Hyperkinesis
Last reviewed: 23.04.2024
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Causes of the hyperkinesis
The causes of hyperkinesis, like many other motor anomalies, are associated with partial dysfunction of the cerebral motor apparatus, motoneurons and inhibitory neurons of the motor 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 arising motor reactions of the organism. The inconsistency of the operation of the motor centers of the cerebral cortex, the nuclei of the motor analyzer (located in the subcortex), the cerebellar dentate nuclei and the conducting pathways distorts the impulses of the motor neurons that enter the muscles. Because of these violations, involuntary motor skills of the person acquires an abnormal character, and then extrapyramidal hyperkinesis is diagnosed.
If an organic or functional pathology affected the motor centers of the reticular zone of the brainstem, then stem dystonic hyperkinesis develops, and subcortical motor structures defeat causes subcortical hyperkinesis: choreic, athetoid, and myoclonic.
The biochemical mechanism of unconscious human movements plays an important role, which is based on such basic neurotransmitters as dopamine, acetylcholine and gamma-aminobutyric acid (GABA). The dopamine synthesized by the axons of brain nerve cells refers to stimulators of motor activity, and its action is counterbalanced by neurotransmitters-antagonists - acetylcholine and GABA. If gamma-aminobutyric acid is the main inhibitory neurotransmitter of the central nervous system, acetylcholine excites neurons of the autonomic nervous system and ensures the transmission of nerve impulses from the motor nerves to receptors of postsynaptic membranes of peripheral nerve endings of muscles. In addition, in the transmission of motor nerve impulses, other "chemical intermediaries" are involved: adrenaline, noradrenaline, serotonin, glycine, glutamic and aspartic acid.
Neurophysiologists have established that the imbalance in the production of these neurotransmitter substances by the body and, consequently, the change in the response of their receptors may be the cause of motor disorders. Also, the emergence of extrapyramidal hyperkinesis has a direct relationship with the functioning of the basal ganglia - the regulating motor functions of the structures of the subcortex of the forebrain. The defeat of these neuronal knots and the disruption of their connections to the spinal cord causes uncontrolled hyperactivity of various muscle groups.
All this can occur as a result of cerebral vascular lesions (chronic cerebral ischemia); Vascular compression of the nerves that go to the muscles; infantile cerebral palsy; diseases of the endocrine system (hyperthyroidism); autoimmune and hereditary pathologies (rheumatism, multiple sclerosis, systemic lupus erythematosus). Among the organic causes of hyperkinesia also appear craniocerebral injuries, tumors, neuroinfections (meningitis, encephalitis) or toxic (primarily, medicamental) effects on the structures of the brain.
Symptoms of the hyperkinesis
Chronic hyperkinesis is considered the most common type of cerebral motor disorders. It is a mechanical impulsive movement of the facial and cervical musculature, which have the appearance of frequent blinking and closing eyes, stereotyped grimaces, convulsive monotonous slopes or turns of the head, etc. As specialists note, this kind of hyperkinesis becomes more pronounced when a person is worried or in a state of emotional overexcitation. For example, ticic hyperkinesis can have a reflex character and appear as a response of a person to a too loud sound or a sudden flash of light.
Also, the symptoms of this type of hyperkinesia can be manifested 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 beginning of a tick for a fraction of a second, but for this it takes a huge effort, after which paroxysm is inevitable (that is, the attack develops more strongly and lasts longer). But none of the types of hyperkinesis, including tics, do not make themselves felt in a state of sleep.
Choreiiform hyperkinesis, which also has such names as choreic hyperkinesis, generalized hyperkinesis or chorea, are manifested in the form of arrhythmic expressive movements of facial muscles in the eyebrows, eyes, mouth, nose, and limb muscles.
Gemifacial spasms or hyperkinesis of the face, as a rule, are observed on one side of the face: convulsive irregular rhythmic contractions of the facial muscles can vary from intermittent to almost constant. Hyperkinesis of the whole face is called paraspasm. When facial hyperkinesis affects the muscular ring around the eyes, the person is constantly involuntarily squeezed, and in this case the blepharospasm is diagnosed. If the circular or radial muscles of the mouth contract (with the involvement of the mandibular musculature), then this pathology is called orofacial dystonia or oral hyperkinesis, which is visually perceived as grimace. In violation of the innervation of the chin-lingual, silo-tongue and longitudinal muscles of the tongue, hyperkinesis of the tongue appears, and patients with this problem often, in addition to the will, poke out the tongue out.
Symptoms of hyperkinesia of a choreic character often manifest themselves in the elderly with senile atrophy of brain regions (due to cerebral circulation disorders), infections and brain traumas, with Bechterew's choreic epilepsy, with genetically determined Huntington's disease. If quite frequent involuntary movements with a large amplitude swing appear in the limbs on one side of the body, neurologists on these symptoms determine ballistics, which can even speak of a brain tumor.
This kind of abnormal motility, like athetoid hyperkinesis, has very characteristic features in the form of unhurried bizarre bending of the fingers, acid and feet, but spasms often seize the face, neck and torso. And such clinical cases are defined as choreoathetoid hyperkinesis or choreoatosis. With these kinetic disorders, over time, a significant limitation of the mobility of the joints and muscles (contractures) can develop.
A trembling hyperkinesis (tremor) is a very frequent, rather rhythmic, low-amplitude movements of the head (up-down and left-right), hands (especially hands and fingers), and often the entire body. In some, the tremor may become more intense in a calm state, while others may try to perform any purposeful actions. Typical trembling hyperkinesis is the most revealing symptom of Parkinson's disease.
Hyperkinesis of a slow type can appear against the background of low muscle tone of some muscles and spastic contractions of others, and this is dystonic hyperkinesis. It is this type of motor pathology that is observed in patients with hyperkinetic cerebral palsy. Also, neurologists are allocated twisting (torsion) spasm or deforming muscular dystonia, in which any action provokes sudden uncontrolled irregular spiral movements of the neck musculature (spasmodic torticollis) and trunks that force a person to take very fanciful static poses. And the more extensive the process, the higher the degree of motor limitation of the patient, which after some time leads to the permanently deformed spatial position of the body.
The symptomatology that distinguishes myoclonic hyperkinesis is manifested in sharp and rapid twitches-synchronous or sequential shock-point contractions of one or several muscles of different localization (first of all, of the tongue, the facial part of the head and neck). Then comes muscle relaxation, often accompanied by tremors. A significant part of such motor dysfunctions is caused by genetic degenerations of the brain structures and has a family history.
As specialists note, neurotic-like hyperkinesis manifested by twitching of individual muscles of the whole body is more characteristic for children, and it must be clearly differentiated from the neurosis of compulsive movements. And here the correct diagnosis solves everything.
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Diagnostics of the hyperkinesis
Diagnosis of hyperkinesia of extrapyramidal origin is not an easy task, but neurologists solve it based on:
- listening to patient complaints and collecting anamnesis;
- examination of the patient to determine the level of his normal and range of abnormal movements;
- general and biochemical blood analysis;
- electrocardiograms;
- electroencephalograms;
- electromyograms (determination of the rate of passage of nerve impulses);
- ultrasound cerebral angiography (studies of the state of the cerebral vascular system);
- computer and magnetic resonance imaging of the brain.
In the case of patients with atherosclerosis, endocrine system diseases, autoimmune pathologies, tumoral foci in the brain, specialists of the appropriate medical profile are involved in the diagnosis.
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Treatment of the hyperkinesis
In most clinical cases, the treatment of hyperkinesis involves considerable difficulties, since it is simply impossible to restore damaged structures of the cortex and subcortex of the brain in extrapyramidal motor disorders. So symptomatic drug therapy is aimed at improving the condition of patients and reducing the intensity of manifestations of pathology.
Among the pharmacological agents with which hyperkinesis is treated in adults, adrenoblocking drugs (alpha and beta-blockers of adrenaline receptors) should be mentioned above all. So, with choreiform hyperkinesia, neurologists prescribe Propranolol (Anaprilin, Athenol, 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, Antepesin, Rivrotil) is considered to be an effective means for relaxing muscles by increasing the activity of GABA, it also acts as a sleeping pill. The standard daily dose is 1.5 mg (three times), the optimal dose is no more than 6-8 mg per day.
Neuroleptic drug Trifluoperazine (Triftazin, Terfluzin, Aquil, Kalmazin, Floazin, etc.) has adrenolitic properties and has a retarding effect on the central nervous system; is taken at 0,03-0,08 g per day. Among the side effects of this drug extrapyramidal hyperkinesises, in particular, tremor, so at the same time appointed a drug against Parkinson's disease, for example, Cyclodol.
Cyclodol (Trihexyphenidyl, Parkopan, Romparkin) refers to cholinolytics and helps to reduce the severity of hypertension of muscles. Cyclodol tablets should be taken after a meal - 0.5-1 mg per day, with a gradual increase in the dose to 5-10 mg per day. The use of this medication is accompanied by dry mouth, increased heart rate, visual impairment.
Stimulates the receptors of dopamine and serotonin of the central nervous system and simultaneously inactivates the adrenoreceptors of muscle cells with the drug Vazobral, which is usually taken 1-2 tablets twice a day (during meals).
The anticonvulsant Gabapentin (Gabagam, Gabalept, Gabantin, Neurontin, etc.) is an analogue of gamma-aminobutyric acid (GABA) and, as a result, reduces the pathological activity of the neurotransmitters. The drug is prescribed at the age of over 12 years - 300 mg (one capsule) three times a day. Side effects of gabapentin: tachycardia, increased blood pressure, dizziness and headache, fatigue, sleep disturbances.
Also, to increase the content of gamma-aminobutyric acid in the central nervous system, valproic acid-based preparations - Apileptsine (Depakin, Orphyril, Convulex) are prescribed. The initial single dose for adults - 0.3 grams, daily - 0.9 g. The most frequent side effects are expressed by nausea, vomiting, diarrhea, stomach pain, drowsiness, skin rashes.
In the treatment of trembling hyperkinesis for the neutralization of acetylcholine, the already mentioned Cyclodole is prescribed, and for the activation of the action of dopamine the same remedies are used as in Parkinson's disease: Levodopa - 125 mg or 250 mg per day; Pramipexole (Mirapex) - one tablet (0.375 mg) per day, in three divided doses.
It is considered useful for hyperkinesis exercises of physical therapy, massage and various water procedures - to alleviate the symptoms. And in cases of torsion hyperkinesis, special orthopedic footwear may be needed, which corrects the pathological position of the foot.
Treatment of ticosis hyperkinesis
Drug treatment of ticosis hyperkinesis includes pharmaceuticals based on analogues or derivatives of GABA (see the previous section), as well as drugs that improve cerebral circulation.
Nootropic drug Pantokalcin (calcium gopentenate) enhances the action of endogenous gamma-aminobutyric acid and thereby reduces the stimulating effect of dopamine, noradrenaline and serotonin on the neuromuscular synapses of the neurotransmitter system. This drug is prescribed for 1.5-3 g per day for adults, and for children 0.75-3 g; the duration of treatment can be from one month to six months. Side effects occur rarely and have the appearance of a skin allergy and a cold.
Increases the activity of GABA-ergic receptors of the central nervous system and the drug Aquifen (Phenibut, Bifren, Noofen) based on aminophenylbutyric acid hydrochloride. It is prescribed for oral administration: adults and adolescents after 14 years - 0.25-0.5 g three times a day; children from 8 to 14 years - to 0.25 grams, from 3 to 8 years - to 0.05-0.1 g three times a day.
To improve the blood supply to the brain in tics, Piracetam (Piramem, Cerebropan, Cyclotzetum, etc.) is prescribed, which not only activates the oxidation-reduction process in the tissues, but also increases the production of dopamine and acetylcholine. The drug should be taken on a tablet (0.4 g) three times a day (before eating); the maximum daily dose is 4.8 g.
Treatment of hyperkinesias in cerebral palsy
Patients with infantile cerebral palsy with hyperkinesis (i.e. Spastic form of cerebral palsy) undergo complex treatment, including with the help of medications.
For the removal of muscle spasms, a sedative Diazepam (Valium, Relanium, Seduxen) can be prescribed - 5-10 mg twice a day. Pregnant and children under three years of age, this drug is contraindicated, and its side effects may manifest as drowsiness, weakness, headache, dry mouth, nausea and increased activity of hepatic transaminases.
Treatment of hyperkinesias in cerebral palsy suggests the use of anticonvulsants - gabapentin (see above) or Acediprol. So, Acediprol (other trade names - Apilepsin, Convulex, Diplexil, Orphilept, Valporin), produced in tablets of 0.3 g and as a syrup, relaxes muscles well with convulsive contractions, and it is prescribed as a child (20-30 mg each per kilogram of body weight per day), and adult patients (not more than 2.4 g per day). There may be side effects such as nausea, vomiting, diarrhea, stomach pain, anorexia, cutaneous feeding.
Among the drugs used to reduce the effect of the exciting neurotransmitter acetylcholine in patients with athetoid hyperkinesis in cerebral palsy, doctors prefer Cyclodol (see above) and Procyclidine, which should be ingested 2 mg three times a day.
In addition, the intramuscular administration of Botox is practiced, which relieves muscular spasms for about three months, cramping movements in cerebral palsy.
Prevention
Prevention of hyperkinesis pursues one goal - to support the maximum physiological functioning of the motor apparatus of the brain and the muscle system that is "directed" by it. The benefits of exercise, rational treatment, and adequate nutrition are evident. In some cases, acupuncture can help. Experts advise the use of vitamins B, vitamins C and E, as well as essential fatty acids (oleic, linoleic, arachidonic, etc.).
Hyperkinesis requires qualified medical care, and their treatment can be lifelong.
Forecast
Prognosis of hyperkinesia, since this type of CNS pathology develops for many reasons, including those in which today's medicine is powerless, for example, damage to the fetal brain, neurodegenerative, autoimmune or genetically determined diseases. In such cases, the forecast can not be positive by definition.