Chorea minor. Causes of chorea in children

Description:

Rheumatic (minor chorea, acute chorea, Sydenham's chorea) is observed almost exclusively in children, mainly in the cold season. Girls get sick almost twice as often as boys.

Symptoms:

Its main manifestation is movement disorders in the form of twitching of the arms and legs (so-called choreic hyperkinesis). The origin of the disease is associated with a previous streptococcal infection; chorea minor is believed to be initial symptom and may precede the formation of rheumatic heart defects. Besides. a family predisposition to chorea minor was noted; Among the patients, girls predominate, which is associated with the action female hormones. The development of clinical manifestations of hyperkinesis during chorea is associated with damage to the nerve structures responsible for coordination of movements and normal muscle tone - the cerebral cortex, cerebellum and some deep brain structures (basal ganglia).

The clinical manifestations of chorea are characterized by muscle weakness, incoordination of movements and, most importantly, choreic. Movements during hyperkinesis are fast, irregular, randomly distributed, and vary greatly in frequency and intensity, which creates the impression of “ragged” movement. They are most often expressed in the face, hands and feet. They can be either one-sided or symmetrical. The most common hyperkinesis is hyperkinesis of the larynx and tongue, which is manifested by slurred speech and impaired swallowing. The muscles of the trunk are usually not involved in hyperkinesis, with the exception of damage to the diaphragm, leading to intermittent, irregular breathing. The severity of hyperkinesis varies from slight grimacing, awkwardness and blurred movements to a “choreic storm” with massive pathological movements in the face, arms and legs.

The disease occurs in the form of attacks of hyperkinesis, interrupted by intervals with normal movements and behavior. Average duration attack lasts 12 weeks, usually 4-6 months, occasionally the disease can drag on for 1-2 years. A third of patients who have had minor chorea subsequently develop heart disease. Some patients may have long-term neurological mental disorders after attacks of chorea and formation heart defect- weakness, lethargy,...

With chorea minor, mental disorders are possible, manifested in emotional instability, anxiety, impulsiveness of actions; Possible decrease in memory and concentration. These disorders often occur at the very beginning of the disease and persist in the intervals between attacks of hyperkinesis. With adequate treatment of the disease, they disappear completely.

Causes:

The development of the disease is caused by the induction by group A hemolytic streptococcus of specific antibodies that cross-react with cytoplasmic antigens of neurons of the caudate and subthalamic nuclei and cause damage to these structures of the central nervous system; a certain importance in the pathogenesis of the disease is also attached to changes vascular wall arterioles and small arteries of the brain.

Morphological examination reveals diffuse degenerative changes neurons in subcortical nuclei and bark cerebral hemispheres against the background of perivascular infiltration and small embolic foci in the brain.

Chorea minor is a rheumatic abnormality. It is expressed in bright, uncontrollable movement disorders. The nature of the occurrence of this nervous pathology has repeatedly baffled doctors. Today, doctors have come to the conclusion that the anomaly develops against a rheumatic background.

The main root cause of the development of this anomaly is a relapse of scarlet fever or tonsillitis.

Factors in the development of the disease

It is noteworthy that girls are at greater risk of developing chorea minor than boys. Reasons for the development of this disease long time were a real mystery for doctors. Now doctors have come to the conclusion that the root cause of the development of chorea minor is the penetration of streptococcal bacteria from group A into the body. The disease can begin to progress even against the background of tonsillitis, when bacteria, traveling through the blood, penetrate the connective tissue.

If an infectious pathogen penetrates the central nervous system, then natural cause This is a disruption of the functioning of the GM. This leads to impaired coordination of movements and muscle tone.

The duration of the anomaly is 3−6 weeks.

Death is quite rare. The reason for this is damage to the cardiovascular system.

How does the pathology manifest itself?

The symptoms of chorea minor are quite specific and the disease can be diagnosed already at the dawn of its development.

Lesser chorea, being a “juvenile” anomaly, develops extremely rarely after puberty. Girls are again at risk. Minor chorea almost never occurs in adult young ladies. The exception is individuals who are prone to relapses during pregnancy.

Main signs

The main symptoms of minor chorea include uncontrolled motor passages. They are expressed in nervous twitching of the upper and lower limbs, which is called in medicine choreic hyperkinesis.

According to some researchers of this pathology, rheumatic cardiac anomalies can develop against the background of minor chorea.

The fact that girls are more susceptible to this disease is explained by the influence of female hormones.

Clinical signs

Subsequently, the symptoms of minor chorea manifest themselves in:

Muscle weakness.
Impaired motor coordination.
The presence of choreic hyperkinesis.

A sick child moves quickly, but not rhythmically. Motor passages are characterized by roughness, awkwardness and random distribution. From the outside it seems that the movements are very “ragged”.

Hyperkinesis can be either symmetrical or unilateral. They are expressed in facial expressions, feet, and hands. Laryngeal hyperkinesis is very common. Against this background, a person suffers from slurred speech and swallowing is impaired.

The muscles of the trunk are rarely involved in hyperkinesis. In this case, rapid, almost interrupted breathing is observed. The severity of abnormal manifestations may vary. In some cases, there is a slight grimacing. Sometimes the patient suffers from violent pathological motor passages.

Diagnosis of the disease

You can pre-diagnose minor chorea immediately. To clarify the diagnosis, the specialist must collect an anamnesis of the patient’s life. For this purpose they are used special methods research. In addition, a person suffering from this disease laboratory conditions blood is taken for analysis. It is in the blood test that the number of markers is revealed rheumatoid factor, as well as reactive protein and streptococcal infection.

The key research method is the electroencephalogram. This procedure assumes that GM activity is examined using waves. Then, for research skeletal muscles The doctor prescribes electromyography to the patient.

For detection focal changes GM is prescribed CT.

Features of helping the patient

Treatment of minor chorea should be timely and correct. It is assumed that a person at risk is registered with the attending physician even before the occurrence of specific disorders.

All instructions and wishes of the specialist must be strictly followed. In some cases, the doctor recommends surgery to remove the tonsils. It’s better to do this, because otherwise the child will get a sore throat very often.

Impulsive uncontrolled actions are stopped by taking antipsychotics.

Important to consider

Minor chorea is characterized by paroxysmal manifestations. Average duration the abnormal process is twelve weeks. In some cases pathological period lasts twelve months.

Against this background, a sick child often complains of:

lethargy and apathy;
hyperfatigue;
sleep disturbances (most often drowsiness is observed);
hallucinations.

A child’s “strange” behavior is not always mischief.

If a child suddenly begins to wrinkle his forehead, spill the contents of a spoon before reaching his mouth, knock over the plate on himself and grimace, there is no need to rush to punish him or take him to a psychologist or priest. It is these signs that are the first signs in the development of chorea minor.

Therefore, if a child suffers from private sore throats, it is recommended to immediately consult a good pediatric doctor.

Conclusion

The prognosis for minor chorea, unfortunately, is not very encouraging. Patients often die from dementia or cachexia.

Prevention of the disease is possible. To do this, you need to promptly treat colds, and even better, prevent their occurrence.

Minor chorea (chorea minor; synonym: Sydenham's chorea, infectious chorea, rheumatic chorea).

Etiology. Currently, the rheumatic nature of chorea minor is beyond doubt; the disease is considered the most common and best studied form of rheumatic encephalitis. The development of minor chorea is often preceded by tonsillitis, a rheumatic attack with damage to the heart, and less often joints, but minor chorea may also be the first clinical manifestation of rheumatism.

The development of minor chorea should be considered as an actively ongoing rheumatic process, even if there are no other clinical manifestations(temperature, ROE, heart changes).

Prevalence. Chorea minor most often affects children aged 5-15 years, girls are approximately 2 times more likely than boys. At the age of 15-25, almost exclusively women are affected, and mostly these are relapses of chorea observed in childhood. It has been noted that asthenic, fragile, and hyperexcitable children are more likely to develop chorea minor. In the warm dry time years, manifestations of chorea minor are observed much less frequently than in cold, rainy months.

Pathological anatomy. Fatalities with rheumatic chorea they are rarely observed and occur with severe rheumatic heart disease or from accidental causes. The brain is swollen, noted focal fibrosis soft meninges.

Histologically, the brain usually shows disorganization connective tissue walls of small vessels and capillaries in the form of mucoid swelling, fibrinoid transformation, sclerosis and hyalinosis, developing against the background of increased tissue and vascular permeability. With a long duration of the disease, small scars are found in the cortex and other parts of the brain - foci of capillary fibrosis (Fig. 1).

In small vessels and capillaries, endothelial proliferation occurs, endovasculitis and microthrombi are observed. Constant signs such as vascular dystonia with their tortuosity, intussusception or aneurysmal protrusion of the wall, hyperemia, stasis, formation of hyaline thrombi and perivascular edema. Near the altered vessels, a focal rarefaction of nerve cells develops with the proliferation of glia.

In some cases, with rheumatic chorea, productive encephalitis is observed with the formation of inflammatory nodules in the brain tissue - nonspecific gliogranulomas, consisting of lymphoid cells, histiocytes, single neutrophils and glial elements (Fig. 2).

Vascular and inflammatory changes in chorea are localized in the subcortical nodes (striatal and caudate bodies, thalamus opticum), in the hypothalamic region, cerebellar peduncles, middle and medulla oblongata, but often spread to the cortex and other parts of the brain.

Many authors attach great importance to the dystrophy of small nerve cells of the subcortical ganglia and the internal granular layer of the cerebral cortex, in which chromatolysis, karyocytolysis with the formation of shadow cells, hydropic degeneration, lipofuscin deposition, and neuronophagia are observed.

Severe hyperplasia of glial elements is also detected: proliferation and hypertrophy of astrocytes, proliferation of dense and drainage oligodendroglial cells, significant hyperplasia and dystrophy of microglia.

In cases with an acute malignant course of rheumatic chorea, vascular, inflammatory and dystrophic changes are most clearly revealed. Micronecrosis of the brain substance, diapedetic hemorrhages occur, localized in the subcortical nodes and brain stem, amoeboid forms of astrocytes appear.

With chorea and non-choric hyperkinesis in children, special attention is drawn to changes in nerve fibers in the form of swelling, vacuolization and the formation of terminal flasks (Fig. 3), localized in the subcortical ganglia, subthalamic region, midbrain and medulla oblongata. The nerve fibers of other parts of the brain remain unchanged. At acute course The disease causes deeper damage to the nerve fibers up to their segmental disintegration. Such changes in nerve fibers do not occur in rheumatism that occurs without chorea. Apparently, it is the damage to the nerve fibers of certain parts of the brain that is the morphological substrate of choreic and non-choreic hyperkinesis. Vascular, inflammatory and dystrophic changes in the brain are nonspecific. They are also observed in rheumatism without chorea and cause a variety of clinical forms and manifestations of chorea disease.

About the changes internal organs for chorea, see Rheumatism.

Pathogenesis minor chorea is considered from the position modern ideas about rheumatism as a chronic autoallergic lesion of connective tissue, mainly its interstitial substance, with secondary changes V parenchymal organs. In the nervous system, chorea minor also affects its connective tissue components - vessels, meninges, stroma of the plexus chorioideus. Nerve cells and the fibers suffer a second time. The importance in the pathogenesis of chorea minor has been established not only morphological changes, but also functional disorders of vascular reactivity and vascular tone. In many patients, plethysmography (Fig. 4) and oscillography revealed low peripheral vascular tone and increased vasomotor lability. The diffuseness of cerebral damage in chorea minor is detected by electroencephalography, and a dependence is noted not on the severity of the clinical symptoms of the disease, but on the duration of the disease with rheumatism.

Rice. 4. Finger plethysmogram of a patient with chorea minor. Pronounced undulation of the curve. Short vascular tone. Deep reactions in response to irritation by cold.

Course and symptoms. Clinical symptoms minor chorea develops gradually; in most patients - at normal temperature and the absence of pronounced changes in the blood. Increased temperature and high ROE are observed in patients with current rheumatic carditis. Heart changes, most often endocarditis with damage mitral valve, are observed in approximately half of patients with chorea minor. Complex therapy of rheumatism and seasonal prevention(bicillin, aspirin) significantly changed clinical forms and the course of rheumatism: severe heart damage is now much less common, the number of attacks and active forms has decreased.

Minor chorea is the first clinical manifestation of rheumatism in many children. Changes in the heart, most of them not severe, can become apparent later, sometimes after several years. In a significant proportion of patients with chorea minor, changes in the heart are expressed only by a slight expansion of its boundaries, functional murmurs at the base, and irregular contractions, and all these disorders are reversible and can stop completely. Most patients experience lability of vasomotors, positive symptoms of pinch, tourniquet, and positive cup test, which is explained by the increased vascular permeability characteristic of rheumatism. The excitability of vasomotors is also increased. The blood is unremarkable, sometimes there is moderate leukocytosis, lymphocytosis, eosinophilia, a slight decrease in hemoglobin content and the number of red blood cells. ROE is normal, sometimes moderately accelerated. There are no changes in the urine.

Various lesions of the central nervous system in chorea minor can be grouped into the following typical triad of symptoms: mental changes, choreic hyperkinesis and decreased muscle tone.

Changes in the psyche belong to the early, first manifestations of chorea, but they can be correctly assessed only with the onset of pronounced hyperkinesis, because the observed neurosis-like syndrome itself (increased irritability, touchiness, tearfulness, unmotivated mood swings, “whims”, absent-mindedness, forgetfulness, inattention, sometimes stubbornness, not previously characteristic of the patient, restless and short sleep with slow falling asleep and easy awakening) is characteristic of many diseases, especially in children. Affective outbursts can occur at the slightest provocation. Episodic conditions described psychomotor agitation with disorders of consciousness, hallucinations, delusional ideas. Psychosensory disorders with chorea minor are expressed by a violation of optical-spatial synthesis.

Gradually, these phenomena are joined and intensified by motor disturbances - awkwardness and imprecision of movements, motor restlessness, grimacing, hyperkinesis. The handwriting changes, the writing becomes sloppy, blots and blots appear, letters slip, and their size becomes uneven. Violent movements are expressed in the muscles of the face, neck, torso, and in the proximal and distal parts of the arms and legs. Hyperkinesis gradually increases in intensity and makes it increasingly difficult to perform targeted movements. Not only writing becomes difficult, but also walking, eating independently, and even the ability to pick up and hold an object in your hand. The spread of hyperkinesis to the muscles of the larynx causes speech impairment, which becomes blurred, dysarthric, and sometimes whispery. The patient sometimes makes muttering, inarticulate sounds. In severe forms, patients completely stop speaking (trochaic mutism). Hyperkinesis prevents the patient from sticking out his tongue voluntarily, and if this is successful, the patient cannot keep it stuck out.

Emotional stress, especially unpleasant emotions, sharply increases hyperkinesis. They stop during sleep, but it is difficult for the patient to fall asleep, since hyperkinesis disturbs him. Symptoms of the tongue and eyelids are characteristic - the inability to keep the tongue sticking out with the eyes closed. When inhaling, the abdominal wall retracts instead of the normal protrusion (Czerny's sign). Difficulty fixing gaze leads to constant movements eyeballs: they “run” all the time different directions. The severity of violent movements is very different: from extremely sharp (“motor storm” or “mad dancing”) to barely noticeable, revealed only with a special study.

Muscular hypotonia can also be expressed in to varying degrees. In cases with a very sharp decrease in muscle tone, hyperkinesis is less pronounced and may even be absent. With the so-called chorea mollis - soft, paralytic chorea - a picture of pseudoparalysis is observed, when the patient cannot perform active movements due to muscle atony. Hypotension with minor chorea is caused not only structural changes in the above areas of the brain, but also functional disorders suprasegmental apparatus, primarily the descending systems of the reticular formation of the brainstem and interstitial brain. If hyperkinesis and muscle hypotonia are expressed in only one half of the body, the disease is called hemichorea.

A well-known correlation has been noted between changes in the psyche and focal disorders of the central nervous system: a state of sharp mental arousal is more often observed in patients with severely expressed hyperkinesis, and general lethargy, apathy, lack of initiative - in patients with mild hyperkinesis and noticeable muscle hypotonia.

Tendon reflexes in patients without severe muscle hypotonia remain preserved. With severe muscle atony, tendon reflexes are not evoked, although reflex arc structurally preserved. Chorea minor is characterized by changes in knee reflexes: 1) Gordon's symptom: after hitting the quadriceps tendon with a hammer, the leg freezes for some time in an extension position due to tonic tension of this muscle; 2) the pendulum-like nature of the knee reflex with repeated swinging of the leg with a gradual decrease in the amplitude of movement.

Sensory disorders are not observed with minor chorea. Some patients have severe pain in the joints, muscles, and occasionally along the nerve trunks. The function of the sphincters is not impaired. The fundus is normal. In severe cases, embolism has been described central artery retina.

The cerebrospinal fluid is usually unchanged. In isolated observations it was noted slight increase liquor pressure and a slight increase in cytosis. Lumbar puncture Most patients do not have minor chorea, since this is not necessary for diagnosis, and hyperexcitable patients react with increased hyperkinesis to any irritation that causes pain.

Electroencephalography for chorea minor reveals a diffuse alpha rhythm deficiency throughout the entire cortex, a predominance of irregular slow waves, and the presence in some cases of individual spike-like oscillations. In patients with hemichorea, changes in the EEG are expressed in both hemispheres. With clinical recovery, EEG normalization does not occur in most patients. Changes in the bioelectrical activity of the brain are more pronounced when the disease with rheumatism is significant and with relapses of chorea minor. In cases where chorea minor is the first manifestation of rheumatism in a child, the EEG may be normal.

During minor chorea, periodic intensification and subsidence of neurological symptoms are observed. The longest cases occur with a very slow and gradual development of clinical manifestations with little severity. The more pronounced the muscle hypotonia, the slower the disease progresses; chorea mollis has a protracted, months-long course. Forms with relatively quickly developed hyperkinesis and without sharp decline muscle tone.

In approximately half of patients, minor chorea recurs; the relapse is usually preceded by an exacerbation of the rheumatic process. Relapse most often occurs after 1-2 years. The number of relapses varies: from one or two to many. With improvement general condition, decrease in hyperkinesis are gradually smoothed out mental disorders, but even after recovery, the state of asthenia in people who have suffered minor chorea remains for a long time. During the follow-up examination of such patients, various neurotic disorders: headaches, dizziness, increased fatigue and irritability.

The diagnosis of minor chorea is made primarily on the basis of the gradual development of hyperkinesis and decreased muscle tone in the presence of changes in the psyche and vascular disorders. A history of rheumatism or frequent sore throats confirms the diagnosis, but it should be remembered that minor chorea is often the first clinical manifestation of rheumatism.

Chorea minor differs from other forms of rheumatic encephalitis with hyperkinesis in muscle hypotonia and the nature of violent movements. From hyperkinesis of neurotic origin, minor chorea can be differentiated by rheumatic history, heart changes, increased vascular permeability, gradual development without a clear connection with psychogenic factors.

The prognosis for chorea minor is favorable. Fatalities are rare and are caused not by chorea, but by severe heart damage. Complex therapy and seasonal antirheumatic prophylaxis reduce the possibility of relapses of minor chorea and allow a more favorable prognosis for both cardiac damage and residual neurological effects.

Treatment - see below.

Rice. 1. A scar made of collagen and reticulin fibers in the cerebral cortex (impregnation according to Snesarev).
Rice. 2. Loose glial nodule in the caudate body (Nissl stain).
Rice. 3. Swelling, vacuolization and formation of end flasks in nerve fibers subcortical nodes (impregnation with silver according to Avtsyn).

Sydenham's chorea (Sudenham, 1636) – neurorheumatism (see).

* * *
(by name English doctor Th. Sydenham, 1624–1689; synonyms - dance of St. Vitus, minor chorea, rheumatic chorea) - a manifestation of rheumatic encephalitis with damage to the cerebellum and its peduncles; in modern clinical practice it is extremely rare. Occurs almost exclusively in childhood and adolescence (5–15 years), its appearance at an older age is regarded as central vasculitis nervous system(more often with systemic lupus erythematosus). Associated with the formation of antineuronal antibodies that interact with basal ganglia antigens. Usually occurs several months after acute attack rheumatism, therefore it is often not possible to identify other signs of rheumatism or streptococcal infection in patients. It manifests itself as bilateral or unilateral (hemichorrhea) hyperkinesis, occurring acutely or subacutely, with an increase over 2–4 weeks. When the larynx and tongue are involved, dysarthria and swallowing disorders develop. In mild cases, there may only be grimacing and mannered gestures (a consequence of the patient’s desire to give the appearance of purposeful movements to involuntary movements). In addition, muscle hypotonia is characteristic (with the so-called soft chorea, it “masks” chorea), decreased tendon reflexes, and a “freezing” knee reflex (prolonged choreic contraction of the quadriceps femoris muscle when its tendon is repeatedly tapped). Often identified mental changes(affective lability, anxiety-depressive and obsessive states, decreased attention and memory), autonomic disorders (lability blood pressure, tachycardia). In most cases, hyperkinesis spontaneously regresses within 3–6 months. Relapses of the disease are possible, including during pregnancy, taking oral contraceptives, psychostimulants, levodopa, diphenine. IN long term Some patients who have had Sydenham's chorea exhibit slurred speech, awkward movements, tremors, tics, asthenic, obsessive or anxiety-depressive disorders. Treatment: bed rest in the acute period, small doses of benzodiazepines or barbiturates; in more severe cases, antipsychotics, valproic acid or carbamazepine are used. Glucocorticoids, plasmapheresis, and intravenous immunoglobulin are used. Those who have had Sydenham's chorea require prophylaxis with benzathine benzylpenicillin for 5 years.

T. Sydenham. Schedula monitoria de novae febris ingressu. Londini, 1686; p. 25–28.

Encyclopedic Dictionary in psychology and pedagogy. 2013.

Notes: the presence of two major criteria, or one major and two minor criteria, in combination with evidence documented of a previous infection with group A streptococci, indicates high probability acute rheumatic fever. Special cases:

1. Isolated chorea - with the exclusion of other causes (including PANDAS*).

2. Late carditis - development of clinical and instrumental symptoms valvulitis - if other causes are excluded.

3. Repeated acute rheumatic fever with or without chronic rheumatic heart disease.

* PANDAS is an abbreviation of the English words “Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections” (children’s autoimmune neuropsychiatric disorders associated with streptococcal infection.” This condition is related in pathogenesis to rheumatic chorea, but differs from it in its normal neurological status. The clinical picture is characterized only behavioral disorders in the form of obsessive-compulsive disorder and (or) tic disorder.

Undoubtedly, to the serious achievements of science of the twentieth century. should include the development of prevention of acute rheumatic fever and its relapses. The basis of primary prevention of acute rheumatic fever is timely diagnosis and adequate therapy active chronic infection pharynx (sore throat, pharyngitis). Taking into account the world clinical experience developed adapted to the conditions Russian healthcare recommendations for rational antimicrobial therapy of tonsillitis and pharyngitis.

Secondary prevention is aimed at preventing recurrent attacks and progression of the disease in people who have had an acute rheumatic fever, and involves regular administration of long-acting penicillin (penicillin benzathine). The use of this drug in the form of bicillin-5 made it possible to significantly (4-12 times) reduce the frequency of repeated rheumatic attacks and, consequently, increase the life expectancy of patients with RPS. At the same time, a number of authors pointed out the insufficient effectiveness of bicillin prophylaxis in 13-37% of patients. Joint studies carried out at the Institute of Rheumatology of the Russian Academy of Medical Sciences and the State Research Center for Antibiotics showed that at present a highly effective and safe drug secondary prevention acute rheumatic chorea is benzathine benzylpenicillin, prescribed at a dose of 2.4 million units intramuscularly every 3 weeks. Produced by domestic industry, prolonged dosage form penicillin - bicillin-5 - is currently not acceptable for secondary prevention of ARF, since it does not meet the pharmacokinetic requirements for preventive drugs. In the coming 21st century. Scientists' efforts will be focused on creating and improving a vaccine containing epitopes of M-proteins from “rheumatogenic” strains that do not cross-react with tissue antigens of the human body.

General information

So, what is minor chorea? Lesser chorea is rheumatic disease neurological nature, which manifests itself as excessive physical activity limbs of the patient. This disease is known as rheumatic chorea and Sydenham's chorea, after the scientist who discovered this disease in 1686 and described its symptoms.

This disease manifests itself to a greater extent in children, however, there is evidence of the occurrence of the disease in adults.

Reasons

The main causative agent of the disease is group A hemological streptococcus. This streptococcus is well known to all parents, since it is precisely it that is to blame for the child’s sore throat or other infectious ailments of the upper respiratory tract(VDP).

It is believed that a child who has contracted an infectious disease of the upper respiratory tract immediately enters the risk group, as a potential patient diagnosed with chorea.

However, despite the fact that this reason is one of the main ones, there are a number of factors that can trigger the development of this disease, including:

heredity;
rheumatic diseases in the body;
disruptions in the functioning of the endocrine system;
the presence of carious formations on the teeth;
decreased immunity;
taking certain medications;
cerebral palsy;
insufficient blood supply to the brain

This is far from full list reasons that can provoke chorea. You should know that children aged 5 to 15 years are most susceptible to this disease due to events occurring in their bodies. hormonal changes. Girls especially suffer from the disease, since their concentration of hormonal surges is several times higher.

Symptoms

The main symptoms of minor chorea are the formation of hyperkinesis of varying intensity in the patient.

Hyperkinesis - involuntary movements or muscle contractions

Since the nervous system is affected, in addition to hyperkinesis, the following clinical manifestations of the disease are diagnosed in a small patient:

uncontrolled movements of the limbs (especially evident during writing or drawing);
grimacing;
regular and uncontrollable scratching of the baby, the inability to sit quietly in one place, the need to touch something on the body, etc.;
slurred speech (in especially severe cases it can manifest as complete loss of speech);
shouting some words or sounds;
moodiness;
touchiness;
anxiety;
decreased muscle tone;
when lifting the baby by the shoulders, the head seems to sink into the shoulders (a kind of pressing of the head into the neck occurs);
inability to raise their arms up with their palms facing inward (the child raises them with their palms facing outward);
inability to stick out tongue with eyes closed;
blueness of the feet and hands;
cold extremities;
low blood pressure.

In adults who are childhood Having suffered this disease, a heart defect can be diagnosed.

Diagnostics

This disease is diagnosed using integrated approach to its study.

At the very beginning, the doctor will receive primary data about the patient’s condition, symptoms and thus compile an anamnesis.

To immediate diagnostic measures can be attributed:

clinical blood test;
neurological tests (checking the body's response using neurological methods);
electromyography;
computed tomography;
magnetic resonance imaging;
electroencephalography.

An integrated approach to the study of the disease will allow you to make a timely and accurate diagnosis and prescribe effective treatment.

Treatment

Therapy for chorea minor consists, first of all, in eliminating the cause of the disease, which in most cases is an infectious disease.

The basis of treatment is antibiotic therapy. Penicillin and cephalosporin, as well as drugs based on them, are used as the main antibiotics for the treatment of Sydenham's chorea.

Naturally, as a maintenance therapy for the gastric microflora, the doctor prescribes a course of bifidobacterial drugs (Linex, Bakset). This therapy It is especially necessary for young children, since their fragile bodies are not able to cope with such stomach disorders on their own.

In addition, for the treatment of minor chorea, sedative and tranquilizing drugs may be required, which are prescribed in case of negative reactions from the psycho-emotional state of the child.

In addition, in most cases, it is possible to prescribe anti-inflammatory drugs to reduce inflammation in the diseased body.

In especially severe cases, the patient in mandatory Bed rest is indicated, limiting the entry of bright light and loud sounds into the room.

The entire complex of treatment must be carried out under the supervision of a specialist - a neurologist. Any self-treatment, especially those prescribed based on the results of studying information via the Internet are strictly contraindicated.

Prognosis and prevention for chorea minor

Sydenham's chorea is not a fatal disease and, with proper treatment, goes away in 5-6 weeks.

Naturally, in case reinfection child with streptococcal infection or rheumatism, relapse is possible.

Among the most unpleasant complications, the disease suffered may include:

Heart defect.
Aortic insufficiency.
Mitrine stenosis.

Despite the fact that the disease is not considered fatal, there have been cases of death due to sudden disruptions of the cardiovascular system.

As preventive measures The following should be noted:

timely treatment of infectious diseases and rheumatic diseases;
complete and harmonious physical development baby;
complete and balanced nutrition;
strengthening the child's immunity.

So, chorea minor is not fatal, but unpleasant disease with the presence of complications, so timely contact with a specialist will avoid problems in the future for both you and your baby. Take care of your children and get treatment correctly!

Chorea minor (Sydenham's chorea) is the main form of rheumatic damage to the nervous system in children. It is often the first clinical sign of rheumatism, but can develop against the background of a latent disease or during its inter-relapse period. Children aged 5 to 15 years are most often affected (girls are approximately 2 times more likely than boys).

The etiology and pathogenesis of X. m. are inseparable from other rheumatic lesions. The main etiological role is played by streptococcal infection, which is considered as a trigger mechanism of the disease, including a number of immunological ones, in particular allergic mechanisms. In the formation of pathological reactivity, a significant role belongs to disorders of the adaptation system hypothalamus - pituitary gland - adrenal glands. Humoral and cellular immunological disorders are manifested by an increase in the titer of antistreptolysin-O, antistreptohyaluronidase and antistreptokinase.

Pathological changes are degenerative-toxic and inflammatory in nature. The main changes are localized in the subcortical nuclei and superior cerebellar peduncles; The small cells of the lentiform nucleus are most affected. The cortex, red nuclei, substantia nigra, cerebellum and other structures are also affected. Vasculitis with fibrinoid swelling and hyalinosis of the vascular wall, degenerative changes in neurons, and a microglial reaction are noted.

Clinical picture. Hm. usually develops gradually against the background normal temperature bodies. Febrility in some patients occurs due to other rheumatic lesions. TO initial manifestations First of all, it refers to cerebrasthenic syndrome. Patients experience irritability, mild excitability, and emotional instability. Motor disinhibition and awkwardness of movements gradually increase, objects begin to fall out of hands, and handwriting in school-age children deteriorates significantly. After about 1-2 weeks, hyperkinesis of facial muscles and limbs appears. The patient wrinkles his forehead, closes his eyes, and stretches out his lips. Choreic hyperkinesis in the limbs is fast, impetuous, wide-ranging, and non-stereotypical. IN initial period The disease is more pronounced in the proximal parts of the arms and legs. At rest, hyperkinesis decreases or disappears, and with excitement, physical stress, and fatigue it increases significantly. In the most severe cases, a “motor storm” occurs - the patient is in motion all the time: he is thrown up, sometimes he cannot stay in bed, hits himself, receives multiple bruises, is deprived of the ability to perform purposeful movements, cannot bring food to his mouth, cannot walk , stand, sit. Speech becomes dysarthric, some syllables or words are pronounced too loudly, others in a whisper. However, in many cases, hyperkinesis with X. m. is not clearly expressed and they have to be identified with special techniques. In this case, the simplest and most convenient test is Yuretskaya and Shanko: a child in the Romberg position is asked to stretch out his arms, spread his fingers, close his eyes and stick out his tongue. This test can also be carried out with a dosed physical activity(squatting, running in place, jumping on one leg). As a result of such an examination, it is possible to detect general motor restlessness, twitching of the tongue and fingers.

A constant sign of the disease is muscle hypotonia, up to atony with mild chorea. In these cases, active movements and the implementation of hyperkinesis become impossible. A clinical picture of pseudoparalysis appears. In some cases, the child cannot even hold his head up. The appearance of hyperkinesis in patients with X. m. indicates the positive dynamics of the disease. The cause of the development of muscle hypotonia is functional-dynamic disorders of the descending connections of the limbic-reticular system.

Along with hyperkinesis and muscle hypotonia, psychotic disorders with delusions, hallucinations, and motor excitations can be observed. These patients require hospitalization in a psychiatric department.

At H.m. others are noted neurological symptoms, for example, the “eyes and tongue” symptom, when the patient cannot simultaneously hold eyes closed and sticking out his tongue; Cherny's symptom - a violation of the synergistic movements of the diaphragm and intercostal muscles during breathing, and therefore sinks when exhaling abdominal wall. Changes in tendon reflexes occur (with mild chorea they do not disappear); knee reflexes are pendulum-like in nature, or when they are evoked, the leg freezes in the extension phase at the knee joint. Hypertensive syndrome is sometimes observed, accompanied by headache, vomiting, and slight changes in the fundus. In most patients, H.m. Functional changes in cardiac activity are determined, which then quickly disappear. Some patients have myocarditis or endocarditis, and therefore patients require cardiac evaluation. With a recurrent course of X. m., changes in the heart occur more often and are more severely expressed than at the onset of the disease. The high vascular permeability characteristic of rheumatism is also expressed in chorea. It is detected by checking the symptoms of a pinch or tourniquet, as well as by a cup test. Changes biochemical tests And general analysis blood levels during chorea are determined by the course of the main rheumatic process.

At correct mode and treatment of X. m. lasts about 2 months, mild chorea lasts up to 5-6 months. With more acute development and pronounced hyperkinesis, the regression of symptoms occurs faster than with subacute development and mildly expressed neurological disorders. In approximately half of patients, cancer occurs with relapses, which often occur after 1-2 years; in some patients, multiple relapses are observed after a short period of time (continuously relapsing course). Typically, relapse is preceded by a sore throat or exacerbation of the rheumatic process. In all cases, relapse should be considered as a manifestation of the activity of rheumatism.

Treatment. The main principles of therapy are the combination of antirheumatic drugs with sedatives. Bed rest is established, traumatic factors are eliminated, and adequate nutrition is provided. Antirheumatic drugs include salicylates, butadione, and brufen in age-related doses. The average duration of treatment with these drugs is 4 weeks. Penicillin and ampicillin are also prescribed usual doses. Antihistamines are indicated (suprastin, tavegil, fenkarol, etc.), and it is advisable to change medications every 7-10 days. If therapy is ineffective and in case of relapse, glucocorticoids (prednisone, dexazone, dexamethasone) are indicated; The maximum dose of these drugs is given for 7-10 days. The total duration of treatment is 40 days. Large doses indicated ascorbic acid(0.1-0.2 g 2-3 times a day), B vitamins. Sedatives are prescribed: bromides, valerian preparations, phenobarbital, phenibut. For severe hyperkinesis, haloperidol and chlorpromazine are prescribed for several days. For any form of rheumatism, sanitation of a possible focus of streptococcal infection (tonsils, carious teeth, sinusitis) is indicated. Surgical intervention in these cases is carried out in the interictal period.