Epilepsy and the thyroid gland are such a wedding. The influence of endocrine glands on the development of epilepsy

Myasthenia – chronic illness, characterized by weakness and pathological muscle fatigue, is an autoimmune disease. Many patients experience changes thymus gland(tumors and hyperplasia of gland tissue).
The development of the disease is characterized by a combination of neuroendocrine and immune deficiency. Pathological weakness caused by a violation of neuromuscular impulse transmission. Clinic. The muscles innervated by the cranial nerve are affected more often and earlier. It manifests itself as ptosis, double vision (diplopia), difficulty chewing, swallowing, and weakness of the facial muscles, neck, shoulder girdle, arms, and chest.
In the morning the patient feels healthy. After a few hours, the eyelids droop, the voice becomes quiet, weak, and speech is slurred. The face is amicable, the “Gioconda” smile. The head hangs or tilts to the side, frequent drooling, shortness of breath, weakness in the legs and arms after minor physical activity. Muscle tone is not impaired, tendon reflexes are preserved, sensory disorders No.
Forms of the disease:
1 – generalized
2 – ocular
3 – bulbar
4 – trunk
Influenced external factors(infections, intoxications, physical, nervous - mental stress), changing the dose of medications used is possible sharp deterioration with development myasthenic crisis(this is a sharp, paroxysmal developing muscle weakness with impaired breathing and cardiac function).
Myasthenic crisis (5-10 minutes)- dangerous condition- muscle weakness suddenly occurs, the patient does not breathe on his own, does not speak, and does not swallow saliva. A common cause is infection of the upper respiratory tract(bronchitis, pneumonia) in some cases the cause remains unclear. The course of myasthenic crisis is aggravated by the patient's uncontrolled use of anticholinesterase drugs (proserin).
Nurse tactics:
1. call a doctor or emergency physician.
2. Provide physical and emotional peace.
3. Give your head an elevated position.
4. If breathing and cardiac activity stop, closed cardiac massage is performed.
5. Perform mechanical ventilation when breathing weakens.
6. Prepare proserin for the doctor’s arrival.
Treatment for myasthenic crisis: Proserin 1-2 ml i.v. The effect occurs within 30 minutes and lasts for 2 hours. IN interictal period: prozerin (0.15), calemin are taken orally, the effect after 1 hour lasts 2 – 4 hours.
Patients with myasthenic crisis are usually hospitalized in the department intensive care. It is necessary to ensure the patency of the airways (remove mucus and vomit from the mouth, make sure that there is no retraction of the tongue). In the hospital, they are transferred to mechanical ventilation to avoid death from respiratory failure. Then they urgently take a general one and biochemical analysis blood (to identify signs of inflammation, exclude hypokalemia, and other metabolic changes). If the patient shows signs of infection, antibiotics (cephalosporins) are added. Plasmophoresis is prescribed.
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Some nervous diseases When doctors first visit patients, it is quite difficult to diagnose them. These diseases include myasthenia gravis. The initial complaints voiced by the patient are rapid fatigue. But after rest, muscle fatigue decreases short time recedes, and the patient feels quite normal again.

Meanwhile, myasthenia gravis is a violation of neuromuscular signal transmission from the central nervous system into the striated muscles, causing abnormal cyclic fatigue after minor exercise.

Information about the disease

There are immune-dependent myasthenia gravis and myasthenic syndromes.

The cause of the first is autoimmune diseases; the development of syndromes is caused by a combination of developmental defects: postsynaptic and presynaptic.

These defects are nothing more than disruptions in the synthesis necessary for normal life body substances and defects in the sensory organs. Due to pathologies of organic processes, the function of the thymus gland is disrupted.

Push to launch autoimmune diseases or violations biochemical processes there may be all factors in the body that weaken immune status, namely infectious diseases, stress or injury.

You can select following forms myasthenia gravis:

ophthalmic;
bulbar;
generalized.

Some doctors believe that bulbar myasthenia is combined with ocular myasthenia, and how separate state it is not classified.

The first symptoms of myasthenia gravis eye-shaped- damage to the muscles of the eyelids. Patients complain of drooping eyelids, rapid eye fatigue, and image doubling.

Then signs of bulbar myasthenia appear - the pharyngeal muscles, also innervated by the cranial nerves, atrophy.

Chewing and swallowing functions are impaired, the timbre of the voice will subsequently change, and the ability to articulate speech will disappear.

With generalized myasthenia, all muscles are gradually blocked - from top to bottom - from the cervical and scapular to the dorsal, then the muscles of the extremities are affected. Drooling appears, the patient finds it difficult to care for himself or perform the simplest actions, and a feeling of weakness occurs in the limbs.

The progression of symptoms can stop at any stage.

In children, the disease does not appear before six months of age; in most cases, it is diagnosed in boys over 10 years of age. For them, it takes up to 2 years from the first symptoms – weakness of the eyelid muscles – to the next ones

In adulthood, between 20 and 40 years of age, women are more likely to get sick, and at the age of over 65, the manifestation of the disease no longer depends on gender.

Types of myasthenic syndrome

There are several myasthenic syndromes caused by genetic defects.

All of them are inherited autosomal recessively, except for the autosomal dominant syndrome, which is caused by the slow closure of immune channels:

Lambert-Eaton syndrome is more often diagnosed in men over 40 years of age. Its main symptoms are weakness of the proximal muscles of the extremities while sparing the bulbar and extraocular muscles. Symptoms may precede clinical manifestations, at physical activity– playing sports, muscle weakness can be stopped;
Congenital myasthenic syndrome. Signs – violation of symmetrical movement eyeballs and ptosis of the eyelids;
Symptoms: weakness of facial and skeletal muscles, sucking function is impaired;
Muscle hypotonia and underdevelopment of the synaptic apparatus causes a rare myasthenic syndrome, in which tendon reflexes are reduced. Typical signs conditions – asymmetry of the face, mammary glands and torso;
Myasthenic syndromes can be caused by taking certain drugs: D-penicillamine and antibiotics: aminoglycosides and polypeptides. Improvement occurs 6-8 months after discontinuation of the drug.

The syndrome caused by slow closure of ion channels has the following symptoms:

weakness of the extraocular muscles;
muscle atrophy;
weakness in the limbs.

Treatment of each case of myasthenia gravis is carried out according to a specific algorithm.

Can be used:

corticosteroids;
antibiotics;
anticholinesterol drugs;
plasmapheresis and other types of specific therapy.

Drugs used for one form of the disease are ineffective for other forms.

Myasthenic crisis

The main symptoms of myasthenic crisis are extensive dysfunction of the bulbar muscles, which includes the respiratory muscles, up to the onset of apnea.

The intensity of symptoms increases at a critical rate - brain hypoxia can occur within half an hour.

If emergency treatment is not provided for sudden myasthenic crisis, the patient will suffocate.

The reasons for the development of a crisis may be the following factors:

stressful conditions;
increased physical activity;
flu;
acute respiratory diseases;
metabolic disorders;
intoxication of various etiologies.

These factors provoke blocking neuromuscular conduction, cause loss of excitability in muscles and tendons.

Patients with myasthenia gravis always have a note with them on which it is written that they suffer from such and such a form of the disease and what medications are needed to provide first aid. In most cases, patients carry medications with them - these are proserin and canevin.

If among those around you who have seen a myasthenic crisis develop, there is at least 1 person who knows how to give injections, the person’s life will be saved. But you still need to call an ambulance.

Crisis treatment

The method of treating myasthenic crisis is completely determined by the patient’s condition and how quickly emergency assistance was provided by the specialist who arrived at the scene. brigade.

As quickly as possible, the victim must be placed in intensive care and connected to a ventilator - artificial respiration. Artificial ventilation lungs should be done within 24 hours, no less.

Plasmapheresis effectively restores the condition, but may require intravenous administration immunoglobulin. Together with immunoglobulin, methylprednisolone and potassium chloride are used.

Joint treatment with immunoglobulin, potassium chloride and methylprednisolone is used if there is a history of inflammatory processes.

Antioxidants are used - lipoic acid in particular. They reduce the amount free radicals, accumulated in the blood, reduce the severity of oxidative stress in the body of patients.

Myasthenic crisis (hereinafter - MK) is a life-threatening condition that is characterized by impaired breathing and swallowing to the extent that compensation is impossible without a set of intensive care and resuscitation measures (including intensive ventilation). According to the literature, crisis courses are observed in 30 - 40% of patients with myasthenia gravis and are more common in women.

Molecular basis MK is probably a sharp decrease in the number of functioning acetylcholine receptors (hereinafter referred to as AChRs) due to a massive attack by their autoantibodies.

Differentiate MK from others severe conditions accompanied by respiratory disorders, it is possible according to the presence bulbar syndrome, hypomimia, ptosis, asymmetric external ophthalmoparesis, weakness and fatigue of the muscles of the limbs and neck, decreasing in response to the administration of acetylcholinesterase inhibitors (hereinafter referred to as AChE).

There is an idea that the highest incidence of myasthenia gravis occurs in the first 2 years from the onset of the disease, while there is a group of patients in whom the manifestation of myasthenia gravis debuts. In the literature, there are cases of the development of myasthenia, accompanied by severe respiratory failure, as the first manifestation of myasthenia gravis (most often with a “late” onset of the disease). The trend towards acute development myasthenia in old age was described by K. Osserman, who identified these patients as a separate group in his classification as acute “fulminant” malignant form with late onset of the disease and early atrophy. Currently, many authors note the clinical evolution of myasthenia gravis and the tendency towards significant “aging” of the disease. Thus, researchers note that since approximately the mid-80s of the 20th century, the incidence of diseases in at a young age and increased 3 times in old age. This circumstance underlies one of the current problems diagnosis of myasthenia gravis in the elderly: currently, according to statistics, 4 out of 5 patients with acute onset of myasthenia are late age a diagnosis of stroke, botulism (or polymyositis) is made. In most cases it is possible to determine trigger factor or a combination of several factors leading to the development of crises, however, there is also a “sudden” onset of crises for no apparent reason.

Many authors point to the polyetiological nature of the development of MC, on the one hand, and the absence of any visible reasons crises in some patients with myasthenia gravis, on the other. The literature describes whole line factors (exogenous and endogenous) that can provoke the development of exacerbation and MK. Among the most common causes of the development of urticaria, according to domestic and foreign authors: upper respiratory tract infection (10 - 27% of cases), aspiration (bacterial) pneumonia (10 - 16%), surgery– thymectomy (5 - 17%), initiation of treatment high doses steroids or their withdrawal (2 - 5%), pregnancy and childbirth (4 - 7%); in 35 - 42% of cases they are not found etiological factor crisis.

In most cases, MK occurs suddenly and develops rapidly, leaving no time to change treatment tactics and prevent them, therefore it is important to assess the significance clinical symptoms, immunological, electrophysiological and pharmacological characteristics, which could serve as criteria for predicting the development of MC.

The crisis nature of myasthenia gravis can be predicted already at the onset of the disease. Reliable predictors of a malignant course are facial weakness, bulbar and respiratory disorders, weakness of the muscles of the neck and hands (a symptom of “sagging” of the 3rd to 5th fingers of the hands) and the absence of “classical” oculomotor disorders (double vision) and proximal weakness of the limbs in the clinical pattern of the debut of myasthenia gravis (moreover, such a selective pattern, having formed early, persists throughout throughout the course of the disease and is observed in patients with the most severe course diseases resistant to the main species pathogenetic therapy- GCS, thymectomy (often during the development emergency patients retain the characteristic selectivity of damage to individual muscle groups, having the so-called “partial” type of crisis).

According to the results of the study (from 1997 to 2012) N.I. Shcherbakova et al. (FGBU " Science Center Neurology" RAMS, Moscow):

Crises in patients with myasthenia gravis often develop in the first year from the onset of the disease, which is primarily due to late diagnosis and lack of adequate pathogenetic therapy. Development of the crisis into more late dates The disease is significantly more often associated with the abolition or reduction of the dose of basic GCS therapy, which reflects the objective difficulties of selecting the minimum maintenance dose of steroids.

MK predominates in women at a young age, in men over 60 years of age. With a “late” onset of the disease, the likelihood of developing crises in women and men is the same.

A feature of myasthenia gravis in the elderly is the tendency towards an acute fulminant onset of the disease, up to the manifestation with MK, which, as shown clinical practice, often causes misdiagnosis.

Important predictors of a malignant “crisis” course of the disease should be considered the presence of a selective craniobulbar clinical pattern, a combination of myasthenia gravis with thymoma, and the lack of effect on thymectomy in young people. age groups(up to 40 years), the presence of antibodies (AT) to MTC (specific muscle tyrosine kinase), poor sensitivity of patients to acetylcholinesterase inhibitors.

The titer (concentration) of AT to AChR does not have prognostic value in determining the severity of the disease. The detection of antibodies to MTC in the serum of patients indicates a high risk of developing a malignant crisis course of the disease.

Electrophysiological criterion high risk MK is a decrease in the amplitude of the M response to the first electrical stimulus in the clinically affected muscle in combination with to a small extent decrement (block of neuromuscular transmission), not corresponding to the severity of paresis.

Myasthenic crisis is characterized by life-threatening weakness of the respiratory and bulbar muscles, leading to respiratory arrest.

Treatment. During a crisis, first of all, you should ensure the airway is open, remove mucus from the throat using an electric suction or using a head-down position. Then it is necessary to carry out mechanical ventilation by everyone accessible ways. The use of masks during mechanical ventilation in patients is not recommended due to existing dysphagia. To quickly stop the crisis, proserin is administered - 0.5-1.5 mg (1-3 ml of 0.05% solution) intravenously with preliminary administration of 0.6 mg of atropine (proserin administered intravenously can cause cardiac arrest), after 15 minutes 0.5 mg of proserine is administered subcutaneously. It is possible to administer 60 mg of neostigmine (proserine) into the endotracheal tube or 2.5 mg intramuscularly. Throughout critical period Airway drainage is mandatory. As additional help, prednisolone 90-120 mg per day, immunoglobulin 0.4 mg per day, cardiotonic and symptomatic drugs are used.

To remove autoantibodies to acetylcholine receptors from the body, plasmapheresis and hemosorption are used.

Cholinergic crisis, resulting from an overdose of anticholinesterase drugs (proserin, neostigmine, kalimine, mestinon), is manifested by miosis, excessive salivation, bronchospasm, sweating, agitation, muscle weakness, abdominal pain, diarrhea, fibrillations and fasciculations.

When this condition is diagnosed, all anticholinesterase drugs are immediately discontinued, 1-2 mg (1-2 ml of 0.1% solution) of atropine is administered subcutaneously or intravenously every hour, monitoring the diameter of the pupils. Mechanical ventilation is performed with intermittent positive pressure through an endotracheal tube, the airways are sanitized.

According to the severity of the injury, traumatic brain injury is divided into concussion, contusion and contusion with compression, which determines the tactics and scope of treatment emergency care.

Treatment. All patients with traumatic brain injury are subject to inpatient treatment and observation. If vital functions are preserved, the patient needs to be provided with rest, cold on the head, symptomatic therapy(painkillers, sedatives, hypnotics) and correction of microcirculatory disorders (venotonics, vasoactive drugs, antiplatelet agents). It is advisable early appointment antibacterial therapy.

The use of antipsychotics and narcotic analgesics for prehospital stage and until exclusion intracranial hematoma Not recommended.

Gradual depression of consciousness is usually a sign of intracranial hematoma, compression, swelling or herniation of the brain, which requires surgical intervention, hemostatic therapy (intravenous 1 ml of 12.5% dicinone or etamsylate solution with an interval of 6 hours) and dehydration therapy. Development psychomotor agitation, hyperthermia, comatose state requires nonspecific emergency treatment.

Under the editorship prof. A. Skoromets

"Myasthenic crisis" and other articles from the section

(p. cholinergica) K. caused by an overdose of anticholinesterase drugs (for example, in the treatment of myasthenia gravis), characterized by weakness, arterial hypotension, bradycardia, miosis, vomiting, salivation, convulsions and fasciculations.

- sudden short-term condition in a patient with the appearance of new and intensification of existing symptoms of the disease...
Medical terms
- a sudden, relatively short-term condition in a patient, characterized by the appearance of new or intensification of existing symptoms of the disease. Addisonian - see adrenal...
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- a sudden, relatively short-term condition in a patient, characterized by the appearance of new or intensification of existing symptoms of the disease...
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- S., in which the mediator is acetylcholine...
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- 1. Used to characterize neurons, nerve fibers and their endings, which use acetylcholine as a neurotransmitter. 2...
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- ; pl. cry/zy, R....
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- -and husband. . Sudden onset acute attack illness...
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- crisis m. A sudden sharp deterioration in the patient’s condition against the background of an existing disease; attack...
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- KRISA a, m. KRISA s, w. CRISIS a, m. crise f., lat. crisis. 1. diploma A difficult situation, a condition that requires a decisive turn, a turning point. Sl. 18. A good way to free yourself from some obligations, which...
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author Vyatkina P.

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From the book Complete medical directory diagnostics author Vyatkina P.

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