Leukoencephalopathy – clinical forms, diagnosis. Progressive vascular leukoencephalopathy

Vascular subcortical encephalopathy is characterized by gait disturbances, dysfunction of the pelvic organs, mild or moderate neurological symptoms (usually passing), progressive dementia, volitional and emotional disturbances. The disease develops gradually. Both a continuous progressive course and slow progression with long periods of stabilization are possible. Worsening symptoms are usually directly related to a prolonged increase in blood pressure. The outcome is complete helplessness, inability to self-care and lack of control over the functions of the pelvic organs.
  Dementia has a character typical of vascular diseases of the brain. There is memory deterioration, a decrease in the level of judgment, slowdown and instability of mental processes. “Emotional incontinence” is often detected - a pronounced inability to restrain emotions with a predominance of asthenic reactions. Long periods of stabilization and even temporary regression of existing disorders are possible.
  Depending on the predominant symptoms, dysmnestic, amnestic and pseudoparalytic dementia are distinguished. With dysmnestic dementia, there is a mild decrease in memory and intelligence, a slowdown in physical and mental reactions. Criticism of one's own state and behavior is slightly impaired. The clinical picture of amnestic dementia is dominated by severe memory impairment for current events while retaining past memories. Pseudoparalytic dementia is characterized by a stable, monotonous, complacent mood, minor memory impairments, and a marked decrease in criticism.
  The clinical picture in all forms of dementia is very variable; a predominance of both cortical and subcortical disorders can be detected, while cortical disorders are accompanied by a more noticeable decrease in intellectual-mnestic activity. In some cases, epileptic seizures are observed. Dementia is accompanied by disturbances in the emotional and volitional sphere. Neurosis-like phenomena, increased exhaustion and decreased mood are possible. In the later stages of the disease, there is a limitation of interests, emotional impoverishment and loss of spontaneity.
  Gait disorders, like dementia, progress gradually. At first, the steps become smaller, the patient begins to shuffle his feet, and it is difficult to lift his feet off the ground. Subsequently, the automaticity of walking is disrupted, the gait becomes slow and cautious, all movements are consciously controlled, as if the patient were walking on slippery ice. The following signs of gait disturbances in Binswanger's disease are identified: decreased step length, slower walking, the need for increased stability, difficulty starting to walk, and decreased stability when turning.

Cerebrovascular disease in the early stages is manifested by decreased performance, increased fatigue, decreased mood, sleep disturbances, when the patient wakes up in the middle of the night and then cannot fall asleep. Then the symptoms of cognitive impairment are added, i.e. Memory decreases, thinking slows down, mental calculation becomes difficult, and excessive fussiness appears. Subsequently, persistent headaches, tinnitus, and dizziness occur. Periodically, cerebral crises develop, which occur with severe disruption of brain functions and are manifested by the development of weakness in the limbs on one side, disturbances in speech, sensitivity, and vision. If such symptoms disappear within 48 hours, then they speak of a transient cerebrovascular accident. If the symptoms persist longer, then it is a stroke. In this case, gross dysfunction of the nervous system can persist until the end of life, disabling the patient. A stroke can be ischemic, when the lumen of a vessel is closed by an atherosclerotic plaque or thrombus, or hemorrhagic, when the integrity of the vascular wall is disrupted and hemorrhage occurs in the brain.

Leukoencephalopathy is a chronic disease that has the ability to progress and is caused by the destruction of white matter cells in the brain. This pathology leads to dementia in old people, or dementia.

In 1894, physician Binswanger described in detail the destructive effects of leukoencephalopathy.

This pathology is called Binswanger encephalopathy. In modern medicine, the diagnosis of PML (progressive multifocal pathology) is increasingly being made - this leukoencephalopathy has the etiology of a virus.

Leukoencephalopathy of the brain - what is it?

Destructive cell death in the nervous system of the brain, which is provoked by hypoxia from insufficient blood flow to the organ, leads to microangiopathy. The disease leukoaraiosis, as well as the pathology of lacunar-type infarctions, change the structure of white matter cells.

These changes are the consequences of poor blood circulation in the organ.

Manifestations of leukoencephalopathy are associated with the severity of the disease, and symptoms depend on the type of pathology. The subcortical type is very often associated with frontal lesions, and is detected in epileptic seizures.

The pathology has a chronic form of progress with its relapses. Elderly people suffer from leukoencephalopathy, but cases of this diagnosis being made in younger patients are not uncommon.

The main causes of brain diffusion:

  • Insufficiency of blood flow in the brain (causing ischemia);
  • Lack of nutrition for brain cells due to hypoxia;
  • Causes that are caused by a number of diseases.

Etiology of Binswanger's pathology - leukoencephalopathy

The etiology of the disease leukoencephalopathy is divided into:

  • Congenital etiology;
  • Acquired type of etiology of the disease.

Congenital etiology of leukoencephalopathy is an anomaly during the intrauterine formation of brain cells of the unborn baby.

The reasons for intrauterine incorrect formation of the fetus can be:

  • Lack of oxygen, which provoked hypoxia of brain cells;
  • Infectious diseases in a pregnant woman;
  • Viruses that pass from the mother to the developing child through the placental connection;
  • If the mother has an immunodeficiency pathology.

The acquired etiology of leukoencephalopathy can be due to the following provoking diseases:

  • Consequences of brain cell injury;
  • Effects of toxins on the brain;
  • After pathology - radiation sickness;
  • In case of diseases of liver cells that do not remove all necessary toxic substances from the bloodstream system, which maximally pollutes the biological fluid that carries these elements through the blood supply system to the brain;
  • For malignant neoplasms in organs;
  • In case of lung disease, when the body does not receive the required dose of oxygen;
  • With a high blood pressure index - hypertension;
  • With a low blood pressure index - hypotension;
  • AIDS;
  • Blood cell leukemia;
  • Cancerous tumors in the blood;
  • Pathology lymphogranulomatosis;
  • Pulmonary tuberculosis;
  • Oncological diseases - sarcoidosis;
  • Metastasis of cancer cells to the liver and brain.

Damage to the white matter of the brain in leukoencephalopathy

ICD 10 code

According to the international classification of diseases, tenth revision ICD-10, this pathology belongs to the class:

I67.3 is a progressive pathology of vascular leukoencephalopathy;

I67.4 - hypertensive encephalopathy;

A81.2 - progressive multifocal disease - leukoencephalopathy.

Types of pathology

This classification includes the pathology groups of leukoencephalopathy. Since there are many causes of this disease, the varieties of this pathology also have their own characteristic differences in etiology, in their manifestation and course.

Can be divided into 3 types of leukoencephalopathy:

  • Vascular leukoencephalopathy;
  • Pathology of hypoxic - ischemic type;
  • Leukoencephalopathy of hemorrhagic type.

But a diffuse multifocal form of the disease often occurs.

Vascular leukoencephalopathy

The cause of vascular leukoencephalopathy is hypoxia of cerebral vessels, as well as their ischemia. This etiology implies defective performance of their functions by the vessels of the brain. Violations of the functionality of cerebral vessels most often provoke disturbances or pathologies in the body's blood flow system.

In connection with this etiology, there are several subtypes of vascular leukoencephalopathy:

Leukoencephalopathy of the venous type. This type of pathology is caused by poor circulation of venous blood (what type of blood is this). This type of disease refers to a mild and long period of development. From the moment of the first symptoms, several calendar years may pass until the next stage in the development of the disease.

At the initial stage of mild leukoencephalopathy, a medical course of therapy is carried out, which can permanently save the patient from the pathology.

At an advanced stage, a complicated form of the disease develops quite quickly and leads to irreversible and incurable consequences.

Leukoencephalopathy of atherosclerotic nature. The cause of this type of pathology is atherosclerosis of the arteries. Cholesterol forms atherosclerotic plaques on the walls of the arteries, which leads to poor movement of blood through the vessels, or blockage of the arteries.

In elderly patients, atherosclerosis can develop due to improper functioning of the digestive system, or from poor nutritional habits - consuming large amounts of cholesterol-containing foods.

When cerebral vessels are blocked, oxygen starvation of brain cells begins. This type of pathology can be cured only if it is diagnosed at an early stage of its occurrence.

If atherosclerotic leukoencephalopathy is not diagnosed in a timely manner, it can develop rapidly and very quickly turn into a complicated form, and lead to irreversible processes in the brain and in the body. This pathology is subcortical atherosclerotic leukoencephalopathy.

Leukoencephalopathy of the hypertensive type. Provocateurs of this type of pathology can be: vascular eclampsia, nephritis of the renal type in the acute phase of the disease, jumps in the blood pressure index, and also the most dangerous provocateur is a hypertensive crisis.

A hypertensive crisis causes an acute form of encephalopathy, which immediately leads to irreversible consequences of the brain condition.

It is impossible to predict this type of pathology. Leukopathy of vascular origin has similar symptoms to the pathology of dyscirculatory encephalopathy. An accurate diagnosis of leukoencephalopathy, which has been identified as small-focal, probably of vascular origin, can be made by a specialized doctor - a neurologist, after a comprehensive diagnostic study of the etiology.


Drug therapy will be carried out based on the diagnosis and form of the pathology.

Leukoencephalopathy of hypoxic-ischemic type

Any leukoencephalopathy of a vascular nature can also be classified as a hypoxic-ischemic type, since each of the vascular types of pathology leads to brain hypoxia, which provokes leukoencephalopathy.

But this type of pathology is allocated to a separate category in the classification, due to the fact that leukoencephalopathy is a complicated form of difficult labor in newborn babies.

The hypoxic-ischemic type of encephalopathy occurs in a child during the period of its intrauterine formation, as well as with complications during the birth process.

The development of this pathology is unpredictable, and the consequences are also different. A minimal loss of brain functionality in children can lead to the child’s inattention, with the inability to concentrate and remember the necessary information - this is a mild degree of consequences of the hypoxic-ischemic type of pathology.


More severe complications lead to complete paralysis of the child’s body.

The hypoxic-ischemic type of foci of leukopathy in the brain also includes the perinatal form of leukoencephalopathy.

This encephalopathy develops according to the principle of an adult disease, only there is the only difference - its occurrence occurred in the womb, or in the first time immediately after birth.

Hemorrhagic type of leukoencephalopathy

This type of brain pathology occurs from vitamin deficiency of brain cells. Lack of vitamin thiamine leads to the development of multifocal leukoencephalopathy of a hemorrhagic nature.

This type of pathology proceeds in the same way as the development of other types of encephalopathy, but the etiology of this type is:

  • Pathology in the digestive system that provoked anorexia;
  • Prolonged gag reflex and a large amount of vomit from the body;
  • Hemodialysis;
  • Acquired immunodeficiency syndrome (AIDS).

Progressive multifocal leukoencephalopathy

This pathology is a deadly type of disease and is caused by papillomavirus. Quite often leads to death. This is a pathology that develops in more than 50.0% of AIDS patients.

A progressive multifocal form of leukoencephalopathy manifests itself:

  • Body paralysis;
  • Hemianopia of unilateral type;
  • Peripheral paresis;
  • Defect of personality consciousness;
  • Syndromes of expiramidal types.

Disability with this type of pathology comes quite quickly, since its development occurs rapidly against the background of reduced immunity. There is a decrease in the functionality of the motor apparatus, speech and hearing apparatus.

As the disease progresses, paralysis of parts of the body and partial paralysis of the brain occurs.


Brain damage in progressive multifocal leukoencephalopathy

Periventricular form

This type of pathology occurs from brain hypoxia with chronic insufficiency of blood in the cerebral vessels. Areas of ischemic damage are located not only in the white medulla, but also in the cells of the gray matter.

Localization of this destruction occurs in:

  • Cerebellum;
  • Bilateral pathology in the frontal regions of the cerebral cortex;
  • In the brain stem.

All parts of the brain that are affected affect the development of motor functions. Disorder of these areas leads to paralysis of some parts of the body.

In newborn children, this type of leukoencephalopathy develops a pathology - cerebral palsy. This happens a few hours after the baby is born.

Leukoencephalopathy, in which white medulla disappears

This type is diagnosed in childhood from 2 calendar years to the 6th birthday. This disappearance occurs in the cerebral cortex due to gene mutation. This pathology has a single nonspecific focus, or small-focus lesions that affect all parts of the brain.

Symptoms of this type:

  • No coordination in movement;
  • Paresis of limbs;
  • Decreased memory or loss of memory;
  • Visual impairment - the nerve of the optic organ atrophies;
  • Epilepsy attacks.

Such children have problems with food consumption, they are highly excitable, and also have increased muscle tone.


The pathology manifests itself in apnea, muscle cramps and a coma, which often ends in death.

How long do people live with leukoencephalopathy?

This pathology is the most dangerous disease of brain cells. With a stable course of the pathology, life time is measured according to medical forecasts to be a little more than two calendar years.

In the acute course of the disease, which immediately turned into a complicated form - no more than 30 calendar days.

The average life expectancy for a diagnosis of leukoencephalopathy is no more than 6 calendar months from the moment the exact type of pathology diagnosis is established. In this disease, time can decide the outcome of life - in a positive direction, or lead to death.

The faster the diagnosis is made and the cause of the disease is found, the sooner therapy can begin and save a person’s life.

Features of the disease

Leukoencephalopathy is an incurable brain disease that affects the white matter of the brain. This pathology is a focal lesion, as well as a multifocal lesion of the white matter in the brain.

The etiology of the disease is viruses that are destructive to the body and primarily affect brain cells.

The occurrence of pathology occurs from reduced functionality of the immune system, mainly in very old people, as well as when the body is affected by the pathology of immunodeficiency. With AIDS, leukoencephalopathy develops in any age category.

There is a problem in drug treatment for this type of brain disease.

The thing is that there is a barrier in the brain through which only drugs containing fats can enter the brain cells.

These fat-soluble drugs can affect brain cells, but drugs that can effectively and quickly cure leukoencephalopathy are water-based. Water-soluble medications are not able to cross the brain barrier.

Therefore, to date, pharmacological companies have not been able to develop drugs for medically effective treatment of pathology - leukoencephalopathy.

Signs of development of leukoencephalopathy

Signs of many types of leukoencephalopathy appear gradually. At the beginning of development, attacks of forgetfulness and absent-mindedness appear. A person has difficulty remembering information and pronouncing long and complex words.

There is a constant feeling of self-pity, and the patient cries a lot. The intellectual performance of the brain is significantly reduced.

With the further development of the pathology, insomnia appears, which can alternate with an endless desire to sleep. Muscle tone increases, which together leads to groundless irritability of the patient.

At this stage of the development of the disease, severe tinnitus appears, as well as involuntary twitching of the optic nerve, which leads to unreasonable movement of the pupils.

If complex therapy is not started at least at this stage, then the disease will lead to:

  • Pathologies of psychoneurosis;
  • To muscle fiber spasms;
  • To dementia;
  • To partial memory loss;
  • Pathology: dementia.

Symptoms of leukoencephalopathy

Symptoms of this pathology develop suddenly and progress at a rapid pace, which can lead the patient to the following signs of the disease:

  • Bulbar type palsy;
  • Parkinson's syndrome;
  • Disturbed gait;
  • Hand tremors occur;
  • Signs of body trembling appear.

Patients with such symptoms are not aware of their pathology and brain damage, so it is necessary for relatives to force such people to undergo a diagnosis in a timely manner in order to know how to treat the disease.

Diagnostics

To establish a diagnosis of leukoencephalopathy of brain tissue cells, it is necessary to undergo a number of diagnostic tests:

  • Visual examination by a neurologist and medical history;
  • Laboratory clinical blood test (general);
  • Analysis of blood composition for the presence of psychotropic elements, alcohol, and drug-containing substances in it;
  • MRI and CT (computed tomography, or magnetic resonance imaging) to identify lesions in parts of the brain;
  • Instrumental diagnostics using electroencephalography will reveal a decrease in the brain activity of organ cells;
  • Dopplerography is a technique that detects pathology and disorders in the blood flow system, as well as cerebral vessels;
  • PCR analysis to detect the virus in the body. This analysis determines the DNA of the provoking virus;
  • Brain cell biopsy;
  • Cerebrospinal fluid puncture.

If it is revealed that viruses are the provocateur of leukoencephalopathy, then further diagnosis is carried out using electron microscopy of brain cells.


Dopplerography of head vessels

Differential diagnostic testing is carried out for the following pathologies:

  • The disease is toxoplasmosis;
  • Pathology cryptococcosis;
  • Dementia due to HIV;
  • Leukodystrophy disease;
  • CNS lymphoma disease;
  • Pathology subacute sclerosing panencephalitis;
  • Multiple sclerosis.

Drug therapy for leukoencephalopathy

Leukoencephalopathy is a pathology that is incurable. The goal of drug treatment is to stop the progression of the disease and extend the patient several years of life.

This pathology must be treated comprehensively with the use of medications, as well as:

  • Physiotherapy;
  • Therapeutic exercise;
  • Massage;
  • Manual therapy;
  • Treatment with phytomedicines;
  • Acupuncture.

Drug therapy is selected according to an individual scheme by the treating doctor:

General measures are:

  • Healthy lifestyle;
  • Timely treatment of all pathologies of the vascular system;
  • Culture of nutrition and cessation of bad habits;
  • Adequate stress on the body;
  • Engage in the prevention and treatment of pathologies that have become provocateurs of leukoencephalopathy.

This pathology is incurable and the prognosis for life depends on timely diagnosis and progression of the disease.

With minimal or incorrect treatment, the disease progresses faster - the prognosis is unfavorable, no more than 6 calendar months.

When carrying out drug therapy for viruses, life expectancy increases by 12 - 18 calendar months.

The medical term “leukoencephalopathy” is used to define a group of diseases accompanied by damage to the white matter and a number of deep structures of the brain. Rapid progression leads to the formation of senile dementia.

In children, there are vascular varieties, congenital forms with a long chronic course. The survival time for this type is longer compared to its multifocal counterpart.

MR image of vascular leukoencephalopathy

To distinguish the pathology from a number of other neurodegenerative diseases with similar clinical symptoms, a classification according to ICD 10 has been developed, which clearly distinguishes the forms of the nosology.

What is cerebral leukoencephalopathy

Damage to the white matter of the brain is caused in most cases by viruses. Vascular and discirculatory forms are caused by impaired blood supply to a certain area of ​​the brain. Chronic ischemia causes irreversible changes.

Clinical symptoms of the disease more often occur when affected by papillomaviruses. The probability of nosology in patients with HIV is less than 6%.

Forms of vascular origin progress slowly. The chronic course of the disease is characterized by gradual irreversible tissue damage. Mild ischemia provokes the formation of small necrotic areas. Diffuse location leads to neurological disorders.

Types of leukoencephalopathy

The least dangerous form is focal. Formed by chronic inflammatory processes of vascular origin. Lack of microcirculation in a certain part of the brain provokes hypoxia, a lack of oxygen. The death of white matter zones takes several years to develop.

Morphological changes occur more aggressively in hypertension. An increase in intracranial pressure causes ruptures of small capillaries with areas of necrosis of the brain parenchyma. A type of medical language is called “discircular encephalopathy.” Appears in people over 55 years of age.

Progressive multifocal leukoencephalopathy has an aggressive course. People with pathology live no more than 5 years. Deaths are associated with extensive heart attacks and strokes.

Classification of types of leukoencephalopathy according to ICD 10

A progressive type of vascular origin (Binswanger's disease) is coded with the symbols “I67.3”. Subcortical dementia with code “F01.2” has been excluded from the classification of diseases of the tenth revision.

Progressive multifocal (multifocal) leukoencephalopathy - “A81.2”. The group of the same name includes phenylketonuria, Alexander disease, and Canavan disease. Pathologies of category “IA” are distinguished for reasons, as they are of autoimmune origin - caused by tissue damage by immunoglobulins of the body’s own. Antibodies become aggressive when the structure of the membrane or the genetic information of the cell changes under the influence of viruses, chemical, and physical factors.

Let's look at the complete classification algorithm:

  • Diseases of the circulatory system – “IX. 100-199";
  • Cerebrovascular diseases “I60-69”;
  • Other cerebrovascular diseases - “I67”;
  • Progressive vascular leukoencephalopathy – “I67.3”;
  • Other specified vascular lesions – “I67.8”.

The international classification of the tenth revision is valid. When encoding the diagnosis, dyscirculatory encephalopathy is often encountered, acute cerebrovascular insufficiency NOS cerebral ischemia (chronic).

Clinical symptoms of small focal leukoencephalopathy

Focal symptoms have a subacute course. The initial stages of the disease are identified by neurologists:

  • Visual impairment, speech impairment;
  • Pathology of the innervation of the muscles of one half of the body;
  • Epilepsy attacks;
  • Headaches, dizziness;
  • Ataxia, anopsia.

Differential diagnosis of focal types is carried out to distinguish them from changes in white matter in HIV and dementia. Spinal lesions occur without impairment of mental functions. White matter damage is accompanied by cognitive impairment.

Progressive multifocal leukoencephalopathy

The cause of multifocal white matter damage is the JC virus, which leads to widespread damage to the nervous system. The disease develops against a background of reduced activity of the immune system. Antiretroviral treatment is expensive, so most people die.

Progressive encephalopathy quickly leads to the destruction of the myelin of most nerve cells. The changes are irreversible, the symptoms gradually increase.

About 80% of the country's population are carriers of human polyomavirus type 2, but encephalopathy does not occur. Only immunodeficiencies in AIDS create opportunities for rapid reproduction of the pathogen.

The immunity of older people cannot cope with the activity of polyomavirus (JC) after immunomodulatory or immunosuppressive therapy after treatment of cancer or organ transplant surgery.

In children, the appearance of pathology is observed after the start of therapy for chronic lymphocytic leukemia and Hodgkin's disease.

The 1C virus is transmitted by airborne droplets or fecal-oral routes. The majority of the population is asymptomatic. Provoking factors:

  • HIV infection;
  • Taking immunosuppressants;
  • Lymphogranulomatosis;
  • Leukemia.

Magnetic resonance imaging is the only way to identify pathological foci within the white matter. After the appearance of visual impairment, dysarthria, hemiparesis, and aphasia, neurologists will be able to suggest a diagnosis. Final verification is possible only after a microscopic examination of brain biopsies - tissue sections taken from the site of injury.

Discircular encephalopathy

The chronic progressive course of cerebrovascular pathology is accompanied by diffuse multifocal changes leading to hemiparesis, ischemic stroke, and multiple neuropsychological and neurological disorders.

The progression of dyscirculatory encephalopathy is associated with tissue degeneration and the accumulation of aggressive metabolites.

Before using neuroimaging methods, experts attributed most of the causes of cognitive disorders to dyscirculatory encephalopathy. Practice shows overdiagnosis of nosology cases. Nuclear magnetic resonance indicates only a 20% incidence of white matter lesions in elderly patients with vascular disease.

The main difference between the discircular type and a stroke is that it affects not large cerebral arteries, but small penetrating vessels, arterioles. Diffuse damage to small branches causes a number of morphological changes:

  1. Numerous heart attacks (lacunar);
  2. Diffuse destruction of white matter;
  3. Mixed form.

Early detection of any category prevents progression after proper supportive care is given.

Features of periventricular and residual leukoencephalopathy in children

Chronic lack of oxygen supply and prolonged ischemia of brain tissue leads to damage to subcortical structures, hemispheres, and the brain stem. Pathological foci are found deep in the gray matter and are accompanied by changes in subcortical fibers.

Periventricular encephalopathy is characterized by the predominant localization of pathological foci around the ventricles of the brain.

The residual appearance has congenital and acquired causes. The provoking factor in a child is traumatic injuries to the skull, inflammatory processes inside the skull. A separate type, encephalomyelopathy, occurs due to abnormalities in the structure of the vascular network of the brain.

Symptoms of residual encephalopathy in children:

  • Cerebral palsy;
  • Oligophrenia;
  • Epilepsy;
  • Vegetative-vascular dystonia;
  • Restless sleep.

Practice shows the presence of a latent course of nosology in newborns weighing about four kilograms. Clinical symptoms appear after the onset of active blood supply. Cases of dementia in preschoolers and schoolchildren are associated with injuries to the skull.

How long do people live with encephalopathy?

Life expectancy is determined by the clinical form of the disease, the rate of progression, and individual changes in the human body.

Progressive multifocal encephalopathy is accompanied by death 1-3 years after detection. Maintenance therapy increases survival.

Varieties of vascular origin have chronic progression. People with this variety, with proper treatment, live for decades. Reduces the duration of hypertension, pronounced ischemic foci of the brain structure, hemorrhages inside the brain.

Principles for diagnosing leukoencephalopathy

The best way to verify changes in the white and gray matter of the brain is MRI. Leukoencephalopathy is localized in the brain and spinal cord. The images visualize areas of high intensity with a diameter of three millimeters to three centimeters of irregular round and oval shape. The location of the lesions in the subcortical and periventricular regions determines the mode of T1-weighted sequences with additional contrast (MR angiography). The method diagnoses atrophy, dilation of the ventricular spaces, and fresh pathological zones.

Multifocal leukoencephalopathy

MRI of the brain in leukoencephalopathy reveals areas of varying intensity in the cerebellum, brainstem, parieto-occipital and frontal regions. Infratentorial localization is less common. A brain scan should be combined with a cerebrospinal fluid examination. The analysis allows us to identify pathological agents that are the cause of pathology.

Direct detection of the JC virus and HIV by PCR has an accuracy of close to 100%. If the test is negative, confirmation or exclusion of the diagnosis is possible by biopsy - taking material from the pathological area after detection by MRI with three-dimensional modeling.

Diagnosis of autoimmune conditions and immunodeficiency is mandatory.

Electroneuromyography records a decrease in signal transmission along auditory, visual, and somatosensory nerve fibers. There are specific places where pathology is localized, the identification of which suggests pathology with a high degree of probability.

Destruction of the myelin of nerve sheaths, verification of axon degeneration are signs of neurodegenerative processes. Pathological waves occur at a subclinical stage before the first pronounced symptoms.

To identify pathologies at the beginning of development, an MRI should be done. The procedure qualitatively shows the soft tissue component saturated with water. After exposure to a magnetic field, the liquid begins to resonate, and the radio frequency signal changes. Pulse registration allows you to display a graphic image on the monitor screen after processing by the program.



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