What is orem in medicine? Acute disseminated encephalomyelitis as a demyelinating disease of the central nervous system

Acute disseminated encephalomyelitis (ADEM) is an autoimmune disseminated disease of the brain and spinal cord, which is characterized by the presence of foci of inflammation in the central nervous system, often in combination with demyelination. The disease was first described by the English physician Clifton 250 years ago in patients after smallpox.

The modern definition of ADEM is based on the presence of signs of multifocal damage to the central nervous system with encephalopathy.

Etiology. ADEM most often occurs after viral infections that are accompanied by a rash, or nonspecific viral infections: measles, chicken pox, smallpox, rubella, herpes zoster, influenza, Epstein-Barr virus, cytomegalovirus, herpes simplex virus, coxsackie virus, infectious mononucleosis, mumps, infections respiratory tract, intestinal infections. It is believed that mycoplasma pneumonia, chlamydia or vaccination against rabies, diphtheria, tetanus, chickenpox, measles, influenza, hepatitis B are factors that predetermine the development of the disease. Less commonly, WEEM occurs against the background bacterial infection. There are known cases of spontaneous development of the disease. Traumatic or spinal cord injury accelerates the development of the disease.

Thus, taking into account etiological factors, ADEM is distinguished between post-infectious and post-vaccination.

Pathogenesis. The leading role in the pathogenesis of ADEM is played by the autoimmune response to myelin or other self-antigens through the mechanism of molecular mimicry or nonspecific activation of autoreactive T-cell clones, which is accompanied by the production of autoantibodies, focal or multifocal (disseminated) inflammation of the brain and/or spinal cord. Thus, the development of the disease is based on an autoimmune reaction. Therefore, it is natural that the literature emphasizes the pathogenetic commonality of ADEM and multiple sclerosis. On the other hand, similar pathogenesis is suggestive, but does not indicate, that ADEM is a form of multiple sclerosis.

Pathomorphology. The main symptom of ADEM is the development of disseminated inflammation, perivascular infiltration with lymphocytes, macrophages or monocytes, especially pronounced around small and medium-sized veins. Perivascular demyelination may occur. Degenerative changes in oligodendrocytes are also observed. More often affected white matter brain and spinal cord, but gray matter (cortex, thalamus, hypothalamus), as well as spinal roots and peripheral nerves may also be involved. MRI visualizes hyperintense lesions on T2-weighted images, and tumor-like lesions with perifocal edema may be observed.

Clinic ADEM is extremely polymorphic and is determined by the presence of a multifocal process in the central nervous system. Often the clinical picture is dominated by signs of brainstem encephalitis, acute meningoencephalopathy with meningism, or hemorrhagic leukoencephalitis. ADEM may present with bilateral retrobulbar neuritis along with other neurological disorders. Monosymptomatic optic neuritis as an isolated manifestation of the disease is observed very rarely. Sometimes the disease manifests itself as visual field defects, aphasia, motor and sensory disorders, and ataxia. Sometimes, especially after rabies vaccination, the clinical picture of ADEM includes a combination of signs of encephalomyelitis with damage to the spinal roots and peripheral nerves (polyradiculoneuropathy). The onset of ADEM is sudden, acute, accompanied by an increase in body temperature and general cerebral symptoms: headache, nausea, vomiting, psychomotor agitation, partial or generalized seizures, impaired consciousness. Characteristic symptoms include myalgia, paresthesia, radicular pain, and meningeal symptoms. Focal neurological disorders (damage to the cranial nerves, paresis of the limbs, sensory disorders, ataxia, urinary disorders) depend on the location of the inflammatory process.

OREM current in most cases monophasic, with significant variations regarding the duration of the disease and the duration of recovery of patients. Considering that ADEM in most cases is characterized by the presence of a multifocal lesion in the central nervous system, repeated monofocal lesions are also interpreted as manifestations of ADEM.

However, repeated attacks of ADEM also occur. If relapse of the disease occurs a short time after the initial presentation and is combined with infection or steroid withdrawal, the term multiphasic disseminated encephalomyelitis (MDEM) is used. The presence of relapses and progression of the disease indicates multiple sclerosis.

Diagnosis of ADEM is based on the following clinical criteria:

• a history of viral infections or vaccinations, inflammation of the upper respiratory tract, intestinal infections that may precede the disease itself, or the disease occurs after a few days of the prodromal period (fever, malaise, myalgia, etc.);
• mainly monophasic course of the disease;
• neurological disorders that indicate the presence of disseminated lesions of the central nervous system;
• CT and MRI reveal multifocal changes in the white matter of the cerebral hemispheres, cerebellum, and pons. Foci of damage to the gray matter of the brain (basal ganglia, thalamus, hypothalamus), and cortical lesions can be determined. In ADEM, the corpus callosum is usually not affected. MRI findings in ADEM vary widely from large focal lesions with perifocal edema to none pathological changes at all. After a few weeks of treatment, partial disappearance of areas of inflammation/demyelination is observed. In the case of ADEM, new lesions do not appear. The detection of new foci of demyelination over 6 months indicates multiple sclerosis. However, the diagnosis must be established carefully, referring to the Mac Donald diagnostic criteria;
• changes in the cerebrospinal fluid are characterized by slight lymphocytic pleocytosis and increased protein levels and cerebrospinal fluid pressure. Serological studies antibodies against different viruses are not determined, but polymerase chain reaction (PCR) remains for the most part negative. Evoked potential studies are also uninformative.

Differential diagnosis of ADEM and relapsing-remitting multiple sclerosis is very difficult. In every case when ADEM is suspected, it is necessary to remember the possibility of the first attack of multiple sclerosis. Clinical observations indicate that in 25-35% of cases typical multiple sclerosis subsequently develops. Some authors consider ADEM to be part of the disease spectrum. For differential diagnosis, MRI examination is important: hyperintense, large lesions, which often occupy the entire hemisphere of the brain, are more characteristic of ADEM than of multiple sclerosis. ADEM must also be differentiated from meningoencephalitis and a brain tumor.

Treatment. The mainstay of treatment for ADEM is suppression of the immune response to an infectious agent or vaccination. For this purpose, high doses of corticosteroids are prescribed: 500-1000 mg of methyl prednisolone in 400 ml isotonic solution sodium chloride intravenously for 3-5 days with a further transition to oral administration prednisolone according to an alternating regimen. In case of insufficient effectiveness of corticosteroids, plasmapheresis and treatment using human immunoglobulin for intravenous administration (0.4 g/kg for 5 days) are performed. If an infectious factor that causes the development of ADEM is detected in the blood or other tissues, antibacterial and antiviral therapy is prescribed. Symptomatic therapy is used: dehydration, anticholinesterase, antihistamine, anticonvulsant. In some cases, the use of cytostatics is successful.

Encephalomyelitis is an acute or subacute inflammatory process that affects the brain and spinal cord. Pathological foci can be localized in any part of the nervous system, but more often disseminated, that is, scattered. The symptoms of the disease will depend on their location.

Encephalomyelitis is considered to be closely related to multiple sclerosis. Indeed, these two diseases have much in common: under the influence causative factor the body begins to produce antibodies that attack and destroy myelin, a special protein that is part of all pathways of the nervous system. As a result of this, in the head and spinal cord foci of inflammation are formed. However, multiple sclerosis is a chronic disease, prone to progression and periodic exacerbations. Multiple sclerosis significantly impairs the patient's quality of life and can be fatal. Encephalomyelitis in most cases - acute illness with rapid development and a relatively favorable outcome. Death is extremely rare. It is possible in the acute period with extensive damage to the nervous system, especially when the nuclei of the cranial nerves of the bulbar group are involved. Encephalomyelitis quite often leaves behind symptoms in the form of a certain neurological deficit; they remain for life, significantly worsening its quality. Some become disabled.

Symptoms and types of encephalomyelitis.

The pathways of almost all parts of the nervous system have myelin sheaths. Theoretically, damage can occur in any area. When examined, foci of inflammation can be found everywhere, but for reasons still unknown in different people they can be located predominantly in certain departments. At the onset of the disease the following are observed:

• malaise;
• increased body temperature (in 50% of cases the temperature remains normal);
• signs of a cold (runny nose, sore throat);
• gastrointestinal disorders;
• slight numbness, tingling in the limbs;
• nausea, vomiting;
• lethargy, drowsiness, sometimes giving way to agitation and convulsions.

Subsequently, a picture of predominant damage to a certain part of the nervous system begins to emerge, depending on which the following types encephalomyelitis.

1. Central (predominantly involving the brain):

• paralysis and paresis of the limbs;
• convulsive syndrome such as epileptic seizures;
• speech disorders;
• impaired coordination of movements.

2. Polyradiculoneuropathy (damage to the spinal cord and its roots):

• disturbances of sensitivity on the trunk and limbs (temperature, pain);
• dysfunction pelvic organs(by type of retention, urinary and fecal incontinence);
• trophic changes in the skin (dryness, bedsores);
• pain along the spine and paravertebral muscles, which can spread along the nerve trunks, simulating the picture of lumbago.

3. Opticoencephalomyelitis, or retrobulbar neuritis, is diagnosed when the optic nerve is involved in the process:

• sharp decrease in vision;
• “veil” before the eyes;
• pain in the depths of the orbit, intensifying with movements of the eyeball.

4. Stem with damage to the nuclei of the cranial nerves:

• facial with typical manifestations of neuritis of the facial nerve;
• oculomotor group;
• bulbar, manifested by impaired swallowing, respiratory function and cardiac function.

Sometimes encephalomyelitis may begin with visual impairment or bulbar syndrome, which causes misdiagnosis.

Most often the disease develops acutely. In the initial period, the picture is blurred; only at week 2 certain neurological symptoms begin to clearly emerge, which, with proper and timely treatment regress over time. In a subacute course, the process of increasing manifestations can last up to 2-3 months.

Causes of the disease

Reasons why the immune system begins to produce proteins against its own cells nerve tissue, remains completely unclear. However, it has been noted that encephalomyelitis most often develops after:

• viral infections, especially those accompanied by a rash (measles, rubella, chicken pox, herpes);
• administration of vaccines (post-vaccination encephalomyelitis);
• colds (flu, bronchitis, pneumonia);
• traumatic brain injuries;
• allergic reaction regardless of the cause;
• any situation accompanied by a decrease in immunity.

Possible consequences:

• complete recovery or mild neurological deficit;
• severe disabling defect;
• transition to multiple sclerosis (very often the onset of multiple sclerosis is mistaken for encephalomyelitis).

Treatment of acute disseminated encephalomyelitis

Treatment should begin immediately after diagnosis. The main diagnostic method is MRI of the brain, which allows identifying foci of demyelination. If it is not possible to conduct a study, if encephalomyelitis is suspected, trial therapy is carried out:

1. Purpose hormonal drugs(prednisolone, dexamethasone). For 3-5 days, the drugs are administered intravenously, then intramuscularly for another 3 days. Subsequently, tablet forms are prescribed with a gradual dose reduction. Hormones are given in high doses to suppress the immune response and stop the destruction of myelin.

2. Plasmapheresis, in which the blood is mechanically cleansed of aggressor antibodies.

3. If there is a clear connection with a bacterial or viral infection, antibiotics are used and antivirals.

4. Antiallergic (suprastin, diphenhydramine).

5. Vitamins, especially group B.

6. Symptomatic therapy (analgesics, antipyretics).

7. If necessary, connect to a ventilator and cardiac monitor.

IN recovery period— pine baths, physical therapy, massage, sanatorium-resort treatment.

Traditional treatment

In the acute period of encephalomyelitis, treatment should be carried out in a hospital setting. In this case, potent medications are used, so traditional treatment unacceptable at this stage. During the recovery phase, to avoid unpleasant consequences, and also to maintain the functions of the nervous system after an illness, you can use:

1. Onions with honey. Peel the onion and grate it on a fine grater. Squeeze out the juice and mix with honey (1:1). Take a teaspoon three times before meals for a month.
2. Mumiyo. Not a large number of— Dissolve 5 g in 100 ml of water. Drink 1 teaspoon 3 times a day 1 hour before meals.
3. She-headed mordovnik. Measure out 3 tbsp. spoons of fruit, pour a glass of boiling water into a thermos and leave for 12 hours. Drink in small portions throughout the day. Course 2 months.

Disseminated encephalomyelitis is a rare neurological disease that occurs as a result autoimmune disorders. Disseminated encephalomyelitis develops against the background of viral and infectious diseases, occurring at high temperatures. At timely application In a medical institution, the disease responds well to treatment, without the development of complications in the future.

The Yusupov Hospital performs diagnostics of any complexity. If disseminated encephalomyelitis is suspected, the patient will be examined in as soon as possible. The sooner the diagnosis is made, the sooner treatment can be started. effective treatment. The Yusupov Hospital uses modern equipment.

Disseminated encephalomyelitis syndrome

The human immune system is aimed at protecting the body from the harmful effects of foreign objects (viruses, bacteria, etc.). Elements of the immune system (lymphocytes, leukocytes, macrophages, antibodies) begin to fight pathogenic objects, trying to destroy them. In autoimmune conditions, elements of the immune system begin to attack healthy cells in the body.

Disseminated encephalomyelitis is an autoimmune disease in which pathological processes occur in the brain. The immune system destroys the myelin sheaths of neurons, thereby disrupting the functioning of brain cells.

The trigger for the development of disseminated encephalomyelitis is a viral or infectious disease with an increase in body temperature above 38C. Quite often, the cause of the development of disseminated encephalomyelitis is upper respiratory tract infections. Encephalomyelitis can also be caused by:

• herpes virus,
• Epstein-Barr virus,
• cytomegalovirus,
• chicken pox,
• measles,
• mumps,
• rubella,
• various bacteria.

Disseminated encephalomyelitis is more common in childhood, since the child’s immune system is still immature. Sometimes disseminated encephalomyelitis occurs after vaccination using a weakened live bacterium, which is also an abnormal response of the immune system.

Disseminated encephalomyelitis: symptoms

The first signs of neurological pathology appear one or several weeks after the first episode of fever. Disseminated encephalomyelitis begins as common cold with high fever, body aches. Then headaches arise, which are difficult to relieve with medications. After a short period of time, a more pronounced neurological picture develops:

• confusion,
• numbness in the arms and legs,
• convulsions,
• epileptic seizures,
• speech disorders,
• double vision,
• swallowing disorder
• drowsiness,
• hallucinations,
• breathing disorder,
• coma.

Disseminated encephalomyelitis is characterized by a rapid increase in symptoms, so it is important not to delay a visit to the doctor. The Yusupov Hospital operates 24 hours a day, seven days a week, and will provide assistance at any time needed.

Disseminated encephalomyelitis with cerebellar ataxia

Disseminated encephalomyelitis affects various areas brain. The severity of the clinical picture will depend on the degree of damage to a particular area. Often disseminated encephalomyelitis affects the cerebellum, causing cerebellar ataxia. The pathology is manifested by impaired coordination of movements various groups muscles. Clumsiness in movements and incoordination are accompanied by intermittent speech and impaired coordination of eye movements. Gait is disturbed, involuntary movements of the limbs may occur.

Disseminated encephalomyelitis: diagnosis

The clinical picture of multiple encephalomyelitis is very similar to multiple sclerosis. After laboratory and instrumental diagnostic methods, the diagnosis of “disseminated encephalomyelitis” is established quite accurately. To determine the disease, the cerebrospinal fluid is examined using a lumbar puncture and an MRI is performed.

Cerebrospinal fluid analysis will show increased protein and lymphocyte levels. An MRI will clearly show areas of damage to the white matter of the brain. White matter is nerve fibers covered by the myelin sheath. In disseminated encephalomyelitis, the membrane is destroyed, forming lesions of various sizes. Visualization of the disease on MRI images helps to reliably establish the diagnosis.

Disseminated encephalomyelitis: treatment

Drug therapy is used to treat disseminated encephalomyelitis. The disease is highly treatable. Timely initiation of therapy is the key to rapid recovery and minimization of residual effects. The following drugs are used for treatment:

• corticosteroids,
• plasmapheresis,
• antibiotics,
• maintenance therapy drugs.

Corticosteroids significantly speed up the recovery process for disseminated encephalomyelitis.

At the Yusupov Hospital, patients receive a full range of medical services. The best neurologists in Russia work here, doctors of sciences who have extensive experience in treating neurological diseases (including disseminated encephalomyelitis). The patient can receive treatment in a comfortable hospital, where he will receive round-the-clock qualified assistance. You can make an appointment and get advice from specialists by phone.

What is encephalomyelitis

Encephalomyelitis is an inflammatory process that simultaneously occurs in the brain and spinal cord. In fact, it is a combination of myelitis and encephalitis. As this disease progresses, a person experiences degeneration of myelin, which is a kind of insulating substance for nerve fibers. Thanks to it, the passage of electrical impulses becomes possible. Inflammatory processes also begin in the brain and blood vessels with the formation of necrotic areas.

Causes of pathology

The causes of encephalomyelitis have not yet been thoroughly studied. But during the research, it was noticed that most often the pathology progresses after:

• viral infections, especially those that were accompanied by the appearance of a specific rash on the skin (chickenpox, rubella, herpes);
• colds;
• allergic reaction;
• introduction of specific vaccines;
• traumatic brain injuries.

Scientists believe that encephalomyelitis may be hereditary in some patients. This is due to the fact that in such people some proteins of the nervous tissues have a similar structure to proteins infectious agents. As a result, the immune system mistakenly begins to attack its own myelin cells.

Despite the fact that encephalomyelitis can affect people of all ages, it is most often recorded in childhood. An interesting fact is that in children the disease is much milder than in adults.

Classification of the disease

Currently there is no unified classification of the disease. But experts distinguish several types of encephalomyelitis based on the nature of the inflammatory process, the rate of increase in symptoms, the localization of the lesion and many other factors. To determine what type of disease a patient has, doctors sometimes need to conduct several different examinations.

Based on the form and speed of development, the following types of encephalomyelitis are distinguished:

• acute, in which symptoms increase over several hours;
• subacute, developing over several weeks;
• chronic, constantly progressing over a long time.

Based on the localization of inflammatory and necrotic foci, encephalomyelitis is divided into several types:

• encephalomyelopolyradiculoneuritis, in which all parts of the central nervous system are affected;
• polyencephalomyelitis - characterized by disorders in the nuclei of the cranial nerves and in the gray matter of the spinal cord;
• optoencephalomyelitis - combines damage to the central nervous system and optic nerves;
• disseminated (scattered) encephalomyelitis - is that small foci of inflammation are scattered in different parts of the central nervous system.

Encephalomyelitis is classified as:

• primary - develops as an independent disease;
• secondary - acts as a complication of another pathology.

Primary encephalomyelitis is usually caused by various neuroinfections. The cause may be viruses such as herpes, enterovirus, cytomegalovirus, etc. Most often, the course of such diseases is acute, the symptoms develop very quickly.

Some types of viral encephalomyelitis can be contagious, and loved ones need to take precautions when communicating with the patient.

Secondary encephalomyelitis develops against the background of other diseases or due to the influence of external factors:

• infectious encephalomyelitis:
  • viral - caused by influenza, herpes, rabies, etc. viruses;
  • bacterial - the source is various pathogenic microorganisms (brucella, chlamydia, mycoplasma, toxoplasma, rickettsia);
• post-vaccination - is a side effect of vaccinations, most often against diphtheria, whooping cough, measles, rubella and chickenpox;
• myalgic is a fairly new disease, which is also called post-viral fatigue syndrome.

There are also special autoimmune types of encephalomyelitis, in which the body begins to confuse the myelin sheaths with foreign tissues of viruses and destroys them. These are the following varieties:

• acute, subacute, chronic disseminated encephalomyelitis (differ in the speed of development of demyelination processes in the spinal cord and brain);
• rabies post-vaccination - is a secondary disease, observed 20 days after rabies vaccinations.

Symptoms of encephalomyelitis

Acute disseminated encephalomyelitis develops very quickly. In the first days, this disease may be confused with ordinary flu or ARVI, as a person’s temperature rises sharply, chills, and muscle pain appear. But later other, more serious signs appear that indicate damage to the central nervous system. The first signs of this are cerebral and meningeal symptoms:

1. The patient's intracranial pressure increases, and blood microcirculation in the central nervous system is disrupted. Severe headaches and dizziness are felt almost immediately. The person becomes lethargic, sleepy, and may lose appetite. If you change positions, walk or look at the light, hear loud sounds, the pain in the head will intensify.
2. It is very common to experience persistent nausea. Even after vomiting there is no relief, the patient continues to feel sick.


3. At some point, convulsions may occur, and muscles in different parts of the body begin to contract involuntarily. Most often, this symptom appears in young children and adolescents.
4. The mental state can be either depressed or overexcited. In the latter case, patients may behave aggressively, become very nervous, and perform chaotic and unnecessary actions.
5. In severe cases, consciousness is depressed. Patients begin to delirium, see hallucinations, fall into lethargic state, they become as if stunned, with difficulty perceiving what is happening around them. If the condition worsens, coma may occur.
6. One of the common meningeal symptoms is stiffness (increased stiffness) of the neck muscles. They become uncontrollable, and the patient cannot bend his head down and reach lower jaw to the chest.
7. Brain damage is checked by the Brudzinski test. If a patient lying on his back tilts his chin toward his chest, his legs will involuntarily bend at the knees.

Also, with acute disseminated encephalomyelitis, various focal symptoms appear, which indicate specific affected structures of the central nervous system:

1. Pyramid signs appear very strongly in those patients whose neurons in the cerebral cortex are damaged. Due to them, conscious muscle contractions should normally be produced. But during the disease, people experience paralysis of the lower and upper limbs, the ability to squeeze the hand and make small movements decreases. Patients also experience increased tendon reflexes, and when struck with a special hammer on the knee or elbow, the limbs begin to twitch too sharply. In some cases, facial expressions may be impaired and paralysis of the oculomotor nerve may occur.
2. Cranial nerve damage is usually associated with optic nerve degeneration. Almost 30% of all patients with encephalomyelitis have vision problems. In mild cases, the severity may decrease slightly, and with more serious lesions the person even goes blind. If other nerves are affected, problems may begin with swallowing reflex, hearing loss appears, the sense of smell disappears.
3. Aphasia (partial or complete loss of speech) occurs when the speech centers of the brain are damaged.
4. Isolated transverse spinal cord lesions are observed in a quarter of all patients with encephalomyelitis. External manifestations are sometimes not observed and abnormalities are detected by magnetic resonance imaging. However, urinary and fecal incontinence, paralysis of the arms and legs, and decreased sensitivity in different parts of the body may occur.
5. Damage to the cerebellum manifests itself very characteristic violation coordination. A person may have difficulty walking; it becomes unsteady and unsteady. Fine motor skills are also impaired. During the examination, the patient cannot eyes closed get your finger into the tip of your nose.
6. Polyneuropathy of the extremities manifests itself in a slight decrease in the sensitivity of the arms and legs, and the skin may tingle slightly. Muscle strength also decreases and limbs become weaker.

If acute encephalomyelitis is not treated in time, it can develop into a chronic form, which is much more difficult to get rid of. It is characterized by alternating exacerbations and remissions. But periods of calm can be very short-term, and soon a deterioration in well-being occurs again. At this time, the symptoms completely repeat the course of acute disseminated encephalomyelitis. It is worth understanding that the patient’s condition will only get worse and worse.

Opticoencephalomyelitis, in addition to the main symptoms, is characterized by various lesions of the optic nerve. Patients begin to complain of decreased visual acuity, sometimes a veil appears before the eyes, which prevents them from clearly seeing the surrounding space. Also a common symptom is the appearance of pain in the orbit, which tends to progress as the disease progresses.

A very interesting and recently discovered type of encephalitis is its myalgic form, which doctors otherwise call post-viral fatigue syndrome. Occurs after various viral diseases or vaccinations. Doctors are not always able to determine correct diagnosis, since the symptoms are very similar to a common infectious disease:

• constant feeling of fatigue;
• energy depletion even after a small load;
• aching joints;
• muscle pain;
• depressive states;
• frequent mood changes;
• indigestion.

Video: chronic fatigue syndrome after infectious diseases

Diagnostics

At the first signs of encephalomyelitis, you should consult a neurologist. He will be able to make a primary diagnosis after examining the patient and taking an anamnesis. If a person has precipitating factors such as infectious lesions or a recent vaccination, this most likely indicates encephalomyelitis. Additionally, the doctor prescribes the following studies:

• magnetic resonance imaging (MRI) - allows you to obtain very accurate layer-by-layer images of any part of the body and see tumors, areas of inflammation or necrotization, hemorrhages and other disorders in the central nervous system;
• computed tomography (CT) - helps to examine internal organs, including the brain and spinal cord, using x-rays;
• myelography is an x-ray method for examining the spine using special contrast agents that allow you to see various diseases spinal cord.

The following tests may also be prescribed:

• lumbar puncture with sampling of cerebrospinal fluid, in which it will be visible increased content proteins and lymphocytes;
• blood test for antibody levels, in which IgA and IgE will be elevated.

Differentiation of pathology

During differential diagnosis, it is very important to distinguish encephalomyelitis from multiple sclerosis. The latter disease is chronic and constantly progressive, as a result the myelin sheath of the nerves is also destroyed. It usually begins with focal symptoms, while encephalomyelitis first manifests itself with general cerebral and intoxication signs.

Also, differential diagnosis is carried out with encephalitis, meningitis, tumor formations in the brain, etc.

Treatment

Encephalomyelitis can only be treated under the supervision of a doctor. This is very serious illness and self-prescribing medications or folk remedies can be life-threatening. Each patient is treated individual approach and medications are prescribed based on the cause of encephalomyelitis. If a person is in very serious condition, the following procedures will be necessary:

• artificial ventilation lungs with respiratory dysfunction;
• plasmaphoresis to cleanse the blood of antibodies and various immune complexes;
• tube feeding for impaired swallowing reflex;
• installation of a catheter in the bladder in cases of urinary retention;
• cleansing enemas for paresis of the intestinal tract.

Drug therapy

At drug treatment The dosage and regimen of medications is selected individually by the attending physician. There is a whole range of drugs that are prescribed for different types of encephalomyelitis:

1. Antiviral drugs - prescribed for an infectious cause of the onset of the disease (leukocyte human interferon).
2. Antibiotics - needed in case of bacterial infection (Ampiox, Kefzol, Gentamicin). At chronic tonsillitis Bicillin is prescribed.
3. Margulis-Shubladze vaccine - prescribed for infection with rabies or human acute encephalomyelitis virus. It is carried out in the subacute period for those patients who exhibit small residual effects after the disease.
4. Steroidal anti-inflammatory drugs - necessary due to the autoimmune nature of encephalomyelitis (Prednisolone).
5. B vitamins are prescribed to support the functioning of the nervous system (Neuromultivit).
6. Vitamin C is effective for maintaining and strengthening the immune system and increasing the body's resistance to infections.
7. Diuretics are necessary in the presence of cerebral edema (Furosemide, Diacarb).
8. Antispasmodics - indicated for various tremors and convulsions (Dibazol).
9. Muscle relaxants are prescribed to those patients who have increased muscle tone (Mydocalm, Cyclodol).
10. Nootropic drugs - necessary to restore higher mental functions brain (Encephabol, Piracetam).

Photo gallery: drugs used in the treatment of encephalomyelitis

Folk remedies

Encephalomyelitis is a very serious disease that cannot be treated with traditional medicine. During periods of exacerbation, treatment is carried out only in a hospital with potent medications that are aimed at achieving a quick effect.

During the period of remission or rehabilitation, it is permissible to use traditional medicine, but only after consultation with the doctor.

Potato compress with honey

In some situations, it is possible to use warm compresses on the affected areas of the spine if the disease is not in the acute stage. They are not allowed to be placed in the heart and neck area.

You can use a compress of potatoes with honey:

1. Take a few potatoes, boil them, mash them, mix with two tablespoons of honey and place in cheesecloth.
2. Place the wrapped cake on the skin previously lubricated with nourishing cream. Cover the patient with a blanket or blanket and leave for one hour.
3. After the designated time, remove the compress and wipe the skin dry. It is best to carry out this procedure at night, so that after it the person falls asleep and does not get out of bed until the morning.

Infusion of Mordovnik sharogolatum

The use of Echinops infusion is effective for various lesions of the central nervous system, it promotes recovery motor activity limbs. Skeletal muscles are also toned.

To prepare the medicine you need:

1. Take three tablespoons of fruit and pour a glass of boiling water.
2. Leave for ten hours in a thermos.

Take 2 teaspoons of infusion twice a day before meals. The course of treatment is about two months.

Onion juice with honey

This remedy is excellent for restoring the body's strength after encephalomyelitis. Phytoncides contained in onions have an antibacterial effect. Honey helps eliminate inflammatory processes and improves metabolism.

Onion juice can be made in any convenient way. You can use a juicer, grater or other device. The resulting liquid must be mixed with the same amount of honey. For one month, you need to take one teaspoon of the resulting product three times a day before meals.

Rehabilitation

Patients do not always fully recover from encephalomyelitis. Many people require various rehabilitation procedures to improve the functioning of all parts of the body. Until complete recovery, you should avoid going to saunas, steam baths and sunbathing.

Restorative massage

Only a specially trained person should perform therapeutic massage on patients who have suffered encephalomyelitis. During the procedure, the skin, subcutaneous tissue, blood vessels and nerve endings are treated. Thanks to improved blood circulation, metabolism is restored, the affected limbs begin to return to health faster. normal condition, strength increases in muscles weakened by the disease. Massage will also be useful for those patients who have increased muscle tone, spasms are observed. The attending physician must refer you for the procedure, as there may be contraindications.

Physiotherapy

After encephalomyelitis, there are often cases when patients feel weakness in the limbs and disturbances in gait and motor skills appear. In this situation good results show physical therapy classes. An individual complex is selected for each person, which helps to maximize the use of the affected areas, strengthen the muscle corset and improve blood circulation.

If the patient is in a supine position, he can perform gymnastics directly on the bed. Here are some exercises:

1. Bend your elbows and rest them on the surface of the bed. Rotate the brushes first clockwise, then in the other direction. Then clench your fists and unclench them completely, spreading your fingers in different directions.
2. Stretch your calves while lying down. Point your feet toward you, and then point your toes out. Then perform rotational movements with your foot.

If the patient is able to walk, then it is necessary to perform exercises that consist of bending the torso forward and backward, from side to side and clockwise. You should also try to touch the floor with your fingers. Don't forget about cervical region spine, it needs to be warmed up by performing head rotations.

Video: exercise therapy complex for the lower extremities

Transcranial magnetic stimulation

This procedure is necessary for those people who, after encephalomyelitis, have various paresis and paralysis of the limbs. Using a special device, the motor cortex of the brain is stimulated, and the specialist observes which muscles begin to contract in the patient. Based on the results obtained, it is possible to trace the dynamics of improvement in the conductivity of nerve impulses and identify the remaining areas of the affected motor pathways.

Electrical myostimulation

It is better to carry out this procedure in a clinic with a doctor. With the help of weak electrical impulses, the patient’s muscles are affected, due to which they begin to contract. There is a kind of imitation of a natural process in the body. Thanks to this method, recovery occurs muscle tissue, metabolism is normalized, the functioning of the nervous system improves.

Thermal treatments

If the patient experiences paralysis due to increased tone muscles or when they spasm, the doctor may prescribe warm baths:

1. Turpentine baths, due to essential oils and terpenes, have an irritating effect on the nervous system and promote the production of heparin, prostaglandins and various mediators. Blood circulation and metabolism improve, and the process of restoration of damaged tissue occurs. For a bath with a volume of two hundred liters, you need to add approximately 50 ml of turpentine solution. The water temperature should be 37 o C. Take baths every other day for ten minutes. The course consists of 10 procedures.
2. Mustard baths also have an irritating effect on the skin and nerve endings. Patients' immunity is increased and blood circulation is activated. Add 150 g of mustard to the bath; the water temperature should not be higher than body temperature. The duration of the procedure is five minutes. 10 sessions are carried out every other day.
3. Sage baths, due to evaporation and the influence of essential oils, help accelerate metabolic processes and improve the functioning of the cerebral cortex. Add 50 ml of musk sage concentrate to the bath. The water temperature should be 36–37 o C. Carry out the procedure every other day for fifteen minutes. For myelitis, 10 sessions are indicated.

Video: turpentine baths

Prognosis and possible complications

In almost 70% of cases, encephalomyelitis is completely cured and leaves no consequences. But in some situations, the following residual effects and complications may be observed:

• urinary and fecal incontinence;
• partial paresis of the limbs;
• weakness in arms and legs;
• formation of bedsores;
• visual and hearing impairment;
• impaired coordination of movements;
• aphasia;
• paralysis;
• various mental disorders.

The duration of treatment depends on the timeliness of contacting a doctor and the speed of development of symptoms. The more pronounced the pathological signs were, the more difficult it was for the patient to recover. In most cases, a person’s life span is not shortened and after recovery he can return to his normal rhythm of life. Fatalities, depending on the type of encephalomyelitis, reach from 5 to 20%.

Currently, there have been cases of transition from multiple encephalomyelitis to multiple sclerosis. Scientists cannot yet accurately identify the reasons for this process. This usually occurs in those patients in whom the acute course of the disease has become chronic.

If a woman was pregnant and fell ill with infectious encephalomyelitis, this may affect the condition of the fetus. The ability to give birth is determined individually, depending on the patient’s condition. It also takes into account what medications were taken, since many of them have Negative influence on the development of the child. Sometimes an abortion may be indicated.

An inflammatory lesion of the central nervous system, presumably of an autoimmune nature, is called acute disseminated encephalomyelitis. It manifests itself as a complication of a recent infectious disease or may develop due to immunization. Treatment of the disease occurs under the supervision of a doctor.

The concept of pathology

Acute disseminated encephalomyelitis is quite dangerous illness, which affects the brain and spinal cord. If treatment is not started in a timely manner and in complex cases, death is possible.

It is believed that children are most susceptible to pathology. The average age at which the disease occurs in this category of people is 8 years. It can begin in infancy (3 months) and is most common before age 10 years. In adulthood and old age, the disease begins at 33.9 and 62.3 years, respectively.

There are primary and secondary forms of the disease. In the first case, it appears as a result of a viral infection. Secondary acute encephalomyelitis develops due to the appearance of complications after various ailments of a viral nature or after vaccination.

Classification

Based on the area affected by the disease, the following types of encephalomyelitis are distinguished:

1. Disseminated myelitis. In this case, the functioning of the spinal cord is disrupted.
2. Opticomyelitis and optoencephalomyelitis. They are characterized by a similar pathogenesis, with lesions of both the brain and spinal cord, as well as damage to the optic nerves.
3. Polyencephalomyelitis. With this disease, the functioning of the nuclei of the cranial nerves located in the brain stem is disrupted, and the spinal cord (its gray matter) is also affected.
4. Encephalomyelopolyradiculoneuritis. One of the most common such pathologies. In this case, disturbances in almost all components of the nervous system are observed.

Acute disseminated encephalomyelitis is most often diagnosed. This disease affects different parts of the brain and spinal cord. Pregnancy with acute disseminated encephalomyelitis proceeds as usual.

There is no uniform classification of this disease. In general, the following varieties are distinguished:

• brainstem encephalitis;
• cerebellite;
• neuromyelitis optica;
• optic neuritis;
• acute transverse myelitis;
• acute hemorrhagic leukoencephalitis.

With the first type there are following signs:

• respiratory disorders;
• neuritis of the facial nerve;
• violation of the swallowing process.

Currently, myalgic encephalomyelitis is also distinguished. It develops after vaccination or an illness of viral origin. At the same time, following symptoms:

• muscle pain;
• disorders of the gastrointestinal tract;
• frequent mood changes;
• depression;
• the appearance of pain syndromes in joint areas;
• fast fatiguability after light loads;
• chronic fatigue.

Causes

To date, they have not been fully studied. It is still unknown for what reasons the body begins to produce proteins aimed at fighting the nervous system.

The progression of the disease is noted according to the following:

• colds;
• allergy;
• decrease ;
• introduction of certain types of vaccines;
• viral infections, primarily those that cause various skin rashes: rubella, chickenpox, herpes;
• traumatic brain injuries.

Signs

The disease begins quickly. Symptoms of acute disseminated encephalomyelitis are divided into general cerebral and focal. The first include the following:

• decreased intelligence;
• weakening of memory;
• disturbance of consciousness;
• epilepsy attacks.

In their absence, the diagnosis of “acute disseminated encephalomyelitis” is doubtful.

Focal symptoms manifest as multiple brain lesions. Basically they are combined as follows:

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

Only based on these signs can only a highly qualified doctor make a correct diagnosis.

The two categories of symptoms of acute disseminated encephalomyelitis described above appear within 7-14 days, after which clinical picture becomes less pronounced. As the disease progresses, disturbances in the peripheral nervous system may appear. A condition such as polyneuropathy may appear.

Different symptoms may appear depending on which part of the brain is affected.

Initial signs may appear already during an infectious disease that causes encephalomyelitis, with asthenia and an increase in body temperature. These include:

• tingling sensation in the legs - quite rare;

• disturbances in the gastrointestinal tract;
• increased excitement, sometimes replacing lethargy;
• runny nose, pain and sore throat;
• drowsiness;
• an increase in body temperature is possible, although not necessary;
• headache;
• general malaise.

If the brain is affected, the following signs of the disease may be observed:

• emergence convulsive syndrome, similar to epileptic seizure;
• paresis of limbs;
• paralysis;
• speech disorders.

When the spinal cord roots are damaged, next symptoms:

• pain syndrome, spreading along the spinal column, reminiscent of the clinical manifestations of lumbago;
• the functioning of the pelvic organs deteriorates: there may be a delay in urination, bowel movements, or the opposite picture in the form of incontinence;
• pain and temperature sensitivity of the body decreases;
• trophic changes in the epidermis appear.

When the optic nerve is damaged, the following symptoms are observed:

• pain appears in the orbit, which gradually increases, especially when making sudden movements with the organs of vision;
• a “veil” forms before the eyes;
• vision deteriorates.

The main differences between acute disseminated encephalomyelitis and multiple sclerosis are as follows:

• unlike the latter, autoimmune reactions to myelin antigens do not have a chronic course and are limited to one exacerbation;
• the structure of the lesions in both diseases is the same, however, the inflammatory dynamics and edema are more pronounced in the disease under consideration, oligodendrocytes are less affected.

Diagnostics

To identify the disease, MRI is performed in acute disseminated encephalomyelitis using contrast. Features of the disease are easily detected by a doctor on an image or screen. In the FLAIR and T2 modes, asymmetric hyperintense foci are determined that have poor outlines in both the white and gray matter of the brain, and in the second they may not be expressed. They can be small (up to 0.5 cm), large (more than 2 cm) and medium (having intermediate values). Sometimes there are large confluent lesions with perifocal edema, which cause displacement of surrounding structures. The optic thalamus may also be involved. In large areas of inflammation, hemorrhages are observed. The contrast agent accumulates in the lesions with varying intensity. They can be detected in the spinal cord in a small number of cases, not exceeding 30%. After identifying the disease and treating it, patients are recommended to undergo a repeat MRI after six months. A decrease in areas of demyelination or their complete disappearance indicates a correct diagnosis and the exclusion of multiple sclerosis.

In addition, diagnosis, if necessary, can be performed by performing a lumbar puncture. In this case, the patient is placed on his side with local anesthesia. Between lumbar vertebrae A needle is inserted to withdraw a small amount of cerebrospinal fluid, which is analyzed. If the disease is present, a large number of lymphocytes will be found in it.

Additionally, perimetry, ophthalmoscopy, and consultation with an ophthalmologist may be prescribed.

When making a diagnosis, it is imperative to take into account the presence in the clinical picture of signs of cerebral syndrome or encephalopathy. The latter includes patient complaints of nausea, vomiting, headaches, while disturbances in behavior and consciousness are noted - from stupor and drowsiness up to the development of coma of varying degrees.

Variants of the course of the disease

Currently there are three of them:

• monophasic;
• returnable;
• multiphase.

In the first case, a single episode of neurological impairment occurs and the disease subsequently resolves.

In the recurrent variant, the same symptoms or even their increase are observed 3 months after the onset of the first attack or 30 days after the end of taking corticosteroids.

The multiphase course is characterized by the fact that after the same period of time new complaints and symptoms appear.

Goals of therapeutic treatment

The patient must first of all know that acute disseminated encephalomyelitis is curable. But to achieve this, you need to carry out appropriate treatment, which should be aimed at:

• identification and treatment of infections, which prevents its transformation into multiple sclerosis; every six months you need to check for their presence by doing control immunograms;
• control immune condition organism to select optimal antiviral therapy;
• the maximum possible restoration of the functioning of brain areas affected by inflammation by stimulating remyelination;
• elimination of the aggressive behavior of immunity to the central nervous system with normalization of the first response to the entry of foreign microorganisms into the body.

Treatment of encephalomyelitis

Basic therapy is carried out with anti-inflammatory drugs steroid drugs. Medium or high doses of Prednisolone can be used depending on the patient’s condition, with a gradual reduction.

Corticosteroid therapy is carried out for 2-5 weeks. For warning side effects appoint intravenous administration immunoglobulins. Immune antibodies and immune complexes can be removed from the body using plasmapheresis, which is carried out in difficult cases.

Treatment of acute disseminated encephalomyelitis is aimed at eliminating the causes of the disease. For this purpose, antiviral agents belonging to the group of interferons are prescribed.

Sometimes when bacterial etiology antibiotics may be prescribed for diseases:

• "Kefzol";
• "Gentamicin";
• "Ampioks".

For the treatment of acute disseminated encephalomyelitis, accompanied by rheumatism, bicillin therapy is prescribed.

Mandatory symptomatic therapy. Hemodynamic restoration, artificial ventilation, and resuscitation measures can be performed.

To prevent cerebral edema, the following drugs are administered:

• "Furosemide";
• "Magnesia";
• "Diakarb."

How to eat when diagnosed with acute disseminated encephalomyelitis? Severe dysphagia should be accompanied by tube feeding.

With urinary retention in bladder a catheter is inserted. If intestinal paresis is observed, then enemas are done. If seizures are present, anticonvulsants are prescribed.

For treatment neurological disorders anticholinesterase drugs are prescribed: “Proserin”, “Galantamine”, vitamins B and C.

For convalescence, absorbable drugs are used: Cerebrolysin, Lidazu.

Treatment of disseminated encephalomyelitis may be accompanied by the use of nootropic drugs:

• "Nootropil";
• "Ginkgo biloba".

Doctors can also prescribe neuroprotectors: Mexidol, Semax.

Motor activity is restored through exercise therapy and massage. Transcranial magnetic stimulation is also performed.

In case of exacerbation of the disease, treatment is carried out in a hospital setting. In this case, potent drugs are prescribed medications.

Folk remedies

They can be used, but not during an exacerbation. They are mainly used during the recovery phase to maintain the functioning of the nervous system. Are used following recipes:

1. Ball-headed Echinops. Take 3 tbsp. l. fruits, pour 250 ml of boiling water, place in a thermos, in which they infuse for 12 hours. The resulting infusion is drunk in small portions throughout the day. Treatment is carried out for two months.
2. Mumiyo. 5 g dissolved in 100 ml of water. Take 1 tsp three times a day. 1 hour before meals three times a day.
3. Onions with honey. The onion is peeled and chopped using a grater. The juice is squeezed out, after which it is mixed with honey. Use 1 tsp three times a day. for a month.

They should not be the main method of treatment. Used with the permission of the attending physician.

Main differences in the course of the disease in children and adults

Previous vaccination or previous infectious disease most often causes acute disseminated encephalomyelitis in children. At the beginning of the development of the disease, they often experience fever, which is absent in adults. Children are characterized by encephalopathy syndrome, which occurs in a severe form. In adults, it manifests itself in mild or moderate form with possible appearance hallucinations and delusions.

Children often exhibit signs of meningoencephalitis with the occurrence of ataxia; in adults there are motor and sensory deficits, and radicular syndrome may be observed.

When performing MRI, lesions in children are located in the spinal cord, brainstem, cerebellum, cortex and region of the basal ganglia; periventicular lesions are rare. In adults, the latter are often observed; there is an increase in protein and pleocytosis.

Children go through the recovery process quite quickly. At the same time, adults have a long period of hospitalization with the same recovery.

The mortality rate in children is around 5%, in adults - around 8-25%. Young patients have the most favorable outcome of the disease. Adults are often characterized by a gross residual deficiency.

The disease may be characterized severe course, resulting in the formation of bulbar disorders, which can be fatal.

The consequences of acute disseminated encephalomyelitis may result in residual neurological deficits, leading to profound disability. Age-related changes are a risk factor for repeated exacerbations and transformation of the disease into multiple sclerosis.

Some patients acquire persistent symptoms, manifested in the form of sensory disturbances, visual impairment and paresis.

Prevention

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

• avoid physical overload during the course of the disease;

• give up bad habits and vaccinations;
• Avoid overheating and hypothermia of the body during the vaccination period.

Forecast

Acute period The disease lasts for 1.5-2 weeks. In most cases, the prognosis is favorable. Up to 90% of patients undergo a monophasic course. In the majority of patients (70-90%), symptoms are subject to regression within six months after the onset of the disease, which is associated with remyelination processes.

The prognosis worsens with recurrent and multiphase flow options. In this case, the acute form of the disease becomes chronic, and multiple sclerosis begins to develop.

Finally

Acute disseminated encephalomyelitis is characterized by disruption of the spinal cord and brain. In this case, patients may experience various symptoms depending on the affected areas and age. Diagnosis mainly involves an MRI of these organs. Treatment during an exacerbation is carried out in a hospital, includes taking corticosteroids and, depending on the accompanying ailments, other medications. In consultation with the doctor, herbal medicine can be used in combination for recovery. A more favorable prognosis is for the monophasic variant of the course of the disease and for children, although in adults with timely identified disease and correct implementation treatment - the prognosis is good.

Acute disseminated encephalomyelitis (ADEM) is a single-phase autoimmune demyelinating disease that affects the human nervous system. The disease is characterized by symptoms of brain damage and develops as a result of infection or vaccination; in other cases, ADEM occurs due to unknown reason– idiopathic form of the disease. In rare cases, a return or multiphase ADEM occurs. The main reason for the development of pathology is an autoimmune reaction of the patient’s body to myelin or other antigens, accompanied by an inflammatory process in the brain or spinal cord, or involving both the brain and spinal cord.

You can undergo a diagnosis of ADEM and differentiate the disease from multiple sclerosis at the neurology clinic of the Yusupov Hospital. Verification of the disease is very difficult; some researchers believe that ADEM is one part of the spectrum of multiple sclerosis. Studies have shown that about 30% of patients who have experienced ADEM subsequently suffer from multiple sclerosis.

OREM decoding (neurology)

ADEM is acute disseminated encephalomyelitis, a disease that affects the spinal cord and brain, causing the appearance of diffuse inflammatory lesions in the brain. Acute disseminated encephalomyelitis is caused by a neurotropic filter virus. There is a spontaneous form of the disease without prior infectious infection.

How does ADEM occur (neurology)

ADEM is a disease that is most often diagnosed in children under 10 years of age. Very rarely, acute disseminated encephalomyelitis is diagnosed in infants, the elderly and middle-aged people. ADEM can cause massive damage to brain tissue, progress and lead to disability over several weeks or months. ADEM is characterized by damage to the subcortical white matter and the presence of pathological foci in the gray matter. Diffuse demyelination develops, an autoimmune inflammatory process in the area of ​​the Virchow-Robin space, the function of which is considered to be the regulation of cerebrospinal fluid and the metabolism between cerebrospinal fluid and tissue fluid.

The development of the disease begins with the penetration of the virus, which can enter the body in several ways - through the gastrointestinal tract and upper respiratory tract, into the spinal cord and brain, penetration of the virus occurs through the blood and perineurally. The peripheral nervous system suffers less, the white matter of the brain is mostly affected, and the development of a demyelinating process is diagnosed. The development of ADEM can begin after vaccination against measles, diphtheria, rabies, tetanus, chicken pox, influenza, hepatitis B. The disease develops as a result viral infection: measles, chickenpox, herpes zoster, rubella, Epstein-Barr virus, herpes simplex, coxsackie, mumps, cytomegalovirus, infectious mononucleosis, intestinal and respiratory tract infections, chlamydia, mycoplasma pneumonia and other infections.

WECM starts with high temperature body (38°C - 39°C), severe nausea, vomiting, muscle pain, headache. Signs of damage to brain tissue may appear - seizures, ataxia, partial blindness, strabismus, loss of consciousness and other signs of pathology. IN pathological process Peripheral nerves and spinal roots are involved - the patient suffers from pain and paresthesia develops. Pelvic function disorders, tachycardia appear, and the skin becomes pale. In case of rapid progression of the disease, severe brain damage occurs within a few days. If the disease becomes chronic, when improvement is replaced by exacerbation due to infectious infection, then this form of the disease becomes difficult to differentiate from multiple sclerosis.

Dynamic MRI in ADEM

An MRI scan reveals multifocal lesions in the white matter of the brain (hemispheres, pons, cerebellum). It is also possible to identify foci of damage to the gray matter (thalamus, hypothalamus, basal ganglia), but the corpus callosum is not damaged. Changes detected by MRI may be large lesions accompanied by perifocal edema; in other cases, changes may be absent. Observation over time with timely treatment of ADEM after a few weeks shows the disappearance of individual areas of inflammation in the brain.

Can lesions increase in ADEM (neurology)

In the case of ADEM, new lesions do not appear; if an MRI reveals the appearance of new foci of the inflammatory process (demyelination), this indicates multiple sclerosis. If treatment is not prescribed in a timely manner, the inflammatory process spreads to other parts of the brain, causing disruption of various functions and demyelination of brain cells. ADEM in most cases is characterized by multifocal lesions of the nervous system, which can vary from small to large areas of damage.

At the Yusupov Hospital, much attention is paid to demyelinating diseases, they provide therapy for multiple sclerosis, autoimmune diseases nervous system and many other neurological pathologies. You can make an appointment with a doctor by calling the clinic.

Bibliography

• ICD-10 (International Classification of Diseases)
• Yusupov Hospital
• "Diagnostics". - Brief Medical Encyclopedia. - M.: Soviet Encyclopedia, 1989.
• « Clinical assessment laboratory research results”//G. I. Nazarenko, A. A. Kishkun. Moscow, 2005
• Clinical laboratory analytics. Fundamentals of clinical laboratory analysis V.V. Menshikov, 2002.