vascular compression of the nerves going to the muscles; cerebral palsy; endocrine system diseases (hyperthyroidism); autoimmune and hereditary pathologies (rheumatism, multiple sclerosis, systemic lupus erythematosus). Among the organic causes of hyperkinesis are also traumatic brain injuries, tumors, neuroinfections (meningitis, encephalitis) or toxic (primarily medicinal) effects on the structures of the brain.

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Symptoms hyperkinesias

Tic hyperkinesis is considered the most common type of cerebral movement disorders. It is represented by automatic impulsive movements of the facial and neck muscles, which look like frequent blinking and squinting of the eyes, stereotypical grimaces, convulsive monotonous tilts or turns of the head, etc. As experts note, this type of hyperkinesis becomes more pronounced when a person is worried or in a state of emotional overexcitement. For example, tic hyperkinesis can be reflexive and appear as a person's response to a sound that is too loud or a sudden flash of light.

Also, symptoms of this type of hyperkinesis can manifest themselves in the form of involuntary sounds that arise due to rapid contractile movements of the muscles of the larynx, pharynx or mouth. By the way, most patients manage to restrain the onset of a tic for a split second, but this requires enormous effort, after which a paroxysm is inevitable (that is, the attack develops more strongly and lasts longer). But none of the types of hyperkinesis, including tics, make themselves known in a state of sleep.

Choreiform hyperkinesis, which also has names such as choreic hyperkinesis, generalized hyperkinesis or chorea, manifests itself in the form of arrhythmic expressive movements of the facial muscles in the area of the eyebrows, eyes, mouth, nose, as well as the muscles of the limbs.

Hemifacial spasms or facial hyperkinesis are usually observed on one side of the face: convulsive arrhythmic contractions of the facial muscles can vary from intermittently frequent to almost constant. Hyperkinesis of the entire face is called paraspasm. When facial hyperkinesis affects the muscle ring around the eyes, the person constantly involuntarily closes their eyes, and in this case blepharospasm is diagnosed. If the circular or radial muscles of the mouth contract (with the involvement of the mandibular muscles), then such a pathology is called orofacial dystonia or oral hyperkinesis, which is visually perceived as grimacing. With disorders of the innervation of the genioglossus, styloglossus and longitudinal muscles of the tongue, hyperkinesis of the tongue appears, and patients with this problem often involuntarily stick their tongue out.

Symptoms of hyperkinesis of a choreic nature often appear in old age with senile atrophy of parts of the brain (due to cerebral circulation disorders), with infections and brain injuries, with Bekhterev's choreic epilepsy, with genetically determined Huntington's disease. If fairly frequent involuntary movements with a large amplitude of swing appear in the limbs on one side of the body, then neurologists determine ballism by these symptoms, which may even indicate a brain tumor.

This type of abnormal motor skills, such as athetoid hyperkinesis, has very characteristic signs in the form of unhurried bizarre bending of fingers, toes and feet, but spasms often capture the face, neck and trunk. And such clinical cases are defined as choreoathetoid hyperkinesis or choreoatosis. With these kinetic disorders, significant limitation of joint and muscle mobility (contractures) can develop over time.

Tremors are very frequently repeated, fairly rhythmic, low-amplitude movements of the head (up-down and left-right), arms (especially hands and fingers), and often the entire body. In some people, tremors may become more intense when at rest, while in others, they may become more intense when attempting to perform any purposeful actions. Typical tremors are the most indicative sign of Parkinson's disease.

Slow-type hyperkinesis may appear against the background of low muscle tone of some muscles and spastic contractions of others, and this is dystonic hyperkinesis. This is the nature of motor pathology observed in patients with hyperkinetic cerebral palsy. Neurologists also distinguish twisting (torsion) spasm or deforming muscular dystonia, in which any actions provoke sudden uncontrolled arrhythmic spiral movements of the neck muscles (spasmodic torticollis) and trunk, forcing a person to take very bizarre static poses. And the more extensive the process, the higher the degree of motor limitation of the patient, which after some time leads to a constantly deformed spatial position of the body.

The symptoms that distinguish myoclonic hyperkinesis are manifested in sharp and rapid twitching – synchronous or successive shock-point contractions of one or more muscles of various localizations (primarily, the tongue, facial part of the head and neck). Then comes muscle relaxation, often accompanied by tremor. A significant part of such motor dysfunctions is caused by genetic degeneration of brain structures and has a family history.

As experts note, neurosis-like hyperkinesis, which manifests itself in twitching of individual muscles of the entire body, is more typical for children, and it must be clearly differentiated from obsessive-compulsive disorder. And here, correct diagnostics are crucial.

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Diagnostics hyperkinesias

Diagnosis of hyperkinesis of extrapyramidal origin is not an easy task, but neurologists solve it on the basis of:

• listening to the patient's complaints and collecting anamnesis;
• examination of the patient to determine the level of his normal and range of abnormal movements;
• general and biochemical blood tests;
• electrocardiograms;
• electroencephalograms;
• electromyograms (determining the speed of nerve impulses);
• ultrasound cerebral angiography (study of the state of the vascular system of the brain);
• computed tomography and magnetic resonance imaging of the brain.

In cases where patients have atherosclerosis, endocrine diseases, autoimmune pathologies, or tumor foci in the brain, specialists in the relevant medical profile are involved in making a diagnosis.

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Treatment hyperkinesias

In most clinical cases, the treatment of hyperkinesis is associated with considerable difficulties, since it is simply impossible to restore damaged structures of the cortex and subcortex of the brain in extrapyramidal movement disorders. So symptomatic drug therapy is aimed at improving the condition of patients and reducing the intensity of pathology manifestations.

Among the pharmacological agents used to treat hyperkinesis in adults, the first to be mentioned are adrenergic blocking drugs (alpha- and beta-blockers of adrenaline receptors). Thus, for choreiform hyperkinesis, neurologists prescribe Propranolol (Anaprilin, Atenotol, Betadren, Propamine, etc.) - 20 mg twice a day (a quarter of an hour before meals) or 40 mg at one time. Side effects include dizziness, nausea, vomiting, diarrhea, increased heart rate, general weakness and depressed mood.

Clonazepam (Clonex, Antelepsin, Rivotril) is considered to be quite an effective means of muscle relaxation due to the increased activity of GABA, it also acts as a sleeping pill. The standard daily dose is 1.5 mg (in three doses), the optimal dose is no more than 6-8 mg per day.

The neuroleptic drug Trifluoperazine (Triftazin, Terfluzin, Aquil, Calmazin, Fluazin, etc.) has adrenolytic properties and an inhibitory effect on the central nervous system; it is taken at 0.03-0.08 g per day. Among the side effects of this drug are extrapyramidal hyperkinesis, in particular, tremor, therefore, some drug against Parkinson's disease is prescribed at the same time, for example, Cyclodol.

Cyclodol (Trihexyphenidyl, Parkopan, Romparkin) is an anticholinergic and helps reduce the severity of muscle hypertonicity. Cyclodol tablets are recommended to be taken after meals - 0.5-1 mg per day, with a gradual increase in the dose to 5-10 mg per day. The use of this drug is accompanied by dry mouth, increased heart rate, and visual impairment.

The drug Vasobral stimulates dopamine and serotonin receptors in the central nervous system and simultaneously inactivates adrenergic receptors in muscle cells. It is usually taken 1-2 tablets twice a day (during meals).

The anticonvulsant Gabapentin (Gabagama, Gabalept, Gabantin, Neurontin, etc.) is an analogue of gamma-aminobutyric acid (GABA) and due to this reduces the pathological activity of neurotransmitters. The drug is prescribed for children over 12 years of age - 300 mg (one capsule) three times a day. Side effects of Gabapentin: tachycardia, increased blood pressure, dizziness and headache, increased fatigue, sleep disorders.

Also, to increase the content of gamma-aminobutyric acid in the central nervous system, drugs based on valproic acid are prescribed - Apilepsin (Depakine, Orfiril, Convulex). The initial single dose for adults is 0.3 g, daily - 0.9 g. The most common side effects are nausea, vomiting, diarrhea, stomach pain, drowsiness, skin rashes.

In the treatment of tremor hyperkinesis, the above-mentioned Cyclodol is prescribed to neutralize acetylcholine, and to activate the action of dopamine, the same drugs are used as for Parkinson's disease: Levodopa - 125 mg or 250 mg per day; Pramipexole (Mirapex) - one tablet (0.375 mg) per day, three times a day.

Exercise therapy, massage and various water treatments are considered useful for hyperkinesis to alleviate symptoms. And in cases of torsion hyperkinesis, special orthopedic shoes may be needed to correct the pathological position of the foot.

Treatment of tic hyperkinesis

Drug treatment of tic hyperkinesis includes pharmaceuticals based on GABA analogues or derivatives (see previous section), as well as drugs that improve cerebral circulation.

The nootropic drug Pantocalcin (calcium hopantenate) enhances the action of endogenous gamma-aminobutyric acid and thereby reduces the stimulating effect of dopamine, norepinephrine and serotonin on neuromuscular synapses of the neurotransmitter system. This drug is prescribed at 1.5-3 g per day for adults, and 0.75-3 g for children; the duration of treatment can be from one month to six months. Side effects are rare and have the form of skin allergies and runny nose.

The drug Aquifen (Phenibut, Bifren, Noofen) based on aminophenylbutyric acid hydrochloride also increases the activity of GABA-ergic receptors in the central nervous system. It is prescribed for oral administration: adults and adolescents over 14 years old - 0.25-0.5 g three times a day; children from 8 to 14 years old - 0.25 g, from 3 to 8 years old - 0.05-0.1 g three times a day.

To improve blood supply to the brain in case of tics, Piracetam (Piramem, Cerebropan, Cyclocetam, etc.) is prescribed, which not only activates the oxidation-reduction process in tissues, but also increases the production of dopamine and acetylcholine. The drug should be taken one tablet (0.4 g) three times a day (before meals); the maximum daily dose is 4.8 g.

Treatment of hyperkinesis in cerebral palsy

Patients with cerebral palsy with hyperkinesis (i.e. spastic form of cerebral palsy) undergo complex treatment, including with the help of medications.

To relieve muscle spasms, the sedative Diazepam (Valium, Relanium, Seduxen) can be prescribed - 5-10 mg twice a day. This drug is contraindicated for pregnant women and children under three years of age, and its side effects can include drowsiness, weakness, headache, dry mouth, nausea and increased activity of liver transaminases.

Treatment of hyperkinesis in cerebral palsy involves the use of anticonvulsants - Gabapentin (see above) or Acediprol. Thus, Acediprol (other trade names - Apilepsin, Convulex, Diplexil, Orfilept, Valporin), produced in tablets of 0.3 g and in the form of syrup, relaxes muscles well during convulsive contractions, and it is prescribed to both children (20-30 mg per kilogram of body weight per day) and adult patients (no more than 2.4 g per day). There may be side effects such as nausea, vomiting, diarrhea, stomach pain, loss of appetite, skin irritation.

Among the drugs used to reduce the effect of the excitatory neurotransmitter acetylcholine in patients with athetoid hyperkinesis in cerebral palsy, doctors prefer Cyclodol (see above) and Procyclidine, which should be taken orally at 2 mg three times a day.

In addition, intramuscular injection of Botox is practiced, which relieves muscle spasms that restrict movement in cerebral palsy for about three months.

Prevention

Prevention of hyperkinesis has one goal – to support the maximum physiological functioning of the motor apparatus of the brain and the muscular system “controlled” by it. The benefits of physical exercise, a rational regimen, and proper nutrition are obvious. In some cases, acupuncture can help. Specialists advise using B vitamins, vitamins C and E, as well as essential fatty acids (oleic, linoleic, arachidonic, etc.).

Hyperkinesis requires qualified medical care, and its treatment can be lifelong.

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Forecast

Prognosis of hyperkinesis, since this type of CNS pathology develops for many reasons, including those for which today's medicine is powerless, such as fetal brain damage, neurodegenerative, autoimmune or genetically determined diseases. In such cases, the prognosis cannot be positive by definition.

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