Spicy disseminated encephalomyelitis Is rare neurological disease which can occur at any age, but more often affects children. It is characterized by disseminated demyelinating brain damage, in the occurrence of which autoimmune processes play a key role.
In acute disseminated encephalomyelitis, there is a short, intense attack of inflammation in the brain and spinal cord, and sometimes in the optic nerve, in which the myelin, the sheath that covers the nerve fibers, is destroyed.
In some cases, acute disseminated encephalomyelitis is difficult to distinguish multiple sclerosis, since often the symptoms of demyelination are the same in both cases. In addition, in both cases, there is an autoimmune lesion. nervous system
Manifestations of acute disseminated encephalomyelitis
More than half of the patients had some kind of infectious disease a few weeks before the illness. Most often it is a bacterial or viral infection of the upper respiratory tract. Children may have prolonged and intense headaches. During the course of the disease, patients also have a fever. Acute disseminated encephalomyelitis often begins with signs of an acute respiratory infection.
Headaches, fever, chills are noted, and there may be numbness in the legs and arms. Of the neurological symptoms in acute disseminated encephalomyelitis, confusion, drowsiness and even coma, impaired coordination, double vision, difficulty swallowing, and weakness in the limbs are noted. In adult patients with acute disseminated encephalomyelitis, motor and sensory symptoms are more common.
In general, the diagnosis of acute disseminated encephalomyelitis is supported by the rapid onset of neurological symptoms, often with fever and headache, usually following an upper respiratory tract infection. General cerebral symptoms also appear, as well as moderate meningeal symptoms... A couple of days later, focal neurological symptoms appear. It can be different due to the different localization of lesions in the brain and spinal cord.
Sometimes signs of damage to certain parts of the brain prevail. Spinal symptoms are characterized by paresis of the arms and legs, more often of a central nature, but sometimes there are signs of peripheral paresis. Hemiparesis is common, as well as sensitivity disorders and dysfunctions of the pelvic organs.
Cause of acute disseminated encephalomyelitis
Acute disseminated encephalomyelitis is known to occur after certain infections. In 50-75% - after inflammatory diseases of the upper respiratory tract. The trigger of autoimmune reactions in acute disseminated encephalomyelitis is most likely a known virus or virus with as yet unknown properties.
Occasionally, this disease can begin after vaccination, although very rarely. In such cases, acute disseminated encephalomyelitis occurs 3 months after vaccination. Acute disseminated encephalomyelitis is the immune system's response to infection. But at the same time, the immune system, instead of attacking foreign agents, begins to produce antibodies to the myelin sheath of nerve fibers. As a result, the nerve tissue is destroyed and neurological symptoms occur.
Diagnostics of the acute disseminated encephalomyelitis
Acute disseminated encephalomyelitis can be suspected in any case when there is an infection and the development of more than one neurological symptom often associated with headache, fever, and altered consciousness. These symptoms worsen over several days, making it clear that there is a serious problem.
Magnetic resonance imaging
MRI is an important research method in the diagnosis of acute disseminated encephalomyelitis. On MRI in acute disseminated encephalomyelitis, common multiple changes in the white matter of the brain are noted.
As you know, the white matter of the brain is the nerve fibers that suffer in this pathology. These nerve fibers are covered with a myelin sheath, which is why this part of the brain is called the white matter. Sometimes in acute disseminated encephalomyelitis, MRI can reveal foci in the gray matter of the brain.
Sometimes the affected area can be more than half the volume of the white matter. These changes are characteristic of acute disseminated encephalomyelitis, but not specific. Within a few months, these changes on MRI are almost completely gone.
Lumbar puncture
This method of research consists in the fact that a thin long needle is inserted between the vertebrae in the lumbar region of the patient to take a sample of the so-called. spinal fluid. In acute disseminated encephalomyelitis, the spinal fluid is often elevated level lymphocytes. These cells belong to the immune system.
Sometimes it is possible to isolate the culture of the pathogen from the spinal fluid, which served as a trigger for the development of acute disseminated encephalomyelitis. In acute disseminated encephalomyelitis, the so-called. oligoclonal groups.
These are abnormal groups of proteins in the spinal fluid that indicate an active immune process in areas of the brain that are in contact with the spinal fluid. These oligoclonal groups are common in multiple sclerosis.
Treatment of acute disseminated encephalomyelitis
Acute disseminated encephalomyelitis - rare disease and there are currently no clinical trials of any treatment that can be compared to placebo or to each other. Currently, steroid drugs, in particular methylprednisolone, are used in acute disseminated encephalomyelitis. Usually, these drugs are prescribed intravenously in courses of 5-7 days, with the transition to oral administration. The goal of this treatment is to suppress the body's autoimmune response.
Unfortunately, steroid drugs have serious side effects, in particular, increased blood glucose levels, decreased potassium levels, sleep disturbances, weight gain, increased blood pressure, etc.
If methylprednisolone is intolerant, immunoglobulin may be prescribed. The activity of this component of the immune system in acute disseminated encephalomyelitis is reduced. The course of such treatment is on average 5 days. Of the complications of such therapy, one can name the risk of infection, allergic reactions. There may also be shortness of breath as a result of excess fluid in the body.
Another of the proposed methods of treatment for acute disseminated encephalomyelitis is plasmapheresis. This method consists in the fact that blood is taken from the patient, and a liquid part is separated from it - plasma, in which there are antibodies that destroy the myelin sheath. After that, instead of plasma, a solution similar in composition to it is introduced. The course of such treatment lasts 10-14 days, and sessions are held every other day. In very rare cases, chemotherapy may be prescribed, such as mitoxantrone or cyclophosphamide, when no other method is effective.
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Multiple encephalomyelitis (SEM)- 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 disorders, disorder of the function of FMN and pelvic organs, impaired consciousness and speech). The diagnosis is based on the comparison of clinical data and the results of MRI of the brain. Treatment of disseminated encephalomyelitis is complex, carried out in a stationary manner, in the acute period it may require resuscitation.
General information
Multiple encephalomyelitis is an acute autoimmune inflammatory-demyelinating pathology with disseminated lesions of both the central and peripheral nervous systems. The difference between SEM and a number of other demyelinating diseases is its reversible nature. pathological changes and the possibility of complete disappearance of the resulting neurological deficit under the influence of therapy. For the first time, disseminated encephalomyelitis was described 250 years ago by an English therapist who observed signs of encephalomyelitis in patients with smallpox. In modern neurology, this is a fairly common disease. Thus, according to 2011 data, 50 cases of SEM were diagnosed only among the adult population of Moscow. Multiple encephalomyelitis can affect people of different age groups, but it is more common in children than in adults. V childhood it usually has a milder course.
The causes of disseminated encephalomyelitis
Primary disseminated encephalomyelitis usually 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, which is close to the rabies virus and has no analogues among the known viruses. It was named the OREM 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, herpes or enterovirus infection. Secondary disseminated encephalomyelitis can be toxic, post-vaccination or post-infectious in nature. Post-vaccination SEM can develop after vaccination against rabies, whooping cough, diphtheria, and measles. There are known cases of encephalomyelitis after the administration of the anti-influenza vaccine. In rare cases, SEM occurs some time after the bacterial infection(mycoplasma pneumonia, toxoplasmosis, chlamydia, rickettsiosis).
In addition to these etiofactors, an unfavorable premorbid background - depletion of the immune system due to chronic stress, hypothermia, trauma, illness or surgery - is of great importance in the occurrence of disseminated encephalomyelitis. In addition, researchers believe the presence of a hereditary predisposition, expressed in the similarity of proteins of nerve tissues with proteins of some infectious agents or in the features of the functioning of the immune system.
The pathogenesis of disseminated encephalomyelitis
The main pathogenetic substrate of SEM 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 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 spinal roots and peripheral nerve fibers. As a result of demyelination, the function of the affected nerve structures is lost.
Morphologically, perivascular infiltration by macrophages, lymph and monocytes, disseminated inflammation, perivascular demyelination, and oligodendrocyte degeneration are noted. The predominantly white matter of the cerebral and spinal structures is affected, but the involvement of the gray medulla is also possible. Demyelination foci in the central nervous system can be visualized using MRI.
It should be noted that there is almost complete pathogenetic similarity between SEM 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 remission and exacerbations. However, the onset of multiple sclerosis can completely mimic the SEM pattern. Multiple encephalomyelitis, in turn, can lead to chronic demyelinating process with the outcome in multiple sclerosis.
Multiple encephalomyelitis symptoms
In typical cases, disseminated encephalomyelitis manifests as severe encephalopathy. In 50-75% of patients, impairments of consciousness develop, ranging from stunnedness to coma. Psychomotor agitation, dizziness, headache, nausea, meningeal syndrome. Often, a detailed clinical picture is preceded by a period of prodrome in the form of myalgias, fever, headache, and general weakness. Characterized by a rapid increase in neurological symptoms, the severity of which reaches a maximum within a few days.
Focal symptoms of disseminated encephalomyelitis are very variable and depend on the topic of the lesions. There may be ataxia, hemiplegia, oculomotor disorders and damage to other cranial nerves, visual field limitations, aphasia or dysarthria, sensory disturbances (hypesthesia, paresthesia), pelvic disorders. Defeat optic nerve proceeds as a retrobulbar neuritis. According to various sources, from 15% to 35% of SEM cases are accompanied by generalized or partial seizures. In about a quarter of cases, spinal symptoms (peripheral paresis, Brown-Séquard syndrome) are noted. Radicular pain syndrome, polyneuropathy, polyradiculopathy may occur. With the development of severe lesions of the brain stem with bulbar disorders, patients need a resuscitation aid.
In addition to the acute monophasic course, disseminated encephalomyelitis can have a recurrent and multiphase course. Recurrent disseminated encephalomyelitis is said to be when, 3 or more months after the first episode of SEM, its clinic is resumed without the appearance of new symptoms and fresh foci of demyelination according to MRI data. Multiphasic disseminated encephalomyelitis is characterized by the onset of a new episode of the disease no earlier than 3 months later. after the permission of the previous one and not earlier than 1 month. after the end of steroid therapy, subject to the detection of new foci on MRI against the background of resolution of old inflammatory areas.
Diagnostics of the disseminated encephalomyelitis
Bright clinical picture, acute course, polymorphism and polysystemicity of symptoms, indications of a previous infection or immunization give the neurologist the opportunity to preliminarily diagnose SEM. Differentiating disseminated encephalomyelitis is necessary from encephalitis, viral meningitis, myelitis, stroke, multiple sclerosis, Balo concentric sclerosis, rheumatic lesions of the central nervous system due to systemic vasculitis, etc.
Additionally, an ophthalmologist's consultation, ophthalmoscopy, perimetry are carried out. Lumbar puncture can reveal high blood pressure cerebrospinal fluid. The study of cerebrospinal fluid determines an increase in protein levels, lymphocytic pleocytosis. PCR study of cerebrospinal fluid, as a rule, gives negative result... In about 20% of cases, the cerebrospinal fluid remains unchanged.
Most reliable method MRI of the brain is used to diagnose disseminated encephalomyelitis. In the T2 and FLAIR modes, poorly delineated asymmetric hyperintense foci in the white, and often in the gray matter of the brain, are determined. They can be small (less than 0.5 cm), medium (0.5-1.5 cm) and large (more than 2 cm) in size. In some cases, large confluent foci with perifocal edema are recorded, causing a mass effect - displacement of the surrounding structures. Additional involvement of the optic hillocks is possible. Hemorrhages may occur in large inflammatory areas. Accumulation contrast agent in the foci has a different intensity. In 10-30% of cases, the foci are found in the spinal cord.
All patients who underwent an acute episode of SEM after 6 months. re-passage of MRI is recommended. The disappearance or reduction of demyelination sites during this period is the main confirmation of the diagnosis of multiple encephalomyelitis and allows 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%.
Multiple encephalomyelitis treatment
Basic pathogenetic therapy SEM is performed with anti-inflammatory steroid drugs. Depending on the severity of the condition, treatment is started with high or medium age doses of prednisolone. As the symptoms regress, the dose is gradually reduced. Treatment with corticosteroids is continued for 2 to 5 weeks. The negative effect of steroid therapy is immunosuppression. To level it in parallel, assign intravenous administration immunoglobulins. In severe cases, it is necessary - hardware removal of immune complexes and antibodies from the blood.
Etiological treatment of disseminated encephalomyelitis is carried out antiviral drugs(analogs of interferon). In rare cases, proven bacterial etiology SEM is prescribed antibiotics (ampicillin + oxacillin, cefazolin, gentamicin, etc.). With the development of the disease against the background of rheumatism, bicillin therapy is performed.
Symptomatic therapy is a vital part of treatment. According to the indications carry out resuscitation measures, Mechanical ventilation, normalization of hemodynamics. If disseminated encephalomyelitis is accompanied by severe cerebral symptoms, then it is necessary to prevent cerebral edema (administration of magnesium, acetazolamide or furosemide). Severe dysphagia is an indication for tube feeding, urinary retention - for catheterization of the bladder, intestinal paresis - for enemas, convulsions - for the appointment of anticonvulsants, etc.
Therapy of neurological disorders in the acute phase of disseminated encephalomyelitis includes the administration of vitamins gr. B, ascorbic acid, anticholinesterase drugs(galantamine, neostigmine), with muscle spasticity - tolperisone hydrochloride. During the recovery period, 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 SEM lasts an average of 1.5-2 weeks. Approximately 67% of patients achieve complete clinical recovery within a few weeks. In some patients, persistent symptoms persist to varying degrees - paresis, sensory disturbances, visual disturbances. In some cases, a severe course of encephalomyelitis with the development of bulbar disorders leading to death. The prognosis is complicated if there is disseminated encephalomyelitis with recurrent and multiphase course, chronization of the demyelination process with the development of multiple sclerosis. Moreover, the signs that allow predicting the future transition of SEM to multiple sclerosis have not yet been determined.
Causes of occurrence
The reasons why the immune system begins to produce proteins against the cells of its own nervous tissue remains completely unclear. However, it has been noticed that encephalomyelitis most often develops after:
- viral infections, especially those accompanied by a rash (measles, rubella, chickenpox, herpes);
- administration of vaccines (post-vaccination encephalomyelitis);
- colds(influenza bronchitis, pneumonia);
- 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 debut of multiple sclerosis is mistaken for encephalomyelitis).
Encephalomyelitis symptoms
The disease usually begins acutely, often with high temperature, headaches appear, sometimes agitated state, paresthesia. In the future, the neurological picture develops rather quickly; all parts of the central nervous system are affected, but in some cases the brain suffers more, in others the brain stem and spinal cord. Of the cranial nerves II, III, VI and VII pairs... Formidable, life-threatening, phenomena occur in the first period of the disease with damage to the trunk - a violation of breathing, swallowing. Frequent lower spastic paraplegia with impaired sensitivity in the type of conductor, urinary retention. Brown-Séquard syndrome is often noted. With the involvement of the radicular-neuritic segment in the process, tendon reflexes decrease or fall out. Cerebellar; extrapyramidal disorders are rare. Keep in mind the possibility lightning-fast forms the course of the disease with rapid brain involvement and brain stem, what in short term leads to death. V cerebrospinal fluid note a slight increase in protein and pleocytosis. The blood is often not changed, but there may be a mild leukocytosis (up to 13,000), a slight shift to the left, mainly in the acute and subacute period.
Some authors do not distinguish acute encephalomyelitis from acute multiple sclerosis. The group of encephalomyelitis also includes disseminated myelitis, when the process is limited only to the spinal cord. Clinically, there are several lesions within spinal cord(cervicothoracic and thoracic localization) with motor and sensory disorders.
After acute period Gradually, complete or partial recovery occurs. However, persistent residual effects can be observed, more often in the form of atrophy of the optic nerves and paresis of the extremities.
Diagnostics
A preliminary diagnosis is made on the basis of an analysis of specific symptoms and a thorough history taking, in which attention is paid to provoking factors (acute viral disease, vaccination). To clarify the diagnosis, magnetic resonance imaging is mandatory. In the case of acute disseminated encephalomyelitis, multiple, often confluent diffuse asymmetric foci of lesions in the brain and spinal cord are found.
Classification
Distinguish between primary and secondary encephalomyelitis. The most common etiological factor acute primary encephalomyelitis is a viral infection. The occurrence of secondary encephalomyelitis is usually considered as a complication of common infectious diseases or is a post-vaccination complication.
By preferential defeat the process usually distinguishes the following types of the disease:
- enis the most common form of encephalomyelitis, which is characterized by damage to almost all parts of the nervous system;
- with polyencephalomyelitis, nuclear damage is characteristic cranial nerves brain stem and gray matter spinal cord;
- opticoencephalomyelitis and opticomyelitis are forms of the disease similar in pathogenesis, which are characterized by a combination of manifestations of optic neuritis with signs of damage to the brain and spinal cord;
- with disseminated myelitis, the spinal cord is affected at different levels.
Patient actions
When this diagnosis is confirmed, urgent treatment should be prescribed, because encephaloemyelitis can have very serious consequences.
Treatment encephalomyelitis
Corticosteroids or ACTH. In case of respiratory disorders - resuscitation measures. In the residual stage - rehabilitative therapy. Muscle relaxants (midocalm) and other drugs that improve cerebral circulation are used as drug therapy.
Complications
Complications of encephalomyelitis are often pneumonia, cystitis, pyelonephritis, bedsores.
Prophylaxis encephalomyelitis
Avoid hypothermia and overheating during vaccination. Do not drink alcohol while vaccinating. People who are vaccinated should be exempted from night shift and physical reboots.
Infections are one of the most common reasons many diseases. Viruses and bacteria are so small that it is impossible to notice the danger with the naked eye. In addition, sick people can spread the infection long before the appearance of any signs of trouble in the body. But the immune system's response to infection also plays a significant role. In some cases, the latter causes much more negative consequences to humans than viruses and bacteria themselves. Such diseases include acute disseminated encephalomyelitis.
What is encephalomyelitis
The brain and spinal cord are the main leaders of all aspects of the body's life: cell division and renewal, the metabolic process, analysis of all types of information coming from outside. The main mechanism of communication between the nervous system and other organs and tissues is an electrical signal. In this case, all incoming information is sent to the center nerve cells(neurons) by short appendages- dendrites. Response information is sent to long process- to the axon.
Neuron - the basic unit of the nervous system
The path of the nerve signal can be quite arduous. Very often, the brain does not independently transfer tasks to organs and muscles, but acts indirectly. The spinal cord stands out among the subordinates. Most of the electrical signals pass through it. The speed of information transfer in the body is high. The main mechanism is the presence of specific electrical isolation in neurons. This role is played by a fat-like substance - myelin. The myelin sheath is not continuous and continuous. Between the covered areas are the bare ones. The latter are called Ranvier interceptions. It is thanks to them electrical impulse overcomes the length of the nerve processes with great speed.
Interceptions of Ranvier provide a high speed of transmission of nerve impulses
Multiple encephalomyelitis - specific disease nervous system, characterized by inflammation of the myelin sheath against the background of a viral infection and the appearance of many negative signs. In this case, all components are involved in the pathological process: the spinal cord, brain, cranial and peripheral nerves. The disease occurs both in childhood and in adults.
Synonym for the disease: demyelinating encephalomyelitis.
Classification
Multiple encephalomyelitis has many forms:
Causes and factors of development
Multiple encephalomyelitis is directly related to the infection of the body with a virus. Various diseases can act as the main triggering factor:
Damage to the nervous system in these cases is necessarily preceded by the development of inflammation at the site of the virus entering the body. The process in the skin, nasopharynx, paranasal sinuses, intestines is only a facade of the disease. Symptoms are the tip of the iceberg. The presence of a virus in the blood - viremia - is hidden from the naked eye.
Nervous tissue is very sensitive to the effects of various pathological agents. Viruses in the process of life emit many harmful substances... Infection can not only disrupt the finely regulated blood flow in the spinal cord and brain. It penetrates the neurons themselves. These tiny life forms are able to overcome the powerful blood-brain barrier.
The latter is a specific structure, like a high fence, behind which nerve tissue is hidden. The fence is played by special small nerve cells - neuroglia: astrocytes and oligodendrocytes. Their scions cover so tightly blood vessels that most of the blood components are unable to penetrate through them. In a similar way the brain is protected from bacteria, viruses, toxins, as well as immune guard cells and their products - proteins and antibodies.
The aggregate of auxiliary cells of the nervous tissue (neuroglia) makes up about 40% of the volume of the central nervous system
The harmful effect of the virus leads to the appearance of large gaps in the powerful fence. Through them, both the hostile particles themselves and immune cells... The first target on their way is the myelin sheath of neurons. Pathological effects lead to the loss of electrical isolation of nerve cells. As a result, there are problems with the delivery of regulatory signals to the muscles, internal organs, the skin. In this case, the appearance of myelin changes significantly. In severe cases, the fat-like shell resembles a sieve.
The destruction of myelin leads to a loss of the speed of the nerve impulse
The place of localization of the process determines which regulatory functions will suffer. In addition, inflammation most often damages myelin in several places of the nervous system at once. Because of this characteristic, the disease has the adjective "scattered" in its name.
Video: encephalomyelitis and its manifestations
Signs of disseminated encephalomyelitis
Multiple encephalomyelitis causes the development of several groups different signs... The first is a typical consequence of the inflammatory process and includes:
- fever;
- chills;
- aching muscles and joints;
- marble pattern of the skin;
- pallor;
- general weakness;
- increased fatigue.
The second group of signs is universal for any disease of the nervous system, including multiple sclerosis:
The third set of signs will help not only to establish the presence of inflammation in the nervous system, but also to determine the part of the spinal cord or brain that has been attacked by the pathological process.
Table: focal signs of disseminated encephalomyelitis
| Optic nerve fibers | Neurons of the upper layers of the cerebral hemispheres | Brain stem neurons | Cranial nerve neurons | Cerebellar neurons | Spinal cord neurons | Spinal cord roots | Spinal cord peripheral nerves |
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Photo gallery: symptoms of encephalomyelitis
Nystagmus occurs when damaged oculomotor nerve 
Damage to nerve cells at the level of the spinal cord leads to a decrease in muscle mass 
Paralysis of the muscles of the larynx creates serious breathing and voice problems 
Nerve palsy leads to facial asymmetry 
The demyelinating process very often affects the optic nerves, due to which there is a loss of visual fields
Diagnostic methods
Recognizing disseminated encephalomyelitis is a challenge for an experienced neurologist. In some cases, the help of an infectious disease specialist may be required. The following tests and instrumental methods help to establish the correct diagnosis:
- objective examination - reveals common signs inflammatory disease(fever, pallor, rapid pulse);
- neurological examination - establishes disorders of the spinal cord and brain (paresis, paralysis, gait and coordination disorders, visual impairments, hearing, speech, swallowing);
- ophthalmological examination is the main way to establish changes in fields and visual acuity, as well as damage to the optic nerve head in the fundus;
- a general blood test - detects signs of inflammation (an excess of white blood cells, a high rate of erythrocyte sedimentation to the bottom of the test tube);
Lymphocytes are the main defenders of the body against viruses
- biochemical blood test - allows you to identify the causative agent of the disease, while you can detect both antibodies against viruses and the infectious agent itself;
- polymerase chain reaction- with a high probability allows you to establish the source pathological process in the spinal cord and brain;
- examination of cerebrospinal fluid obtained through a puncture at the lumbar level of the spine - allows you to establish the viral nature of the disease by its content a large number lymphocytes;
- electroneuromyography is the main method for studying the activity of brain neurons and their processes, the movement of an electrical signal is recorded in the form of a graph, a change in the appearance of which makes it possible to establish the degree of damage to nerve cells;
- magnetic resonance imaging is the main method used to identify pathological foci of the disease in the tissue of the spinal cord and brain, the resulting picture allows one to speak about the severity of demyelination of nerve cells, as well as observe the effect of the treatment.
MRI is the main diagnostic method for disseminated encephalomyelitis
Differential diagnosis is carried out with the following diseases:
Treatment options for disseminated encephalomyelitis
Therapy for demyelinating diseases of the spinal cord and brain - complex different methods aimed at eliminating inflammation, eliminating its causes, as well as improving metabolism in the nervous tissue. Treatment is carried out under the guidance of a specialist in the specialized department of the hospital. In severe cases, resuscitation may be required.
Medication
To eliminate the phenomena of the disease, the following drugs are first of all prescribed:
- Steroid hormones. They have the most powerful anti-inflammatory effect. Also, these drugs are able to suppress aggressive behavior the immune system. These medicines include Prednisolone, Metipred, Dexamethasone, Hydrocortisone.
- Antiviral drugs. They actively fight the infection that has already penetrated into the nerve cells. To solve this problem, preparations containing interferon are best suited (Interferon-alpha, Interferon-beta, Cycloferon).
- Metabolic agents. They improve the metabolism in neurons and promote the formation of the myelin sheath (Piracetam, Phezam, Mexidol, Actovegin).
- Vitamins of group B. They help the formation and delivery of the nerve signal to the addressees (Pyridoxine, Thiamin, Riboflavin, Cyanocobalamin).
- Vasoactive drugs. Improves blood circulation in the vessels of the brain (Trental, Curantil).
- Diuretic medicines. Used to eliminate inflammatory edema of the nervous tissue (Diacarb, Lasix, Furosemide).
- Non-steroidal anti-inflammatory drugs. Necessary to eliminate fever and other inflammation (Ibuprofen, Nimesulide, Paracetamol).
- Anticonvulsants. Used to eliminate muscle cramps(Relanium, Depakin).
Photo gallery: drugs for the treatment of disseminated encephalomyelitis
Cycloferon contains interferon protein, which has antiviral activity 
Actovegin improves metabolic processes in the nervous tissue 
Milgamma is a complex vitamin preparation 
Trental improves blood circulation in the vessels of the brain 
Diacarb prevents the accumulation of excess fluid in the nervous tissue 
Nise is an effective pain reliever and antipyretic drug 
Depakine is used to prevent seizures 
Prednisolone is a powerful anti-inflammatory drug
Physiotherapy
Physiotherapy procedures have a beneficial effect on the activity of the nervous system. The following techniques are used:
Plasmapheresis has an effective effect. With the help of special filters, the blood is cleared of antibodies - one of the factors in the development of the disease.
The patient's blood is cleared of harmful impurities, and then returns to the body
Encephalomyelitis - serious illness requiring the attention of a specialist. Self-medication or application folk remedies is not only ineffective, but can also aggravate the situation.
Complications and prognosis
Vivid manifestations of the disease are observed within 10-14 days, after which, as a rule, they decline. The entire healing process takes several months. Sixty-seven percent of the time negative signs completely eliminated, the work of the nervous system is restored. However, there is a possibility that some of the disorders will remain forever.
In addition, in the presence of a special predisposition, encephalomyelitis can turn into an irreversible demyelinating process - multiple sclerosis. At severe course the disease may develop the following complications:
The virus that caused damage to the myelin sheath of neurons in a woman during pregnancy can have a variety, including extremely Negative influence on the fetus. The herpes virus, rubella can lead to the formation of severe anatomical abnormalities, spontaneous miscarriage in early dates and stillbirth.
Life expectancy is determined by the nature of the disease and the severity of neurological disorders. The ability to bear and give birth to a child depends on the same circumstances.
Prophylaxis
The main method of preventing encephalomyelitis is vaccination against infectious agents. Chicken pox, rubella, flu - diseases fraught with many severe complications... The formation of immunity against such pathologies is one of the major achievements modern medicine.
The vaccine forms acquired immunity against infections
Acute disseminated encephalomyelitis (Wholesale electricity market, ODEM) is an inflammatory demyelinating disease of the central nervous system, which is believed to be caused by a hypersensitivity reaction of T cells. It is one of the many syndromes that can develop after vaccination or microbial infection and has a latency period (1–2 weeks). Typical manifestations of this demyelinating lesion on MRI are predominantly periventricular white matter involvement. Likewise, albeit to a lesser extent, the gray matter of the basal ganglia and spinal cord may be affected.
Epidemiology
Usually acute disseminated encephalomyelitis occurs in children or adolescents (usually younger than 15 years old). However, the literature describes cases of ADEM in any age groups... Some studies have noted seasonal peaks in incidence in winter and spring, which is in good agreement with the infection theory of ADEM. Less than 5% of all reported cases of ADEM occurred after vaccination. Unlike many other demyelinating diseases (eg multiple sclerosis or Devik's disease), there is no greater predisposition in women, and, on the contrary, slightly predominates in men.
Clinical picture
Usually it proceeds as a monophasic disease, while individual foci of brain damage can be at different stages of development. In 10% of cases, a relapse develops within the first three months. Unlike multiple sclerosis, symptoms are more systemic in nature, and include fever, headaches, depression of the level of consciousness up to coma, convulsions and neurological deficits in the form of hemiparesis, lesions of the cranial nerves, movement disorders, behavioral changes in the form of depression, delirium or psychosis.
Pathology
Acute disseminated encephalomyelitis (AEM, OEM) occurs as a result of a cross-immune response to the antigens of the virus, which provokes autoimmune damage to the central nervous system. In half of the confirmed cases, IgG antibodies Anti-MOG (myelin-oligodendrogliocytic glycoprotein) are detected. Pathological sign is a limited perivenular inflammation (in the English literature - sleeves of demyelination), which is also characteristic feature multiple sclerosis. However, multiple sclerosis usually presents as confluent areas of completely demyelinated areas infiltrated by macrophages and reactive astrocytes.
Markers
- cerebrospinal fluid
- pleocytosis
- possibly an increase in myelin basic protein
- anti-MOG antibodies
Diagnostics
Manifestations range from small punctate lesions to tumor-like lesions that have less mass effect than expected for a similar lesion size and are localized in both the infra- and supratentorial white matter of the brain. Unlike multiple sclerosis, lesion corpus callosum not typical for disseminated encephalomyelitis. Lesions are usually bilateral, but asymmetric. The defeat of the cerebral cortex, subcortical gray matter (especially the thalamus and trunk) occurs, but not often, and, if present, makes it possible to differentiate the lesion from multiple sclerosis. In addition to gray matter lesions, antibodies against the basal ganglia may form, causing more diffuse lesions... Spinal cord involvement occurs only in a third of cases and manifests itself in the form of confluent intramedullary lesions of various sizes and degrees of contrast enhancement.
CT scan
The lesions represent loosely demarcated areas of reduced density in the white matter, which may have annular contrast enhancement.
Magnetic resonance imaging
MRI is more sensitive than CT and demonstrates features of a demyelinating process:
- T2: manifested by subcortical areas of increased signal, surrounded by perifocal edema; possible involvement of the thalamus and brainstem
- T1 with paramagnets: point or ring-shaped contrast enhancement (amplification in the form of an open ring is possible); lack of amplification does not exclude the diagnosis
- DWI: limitation of diffusion around the periphery is possible; the central part of the lesion (which, although it has a high signal on T2 and a low signal on T1 weighted images), has neither diffusion limitation (in contrast to a brain abscess), nor the absence of a signal expected with cysts, which is due to an increase in the content of intracellular water in demyelination zone.
The transfer of magnetization can be useful in differentiating the WECM and RS.
Differential diagnosis
- Susack's syndrome (retinochleocerebral vasculopathy)
- multiple sclerosis
- Marburg variant
- acute hemorrhagic leukoencephalitis (Hirst's disease)
Last updated: 17/05/2017
Literature
- Morimatsu M. Recurrent ADEM or MS ?. J Intern Med. 43 (8): 647-8. J Intern Med
- Honkaniemi J, Dastidar P, Kähärä V, Haapasalo H. Delayed MR imaging changes in acute disseminated encephalomyelitis. AJNR. American journal of neuroradiology. 22 (6): 1117-24. Pubmed
- Inglese M, Salvi F, Iannucci G, Mancardi GL, Mascalchi M, Filippi M. Magnetization transfer and diffusion tensor MR imaging of acute disseminated encephalomyelitis. AJNR. American journal of neuroradiology. 23 (2): 267-72. Pubmed
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- Garg RK. Acute disseminated encephalomyelitis. Postgraduate medical journal. 79 (927): 11-7. Pubmed
- Hynson JL, Kornberg AJ, Coleman LT, Shield L, Harvey AS, Kean MJ. Clinical and neuroradiologic features of acute disseminated encephalomyelitis in children. Neurology. 56 (10): 1308-12. Pubmed
- Wong AM, Simon EM, Zimmerman RA, Wang HS, Toh CH, Ng SH. Acute necrotizing encephalopathy of childhood: correlation of MR findings and clinical outcome. AJNR. American journal of neuroradiology. 27 (9): 1919-23.
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