Brain diseases due to HIV infection. MRI aspects of neuroimaging of central nervous system lesions in HIV infection Treatment of meningitis in HIV

Tuberculous meningitis is a chronic disease of the membranes of the brain and brain tissue caused by Koch's bacillus. It is clinically characterized by a gradual onset, the appearance of meningeal symptoms, signs of encephalitis and characteristic changes in the cerebrospinal fluid.

The causative agent is Koch's bacilli, which are strictly anaerobic and cannot grow in a normal environment. The process is metastatic, the main concentration of bacilli is localized in the diseased organ, as well as in the bone marrow. Less commonly, the process moves from the brain to the dura mater of the brain or spinal cord, causing osteomyelitis.

Tuberculous meningitis: clinical picture

Tuberculous meningitis clinically passes through three stages. The disease is preceded by a prodromal (preparatory) stage of varying lengths, usually about 2-3 weeks. Signs of infection during this period include slight general malaise, mood swings, apathy, and irritability.

Tuberculous meningitis: Stage I

Mild fever with headache, vomiting and constipation. The patient has pale skin, a frightened appearance, often sunken eyeballs, and sharpened cheekbones. The neck has limited mobility. In terms of heart rhythm, bradycardia (slow pulse) is noted. Physiological reflexes are enhanced. At the end of this stage, which lasts 7-10 days, fever appears and objective meningeal signs appear.

Tuberculous meningitis: stage II

All symptoms manifest themselves even more, basilar symptoms occur: strabismus, ptosis (drooping) of the eyelids, double vision (diplopia). The patient loses control of urination, and signs of consciousness disorder appear.

Tuberculous meningitis: Stage III

During the third week, in addition to existing clinical symptoms, signs of encephalitis dominate. They are characterized by:

qualitative and quantitative disorders of consciousness - irritability, anxiety, lethargy, apathy, drowsiness, stupor, coma;
focal symptoms - hemiparesis and hemiplegia;
muscle cramps, sensory disorders.

Basilar signs become even more pronounced. An adult patient dies in a coma between 3-5 weeks of illness, children - between 20 and 25 days of illness.

The diagnosis is made based on the history of latent or active tuberculosis in the body, clinical symptoms and analysis of cerebrospinal fluid. Typically, treatment lasts from nine to twelve months.

Tuberculous meningitis in HIV-infected individuals is one of the most severe manifestations of tuberculosis (TB). The risk of developing extrapulmonary tuberculosis, including tuberculous meningitis, especially increases in the last stages of HIV infection/AIDS. Prolonged fever, systematic headaches, vision problems, swelling of the fundus of the eye and other symptoms of unknown origin, as well as a sharp decrease in CD4 (the greatest risk is below 200 cells) - all this should be a reason to immediately consult a doctor, if until then The HIV-infected patient did not attach importance to systematic examinations.

Only early detection and timely administration of antiretroviral therapy (ART), along with adequate antimycobacterial therapy, can give a completely favorable prognosis for recovery from tuberculous meningitis in HIV-infected people.

This article is for informational purposes only. Any symptoms should be thoroughly examined in specialized institutions.

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The brain of HIV-infected people is at particular risk. We are talking not only about progressive oncological tumors, but also about meningitis and other inflammatory processes. What causes these pathologies, and which of them are the most common?

Why does brain damage occur in HIV and what does it lead to?

HIV cells enter the head through the blood. In the early stages, this is expressed through inflammation of the membrane of the hemispheres. The so-called meningitis is expressed by acute pain that does not subside for several hours, as well as severe fever. All this happens in the acute phase of the immunodeficiency virus. How does HIV affect the brain, what can happen next? Infected cells actively multiply and divide, causing complex encephalopathies with an unclear clinical picture. At later stages, brain damage due to HIV can take on a completely different character. They develop into cancer, which is asymptomatic in the first few stages. This is fraught with death, because it is impossible to quickly begin treatment in this case.

Common types of brain damage due to HIV infection

Here are the most common pathologies that can develop in people with the immunodeficiency virus after the affected cells enter the hemispheres and surrounding tissues:

Associated dementia. In healthy people, it can appear after sixty years of age. If HIV infection is firmly established in the body, brain damage of this type develops regardless of age. The classic manifestations of this psychomotor disorder are dementia, partial or complete loss of cognitive ability, and so on.
Meningitis in HIV-infected people can occur both in the initial stages and in the acute phase. It can be aseptic or bacterial. The first one most often has an infectious form. Its causative agent can be not only the human immunodeficiency virus, but also other viruses that accompany it, such as herpes or cytomegalovirus. Damage to the membrane in this disease can be fatal if not treated properly.
Associated encephalopathy. Often manifests itself in children infected with AIDS. In addition to high intracranial pressure, it is characterized by such signs as increased muscle tone and delayed mental development.
Kaposi's sarcoma is a serious and dangerous disease, which is characterized by its main localization in brain tissue. It is worth noting that with this pathology, numerous areas of the skin are also affected. Small growths that resemble ulcers can cover the face, limbs, palate, and other areas of the mouth. Such changes in the brain with HIV and AIDS are diagnosed exclusively visually. Experienced medical experts assure that it is extremely difficult to confuse Kaposi's sarcoma with other diseases, so taking a biopsy is not necessary. It is impossible to cure this disease; you can only slightly relieve its symptoms or temporarily stop the spread of the rash.

Please note that if an HIV-infected person has a disease in the brain, he needs strict medical supervision, as well as strict adherence to all instructions. This will help maintain quality of life and significantly extend it.

A fairly popular complication that occurs with HIV infection is.

HIV is one of the most dangerous diseases today, and it is not yet possible to cure it. To understand why this happens, you need to find out which ones.

The lungs are particularly at risk with HIV. This disease very quickly affects these organs. However, there may not always be a prognosis in such cases.

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Diagnosis and treatment of neurological manifestations of neuroAIDS

Human immunodeficiency virus disease can occur in the form of hidden carrying of the virus, as well as in the form of acquired immunodeficiency syndrome, which is the extreme stage of HIV.

With the development of HIV and AIDS, almost all systems of the human body are affected and affected. The main pathological changes are concentrated in the nervous and immune systems. Damage to the nervous system caused by HIV is called neuroAIDS.

It is observed intravitally in approximately 70% of patients, and posthumously in%.

Causes and pathogenesis of the disease

The pathogenetic mechanisms of the effects of HIV on the nervous system have not yet been fully studied. It is believed that neuroAIDS occurs due to direct and indirect effects on the nervous system.

There is also an opinion that the reason lies in impaired regulation of the response process from the immune system. The direct effect on the nervous system is carried out through penetration into cells that carry the CD4 antigen, namely neuroglia of the brain tissue, cells of the lymphocyte membrane.

At the same time, the virus can penetrate the blood-brain barrier (the physiological barrier between the circulatory system and the central nervous system). The reason for this is that viral infection increases the permeability of this barrier, and that its cells also have CD4 receptors.

It is believed that the virus can penetrate brain cells through cells that can capture and digest bacteria that easily pass the blood-brain barrier. As a result of this, only neuroglia are affected, while neurons, due to the fact that they do not have CD4 receptors, are not damaged.

However, due to the fact that there is a connection between glial cells and neurons (the former serve the latter), the function of neurons is also impaired.

As for the indirect influence of HIV, it occurs in various ways:

as a result of a rapid decrease in immune defense, infections and tumors develop;
the presence in the body of autoimmune processes that are related to the production of antibodies to nerve cells that have built-in HIV antigens;
neurotoxic effects of chemicals produced by HIV;
as a result of damage to the endothelium of cerebral vessels by cytokines, which leads to disturbances in microcirculation, hypoxia, which causes the death of neurons.

Primary and secondary neuroAIDS

There are two groups of neurological manifestations that are associated with HIV infection: primary and secondary neuroAIDS.

In primary neuroAIDS, HIV directly affects the nervous system. There are several main manifestations of the primary form of the disease:

Secondary neuroAIDS is caused by opportunistic infections and tumors that develop in an AIDS patient.

Secondary manifestations of the disease are expressed as follows:

Most often, patients with neuroAIDS have the following tumors in the central nervous system:

Features of the clinical picture

Primary neuroAIDS often occurs without symptoms. In rare cases, neurological symptoms may appear 2-6 weeks after HIV infection. During this period, patients experience fever of unknown origin, swollen lymph nodes, and skin rashes. In this case the following appears:

Aseptic meningitis. Occurs in a small number of patients with HIV (about 10%). The clinical picture is similar to serous meningitis. With aseptic meningitis, the level of CD8 lymphocytes in the cerebrospinal fluid increases. When viral meningitis has another cause, the number of CD4 lymphocytes increases. In rare and severe cases, it can lead to mental illness and disturbances of consciousness.
Acute radiculoneuropathy. Caused by inflammatory selective damage to the myelin sheath of the roots of cranial and spinal nerves. This condition manifests itself in tetraparesis, sensitivity disorders of the polyneuric type, radicular syndrome, damage to the facial and optic nerves, and bulbar syndrome. Signs begin to appear and gradually become more intense both after a few days and after a few weeks. When the condition stabilizes over the course of a few days, the intensity of symptoms begins to decrease. Only 15% of patients have sequelae after acute radiculoneuropathy.

Certain forms of neuroAIDS make themselves felt at the open stage of HIV infection:

HIV encephalopathy (AIDS dementia). The most common manifestation of neuroAIDS. The presence of behavioral, motor, and cognitive disorders is noted. In approximately 5% of HIV patients, encephalopathy is the primary symptom indicating the presence of neuroAIDS.
HIV myelopathy. It is expressed in dysfunction of the pelvic organs and lower spastic paraparesis. The peculiarity is the slow progression and differences in the severity of symptoms. About a quarter of people with HIV are diagnosed with this disease.

Establishing diagnosis

NeuroAIDS occurs quite often, in most patients with HIV, so all carriers of the infection are recommended to undergo regular examination by a neurologist. HIV encephalopathy initially manifests itself in impaired cognitive functions, so in addition to studying the neurological status, it is also necessary to conduct a neuropsychological examination.

In addition to the basic studies that patients with HIV undergo, to diagnose neuroAIDS it is necessary to turn to tomographic, electrophysiological and liquorological research methods.

Patients can also be referred for consultation to a neurosurgeon, psychiatrist, and other specialists. The effectiveness of treatment of the nervous system is analyzed for the most part using electrophysical research methods (electromyography, electroneuromyography, evoked potential research).

Disturbances in the nervous system in neuroAIDS, as well as the study of their course and the results of therapy, are studied using computed tomography and magnetic resonance imaging.

An analysis of cerebrospinal fluid, which is collected using a lumbar puncture, is also often prescribed. If the patient, in addition to neurological manifestations, a decrease in the number of CD4 lymphocytes, has an increased protein level in the cerebrospinal fluid analysis, a decreased glucose concentration, and moderate lymphocytosis, then we are talking about the likelihood of developing neuroAIDS.

Complex treatment

Treatment of neuroAIDS and stopping its development are inseparable from the treatment of HIV infection, and form its basis. Patients are prescribed antiretroviral therapy with medications that have the ability to pass through the blood-brain barrier and, as a result, block the development of HIV, stop the increase in immunodeficiency, reduce the intensity and severity of neuroAIDS symptoms, and reduce the likelihood of infections.

The most studied is the use of Stavudine, Zidovudine, Azidotimidine, Abacavir. Since the drugs are quite toxic, the prescription must occur with the consent of the patient, and according to an individual program.

It is also necessary to treat each specific form of neuroAIDS:

The use of plasmapheresis and corticosteroid therapy is also effective. Treatment of tumors may require surgery, and consultation with a neurosurgeon is necessary.

In the situation of early detection of neuroAIDS (in the primary stages), and the presence of adequate treatment for the manifestations of the disease of a neurological nature, there is a possibility of slowing down the development of the disease. Often the cause of death in patients with neuroAIDS is stroke, opportunistic infections, or malignant tumors.

This section was created to take care of those who need a qualified specialist, without disturbing the usual rhythm of their own lives.

Brain damage due to HIV infection

The article describes the features of the pathogenesis and clinical course of strokes in HIV positive patients.

The nervous system is affected by the human immunodeficiency virus in 80–90% of cases, even in the absence of characteristic changes in the peripheral blood and other organs. Moreover, in 40–50% of cases, neurological complications are the first manifestations of symptoms of HIV infection, i.e. the patient learns about his first manifestations of neuroAIDS precisely by the onset of problems with the nervous system (severe memory deterioration, weakening of attention and ability to concentrate, decreased intelligence, progressive dementia, hemorrhagic and ischemic strokes, etc.).

Numerous complications in patients with symptoms of HIV infection can be caused by:

Various opportunistic infections, and even

Side effects of antiretroviral drugs

In the brains of patients with HIV infection, strains of the virus are found that infect cells that have CD4 receptors on their surface. They damage the white matter of the brain using neurotoxins produced by their own cells that are activated or infected by the virus. In addition, infected cells inhibit the growth of new nerve cells in the cerebral cortex, i.e. have a neurotoxic effect.

As an example, we present statistics of observations of 1600 patients with symptoms of HIV infection aged 35–45 years. The number of strokes in HIV positive patients exceeded the statistics of uninfected people by more than 30 times!

Thus, we can conclude that patients with symptoms of HIV infection are at high risk of stroke.

The main forms of disorders that are observed in HIV-positive individuals are large ischemic strokes of the white and gray matter of the brain, or many small ischemic strokes that regress within 2-3 weeks.

Since CD4 receptors are located in various cells of the brain and spinal cord, almost the entire human central nervous system is subject to HIV attack. And after strokes of varying severity, the destruction caused contributes to secondary damage to the nervous tissue.

In patients with injection drug use, these lesions are superimposed by an allergy to foreign substances and damage to the vessel walls by small foreign impurities, which leads to a narrowing of the lumen of the vessel and its thrombosis with further possible ischemic stroke or rupture of the vessel.

Due to neglect of the sterility of injections, purulent-septic complications are not uncommon.

In patients who have been using drugs for a long time, dilatation of small veins in all parts of the brain is often observed, the walls of blood vessels are clogged and partially stretched and disintegrated, and minor hemorrhages and thrombosis are frequent. We can say that the “preparation” for an ischemic stroke was carried out to the highest standards, nothing was missed!

Patients with symptoms of HIV infection quite often experience either an ischemic stroke or a transformation of an ischemic stroke into a hemorrhagic one. Primary hemorrhagic stroke itself is quite rare. Spontaneous spinal hemorrhages also sometimes occur.

Hemorrhagic stroke is more common in patients with Kaposi's sarcoma metastases to the brain.

A study conducted in one American clinic over a 10-year period showed that the number of strokes in people with symptoms of HIV infection increased by 67%. (All strokes were ischemic.) At the same time, in the control group (patients not infected with HIV), the number of strokes decreased by 7%.

All patients had severely reduced immunity: 66.7% of patients had a CD4 level below 200/μl, 33.3% had a CD4 level of 200–500/μl.

Symptoms of HIV encephalopathy and prognosis

Slowly progressing HIV infection affects more than just the body's immune system. The virus spreads to all vital organs of the human body. In nine cases out of ten, the virus attacks the patient’s nervous system, and HIV encephalopathy develops.

What is HIV?

The immunodeficiency virus causes irreversible changes in the cellular structure, as a result of which the body loses the ability to resist other infectious diseases.

The virus can live in the body for a long period – up to fifteen years. And only after such a long period of time will the development of immunodeficiency syndrome begin.

The number of virus carriers is growing steadily every year. The route of transmission of the virus is exclusively from person to person, animals are not carriers, and even in laboratory conditions it was not possible to inoculate the virus into an animal, with the exception of some monkeys.

The virus is found in human body fluids. Routes of HIV infection:

unprotected sexual intercourse;
blood transfusion;
from sick mother to child.

The possibility of transmission of the virus through household, airborne droplets or saliva has not yet been proven. The virus is transmitted only through blood or sexual contact. The risk group includes homosexuals, drug addicts and children of sick parents.

Infection of a child occurs through the passage of the baby through the birth canal, as well as through breastfeeding. However, quite a lot of cases have been described in which absolutely healthy children were born to HIV-positive mothers.

HIV symptoms and diagnosis

Due to the long incubation period, symptomatic detection of the virus is impractical. Infection can only be diagnosed using a laboratory method - this is the only way to reliably determine a patient’s HIV status.

Since the virus attacks the patient's immune system, the symptoms and prognosis of the disease are quite vague and characteristic of various diseases. The initial signs are similar to those of ARVI or influenza:

difficulty breathing;
pneumonia;
sudden weight loss;
migraine;
blurred vision;
inflammatory diseases of the mucous membranes;
nervous disorders, depressive states.

When the virus is transmitted from an infected mother to an infant, the disease develops very rapidly. Symptoms increase rapidly, which can lead to death in the first years of a child’s life.

Development of the disease

The disease does not appear immediately. It can take ten years from the moment of infection with the virus to the development of immunodeficiency. The following stages of disease development are distinguished:

incubation period;
infectious period;
latent period;
development of secondary diseases;
AIDS.

The incubation period is the period of time between a person becoming infected and the ability to determine the presence of the virus in the blood using laboratory methods. As a rule, this period lasts up to two months. During the incubation period, the presence of the virus in the patient’s blood cannot be detected by analysis.

After the incubation period, the infectious period begins. During this period of time, the body actively tries to fight the virus, so symptoms of infection appear. Typically, patients report fever, flu-like symptoms, and respiratory and gastrointestinal infections. The period lasts up to two months, but symptoms are not present in every case.

During the latent period of disease development, there are no symptoms. During this period of time, the virus infects the patient’s cells, but does not manifest itself in any way. This period can last a long time, up to flying.

The latent period of the virus in the body is replaced by the stage of the addition of secondary diseases. This is due to the reduction of lymphocytes responsible for the body’s immune defense, as a result of which the patient’s body is not able to resist various pathogens.

The last period of disease development is AIDS. At this stage, the number of cells that allow the body to provide complete immune protection reaches a critically low value. The immune system completely loses the ability to resist infections, viruses and bacteria, resulting in damage to internal organs and the nervous system.

Pathologies of the nervous system in HIV

Damage to the nervous system during HIV infection can be primary or secondary. An attack on the nervous system can occur both at the initial stage of infection by the virus, and as a result of the development of severe immunodeficiency.

The primary lesion is characterized by the direct effect of the virus on the nervous system. This form of complication occurs in children with HIV.

Secondary lesions develop against the background of immunodeficiency. This condition is called secondary neuro-AIDS. Secondary lesions develop due to the addition of other infections, the development of tumors and other complications caused by immunodeficiency syndrome.

Secondary disorders can be caused by:

autoimmune reaction of the body;
the addition of an infection;
tumor development in the nervous system;
changes in vascular nature;
toxic effects of drugs.

Primary damage to the nervous system during HIV infection may be asymptomatic. It should be noted that often damage to the nervous system is one of the first symptoms of HIV infection in a patient. In the early stages, the development of HIV encephalopathy is possible.

Encephalopathy due to HIV

Encephalopathy is a degenerative lesion of the brain. The disease develops against the background of serious pathological processes in the body, for example, HIV encephalopathy. The disease is characterized by a significant decrease in the amount of nervous tissue and disruption of the functioning of the nervous system.

Encephalopathy is often a congenital pathology. Cases of encephalopathy are common in newborns with HIV.

Symptoms of this pathology vary depending on the severity of brain damage. Thus, all symptoms are divided into three conditional groups, depending on the nature of the disease:

Stage 1 – there are no clinical manifestations, but laboratory tests reveal changes in the structure of brain tissue;
Stage 2 – mild brain disorders are observed;
Stage 3 is characterized by pronounced nervous disorders and impaired brain activity.

The symptoms of encephalopathy in HIV are no different from the signs of this disease that appears against the background of other pathologies. Starting from the second stage of development of encephalopathy, the following symptoms are distinguished:

constant migraines and dizziness;
mental instability;
irritability;
disturbance of mental activity: weakening of memory, inability to concentrate;
depression and apathy;
speech disorder, facial expressions;
disturbances of consciousness, character changes;
trembling fingers;
deterioration of vision and hearing.

Often these symptoms are accompanied by sexual dysfunction and loss of libido.

Dementia in HIV-infected people

HIV encephalopathy belongs to a whole group of diseases characterized by cognitive impairment. These diseases are collectively called AIDS dementia (dementia).

Encephalopathy in HIV often develops as a result of drug therapy. This form of nervous system disorder occurs in infants born with HIV.

Drug addicts and people who abuse alcohol are susceptible to encephalopathy. In this case, the disease develops due to the toxic effects of drugs and alcohol on the patient’s nervous system.

Pathologies of the nervous system with HIV develop differently in each patient. Sometimes it can be difficult to diagnose the presence of a disorder at the initial stage. In this case, doctors pay special attention to depression, apathy or sleep disorders in the patient.

AIDS dementia expresses itself in different ways, but the outcome for any disease of the nervous system associated with HIV is the same - it is dementia. Thus, the final stage of development of encephalopathy or other neurological disorder in patients is a vegetative state. Patients develop complete or partial paralysis; the patient cannot care for himself and needs care. The outcome of progressive dementia in patients is coma and death.

It should be noted that dementia in patients is the exception rather than the rule; it occurs in no more than 15% of patients. The development of pathological disorders of mental activity occurs over a very long time. With severe immunodeficiency, dementia often does not have time to acquire a severe form due to death.

However, mild symptoms of cognitive impairment are observed in every second case of HIV infection.

Stages of dementia

Dementia develops over a long period and consists of several stages. However, not every patient goes through all stages; most cases experience mild cognitive impairment.

Normally, patients do not have any mental or motor impairment. This is an ideal case in which damage to the nervous system by the virus is not observed.

The subclinical stage is characterized by mild cognitive impairment, characterized by mood swings, depression and impaired concentration. Patients often experience slight inhibition of movement.

A mild form of dementia is characterized by slow mental activity, the patient speaks and moves slightly inhibited. The patient can fully care for himself without assistance, but complex intellectual or physical activities cause some difficulty.

The next stage of dementia development, middle, is characterized by impaired thinking, attention and memory. Patients can still look after themselves independently, but already have serious difficulties with communication and mental activity.

At a severe stage, the patient has difficulty moving without assistance. There is a severe disturbance in thinking, as a result of which any social interactions with others are very difficult. The patient does not perceive information and experiences serious difficulties when trying to talk.

The final stage of dementia development is vegetative coma. The patient is unable to perform basic actions and cannot cope without outside help.

Diagnostic methods

Since pathology causes a change in the volume of nervous tissue, the disease is diagnosed using the following methods:

Based on the lumbar puncture, a decision is made on the advisability of further research. This analysis reveals the presence of changes in the nervous system.

MRI (magnetic resonance imaging) can successfully identify pathological changes in the white matter of the brain. To obtain an accurate picture, it is necessary to conduct examinations of the brain, as well as the neck and eyeball.

REG (rheoencephalography) is an examination carried out by a non-invasive method, with the help of which it is possible to obtain complete information about the condition of the main arteries and vessels of the patient’s nervous system.

Dopplerography is mandatory. This examination is necessary to assess the condition of the blood vessels in the brain. Changes in encephalopathy primarily affect the main vertebral and cerebral arteries, changes in which are shown by Doppler ultrasound.

Therapy and prognosis

Timely treatment of the underlying disease will help to avoid the development of neurological disorders in HIV. Typically, dementia caused by encephalopathy develops only if the patient is not treated therapeutically.

Any damage to the nervous system caused by HIV is treated with potent antiviral drugs (for example, zidovudine).

To date, the best results in the treatment of nervous system diseases associated with HIV are shown by HAART therapy. This therapy is based on the simultaneous use of two groups of antiretroviral drugs.

Timely treatment can stop further development of encephalopathy and dementia. In some cases, it is possible to stop the progression of dementia, and in others, it is possible to delay the development of cognitive impairment for a long time.

HIV encephalitis also involves taking antidepressants to correct the patient's mental state. At the initial stages of development of the disorder, patients experience depressive states and sleep disorders, which should be combated with the help of special medications.

It is impossible to say unequivocally what the prognosis for patients with HIV encephalopathy is. This depends on the characteristics of the damage to the nervous system and brain in a particular patient.

Prevention of pathologies of the nervous system

It is still not clear how exactly the virus provokes the development of diseases of the nervous system. However, AIDS dementia is a pressing problem for HIV-infected people, whose number is increasing every year.

There are no preventive methods against the development of encephalopathy and other neurological changes. The patient must be attentive to his own health. Reasons to contact the clinic for help are the following conditions:

depression and apathy;
mental instability;
frequent mood changes;
sleep disorders;
headache;
visual disturbances and hallucinations.

Timely treatment will avoid or significantly delay the onset of severe symptoms of dementia. However, the patient must help himself.

Together with drug therapy, patients are shown careful control of their own emotions. Patients should remain mentally and physically active. To do this, it is recommended to be in society, play sports and give your own brain an intellectual challenge. To stimulate brain activity, patients are shown educational tasks, riddles, and reading complex literature in large volumes.

It should be remembered that symptoms of nervous system disorders often do not appear until the later stages of immunodeficiency. However, in some cases, minor memory impairment and distracted attention characteristic of encephalopathy may appear before the first symptoms of immunodeficiency appear. Drug therapy for HIV helps not only to prolong the patient’s life, but also to avoid the development of severe dementia.

The information on the site is provided solely for popular informational purposes, does not claim to be reference or medical accuracy, and is not a guide to action. Do not self-medicate. Consult your healthcare provider.

The article outlines the main aspects of neuroimaging of some viral infections of the central nervous system, including HIV infection, as well as MRI syndromes of pathology associated with HIV infection. A catamnesis of the formation of HIV-induced dementia in a child is presented. The necessity of having high-field (at least 3 Tesla) MR tomographs in large psychiatric hospitals with a modern approach to neurovisualization of psychiatric pathology is substantiated.

Shilov G.N., Krotov A.V., Dokukina T.V. State Institution "Republican Scientific and Practical Center for Mental Health"

Over the past decades, the spread of acquired immunodeficiency syndrome (AIDS) has increased significantly, which explains the close attention to this pathology of various specialists, including neuropsychiatric doctors.

In this regard, it should be remembered that damage to the central nervous system occurs in 30-90% of all cases of HIV-infected people, and in 40-90% of them the disease can manifest itself as mental and/or neurological symptoms, which, unfortunately, become obvious, as a rule, in the terminal period of development of the disease, especially since diagnosis in the early stages of development of the pathological process, when treatment and preventive measures are most effective, is difficult.

Magnetic resonance imaging for HIV

It is believed that changes in the brain in HIV-infected and AIDS patients can be caused by various factors, such as various types of opportunistic infections, tumor process, cerebrovascular diseases, demyelinating process, as well as the direct effect of the immunodeficiency virus, and lesions of the central nervous system can develop both simultaneously or in parallel with HIV infection, and metachronously, i.e. some time after infection. It is well known that opportunistic infections are the most common in AIDS patients, i.e. in approximately 30% of patients. These include toxoplasmosis, herpetic, cytomegalovirus, cryptococcal, tuberculosis, papovavirus and other infections.

It should also be noted that the clinical manifestations of brain damage in AIDS depend to a greater extent on the localization of changes in the central nervous system than on the etiology. So, in particular, both single and multifocal lesions can occur, which can be accompanied by mass effect.

It is known that the main most informative methods of neuroimaging at present are X-ray computed tomography (CT) and magnetic resonance imaging (MRI). When CT diagnoses AIDS, as a rule, either no changes in the brain matter are detected, or mild atrophy is detected with areas of low density in the white matter.

MRI diagnosis of AIDS, as well as in inflammatory diseases in persons with unchanged immunity, is based primarily on the assessment of direct signs of the pathological process and the nature of the enhancement, which, by the way, may be less clearly expressed than usual. Most often, brain damage in immunodeficiency (without signs of another neuroinfection) is manifested by diffuse atrophy, which is observed in 31% of subjects with asymptomatic HIV infection and in 70% of patients with clinical manifestations of AIDS.

Damage to the central nervous system in HIV

A special place in the clinical and neurological manifestations of AIDS is given to cytomegalovirus infection (CMV). It has been suggested that it is the combination of HIV and CMV infections that leads to the development of AIDS-associated encephalopathy and dementia. At the same time, it should be especially emphasized that the picture of HIV encephalopathy is most clearly manifested in children, which is apparently associated with the immaturity of the brain substance and its extreme vulnerability, both at the stage of infection and in the future. In these cases, HIV encephalopathy, as well as other serious manifestations of cell-mediated immune deficiency, develop over a relatively short period of time (5-8 years). It is obvious that one of the early symptoms of HIV encephalopathy is behavioral changes. Naturally, the appearance of such symptoms first of all requires the mandatory inclusion of psychoneurological specialists in the complex of examination of such children.

One of the common manifestations of central nervous system damage during HIV infection is subacute HIV encephalitis, characterized by a pronounced atrophic process, primarily in the cerebral cortex. In an MRI study, it is manifested by expansion of the subarachnoid space and ventricles of the brain. Focal lesions of the central nervous system are also possible, when microscopic examination reveals parenchymal and perivascular infiltration of lymphocytes and macrophages around the veins and capillaries in the projection of the semioval centers, basal ganglia and pons. In this case, in the subcortical sections of the white matter of the frontal and parietal lobes, foci caused by demyelination of intracortical fibers can be visualized. It should also be noted that intravenous contrast is not effective in this case. Changes are often two-way. It should be especially emphasized that the described picture is nonspecific and also occurs with CMV infection, which can also manifest itself as diffuse damage to the deep white matter (the lesions, as a rule, have clear contours, without perifocal edema). It is also possible to develop ventriculitis with the involvement of the periventricular white matter in the process, but in this case there is an accumulation of the contrast agent.

Tumors are relatively rare and, as a rule, have an atypical course (first of all, of course, it is necessary to mention lymphoma). Usually the tumor has the appearance of a solid node, but in half of the cases there is a multifocal lesion, with the possibility of spreading to the membranes of the brain. Most often, characteristic changes are localized in the periventricular region, however, the basal ganglia with the septum pellucida and the corpus callosum can also be involved in the process, and pronounced perifocal edema is almost always observed. The tumor itself is characterized by a moderately hypointense signal on T1-weighted images (WI) and a moderately hyper- or isointense signal on T2-weighted images on MRI, and after intravenous administration of contrast, a ring-shaped or solid-type change in signal intensity is observed.

Brain damage due to HIV

Of particular note is the role of magnetic resonance spectroscopy (MRS) in the diagnosis of AIDS, which is capable of not only accurately differentiating the above pathology based on its chemical profiles, but also predicting and monitoring the effectiveness of antiviral therapy. However, it should also be noted that to perform MRS, a high-field MRI with a magnetic field strength of at least 3 Tesla is required.

We present an observation of an HIV-infected child.

Child P., 8 years old, was admitted to the children's department of the State Institution "Republican Scientific and Practical Center for Mental Health" on the referral of a child psychiatrist from the Minsk City Clinical Children's PND, accompanied by his mother and grandmother, with complaints of behavioral disturbances in the form of emotional lability, increased fatigue, absent-mindedness, lack of educational motivation, disturbances in speech (blurredness), writing (cannot keep up with a line), impaired concentration, increased distractibility. His condition changed in the spring of 2010. He was not registered with a psychiatrist. He has been disabled since childhood due to a somatic disease since 08/24/10. He has been registered with a pediatrician since 06/30/10. The child was registered late because the mother hid this condition of the child.

History: Child from 2nd pregnancy. Childbirth 1 is rapid, large fetus. He screamed right away.

Birth weight - 4100 g. Discharged from the hospital on time. At home I was a calm child. Early development was unremarkable. He began to hold his head up by 1 month. He started sitting at 6 months and began walking independently at 10 months. The first words appeared by 6 months, phrasal speech by one year.

He was enrolled in kindergarten at the age of 2, adapted well, had contact with children, and completed the kindergarten curriculum.

I went to school at the age of 6, studied according to the general education school program until 3rd grade (with “excellent” grades). In April-May 2010, I began to experience difficulties in studying due to increased fatigue and inability to concentrate on the educational material. Since September 2010, I studied at home according to the 4th grade general education program.

According to the mother, in the maternity hospital the ELISA-HIV blood test was negative. After clinical manifestations of the disease in the form of disturbances in gait, speech, and writing, the boy from the neurological department of the Lida TMO was sent for examination to the Grodno Regional Clinical Infectious Diseases Hospital, from where he was discharged with a diagnosis of HIV infection. Clinical stage 4 (AIDS). S-3 (SD-4 - 2 cells). Progressive multifocal leukoencephalopathy.

Among the diseases suffered, the following were noted: ARVI, chicken pox at 3 years old, stomatitis, pneumonia (in 2007 it was a protracted course, treated as an inpatient), frequent bronchitis.

Injuries, surgeries, and seizures are denied.

Allergies to flowering herbs, mosquito bites, pollen, sweets.

Mother: 28 years old - infected with HIV since 2006. Currently undergoing chemotherapy for non-Hodgkin's lymphoma.

Father: 37 years old - according to mother - healthy. Has not lived with family since the birth of the child.

The mother has been married since 2003, the child has been transferred to his stepfather’s surname.

The mother's second husband is not infected with HIV.

Heredity is psychopathologically (according to the mother) not burdened.

Neurological status: complaints of speech and writing disorders. FMN D=S.

The pupils are equal in size. There is no nystagmus. Full range of eye movements. Convergence is slightly reduced. The face is symmetrical. Tongue in the midline. CHP D=S.

Movements in the limbs are in full range. Muscle strength is sufficient. Muscle tone is slightly reduced, D=S. No pathological signs were identified.

Does not perform coordination tests: adiadochokinesis is noted. Unstable in the Romberg position (mild static ataxia). The gait is uncertain. There are no meningeal signs.

Somatic status:

Highly nourished child. Skin with elements of allergic dermatitis. Visible mucous membranes are clean. In the lungs - vesicular breathing. Heart sounds are rhythmic. The abdomen is soft and painless. Physiological functions are normal.

Mental status:

Conscious. Oriented partly to the place and completely to his own personality (he did not name the day, month and year - when asked, he began to list the seasons in the wrong sequence; he lists the days of the week correctly). Speech is fast and slurred. The vocabulary is sufficient, but awareness is reduced.

Knows basic colors. Summarizes and classifies using, “selecting the 4th extra” is not available. He does not understand the hidden meaning of proverbs and sayings. He reads quickly, but does not understand the essence of what he read and does not retell the text. Fine motor skills of the hands are impaired, shows the basic figures, but has difficulty working with the Seguin board. Self-service skills have been developed, but he only partially uses them independently. The mood is labile. Gets tired and exhausted quickly. Cannot explain changes in his behavior. Criticism reduced. I stayed in the department with my grandmother, because... needs specific and additional care.

Results of examination of the central nervous system for HIV,

RCT of the brain dated May 24, 2010.

The study was carried out using the usual technique, without contrast enhancement, with a section thickness of 5 mm. Pathological formations and foci of brain matter with altered density are not visualized. The midline structures of the brain are not displaced. The ventricular system is not dilated or deformed. The subarachnoid spaces and sulci of the brain are not expanded. The sella turcica is of regular shape and normal size; no destructive changes in the bones that form it have been identified. The cisterns at the base of the brain are not changed. No bone pathology was detected, the paranasal sinuses were airy.

Conclusion: Structural pathological changes in the brain were not identified.

MRI of the brain in Minsk on September 22, 2010. It was carried out on an “Obraz 2 M” tomograph (RF, 1998) with a magnetic field strength of 0.14 Tesla

No pathological space-occupying formations were identified in the cranial cavity. In the white matter of the brain (mainly in the semioval bodies), a diffuse hyperintense MR signal in the T2 image is detected on both sides (Fig. 1,2,3). After administration of a contrast agent (Omniscan 20 ml), areas of pathological accumulation are not detected. The midline structures are not displaced. Cortical grooves and basal cisterns are moderately dilated. The lateral ventricles are somewhat dilated and symmetrical. The fourth ventricle is of normal size and shape and occupies a mid-position. The craniospinal junction is without features. The pituitary gland is of normal size and shape.

Conclusion: The MR picture may be consistent with HIV-associated encephalitis.

Speech therapist's report: speech articulation disorder (rotacism).

Psychologist's conclusion: the level of intellectual development corresponds to mild mental retardation (72/58/62) - regression. Violation of the emotional sphere, monotony. Fluency, slurred speech.

The logical structure of thought processes is disrupted, incoherence is noted. Reduced control over criticism of one's behavior. The volume and concentration of attention suffers, and rapid exhaustion is noted. Reduced mnestic function.

Taking into account the anamnesis (HIV-infected, behavior has changed in the form of increased fatigue, hyperactivity, lack of educational motivation), the clinical picture and objective data (lability of the psycho-emotional sphere, difficulties in concentrating voluntary attention and exhaustion of attention, difficulties in communication and learning), we can put diagnosis:

Organic personality disorder due to HIV infection. F.07.14.

dementia due to HIV infection (HIV encephalopathy). F.02.4

Treatment performed after MRI of the brain:

1. Antiviral - “zidovudine”, “paleyvudine”, “efavir”

2. Immunomodulators - “immunofan”, “gepon”

3. Antifungal drugs - “fluconazole”

This observation allows us to draw the following conclusions: 1. unlike MRI, CT cannot effectively visualize CNS lesions in HIV-infected patients, while MRI is more sensitive 2. the examination plan for children with mental retardation and other behavioral disorders requires mandatory inclusion in their examination not only of specific research methods generally accepted for psychiatry, neurology and infectious diseases, but also of such a neuroimaging method as MRI, given its high informativeness and harmlessness (especially since we are talking about pediatric patients). 3. for a full examination of patients, it is preferable for a large mental hospital to have in its diagnostic arsenal a high-field (at least 3 Tesla) MRI, which would allow not only to reliably exclude the neurological (organic origin) component of mental pathology, but also to differentiate various types of mental pathology into based on its chemical profile (i.e., conduct MRS), as well as predict and monitor the effectiveness of the therapy.

Bibliography:

1. Lobzin Yu.V. Guide to infectious diseases. - St. Petersburg: Foliant, 2000. P. 74 82.

2. Mikhailenko A.A., Osetrov B.A. Differential diagnosis of nerve

diseases: A guide for doctors / Ed. GA. Akimova, M.M. Odinaka.-SPb.: Hippocrates, 2001. P. 635 647.

3. Melnichuk P.V., Shulman D.R. Neurological manifestations of HIV infection. Diseases of the nervous system / Ed. N.N. Yakhno, D.R. Shtulman. - M., Medicine, 2003.P.399-408.

4. Trofimova T.N., Ananyeva N.I. and others. Neuroradiology. SPb.: Publishing house SPbMAPO, 2005. P. 264-271

5. David D. Stark, Willam G. Bradley. Magnetic resonance imaging. / 2nd edition. Mosby-Year Book Inc., 1992.

6. Steiner I., Budka H. et all. Viral meningoencephalitis: a review of diagnostic methods and treatment recommendations./ European journal of neurology. - Vol.1, No. 2 - 2010

7. Dun V., Bale JF Jr. et all. MRY in children with postinfectious disseminated encephalomyelitis. - Magn Reson Imaging 1986; 4:25-32.

8. Tyler K.L. Emerging viral infections of the central nervous systems. Arch Neurol 2009;66:1065-1074.

9. Yin EZ, Frush DP et all. Primary immunodeficiency disorders in pediatric patient: clinical features and imaging findings. AJR Am J Roentgenol 2001; 176:1541–1552.

31 05 2016

The immunodeficiency virus causes irreversible changes in the cellular structure, as a result of which the body loses the ability to resist other infectious diseases.

The virus can live in the body for a long period – up to fifteen years. And only after such a long period of time will the development of immunodeficiency syndrome begin.

The virus is found in human body fluids. Routes of HIV infection:

unprotected sexual intercourse;
blood transfusion;
from sick mother to child.

HIV symptoms and diagnosis

difficulty breathing;
pneumonia;
sudden weight loss;
migraine;
blurred vision;
inflammatory diseases of the mucous membranes;
nervous disorders, depressive states.

When the virus is transmitted from an infected mother to an infant, the disease develops very rapidly. Symptoms increase rapidly, which can lead to death in the first years of a child’s life.

Development of the disease

incubation period;
infectious period;
latent period;
development of secondary diseases;
AIDS.

Pathologies of the nervous system in HIV

The primary lesion is characterized by the direct effect of the virus on the nervous system. This form of complication occurs in children with HIV.

Secondary disorders can be caused by:

autoimmune reaction of the body;
the addition of an infection;
tumor development in the nervous system;
changes in vascular nature;
toxic effects of drugs.

Encephalopathy due to HIV

Encephalopathy is often a congenital pathology. Cases of encephalopathy are common in newborns with HIV.

Symptoms of this pathology vary depending on the severity of brain damage. Thus, all symptoms are divided into three conditional groups, depending on the nature of the disease:

Stage 1 – there are no clinical manifestations, but laboratory tests reveal changes in the structure of brain tissue;
Stage 2 – mild brain disorders are observed;
Stage 3 is characterized by pronounced nervous disorders and impaired brain activity.

constant migraines and dizziness;
mental instability;
irritability;
disturbance of mental activity: weakening of memory, inability to concentrate;
depression and apathy;
speech disorder, facial expressions;
disturbances of consciousness, character changes;
trembling fingers;
deterioration of vision and hearing.

Often these symptoms are accompanied by sexual dysfunction and loss of libido.

Dementia in HIV-infected people

HIV encephalopathy belongs to a whole group of diseases characterized by cognitive impairment. These diseases are collectively called AIDS dementia (dementia).

Encephalopathy in HIV often develops as a result of drug therapy. This form of nervous system disorder occurs in infants born with HIV.

Drug addicts and people who abuse alcohol are susceptible to encephalopathy. In this case, the disease develops due to the toxic effects of drugs and alcohol on the patient’s nervous system.

However, mild symptoms of cognitive impairment are observed in every second case of HIV infection.

Stages of dementia

Dementia develops over a long period and consists of several stages. However, not every patient goes through all stages; most cases experience mild cognitive impairment.

Normally, patients do not have any mental or motor impairment. This is an ideal case in which damage to the nervous system by the virus is not observed.

The subclinical stage is characterized by mild cognitive impairment, characterized by mood swings, depression and impaired concentration. Patients often experience slight inhibition of movement.

The final stage of dementia development is vegetative coma. The patient is unable to perform basic actions and cannot cope without outside help.

Diagnostic methods

Since pathology causes a change in the volume of nervous tissue, the disease is diagnosed using the following methods:

lumbar puncture;
dopplerography.

Based on the lumbar puncture, a decision is made on the advisability of further research. This analysis reveals the presence of changes in the nervous system.

Dopplerography is mandatory. This examination is necessary to assess the condition of the blood vessels in the brain. Changes in encephalopathy primarily affect the main vertebral and cerebral arteries, changes in which are shown by Doppler ultrasound.

Therapy and prognosis

Any damage to the nervous system caused by HIV is treated with potent antiviral drugs (for example, zidovudine).

Timely treatment can stop further development of encephalopathy and dementia. In some cases, it is possible to stop the progression of dementia, and in others, it is possible to delay the development of cognitive impairment for a long time.

Prevention of pathologies of the nervous system

depression and apathy;
mental instability;
frequent mood changes;
sleep disorders;
headache;
visual disturbances and hallucinations.

Timely treatment will avoid or significantly delay the onset of severe symptoms of dementia. However, the patient must help himself.

Summary

According to official data from the Ministry of Health of Ukraine, the number of people newly diagnosed with HIV infection/AIDS in the period from 1987 to November 2009 is: HIV infection - 156,404, AIDS - 30,767, deaths - 17,454. According to official estimates from the World Health Organization and UNAIDS, in 2005–2006. About 45 million people on the planet are infected with HIV. The average HIV infection rate in Ukraine is 58 cases per 100 thousand population.

One of the target organs of HIV is the nervous system: only 1/10,000 of the peripheral blood lymphocytes of AIDS patients are infected with the virus, while in brain tissue HIV affects every hundredth cell. Accordingly, one of the common manifestations of HIV/AIDS is damage to the nervous system. Neurological complications of HIV infection can be either caused by the retrovirus itself or due to opportunistic infections, tumors, cerebrovascular pathology, and the toxic effects of antiretroviral drugs.

It is known that the direct damage consists of infection and destruction of cells of the nervous system that have the CD4 receptor. These include: astrocytes, oligodendrocytes, microglia, monocytes, fibroblast-like brain cells, endothelial cells of blood vessels, neurons. In addition, glial cells are affected not only due to infection, i.e. penetration of HIV into the cell itself, but also due to their membrane lysis by the gp120 protein. Glycoprotein gp120 plays a key role in the pathogenesis of HIV neuronal damage by blocking neuroleukin (a lymphokine with a neurotrophic effect). Under the influence of gp120, astrocytes do not retain glutamate at synapses, which leads to increased Ca2+ ion load and cytotoxic effect.

Each link in the pathogenesis subsequently leads to the emergence in patients of a special clinical picture with a characteristic neurological deficit, depending on the point of application. Thus, a decrease in the neurotrophic influence of bioregulatory substances of the hypothalamic-pituitary complex leads to a disruption of mediator metabolism. Deficiency of gamma-aminobutyric acid and glycine subsequently leads to the development of epileptic seizures. Serotonin depression leads to antiserotonin ataxia. Violation of vasopressin metabolism leads to memory impairment. Damage to the endothelial cells of the choroid plexus of the meninges and the ependyma of the ventricles leads to the development of inflammation of the mesenchymal elements of the nervous tissue and secondary demyelination, which will subsequently be clinically manifested by the development of virus-induced vasculitis. Depression of cellular immunity leads to the development of opportunistic infections and neoplastic processes in patients.

There are several hypotheses that can explain the easy penetration of HIV through the BBB. According to one hypothesis, direct damage to the central nervous system itself can occur due to perineural penetration of the virus into glial cells. Indirect damage also occurs - when the virus penetrates from the cells of the immune system into the nervous system (the “Trojan horse” mechanism). It is possible for the virus to penetrate the endothelial cells of cerebral capillaries that carry the CD4 antigen on the membrane. It is also assumed that there are genetic variants of HIV that have a specific neurotropic effect.

CD4 receptors are located not only in neuroglial cells, but also in endothelial cells of the choroid plexus of the meninges and ventricular ependyma. This can subsequently lead to HIV-associated vascular lesions of the spinal cord and brain. Since the pathological process is localized endovascularly, primary vasculitis and vasculopathy may occur. Primary HIV-associated vasculitis of the brain and spinal cord can subsequently lead to secondary damage to the nervous tissue. It is known that thrombocytopenia, which often develops during HIV infection, increases the risk of developing hemorrhagic complications, which causes disturbances in blood rheology and hypercoagulation. Histological studies in HIV-infected patients revealed infiltration of the vessel wall with leukocytes, edema and proliferative changes in the intima. All this leads to a narrowing of the lumen of the vessel and its thrombosis with further possible infarction, rupture of the vessel and hemorrhage. Very often, an HIV-infected patient experiences a transformation of an ischemic stroke into a hemorrhagic one. In HIV-associated vasculitis, multifocal lesions develop. This gives grounds to talk not just about vasculitis, but about the meningovascular productive form of neuro-AIDS.

Approximately 40% of HIV-infected people have abnormal cerebrospinal fluid (CSF), usually with mild pleocytosis (5-50 cells/mm3), increased protein (500-1000 mg/L) and normal glucose concentrations. These changes are not specific. Half of clinically healthy HIV-infected patients have pleocytosis or increased protein in the CSF, and in 20% the CSF grows HIV on tissue culture, often in high titers. Later, pleocytosis decreases, while the amount of protein may increase, decrease, or remain unchanged. As in peripheral blood, the CSF CD4:CD8 ratio is low, especially late in the infection. The virus titer in the CSF also decreases in the late stage. These changes in the CSF are moderate and not constant, so based on them it is difficult to predict the course of the disease and the effectiveness of therapy.

Anti-HIV is usually detected in the CSF in high titres. Comparison of antibody titers in blood and CSF indicates that antibodies may be synthesized in the CNS. Antibodies to HIV in the CSF belong to the IgG class, but in some patients it was possible to find antibodies of the IgA and IgM classes. Antibody synthesis in the central nervous system begins early, immediately after infection of the meninges. Oligoclonal antibodies can also be detected in the CSF; they correspond to HIV epitopes and have a different migratory ability than serum antibodies. Pleocytosis and protein concentration correlate poorly with anti-HIV antibodies in the CSF and the presence and number of oligoclonal bands. Patients with a positive CSF culture for HIV have both anti-HIV antibodies in the CSF and oligoclonal bands. In patients with AIDS, antibody synthesis in the CSF is markedly lower than in HIV-infected patients without AIDS. The concentrations of p24 antigen and anti-p24 antibodies in the CSF and serum change in parallel, but the concentration of p24 in the CSF is usually higher. The concentration of p24 is maximum in the AIDS-dementia complex, but usually the concentration of antigens and antibodies poorly correlates with the severity of clinical symptoms and the effectiveness of therapy.

In the clinical picture, a characteristic series of symptom complexes can be identified: meningism, pyramidal insufficiency, cerebellar ataxia, convulsive syndrome, AIDS-dementia complex, a symptom complex characteristic of encephalitis, meningitis. Clinical observations show that in the early stages of HIV infection, the most common are reactive neurotic states and manifestations of asthenovegetative syndrome. Patients have a variety of neurotic disorders, as well as increased fatigue, absent-mindedness, forgetfulness, deterioration of mood, narrowing of interests, sleep disorders, various phobias, and autonomic lability. In later stages of the disease, damage to the nervous system comes to the fore, mainly due to opportunistic infections.

Diseases of the central nervous system resulting from direct damage by a retrovirus

Acute aseptic meningoencephalitis

This syndrome is detected in 5-10% of HIV-infected people immediately before seroconversion and during or after mononucleosis-like syndrome. Patients are worried about headache, fever, mental status disorders, focal or generalized seizures are determined. With the exception of transient facial paralysis (Bell's palsy), focal or lateralized nervous system symptoms are rare. There are reports of acute myelopathy with paraparesis and severe pain, lack of sensory disturbances, urinary incontinence and spinal myoclonus (rhythmic contractions of the abdominal muscles) in the early stages of infection. In the CSF, it is possible to detect pleocytosis, a moderate increase in protein and a normal amount of glucose - changes similar to those detected in seropositive clinically healthy HIV-infected patients. Laboratory diagnosis of HIV infection is based on isolation of virus or p24 from serum or CSF or, later, serologic evidence of seroconversion (usually 1 or 2 months later). Acute meningoencephalitis is a self-limiting disease and requires only symptomatic therapy.

Complex "AIDS - dementia" (AIDS - Dementia Complex, ADC)

ADC, also called "HIV encephalitis", "HIV encephalopathy", "subacute encephalopathy", occurs exclusively during the AIDS phase. This most common neurological disease in AIDS patients may also be the first symptom of AIDS in HIV-infected people. Early symptoms are apathy, inattention, forgetfulness, impaired concentration, decreased intelligence, autism, which together is very similar to depression. Patients may also exhibit disorientation, confusion, hallucinations, or psychosis. Initial examination at the patient's bedside does not reveal any disorders, but neurophysiological research already during this period shows a violation of the accuracy and speed of motor functions, including visual-motor functions, fluency of speech, short-term memory, and difficulty in solving complex situational problems. This distinguishes ADC in the early phase from banal depression. In patients, the pace of thinking and reaction speed are significantly reduced. When dementia becomes apparent, cortical symptoms (such as aphasia, apraxia, and agnosia) are also not primary; therefore, some neurologists classify ADC as subcortical dementia as opposed to cortical dementia such as Alzheimer's disease. Oculomotor disturbances are common in the early phase of ADC. Increased “physiological” tremor is also often detected. Patients typically have an unsteady gait that is difficult to classify as ataxia, sensory ataxia, spastic apraxic, or functional. Some patients have gait disturbance and lower limb dysfunction associated with vacuolar myelopathy. ADC may progress gradually or stepwise with sudden deterioration, sometimes in combination with systemic manifestations of the disease.

The diagnosis of ADC is made by excluding competing diagnoses that may lead to impaired consciousness, psychosis, or dementia in patients with AIDS. Blood tests, CSF, and head computed tomography (CTG) are of decisive importance. These diseases include not only infections and tumors of the central nervous system, but also side effects of drug therapy and nutritional imbalances. In patients with ADC, CTG is either normal or reveals brain atrophy. Magnetic resonance imaging (MRI) shows brain atrophy. Later, areas of softening and diffuse changes in the white matter appear, best identified by T2-mode MRI. These changes are not specific. Positron emission tomography of the head shows abnormalities in glucose metabolism. In the early phases, it is possible to detect hypermetabolism in the basal and thalamic ganglia, later - hypometabolism in the gray matter of the cortex and subcortical formations. The CSF may be normal or have mildly increased numbers of cells, protein, or oligoclonal antibodies. High levels of b2-microglobulins are detected frequently and correlate with the severity of ADC.

Almost half of patients with ADC, especially those with severe disease, have vacuolar myelopathy. In addition to the latter, the severity of ADC is correlated with: the number of multinucleated cells, pallor of the centrum semiovale, and the presence of HIV in the brain. Pathological changes confirm that with proper treatment, some or all symptoms can be reversible.

Progressive encephalopathy (PE)

Progressive encephalopathy is a CNS disorder in children that is clinically similar to ADC in adults. It is detected in almost half of infected children. Less than 25% of infected children have normal neuropsychic development, 25% have stable (non-progressive) encephalopathy, possibly caused by complications of the perinatal period.

PE manifests itself between the ages of 2 months and 5.5 years, on average at the age of 18 months. The onset of the disease is usually gradual, although it can be acute. In some children, PE is the first manifestation of HIV. In sick children, a delay (or involution) of mental and physical development is noted. Special studies reveal delayed intellectual development, decreased rates of brain growth, and symmetrical motor impairment. Initially, children are sedentary, apathetic, and later develop mutism and dementia. Half of children with PE develop acquired microcephaly. At the onset of the disease, hypotonia and hyporeflexia are noted, subsequently progressing to pseudobulbar palsy and quadriplegia. Children who do not receive treatment may deteriorate quickly, or gradually, or in steps. Death usually occurs within a year after diagnosis. Like ADC, PE appears in the late phase of the disease, when the patient has signs of immunodeficiency. CTG may be normal, but most often it is possible to detect brain atrophy. On CTG with intravenous contrast in children under 5 years of age, one can see increased contrast in the basal ganglia and frontal lobes of the brain, and calcifications. These changes may progress. MRI reveals increased signal levels in the paraventricular white matter.

Children with PE may have moderate lymphocytic pleocytosis (5-25 cells/mm3) and increased protein content in the cerebrospinal fluid (500-1000 mg/l). As in adults, a higher titer of antibodies is detected in the cerebrospinal fluid compared to serum, which confirms their intracerebral synthesis. In children with PE it is also possible to detect exceptionally high levels of p24 in the CSF. Tumor necrosis factor concentrations in serum, but not CSF, correlate with clinical symptoms. Three quarters of children with PE have high serum TNF concentrations, and 95% of HIV-infected children with high TNF levels have PE.

Opportunistic infections of the central nervous system, conditions resulting from cerebrovascular disorders, neoplasms

Diseases of the brain parenchyma

Toxoplasmosis. Toxoplasma gondii- the most common cause of focal damage to the central nervous system in patients with AIDS. Approximately 10% of AIDS patients have CNS toxoplasmosis. Most cases result from reactivation of a latent infection. In AIDS patients with a positive Sebin-Feldman test, but without clinical manifestations of toxoplasmosis, the latter will develop in the future in 30%. Although not common, a small number of patients with CNS toxoplasmosis have a negative Sebin–Feldman test, so negative dye tests do not negate toxoplasmosis. Changes in titer value, such as a 4-fold increase in paired sera, are unusual. Extracerebral manifestations of toxoplasmosis, such as chorioretinitis, are rare and do not correlate in any way with damage to the nervous system.

CTG and MRI play a crucial role in diagnosis. CTG reveals areas of damage to the brain substance with edema, more intense staining with intravenous contrast, often in the form of rings. Absence of change on CTG is unusual. Lesions are most often found in the basal ganglia. Other diseases can give a similar picture, and it is possible that the patient simultaneously has several diseases of the brain parenchyma, giving a picture of multiple lesions.

It is preferable to be confident in the diagnosis of brain toxoplasmosis before starting treatment. A brain biopsy is of some importance. The latter also has a known risk - due to the possibility of infection or bleeding. A brain biopsy should only be considered if a 2-week trial of treatment fails. It is difficult to make a diagnosis of toxoplasmosis using a biopsy. Histologically, inflammation in the abscess caused by Toxoplasma gondii may resemble lymphoma. Detection of trophozoites (or tachyzoites) by the immunoperoxidase method, which has diagnostic value, is often difficult. An open brain biopsy is preferable to a needle biopsy, but even in this case the diagnosis may not always be established. It is possible to isolate the pathogen biologically (injecting a brain sample into mice) or in tissue culture.

Thus, most patients begin to receive treatment for toxoplasmosis without a specific diagnosis of CNS toxoplasmosis.

In the diagram presented in table. 1, sulfadiazine can be replaced by one of the following drugs:

- clindamycin, 600 mg IV or orally 4 times a day for 6 weeks;

- azithromycin, 1200 mg orally 1 time per day for 6 weeks;

— clarithromycin, 1 g orally 2 times a day for 6 weeks;

- atovaquone, 750 mg orally 4 times a day for 6 weeks.

Some patients require a very long course of intensive treatment for acute infection. There are no standard recommendations regarding the duration of treatment: the decision to switch to another course of treatment is made based on clinical indications and CT results, if available.

Improvement occurs within 10 days and is verified by the positive dynamics of CTG and MRI. In this case, it is finally established that pathological changes in the central nervous system were caused by Toxoplasma gondii. Since swelling of the brain tissue also occurs with this pathology, doctors often prescribe glucocorticoids for the entire duration of treatment. Glucocorticoids improve the course of many diseases of the brain parenchyma in HIV. Thus, improvement in the case of combination therapy does not mean that pathological changes in the central nervous system were due to Toxoplasma gondii.

CNS toxoplasmosis in patients with AIDS often recurs after cessation of treatment. Most patients require ongoing maintenance therapy. For secondary prevention, use half the doses of drugs included in effective regimens used to treat acute toxoplasmosis; treatment is continued until the CD4 lymphocyte count remains > 200 per μl for 3 months.

Primary CNS lymphoma. Primary CNS lymphoma is detected in two percent of AIDS patients. The tumor has antigenic markers of B cells and is multicentric. Neurological symptoms may indicate focal or diffuse central nervous system disease. The most typical should be considered hyperventilation, in some patients in combination with uveocyclitis. These symptoms may be important for the presumptive diagnosis of CNS lymphoma. Primary lymphoma can occur in patients with immunodeficiencies due to causes other than HIV. These patients have a high titer of antibodies to the Epstein-Barr virus (EBV), and EBV-specific nucleic acids and proteins are detected in tumor cells. In tissue culture, EBV has the ability to transform B lymphocytes. It is possible that EBV may be the cause of primary CNS lymphoma. Since the EBV genome and its mRNA are present in tumor cells of patients with AIDS, EBV can cause primary CNS lymphoma in patients with AIDS.

CTG reveals one hyper- or isodense lesion or more with signs of edema of the brain substance. The lesions may be unilateral or bilateral. Rarely, the lesion is of low density (hypodense) and does not contrast with intravenous contrast. Some lesions have a ring-shaped appearance with intravenous contrast and resemble toxoplasmosis. MRI is more sensitive than CTG. Changes on CTG are not specific for lymphoma. Angiography usually reveals the presence of a nonvascularized mass, although some tumors stain homogeneously. Lumbar puncture is potentially dangerous. Cytological examination of the CSF reveals tumor cells in only 10-25% of patients. In these patients, high levels of b2-microglobulins can be detected, but in patients with AIDS these changes are not specific. Definitive diagnosis requires a brain biopsy. In case of a single lesion, biopsy is the method of choice for diagnosis; in case of multiple lesions, treatment for suspected CNS toxoplasmosis is usually attempted, and in case of failure, biopsy is used.

Primary CNS lymphoma in patients with AIDS significantly decreases in size under the influence of corticosteroids, it is sensitive to X-ray radiation, but the average survival does not yet exceed 2 months, while patients with non-AIDS lymphoma survive for 10-18 months. In contrast to other types of brain tumors, surgical decompression is more likely to harm the patient. Highly effective antiretroviral therapy can cause fairly stable remission of primary CNS lymphoma.

Progressive multifocal leukoencephalopathy (PML). Like primary CNS lymphoma, PML can occur in patients with immune compromise due to causes other than HIV (eg, corticosteroid use). Currently, 20% of patients with PML have AIDS; however, as the number of AIDS patients increases, this percentage will increase. PML occurs in 2-5% of AIDS patients. These patients exhibit progressive dementia and focal neurological symptoms.

CTG usually reveals one or more hypoattenuating lesions that do not enhance with intravenous contrast. Damage often begins at the gray/white matter interface and progresses progressively into the white matter. MRI is usually more sensitive than CTG and is more likely to detect large and multiple lesions. CSF studies are not informative, except for detecting an increased concentration of myelin basic protein.

The diagnosis is based on a biopsy, which reveals: a) demyelination; b) large astrocytes with abnormal, sometimes multiple, nuclei; c) oligodendroglia with eosinophilic intranuclear inclusions. Pathological changes resemble those detected in PML caused by causes other than AIDS. JC virus, a member of the Papovaviridae, infects glial cells, especially oligodendroglia (by comparison, HIV infects macrophages and microglia). Because abnormal astrocytes may be mistaken for glioma or the patient may be mistaken for having cytomegalovirus (CMV) infection, diagnosis depends on immunohistochemical detection of JC virus in the biopsy specimen. The JC virus Gis-activating regulatory element is active in neonatal glioma tissue culture; JC virus-stimulated T-antigen expression in mice leads to dysmyelination. This confirms that JC virus causes PML.

There is no sufficiently effective treatment. The average life expectancy is 4 months, but some patients with AIDS have longer survival times after diagnosis of PML than patients without AIDS.

Stroke. Hemorrhagic, thrombus-related, or thromboembolic strokes are uncommon in HIV-infected people. Hemorrhagic stroke is more common in patients with severe thrombocytopenia (especially in patients with hemophilia) and with metastases of Kaposi's sarcoma to the brain. Strokes associated with thrombosis occur in patients with angiitis. The development of granulomatous angiitis may be associated with herpetic lesions of the face, but it also occurs in patients with AIDS who have not had a herpetic infection. In some patients, the cause of strokes associated with thrombosis cannot be determined. Perhaps some of them had “anticoagulant lupus”, anticardiolipin antibodies. The presence of anticoagulant lupus is usually explained by a high partial thromboplastin time, a false-positive VDRL test, and a low platelet count. The presence of anticardiolipin antibodies in the diagnosis of this syndrome is not clear. Thromboembolic stroke has been reported in patients with infective endocarditis with marasmus or nonbacterial endocarditis with thromboembolic syndrome, which may be associated with Kaposi's sarcoma. An association between thrombocytopenic purpura and AIDS cannot be ruled out. The full pentad of symptoms of thrombocytopenic purpura includes (all 5 symptoms are not necessary in patients with AIDS): thrombocytopenia, microangiopathic hemolytic anemia, kidney pathology, fever, neurological pathology (usually progressive).

Herpes virus infection. Herpes viruses include CMV, herpes zoster virus (HZV), and herpes simplex viruses type 1 and 2. These viruses can cause diseases of both the brain parenchyma and its membranes. When they develop in patients with HIV infection, they are usually referred to as “secondary viral encephalomyelomeningitis.” Other nonherpetic viral infections associated with immunodeficiency, such as measles, enteroviral encephalitis, and enteroviral myositis, have not been reported in AIDS.

CMV infection has a unique manifestation in HIV-infected people. Retinitis is found in 20-25% of AIDS patients. Most often it is caused by CMV. Retinal damage consists of permeation of the vascular area with hemorrhagic exudate. Adrenal insufficiency is common in patients with disseminated CMV infection. CMV encephalitis may present with focal, multifocal, or generalized neurological symptoms. CTG and MRI may be normal. A quarter of AIDS patients have histological signs confirming the presence of CMV infection: neuronal necrosis, eosinophilic inclusions in the nuclei. CMV can also cause severe motor polyradiculopathies. CMV-positive multinucleated (cytomegalic) cells are found in the subpial, sub-ependymal areas and nerve roots. CMV can also cause acute polyradiculopathy.

Herpes zoster usually results from reactivation of a latent infection and occurs at different stages of HIV. Patients with AIDS more often have disseminated herpes and postherpetic neurological syndrome, as well as multifocal leukoencephalitis with focal or lateralized neurological symptoms, signs of hydrocephalus on CTG. CSF may be normal. Pathologically, ventriculitis and focal necrosis with intracellular inclusions in ependymal cells and glia are determined. Cerebral granulomatous angiitis, as a consequence of a herpetic infection, is manifested by fever, impaired consciousness, and ischemic strokes. Finally, patients may have myelitis caused by HZV.

People with AIDS often have extensive skin ulcers caused by the herpes simplex virus (HSV). In this case, the risk of HSV encephalitis is very high. HSV-2 commonly causes perirectal and genital ulcers, as well as meningitis and myelitis.

See table. 2-5.

Non-steroidal anti-inflammatory drugs are prescribed for pain relief. If these do not help, amitriptyline, carbamazepine or phenytoin can be prescribed.

Diseases of the meninges

Cryptococcosis and other fungal infections. These diseases most often occur in the late stages of HIV infection. Meningitis caused by Curtosossus neofortans, occur in 5-10% of AIDS patients, most often in intravenous drug addicts and bird owners. Other fungal infections are more rare in people with AIDS. Disseminated histoplasmosis and coccidioidomycosis are more often observed in residents of endemic areas. Other fungal diseases that may occur in people with AIDS include aspergillosis, candidiasis, and mucormycosis.

Patients with cryptococcal meningitis usually present with fever (65%), headache or head discomfort (75%), stiff neck (22%), impaired consciousness syndrome (28%), and focal neurological symptoms or seizures (< 10 %). У некоторых больных может быть только лихорадка или только головная боль без каких-либо неврологических изменений. КТГ обычно в норме, за исключением случаев, когда развиваются грибковые абсцессы или гидроцефалия. В некоторых случаях СМЖ не изменяется. Для этиологической расшифровки при криптококковых менингитах применяются окрашивание СМЖ тушью (положительный результат в 72-100 % случаев), выявление криптококкового антигена (положительный в 90-100 %). В сыворотке криптококковый антиген удается выявить в 95-100 % случаев. Встречаются ложноотрицательные результаты, возможно, в связи с низкой концентрацией криптококкового антигена, инфекцией, вызванной необычным серотипом. Ревматоидный фактор может приводить к ложноположительным результатам. Диагностика криптококкового менингита может потребовать проведения повторных люмбальных пункций с попыткой выделения культуры гриба.

Lifelong secondary chemoprophylaxis is necessary; for this you can use fluconazole, 200 mg orally 1 time per day; An alternative drug for long-term secondary chemo-prevention is itraconazole, 200 mg orally once a day for life.

There is no specific evidence yet to support continuation or cessation of prophylaxis after improvement in immune system function (CD4 > 200 in 1 μl).

When treating patients receiving methadone maintenance therapy, it is necessary to be aware of the interaction between fluconazole and methadone.

Lymphomatous meningitis. Patients with AIDS often develop non-Hodgkin's lymphoma with B-lymphocyte markers. Tumor cells morphologically resemble cells of primary CNS lymphoma, but contain the EBV genome and the proteins encoded by it. Cancer is most often extranodal; the meninges are involved in the pathological process in 10-30% of cases. Paraspinal localization with the development of symptoms of spinal cord compression occurs in 10% of patients. In the meningeal form, it is possible to identify cranial nerve palsies, radiculopathy and headache. In the CSF, pleocytosis, increased protein concentration, and in isolated cases, hypoglycorachia are detected. Diagnosis is based on cytological examination of the CSF. Treatment consists of combined chemotherapy and radiotherapy.

Disseminated tuberculosis. HIV-infected people who test positive for purified protein derivative are at high risk of developing disseminated tuberculosis (TB) and should receive isoniazid for prophylaxis. 2% of HIV-infected people have active tuberculosis. Active disease can occur at any stage of HIV infection and is most often, but not always, the result of activation of latent infection. Patients may experience meningeal symptoms (fever, headache, stiff neck). There may also be symptoms of spinal cord compression due to infection. Cases of myelopathy with isolation of mycobacteria on spinal cord biopsy have been reported. Finally, in patients with disseminated tuberculosis, signs of adrenal insufficiency can be identified.

The skin test is negative in 70% of AIDS patients with active tuberculosis. Chest radiography often reveals pathology, with changes localized in the lower and middle lobes, and not in the upper, as is usually the case with tuberculosis. A tumor-like formation in the brain (tuberculoma) can be detected by CTG. In the CSF it is possible to detect mononuclear cytosis, increased protein levels and, rarely, hypoglycorrhachia. With CSF microscopy, acid-fast bacilli can be detected in 37% of cases, and the pathogen can be isolated in 45-90% (this takes 1-2 months). Newer tests have been developed for the rapid detection of mycobacterial antigen.

The course of tuberculosis in HIV-infected people is more severe, its treatment is more complex, and the frequency of side effects is higher. For these reasons, all patients with active tuberculosis should be tested for HIV. HIV-infected patients with acid-fast bacilli on a smear or biopsy should receive anti-tuberculosis therapy for as long as bacteriological testing is carried out, despite the fact that some patients will be diagnosed with Mucobacterium avium intracellulare, but not M. tuberculosis.

In HIV-infected patients with coinfection M. tuberculosis there is a high risk of developing active TB, so they need to undergo preventive treatment with isoniazid at a dosage of 5 mg/kg (but not more than 300 mg/day) once a day, a course of 6 months.

Syphilis. There are strict epidemiological patterns between syphilis and AIDS. This means that all patients with syphilis must also be tested for HIV. Symptoms of syphilis can occur at any stage of HIV infection. Syphilis of the nervous system can manifest as ischemic stroke, meningitis, Bell's palsy, optic neuritis, polyradiculopathy and dementia. Since more than 25% of HIV-infected people with neurosyphilis have negative “nonspecific” antitreponemal tests (VDRL, RPR), recognition of syphilis depends on positive “specific” antitreponemal tests (FTA-abs, MNA-TP, TRNA). Both types of tests are designed to detect circulating antitreponemal antibodies in the blood. Most likely, there are more false positives and false negatives with HIV than with syphilis testing in people uninfected with HIV. The VDRL test can be successfully used to monitor the effectiveness of syphilis therapy in HIV-infected people. It is generally accepted to use routine and VDRL testing of CSF to diagnose neurosyphilis. Both of these tests produce a higher number of false positive and false negative results in HIV-infected people.

Neurosyphilis is treated with large doses of penicillin G (2-4 million units intravenously every 4 hours for 10-14 days). HIV-infected patients with FTA-abs-positive serum and a positive VDRL test with CSF should receive treatment as indicated. Other indications for high-dose intravenous penicillin for syphilis are unclear. There are reports of unsuccessful use of long-acting penicillins administered intramuscularly in the treatment of secondary syphilis in HIV-infected patients.

Spinal cord diseases

Vacuolar myelopathy. This disease occurs exclusively in patients with AIDS, affecting approximately 20% of patients. Although myelopathy is often associated with ADC, the disease can occur in patients with AIDS and without dementia. Gait disturbance in combination with spastic paraparesis and sensory ataxia is noted. Neurological examination reveals hyperreflexia, muscle spasticity, impaired vibration sensitivity in the legs and instability in the Romberg position. After a few weeks or months, urinary incontinence occurs. CSF examination is not informative. Evoked auditory and visual brainstem potentials were normal. A universal delay in somatosensory evoked potentials of the posterior tibial nerve is always found. This can be detected long before the clinical manifestation of the disease. Differential diagnosis includes spinal cord compression due to lymphoma or tuberculosis, infectious myelitis such as HIV seroconversion, herpes infection and HTLV-1, and myeloradiculopathy. Pathomorphological examination reveals demyelination and vacuolization of the white matter of the posterior and lateral cords and a small number of macrophages with fatty inclusions. Electron microscopy reveals that the vacuoles are the result of intramyelin edema. HIV antigens can rarely be isolated from spinal cord tissue of patients with vacuolar myelopathy. The most severe changes can be detected in the thoracic spinal cord.

Neuropathy of the cranial nerves. Neuropathy of the cranial nerves (most often in the form of isolated unilateral paresis of the facial nerve) occurs in 10% of HIV-infected people throughout their illness in combination with either isolated HIV infection or damage to the meninges. In addition, orbital tumors (eg, lymphoma) may cause early oculomotor paralysis. Lower motor neuron palsy of the facial nerve usually occurs in the middle phase of infection and resembles Bell's palsy. Recovery is usually observed without any treatment.

Neuromuscular diseases

Approximately 30% of people with AIDS have neuromuscular diseases. Deficiency of cobalamin, α-tocopherol, syphilis, thyroid dysfunction, side effects of drugs such as zidovudine, vincristine, disulfiram can lead to symptoms of a neuromuscular disease and require special treatment.

Five neuropathic syndromes have been described in patients with AIDS: Guillain-Barré, chronic demyelinating polyneuropathy, multiple mononeuritis, distal sensory peripheral neuropathy, acute polyradiculopathy.

Guillain-Barre syndrome. This syndrome occurs mainly in the early and middle phases of infection. As with Guillain-Barré syndrome not associated with HIV infection, these patients sometimes require artificial ventilation due to developing acute respiratory failure. The examination reveals weakness, areflexia with normal sensitivity. Hepatitis B surface antigen detection and abnormal liver tests are routine. High levels of protein are detected in the CSF. In many, but not all patients, pleocytosis is also detected in the CSF, which may be a consequence of HIV infection itself. The presence of pleocytosis in patients with Guillain-Barré syndrome should raise suspicion of HIV infection. Nerve conduction may be normal or slow with depression or conduction block. When axons are involved in the process, neuromyography reveals symptoms of denervation. A biopsy of peripheral nerves either reveals no changes or segmental demyelination can be detected. Perineural cells may be vacuolated. The degree of inflammation may vary. CMV infection of Schwann cells is possible, especially pronounced in the area of the proximal roots. Careful monitoring of vital functions in these patients is the key to successful treatment of Guillain-Barré syndrome. A decrease in vital capacity of less than 1 liter is usually an indication for artificial ventilation. Although some patients experience spontaneous recovery, treatment by replacing the patient's plasma with donor plasma is the method of choice.

Chronic inflammatory demyelinating polyneuropathy (CIDP). This syndrome occurs mainly in the middle stage of infection, although it can also occur in patients with AIDS. Patients are concerned about progressive constant or intermittent weakness. The examination reveals weakness in the proximal and distal muscle groups, normal (or relatively normal) sensitivity and areflexia. More often there is weakness in the facial muscles. The CSF reveals proteinorachia and pleocytosis, which most often results directly from HIV infection. It is impossible to accurately differentiate CIDP in HIV from idiopathic one only on the basis of the presence of pleocytosis, although HIV infection can be assumed. In a third of patients, the concentration of myelin basic protein increases in the CSF. The correct diagnosis depends on the results of HIV testing. Nerve conduction studies reveal decreased conduction with conduction block and depression indicative of segmental demyelination. Electromyography, when axons are involved in the process, reveals demyelination. On nerve biopsy, demyelination, macrophage infiltration, perivascular and endoneurial inflammation are evident. Vacuolation of perineural cells can be significant. HIV antigens cannot be detected in nerve biopsies. CIDP is difficult to differentiate from Guillain-Barré syndrome, lymphomatous infiltration of nerve roots, and toxic neuropathy caused by drugs (such as vincristine, disulfiram, isoniazid, dapsone). With treatment with corticosteroids and plasmapheresis, CIDP regresses. In some cases, spontaneous recovery occurs. Improvement may correlate with normalization of cell counts and protein in the CSF. The causes of CIDP are unknown.

Multiple mononeuropathy. The rarest form of neuropathy. It is characterized by suddenly developing lesions of large isolated nerve trunks. The process may involve cranial nerves. The cause is usually acute inflammation or disruption of the blood supply to the nerves. This syndrome is clinically difficult to distinguish from compressive neuropathy, progressive polyradiculopathy, and when many nerves are involved, from CIDP.

Progressive polyradiculopathy. With this syndrome, which usually develops in the late stage of HIV, progressive sensorimotor insufficiency and areflexia appear acutely or subacutely, localized at the level of the lumbosacral spinal cord with the development of dysfunction of the sphincters of the bladder and rectum. Patients are unable to move independently and have urinary retention.

With this syndrome, death most often occurs within a few months. In half of the cases, pleocytosis, high protein content and decreased glucose levels can be detected in the CSF. In half of the patients, CMV can be isolated from the CSF using a virological method. The electromyogram reveals acute denervation (fibrillation and positive sharp waves). Differential diagnosis includes acute spinal cord compression, meningeal lymphomatosis, and neurosyphilis. With virological examination of sectional material, in many cases it is possible to detect CMV infection of endoneurial cells of the dorsal roots of the spinal cord and endothelial cells. Early administration of ganciclovir leads to reversal of the disease in a number of patients.

Damage to the autonomic nervous system (ANS)

Damage to the ANS, usually mild, occurs late in the infection and is manifested by orthostatic hypotension. Damage to both the sympathetic and parasympathetic divisions of the ANS occurs. There is a poor correlation with other neurological manifestations of HIV. Adrenal insufficiency may also occur.

Bibliography

1. Katlama C. et al. Pyrimethamine-clindamycin vs. pyrimethamine-sulfadiazine as acute and long-term therapy for toxoplasmic encephalitis in patients with AIDS // Clinical Infectious Diseases. - 1996. - 22(2). - 268-275.

2. Dannemann B. et al. Treatment of toxoplasmic encephalitis in patients with AIDS. A randomized trial comparing pyrimethamine plus clindamycin to pyrimethamine plus sulfadiazine. The California Collaborative Treatment Group // Annals of Internal Medicine. - 1992. - 116(1). - 33-43.

3. Chirgwin K. et al. Randomized phase II trial of atovaquone with pyrimethamine or sulfadiazine for treatment of toxoplasmic encephalitis in patients with acquired immunodeficiency syndrome: ACTG 237/ANRS 039 Study. AIDS Clinical Trials Group 237/Agence Nationale de Recherche sur le SIDA, Essai 039 // Clinical Infectious Diseases. - 2002. - 34(9). - 1243-1250.

4. Fine H.A., Mayer R.J. Primary central nervous system lymphoma // Annals of Internal Medicine. - 1993. - 119(11). - 1093-1104.

5. Hoffmann C. et al. Survival of AIDS patients with primary central nervous system lymphoma is dramatically improved by HAART-induced immune recovery // AIDS. - 2001. - 15(16). - 2119-2127.

6. Hoffmann C. et al. Response to highly active antiretroviral therapy strongly predicts outcome in patients with AIDS-related lymphoma // AIDS. - 2003. - 17(10). - 1521-1529.

7. McGowan J.P., Shah S. Long-term remission of AIDS-related primary central nervous system lymphoma associated with highly active antiretroviral therapy // AIDS. - 1998. - 12(8). - 952-954.

8. Hoffmann C. et al. Successful autologous stem cell transplantation in a severely immunocompromised patient with relapsed AIDS-related B-cell lymphoma // European Journal of Medical Research. - 2006. - 11(2). - 73-76.

9. Whitley R.J. et al. Guidelines for the treatment of cytomegalovirus diseases in patients with AIDS in the era of potent antiretroviral therapy: recommendations of an international panel. International AIDS Society-USA // Archives of Internal Medicine. - 1998. - 158(9). - 957-969.

10. Foscarnet-Ganciclovir Cytomegalovirus Retinitis Trial: 5. Clinical features of cytomegalovirus retinitis at diagnosis: studies of ocular complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group // American Journal of Ophthalmology. - 1997. - 124(2). - 141-157.

11. Jacobson M.A. et al. Phase I study of combination therapy with intravenous cidofovir and oral ganciclovir for cytomegalovirus retinitis in patients with AIDS // Clinical Infectious Diseases. - 1999. - 28(3). - 528-533.

12. Martin D.F. et al. Oral ganciclovir for patients with cytomegalovirus retinitis treated with a ganciclovir implant. Roche Ganciclovir Study Group // The New England Journal of Medicine. - 1999. - 340(14). - 1063-1070.

13. Conant M.A. et al. Valaciclovir versus aciclovir for herpes simplex virus infection in HIV-infected individuals: two randomized trials // International Journal of STD and AIDS. - 2002. - 13(1). — 12-21.

14. Ioannidis J.P. et al. Clinical efficacy of high-dose acyclovir in patients with human immunodeficiency virus infection: a meta-analysis of randomized individual patient data // Journal of Infectious Diseases. - 1998. - 178(2). - 349-359.

15. Chang E., Absar N., Beall G. Prevention of recurrent herpes simplex virus (HSV) infections in HIV-infected persons // AIDS Patient Care. - 1995. - 9(5). - 252-255.

16. Safrin S. Treatment of acyclovir-resistant herpes simplex virus infections in patients with AIDS // Journal of Acquired Immune Deficiency Syndrome. - 1992. - 5, Suppl. 1. - S29-S32.

17. Gnann J.W. Jr., Whitley R.J. Clinical practice: herpes zoster // The New England Journal of Medicine. - 2002. - 347(5). - 340-346.

18. Saag M.S. et al. Practice guidelines for the management of cryptococcal disease. Infectious Diseases Society of America // Clinical Infectious Diseases. - 2000. - 30(4). - 710-718.

19. Bucher H.C. et al. Isoniazid prophylaxis for tuberculosis in HIV infection: a meta-analysis of randomized controlled trials // AIDS. - 1999. - 13(4). - 501-507.

20. Gallant J.E., Moore D., Chaisson R.E. Prophylaxis for opportunistic infections // Annals of Internal Medicine. - 1995. - 122(9). - 730-731.

21. Havlir D.V. et al. Prophylaxis against disseminated Mycobacterium avium complex with weekly azithromycin, daily rifabutin, or both. California Collaborative Treatment Group // The New England Journal of Medicine. - 1996. - 335(6). - 392-398.