Myalgic encephalomyelitis symptoms. Encephalomyelitis. Infusion of Mordovnik sharogolatum

Disseminated encephalomyelitis (DEM)- an acute autoimmune inflammatory process that diffusely affects various parts of the central and peripheral nervous system and leads 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.

General information

Disseminated encephalomyelitis is an acute autoimmune inflammatory demyelinating pathology with disseminated damage to both the central and peripheral nervous systems. The difference between REM and a number of other demyelinating diseases is the reversible nature of the pathological changes and the possibility of complete disappearance of the resulting neurological deficit under the influence of therapy. Disseminated encephalomyelitis was first described 250 years ago by an English physician who observed signs of encephalomyelitis in patients who had suffered smallpox. In modern neurology, this is a fairly common disease. Thus, according to 2011 data, 50 cases of REM were diagnosed among the adult population of Moscow alone. Disseminated encephalomyelitis can affect people of different age groups, but is more common in children than in adults. In childhood it usually has a milder course.

Causes of disseminated encephalomyelitis

Primary disseminated encephalomyelitis, as a rule, has a viral etiology. Attempts to identify a specific pathogen led to the fact that domestic scientists isolated a virus from the blood and cerebrospinal fluid of patients that is close to the rabies virus and has no analogues among known viruses. It is called the ADEM virus. However, such a virus is not detected in all patients.

Often, disseminated encephalomyelitis occurs after an acute respiratory viral infection: chickenpox, rubella, influenza, measles, infectious mononucleosis, herpetic or enterovirus infection. Secondary disseminated encephalomyelitis can be toxic, post-vaccination or post-infectious in nature. Post-vaccination REM can develop after vaccination against rabies, whooping cough, diphtheria, measles. There are known cases of encephalomyelitis after administration of the influenza vaccine. In rare cases, REM occurs some time after a bacterial infection (mycoplasma pneumonia, toxoplasmosis, chlamydia, rickettsiosis).

In addition to these etiofactors, an unfavorable premorbid background is important in the occurrence of disseminated encephalomyelitis - depletion of the immune system due to chronic stress, hypothermia, 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. The white matter of the cerebral and spinal structures is predominantly affected, but the gray matter of the brain may also be involved. 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 are noted. 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. In approximately a quarter of cases, spinal symptoms are noted (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

A clear clinical picture, an acute course, polymorphism and polysystemic 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 testing of cerebrospinal fluid usually gives a negative result. In approximately 20% of cases, the cerebrospinal fluid remains unchanged.

The most reliable method for diagnosing disseminated encephalomyelitis is brain MRI. 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 varying intensity. 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 for REM is carried out 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, intravenous immunoglobulins are prescribed in parallel. In severe cases, hardware removal of immune complexes and antibodies from the blood is necessary.

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

Symptomatic therapy is a vital element of 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. Some patients retain varying degrees of severe, persistent symptoms - paresis, sensory disturbances, visual disturbances. In some cases, a severe course of encephalomyelitis is possible with the development of bulbar disorders, leading to death. 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.

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What is acute disseminated encephalomyelitis?

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 membrane performs a nutritional and protective function, ensuring the vital activity of 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 some connective tissue proteins.

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 viral infections of the 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 proves that a 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.

Genetic characteristics have a leading role in the development of acute disseminated encephalomyelitis, such as a hereditary tendency to autoimmune reactions (one of the relatives suffered from diseases such as rheumatoid arthritis, systemic lupus erythematosus, etc.) or the genetic similarity of the molecules of proteins in the nervous tissue with those or other 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 the genetic nature of the disorders).

In addition, the development of acute disseminated encephalomyelitis is facilitated by the presence of foci of infection in the body, concomitant chronic diseases, trauma, 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 - characterized by 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 in complete recovery, and residual effects of varying severity often remain:

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

Diagnostics

To clarify the diagnosis, magnetic resonance imaging is mandatory. 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.

Analysis of cerebrospinal fluid shows an increased content of protein and cellular elements of the lymphocytic series, the 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 are microorganisms of 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.

Pathogenetic treatment also includes vitamin therapy. 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, cerebral edema is prevented (furosemide, Diacarb, magnesium sulfate according to standard regimens). 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. In extremely severe conditions, mucus may accumulate in the trachea. In such cases, hardware suction is performed.

For the treatment of neurological disorders in the acute phase, dibazole, anticholinesterase substances (Proserin, galantamine) are used; for increased muscle tone - 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.

The myelin sheath is a protective layer that 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 an English specialist connected chickenpox and its 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 suffering a viral disease, 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 and decreased reactivity of the body.

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, there may be some specific symptoms that occur in rare cases, such as 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 the nerve roots emanating from it. 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, are 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 study is necessary, since in the case of repeated detection of symptoms of the disease, we are not talking 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 the use of 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, usually 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.

At the stage of restoring the motor functions of the body, the patient is prescribed massage, physical therapy and stimulation of the cerebral cortex using magnetic impulses (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 with neurological changes, including 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 to repeat the MRI of the head and consult a good specialist.

So, the diagnosis of REM is not the same as multiple sclerosis, but under unfavorable conditions it can 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.

Disseminated encephalomyelitis is an acute inflammatory lesion of the central nervous system, which is presumably autoimmune in nature.

As a rule, this disease is a complication of a recent infectious disease or develops as a consequence of immunization. To cope with this disease, it is very important to consult a doctor in time. The specialist will make an accurate diagnosis and select adequate therapy.

The essence of the disease

Encephalomyelitis is considered a dangerous disease that combines damage to the spinal cord and brain. In severe cases, this disease even leads to death. In this case, complete recovery can be observed. The prognosis depends on the activity of the abnormal process, the cause of the disease, and the adequacy of therapy.

Currently, it is customary to distinguish between two main forms of this pathology – primary and secondary encephalomyelitis. In the first case, the disease most often results from a viral infection. When secondary encephalomyelitis appears, we are talking about a complication of common infectious pathologies. It can also develop after vaccination.

Types of violations and points of main impact

Depending on the area of ​​damage, the following types of encephalomyelitis are distinguished:

However, disseminated encephalomyelitis is most often diagnosed. This form of the disease is characterized by the appearance of lesions that affect different parts of the brain and spinal cord.

Causes and risk factors

The causes of the development of disseminated encephalomyelitis are not fully understood. Scientists are still wondering why the immune system begins to synthesize proteins aimed at fighting nervous tissue.

However, the studies carried out allowed us to establish some regularities. Thus, the disease most often progresses after such events:

• viral infections– especially those that provoke the appearance of specific rashes on the skin. Such diseases include herpes, chickenpox, rubella;
• introduction of specific vaccines;
• reducing the body's reactivity;
• allergy;
• colds.

Complex of symptoms

All manifestations of disseminated encephalomyelitis can be divided into 2 main categories - focal and cerebral. Thus, focal symptoms are represented by a significant variety of brain lesions. There are also certain combinations in the form of the following syndromes:

• pyramidal;
• cerebellar;
• extrapyramidal;
• oculomotor disorders.

All of these syndromes have a large number of manifestations, so only a qualified specialist can make an accurate diagnosis.

• appearance;
• disturbances of consciousness;
• cognitive impairment– weakening of memory, decreased intellectual capabilities.

Also, against the background of this process, certain symptoms of dysfunction of the peripheral nervous system may appear. A fairly common condition in this case is.

Some people experience initial signs, which may include the presence of, which caused the appearance of disseminated encephalomyelitis, with an increase in temperature and.

Diagnosis and approach to therapy

Making an accurate diagnosis is not too difficult. Doctors usually perform it using contrast.

The clinical features of this disease can be easily seen on the screen or in photographs. If necessary, your doctor may prescribe a lumbar puncture.

Goals of therapy

With the development of disseminated encephalomyelitis, treatment should solve the following problems:

Treatment methods

Basic therapy of the disease is carried out with the help of anti-inflammatory steroid drugs. Depending on the complexity of the person’s condition, high or medium doses of Prednisolone are used. As the symptoms of the disease develop, the volume of the drug is gradually reduced. Corticosteroid therapy should be continued for 2-5 weeks.

It is important to take into account the negative aspects of such treatment, one of which is immunosuppression. To cope with this side effect, intravenous immunoglobulins are prescribed in parallel. In difficult cases, plasmapheresis is required. In this case, immune complexes and antibodies are removed from the body using a special device.

Etiological therapy for disseminated encephalomyelitis is carried out using antiviral drugs. Interferon analogues are usually used for this purpose.

In rare cases, when the disease is of bacterial origin, antibacterial drugs are used. The doctor may prescribe Ampiox, Gentamicin, Kefzol. If the pathology develops against the background of rheumatism, bicillin therapy is indicated.

A mandatory component is symptomatic therapy. According to indications, resuscitation measures, artificial ventilation, and hemodynamic restoration can be carried out. If the disease is accompanied by cerebral manifestations, you need to pay attention to prevention. For this, Diacarb, Magnesia, Furosemide can be administered.

For severe dysphagia, tube feeding is used. If a person has urinary retention, a catheter is inserted into the bladder.

In case of intestinal paresis, enemas should be done. is an indication for the prescription of anticonvulsant drugs.

To cope with neurological disorders that often accompany exacerbation of disseminated encephalomyelitis, you need to use B vitamins, ascorbic acid, and anticholinesterase drugs. These include Galantamine, Prozerin. For muscle spasms, the use of Mydocalm is indicated.

During convalescence, you need to use absorbable agents - Lidaza, Cerebrolysin.

Also during this period, nootropic drugs are indicated - Ginkgo biloba, Nootropil. In addition, doctors often prescribe neuroprotectors - in particular, Semax or.

To restore motor activity, you need to do massage and therapeutic exercises. Transcranial magnetic stimulation has a good effect.

During the period of exacerbation of encephalomyelitis, treatment is carried out in a hospital setting. During this period, potent drugs are used, and therefore traditional therapy is not used.

Folk remedies for restoring the body

During the recovery phase, effective recipes can be used to maintain the functioning of the nervous system:

1. Onions with honey. The onion needs to be peeled and chopped using a grater. Squeeze out the juice and mix in equal parts honey. Take a small spoon three times a day. This should be done before meals for a month.
2. Mumiyo. Literally 5 g of the product must be dissolved in 100 ml of water. Take a small spoon three times a day an hour before meals.
3. Ball-headed Echinops. To make the product, you need to take 3 large spoons of the fruits of this plant, pour 250 ml of boiling water and leave in a thermos for 12 hours. Drink small portions throughout the day. The course of treatment should be 2 months.

Complications and consequences

Some patients have persistent symptoms, which manifest themselves as visual impairment or sensory disturbances.

In some cases, disseminated encephalomyelitis is characterized by a severe course, the consequences of which result in, which can lead to death.

Forewarned and forearmed!

To prevent the development of the disease, you must adhere to the following rules:

• avoid hypothermia and overheating during the vaccination period;
• refrain from drinking alcohol during vaccinations;
• Avoid physical overload during this period.

Disseminated encephalomyelitis is a very serious disease that can cause dangerous consequences. To avoid this, it is important to promptly consult a doctor who will select complex therapy.