Acute disseminated encephalomyelitis. Disseminated encephalomyelitis: real clinical picture and possible treatment outcome

Encephalomyelitis (acute disseminated, disseminated, myalgic) - pathology of the central and peripheral nervous system, consisting in . Formed at any age, there is no special attachment to gender. Sometimes it ends in death.

The reasons for the development of such a disease can be:

1. Traumatic brain injury;
2. Viral or bacterial infection (complication of rubella, smallpox and other pathologies);
3. Diseases of the immune system associated autoimmune diseases, reduction of defensive reactions;
4. Vaccination, in in this case This refers to the introduction of diphtheria, measles;

Factors contributing to the progression of the disease are constant, chronic stress, hypothermia, the postoperative period, hereditary predisposition, poor nutrition and consumption of foods low in essential nutrients, vitamins, and microelements.

However, it is worth noting that the exact cause of the development of this kind of inflammation has not yet been determined, but it has been noted that acute encephalomyelitis occurs precisely after a viral infection.

Pathogenesis is based on development autoimmune changes in organism. When viruses penetrate, the immune system produces antibodies and thus fights foreign agents. The problem is that the DNA of viruses, their protein component is similar in composition to the myelin sheath, their own already produced antigens recognize it as a harmful substance, begin to destroy it, and an inflammatory reaction develops.

Mainly involved in the process. Under microscopy it is observed leukocyte infiltration, focal inflammation, oligodendrocyte degeneration.

From an etiological and pathogenetic point of view, two common diseases are similar: disseminated encephalomyelitis and multiple sclerosis. The causes and mechanism of development are almost the same, but the main difference is the course of the disease. The first pathology is reversible; there is a possibility that the organ structure will return to previous state. In multiple sclerosis, the course is chronic, irreversible and most often leads to further complications.

Classification and symptoms

International classification diseases of the tenth revision, which all attending physicians adhere to, unites myalgic encephalomyelitis, encephalitis and myelitis into one category and divides it into the following groups:

1. Acute disseminated encephalitis is an inflammation of the central nervous system, the lesion is mainly viral in nature.
2. Tropical spastic paraplegia - symmetrical with demyelination of white matter spinal cord;
3. and meningomyelitis, not classified in other categories - the etiological factor is microorganisms such as meningococci, Koch's bacillus, rickettsia, streptococci, staphylococci;
4. Myelitis or acute disseminated encephalomyelitis of unspecified origin - this diagnosis placed in the absence of data on the possible cause of development.

Some sources limit the division to two positions: primary and secondary. Primary disease is considered as original by viruses. Secondary pathology becomes a complication of injury, the development of an infectious focus in another part of the body, or a consequence of an inadequate response to vaccination.

With encephalomyelitis, symptoms depend on which part of the nervous system is affected. In the first stages, the clinical picture is general; it includes headaches, general malaise, drowsiness even with unchanged sleep patterns, disorders gastrointestinal tract, and Clinical signs ARVI - sore throat, fever, runny nose and others. Further symptoms vary.

When the brain is involved in a pathological process, the patient complains of a change in speech, complete or partial impairment motor activity limbs, convulsions. Very severe cases the psyche changes.

With inflammation occurring in the area of ​​the spinal cord and its roots, the patient is concerned about changes in the skin in the form trophic ulcers, decreased sensitivity to thermal, painful stimuli, incontinence of bowel movements or, conversely, decreased volume of urine and constipation, pain spreading along the spine.

When changing the structure optic nerve Vision decreases sharply, the patient speaks of a “veil before the eyes,” and pain increases.

Myalgic encephalomyelitis can affect the sensory and motor nuclei of twelve pairs cranial nerves, in this case the patient suffers from problems with swallowing, breathing and other necessary processes. Characteristic permanent shift moods, depression, changes in behavior, in thinking.

Diagnostics

The preliminary diagnosis in almost 100% of cases coincides with the clinical one, since the clinical picture is clearly expressed, especially in the first fourteen days from the onset of inflammation. The doctor listens carefully to complaints and carries out general examination, noting possible redness mucous membrane of the oropharynx, increased body temperature, increased pain when moving the eyeballs.

According to the standard, blood, urine, and in some cases stool tests are prescribed (if there is a change in stool or gastrointestinal disorders). In the first seven days of the acute period, an increase in leukocytes, an increase in the erythrocyte sedimentation rate, and anemia are observed in the general blood test. In urine in the absence accompanying pathologies usually there are no changes or deviations from the norm. It is very important to carry out immunological tests (complement fixation reaction, linked immunosorbent assay and others) to detect antibodies to specific pathogen. If bacteria that cause myalgic encephalomyelitis are detected, their sensitivity to antibiotics is checked to build a further treatment plan.

In order to differentiate this pathology from the development of benign and malignant neoplasm, multiple sclerosis, systemic vasculitis and other similar diseases is carried out instrumental diagnostics, including computer and magnetic resonance imaging, electroencephalography, myography for paresis and paralysis of the limbs. Sometimes Doppler ultrasound examination of the cerebral vessels is used to study the vessels, since disruption of the structure and blockage of the lumen of the artery leads to disruption of tissue trophism and further problems.

Consultation with an ophthalmologist is necessary.

Treatment

For disseminated encephalomyelitis, treatment is based on the use of steroidal anti-inflammatory drugs (Prednisolone). Their dosage depends on the age of the patient, individual characteristics organism, the presence of concomitant pathologies and the severity of the ongoing process. The main side effect of these drugs is an additional decrease in immunity. That is why the use of glucocorticosteroids is combined with the use of immunomodulators and immunoglobulins.

In the case of a high concentration of autoantibodies that destroy healthy tissue, plasmapheresis is prescribed, that is, purification of the plasma from such protein bodies and immune complexes.

Therapy that destroys the main etiological factor consists of prescribing antibiotics wide range actions, antiviral medicines, namely interferon analogues. The effectiveness of other similar drugs has been little studied and practically unproven.

Often, when the nuclei of the cranial nerves are affected, resuscitation measures, artificial ventilation, stabilization of hemodynamic parameters. If swallowing is impaired, it is necessary parenteral nutrition with introduction into the body specialized mixtures, enriched with proteins, lipids, carbohydrates. Prevention of cerebral edema is necessary.

Since myalgic encephalomyelitis also occurs against the background of hypo- and vitamin deficiency, impaired tissue trophism and oxygen delivery, the doctor should prescribe group B drugs and nootropics. For paresis and convulsions, appropriate medications are prescribed.

Further rehabilitation of patients involves massage, physiotherapy and therapeutic exercises.

Prognosis and prevention

Complications of the disease can include bedsores due to decreased physical activity, inflammation Bladder And urethra, pyelonephritis.

The prognosis is favorable in most cases. With timely diagnosis and adequate treatment After a certain period of time, the functions of the central and peripheral nervous systems are completely restored. The consequences of the inflammatory process in the area of ​​the nuclei are more severe, as vital processes are disrupted, in which case death is possible.

Prevention includes timely treatment viral and bacterial pathologies, balancing work and rest, rationalization of nutrition, regular medical examination (dispensary examination). Vaccination should be carried out in the absence of contraindications with full control of the person’s well-being.

Disseminated encephalomyelitis(SEM)- acute autoimmune inflammatory process, diffusely affecting various areas central and peripheral nervous system and leading to reversible demyelination. Clinically, disseminated encephalomyelitis is characterized by rapidly increasing variable polymorphic neurological symptoms (sensory and motor impairments, dysfunction of the cranial nerve and pelvic organs, impaired consciousness and speech). The basis of diagnosis is a comparison of clinical data and MRI results of the brain. Treatment of disseminated encephalomyelitis is complex, carried out inpatiently, and in the acute period may require resuscitation.

In addition to these etiofactors, important in the occurrence of disseminated encephalomyelitis has an unfavorable premorbid background - depletion of the immune system due to chronic stress, hypothermia, suffered trauma, illness or surgery. In addition, researchers believe the presence of a hereditary predisposition, expressed in the similarity of proteins in nerve tissue with proteins of certain infectious agents or in the peculiarities of the functioning of the immune system.

Pathogenesis of disseminated encephalomyelitis

The main pathogenetic substrate of REM is an autoimmune reaction. As a result of the similarity of the protein antigens that make up infectious agents with myelin and other proteins of the nervous tissue, the immune system begins to produce antibodies to its own structural elements of the nervous system. This process is systemic in nature and leads to the destruction of myelin both in the spinal cord and brain, as well as in the spinal roots and peripheral nerve fibers. As a result of demyelination, the function of the affected nerve structures is lost.

Morphologically, perivascular infiltration with macrophages, lymphocytes and monocytes, disseminated inflammation, perivascular demyelination, and degeneration of oligodendrocytes are noted. Affected predominantly white matter cerebral and spinal structures, but gray may also be involved medulla. Foci of demyelination in the central nervous system can be visualized using MRI.

It should be noted that there is almost complete pathogenetic similarity between REM and multiple sclerosis. The main difference between them is that the first is an acute and predominantly reversible process, and the second is a chronic progressive disease with periods of remissions and exacerbations. However, the onset of multiple sclerosis can completely mimic the pattern of SEM. Multiple encephalomyelitis, in turn, can lead to chronicity of the demyelinating process resulting in multiple sclerosis.

Symptoms of disseminated encephalomyelitis

In typical cases, disseminated encephalomyelitis manifests as severe encephalopathy. 50-75% of patients develop disturbances of consciousness, ranging from stupor to coma. Psychomotor agitation, dizziness, headache, nausea, meningeal syndrome. Often the full clinical picture is preceded by a prodrome period in the form of myalgia, fever, headache, and general fatigue. Characterized by a rapid increase in neurological symptoms, the severity of which reaches a maximum within a few days.

The focal symptoms of disseminated encephalomyelitis are very variable and depend on the topic of the lesion. Ataxia, hemiplegia, oculomotor disorders and damage to other cranial nerves, limitations of visual fields, aphasia or dysarthria, sensory disturbances (hypoesthesia, paresthesia), and pelvic disorders may be observed. Damage to the optic nerve occurs as retrobulbar neuritis. According to various data, from 15% to 35% of cases of REM are accompanied by generalized or partial seizures. Approximately a quarter of cases have spinal symptoms ( peripheral paresis, Brown-Séquard syndrome). Radicular pain syndrome, polyneuropathy, and polyradiculopathy may occur. With the development of severe brainstem lesions with bulbar disorders, patients require resuscitation assistance.

In addition to the acute monophasic course, disseminated encephalomyelitis can have a recurrent and multiphasic course. Recurrent disseminated encephalomyelitis is said to occur when, 3 or more months after the first episode of REM, its clinical picture is resumed without the appearance of new symptoms and fresh foci of demyelination according to MRI. Multiphasic disseminated encephalomyelitis is characterized by the occurrence of a new episode of the disease no earlier than after 3 months. after resolution of the previous one and not earlier than 1 month. after the end of steroid therapy, provided that new lesions are detected on MRI while old inflammatory areas have resolved.

Diagnosis of disseminated encephalomyelitis

Vivid clinical picture, acute course, polymorphism and polysystemicity of symptoms, indications of a previous infection or immunization give the neurologist the opportunity to preliminarily diagnose REM. It is necessary to differentiate multiple encephalomyelitis from encephalitis, viral meningitis, myelitis, stroke, multiple sclerosis, Balo concentric sclerosis, rheumatic lesions of the central nervous system due to systemic vasculitis, etc.

Additionally, consultation with an ophthalmologist, ophthalmoscopy, and perimetry are carried out. Lumbar puncture may reveal increased cerebrospinal fluid pressure. Cerebrospinal fluid examination reveals increased protein levels and lymphocytic pleocytosis. PCR study of cerebrospinal fluid, as a rule, gives negative result. In approximately 20% of cases, the cerebrospinal fluid remains unchanged.

Most reliable method MRI of the brain is used to diagnose disseminated encephalomyelitis. In T2 and FLAIR modes, poorly defined asymmetric hyperintense foci are detected in the white, and often in the gray matter of the brain. They can have small (less than 0.5 cm), medium (0.5-1.5 cm) and large (more than 2 cm) sizes. In some cases, large confluent lesions with perifocal edema are recorded, causing a mass effect - displacement of surrounding structures. Additional involvement of the optic thalamus is possible. Hemorrhages may occur in large inflammatory areas. The accumulation of contrast agent in the lesions has different intensities. In 10-30% of cases, lesions are detected in the spinal cord.

All patients who suffered an acute episode of REM, after 6 months. A repeat MRI is recommended. The disappearance or reduction of areas of demyelination during this period is the main confirmation of the diagnosis of “multiple encephalomyelitis” and allows one to exclude multiple sclerosis. At the same time, the complete disappearance of inflammatory areas is recorded in 37-75% of cases, and a reduction in their area - in 25-53%.

Treatment of disseminated encephalomyelitis

Basic pathogenetic therapy REM is performed with anti-inflammatory steroid drugs. Depending on the severity of the condition, treatment begins with high or average age-specific doses of prednisolone. As symptoms regress, the dose is gradually reduced. Treatment with corticosteroids is continued for 2 to 5 weeks. A negative effect of steroid therapy is immunosuppression. To level it out, they are prescribed in parallel intravenous administration immunoglobulins. In severe cases it is necessary - hardware removal from the blood of immune complexes and antibodies.

Etiological treatment of disseminated encephalomyelitis is carried out antiviral drugs(interferon analogues). IN in rare cases proven bacterial etiology REM is prescribed antibiotics (ampicillin + oxacillin, cefazolin, gentamicin, etc.). When the disease develops against the background of rheumatism, bicillin therapy is performed.

Symptomatic therapy is vital necessary element treatment. According to indications, resuscitation measures, mechanical ventilation, and normalization of hemodynamics are carried out. If disseminated encephalomyelitis is accompanied by severe cerebral symptoms, then prevention of cerebral edema (administration of magnesium, acetazolamide or furosemide) is necessary. Severe dysphagia is an indication for tube feeding, urinary retention for bladder catheterization, intestinal paresis for enemas, convulsions for the prescription of anticonvulsants, etc.

Therapy of neurological disorders in the acute phase of disseminated encephalomyelitis includes the administration of vitamins G. B, ascorbic acid, anticholinesterase drugs (galantamine, neostigmine), for muscle spasticity - tolperisone hydrochloride. During the period of convalescence, absorbable drugs (hyaluronidase, aloe extract), nootropics (pyritinol, piracetam, ginkgo biloba), neuroprotectors (meldonium, Semax, ethylmethylhydroxypyridine succinate) are used. To restore motor function, they resort to massage and exercise therapy, transcranial magnetic stimulation.

Prognosis of disseminated encephalomyelitis

The acute period of REM lasts on average 1.5-2 weeks. Approximately 67% of patients experience complete clinical recovery within a few weeks. In some patients it persists varying degrees severe persistent symptoms - paresis, sensory disturbances, visual disturbances. IN in some cases a severe course of encephalomyelitis with the development of bulbar disorders leading to death is possible. The prognosis is complicated if there is multiple encephalomyelitis with a recurrent and multiphase course, chronic demyelination with the development of multiple sclerosis. Moreover, the signs that make it possible to predict the future transition of REM to multiple sclerosis have not yet been identified.

Acute disseminated encephalomyelitis is a rare but serious chronic disease that resembles multiple sclerosis in its manifestations. Correct treatment helps to effectively keep the symptoms of the disease under control.

At the Yusupov Hospital, treatment of acute disseminated encephalomyelitis is carried out according to modern standards, using glucocorticoids and symptomatic drugs. Patients are treated by highly qualified doctors who have great experience in the treatment of this pathology.

In parallel with drug therapy, we use the full range of necessary rehabilitation measures. They help restore impaired functions of the nervous system, return the patient to normal life, and ensure his psycho-emotional well-being.

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*The information on the site is for informational purposes only. All materials and prices posted on the site are not a public offer, defined by the provisions of Art. 437 Civil Code of the Russian Federation. For accurate information, please contact the clinic staff or visit our clinic.

Acute disseminated encephalomyelitis (ADEM, another name is acute disseminated disseminated encephalomyelitis, ADEM) - rare disease, which resembles an exacerbation of multiple sclerosis. These two diseases are similar: the same disorders occur in the nervous tissue, which manifest themselves in approximately the same symptoms.

What happens in the body during ADEM?

Acute disseminated encephalomyelitis, like, is a demyelinating disease.

The long processes of nerve cells are like wires that carry electricity. Like every wire in your apartment, they have special “insulation”. It's called the myelin sheath. But the myelin sheath is no ordinary insulation. It is not continuous: it has breaks located at certain, approximately equal, intervals. Thanks to them, the electrical impulse seems to “jump” along the nerve fiber and reaches the target much faster.

In acute disseminated encephalomyelitis, the myelin sheath is destroyed. The propagation of nerve impulses is disrupted. This is the cause of neurological symptoms.

Why does acute disseminated encephalomyelitis occur?

Most often, the disease is provoked by viral infections: mumps (mumps), chicken pox, measles, rubella. Sometimes bacterial infections, such as Lyme disease, act as a provoking factor. There are cases where ADEM developed after the administration of vaccines. Sometimes the disease occurs for no apparent reason.

In acute disseminated encephalomyelitis, the immune system begins to attack the myelin sheaths of its own nerve cells. In other words, ADEM is an autoimmune pathology.

What are the signs of ADEM?

ADEM may manifest itself different symptoms, depending on which part of the brain is affected:

• Movement disorders - usually weakening in one half of the body (with damage to the cerebral cortex).
• Impaired coordination of movements. They become awkward and inaccurate. It is difficult for a person to maintain balance while standing or while walking (with damage to the cerebellum).
• Muscle tone disorders, lethargy. Symptoms resembling Parkinson's disease arise (when the nerve centers located deep in the cerebral hemispheres are damaged - they also suffer in Parkinsonism).
• Eye movement disorders. It becomes impossible to turn eyeballs in any direction due to damage to the nerve centers that regulate the functioning of the extraocular muscles.

In addition, general symptoms of brain damage occur: epileptic seizures, attention, thinking.

The difference between ADEM and multiple sclerosis is that all symptoms occur once and go away after a while. Multiple sclerosis - chronic pathology, in which exacerbations develop periodically.

What examination is prescribed for ADEM?

The main diagnostic method is magnetic resonance imaging (MRI). The images show clearly visible lesions in the brain. Usually the doctor does not doubt the diagnosis.

The neurologist may also prescribe a spinal tap. The patient is placed on his side and local anesthesia and a needle is inserted between the lumbar vertebrae. A small amount of cerebrospinal fluid is obtained and sent for analysis. They find it increased amount immune cells-lymphocytes.

Treatment of ADEM

The main method of treating acute disseminated encephalomyelitis is the use of adrenal hormones (glucocorticoids). They suppress immune cell activity and inflammation in the brain. In rare cases, if the disease is severe, the doctor prescribes blood purification using plasmapheresis.

In addition, medications are prescribed that help fight the symptoms of ADEM: anticonvulsants, diuretics to eliminate edema, etc.

Rehabilitation treatment after suffering from ADEM includes physiotherapy, massage, physical therapy. It helps to quickly restore the functions of the nervous system and return to normal activities. At the Yusupov Hospital, rehabilitation is given increased attention, here this direction is developed very well.

In most cases, complete recovery occurs and all symptoms disappear. The impaired functions of the nervous system are restored. Rarely with very severe course ADEM patients die.

Sometimes after some time the symptoms of acute disseminated encephalomyelitis recur again. In this case, they speak of a recurrent form of the disease.

Bibliography

• ICD-10 (International Classification of Diseases)
• Yusupov Hospital
• Gusev E.I., Demina T.L. Multiple sclerosis // Consilium Medicum: 2000. - No. 2.
• Jeremy Taylor. Health according to Darwin: Why we get sick and how it is related to evolution = Jeremy Taylor “Body by Darwin: How Evolution Shapes Our Health and Transforms Medicine.” - M.: Alpina Publisher, 2016. - 333 p.
• A.N. Boyko, O.O. Favorova // Molecular. biology. 1995. - T.29, No. 4. -P.727-749.

Disseminated encephalomyelitis is a pathology in which the lesions are diffusely scattered (disseminated) throughout the nervous tissue of the spinal cord and brain, so the name itself indicates the severity of the disease.

In medicine, acute processes are usually called processes that occur suddenly, are characterized by pronounced symptoms and can have the following outcomes:

• complete recovery;
• recovery with the formation of a defect;
• transition to a chronic form;
• death of the patient.

• the immediate cause of the disease;
• process activity;
• the initial state of the patient’s body;
• timeliness and adequacy of treatment.

What is acute demyelinating encephalomyelitis?

Myelin is a sheath surrounding nerve fibers through which nerve impulses are carried, like wires. This sheath consists of specialized glial cells (the so-called neuroglia), and promotes the rapid transmission of information along nerve fibers (myelination of the fiber increases the speed of impulse transmission by 5-10 times).

In addition, the shell provides nutritional and protective function, providing vital activity nerve fibers. So demyelination of the fiber leads to disruption of the functioning of neurons, and with a long course of the disease - to the gradual degeneration of nerve fibers and death of nerve cells.

The group of demyelinating diseases of the nervous system also includes multiple sclerosis, Schilder's leukoencephalitis, Balot's concentric sclerosis and acute hemorrhagic leukoencephalitis. Therefore, when diagnosing acute disseminated encephalomyelitis, these diseases should be excluded.

What is the mechanism of development of acute disseminated encephalomyelitis?

This happens when the body perceives some of its elements as foreign. There is a whole group of diseases with a similar development mechanism: systemic lupus erythematosus, rheumatoid arthritis, rheumatism and many others.

To date, three mechanisms for the occurrence of autoimmune aggression are known. In some cases, a violation of immunological tolerance occurs when a foreign antigen is ingested, similar in composition to certain proteins of the body. Autoaggression in rheumatism occurs due to the similarity of the antigenic composition of the causative agent of scarlet fever and certain proteins connective tissue.

Another mechanism: a change in the antigenic composition of tissue damaged by the inflammatory process, as a result of which the tissue is no longer recognized as its own. And finally, some tissues are not recognized by the immunological system because they normally never come into contact with it due to the existence of a specific barrier.

Thus, the blood-brain barrier separates the blood and the cells of the central nervous system, so when it is disrupted, autoimmune reactions can occur.

Unfortunately, the mechanism of development of autoaggression in demyelinating diseases of the nervous tissue has not been fully studied, although no one doubts the autoimmune nature of the occurrence of acute disseminated encephalomyelitis.

It is believed that all three mechanisms have a certain significance in the development of pathology, with the leading one being the similarity of the antigenic composition of some infectious agents (viruses, bacteria, rickettsiae) with proteins of nervous tissue. With a long course of acute disseminated encephalomyelitis, secondary reactions are especially strong when destroyed myelin enters the blood and provokes an increased immune response.

Causes of acute disseminated encephalomyelitis

In approximately 25-30% of patients, the pathology is caused by a specific pathogen - human acute encephalomyelitis virus (HAEV) . In other cases - nonspecific infectious and non-infectious agents.

The most common causative agents of the disease are measles, rubella, chickenpox, influenza, and unrecognized viruses viral infections upper respiratory tract or gastrointestinal tract.

Less commonly, the impetus for the development of the disease is vaccination (post-vaccination disseminated encephalomyelitis). Most often, the disease develops after vaccination against rabies or whooping cough. Cases of acute disseminated encephalomyelitis after the administration of measles and influenza vaccines have also been described.

It is extremely rare that disseminated encephalomyelitis develops after a bacterial infection (streptococci, staphylococci), rickettsiosis, toxoplasmosis, or diseases caused by spirochetes.

However modern research prove that previous infection or vaccination is only an impetus for the development of the disease. In order for this severe pathology to develop, a complex of predisposing factors must be present.

The leading role in the development of acute disseminated encephalomyelitis is played by genetic characteristics, such as a hereditary tendency to autoimmune reactions (one of the relatives suffered from diseases such as rheumatoid arthritis, systemic lupus erythematosus, etc.) or genetic similarity of nervous tissue protein molecules with certain infectious agents.

In approximately 2-5% of patients with acute disseminated encephalomyelitis, an unfavorable family history of demyelinating diseases of the nervous system can be traced (given that these pathologies are relatively rare, these figures prove genetic character violations).

In addition, the development of acute disseminated encephalomyelitis is facilitated by the presence of foci of infection in the body, accompanying chronic diseases, injuries, stress, physical and nervous exhaustion.

Predisposing factors also include age and gender. Despite the fact that the disease can occur at any age, the diagnosis of “acute disseminated myelitis” is most common in childhood and adolescence, with boys being sick more often than girls.

Symptoms

The disease begins suddenly and violently, and often at the very beginning resembles an acute infectious disease - characteristic high fever and symptoms of intoxication (weakness, lethargy, loss of appetite). In addition to general infectious symptoms, acute disseminated encephalomyelitis syndrome includes the following groups of symptoms:
1. General cerebral symptoms.
2. Meningeal symptoms.
3. Focal symptoms.

General cerebral and meningeal symptoms of acute disseminated encephalomyelitis

The mechanism of occurrence of cerebral symptoms in acute disseminated encephalomyelitis is quite complex and includes increased intracranial pressure, neurointoxication, and impaired microcirculation in brain tissue. The severity of these symptoms indicates the severity of the disease and has a certain prognostic value.

The most common cerebral symptoms in acute disseminated encephalomyelitis include:

• headache;
• nausea and unrelieved vomiting;
• drowsiness;
• disturbance of consciousness (stupefaction, in extremely severe cases turning into a coma);
• convulsive syndrome.

The pathology of other pairs of cranial nerves in acute disseminated encephalomyelitis most often manifests itself as double vision, asymmetry and impaired facial sensitivity. Much less common are hearing and smell disorders, dysarthria (speech impairment caused by decreased motor function of the articular apparatus), and dysphagia (impaired swallowing, choking).

Polyneuropathy of the extremities is manifested by local sensitivity disorders, paresthesia (the sensation of crawling) and so-called flaccid paralysis, that is, paralysis combined with a significant decrease in muscle tone and trophic disorders.

20-25% of patients with acute disseminated encephalomyelitis show signs of isolated transverse spinal cord lesions. In this case, there are no focal symptoms from the brain, so the pathology of the central nervous system is detected only by magnetic resonance imaging.

Signs of transverse spinal cord lesions depend on the level of the lesion, and are manifested by symmetrical paralysis of the limbs, sensory pathology and so-called pelvic disorders (impaired urination and defecation, sexual dysfunction).

Course and prognosis of acute disseminated encephalomyelitis

In 50-76% of patients (according to various sources), the disease ends full recovery, there are often residual effects of varying severity:

• paresis;
• paralysis;
• sensitivity disorders;
• impaired coordination of movements;
• aphasia;
• various mental disorders;
• autonomic disorders;
• tendency to have convulsive seizures.

Diagnostics

To clarify the diagnosis in mandatory Magnetic resonance imaging is performed. In the case of acute disseminated encephalomyelitis, multiple, often confluent, diffuse, asymmetrical lesions are found in the brain and spinal cord. Upon repeated examination, in the absence of fresh lesions, a gradual restoration of the nervous tissue is observed over time.

Cerebrospinal fluid analysis shows increased content protein and cellular elements of the lymphocytic series, glucose content is normal. In approximately half of patients (mostly adults), specific antibodies can be detected.

In those rare cases when the causative agents of acute infectious encephalomyelitis were microorganisms bacterial origin, antibiotics are prescribed in age-specific dosages. Preference is given to drugs from the group of penicillins (ampicillin, Ampiox), cephalosporins (Kefzol) or aminoglycosides (gentamicin).

If the disease occurs against the background of rheumatism, or there is reason to believe that acute disseminated encephalomyelitis was provoked by chronic tonsillitis, standard bicillin therapy regimens for rheumatism are prescribed.

If the causative agent of the disease turns out to be the rabies virus (post-vaccination encephalomyelitis) or the HME virus (human acute encephalomyelitis virus), then, in the case of pronounced residual effects, vaccination against acute encephalomyelitis and multiple sclerosis is carried out in the subacute period using the Margulis-Shubladze vaccine.

Basic pathogenetic treatment of acute disseminated encephalomyelitis

For mild to moderate cases of the disease, age-average doses of corticosteroids are used for 3-7 days. Then, as the process subsides, the doses are reduced. The duration of therapy ranges from 2 to 4-5 weeks or more.

Pulse therapy (a course of high doses of corticosteroids) is often used. In extremely severe cases, plasmapheresis is used (hardware purification of blood from antibodies and immune complexes).

In the presence of concomitant foci of infection, hormonal therapy should be combined with the prescription of broad-spectrum antibiotics.

TO pathogenetic treatment Vitamin therapy also applies. B vitamins and vitamin C begin to be taken in the acute period, and continue in the early convalescence phase. Good clinical results were shown by a course of vitamin B 12 (cyanocobalamin).

Treatment and prevention of complications of acute disseminated encephalomyelitis in the initial stage of the disease

In case of severe cerebral symptoms, prevention of cerebral edema is carried out (furosemide, Diacarb, magnesium sulfate according to standard schemes). If necessary, resuscitation measures and intensive therapy are carried out (inhalation of a mixture of nitrogen and oxygen, administration of sodium hydroxybutyrate, emergency normalization of hemodynamics).

In case of severe dysphagia, feeding is performed through a tube, and in case of pelvic disorders accompanied by urinary retention, catheterization of the bladder is carried out with mandatory rinsing with disinfectant solutions. It is necessary to constantly monitor bowel function and, if necessary, regularly use enemas. At extremely severe conditions accumulation of mucus in the tracheal lumen is possible. In such cases, hardware suction is performed.

For the treatment of neurological disorders in the acute phase, dibazole, anticholinesterase substances (Prozerin, galantamine) are used, with increased tone muscles – Mydocalm, Cyclodol.

Pathogenetic and symptomatic treatment of acute disseminated encephalomyelitis in the early convalescence phase

To combat cerebrovascular disease, courses of nootropics such as Encephabol (orally) or piracetam (orally or intravenously) are prescribed.

Rehabilitation measures for acute disseminated encephalomyelitis are aimed mainly at the correction of motor and speech disorders.

A dangerous pathology that can cause damage to the spinal cord and brain is disseminated encephalomyelitis (DEM). This disease is a demyelinating disease that affects both the central and peripheral nervous systems.

So what is it - SEM? Acute disseminated encephalomyelitis is characterized by the production of antibodies in the human body, which begin to destroy the myelin sheath of the brain and spinal cord. As a result of such an attack, all affected areas cease their normal functioning. This disease is not just dangerous, but deadly and requires close attention.

Myelin sheath - protective layer, which surrounds the fibers of the peripheral and central nervous system

The first mention of a disease called acute disseminated encephalomyelitis dates back to 1767. It was then that the English specialist contacted chicken pox and subsequent consequences with this disease.

If we compare multiple encephalomyelitis and multiple sclerosis, they have a lot in common, but they are far from the same thing. So, in the case of REM, as with sclerosis, the basis of the disease is the body’s protective reactions that occur to myelin antigens. The difference between multiple encephalomyelitis and multiple sclerosis is that REM is characterized by one exacerbation during the entire period of the disease, while in multiple sclerosis such exacerbations have a chronic course.

It is important to understand that multiple encephalomyelitis (MEM) and multiple sclerosis (MS) are interrelated, as there is a possibility of MEM converting to MS.

What is the reason for the emergence of SEM? There is still no clear answer to this question, but many factors point to its viral nature.

SEM image of the brain

There were a large number of attempts to identify the encephalomyelitis virus, but as a result it was found that not all patients had this virus, which was called the ADEM virus. Some patients acquired acute disseminated encephalomyelitis after an illness viral in nature, these include:

• chickenpox;
• rubella;
• measles;
• mononucleosis;
• ARVI;
• herpetic infection.

In addition, REM can develop against the background of vaccination against:

• rabies;
• whooping cough;
• diphtheria;
• measles;
• flu

There are cases of the disease developing against the background of:

• toxoplasmosis;
• chlamydia;
• rickettsiosis;
• mycoplasma pneumonia.

In addition, there have been cases of the development of REM after traumatic brain injury, allergic reactions reducing the body's reactivity.

When the spinal cord is affected

Symptoms

Acute disseminated encephalomyelitis differs in the nature of damage to one or another part of the central nervous system or PNS and is classified as follows:

• central;
• polyradiculoneuropathy;
• optoencephalomyelitis;
• stem;
• myalgic encephalomyelitis.

Accordingly, each of the above types is characterized by special symptoms, however, at the initial stage the symptoms are general, including:

• headache;
• drowsiness;
• general painful condition;
• sore throat;
• runny nose;
• temperature increase;
• increased excitability (occurs sometimes);
• stomach upset.

In addition, it is possible that some specific symptoms that occur in rare cases, for example, colic in the legs. 60–80% of patients experience comatose states which can ultimately lead to death.

Central

This type of disease develops when parts of the brain are damaged and is characterized by:

• difficulty speaking;
• paralysis of the trunk;
• paresis of the limbs;
• convulsions (epileptic seizure).

Polyradiculoneuropathy

This type of disease occurs when the encephalomyelitis virus has affected areas of the spinal cord and those emanating from it. nerve roots. Symptoms characteristic of this disease:

• decreased pain threshold;
• acute pain in the spine;
• urinary or fecal incontinence;
• skin changes.

Opticoencephalomyelitis

Observed when the optic nerve is damaged, and includes:

• blurred vision;
• pain in the eyes when rotating the eyeballs;
• the presence of a “veil” before the eyes.

Stem

This type of disease has much in common with the central one, since in this case the brain is affected, however, not the entire brain, but only the nuclei of the cranial nerves. The disease is characterized by:

• neuritis of the facial nerve;
• difficulty swallowing functions;
• difficulty breathing.

Myalgic

Myalgic encephalomyelitis, or otherwise post-viral fatigue syndrome, is characterized by specific symptoms:

• fatigue;
• depression;
• shoulder pain;
• change of mood;
• muscle pain;
• disruption of the gastrointestinal tract.

The development of the disease occurs against the background of vaccinations or as a result of a viral disease.

Watch the video: on the road to recovery from acute disseminated encephalomyelitis

Diagnosis of the disease

Multiple encephalomyelitis and multiple sclerosis have much in common, including at the diagnostic level. In addition to sclerosis, acute encephalomyelitis is similar to diseases such as:

• encephalitis;
• viral meningitis;
• transverse myelitis;
• a brain tumor;
• Balo's sclerosis;
• systemic vasculitis.

For diagnostics use:

• cerebrospinal fluid analysis;
• magnetic resonance imaging (MRI);
• computed tomography (CT);
• ophthalmoscopy;
• perimetry.

Additionally, a consultation with an ophthalmologist is possible.

When collecting cerebrospinal fluid, the doctor pays attention to the pressure under which the fluid flows out. If the liquid spurts out, we can talk about the presence of a disease.

Among other things, an increased amount of protein indirectly indicates the presence of a disease such as acute encephalomyelitis, but disseminated encephalomyelitis does not always cause an increase in protein in the spinal cord, so the study is carried out comprehensively.

Thus, during MRI or CT diagnostics, the nature of the lesion in the white and gray matter of the brain, as well as the extent of the area, is determined. As a rule, large lesions are characteristic of acute encephalomyelitis.

MRI diagnostics is indicated for persons who have had REM. So, after six months, a repeat examination is necessary, since if symptoms of the disease are re-identified we're talking about not about REM, but about multiple sclerosis.

Treatment

The concepts of symptoms and treatment of a disease have a vital connection, since when the first symptoms appear, it is necessary to diagnose the disease as quickly as possible and begin immediate treatment in order to minimize the risk of death.

The basis of treatment is taking steroid drugs, the dosage of which differs depending on the severity of the disease. Gradually, as the patient's condition improves, the dose of the medicine is reduced.

This type of treatment has a number of side effects, in particular – suppression of the patient’s immunity. To eliminate this, the patient is prescribed drugs from a series of immunoglobulins, and in especially severe cases, it is possible to remove produced antibodies from the patient’s blood.

In addition to the main treatment, the patient is shown:

• antiviral drugs (interferon-based);
• taking B vitamins, ascorbic acid;
• drugs that eliminate cerebral edema;
• nootropics;
• neuroprotectors.

Since acute encephalomyelitis affects the most important human organ, the patient may require resuscitation, as a rule, this is artificial ventilation, connecting the patient to a cardiac monitor and normalizing hemodynamics.

In addition, in some cases it is possible to probe the patient's nutrition and catheterize the bladder, prescribe an enema and anticonvulsant drugs.

During the recovery phase motor functions body, the patient is prescribed massage, physical therapy and stimulation of the cerebral cortex using magnetic pulses (done non-invasively).

ethnoscience

Unfortunately, treatment with folk remedies for this disease is unacceptable. Naturally, it will be useful to introduce some herbs or tinctures as concomitant therapy, but only on the recommendation of the treating specialist. For such a disease, treatment with folk remedies, excluding conventional therapy, will lead to death in 90% of cases.

Predictions and consequences

As a rule, acute encephalomyelitis is characterized by a short duration of 1–2 weeks. However, if not properly treated, it can lead to irreversible consequences. The prognosis of the disease is such that 60–70% of patients are completely cured of this disease, and the remaining 40–30% are diagnosed neurological changes, up to the acquisition of disability or death.

Consequences:

• paresis of the limbs;
• disturbances of vision and sensations;
• bulbar disorders (problems with swallowing).

As for the development of the disease during pregnancy and after childbirth, it is worth noting that in women who have had this disease, the risk of relapse increases after delivery, and during pregnancy, on the contrary, it decreases. For such cases it is recommended rerun MRI of the head and consultation with a good specialist.

So, the diagnosis of REM is not the same as multiple sclerosis, but when unfavorable conditions may become one. For this reason, the main recommendation for treating this disease is not to delay it. Because the consequences could be more dire. Take care of your health and do not neglect going to a specialist.