Hyena bar disease symptoms. Guillain-Barré syndrome: signs, diagnosis, treatment Definition of disease. Causes of the disease

Guillain-Barré syndrome is considered one of the serious neurological diseases, when the human immune system changes polarity and destroys its own cells - neurons. This leads to autonomic dysfunctions and, in the absence of timely assistance, to paralysis. The disease has its own symptoms, which allows you to recognize the disease and start its treatment in time. According to statistics, about 2% of people are affected by pathology. More than 80% of them are completely cured thanks to modern therapeutic methods.

The reasons

This syndrome has been known to medical science for over 100 years. But until today, the exact causes of the pathology and all the factors that provoke its occurrence have not been fully clarified.

Classically, it is believed that the cause of the disease lies in the failure of the functioning of the human immune system. With healthy immunity, when foreign cells enter the body, an internal “alarm” is triggered and the fight against infections begins, the rejection of dangerous elements. When Guillain-Barré syndrome occurs, defense mechanisms misfire, confusing "us" and "them": they take human neurons for foreign cells and fight them. It turns out that the human immune system destroys the nervous system. This conflict leads to pathology.

Why such "failures" in the protection of the body occur is also a little-studied question. The reasons for which the disease can develop are rooted in various traumas and diseases. Common "triggering" factors are:

1. Traumatic brain injury.

Physical damage that caused swelling of the brain or tumors in it is especially dangerous. The likelihood that the syndrome will affect the nervous system is quite high. Therefore, doctors take into account the presence of traumatic brain injuries, both in the diagnosis of GBS itself, and in control examinations of a person who has already recovered from brain edema, as a preventive measure.

2. Viral infections.

The human body successfully copes with many infections. However, with frequent viral diseases or too long treatment, immunity weakens. If the treatment of an infectious-inflammatory process was delayed or strong antibiotics were used, the risk of provoking GBS doubles. The immune system begins to mistakenly perceive neurons as infectious agents and sends a command to leukocytes to destroy the top layer of nerve cells. As a result, the myelin coating of neurons loses its structure, and nerve signals enter the tissues fragmentarily, gradually disappearing altogether. This is the reason for the failure of the functioning of organs and paralysis of parts of the body.

3. Predisposition is hereditary.

The syndrome is studied not only by the anamnesis of a person's life, but also by his predisposition to changes in the polarity of the immune system. If the pathology of Guillain-Barré has already been encountered in the family, the patient automatically falls into the risk zone: the slightest head injury or minor infectious diseases can become a trigger for the onset of the disease.

Other reasons are possible. GBS has been observed in people with various allergies, after vaccination against diphtheria or polio, who underwent complex surgery or chemotherapy.

Symptoms

Guillain-Barré neuropathology has symptoms of three forms of the development of the disease:

• acute, when the signs rapidly manifest themselves in a matter of days;
• subacute, when the disease "swings" from 15 to 20 days;
• chronic, sluggish and the most dangerous because of the difficulty in diagnosing and timely prevention of irreversible processes.

Initially, Guillain-Barré syndrome is accompanied by symptoms similar to a viral respiratory infection:

• a sharp increase in body temperature;
• catarrhal inflammation in the upper respiratory tract;
• joint pain and general weakness.

Often the onset of the disease is accompanied by gastrointestinal disorders.

But there are other clear symptoms that help not to confuse SARS and the syndrome:

1. Weakness of the limbs.

Destroying nerve cells lead to a decrease and even loss of sensitivity and signal transmission to muscle tissues.

First, symptoms in the form of discomfort appear in the lower legs, then discomfort spreads to the feet, while also appearing in the hands. A person feels a "tingling" in the joints of the fingers and alternating aching pain with numbness. Loss of control and coordination during simple actions: it is difficult for a person to hold a spoon or write with a pen on paper.

It is characteristic that the symptoms appear symmetrically: muscle weakness or tingling in the fingers appears simultaneously in both legs or arms. This excludes a number of other diseases associated with disorders of the human muscle structure or musculoskeletal system.

2. Visually noticeable increase in the abdomen.

Symptoms are also expressed by a strongly protruding abdomen. This is explained by the fact that the sick person has to completely rebuild from the upper to the abdominal type of breathing. This happens due to weakness in the diaphragm: it is becoming more and more difficult for the patient to enter and exhale with the chest.

3. Difficulty swallowing.

Weakened pharyngeal muscles interfere with the normal swallowing reflex. A person can easily choke on their own saliva. It is increasingly difficult for the patient to eat and chew - the muscles of the mouth are gradually weakened too.

4. Incontinence.

It is difficult for the patient to control the bladder or accumulated gases in the intestines.

Guillain-Barré syndrome affects almost all internal organs. Therefore, attacks of tachycardia, hypertension, visual impairment and other manifestations of body dysfunction are possible.

Why is the SGB dangerous?

Medical studies show statistics in which the disease most often develops gradually, over several weeks. A slight weakness in the limbs intensifies after a couple of weeks, and only then the syndrome begins to really bother the person.

On the one hand, this gives some time for consultations with doctors and clarification of the disease. But on the other hand, it threatens with untimely diagnosis and complication of treatment in the future. After all, the symptoms appear very slowly and in this form can easily be mistaken for the beginning of another disease.

In the acute form, the syndrome develops so quickly that after a day a large part of the body can become paralyzed. After tingling in the limbs, weakness appears in the shoulders, back, hips. The longer help is not provided, in the form of medical and hardware treatment, the more likely it is that the paralysis will not remain forever.

In the case of the acute form of GBS, when the syndrome develops rapidly, obvious difficulties in breathing are noticeable after a few hours. With a hyperdynamic course of the syndrome, you should immediately go to the hospital, where the patient can be helped, for example, by connecting to artificial respiration.

Treatment

Guillain-Barré pathology is successfully eliminated in more than seventy out of a hundred cases. Modern treatment of the syndrome is carried out at several levels:

• symptomatic;
• resuscitation;
• preparation;
• blood-purifying;
• muscle recovery;
• preventive.

With the acute development of the syndrome, in the first place, of course, treatment is carried out aimed at eliminating acute symptoms that require resuscitation procedures:

• connection to an artificial respiration apparatus in case of impaired lung function and a weak diaphragm;
• the use of a catheter for problems with urine output;
• installation of a tracheal tube and probe for problematic swallowing.

Symptomatic treatment includes the use of medications:

• laxatives for constipation;
• antipyretic, if the body temperature exceeds 38-39 degrees;
• medicines that regulate heartbeat and blood pressure;
• eye drops from overdrying of the mucous membrane of the eye in violation of the motor function of the eyelids.

Progressive syndrome can be stopped by hardware blood cleansing (plasmapheresis), in which part of the volume of circulating plasma is removed from the blood. Instead of plasma, isotonic sodium solution or other substitutes are injected into the blood.

The introduction of immunoglobulin intravenously is widely used. If the syndrome is not burdened with complications, this method gives positive results in a few months, and the patient has every chance to regain his normal healthy state.

Rehabilitation

Since Guillain-Barré syndrome causes damage not only to neurons, but also to the circumosseous muscles, a recovering patient sometimes has to re-learn how to walk, hold a spoon, etc.

In order to restore normal muscle activity, traditional treatment is used:

• massage and rubbing;
• physiotherapy;
• electrophoresis;
• taking baths for relaxation and a contrast shower for muscle tone;
• radon baths;
• application with beeswax or paraffin;
• medical gymnastics, etc.

At the recovery stages, treatment with a health-improving diet and vitamin therapy is prescribed. The body intensively replenishes the reserves of vitamin B, potassium, calcium and magnesium.

Patients who have had Guillain-Barré disease remain registered with a neurologist. They periodically undergo a preventive examination, the main task of which is to identify the prerequisites for a relapse.

Timely treatment can restore a person's ability to live a full life: to serve himself and not be afraid of an active lifestyle.

We bring to your attention a detailed video about this syndrome:

Guillain-Barré Syndrome- symptoms and treatment

What is Guillain-Barré Syndrome? We will analyze the causes of occurrence, diagnosis and treatment methods in the article of Dr. Zhuykov A.V., a neurologist with an experience of 19 years.

Definition of disease. Causes of the disease

Guillain-Barré Syndrome (GBS)- an acute autoimmune disease of the peripheral nervous system, characterized by muscle weakness. This disorder encompasses a group of acute disorders of the peripheral nervous system. Each variant is characterized by features of the pathophysiology and clinical distribution of limb and cranial nerve weakness.

In 70% of patients with GBS, a previous infectious disease was observed before the onset of neurological symptoms.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Guillain-Barré Syndrome Symptoms

Symptoms of acute respiratory viral infections or disorders of the gastrointestinal tract are observed in 2/3 of patients. The first symptoms of GBS are paresthesia of the fingers of the extremities, followed by progressive weakness of the muscles of the lower extremities and gait disturbance. The disease progresses over several hours or days, weakness of the upper limbs and cranial nerve palsy develop. The paralysis is usually symmetrical and, of course, of a peripheral nature. In half of patients, pain may be the initial complaint, making diagnosis difficult. Ataxia and pain are more common in children than in adults. Urinary retention is observed in 10%-15% of patients. Damage to the autonomic nerves is manifested by dizziness, hypertension, excessive sweating and tachycardia.

An objective examination reveals ascending muscle weakness, as well as areflexia. Tendon reflexes of the lower limbs are absent, but reflexes of the upper limb may be elicited. Muscle weakness can also involve the respiratory muscles. Damage to the cranial nerves is noted in 35-50%, autonomic instability in 26%-50%, ataxia - in 23%, dysesthesia - in 20% of cases.

The most common signs of autonomic dysfunction are sinus tachycardia or bradycardia and arterial hypertension. In patients with severe autonomic dysfunction, changes in peripheral vasomotor tone with hypotension and arterial pressure lability are observed.

Infrequent variants of the clinical course of the disease include fever at the onset of neurological symptoms, severe sensory impairment with pain (myalgia and arthralgia, meningismus, radicular pain), sphincter dysfunction.

The possibility of GBS should be considered in any patient with rapid onset of acute neuromuscular weakness. At an early stage, GBS should be distinguished from other diseases with progressive symmetrical muscle weakness, including transverse myelitis and myelopathy, acute toxic or diphtheritic polyneuropathy, porphyria, myasthenia gravis, and electrolyte disturbances (eg, hypokalemia).

The pathogenesis of Guillain-Barré syndrome

The neurophysiological processes underlying GBS are divided into several subtypes. The most common subtypes include:

• acute inflammatory demyelinating polyradiculopathy;
• acute motor axonal neuropathy;
• acute motor and sensory axonal neuropathy;
• Miller-Fisher syndrome, as a variant of GBS, is characterized by a triad of signs: ophthalmoplegia, ataxia and areflexia.

It is believed that GBS develops as a result of the production of antibodies against the protein of the infectious agent, which cross-react with gangliosides of human nerve fibers. Autoantibodies bind to myelin antigens and activate complement, forming a membrane attack complex on the outer surface of Schwann cells. Damage to the sheaths of the nerve trunks leads to conduction disturbances and muscle weakness (at a later stage, axonal degeneration can also occur). The demyelinating lesion is seen along the entire length of the peripheral nerve, including the nerve roots.

All types of nerves are affected, including autonomic, motor and sensory fibers. Involvement of motor nerves occurs much more often than sensory ones.

Complications of Guillain-Barré syndrome

Patients with GBS are at risk for life-threatening respiratory complications and autonomic disorders.

Indications for transfer to the intensive care unit include:

• rapid progression of motor weakness with damage to the respiratory muscles;
• ventilation respiratory failure;
• pneumonia;
• bulbar disorders;
• severe autonomic failure.

Treatment complications requiring intensive care include fluid overload, intravenous immunoglobulin anaphylaxis, or hemodynamic disturbances during plasmapheresis.

15%-25% of children with GBS develop decompensated respiratory failure, which requires mechanical ventilation. Respiratory disorders are more common in children with rapid disease progression, upper limb weakness, autonomic dysfunction, and cranial nerve involvement. Tracheal intubation may be required in patients to protect the respiratory tract, mechanical ventilation. In GBS, rapid progression, bilateral facial paralysis, and autonomic dysfunction predetermine an increased likelihood of intubation. Planning for early intubation is essential to minimize the risk of complications and the need for emergency intubation.

Autonomic dysfunction increases the risk of endotracheal intubation. On the other hand, dysautonomy may increase the risk of hemodynamic reactions to drugs used to induce anesthesia during intubation.

Signs indicating the need for mechanical ventilation:

1. ventilation respiratory failure;
2. increasing oxygen demand to maintain SpO2 above 92%;
3. signs of alveolar hypoventilation (PCO2 above 50 mm Hg);
4. a rapid decrease in vital capacity by 50% compared with the initial level;
5. inability to cough

Autonomic dysfunction is the main factor in mortality in GBS. Fatal cardiovascular collapse due to autonomic dysfunction occurs in 2%-10% of severely ill patients. Monitoring of heart rate, blood pressure, and electrocardiogram should continue for as long as patients require respiratory support. Transcutaneous pacing may be required for severe bradycardia. Hypotension is corrected by circulating blood volume (CBV) replenishment, and if the patient is unresponsive to CBV replacement, α-agonists such as norepinephrine, mezaton, epinephrine are used.

In unstable hemodynamics, continuous recording of arterial and central venous pressure should be carried out to control the volume of infusion therapy.

Arterial hypertension may occur, but this complication does not require special treatment unless it is complicated by pulmonary edema, encephalopathy, or subarachnoid hemorrhage.

Diagnosis of the Guillain-Barré syndrome

Instrumental diagnostics

Lumbar puncture

On lumbar puncture, CSF results usually show an elevated protein level (>45 mg/dL), without pleocytosis (<10 клеток/мм3) (белково-клеточная диссоциация). Иногда уровень белка может оставаться нормальным, при умеренном повышении количества клеток (10-50 клеток/мм3). Цитоз выше, чем 50 клеток/мм3, свидетельствует против диагноза ГБС. В ряде случаев могут быть необходимы повторные люмбальные пункции для уточнения диагноза.

Neurofunctional diagnostics

ENMG (Electroneuromyography)- the only instrumental diagnostic method that allows confirming the diagnosis of GBS and clarifying the nature of pathological changes (demyelinating or axonal) and their prevalence.

Needle electromyography is characterized by the presence of signs of the current denervation-reinnervation process in polyneuropathy. Examine the distal muscles of the upper and lower extremities (eg, tibialis anterior, extensor digitorum common), and if necessary, proximal muscles (eg, quadriceps femoris).

ENMG study in patients with GBS depends on the clinical manifestations:

• with distal paresis, long nerves on the arms and legs are examined: at least four motor and four sensory (motor and sensory portions of the median and ulnar nerves; peroneal, tibial, superficial peroneal and sural nerves on one side).

Assessment of the main ENMG parameters:

• motor responses (distal latency, amplitude, shape and duration), the presence of conduction blocks and dispersion of responses; the speed of propagation of excitation along the motor fibers in the distal and proximal areas is analyzed.
• sensory responses: amplitude and speed of excitation conduction along sensory fibers in the distal regions.
• late ENMG phenomena (F-waves): latency, form and amplitude of responses, chronodispersion value, dropout percentage are analyzed.
• with proximal paresis, it is mandatory to study two short nerves (axillary, musculocutaneous, femoral, etc.) with an assessment of the parameters of the motor response (latency, amplitude, shape).

The first signs of the denervation process appear two to three weeks after the onset of the disease, the signs of the reinnervation process - a month later.

Treatment of Guillain-Barré syndrome

General supportive care and care

Patients requiring intensive care require meticulous general care. Constipation is observed in more than 50% of patients with GBS as a result of dynamic intestinal obstruction.

Paracetamol is used for pain. Katadolon and tramadol are used for severe pain syndrome. For neuropathic pain, carbamazepine and gabapentin are effective.

In the treatment of GBS, various types of immunomodulatory therapy are being undertaken.

Intravenous immunoglobulin is given as a daily infusion (at a dose of 0.4 g/kg/day) for 5 days during the first 2 weeks of illness. A second course of immunoglobulin may be required in 5%-10% of patients, with a negative trend after initial improvement. The mechanism of action of intravenous immunoglobulin is probably multifactorial and is believed to include modulation of complement activation, neutralization of idiotypic antibodies, suppression of inflammatory mediators (cytokines, chemokines).

Side effects of immunoglobulin include headache, myalgia and arthralgia, flu-like symptoms, and fever. Patients with IgA deficiency may develop anaphylaxis after the first course of intravenous immunoglobulin.

Plasmapheresis promotes the removal of antibodies involved in the pathogenesis of GBS. During each session, 40-50 ml/kg of plasma is replaced with a mixture of 0.9% sodium chloride solution and albumin. Plasmapheresis leads to a reduction in recovery time and a decrease in the need for mechanical ventilation. These benefits are evident if plasmapheresis is performed within the first two weeks of illness onset. Complications associated with plasmapheresis include hematoma at the site of venipuncture, pneumothorax after catheterization of the subclavian vein, and sepsis. Plasmapheresis is contraindicated in patients with severe hemodynamic instability, bleeding, and sepsis.

The combination of plasmapheresis and immunoglobulin has shown no clinical benefit.

Corticosteroids should not be used in the treatment of GBS, as they do not hasten recovery, do not reduce the likelihood of mechanical ventilation, and do not affect the long-term outcome.

Forecast. Prevention

GBS remains a serious disease despite improved treatment outcomes. Compared with adults, children often have a more favorable course of the disease, with a complete rather than a partial recovery. The causes of adverse outcomes in GBS are respiratory failure, complications of mechanical ventilation (pneumonia, sepsis, acute respiratory distress syndrome and thromboembolic complications), cardiac arrest secondary to dysautonomia.

Recovery usually begins two to four weeks after symptoms stop progressing. The average time from the onset of the disease to complete recovery is 60 days. Data on the long-term outcome of GBS are limited. 75% - 80% of patients recover completely. About 20% of patients cannot walk after six months.

The younger age group (less than 9 years), rapid progression and maximum muscle weakness, the need for mechanical ventilation are important predictors of long-term motor deficit.

Guillain-Barré syndrome is a severe autoimmune disease that affects the peripheral nervous system. The most common manifestation is acute tetraparesis, when the movements of all four limbs become almost impossible. Other movements also stop, including swallowing, the ability to lift the eyelids, and spontaneous breathing. Despite this, the course of the disease is benign, most cases end in recovery. Less common is the transition to a chronic course or relapses. Guillain-Barré syndrome occurs in all countries, regardless of their level of development, with the same frequency - about 2 cases per 100 thousand population, there is no gender dependence. The disease can affect patients of all ages.

Why does the syndrome occur?

The leading mechanism of development is autoimmune. In most cases, the onset of the disease occurs in the first three weeks after an acute respiratory or intestinal infection. Since a sufficient amount of time has passed since the moment of the disease, and the symptoms characteristic of the infectious process have time to pass, the patients themselves, as a rule, do not associate these conditions with each other. The cause may be pathogens such as:

• Epstein-Barr virus or human herpes type 4;
• mycoplasma;
• campylobacter, which causes infectious diarrhea;
• cytomegalovirus.

The researchers found that the "sheath" of these pathogens is similar to the myelin sheath of the axon of peripheral nerves. This similarity causes the nerves to be attacked by antibodies that are initially produced and circulate in the blood in response to the appearance of an infectious agent. This phenomenon is called "molecular mimicry" and explains why immune complexes attack the body's own tissues.

Cases are described when the syndrome occurs after vaccination, after surgical operations and abortions, hypothermia, stress. In some cases, the cause cannot be found.

How does the syndrome manifest itself?

Within a few days, up to a maximum of 1 month, muscle weakness in the legs increases, difficulties arise when walking. Further, the hands weaken, the mimic muscles suffer last. Such symptoms have a separate name - Landry's ascending paralysis.

But sometimes the paralysis starts from above, from the arms, spreading down, but all the limbs are always affected.

Every fifth case is accompanied by paralysis of the muscles of the body, namely the diaphragm and intercostal muscles. With such paralysis, breathing becomes impossible, artificial ventilation of the lungs is required.

A frequent manifestation is bulbar syndrome or bilateral paralysis of the muscles of the soft palate, when swallowing and clear speech are impossible.

Along with motor fibers, sensory ones are sometimes also affected. Sensitivity disorders develop, tendon reflexes decrease, pain in the extremities disturbs. The pains are pronounced "neuropathic" in nature - burning, feeling the passage of current, tingling. Pelvic disorders are rare, but the most common is urinary retention, which in some cases is combined with excess urine production.

Autonomic dysfunction joins, which is manifested by fluctuations in blood pressure, palpitations, other cardiac arrhythmias, sweating, and lack of intestinal motility.

Classification

There are several forms depending on whether the myelin sheath or axon is damaged, according to the severity of the course and the prognosis:

• acute inflammatory demyelinating polyneuropathy or AIDP, when the myelin sheath is destroyed;
• acute motor or sensory-motor axonal neuropathy, when axons are destroyed;
• rare forms - Miller-Fisher syndrome, acute pandysautonomy and others, the frequency of which does not exceed 3%.

Diagnostic measures

• muscle weakness in the limbs, which progresses;
• decrease or absence of tendon reflexes from the first days of illness.

WHO also highlights additional signs confirming the diagnosis, which include:

• symmetry of the lesion;
• symptoms increase no more than 4 weeks;
• sensory disturbances of the "gloves and socks" type;
• involvement of the cranial nerves, especially the facial;
• possible spontaneous restoration of functions after stopping the progression of the disease (the so-called "plateau");
• the presence of vegetative disorders;
• absence of hyperthermia (if there is a fever, then it is caused by other infections);
• an increase in the amount of protein in the cerebrospinal fluid, while its cellular composition does not change (protein-cell dissociation).

The final diagnosis is impossible without electroneuromyography or ENMG. This study reveals which part of the nerve is damaged - the myelin sheath or the axon. ENMG also accurately determines the extent of the lesion, its severity and the possibility of recovery.

Since, in addition to the Guillain-Barré syndrome, there are a number of acute, subacute and chronic polyneuropathies, electromyography allows differential diagnosis between them and contributes to the development of the correct treatment tactics.

Often, a lumbar puncture is necessary for diagnosis, followed by a study of the cerebrospinal fluid, and such tests as can be informative:

• blood for autoantibodies to neuronal structures;
• blood for class A gamma globulins (especially if immunoglobulin therapy is planned);
• biomarkers of neurofilament (part of the cytoplasm of a neuron);
• tau protein markers (a special protein that destroys a neuron).

Specialists of the CELT clinic additionally use their own algorithms for differential diagnosis, which make it possible to reliably distinguish Guillain-Barré syndrome from other diseases that cause progressive muscle weakness in all limbs or tetraparesis.

Our doctors

Treatment rules

To date, two main pathogenetic methods for the treatment of Guillain-Barré syndrome are known, and both are successfully used by CELT specialists. These are plasmapheresis and intravenous immunotherapy. These methods can be used in isolation or used in combination, it all depends on the specific clinical situation. Treatment is aimed at removing the immune complexes circulating in the patient's blood or neutralizing them. Both methods of treatment are equivalent, almost always lead to recovery. Treatment stops the process of destruction of peripheral nerves, reduces the duration of the recovery period, and helps to reduce neurological deficits.

Plasmapheresis is a blood purification operation. Most often, hardware plasmapheresis is used on continuous separators, during which the blood taken from the body is divided into formed elements (or blood cells) and plasma (or serum). All toxic substances are in the plasma, so it is removed. The same blood cells are returned to the person, diluted if necessary with plasma-substituting solutions or donor plasma. The duration of the procedure is about one and a half hours, the entire course consists of 3 or 5 sessions. No more than 50 ml / kg of plasma body weight is removed at a time.

In the process of treatment, blood parameters are monitored: electrolytes, hematocrit, clotting time, and others.

Intravenous immunotherapy is the administration of a preparation of human immunoglobulin class G. These immunoglobulins stop the production of antibodies to one's own nerves, while reducing the production of substances that support inflammation. These drugs are indicated for the pathogenetic treatment of Guillain-Barré syndrome in both adults and children.

Along with specific treatment, careful patient care is provided, including the prevention of pressure sores, pneumonia, and contractures. Treatment of associated infections is often required. Prevention of venous thrombosis is carried out, feeding through a tube is carried out, excretory function is controlled. Recumbent patients undergo passive gymnastics, as well as early verticalization, which avoids blood flow disorders. With the threat of developing contacture (immobility of the joints), paraffin procedures are possible. If necessary, motion simulators based on biofeedback are used.

Patients with damage to the myelin sheaths recover faster, while axonal damage requires a longer rehabilitation period. Axonal lesions often leave behind a neurological deficit that is difficult to correct.

Prevention

The main method is the complete cure of infections that we consider banal, familiar. Guillain-Barré syndrome often develops with a slight weakening of the immune system, which is possible in every person.

The easiest way to be on the safe side is to check your current immune status. It will take only a few days, and the detected deviations can be treated in time.

The doctors of the CELT clinic have at their disposal not only the latest diagnostic equipment, but also the latest treatment methods that have received worldwide recognition. The main role in prevention belongs to the patient who seeks examination and treatment in a timely manner.

Guillain-Barré syndrome is a group of acute autoimmune diseases characterized by rapid progression. The period of rapid development is approximately one month. In medicine, this disorder has several names - Landry's palsy or acute idiopathic polyneuritis. The main symptoms are muscle weakness and lack of reflexes, which occur against the background of extensive nerve damage (as a result of an autoimmune process). This means that the human body accepts its own tissues as foreign, and the immune system forms antibodies against the affected nerve sheaths.

Diagnosis is based on a hardware study of the patient and the presence of specific signs on at least one limb. This disorder affects people of any age group, regardless of gender, but it is most often seen in people of middle age from 30 to 50 years, but, nevertheless, it is often observed in children.

Treatment of the disease is carried out only in a hospital, as very often patients require artificial ventilation of the lungs. The prognosis after therapy, rehabilitation and recovery is favorable in half of the cases.

Etiology

In most cases, the reasons for the expression of Guillain-Barré syndrome are unclear, since it refers to autoimmune processes. But experts identify several predisposing factors:

• complex course of infectious diseases;
• damage to the upper respiratory tract;
• infectious nature;
• complications from surgery or vaccination;
• craniocerebral diseases or injuries resulting in swelling or neoplasms in the brain. That is why the likelihood of the syndrome affecting the human nervous system is high;
• genetic predisposition. If one of the close relatives was diagnosed with this disease, then the person automatically falls into the risk zone. For this reason, the disease can manifest itself in a newborn child and school-age children;
• infections belonging to the group of viruses.

Experts agree that Guillain-Barré syndrome is expressed during or after the course of the above diseases.

Varieties

Currently, there are several forms of the course of this disorder:

• demyelinating - occurs in most cases. It got its name because during the course, an element such as myelin is significantly damaged;
• axonal - characterized by a violation of the processes that feed the nerves - axons. The main symptom is weakness in the joints and muscles;
• motor-sensory - the flow is similar to the previous form. Signs include weakness and significant numbness of the skin.

A separate type of syndrome is one that affects vision. At the same time, it is quite difficult for a person to move his eyes, his visual acuity is disturbed, and there is unsteadiness while walking.

Depending on the development, Guillain-Barré syndrome is characterized by:

• gradual course - weakness increases within a few weeks, after a person ceases to perform elementary functions, for example, holding cutlery while eating or writing with a pen. This course is good because a person has time to consult a doctor. The danger lies in untimely treatment and the threat of complications, especially in children or pregnant women;
• acute development - the disease develops so quickly that in a day a person can be partially paralyzed. The spread of weakness begins with the lower extremities and gradually passes into the shoulders, back and pelvis. The more it spreads, the more likely it is to become paralyzed.

Symptoms

The main symptom of Guillain-Barré syndrome is rapidly progressive weakness, which stops its development after a month from the first manifestation of other symptoms. It most often affects the lower extremities, and after three weeks of leakage, it passes to the upper ones. First, discomfort is felt by a person in the shin area, after which the feet are affected and at the same time the hands are affected. It is noteworthy that weakness, numbness and tingling are simultaneously manifested in both the lower and upper limbs. In addition, the following signs are observed, but they occur on an individual basis:

• difficulty during swallowing, not only when eating food, but also when taking liquids;
• violations of respiratory functions, up to the point that a person cannot breathe on his own;
• the occurrence of pain of varying intensity in the back and affected limbs. Such a symptom is difficult to treat;
• heart rate disorder, in some it can be very fast, in others it can be slowed down;
• paralysis of the muscles of the face;
• loss of tendon reflexes;
• lack of sensitivity in the feet and hands;
• increased sweating;
• fluctuations in blood pressure;
• possible occurrence of uncontrolled emission of urine;
• shaky and unsteady gait;
• changes in the volume of the abdomen. This happens because it is difficult for a person to breathe with the help of the diaphragm, and he is forced to use the abdominal cavity;
• impaired coordination of movements;
• decreased visual acuity - most often there are bifurcation and strabismus.

Such symptoms are inherent in both adults and children and newborns.

Complications

For any person, there is a possibility of death, due to the possible occurrence or complete cardiac arrest. In addition, there is a high probability that paralysis will remain until the end of life. When diagnosing this syndrome in a pregnant woman, there is a risk of miscarriage or death of the fetus in the womb.

Diagnostics

The main task of a specialist during diagnosis is to exclude other diseases of a neurological nature, which may be, and various lesions of the central nervous system. Determination of the diagnosis consists in the following activities:

• collection by the doctor of complete information about previous diseases and clarification of the first time of occurrence of unpleasant symptoms;
• implementation of a neurological examination, which consists in assessing motor reflexes, sensitivity of the affected limbs, eye movements, gait, as well as the reaction of the heart to a sharp change in body position;
• blood test - carried out to detect the presence of antibodies and detect the inflammatory process;
• cerebrospinal fluid sampling - for this, a puncture is performed, i.e. a puncture in the lumbar back, during which up to two milliliters of fluid is collected to count blood cells, proteins and the presence of antibodies in it;
• daily monitoring of blood pressure;
• studies of respiratory functions - using spirometry;
• conducting ENMG. This will allow the specialist to assess the passage of the nerve impulse. With this syndrome, it will be slow, as myelin and axon pathology are exposed;
• additional consultations with specialists such as an immunologist and an obstetrician-gynecologist.

In addition, another sign to confirm the diagnosis is the presence of weakness and lack of reflexes in more than one limb. After receiving all the diagnostic results, the specialist prescribes the most effective individual therapy tactics.

Treatment

The main goal of the treatment is:

• restoration of vital functions;
• elimination of symptoms of an autoimmune disease using specific techniques;
• the rehabilitation period of the patient;
• prevention of complications.

The first thing to do is to place the patient in a hospital, and if necessary, connect him to a lung ventilator, install a catheter in case of violation of urine emission, use a special tube or probe if swallowing is difficult. If the paralysis is clearly expressed, it is necessary to provide proper care - change the position of the human body every two hours, take hygiene measures, feed, monitor the functioning of the intestines and bladder.

Specific treatment is to use:

• plasmapheresis, i.e., blood purification from antibodies - from four to six operations can be performed, the interval should be one day. Thanks to its use, it is possible to reduce the severity of paralysis. The course of therapy will be different for children and adults;
• injections of immunoglobulin (protective antibodies), which were taken from healthy people - are used once a day for five days. Its use improves prognosis.

To eliminate symptoms, the patient is prescribed:

• drugs to restore normal heart rhythm;
• antibiotics if infection occurs;
• heparin - to avoid the occurrence of blood clots;
• hormonal medications;
• antioxidants - improve metabolism.

Since Guillain-Barré syndrome has a negative effect on the muscles, sometimes a person has to re-learn how to perform elementary movements. For this purpose, rehabilitation methods are used:

• a course of therapeutic massage of the affected limbs;
• the use of physiotherapy;
• taking contrast and relaxing baths that will restore muscle tone. Radon baths are often used;
• compress based on wax and paraffin;
• performing physical therapy exercises;
• a special diet enriched with vitamins and nutrients (potassium, calcium and magnesium).

After the normalization of the patient's state of health, he must be registered with a neurologist. In addition, it will be necessary to undergo preventive examinations in order to identify the prerequisites for a relapse of the disease at an early stage. If the treatment was started in a timely manner, it makes it possible to return the patient to a full, active life.

Synonyms:acute demyelinating polyradiculo(neuro)pathy, acute post-infectious polyneuropathy, Landry-Guillain-Barré syndrome, obsolete. Landry's ascending paralysis.

The term Guillain-Barré syndrome is an eponym (i.e. giving a name) for a set of syndromes of acute inflammatory polyradiculoneuropathy of an autoimmune nature, a characteristic manifestation of which is a progressive symmetrical flaccid paralysis in the muscles of the extremities and muscles innervated by cranial nerves (with the possible development of dangerous respiratory and swallowing disorders) with or without sensory and autonomic disorders (unstable blood pressure, arrhythmias, etc.). ) .

Along with the fact that Guillain-Barré syndrome is classically presented as a demyelinating polyneuropathy with ascending weakness, called acute inflammatory demyelinating polyneuropathy and accounting for 75-80% of cases, Several atypical variants or subtypes of this syndrome have been described and identified in the literature, representing a heterogeneous group of immune-dependent peripheral neuropathies. : Miller-Fisher syndrome (3 - 5%), acute motor axonal polyneuropathy and acute sensorimotor axonal polyneuropathy (make up 15-20%), and more rare acute sensory polyneuropathy, acute pandysautonomy, acute cranial polyneuropathy, pharyngo-cervico-brachial variant. As a rule, these variants are clinically usually more difficult than the main one.

EPIDEMIOLOGY

Guillain-Barré syndrome most common acute polyneuropathy. The incidence is 1.7 - 3.0 per 100,000 population per year, approximately equal in men and women, has no seasonal fluctuations, and is more common in old age. The incidence at the age of 15 years is 0.8 - 1.5, and at the age of 70 - 79 years it reaches 8.6 per 100,000. Mortality ranges from 2 to 12%.

ETIOLOGY and PATHOGENESIS

Etiology of the disease not completely known.

Guillain-Barré syndrome is post-infectious autoimmune disease.

1 - 3 weeks before the development of the syndrome, 60 - 70% of patients have respiratory or gastrointestinal infections, which can be:
viral nature(cytomegalovirus, Epstein-Barr virus)
bacterial nature(caused by Campylobacter jejuni)
mycoplasmal nature

The syndrome is much less common:
after peripheral nerve injury
surgical interventions
vaccinations
with tick-borne borreliol (Lyme disease)
sarcoidosis
systemic lupus erythematosus
AIDS
malignant tumors

Both cellular and humoral immune mechanisms likely play a role in the development of the disease.

infectious agents, apparently trigger an autoimmune reaction directed against peripheral nervous tissue antigens (lemmocytes and myelin), in particular with the formation of antibodies to peripheral myelin - gangliosides and glycolipids, such as GM1 and GD1b, located on the myelin of the peripheral nervous system.

!!! The titer of antibodies to GM1 and GD1b correlates with the clinical course of the disease.

Also, apparently an immunological cross-reaction is possible between Campylobacter jejuni lipopolysaccharides and GM1 ganglioside. There is still no final opinion on the nature of the antigen or antigens that cause the development of cascade immune reactions.

The myelinated nerve fiber consists of an axial cylinder (actually a process containing cytoplasm) covered with a myelin sheath.

Depending on the purpose of the lesion, they distinguish:
demyelinating variant diseases (more common)
axonal variant diseases

the disease affects the myelin sheaths of axons, demyelination is observed without the involvement of the axial cylinders of axons, and therefore the speed of conduction along the nerve fiber decreases with the development of paresis, but this condition is reversible. These changes are detected primarily at the junction of the anterior and posterior roots of the spinal cord, while only the anterior roots may be involved (which explains the variants with purely motor disorders), and other parts of the peripheral nervous system may also be involved. The demyelinating variant, in particular, is characteristic of the classic Guillain-Barré syndrome.

The axonal variant of the lesion is much less common. , more severe, in which degeneration of the Waller type (distal to the site of the lesion) of the axial axon cylinders develops with the development, as a rule, of severe paresis or paralysis. In the axonal variant, the axonal antigens of the peripheral nerves are primarily attacked by the autoimmune attack, and a high titer of GM1 antibodies is often found in the blood. This variant, in particular, observed in acute sensorimotor axonal polyneuropathy, is characterized by a more severe and less reversible course of the syndrome than in the first case.

Most cases of Guillain-Barré syndrome are characterized by self-limiting autoimmune damage., in particular, due to the elimination of autoantibodies after a certain time, i.e. reversible nature of the lesion. For the clinic, this means that if a seriously ill patient with paralysis, swallowing disorders and respiratory failure is given adequate non-specific supportive therapy (prolonged mechanical ventilation, prevention of infectious complications, etc.), then recovery can often be as complete as when using specific therapy, but will come in more late dates.

CLINIC

The main manifestation of the disease is:
progressive over several days or weeks (average 7-15 days) relatively symmetrical flaccid tetraparesis - weakness in the arms and legs with low muscle tone and low tendon reflexes
tetraparesis initially more often involves the proximal legs, which is manifested by difficulty climbing stairs or getting up from a chair
only after a few hours or days the hands are involved - "ascending paralysis"

The disease can quickly (within a few hours) lead to paralysis of the respiratory muscles.

Often the initial manifestation of Guillain-Barré syndrome is paresthesia(an unpleasant feeling of numbness, tingling, burning, crawling) in the tips of the fingers and toes.

The following variants of the onset of the disease are less common:
Paresis primarily develops in the arms ("descending paralysis").
Paresis develops in the arms and legs at the same time.
The hands remain intact during the course of the disease (paraparetic variant of the syndrome).
Initially, the paralysis is unilateral, but after a while, the defeat of the other side is sure to join.

Depending on the severity of symptoms, there are:
mild illness- can walk more than 5 m without assistance
the average degree of the disease- moderate paresis is noted (the patient cannot walk confidently without support or cannot walk more than 5 m on his own), pain and sensitivity disorders
severe disease- cases are considered, accompanied by paralysis or severe paresis of the limbs, often with respiratory disorders

The course of the disease
escalation phase within 7 - 15 days it is replaced by a plateau phase (stabilization of the process), lasting 2 - 4 weeks, and then recovery begins, lasting from several weeks to months (sometimes up to 1 - 2 years).

Complete recovery occurs in 70% of cases.
Rough residual paresis of the extremities and sensory disturbances persist in 5–15% of patients.
In 5 to 10% of cases, the syndrome recurs, often after completion of a course of treatment, or is provoked by a respiratory or intestinal infection.

Clinical variants of the disease

In a typical case of Guillain-Barré syndrome:
sensory disturbances, as a rule, are moderately expressed and are represented by paresthesia, hypalgesia (reduced sensitivity), hyperesthesia (increased sensitivity) in the distal extremities of the "socks and gloves" type, sometimes mild violations of deep sensitivity, pain in the muscles of the shoulder and pelvic girdle, back, radicular pain, symptoms of tension (may persist against the background of regression of paralysis).
myalgias usually subside spontaneously after a week
with the upward direction of development, paresis captures the muscles
legs, arms, torso
respiratory muscles
cranial muscles, mainly: mimic (characterized by bilateral lesions of the facial nerves)
bulbar with the development of aphonia - loss of sonority of the voice, dysarthria - speech disorders, dysphagia - swallowing disorders up to aphagia - inability to swallow
less often, the external muscles of the eyes - paresis of the abduction of the eyeball
may be involved flexors of the neck and muscles that raise the shoulders, weakness of the intercostal muscles and diaphragm with the development of respiratory failure.
characteristic are shortness of breath on exertion, shortness of breath, difficulty swallowing, speech disorders.
all patients have loss or sharp depression of deep tendon reflexes, the degree of which may not correspond to the severity of paralysis
is also developing muscle hypotonia and malnutrition (in the late period)
autonomic disorders in the acute period occur in more than half of the cases of the disease, and are often the cause of death; there is a violation of sweating, intestinal paresis, an increase or decrease in blood pressure, orthostatic hypotension, tachycardia or bradycardia, supraventricular, ventricular arrhythmias, cardiac arrest.

In 17 - 30% of patients may develop (acutely, within hours and days) respiratory failure requiring mechanical ventilation, as a result of damage to the phrenic nerve, paresis of the diaphragm and weakness of the respiratory muscles. With paresis of the diaphragm, paradoxical breathing develops with retraction of the abdomen on inspiration.

Clinical signs of respiratory failure are:
rapid breathing (tachypnea)
sweat on the forehead
weakening of the voice
the need to pause for breath during a conversation
weakening of the voice
tachycardia with forced breathing
also with paresis of the bulbar muscles, it is possible to develop a violation of the patency of the respiratory tract, a violation of swallowing (with the development of aspiration) and speech

In the initial stage of the disease, fever is usually absent.

ATYPICAL VARIANTS of Guillain-Barré Syndrome

Miller-Fisher Syndrome- occurs in 5% of cases of Guillain-Barré syndrome.
Appears:
motor ataxia - gait disturbance and ataxia (coordination disorder) of the trunk muscles
ophthalmoplegia involving the external, rarely internal muscles of the eye
areflexia
typical muscle strength
usually results in full or partial recovery within weeks or months
rarely, in severe cases, tetraparesis, paralysis of the respiratory muscles can join

Acute sensory polyneuropathy
Appears:
rapid onset with severe sensory disturbances and areflexia, rapidly involving the extremities and symmetrical in nature
sensitive ataxia (impaired coordination of movements)
the prognosis is often favorable

Acute motor axonal polyneuropathy
Closely associated with C. jejuni intestinal infection, with about 70% seropositive for C. jejuni.
It is clinically manifested by: purely motor disorders: increasing paresis of the ascending type.
Diagnosed by electromyography for purely motor axonopathy.
This type is characterized by a higher proportion of pediatric patients.
In most cases, the prognosis is favorable.

Acute sensorimotor axonal polyneuropathy
It usually presents with rapidly developing and severe tetraparesis with prolonged and poor recovery.
As well as acute motor axonal polyneuropathy, it is associated with diarrhea caused by C. jejuni.

Acute pandysautonomy
Occurs rarely.
It proceeds without significant motor or sensory disturbances.
Disorders of the function of the autonomic nervous system are manifested:
severe postural hypotension
postural tachycardia
fixed pulse
constipation
urinary retention
sweating disorders
decreased salivation and lacrimation
pupillary disorders

Pharyngo-cervico-brachial variant
It is characterized by isolated weakness in the facial, oropharyngeal, neck, and upper limb muscles without involvement of the lower limbs.

Acute cranial polyneuropathy
It is manifested by the involvement of only cranial nerves in the pathological process.

COMPLICATIONS
Paresis and paralysis in the limbs, neck.
Persistent loss of sensitivity.
Thrombosis of deep veins of the leg.
In 5% of patients, chronic inflammatory demyelinating polyradiculoneuropathy with a relapsing or progressive course, sensitive to corticosteroids, subsequently develops.
Death due to respiratory failure, pneumonia, pulmonary embolism, cardiac arrest, sepsis, respiratory distress syndrome, dysfunction of the autonomic nervous system.

DIAGNOSTICS

Polyradiculoneuritis should be suspected with the development of a relatively symmetrical increasing muscle weakness in the limbs. Characteristic of the disease is acute or subacute ascending flaccid tetraparesis with areflexia.

Main diagnostic criteria for Guillain-Barré syndrome:
increasing muscle weakness in at least two limbs
a significant decrease in muscle strength, up to a complete loss, of tendon reflexes

Additional diagnostic criteria are:
decrease in the speed of conduction of nerve impulses through the muscles with the formation of a conduction block during EMG
protein-cell dissociation in the cerebrospinal fluid

Supporting the diagnosis:
disease progression within 4 weeks
start of recovery in 2 - 4 weeks
relative symmetry of symptoms
lack of pronounced sensory disturbances
cranial nerve involvement (primarily bilateral facial nerve involvement)
autonomic dysfunction
absence of fever at the onset of the disease
not characteristic of pelvic disorders
(neurogenic urinary disorders)

Study of cerebrospinal fluid
during the 1st week of the disease, the protein content in the cerebrospinal fluid remains normal
starting from the 2nd week, protein-cell dissociation is detected - an increased protein content with normal or slightly increased cytosis (no more than 30 cells in 1 μl.)
with higher cytosis, another disease should be sought
against the background of a high level of protein, the appearance of congestive nipples of the optic nerves is possible

Electromyographic study
It allows to identify the peripheral nature of the lesion, as well as to differentiate the demyelinating and axonal variant of the disease.
With demyelinating variant the disease is characterized by: a decrease in the amplitude of the M-response against the background of signs of demyelination of nerve fibers - a decrease in the speed of conduction along motor fibers by more than 10% of normal, lengthening of the distal latency, partial blocks of conduction.
With axonal a decrease in the amplitude of the M-response is detected against the background of a normal conduction velocity along the motor fibers (or a decrease in velocity, but not more than 10%), a normal value of the distal latency, and an F-response.

Determination of plasma autoantibodies
It has limited diagnostic value.
Usually not performed as a routine study.
Investigated for scientific purposes and may be useful in complex, diagnostically unclear cases, in particular for the diagnosis of acute axonal lesions.
Antibodies to glycolipids (ganglioside GM-1 and GQ1b) are detected in blood plasma in 60-70% of patients in the acute phase of the disease.
GM1 antibodies are often found in both motor axonal neuropathy and acute inflammatory demyelinating polyneuropathy (classic). Previous intestinal infection with C. jejuni is strongly associated with high titers of anti-GM-1 antibodies.
Antibodies to GQ1b are found in patients with Guillain-Barré syndrome with ophthalmoplegia, including patients with Miller-Fischer syndrome.

DIFFERENTIAL DIAGNOSIS

The possibility of the following diseases, which may be accompanied by a similar clinical picture, should be excluded:
tumors and vascular myelopathy of the spinal cord
stem or spinal stroke
diphtheria polyneuropathy
periodic paralysis
polymyositis
polio
botulism
myasthenia gravis
hysteria
polyneuropathy of "critical conditions"
Wernicke's encephalopathy
stem encephalitis

TREATMENT

Treatment of Guillain-Barré syndrome includes two components:
non-specific- maintenance therapy
specific - plasmapheresis therapy or pulse therapy with class G immunoglobulin.

!!! Due to the possibility of developing decompensation with severe respiratory failure within a few hours, as well as cardiac arrhythmias, it is necessary to treat Guillain-Barré syndrome in the acute phase as an emergency.

In cases of development of acute respiratory failure in a medical institution, it must be possible to conduct long-term artificial ventilation of the lungs.

In severe cases with early development of acute respiratory failure, treatment is carried out in an intensive care unit or intensive care unit:
conduct hourly monitoring VC, blood gases, blood electrolytes, heart rate, blood pressure, the state of the bulbar muscles (the appearance and increase of swallowing disorders that do not bring relief to cough, hoarseness, speech disorders)
with bulbar palsy with swallowing disorders, choking, pouring out the drink through the nose, the introduction of a nasogastric tube is indicated, and often intubation (to prevent aspiration and aspiration pneumonia)
tracheal intubation indicated with mechanical ventilation with the development of respiratory failure, if the VC drops below 12 - 15 ml / kg, and with bulbar paralysis and violations of swallowing and speech below 15 - 18 ml / kg.
with no tendency to recover spontaneous breathing within 2 weeks, a tracheostomy is performed

!!! Corticosteroids are not currently used because they have been shown to be ineffective. They do not improve the outcome of the disease.

SPECIFIC THERAPY

Specific therapy using plasmapheresis or intravenous administration of high doses of immunoglobulin begins soon after diagnosis. Approximately equal effectiveness of both methods of treatment is shown, as well as the absence of an additional effect from a combination of these methods. Currently, there is no consensus on the choice of specific therapy.

With a light flow Guillain-Barré syndrome, taking into account the fact that there is a high probability of spontaneous recovery, the treatment of patients can be limited to non-specific and supportive therapy.

With an average severity of the process, and especially in severe cases, specific therapy begins as early as possible.

Treatment with immunoglobulin has some advantage over plasmapheresis, since it is easier and more convenient to use, has a significantly lower number of side effects, is easier on the patient, and therefore immunoglobulin is the drug of choice in the treatment of Guillain-Barré syndrome.

Intravenous pulse therapy with immunoglobulin
Intravenous pulse therapy with immunoglobulin (IgG, preparations - octagam, sandoglobulin, intraglobulin, human normal immunoglobulin) is indicated for patients who are unable to walk more than 5 m without assistance, or more severe (with paralysis, respiratory and swallowing disorders) patients with maximum the effectiveness of the drug at the beginning of therapy within 2 to 4 weeks from the onset of the disease. It is administered intravenously at a dose of 0.4 g / kg / day for 5 days (total course dose of 2 g / kg or about 140 g). An alternative scheme for the administration of the same course dose: 1 g / kg / day in two administrations for two days. Its use is limited by its high cost.

Plasmapheresis
Plasmapheresis administered in the phase of disease progression (approximately in the first two weeks) almost doubles the recovery process and reduces the residual defect. It is prescribed in moderate and severe cases according to the scheme of 4 - 6 sessions every other day, with an exchange of 50 ml / kg per session (at least 35-40 ml of plasma per kg of body weight), in total for the course a total of 200 - 250 ml / kg (at least 160 ml of plasma per 1 kg of body weight per course). In mild cases and in the recovery phase, plasmapheresis is not indicated. Plasmapheresis showed a rather high efficiency when administered to seriously ill patients, when therapy was started more than 30 days after the onset of the disease.

In 5-10% of patients, a relapse of the disease occurs after the end of treatment with plasmapheresis or immunoglobulin.. In this case, either resume treatment with the same method, or use an alternative method.

NON-SPECIFIC THERAPY

It is necessary to prevent deep vein thrombosis of the lower leg in bedridden patients (especially with paralysis in the legs):
oral anticoagulants of indirect action phenylin or warfarin are used in doses that stabilize the INR at the level of 2.0, or fraxiparine (nadroparin) 0.3 ml. s / c 1 - 2 times / day, or sulodexide (Wessel Due F) 2 times a day, 1 ampoule (600 LSU) / m for 5 days, then orally 1 caps (250 LSU) 2 times a day
prophylaxis is carried out before the patient begins to get out of bed
if thrombosis has developed before the start of therapy, prophylaxis is carried out according to the same scheme
also apply bandaging with an elastic bandage of the legs to the middle of the thigh (or use stockings with graduated compression) and raising the legs by 10-15
shows passive and, if possible, active "walking in bed" with bending the legs, emitting walking for 5 minutes 3-5 times a day

With paresis of the facial muscles, measures are taken to protect the cornea:
instillation of eye drops
eye patch for the night

Prevention of contractures and paralysis:
for this, passive exercises are carried out 1 - 2 times a day
ensure the correct position in bed - comfortable bed, foot supports
massage the limbs
subsequently connect active physiotherapy exercises

Prevention of bedsores:
change position in bed every 2 hours
wipe the skin with special compositions
use anti-decubitus mattresses

Prevention of lung infection:
breathing exercises
the earliest possible mobilization of the patient

With a decrease in lung capacity, difficulty in separating bronchial secretions:
massage is shown (effleurage and vibration with simultaneous rotation of the body in the supine position) every 2 hours during the day.

Symptomatic therapy:
antiarrhythmic
hypotensive
analgesic

With arterial hypotension, a drop in blood pressure (approximately blood pressure 100 - 110/60 - 70 mm Hg and below):
in / in the introduction of colloid or crystalloid solutions - isotonic solution of sodium chloride, albumin, polyglucin
with insufficient effect in combination with corticosteroids: prednisone 120-150 mg., Dexazone 8-12 mg
in case of insufficiency of these funds, vasopressors are used: dopamine (50-200 mg is diluted in 250 ml of isotonic sodium chloride solution and injected at a rate of 6-12 drops / min), or norepinephrine, or mezaton

Use for moderate pain simple analgesics and non-steroidal anti-inflammatory drugs.

For severe pain syndrome, tramal or cabamazepine (tigretol) or gabapentin (Neurontin), possibly in combination with tricyclic antidepressants (imipramine, amitriptyline, azafen, etc.).

Classes with a speech therapist for the treatment and prevention of speech and swallowing disorders.

Rehabilitation

Rehabilitation includes massage, therapeutic exercises, physiotherapy. Transcutaneous muscle stimulation is performed for muscle pain and paresis of the limbs.

FORECAST

Unfavorable prognostic factors include:
elderly age
rapid progression of the disease in the initial phase
development of acute respiratory failure with the need for mechanical ventilation
history of intestinal infection with C. jejuni

Although most patients with Guillain-Barré syndrome have a good recovery with adequate therapy, 2-12% die from complications and a significant proportion of patients have persistent motor deficits.

Approximately 75-85% have a good recovery, 15-20% have a moderate motor deficit, and 1-10% remain profoundly disabled.

The rate of recovery of motor functions can vary and take from several weeks to months. With axonal degeneration, recovery may take 6 to 18 months. In general, slower and less complete recovery will be seen in older patients.

Mortality in Guillain-Barré syndrome is largely determined by capacity of the hospital to conduct modern non-specific maintenance therapy (long-term mechanical ventilation, prevention of infectious complications, etc.), and in modern hospitals is about 5%. Previously, mortality was up to 30% due to the development of respiratory failure and secondary complications.

PREVENTION

Specific methods of prevention missing.

Patients are recommended avoid vaccinations within 1 year from the onset of the disease, as they can provoke a relapse of the syndrome.
In the future, immunizations are carried out if there are appropriate justifications for their need for this.

If Guillain-Barré Syndrome develops within 6 months of any vaccination it makes sense to advise the patient to refrain from this vaccination in the future.