Encephalopathy in HIV - symptoms and diseases. VIL-encephalopathy: causes, symptoms, peculiarities of interruption and elimination of brain encephalopathy in HIV infection

By and large, VIL-infection is hostile not only to the immune system of the organism. Virus expands on all life is important to the organisation's body. In nine vipadki from ten, the virus is hostile to the nervous system of the sick person, VIL-encephalopathy develops.

Virus to immunodeficiency is a vicious change in the clinical structure, as a result of which organisms are involved in health to the support of those who become ill and infectious in nature.

Virus can live in organism trivial period - right up to fifteen years. I only through this kind of term is considered a development to the syndrome of immunodeficiency.

The number of noses in a virus with dermal fissure is unrepentantly growing. The transmission of viruses to the virus is entirely different from people to people, creatures cannot be brought into laboratory minds without reaching into the beasts of a virus, behind the blame of the mavericks.

Virus takes revenge in the homelands of human organism. VIL Infected Hoes:

  • unprotected article contacts;
  • blood transfusion;
  • from a sick mother to a child.

Possibility of transmission to the virus by a little bit, by a drift-droplet path, for it has not yet been brought about with a drip. The virus is transmitted only through shelter or contact. Homosexuals, drug addicts and sick children are in the group of risiks.

Infected children are seen by the path of passage through the family paths, as well as during breastfeeding. On the other hand, it is described vipadks to finish it, if VIL positive mothers have absolutely healthy children.

VIL symptoms and diagnostics

For rakhunok trivial incubation period, symptomatic of the virus є underestimated. Infection can only be diagnosed by a laboratory method - a single method reliably determines the patient's VIL status.

So as the virus is hostile to the patient's immune system, the symptoms and prognosis of ill health are typical for children with ill health. On the cob, there are signs similar to the symptoms of GDVI for influenza:

  • difficulty in dikhannya;
  • pneumonia;
  • Rizke reduction of the vagi;
  • mіgrenі;
  • collapse of the gap;
  • fired up mucous membranes;
  • nerves, depressions.

When a virus is transmitted from an informal mother to a child, the disease will develop even more rapidly. Symptoms quickly grow, which can lead to a lethal result in the life of a child.

development of an affliction

The ailment does not appear immediately. From the moment of infection with the virus, a dozen rockets can pass before the development of immunodeficiency. See the advancing stage of development of the disease:

  • incubation period;
  • infectious period;
  • latency period;
  • development of secondary zahvoryuvan;
  • SNID.

An incubation period is called an hour, between infected people and the possibility of the appearance of a virus in the blood laboratory methods... As a rule, the period is three times as long as two months. Before the hour of the incubation period, the appearance of the virus in the patient's blood is uncomfortable during the analysis.

Pislya incubation, infestation period. In a whole hour, the organism is actively fighting against the virus, which causes the symptoms of infection. As a rule, patients mean a fever, signs of flu, infections dikhalnyh noblesі shlunkovo-intestinal tract. The period is usually up to two months, however, the symptoms are present in the skin.

During the latency period for the development of ailments, the symptoms are on the day. At the end of the hour, the virus is hostile to a sick person, ale niyak does not manifest itself. The whole period can be a trivial hour, up to 15-20 years.

The latency period of the known virus in the organism changes to the stage of the acquisition of secondary illnesses. The price is summed up by the speedy lymphocytes, who are being considered for the immune system of the organism, as a result of which the organism of the sick is not in the age of the children of the old children.

The remaining period for the development of ailments - tse SNID. At the end of the day, there are a number of cells that allow you to prevent the body from reaching a critically small value. The immune system will increase the ability to support infectious diseases, viruses and bacteria, as a result of which there will be a fight internal organsі nervous system.

Pathology of the nervous system in VIL

Disruption of the nervous system in case of HIV infection is primary and secondary. A blow to the nervous systems can occur at the cob stage of a virus infection, as well as the development of a viral immunodeficiency.

Primary damage is characterized by a non-infused virus on the nervous system. Qia form of accelerated learning in children with VIL.

Secondary tests develop on the development of immunodeficiency. Tsey stan is called the secondary neuro-SNID. Secondary treatment develops in cases of infection, the development of fluff and those who suffer from immunodeficiency syndrome.

Second failure can be a wiklican:

  • autoimmune reaction to the body;
  • admission to infection;
  • development of chubby in the nervous system;
  • snakes of the judgment character;
  • toxic dієu lіkіv.

Primary lesion of the nervous system with HIV infection can be asymptomatic. It means that often the nervous system is affected, one of the first symptoms of HIV infection in a sick person. At the early stages of vigorous development of VIL-encephalopathy.

Encephalopathy in VIL

Encephalopathy is called dystrophic lesion of the brain. Ailments develop on aphids of serious pathological processes in the body, for example, VIL-encephalopathy. Ailments are characterized by significant changes in the number of nerve tissue and damage to the functioning of the nervous system.

Often encephalopathy is a congenital pathology. Variations of encephalopathy are not often observed in newborn children with VIL.

Symptoms of a general pathology develop as a severity of brain damage. In such a rank, all the symptoms are divided into three groups, depending on the nature of the disease:

  • Stage 1 - clinical manifestations of the day, however, during laboratory monitoring, a change in the structure of the tissue appears in the brain;
  • Stage 2 - a slight turn of brains is prevented;
  • Stage 3 is characterized by a wide range of nervous breakdowns and breakdowns of cerebral activity.

Symptoms of encephalopathy in VIL do not appear to be indicative of a series of ailments, which appeared on the other pathologies. Correcting the development of encephalopathy from another stage, I see the onset of symptoms:

  • post-wrinkle and spoiled;
  • mental instability;
  • gratitude;
  • deterioration of rosum activity: weakening of memory, lack of respect for concentration;
  • depression and apathy;
  • damaged movi, mіmіki;
  • destruction of svidomost_, character;
  • three fingers;
  • loss of hearing and hearing.

Often, up to the number of symptoms, the deterioration of the statutory functions and the loss of libido occur.

Dementia at VIL-Informants

VIL-encephalopathy is referred to a whole group of illnesses, which are characterized by cognitive impairment. Tsі zagvoryuvannya publicly called SNID-dementia (dementia).

Encephalopathy in VIL often develops as a result of drug therapy. It is a form of destruction of the nervous system and is spared by the nemovlyat, the people who are married to VIL.

Encephalopathy of drug addicts and people who are ill with alcohol. In general, ailments develop as a result of a toxic infusion of drugs and alcohol on the patient's nervous system.

Pathology of the nervous system in VIL develops in a skin patient in a reasonable way. Inodi buv smoothly diagnose the appearance of damage on the cob stage. In general, patients come to especially respect for depression, apathy, or for a sleep disturbance in a patient.

SNID-dementia is lucid in a simple way, however, the result of any illness of the nervous system with VIL of the same is the whole bewilderment. In such a rank, the stage of development of encephalopathy is concluded, or the development of neurological damage in ailments - a vegetative state. The ailments develop a more or less partial parallel, the patient cannot independently serve himself and will need to look. The result of progressive dementia in ailments is a coma and death.

Slide it means that dementia in ailments is more expensive than vinyats, but as a rule, it’s not more than 15% of patients. The development of pathological breakdowns of rosum activity is seen in a stretch for more than a trivial hour. With advanced immunodeficiency, dementia often does not rise to the importance of form in conjunction with a lethal result.

Protest, mildly evolving symptoms of cognitive disorders are susceptible to another type of skin infection of VIL infection.

stages of dementia

Dementia is developed over a trivial period and is stored in decile stages. Protest, it is not a skin patient to go through all stages, in most cases, easy cognitive problems are prevented.

At normi in the patients on the daytime, whether the psyche is damaged or the activity of the psyche. Tse is ideal vipadok, in case of damage to the nervous system and the virus is not spared.

The subclinical stage is characterized by mild cognitive deterioration, which is characterized by a minuscule attitude, a depressive camp and a disordered concentration of respect. Often, at the same time, patients with a lot of people have an easy way of getting rid of them.

For an easy form of dementia, it is characterized by a high level of activity, a patient to talk and to collapse a little flaky. The patient will help myself without outside help, ale foldable intellectual physical activity wiklikaє deyake difficulty.

The stage of development of dementia, middle age, has come, characterized by loss of purpose, respect and memory. It is a good idea to serve yourself independently, even if it is difficult for you to do it yourself.

At an important stage, the patient is forced to intercourse without outside help. There is a stronger loss of misery as a result of any social interaction with more difficulties. The patient does not receive information and is aware of the foldability when trying to grow.

The final stage of the development of perplexity is a vegetative coma. The patient is not in the snake of the viconatie of the elementary diy and cannot do without outside help.

diagnostic methods

So, the pathology of the wicker can be diagnosed by the following methods:

  • lumbar puncture;
  • dopplerography.

On the basis of carrying out the lumbar puncture, a decision is taken about the professionalism of the present educators. Tsey analysis allows the manifestation of changes in the nervous system.

MRI (magnetic resonance imaging) allows you to successfully reveal pathological changes in the brain. To reject the exact picture, it is necessary to carry out a thoroughness of the brain, as well as a full-time apple.

REG (rheoencephalography) is a complete system, carried out by a non-invasive method, for the help of which it is necessary to provide information about the main arteries and the brain of the patient's nervous system.

Dopplerography is recognized in a generalized order. This is necessary to assess the size of the brain. Snakes in case of encephalopathy brain arteries, Zmini in which dopplerography is shown.

Therapy and prognosis

To unify the development of neurological damage with VIL, you can also use a quick therapy of the main disease. As a rule, dementia, caused by encephalopathy, develops only in every day of the patient's therapeutic treatment.

Be-like damage to the nervous system with VIL, chase after the help of the strong anti-tartar drugs(For example, zidovudine).

On the current day, the most beautiful result of the treatment of the nervous system with VIL is showing HAART therapy. This therapy is based on two groups of antiretroviral drugs at once.

You will be able to get rid of any further development of encephalopathy and dementia right away. For some people, there is a zupiniti of progress in dementia, and for others - for a line of development of cognitive damage to a trivial term.

VIL-encephalitis is also the transmission of antidepressants for the correction of the mentally ill. on cob stages The development of deterioration is associated with depressive conditions and the development of sleep in patients, who are struggling for the additional help of special drugs.

It is unambiguous to say about those prognosis for patients with VIL-encephalopathy. Tse lay down the peculiarities of the nervous system and the brain in a particular patient.

Prevention of pathologies of the nervous system

Until now, the fever has not been identified, as the virus itself provokes the development of ailments of the nervous system. Protest, SNID-dementia є an urgent problem of VIL-information, such as skin rock is growing more and more.

Prophylactic methods for the development of encephalopathy and other changes of neurological nature are not known. The patient is guilty of being respectfully put to health. The drive for the beetle up to the market is behind the help of such a station:

  • depression and apathy;
  • mental instability;
  • frequent change in mood;
  • disturbed sleep;
  • headaches;
  • the destruction of the dawn and the hallucinations.

Nowadays it is possible to allow uniqueness, or altogether, to write, show important symptoms of dementia. However, the patient is guilty of his own free will.

Spilno with drug therapy, we are sick of indications of retail control of vlastnyh emotsіy. The guilty patients become mentally and physically active. For the whole it is recommended to buy in a suspension, go in for sports and give an intellectual boost to the brain. To stimulate the brain activity of the ailments, we show the development of ideas, riddles, reading of folding literature in the great registers.

As a result of memory, the symptoms of disorders of the nervous system often do not appear until the stage of immunodeficiency. Protest, in some cases of minor damage to memory and growth of respect, characteristic of encephalopathy, may appear before the first symptoms of immunodeficiency appear. Medication therapy for VIL supplementation does not only promote life for a sick person, but also does not develop the development of dementia.

It's easy to add your good robot to the knowledge base. Vicorize the form

Students, postgraduates, young people, who are victorious to develop the knowledge base in their own lives and robots, will be your best friend.

Posted on http://www.allbest.ru/

Saint Petersburg State University

Faculty of Medicine

Department of Infectious Diseases, Epidemiology and Hygiene

VIL-encephalopathy

St. Petersburg

Entry

Epidemiology VIL / SNIDu

VIL. Zagalny characteristic of the zabudnik

Neurotropic activity VIL

Pathomorphology of VIL-encephalopathy

Misce VIL-encephalopathy in the classification of VIL-Infections

Clinical picture and overbig VIL-encephalopathy

Diagnostics of VIL-encephalopathy

Differential diagnosis VIL-encephalopathy

Principles of therapy and treatment of VIL-encephalopathy

visnovok

List of Literature

sik list-forgiven

VIL - virus to human immunodeficiency.

SNID is a syndrome of full-bodied immunodeficiency.

SDK - SNID-dementia complex.

CNS - Central Nervous System.

CSF - spinal cord.

Hematoencephalic bar'єr - hematoencephalic bar'єr.

HAART is a highly active antiretroviral therapy.

Entry

VIL-infection - a progressively anthroponous disease with a highly percutaneous infection mechanism, characterized by specific lesions immune system with the development of immunodeficiency, which can manifest itself as oportophysical infections, evil new creatures and autoimmune effects.

Over the last 30 years, the breadth and disease on the VIL-infection has grown significantly, but absolutely effective drug It’s dumb, I’ll look at the visibility of the virus, the vaccine doesn’t reboot in the stage of development, if the children of the early days and went to the stage of clinical viprobuvan - that on this day the problem of VIL is an urgent problem.

Epidemiology VIL / SNIDu

Until the end of 2002, according to estimates, 42 million adults and children bully informed VIL were suffering at SNID. Of these, 28.5 million (68%) were residents of African regions that were rooted in the Sahari during the day, and 6 million (14%) were residents of Pivdennaya and Pivdenno-Shidnoi Asia. In 2002, for estimates, we can talk about 5 million new types of information about VIL middle-aged and children, and 3.1 million people died as VIL / SNIDu. 2.4 million (77%) of the number of deaths were reported in the regions of Africa on the first day of the Sahari. Tsi regions are characterized by the most favorable indicators (9% before the end of 2002) of the widening of seropositive reactions to VIL in the middle-aged (15-49 years) population.

In 2001, from 25 countries with an indicator of the widening of seropositive reactions to IL in older adults, more than 5% of 24 countries were in the regions of Africa that were roasted for a day from the Sahari. One land from the region of Bula Gaitia. In 9 regions (in Africa for the first half of the day from the Sahari), the rate of seropositive reactions to ILI became 15% or more. Such a rank, the land of Africa, roztasovani for the day off from the Sahari, bears the greatest tyagar of the VIL / SNIDu Epidemic. Protest of VIL significant increases in some regions of the other regions with an indicator of seropositive reactions of 1-5%, for example: Cambodia, M'yanmi, Thailand (region of Pivdenno-Shidnoy Asia), as well as Panama Belizi, Guatemala, Surinami (American Region). The prevalence of seropositive reactions to VIL, mabut, is stabilizing in the regions of Africa, which have been growing for the first time from the Sahari, and increasingly among the population of some of the great great countries, for example, the Russian Federation.

The sickness rate at SNID in the Russian Federation (according to the data for 2007) was 6.46 per 100,000 population, and VIL-Infikovanih - 16 per 100,000 population.

Clinical manifestations of the nervous system and develop at the early stages of HIV infection in 40% of patients, and in 4-5% of them neurological symptoms are the oldest clinical manifestations of the disease. For autopsy data, pathomorphological changes in the nervous system are observed in 70-80% of patients who have died of SNID. lost morphological preliminaries allow to respect, that the pathology of the nervous system can be found in the transition to a large number of diseases in the SNID (Mikhailenko A.A., Osetrov B.A., Golovkin V.I., 1993; Price R., Brew V., 1988; Maj M . et al, 1994; Heaton et al, 1995; Zeifert P., 1996).

Due to the frequency of the defeat of the organs and systems in HIV infection / SNID, the nervous system stands on a different pathway of the immune system. It is linked to a great number of pathogenetic mechanisms of the central and peripheral nervous systems.

VIL. commonI am a character

Human immunodeficiency virus (VIL) goes down to the Retroviridae family, and Lentivirinae family - genus Lentivirus.

Zrіliy vіrіon with a diameter of close to 100 іm. In structures ВІЧ_1, they develop an envelope, a matrix sphere, an envelope of a nucleotide, genomic RNA, a fragment of the integration and nucleoprotein complex is included in the structure, as well as laterality. With an average increase in the electronic microscope, the nucleus and the shell of the virus are visible. The name of the virus membrane is permeated with viny beads (enveloped beads) gp41 and gp120 (which I will call the word "glicoprotein") from movlyav. Masoyu 41 і 120 kD. Cycles on the surface of the membrane of the virus form 72 sprouts, and the skin contains 3 gp120 molecules.

The nucleotide shell is folded into the bilka (p24) molecules molecular weight 24 kD. The middle nucleotide is replaced by the virus genome (two RNA molecules), block with a molecular weight of 7 kD and a complex of enzymes: vortex transcriptase, RNase, protease.

The genome of HIV_1 is composed of 9 genes: three structural (gag - group_specific; pol - polumerasae; ENV - envelope), characteristic of all retrovirals, and six regulatory (tat - transactivation; rev - regulator of expression of virus proteins; nef-negative regulatory factor , as well as vpr, vpu for ВІЧ_1; vрх for ВІЧ_2 with little functionality). For its budovy genome, VIL is in many ways similar to those of retroviruses.

The tat gene is the most active regulator, which will make it possible to make the replication of the virus 1000 times stronger. Win also regulates the expression of cell genes. The rev gene vibrating activates the synthesis of structural proteins in the virus. At the lower stages of viral infection, the rev gene supports the synthesis of regulatory proteins. The nef gene, during the interaction with LTR, ensures the transcription of viral genomes, preventing transcription between viruses and organisms. Synchronous function is tat and nef to increase the replication of the virus, but do not lead to the bend of the infected virus of the virus.

The structural genes gag, pol and ENV ensure the synthesis of protein vitamins: 1) envelope genes (ENV) encode the translation of the envelope precursor protein to the virus gp160, which is then split into gp120 and gp41; 2) group-specific genes (gag) encode the translation of the precursor protein of the inner part of the virus (nucleotide and matrix) from the virus. weight 55 kD, which can be split into p24 / 25, p7 / 9, p13, p15, p17 / 18; 3) gene pol code of the enzyme system and virus, vorotnu transcriptase (p66 / 51), integrali (p31 / 33), ribonuclease H (p15).

Bilki virion in the body of the information people and start the immune response and the synthesis of immunoglobulins.

In addition to structural and regulatory genes, up to the VIRON VICh_1 store, there is an LTR, and to the ВІЧ_2 store, the additional gene X.

VIL develops in a high genetic minority, yak in 30-100, and for deyakim danimi, in 1 million. Raziv vische, nіzh in a virus grip. It is not only related to virus strains, seen from other ailments, ale and to strains, seen in times of disease from one or the same ailment.

VIL unstable at the most recent middle-class. It is practical to increase the temperature of 56 ° C for 30 minutes, when boiling - after 1-3 minutes, when injected with chemical agents, allowed for disinfection (3% of the solution,% peroxide, 5 % of hypochlorite, 1% of glutaraldehyde, 70% of ethyl alcohol, etc.). The virus is tolerably stable to ionizing radioactivity, ultraviolet detection and freezing at minus 70 ° C.

However, it is possible that the virus can be taken from the hanging mill for a long period of time and for several days, ale only in the streets, so that the virus can be found in high concentrations: in the blood and in the sperm.

VIL infection of cells, on the surface - CD4 antigen. Tse T-helpers are a subpopulation of T-lymphocytes, which play a role in the immune system. Їх is called CD4 + T-lymphocytes.

In the rest of the rock bulo is also revealed, for the penetration of VIL into the cell on the surface of the necessary and inspirational molecules, called chemokin. Patients, in some germs of specific chemokines (for example, CCR5), are more resistant to HIV infection. In those who are susceptible to molecular changes in chemokine receptors, SNID develop more rapidly.

Neurotropic activity VIL

The main reason for the lesion of the nervous system is the spore rate of the viral membrane glycoprotein gp 120 (or gp 105 in IL-2) to the cell receptor of astrocytes CD4. Mechanism of penetration of a virus into a cell of two components: 1) modification of the cell membrane with a gp 120-CD4 complex for the development of zones for gp 41 - more than one viral enveloped cell; 2) block gp 41 cells are lodged in the middle of cells. In addition, the main cells are not only affected by the information, but the penetration of the virus (VIL) into the middle of the cell, but rather the membrane lysis with the gp 120 bottle.

More power, less on astrocytes, CD4 receptor on T4-lymphocytes-helpers / inductors. In normal spinal cord (spinal cord), boules have immunocompetent cells, including T-helpers. The cytological characteristic of liquor and blood does not appear either in the critical or in the functional relationship. So, in the spinal cord helper cells - 70 ± 9%, suppressors - 20 ± 1%, and in the blood - 44 ± 11% and 20 ± 7% apparently (Brinkman C.I., 1983). With a wide range of peripheral lymphocytes in the reaction of blast-transformation, they react to cerebral antigens of blood and blood speech, and lymphocytes of CSF to normal cerebral antigens, naturally, do not react (Malashkhia Yu.A., 1986). In addition, in the presence of natural blood cells (NK), the cytotoxicity of T-leukemic cells is also present and can be captured by such a rank brain as a development of lymphomy. Otzhe, for the development of T-lymphoma, the brain needs a virus, a vibrating enemy ЄK. Such a virus, yak vidomo, is oncoretrovirus HTLV-1. Obviously, it is also possible to achieve great vm_st helpers-С04 + in liquor and іth damage of VIL in order to reduce the immune system and development of opaque neuroinfections: cryptococcal menіngіtu, herpetic menіnіtu.

Investigations of VIL microglial cells produce low molecular weight peptides, which infuse toxicly into astrocytes. Mechanism of low molecular weight toxin dressings with rearrangement of NMDA receptors in astrocytes, which disrupts metabolism and functions. The growth of astrocytes, as they take an active part in the exchange of the wakeful neurotransmiter of glutamate (sprouting, do not get the fast accumulation of glutamate), to bring up to the overwhelming accumulation of it in the extracellular extracellular nerve In a cascade of pathobiochemical reactions (including and activation of peroxide oxidation of membrane lipids), in a whole cascade of pathobiochemical reactions, to destroy the membranes, in the endosceum, to the bend of the nerve cells.

In the minds of the increase in the penetration of the hematoencephalic barrier of the penetration of fragments of the neuronal membranes into the bloodstream into the bloodstream, the autoantitils are established, as the membranes of the nerve cells are eluted. Can і intrathecal (in the boundaries of the central nervous system) production of cych antibodies, which take part in the autoimmune process. It is transmitted that such a mechanism is the basis of the primary lesion to the brain - VIL-encephalopathy (Gullian D, 1990; Zakharova M.N., Zavalishin I.A., 1997).

Endothelial cells of vertebral fossils, membranes to the brain and endothelium cells may carry the CD4 receptor on their surface. To develop in case of severe vascular induction of vasculitis of the brain and spinal cord to the inflammation of mesenchymal elements of the nerve tissue and secondary demineralisation, as well as clinically manifested rosaceous sclerosis syndrome

There are 100 cells of neurogly on astrocytic seizures, 61, oligodendrocytes - 29, and microglial cells - 10. In addition, all the stinks of the brain are clearly connected with neurons and diseases in the liver, which is the main target of neuropathy. , 1983).

According to the theory of sub-baseline development, viral antigens are responsible for one hour of interaction with target cells (CD4 +) and cells of the head complex of hystosity (HLA). Indeed, in the latest polypeptide lancers gp 120, HLA-DR, HLA-DQ and CD4, one and the same tetrapeptide Arg-Phen-Asp-Ser is revealed. Antibody to cytokine tetrapeptide in case of HIV infection in human organisms reacts overly with CD4 + cells, causing an autoimmune component of gluotoxic reactions.

Humoral immunity with neuro-AIDS, like і clerical, even uncommon. On the cob get sick, yak i with bagatokh neuro in Russian infections In the spinal cord, there is IgM (in the normal range) and it grows instead of IgG, as the concentration decreases, it decreases, and there is an increase in IgA. However, polyclonal hyperimmunoglobulinemia in functional deficiency. Є disproportion of immunoglobulin subclasses of immunoglobulin subclasses: zmist IgG1 and IgG3 increased, and IgG2 and IgG4 decreased. Progressive lowering of IgG2 in the spinal cord back of the brain for the development of optic meningoencephalitis, activation of latent infections (prostate and operative herpes, cytomegal and other).

Another important aspect of destruction humoral immunity(Belgesov N.V. z spivavt, 1991) і, possibly, neuroendocrine regulation of the immunological bar'er of the brain, є blocking with antibodies up to gp 120 dilanoks of clitin and іх postulated receptors, sensitive to peptide hormones cystic brain and thistle. In 1984, Wybran showed the ability to synthesize in the tissue the brain (in the hypothalamus) a thymosidin-like hormone differentiating the stem cells of the CSF cells into T-lymphocytes. Mikhailenko A.A., Osetrov B.A., Golovin V.I, 1993, showed that with such a SNID-associative discomfort, yak rosy sclerosis, Cystkovozygous cells do not react with differentiation on thymus hormones, but react on myelopeptides like dalartin. It is not included that the restoration of the T-lanka of the immune bar is guilty of being carried out for the additional hormones (factors) of the cystic brain and only for the additional preparation of the type of thymalin or thymogen. This is due to the fact that macrophages of the central nervous system, as well as macrophages in the zagala, are the cells of cystocytic motility. For the restoration of the function of the neuroglial complex, it is also necessary to prepare the cystic brain.

Creation of immune-regulating hormones (interferon, thymosin, etc.) The complex SNID-dementia, for its territorial protection, is much wider, lower than the middle virus-induced cytopathic midway between the ruining of the nervous system. Dementia in neuro-SNID is abundant in chomu є the result of a decrease in the neurotrophic inflow of bioregulatory cerebral rhechovins, for example, vasopresin, a peptide of memory (Ashmarin M.G. et al., 1977). Spinal lesions (ALS syndrome, amyotrophies and inn.) Associated with shortcomings of the only neuropeptide - thyroliberin, widely distributed in the central nervous system, including the spinal cord (Schally, 1978 and in.). Neurotrophic infusion of peptides into the brain can appear either without a median (synthesis of neuronal nucleotides), or mediately - through an imbalance in the amino acids of the spinal cord. Transferring GABA and glycin to galvanic influx is not only on the electrogenesis of neurons, but on neuroallergic and autoimmune processes. Tryptophan, a mediator of serotonin, is also a galvanic immunological reaction. The encephalitic reaction in the form of epileptics is tied by the court to the [offensive] depression of GABA-ergic infusion (deficiency of GABA and glycine). Atactic dressing syndrome is not only due to cerebral lesions, but not enough serotonin (say: antipsychotic antiserotonin ataxia). Thus, the pathogenesis of neuro-SNID is foldable, multicomponent, and not only because of the non-mediated introduction of VIL in the central nervous system, but because of the impairment of the functions of the immune and endocrine systems of the brain.

pathogenetic factor , Scho to develop to the level of the nervous system at the early stages of VIL-infection, can be systematized by the advancing rank.

CNS lesion syndrome.

1. Pervinne (bezposredn) diyu VIL.

2. Autoimmune reactions.

3. Oporunistic and secondary infections.

4. Pukhlini.

5. Sudinni accelerated.

6. Psychogenic officials.

7. Iatrogenic causes.

Whores penetration of VIL in the central nervous system still not encrypted. Some of the extensions of such hypotheses:

1) VIL is consumed in the central nervous system for the help of infected macrophages, which penetrate through the hematoencephalic bar (variant of the "Trojan horse");

2) VIL penetrates into the central nervous system through nerve fibers;

3) IL penetrates into the central nervous system through the slits between the endothelial cells of the capillaries and the information cells of the neuroglia.

Pathological changes in the nervous system, viclikans without a median VIL, occur at any stage of infection.

Deyakі forms of primary-viral lesions of the nervous system and develop in case of viral-infectious diseases even in the stage of the first manifestations of ailment in the period of seroconversion, іnch neurological syndromes develop at higher progression of diseases

Pathomorphology VILencephalopathy

With pidgostroma VIL-encephalitis, an atrophic process in the brain is indicated, it is easy to reduce the enlargement of the furrows and the reduction of measles great pіvkul and expansion of the slurry system. Atrophy of the brain can be found in the presence of an additional computer tomography. When you look at the brain, it is also the bliss of the great speeches of the great festivals.

With microscopic dosage, a picture of an acute meningoencephalitis appears. In the brain and spinal cord, perivascular infiltration appears everywhere; Vona is more pronounced in the bile of speech in the brain, lower in the cortex; in the big world, there are lobbies and strongholds, educational institutions, a lozenge, a city of war. Mononuclear cells, macrophages with pyroplasmic cytoplasm and macrophages appear at the warehouse of perivascular infiltrations, and also microgliocytes.

An important pathomorphological peculiarity of the acute HIV-encephalitis is the presence in the infiltrates of large-nucleus giant cells, which is tied to one of the other biological authorities of the VIL - the pressure on the infection of the cyclinous cells Bagato-nuclear cells є important and important characteristic feature morphological changes in the brain (and spinal cord) in case of VIL-encephalitis, which are authoritative (Price R.W, Brew B.J., 1988) vvazhayut right in the right term "multinucleate encephalitis" for yogic development. Look at the early ages at the progression of nuclear-powered cells to disperse. It is transmitted, that the cells can be either infected by macrophages, or by histiocytes, or by T-helpers, such as they have absorbed T4-epitope; The remainder of the boiling process is supported by the formation of nuclear giant cells from T4-cells in their cultures.

Besides perivascular infiltration in the speech of the brain, microglial vascular sites appear, along with necrosis, demyelination and astrocytic gliosis.

In addition to immunochemical methods, it has been shown that cells of perivascular infiltrates replace nuclei and membranes of VIL (p24 and P41), however, the number of viral antigen is not the same in children; VIL antigens appear in the main and endothelial cells, as well as in the nucleated cells; in the nerve cells of the VIL antigen appear rarely. In such a rank, VIL does not show a clear neurotropism, causing a system of macrophages-monocytes in the role of cytin-targets.

Є Possibility of those that infiltration of brain tissue by macrophages is superimposed on cytokines, such as a factor of necrosis of fluff, as well as peroxidases and strong acid radicals, which can lead to the development of malnutrition.

In case of VIL-infection in the brain, there are also some changes that are not, however, VIL-specific. Until the number of such changes, vacuolar leukoencephalopathy is recognized, spongy changes and losses to the pigment of black substance.

Vacuolar leukoencephalopathy is represented by vacuolization of the phytoplasmic speech often great ponds of the brain, corpus callosum, white speech of the corn and pons. Histological predictions give allowance, but vacuoles may be the result of degeneration of oligodendrocytes or intraaxonal degeneration.

Spongiform changes are presented to the statements of a great number of other vacuoles in the superficial measles balls and periventricular areas of the brain; zim zminam supravodzhu reactive astrocytic gliosis and a decrease in the number of nerve cells. Some changes occur with Alzheimer's ailments and with alcoholic encephalopathy. Transmitting, spongyform changes can lead to brain damage or toxic talk that is obvious in the CSR.

The depigmentation of the black substance is revealed in 90% of the ailments on SNID. Microscopically, the degeneration of the black substance in the gross changes of the nucleus and cytoplasm and cytolysis from the surplus of melanin granules on the microscopy of the cells is microscopically indicated. The reason for the cich is not home.

The pathomorphological picture of acute HIV-encephalitis in the general world is clinically promoted to develop dementia of the subcortical type and to experience neurological disorders with it.

The stage of dementia swelling is the number of nucleated cells.

Small. 1. MRI picture of VIL-encephalopathy (atrophy of the brain, enlargement of its sores and shlunochkiv).

Misce VIL-encephalopathyії in the classification of VIL-Infections

I see five last stages of VIL-infection (Pokrovsky, 2001):

Stage 1 - incubation stage, three times a length of 2-6 times and more;

Stage 2 - the stage of the first manifestations, including:

2 "A" - asymptomatic, if there are clinical manifestations of VIL -infectious diseases or of opportunistic illnesses on the day, and I believe that VIL is diagnosed as anti-virus.

2 "B" - gostra VIL-infection without secondary ailments (manifest clinically, in a greater degree similar to the symptoms of other infections).

2 "B" - GOST VIL-infection with secondary illnesses (on the hourly decrease of T4 lymphocytes, secondary illnesses develop - angina, bacterial pneumonia, candidiasis, herpes - I tend to get sick. The triviality of the classy manifestations of the hospitality of the VIL-Infections becomes 2 - 3.

Stage 3 is latent. Most of the progress of immunodeficiency. We are one of the key manifestations of improving lymph nodes, as it may not be. The triviality of the latent stage from 2-3 to 20 and more rocks, in the middle 6-7 years. Decrease in the deed of lowering the level of T4-lymphocytes.

Stage 4 - the stage of secondary illnesses. Trivial replication of VIL, which can lead to the bend of T4 lymphocytes and to the development of secondary (oporitic) illnesses, infectious and / or oncological ones on aphids. Symptoms at the stage may be a werewolf character, so that they can pass by themselves, or as a result of treatment. Falling from the severity of secondary ailments see the onset of the stage.

4 "A" - for non-typical bacterial, fungal and varicose mucous and skinny curvatures, igniting diseases of the upper dichny nobles.

encephalopathy HIV disease clinical

4 "B" - more important and trivial education, Kaposi's sarcoma, vaginosis (10% more), damage to the peripheral nervous system and internal organs.

4 "B" - important, clutter up the life oportunistic illnesses.

Stage 5 - thermal. To carry the organs and systems with a non-negotiable broach. Navіt adequately carried out anti-tress therapy and treatment of opportunistic illnesses is not effective, and illnesses are not effective for a long period of time.

Damage to the nervous system can be accelerated at any stage of VIL-infection: in the subclinical phase - in 20% of the ailments, in the stage of the open-cut clinical picture of ailments - in 40-50%, in 30--90% of the cases. Virus to immunodeficiency of people can spend a trivial hour in the body without suffering symptoms of ailment.

The lesion of the nervous system in HIV infection and SNID, as has already been said before, is malignant and developing in 50-80% of patients, and in 10-45% of patients with neurological symptoms of onset presentation. With pathomorphological delayed lesions of the nervous system, 80-90% show up.

The dissection of the nervous system can be the first, without the middle, we will pick out the cytopathic diseases of the virus (9%), the second ones, we will explain the opportunistic infections, which develop in patients with CHID in the minds of the immune system, 22% trivial by VIL himself (8%). It also sees the damage of the nervous system, cleverly related to HIV infection, and to stress situations, including the appearance of information about the strong infection of HIV, toxic in the case of alcoholic, drug-related speech disorders.

The first neuro-AIDS, injecting the VIL itself, can be manifested in the viglyadі of the onset key forms:

SNID-dementia (VIL-encephalopathy),

Meningit,

Meningoencephalitis,

Vascular neuroAIDS,

Vacuolar myelopathy due to the type of viscid or transverse myelitis,

Symmetric distal sensory polyneuropathy,

Chronic ignition demiєlіnіyucha polyneuropathy,

Gostra igniting demilinizucha polyneuropathy (OVDP) for the type of Gin-Barre syndrome,

Encephalomyelopolyneuropathies,

· ALS-like syndrome (ALS - bichny amіotrophic sclerosis).

CLINIC CARDSina and out of VIL-encephalopathy

Symptomatic VIL-infection of the central nervous system.

At the end of the day, it was established that early asymptomatic infection of the central nervous system and virus is the rule. Tsei visnovok runtutsya on prelіgennі SMR in seropositive clinically healthy individuals. At the same time, there is an increase in the number of cells, the increase in the number of cells and immunoglobulins, signs of intrathecal ("zabar rni") synthesis of antibodies to HIV, due to the development of spinal cord disease in people in the course of the disease.

Symptomatic CNS infection can be developed at once from different organs and systems. At the hostess period, you will go to VIL-virusemia.

Asymptomatic VIL-infection has a reversible character.

It is unclear, for which minds asymptomatic VIL-infection transforms into clinically manifestny aseptic meningitis or encephalitis.

Gostriy encephalitis and meningoencephalitis.

Gostry meningoencephalitis is seen as the best goste, important and rare form of primary CNS lesion in case of HIV infection. The development of VIL-meningoencephalitis grows in an hour, or to navigate before the change of serological tributes. On the ear of a hospitable meningoencephalitis of the world psychotic in viglyadi passing svidomostі (right up to the Komi), epileptic seizures.

With somatic obesity in ailments, lymphadenopathy, splenomegaly, maculo-papulogenous viscous, and kropivyanka can be generalized.

In the spinal cord, there are nonspecific ignition symptoms, CT signs of damage to the brain.

Neurological symptomatology with a prolonged period of time can be recognized. However, in a small part of the sick, they suffered a meningoencephalopathy, a possible development of chronic VIL-encephalopathy.

At the hospital stage, differential diagnosis is carried out with encephalitis, herpes simplex virus. The rest can be made, as long as 3 days with a repeated CT scan, there will be no pathology in the brain in the view of the decrease in health.

The host period is approximately 1 day long, and there are no different neurological inheritances. Gostriy encephalitis is associated with direct lesions of the brain with the virus of human immunodeficiency.

VIL-dementia (VIL-encephalopathy, complex SNID-dementia, pidgostria encephalopathy) It is an unprecedented manifestation of VIL-infection, which can be promoted at various stages of illness.

VIL-dementia is a special clinical syndrome of pidcortical frontal dementia, interfacing with no middle virus on the brain and appear as cognitive, ruddy and behavioral disorders. є by ourselves frequent syndrome primary lesion of the central nervous system in VIL-infection / SNID.

VIL-dementia is prone to develop in sick people when there are opaque infections or puffins (on the most common immunosuppression and systemic manifestations of VIL / SNIDu), ale in the first vapors. In some cases, such signs of viral infections, such as lymphadenopathy, nezduzhannya, vaginosis, oral candidiasis, are suspected; in some of them there may be laboratory signs of immunodepression. It is possible that dementia develops in 90% of patients with SNID (Pumarola-Sune et al., 1997).

Cob symptoms of ailments can be damage in the cognitive sphere, in the first place, difficult concentration of respect and damage to memory. It’s a good idea to fix the second thought or to change it, it’s a lot of them to skary on the "goodness" of the message. The robotic age is growing for the sick more and more; in order to fit in with this wicked robot, it will take more and more an hour. Destruction of memory and difficult repairs in zoosereduction leads to obvious mistakes in robots, in connection with which winners the need to use notes, write down the plan of the paper on a sheet of paper. In quiet people, if a professional or a bobbing activity of a patient's increased respect and activity, an increase in dementia can manifest itself significantly earlier. In the largest types of change of cognitive performance and specialty of change, the first to help are close friends and family members of the sick. Until the number of such changes, there are elements of social obscenity and apathy.

Depressive syndrome is susceptible to occur in such ailments older, less can be ochіkuvati; In some cases, agitated organic psychosis is referred to, as can be overwhelmed by signs of ailment. Such patients are destroyed, hyperactive, the hypocritical camp can develop.

At the early stages of ailment, formal psychological tests may not be able to evolve, whether it appears to be adequate. With a little progressing ailments, it is difficult to see tests that are straightforward to the assessment of respect, tests with a selection of counterparts for the quickening of understanding of numbers, tests for solutions of intellectual establishments. Start to override the trust of the misery, apathy. Ailments grow up to the extent that they become ill, they cannot correctly assess the situation, which has gone wrong. Rukhovi rozladi can develop in the early stage of VIL-dementia. There are skargi for the destruction of the ruins and coordination of the rucks. Sickness starts to miss speeches often, hands become less smart and precise, handwriting deteriorates, communication and articulation are destroyed.

The destruction of the coordination of rukhiv leads to frequent spitting, or falls, when walking ailments, they show special protection. Symptoms of oral automatism appear - proboscis and nasolabial reflexes, mensh often appears hapal reflex. Perceptibly є hyperreflexia. The collapse of the last anti-tilt of the hands and feet (adiadochokinesis). There are okoruhiv razladi: trust of rukhiv real apples, The smoothness of the collapsed eyes will break down, the integrity and inaccuracy of the fall of the apples will appear. In general, there is an ataxia, how to appear in ruined walking along a straight line. There is a build-up and weakness of nig, at the same time, at the same time, intertwining the power of independent oversupply of a sick person. At the lowest stage of ailments, you get sick є the deterioration of the disease and defecation.

In the thermal stage, the sickness camp becomes "vegetative". It is a problem to lie in a bed, not self-sucking, not controlling the function of the pelvic organs, proteas, for the sake of periods of doubt, є singing riven of sleep; the comatose stump of the bandage was tied with infectious and quickened ones.

Table 1. International VIL-Dementia Scale (IHDS) for the assessment of the severity of the country (Sidtis, Price, 1990):

Normal mental and psychological functions.

Stage 0.5 (subclinical / double-valued)

Slightly swelling symptoms with sparing activity and health to the point. The move and the strength are normal.

Stage 1.0 (mild / mild)

Bezperechni signs of functional deficiencies: zdatny vikonuvati all, ale lishe in singing boundaries. You can walk without outside help.

Stage 2.0 (pomirna)

Pratsyuvati and vikonuvati foldable aspects of all-round performance is impossible, albeit vikonuє basic conditions for self-service. Hospitalization is not required, however, when walking, you can only need one support (a reed, a policeman).

Stage 3.0 (swept / important)

Significant intellectual abnormal defect (cannot walk without outside help).

Stage 4,0 (kintseva / thermal)

Stan, close to vegetative. Intellectual and social intelligence in the embryonic stage. Mayzhe abo call names. Paresis abo parallel lower kintzivok with subordinate (slash and feces) non-trivial.

Early neurological problems are manifested in 8-12 months. at the moment of infection with the presence of VIL-anti-til. In a larger term, there is a secondary neuroAIDS as the result of a developed immune deficiency and activation of optic infections. Yogo klinichny forms are also recognized as significant differences. In the whole stage, there may be a progressive multifocal leukoencephalopathy with an increase in dementia and malignant hyperkeys; meningitis abo meningoencephalitis, accumulation of toxoplasmosis, fungal, cryptococcal, herpetic, cytomegalovirus, protozoal, tuberculous infection; abscesses to the brain (cryptococosis, tuberculosis, toxoplasmosis); cerebral vasculature with cerebral infarctions; polyradiculoneuropathy; new central nervous system (lymphoma to the brain, Kaposi's sarcoma, nondifferentiated pukhlini).

Perebіg and the progress of VIL-encephalopathy is practically not transferable, and the factor, which is, of course, not established. Clinical symptomatology can become a stable stretch of bagatokh months, proteine ​​SNID-dementia is rapidly progressing.

Diagnostics of VIL-encephalopathy

V CLINIC PRACTICE Diagnostics of VIL-encephalopathy is based on the background of such tributes.

1. Epidemiological data. Necessity to a group of patients: homosexuality, individuals who were carried out internally infusion or blood transfusions and drugs, children or heterosexual partners of VIL-infused individuals.

2. Somatic signs of VIL-infection.

3. Asymptomatic brought VIL-infection (high titer of antibodies to VIL in the blood (IFA, immunoblot), VIL seen behind additional PLR).

4. SNID-association complex (stages 4A and 4B) according to V.I. Pokrovsky.

5. The picture SNIDu (stage 4B, terminal stage) has been rejected.

6. Clinical and neurological signs (including neuropsychological conditions and cognitive tests).

Table 2. Diagnostic scale of VIL-dementia (AIDS Reader 2002; 12:29).

Maximum number of points

Assessment of memory protection (ear): patients name 4 words (for example, droplets, dog, greenery, peach) and ask to repeat them over the drug.

Evaluation of the psychomotor reaction speed: hour (in seconds), as it is necessary for patients to write the alphabet. Number of points:<21 сек = 6 баллов; 21,1-24 сек = 5 баллов;

24.1-27 sec = 4 bali; 27.1-30 sec = 3 bali; 30.1-33 sec = 2 bali; 33.1-36 sec = 1 point; > 36 sec = 0 points

Assessment of memory protection (result): ask the patient to repeat 4 words, as they called them on the cob; If a patient cannot guess a word, it is permissible to give a semantic clue, for example: "tvarina" (dog), "color" (green) and ін. For kozhne, the word narahoyut 1 point is correctly named.

Design: the patient is asked to copy the image of the cube during the hour.

Number of points:<25 сек = 2 балла, 25-35 сек = 1 балл, >35 sec = 0 points.

* Dementia is characterized by 7 points and less (from 12), but the specificity of this technique is not so, that for the establishment of an accurate diagnosis it is necessary to further neurological conditions.

7. Dementia.

8. Rukhovi destructiveness (destructive ruchus, tremor, ataxia, paraparesis).

9. Behavioral damage (social disability, organic psychosis).

10. neurodiagnostic dosage. Computer tomography abo nuclear magnetic resonance. CT scan of the brain reveals atrophy of measles in the brain with the enlargement of the bovine sulci and the slurry system; MRI T2-rezhimі mozhna viyaviti vіdnosno simetrichnі difuznі abo multifokalnі gіperіntensivnі zmіni bіloї rechovini in periventricular oblastі i semіovalnogo tsentrі of nerіvnimi edges scho not viklikayut weight-efekta i not nakopichuyut contrast abo bіlsh drіbnі asimetrichnі vognischa in bіlіy rechovinі i basal ganglia.

11. Immunological data. Change in the number of CD4 / CD8 lymphocytes in peripheral blood, which are signs of lack of function of T-lymphocytes, macrophages.

12. Serological data. Antibody to VIL in syrovatz blood.

13. Seeing a virus. VIL visualization from blood, spinal cord to the brain, detection of VIL antigens. It means that if SMR pathology is present, it can be seen, but in 20% of patients there is a slight pleocytosis (no more than 50 cells in 1 μl), and in 60% of patients - more There is also a tribute about the improvement in the spinal cord formation of B2-microglobulin, neopterin, chinolinate, which is mainly due to the severe clinical manifestations.

14. Pathomorphological dosage (biopsy or autopsy). Zmіna of bіloї speech: pyatonuclear cells and macrophageal infiltration.

15. In case of a clinically diagnosed diagnosis, it is also the case that the causes of the central nervous system damage (including infections, new diseases, cerebrovascular ailments, neurological psychiatric problems, drug addiction)

Yaksho є dan, that it is possible to relate to the manifestation of a depressive episode, or to the malignancy of a patient with biologically active speech disorders (BAD), then the diagnosis of VIL-encephalopathy is guilty of being diagnosed before a decrease in depression

DdifferentialI diagnostics of VIL-encephalopathy

Table 3. Differential diagnosis of VIL-encephalopathy and methods of improvement.

ailing

Diagnostic method and comments

neurosyphilis

Pre-treatment for anti-spinal cord and pre-diagnosis of spinal cord (pleocytosis> 45/3); serological data may be atypical for active neurosyphilis.

cytomegalovirus encephalitis

Spinal motility (pleocytosis, one neutrophilic; decrease in glucose levels, alterations in the backbone bottle).

Pre-treatment of spinal cord birth by PLR method for cytomegalovirus, detection of cytomegalovirus antigen (pp65) in blood.

Pre-treatment of blood and spinal cord growth for antibodies (level and index IgG can be adjusted).

MRI (Possibly subpendymal improvement of strength and accumulation of contrast).

It develops mainly on the basis of the smallest organisms (retinitis, colitis, pneumonia, esophagitis).

toxoplasmosis

CT / MRI (one or more in the head, often for everything in the area of ​​the basal nuclei, or the thalamus, a grip on the suspicious tissue, the embryo, which is not too strong for the contrast (middle or middle).

Specific to toxoplasmic IgG in the blood and spinal cord (the amount of antibodies is increased).

(Inodi toxoplasmosis against diffuse microglial nodules encephalitis).

Primary CNS lymphoma

CT / MRI: one, for example, in the room, often for all the order with the lugs, for all the instructions, for the napryak, for the more powerful contrast (partly for the middle, not for the ring-shaped).

Cytological dosage of spinal cord birth.

Pre-treatment of the spinal cord by the PLR ​​method for the Epstein-Barr virus (VIL-associated lymphoma of the central nervous system, viclikana with the Epstein-Barr virus).

Positron-emitting tomography or single-photon emitting tomography (intermediate accumulation of isotopes).

Encephalitis, viklicaniy virus varicella zoster

Spinal spinal cord (swelling of signs of heat).

IgG, specific to the virus varicella zoster, in the blood and spinal cord (IgM may be present). Pre-treatment of the spinal cord by the PLR ​​method for the varicella zoster virus.

In most ailments є operative lichen (in the past hour or in anamnesis).

cryptococky meningit

Dorsal spinal cord (the grip is not adjusted, the number of clines and flakes may be normal), smear contrast is mascara.

Detection of cryptococcal antigen in the blood and spinal cord, sowing in the middle for fungi.

Tuberculous meningitis and other bacterial infections

CSF, seeding, PCR on mycobacterium.

Doslіdzhennya in fallowness due to the situation.

Progressive multifocal leukoencephalopathy

MRI (one little bit of vognisch at a biley speech, a lot of approval is dumb, a bunch of dumb, to the strength of the contrast is dumb).

Pre-treatment of the spinal cord by the PLR ​​method for the JC virus.

Intoxication

Validation of drugs in blood / drug screening.

Metabolic encephalopathy and poganiy zalny stan

The value of the electrical energy indicators, indicators of the function of the liver and the liver, hormones ( thyroid gland, Cortisol), blood analysis.

Hypoxemia (blood gas).

Poganiy zalny stan (postal mode, visnazhennya, hyperthermia).

Depression with pseudodementia

Psychiatrically circumstantial.

Інші forms of subcortical dementia

Normotensive hydrocephalus, parkinsonism, other neurodegenerative stun, subcortical atherosclerotic encephalopathy.

tera principlePII and Likuvannya VIL-encephalopathy

For a glance at the pathogenesis of VIL-encephalopathy, people are guilty of being guilty of suppressed replication of the virus in the central nervous system. The need for penetration of anti-tier forces into the spinal cord back has not been brought about. A number of clinical (Letendre, 2004), virological (de Luca, 2002), pathological and electrophysiological advances have shown that drugs can be reached in the spinal cord with high concentrations, more effective. However, the author didn’t notice the connection between the number of drugs that penetrate into the spinal cord, and their concentration in the spinal cord from the stage of suppression of the viral insertion into the spinal cord (Eggers, 2003). Neurological and cognitive training on HAART (highly active antiretroviral therapy) is more strongly associated with the suppression of viral pressure in the spinal cord, lower in the plasma (Marra, 2003). Whilst, leave unconsciously, the camp of the patients from the VIL-dementia will turn on the HAART ( J Neurovirol 2002; 8:136; J Neurol 2004; 10:350).

For the duration of prospective monitoring of clinical patients, viprobuvan still vvazayut, but in patients with VIL-encephalopathy it is even more important to include more drugs in the antiretroviral regimen that will penetrate into the central nervous system. Permeate any of the upcoming drugs: zidovudine, lamivudine (reach high concentrations in the spinal cord in the cerebrospinal cells; unpublished data), nevirapin and indinavir.

In decilcochles of small pretreatment with VIL-encephalopathy, the presence of selegelin, nimodipin, lexipaphant and antioxidant CPI-1189 was observed. The drugs work on the molecular mechanisms of the pathogenesis of VIL-encephalopathy and to develop in conjunction with antiretroviral therapy. On the other hand, there is a tendency towards clinical and neuropsychiatric conditions, but still cannot be recommended for all ailments.

I'll look at organic exercise Central nervous system in IL-dementia and stiffness of changes in a large variety of cases. ), in case of insomnia - ivadal in 1-2 tables. at night, with an increase in depression - Magne-B6, 1 tab. 2-3 times for dobu abo tranxen 1 tab. 2 times a day. For stimulation of cognitive functions, drugs are prescribed to avenge ginkgo-biloba (tanakan, Memoplant - 1 tab. 2-3 times and every 3-6 months). In children with ailments, it is possible to reject the defect, if they want it, they are still positive in their memory and cognitive functions during the therapy of the survivors. biologic drug To take revenge on the neuropeptides - Cerebrokurin, 2.0 ml in vnutrіshnyyazovo school №20. One of the drugs, which is vicious in ailments with dementia, is gliatilin (holin apfoscerat). Gliatilin is a way to get rid of 40.5% choline, so it can penetrate through the hematoencephalic bar and serve as a donor for the biosynthesis of the neurotransmitter acetylcholine in the presynaptic membranes of cholinergic neurons. In addition, gliatilin, being an intermediary of phospholipid membranes, takes part in anabolic processes that are related to membrane phospholipid and glycerol synthesis, robustly positively infused into the functional staging of the membrane cells of the cystic In case of stagnation of gliality, the psycho-social sphere (the memory of the emotional background, the tolerance of the emotional background, the drastic increase), the memory of the growth of the organ Gliatilin is consumed in 1 capsule (400 mg) 3 times a day, to go. Triviality of courses from 3 to 6 months.

V new period (Yakshcho is used to stabilize the process) dozіnnіly sign of metabolic therapy in viglyadі vobenzim on 5 tabl. 3 times a day, stretching out, maybe 4 tablespoons. 3 times a day, 3 tab. 3 times a day, 2 tables. 3 times a day - 1 day, sometimes 1 table. 1 time a day for 2 teas.

forecast

The prognosis for getting sick, for life - unwillingness. The average triviality of the life of ailing people for the development of dementia is close to 5-6 months (Fischer, 1987; Kennedi, 1988).

For patients who receive HAART, they are statistically more significant in terms of their triviality in life ( AIDS 2003; 17: 1539) and the decrease in indicators of sickness on the VIL-Dementia, protest likuvalny effect HAART is not valid for VIL-dementia ( Brain pathol 2003; 13:104).

perkey

VIL-encephalopathy manifests itself in case of severe immunodeficiency, inability to deceive patients, maladjusting in the society and beating, but it means that the picture of getting overwhelmed and unattractive by people

Not mayuchi on sogodnіshnіy day mozhlivostі usunennya reason (s povnoї elіmіnatsії vіrusu organіzmu іnfіkovanoї) tsіlkom ymovіrno upovіlnennya rozvitku complex SNІD-dementsії Shlyakhov adequate regular i lіkuvannya antiretrovіrusnimi drugs (SSMSC takozh yak mozhut rozglyadatisya varіant profіlaktiki VІL-entsefalopatії) zastosuvannya patogenetichnoї terapії.

Crazy, the main problem is VIL-infection itself, because the primary prevention of disease is effective in the fake and to the reduction of disease, incl. VIL-encephalopathy.

List of Literature

1. Gustov A.V., Ruina E.A., Shilov D.V., Erokhina M.N. Clinical options for the lesion of the nervous system in HIV infection. Magazine "Suchasnі tekhnologii v medіdі". Nizhniy Novgorod, 2010 No. 3, pp. 61-65.

2. Rakhmanova A.G., Vinogradova E.N., Voronin E.E., Yakovlev A.A. Vich infection. St. Petersburg, 2004.S.: 16, 209-244.

3. Є.P. Shuvalov. Infectious diseases- a handler for VNZ. Moscow, 2001.S.: 325, 326.

4. Yakovlev N.A., Zhulev N.M., Slyusar T.A. NeuroAIDS. Neurological problems with HIV infection / SNID. Navchalnyy posibnik for lykariv. "МІА". Moscow, 2005.S.: 67-91.

5. Barlett J., Gallant. J. Clinical aspects of VIL-infection. USA, 2007. C: 527-529.

6. Yvtushenko S.K., Derev'yanko I.M. Diagnostics and lesion of the nervous system in HIV-infected patients with primary and secondary neuro-AIDS (methodical recommendations). Donetsk, 2001.S.: 9-17.

7. Kharris E., Maher D., Graham S. TB / VIL klinichne Kerіvnitstvo. WHO, 2006.S.: 26-29.

8. Robertson K. Handouts for Diagnosing AIDS Dementia. 2007.http: //www.searchthailand.org/en/resources/Free%20Slides/2.%2010th%20Bangkok%20Symposium/01-HIV%20associated%20dementia%20case%20study-Prof.Kevin%20Robertson.pdf

9.http: //www.eurasiahealth.org within the ACED (AIDS Care Education Training) programs.

Posted on Allbest.ru

more documents

    Dyscirculatory encephalopathy yak chronic progressive diffuse or small focal lesions of the brain. Classification of pathology on the type. The main reasons for the development of the KhRMK, the main key picture. Stages of discirculatory encephalopathy.

    presentation, donations 02/27/2016

    Understanding, classification, diagnostics and clinical manifestation of discirculatory encephalopathy. Atherosclerotic (often with lesions of the magistral heads of the head), hypertonic, malignant, venous discirculatory encephalopathy. Likuvannya method.

    presentation, donations 04/20/2017

    The causes of dyscirculatory encephalopathy are lack of blood circulation in the brain, as we have before the stepwise impairment of its functions and diffuse impairment in its structures. Methods of instrumental diagnostics of sickness, preparations for lykuvannya.

    presentation, donations 12/21/2015

    Клінічні signs virus immunodeficiency. Clinical and immunological picture of becoming ill. Laboratory diagnostics of SNID on the basis of key data. Having shown in ailments generalized sarcoma Kaposhi, encephalopathy and cryptococcal meningitis.

    presentation, donations 04/21/2015

    Development of the meningeal syndrome, hypertensive encephalopathy. Damage to cerebral blood circulation. Clinical signs and confirmation of diagnosis of meningitis. Determination of pleocytosis, cell storage, concentration of sugar and chloride. Features of the liquor.

    presentation, donations 04/07/2015

    Understand and zagalny characteristic of syphilis yak classic venereal disease, Yogo klinichna picture and symptoms. Description of the origin and the particularity of the tooth injected into the body. Go to the diagnosis of this disease.

    presentation, donations 04/05/2016

    Characteristics of the chumi plant. Infection transmissions. Klinichna picture of an affliction. Epidemiological peculiarities of the plague. Expanded Chumi in to the lucky day... Symptoms, you see, are not safe and ill. Prevention of ailments and prophylaxis.

    presentation, donations 05/05/2014

    Epidemiology, ethology, class of postresuscitation ailment. Type of renewal of neurological status in the post-toxic period. Pathophysiology to postanoxic encephalopathy. The current principle of intensive therapy. Intracerebral come in.

    presentation, donations 03/26/2016

    Characteristics of Duhring's dermatitis herpetiformis yak mіkhura dermatosis. Epidemiology, ethology, breadth, clinical picture of ailing. Differential diagnosis of dermatitis. Principles of drug therapy, especially muscle therapy.

    presentation, donations 03/01/2016

    Providn_ pathogenetic mechanisms bronchial asthma... Classification and ethological forms of engulfment. A clever picture that accelerated. Statement of diagnosis, differential diagnosis and the principle of diagnosis. Suchasny pidhіd until lіkuvannya zagostren.

Infections of a virus with immune deficiency of people can be contradicted by a sickly wearing virus, as well as a syndrome of a sickly immune deficiency, which is an extreme stage of HIV.

During the development of VIL and SNID, it is practically all the systems and organisms of people that will be used. The main pathological changes in health in the nervous and immune systems. The breakdown of the nervous system in VIL is called neuroSPID.

Approximately 70% of patients experience a survival rate, and 90-100% posthumously.

Causes and pathogenesis of illness

Until now, it is not up to the introduction of pathogenetic mechanisms for the injection of VIL on the nervous system. Vvazhaє, scho neuroAIDS winy through direct і mediated inflow into the nervous system.

Also, I think that the reason to cry is in the broken regulation of the process of changing from the immune system. Direct injection into the nervous system to penetrate through the penetration into cells, which carry the CD4 antigen on them, and the neuroglia of the brain tissue itself, cells of the lymphocytic membrane.

At the same hour, the virus can penetrate through the hematoencephalic bar (physiological bar between the blood and central nervous system). The reason for this is that viral infection increases the penetration of this bar, and those that are in their cells are also CD4 receptors.

I think that the virus can penetrate into the cells of the brain behind the clotting cells of the cells, which can easily catch and overtravel bacteria, as it is easy to pass the hematoencephalic bar. As a result of this, only neuroglia and neurons appear to be hostile, but for this they do not volodyne CD4 receptors, they do not appear.

However, through those connections between glial cells and neurons (first servicing others), the function of neurons is also impaired.

If you want to use an indirect injection of VIL, then you will be able to use it in different ways:

  • as a result of the severe reduction of the immune system, infections and chickens develop;
  • the presence of autoimmune processes in the body, as there are links in the process of viral antigens to nerve cells, which may induce VIL antigens;
  • neurotoxic inflow of chemical words, which are violated by VIL;
  • as a result of the destruction of the endothelium of cerebral sudins with cytokines, it is possible to cause damage to the microcirculation, hypoxia, and to the destruction of neurons.

At the moment, there is no clearness and no single thoughts about the mechanisms of inception and development of VIL and neuro AIDS, problems of wandering around the vision of a virus in laboratory minds. Tse called to the appearance of the singing number of physicians and fakhivts, who invade VIL to incorrect understandings, however, at the same time, they do not prevent VIL infections from being shown.

Primary and Secondary NeuroAIDS

There are two groups of neurological manifestations that are associated with HIV infection: first and second neuro AIDS.

In the case of primary neuroSPID, VIL is injected into the nerve system without interruption. There is a small number of the main manifestations of the primary form of ailment:

  • vacuole;
  • vascular neuroAIDS;
  • multiple;
  • neuropathy of the facial nerve;
  • gostry;
  • lesion of the peripheral nervous system;
  • sensory polyneuropathy;
  • SNID-dementia;
  • igniting demiєlіnіyucha polyneuropathy.

Secondary neuro-AIDS of speculation with opportunistic infections and puffins, which develop in a sick person on SNID.

Secondly, manifest the disease and turn in the offensive:

Most often, neuro AIDS patients are susceptible to such chills in the central nervous system:

  • disseminated Kaposi's sarcoma;
  • lymphome Berkitt;
  • pervinna;
  • undifferentiated chickens.

Features of the classic picture

Primary neuro AIDS is often asymptomatic. In severe cases, symptoms of a neurological nature can appear at 2-6 hours every hour of infection with HIV infection. For an hour and a half, the children have a fever of unknown genesis, the improvement of lymph universities, and the growth of visibility. When tsyom z'yavayutsya:

  1. ... To meet with a small number of patients from VIL (close to 10%). On the klinichniy picture similar to. With aseptic changes in the spinal cord growth, the level of CD8 lymphocytes. If there is a lack of cause, then the increase in the number of CD4 lymphocytes. In small and important cases, it can lead to mental illnesses.
  2. gostra radіkuloneuropathy... Viklikan, we will ignite the vibrations of the muslin shell of the cranial roots and spinal nerves... Tsei stan is manifested in a loss of sensitivity of the polyneuric type, cortical syndrome, severe facial and intramural nerves. Signs of mending the appearance and step by step increase the intensity both through the circle of dib, and through the circle of the press. When the stabilization is established, I will stand on the protesters for about 14-30 days, and fix the decrease in the intensity of symptoms. Only 15% of the patients have a trace of the state radioactive neuropathy.

Okremi forma neuroSPID give nobility about themselves at the early stage of VIL Infections:

  1. (SNID-dementia). The most frequent manifestation of neuro AIDS. The manifestation of behavior, ruddy, cognitive disturbances is indicated. In about 5% of patients with VIL, encephalopathy is the primary symptom, to speak, of the manifestation of neuro AIDS.
  2. VIL myelopathy... To rotate in the damaged functions of the pelvic organs and the lower spastic one. Particularly, in the more severe resistance and visibility in the degree of severity, the manifestation of symptoms. Tse zhvoryuvannya is diagnosed in about four people with VIL.

diagnostics

NeuroSIDs are trained to do it often, in most patients with VIL, it is recommended that all patients with infections should have a regular check-up with a neurologist. VIL encephalopathy sometimes manifests itself in impaired cognitive functions, it is necessary to improve the neurological status, as well as to carry out neuropsychological conditions.

In addition to the main prescriptions, such as passing ailments from VIL, for the diagnosis of neuro AIDS, it is necessary to turn to tomographic, electrophysiological and clinical methods of prescription.

Ailments can also be hired for a consultation before a neurosurgeon, psychiatrist, and also other problems. The effectiveness of stimulating the central nervous system is analyzed by using additional electrophysical methods of dosage (electromyography,).

Disruption in the nervous system with neuro AIDS, as well as the result of the therapy, can be seen for help.

An analysis of the cerebrospinal origin is also often indicated, the parkan which is looking for help. Even if the patient has a neurological character, a decrease in the number of CD4 lymphocytes, in the analysis of the spinal growth period, a decrease in the concentration of glucose, lymphocytosis, lymphocytosis

complex lykuvannya

Dealing with neuro-AIDS and reducing the development of nervousness from diseases of VIL infections, and putting it into the base. to the patients antiretroviral therapy with medicinal drugs, as it may be possible to pass through the hematoencephalic bar, and in the event of a blockage of the development of HIV

  • herpes sores- Tsimeven, Abakavir, Atsiklovir, Sakvinavir.
  • It is also effective є sucking plasmapheresis, corticosteroid therapy. Likuvannya pukhlin can vimagati surgical involvement, and consultation of a neurosurgeon is required.

    In the situation of early manifestation of neuro-AIDS (at the first stages), and in the presence of adequate treatment for the manifestation of ailments of a neurological nature, there is a good chance of developing ailments. The most common cause of death in patients with neuro AIDS is stroke, the manifestation of opportunistic infections, and malignant fluffs.

    The main reason for the development of VIL-encephalopathy (VIL-E) is the infection of the central nervous system with the virus of human immunodeficiency. In case of VIL-encephalopathy, VIL replication is active in macrophages and cells of the microglia of the brain. In neurons, viruses do not appear, they protest, functional and structural neurons, zooming in on other immunopathological mechanisms. Replication of a virus in the central nervous system from the statements of new quasi-species appears in the first world from the hemolymph system (Eggers, 2003). For the description of the sickness earlier, we used the same terms, including “SNID-dementia complex”, “SNID-dementia syndrome”, “SNID-dementia” and “VIL-associations of cognitive-motor complex”. All terms according to the day are synonymous with VIL-encephalopathy. In 2007, the international pre-social group analyzed the nosological forms of VIL-associated neurocognitive disorders and introduced a new category - "Symptomatic neurocognitive disturbance"(Antinori, 2007). Prior to the era of HAART, VIL-encephalopathy developed in approximately 15-20% of patients. In the quiet period, the disease on VIL-encephalopathy decreased, albeit in the lesser world, it didn’t damage the central nervous system, SNID-indicator diseases (Dore, 2003). Oscillations in the deserted lands of the community, the triviality of life of the VIL-informant comes close to the triviality of the life of the population in general, the breadth of the VIL-associated neurocognitive range, 2002, is approaching up to 20-50%.

    VIL-encephalopathy reduces the triviality of the life of the ill (Sevigny, 2007). It is generally known that VIL-encephalopathy is susceptible to affection. However, in the whole world, ART is injected into the function of the brain and a somewhat stable effect, for the time being it is unclear.

    Data is accumulated about the possibility of chronic progression, or, in some cases, re-development of neurocognitive disorders in patients who receive effective antiretroviral therapy (Antinori, 2007; Brew, 2004). The results of the late caution for receiving ART by patients who had no cognitive impairment at the time of inclusion in the pre-admission period, showed that after 5 years the cognitive function was lost to a large number of them (Cole, 2007). Even in one of the few people who participated in the participation in ART of patients with a rather low, albeit growthless number of CD4 lymphocytes, due to the fact that the cognitive function was improved, however, I didn’t add

    In such a rank, it is important to show VIL-encephalopathy in the possession of ART VIL-infected at a time to develop rapidly (Price, 2008). However, it is not less significant from the point of view of the point of departure, the destruction is constantly developed in the clinical practice. In the current hour, the stench develops even at the early stages of immunosuppression, zooming out of HIV infection (Dore, 2003; Sacktor, 2001).

    Before the era of HAART, the number of CD4 lymphocytes was not increased as predictive factors for VIL-encephalopathy, but the situation changed at the same time. In pozdovzhnіh doslіdzhennyah for participation otrimuyut ART patsієntіv without dementsії boule viyavlenі nastupnі prognostichnі factorization VІL-entsefalopatії: nizky rіven osvіti, SNІD-іndikatornі zahvoryuvannya in anamnezі, nizky mіnіmalny rіven lіmfotsitіv CD4 (nadir), Pokhil vіk and takozh sirovatkovі rіvnі FNP-alpha i MCP-1 (type 1 monocyte chemotactic protein) (Robertson, 2007; Bhaskaran, 2008; Sevigny, 2004). Winning and (abo) persistence of viral encephalopathy, non-invasive suppression of viral infection in blood plasma, may be associated with chronic immune activation, so that it is not susceptible to persistence.

    The process of caution, perhaps, will place an infectious process in the central nervous system as a result of an infectious process in hemolymphatic systems. The most important factor in the development of VIL-encephalopathy is the implantation of drugs, deyakі polymorphism genіv, which can code TNF-Alfano MCP-1, and, perhaps, supportive of HCV infection. Not long ago, there were descriptions of the development of important VIL-encephalopathy, with high levels of varietal nesting in the spinal cord ridges, in which ART patients can be purchased, in those cases, in those cases, the inferiority of the lower plasma levels.

    For histological preliminaries in the perivascular space and parenchyma, there was no CD8 lymphocytes, some of them were interrupted by the neurons. Tsei stan bulo interpreted the phenomenon of the renewal of the immune system, rectifying against VIL (Venkataramana, 2006).

    Klinichny show

    VIL-encephalopathy pidkirkovu dementia, as you are inclined to develop with a stretch of decilkoh tizniv or miscellaneous. Gostra symptomatology is directed to the cause of encephalopathy. Likhomanka, visnazhennya, diya tranquilizators, as well as rotten physical condition, for example, in case of oportunistic infection, can supervise the picture of dementia. In cich vipads, the diagnosis of VIL-encephalopathy can only be established after repeated examinations, as it is necessary to carry out a polyphenia to become ill. If you show encephalopathy with the help of relatives, and not the patient himself, it is even more important to feed them. Serious skargi - misery, forgetfulness, difficulty concentrating respect, lack of strength, mild symptoms of depression, dullness of emotions (div. Tables 25.1 and 25.2). Table 25.1. Symptoms VІL-entsefalopatії, vklyuchayuchi danі anamnesis, zіbranі Zi slіv blizkih patsієnta KognіtіvnieZabivchіvost, utrudnennya kontsentratsії uwagi, spovіlnenіst mislennya (spriynyattya, obrobki Informácie) .EmotsіonalnieUtrata pragnennya dіyati, bezіnіtsіativnіst, vіdstoronennya od sotsіalnogo Zhittya, nezdatnіst rozporyadzhatisya svoїmi fіnansami i organіzovuvati svoє Zhittya, prignіchenіst Slowness and complication of the appearance of thin layers (for example, leaves, stagnation of goodies), impaired gait. Table 25.2. Show VIL-encephalopathy There may also be tremors and old people of the course with other crocs. At the lower stage: the strengthening of tendon reflexes, Babinsky's symptom, the improvement of saccadic crumbs of apple apples, the deterioration of the function of sphinkters, including non-limiting slaughter and feces. Dolonno-pidboriddya, hapal and glabellar reflexes. May be a subutnya polyneuropathy. In termіnalnіy stadії: i spasticity tetraplegіya netrimannya sechі i kala.Psіhonevrologіcheskіe sіmptomiZamedlenіe psychomotor (napriklad, pererahuvannya months at zvorotnomu in order) korotkochasnoї pam'yatі torn down (utrudnene vіdtvorennya aurally pererahovanih predmetіv, numbers) gnuchkostі mislennya torn down (by letters utrudnene vimova simple words At the early stage: dullness of emotions, loss of strong special rice, increased handling, lack of performance. At the junior stage: it is not difficult to overhaul the steps in the direct order, disorientation in the hour, space and situation. In the thermal stage: mutism. Loss of svidosti, rigidity of mucous membranes, acute and asymmetric neurological symptoms (for example, hemiparesis, aphasia) are not typical for VIL-encephalopathy. Psychotic symptoms without cognitive abnormalities with a simple diagnosis of VIL-encephalopathy. Psychosis and VIL-encephalopathy rarely develop overnight. Ridko show the manifestation of VIL-encephalopathy and partial and generalized epileptic seizures. For an assessment of the severity of VIL-encephalopathy by step functional breakdowns can be victorious in the classification of the Sloan and Kettering Memorial Center (div. table 25.3) (Price, 1988). Table 25.3. Classification of VIL-encephalopathy at the severity level Stage 0 (Norm). Normal mental and psychological functions. Stage 0.5 (Total / subclinical encephalopathy). There is no destructiveness of greatness and activity; normal stroke; Possibility of control of the collapse of the eyes and limbs. Stage 1 (Mild encephalopathy). The patronage and increased activity of saving, even more difficult for the visitors of folding buildings; є bezpechnі signs of functional, intellectual or rudimentary ruins; You can walk without outside help. Stage 2 (Pomirna encephalopathy). Building up to self-service is saved, but it is unfortunate to see more foldable side-by-side buildings and professional equipment; for walking, you can use a cane. Stage 3 (Vazhka encephalopathy). Serious destruction to the intellect (the ailment is not a staunch quest for novelties and the memory of the story, it’s worthy of it in a special way, it’s impossible to get rid of it, it’s a bit of a baldness); ruins (you can't walk without outside help, you want to trust the ruins of your hands and your hands are weak) Stage 4 (Terminal stage

    summary

    According to the official data of the Ministry of Health Protection of Ukraine, a number of individuals with the first establishment of the diagnosis "VIL-Infections / SNID" in the period from 1987 to the fall of 2009 to become: VIL-pom 404, CI67 454. for the official assessments of the All-Russian Health Protection Organization and UNAIDS, in 2005-2006 p. close to 45 million people on the planet. The average indicator of VIL information in Ukraine becomes 58 vipadkiv per 100 thousand. Population.

    One of the organ-targets of VIL is the nervous system: only 1/10 000 part of lymphocytes of the peripheral blood of ailments on SNID is infected with a virus, at that hour in the tissue of the brain VIL is hostile to the skin honeycomb. Apparently, one of the frequent manifestations of VIL / SNIDu is the lesion of the nervous system. Neurological acceleration of viral infections can be caused by the retrovirus itself, as well as by oportunistic infections, puffs, cerebrovascular pathologies, toxic injections of antiretrovirals.

    Seemingly, without a mediocre improvement in the field of information and destruction of the cytin of the nervous system, which may cause the CD4 receptor. The patients can be carried: astrocytes, oligodendrocytes, microglia, monocytes, fibroblast-like cells of the brain, cells of the endothelium of blood-bearing vessels, neurons. In addition, the main cells are not only affected by the information, but the penetration of the VIL is in the middle of the cell itself, albeit and in every case of their membrane lysis with the gp120 bottle. The glycoprotein gp120 has a key role in the pathogenesis of IL-neuronal ears for the blockade of neuroleukin (lymphocytes, which have a neurotrophic effect). With the infusion of gp120, astrocytes do not absorb glutamate in synapses, until the ionization of Ca2 + and cytotoxic activity is increased.

    Skin lanka pathogenesis should be brought to a diagnosis in patients with a particular clinical picture with a characteristic neurological deficiency. Thus, a decrease in the neurotrophic inflow of the bioregulatory speech of the hypothalamic-hypophysis complex to the weed before the destruction of the mediator exchange. Deficiency of gamma-aminobutyric acid and glucine is carried out every year until the development of epileptics by the court. Depression of serotonin to produce anti-serotonin ataxia. Damaged exchange for vazopressin - until the memory is destroyed. Separation of endothelial cells of the vertebral gossip from the sheaths to the brain and the endothelial cells of the chickens is to produce the development of the firing of the mesenchymal elements of the nerve tissue and the second demilitarization, which will show up during the whole year in the future. Depression of clerical immunity to develop to the development of patients with oportunistic infections and to neoplastic processes.

    There are several hypotheses that can explain the easy penetration of VIL through the hematoencephalic bar. One of the hypotheses, the most uncomfortable lesion of the central nervous system, and can be used for the development of perineural penetration of the virus in the main cells. Small mice and indirect cut - if the virus from the immune system penetrates into the nervous system (the mechanism of the "Trojan horse"). The virus can penetrate into the endothelial cells of the cerebral capillaries, carrying the CD4 antigen on the membrane. The transmission of genetic variants of VIL is also transmitted, as well as a specific neurotropic effect.

    The CD4 receptor is not only in the cells of the neuroglia, but in the endothelial cells of the fox gossips of the brain and endothelial cells of the brain. In this way, it is possible to produce up to VIL-assocyovanimous damage to the spinal cord and to the brain. Oscillations of the pathological process of localization of endovascular, may lead to the diagnosis of primary vasculitis and vasculopathy. The first VIL-association of vasculitis of the brain and spinal cord in the other can lead to the secondary lesion of the nerve tissue. Seemingly, it often develops in case of HIV infection, thrombocytopenia increases the development of hemorrhagic diseases, as well as decreases blood rheology and hypercoagulation. When carrying out histological examinations in VIL-informed patients, the disease was detected with leukocytes, increased and proliferative changes were detected. Everything is to lead to the sound of education of the judgment and thrombosis with advanced infarction, opening of the judgment and hemorrhage. Even more often, a VIL-infected patient is more likely to undergo the transformation of an ischemic insult into a hemorrhagic one. With VIL-associated vasculature, multifocal lesions develop. Tse let us tell you not just about vasculitis, but about Meningovascular productive form of neuro-SNIDu.

    Approximately 40% of VIL-information may change spinal cord ridin (CMP), develop mild pleocytosis (5-50 cells / mm3), increased amounts of alcohol (500-1000 mg / l) and The changes are not specific. Half of the clinically healthy HIV-infected patients may have pleocytosis or the number of cells in the spinal cord is increased, in 20% of CSF there is an increase in HIV on tissue cultures, often in high titers. The increase in pleocytosis will decrease, at that hour, as the number of bites can be reduced, change, or without changes. Yak in peripheral blood, spinal growth in spinal cord CD4: CD8 is low, especially in at the stageінфекції. The titer of the virus in the spinal cord during the stage also decreases. The changes in the spinal cord rotations are of the same kind and not permanent, so it is important to predict the overcoming of the disease and the effectiveness of therapy.

    Anti-HIV appears in the spinal cord and in high titers. The determination of the titer of antibodies in the blood and spinal cord ridin is in the case of those, which antibodies can be synthesized in the central nervous system. Antibodies to HIV in the spinal cord are classified as IgG, but in some ailments it was said to be antibodies of IgA and IgM classes. The synthesis of antibodies in the central nervous system is repaired early, as soon as the inflammation of the cerebral membranes occurs. Oligoclonal antibodies in the spinal cord can also be detected, the stench appears to be HIV-positive and may be seen as a symptom of migraine health. Pleocytosis and concentration of blood is badly correlated with anti-НIV-antibodies in the spinal cord and the number of oligoclonal smogs. Patients with a positive culture of HIV from the spinal origin and anti-HBV antibodies in the spinal cord and oligoclonal swans. In patients with CHIDom, the synthesis of antibodies in the spinal cord is slightly lower, less in VIL -infikovans without CHID. The concentration of p24-antigen and anti-p24-antigen in the spinal cord changes in parallel, while the concentration of p24 in the spinal cord starts to develop. The concentration of p24 is maximal in the case of the complex "SNID - dementia", but the concentration of antigens and antigens is at a premium because of the variability of clinical symptoms and effective therapy.

    In the classic picture, you can see a characteristic number of symptomatic complexes: meningism, pyramidal deficiency, cerebellar ataxia, sudominal syndrome, SNID-dementia complex, symptom complex, characteristic of encephalitis, meningitis. Clinical caution is shown that at the early stages of HIV infection, the most frequent are reactive neurotic conditions and manifest asthenovegetative syndrome. Patients may have a misnomer and neurotic character, as well as become obstinate, unimportant, forgetful, disordered mood, ringing of interest, lack of sleep, autonomy, vegetation. At the larger stages of illness, the first plan is to deal with the nervous system, and moreover, it is overwhelmed by opaque infections.

    Involvement of the central nervous system, which is the result of direct infection with a retrovirus

    Hostry aseptic meningoencephalitis

    Tsei syndrome occurs in 5-10% of HIV-infected patients without prior seroconversion or in the presence of mononucleosis-like syndrome. Ailing headache, a feverish woman, a breakdown in the mental status, focal or generalized court attacks. For the blame of the fact that the facial nerve paralysis is minus (Bell's parallax), the symptoms of the nervous system are severely affected and lateralized. Є Regarding the state of myelopathy with paraparesis and swelling of pain syndrome, in early stagesінфекції. In spinal discs, pleocytosis appears, in addition to the increase in blood pressure and a normal amount of glucose - changes, similar to those in seropositive clinically healthy HIV-positive patients. Laboratory diagnostics of VIL-infection is primed on a visible virus abo p24 from a virus or CSF abo, in larger terms, on serological signs of seroconversion (give 1 or 2 months after that). Gostry Meningoencephalitis is self-limiting to illnesses and only symptomatic therapy.

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

    ADC, also of the title "VIL-encephalopathy", "VIL-encephalopathy", "subacute encephalopathy", is developed in the phase of SNID. Most often, neurological illness in patients with SNID may also be the first symptom of SNID in VIL-infected patients. With early symptoms - apathy, disrespect, forgetfulness, loss of concentration of respect, decrease in intellect, autism, and, in fact, even more depression. Patients can also have a deafening feeling, deafening, hallucination or psychosis. A lot of problems with a sick person does not allow for any problems, even for neurophysiological predictions in the whole period of showing a deterioration in the accuracy and speed of motor functions, including the memory of short motor functions, smoothness ... Tse led ADC in the early phase of a banal depression. In the case of the children, the rate of misdirection and the speed of reaction are decreasing. If dementia is evident, cortical symptoms (such as aphasia, apraxia and agnosia) are also not the main ones; In conjunction with cym deyaki, neurologists classify ADC as subcortical dementia against cortical dementia, such as Alzheimer's disease. Okay roast є frequent in the early ADC phase. It is often the case that there is a "physiological" tremor. In ailments, there is a lack of progress, it is foldable to classify it as ataxia, sensory ataxia, spastic, which is considered to be apraxia, or is functional. Deyakіpatsієnti may be impaired walking and impaired function of lower children, associated with vacuolar myelopathy. ADC can progress stepwise or stepwise with rapt fights, in some cases with systemic manifestations of ailments.

    Diagnosis of ADC is established by a path of success of competing diagnoses, which can lead to the destruction of symptoms, psychosis or dementia in people with SNID. Pre-treatment of blood, spinal cord, computer tomography of the head (CTG) may be of great importance. The disease includes not only infections and chickens of the central nervous system, but also side effects drug therapy, imbalance of living words. In ailments with ADC CTG, either normal or atrophy of the brain appears. Magnetic resonance imaging (MRI) shows atrophy of the brain. In addition, there are middles of growth, diffusion changes in speech, and most often it starts with T2-mode MRI. These changes are not specific. Positron imaging of the head showing impairment of glucose metabolism. In the early phase, hypermetabolism appears in the basal and thalamic ganglia, and hypometabolism in the systemic measles and pediatric statements. CSF can be normal either with an increase in the amount of clintin, or a small amount of oligoclonal antibodies. The high level of b2-microglobulin occurs frequently and is due to the severity of ADC.

    Mayzhe half of the ailments with ADC, especially with severe interruption, maє vacuolar myelopathy. The size of the ADC is correlated: the number of nuclear cells, the presence of the semi-oval center, the presence of HIV in the brain. Pathomorphological changes are confirmed, when correct love Part of all symptoms can be werewolves.

    Progressive encephalopathy (PE)

    Progressive encephalopathy - the central nervous system in children, clinically similar to ADC in older adults. Appear more often at half of the children. Less than 25% of children who are infected may have normal neuropsychic development, 25% have stable (non-progressive) encephalopathy, viclican, and possibly, accelerated perinatal period.

    PE is manifested in the second month - 5.5, in the middle - in 18 months. Earn ear of zhvoryuvannya, start your deeds, if you want you can get good and go. For some children, PE is the first manifestation of VIL. In sick children, it means to take on (or inevitably) pink and physical development. Special support intellectual development, Reducing the rate of growth of the brain, symmetrical lack of strength. A lot of children are low-minded, apathetic, mutism and dementia develop. In half of the children with PE, microcephaly develops. Hypotonia and hyporeflexia, progressing into pseudobulbar parallels and quadriplegias, are indicated on the ear of the disease. The age of children, who doesn’t get rid of the love, can go swiftly, or stepwise, or stepwise. Death is insistent, call out to reach out to fate for the establishment of diagnosis. Yak and ADC, PE are in the early phase of an illness, if the sick person has signs of immunodeficiency. CTG may be normal, however, most often it is injected into atrophy of the brain. On CTG with internal contrasts in children younger than 5 years, it is possible to strengthen the contrast of the basal ganglia and frontal parts of the brain, calcification. The changes can progress. MRI detects changes in signals in the paraventricular bile of speech.

    Children with PE may have a small amount of lymphocytic pleocytosis (5-25 cells / mm3) and displacement instead of a bottle in liquor (500-1000 mg / l). Even in older adults, in liquor, there is a higher titer of antibodies in porous with a strong titer, which supports internal synthesis. In children with PE, it is also possible to see a high level of p24 in the spinal cord. The concentration of the factor of necrosis of chickens in syrovattsi, but not in the spinal cord, corelus key symptoms... Three four children with PE may have a high concentration of TNF in syrovatz, 95% VIL-infected children with a high level of TNF - PE.

    Oportunistic infections of the central nervous system, I will have an inherited cerebrovascular lesion

    Cerebral parenchyma

    Toxoplasmosis. Toxoplasma gondii- the most common reason for the severity of the central nervous system in ailments on SNID. Approximately 10% of ailments on SNID suffer from toxoplasmosis of the central nervous system. Most of the infections are the result of reactivation of latent infections. In ailments on SNID with a positive Sebin-Feldman test, or without clinical manifestations of toxoplasmosis, it remains in 30% of cases. If we do not want to expand it, the number of ailments with toxoplasmosis of the central nervous system is not large. negative test toxoplasmosis is not detected with barvnik. Changes in the size of the title, such as the increase in 4 times in the boys, are unaccountable. Extracerebral manifest toxoplasmosis, such as chorioretinitis, is rare and does not correlate with lesions of the nervous system.

    CTG and MRI play a vital role in diagnostics. CTG is located in the area of ​​speech in the brain with the embankment, in more intensive farbrowns with internal contrasting, often in the eyes of the children. Visibility of changes at KTG є is unaccountable. Vignischa urazhennya appears most often in the basal ganglia. Інші sickness can give me a picture, and it isn’t turned on, but the sick person suddenly has a little sickness in his parenchyma brain, which gives a picture of a lot of battle.

    It is important until the ear of the mother is drawn into the diagnosis of toxoplasmosis in the brain. Singing the meaning of the biopsy to the brain. Ostannya maє and vidomy risik - through the possibility of admission to infection or bleeding. The biopsy of the brain is to blame only for the fact that the second course of trial treatment does not give results. Establish a diagnosis of toxoplasmosis for additional biopsies is important. Histologically burning in abscesses, Toxoplasma gondii, I can nagaduvati lіmphoma. Detection of trophozoites (abo tachizo-ites) by the immunoperoxidase method, diagnostic value, Often important. The diagnosis of biopsies to the brain is more beautiful than the head, and it is not possible to find a diagnosis in any way. It is possible to see the pupil by the biological method (introduced into the brain of the mice), or in the culture of tissue.

    In such a rank, a greater part of the patients started to correct the treatment of toxoplasmosis without the established diagnosis of toxoplasmosis of the central nervous system.

    The schema, presented in table. 1, sulfadiazine can be replaced by one of the most advanced drugs:

    - clindamicin, 600 mg i.v., or in the middle 4 times and for 6 times;

    - azithromicine, 1200 mg every once in a while for 6 weeks;

    - clarithromicin, 1 g vseredin 2 times and 6 times for extra;

    - atovaquone, 750 mg in the middle 4 times and for 6 days.

    Children need more trivial intensive treatment course State Department of Infection... There are no standard recommendations for the triviality of the test: the decision about switching to the other course of the test is to take the best results and CT results, if it is available.

    The polish is infused for 10 days and is verified by the positive dynamics of CTG and MRI. In general, there is a residual rise in the pathological changes in the central nervous system. Toxoplasma gondii... Oscillations in cases of pathology develop and tissue swelling in the brain, drugs often indicate glucocorticoids for the entire term of treatment. Glucocorticoid polypsychiatric overbig the parenchymal brain with VIL. In such a rank, polymorphism in the context of combined therapy does not mean that pathological changes in the central nervous system will be increased. Toxoplasma gondii.

    Toxoplasmosis of the central nervous system in ailments on SNID often recurs after treatment. Most of the ailments will require continuous therapy. For secondary prophylaxis, take half the doses of drugs, which should be included in the effective scheme, which are used for the treatment of toxoplasmosis; Continue to continue until quiet times, as long as the number of lymphocytes CD4 will NOT be reduced to> 200 in 1 μl for 3 months.

    Primary CNS lymphoma. The primary lymphoma of the central nervous system appears in two people with ailments on SNID. Pukhlina MA is an antigenic marker of B-clinical, multicenter. Neurological symptoms can occur on the midline or diffuse central nervous system. Nay-bolsh is a typical step in respect of hyperventilation, among children in common with uveotsiklit. Symptoms may be important for the diagnosis of lymphoma of the central nervous system. Primary lymphoma can be diagnosed in ailments with immune deficiencies, other causes (NOT HIV). In cychs ailing є a high titer of antibodies to the Epstein-Barr virus (EBV), in chickens, the power of EBV nucleic acids and bins begins. In tissue culture EBV the power of transforming B-lymphocytes. It is not included that EBV can be the cause of the primordial lymphoma of the central nervous system. Oscillations of the EBV genome and thiRNA are present in the chubby cells of ailments on SNID, EBV may be the primary disease of the central nervous system and in patients with CHIDom.

    KTG viyavlyaє one hyper- or izodensivny in the fire or more signs of a speech in the brain. Vognischa can be unilateral or bilateral. Ridly in the area there is a decrease in intensity (hypodenseous) and not contrasting with internal contrasting. Deyakis in the middle of the ring-like form with internal contrasting and toxoplasmosis. MRI is more sensitive, less CTG. The changes on CTG are not specific for lymphoma. Angiography evoke the appearance of a non-vascularized mass, so that the deyaky puffs are fired homogeneously. Lumbar puncture is potentially not safe. Cytological dosage of the spinal cord genus of the disease was found in 10-25% of the ailments. In cichs with ailments, there is a high level of b2-microglobulin, but in sick people on SNID, the changes are not specific. Residual diagnosis of biopsy to the brain. With a single vognischі biopsy є by the method of vibration for diagnostics, with multiple staggered times, start trying to get rid of the drive of the transmission of toxoplasmosis of the central nervous system, and in case of failure - vicious biopsies.

    The primary lymphoma of the central nervous system in ailments on SNID significantly changes in the size of the amount of corticosteroids injected, she is sensitive to X-ray vipromynuvannya, but the average life does not change 2 months, in the wrong hour. On the contrary to the other types of brain poohlin, surgical decompression is better for a sick person. Highly effective antiretroviral therapy can reduce the risk of remission of the primary lymphoid of the central nervous system.

    Progressive multifocal leukoencephalopathy (PML). As the primary central nervous system lymphoma, PML can be diagnosed in ailments with immune disorders, vicious diseases, low HIV, causes (for example, corticosteroids). Infection of 20% of ailments from PML may have SNID; However, with an increase in the number of ailments on the SNID, the number of people who are sick will be reduced. PML occurs in 2-5% of ailments on SNID. Cych patients develop progressive dementia and neurological symptoms.

    CTG will develop one hypodenseous in the presence of an increase, or even more, do not contrast with an intravenous contrast. It is the most frequent thing to fix on the cordon of old and common speech, and lastly to expand into the word of speech. MRI is more sensitive, less CTG, more often there are great and many alternatives. The pre-treatment of the spinal cord is not informative, with the blame for the increased concentration of the main library.

    Diagnosis primed on biopsies, yak viyavlya: a) demilinizatsiyu; b) great astrocytes behind abnormal, in one multiple, nuclei; c) oligodendrogly with eosinophilic internal nuclear inclusions. Pathological changes occur in PML, vicious causes of SNID. JC-virus, which is referred to as Papovaviridae, Informations of glial cells, especially oligodendroglia (for children: HIV is an enemy of macrophages and microglia). Oscillations of pathological changes in astrocytosis can be taken for a reason, as there may be no evidence of those who have an ailing cytomegalovirus (CMV) infection, the diagnosis is due to the presence of immunohistochemistry. Gis-active regulatory element JC-virus is active in the culture of tissue of gliomy of the new neoplasm; stimulated by the JC-virus expression of the T-antigen in Misha Veda before desmielinizatsiya. Це підтверджує, шо JC-virus wiklikaє PML.

    finish effective treatment dumb. The average triviality of life - 4 months, ale deyaki sickness from SNIDom may have great terms of vision for the establishment of PML diagnostics, less patients without SNIDu.

    Insult. Hemorrhagic, tied with thrombus confirmation or thromboembolic insult, are not susceptible to VIL-informants. Hemorrhagic stroke often occurs in ailments with severe thrombocytopenia (especially in ailments for hemophilia) and with metastases of Kaposi's sarcoma in the brain. Insult, associated with thrombosis, occurs in patients with angiitis. The development of granulomatous angiitis can be linked to herpetic lesions of an individual, but it is less likely to develop in sick people on SNID, who were not sick on herpetic infections. In some patients, the cause of strokes associated with thrombosis should not be given. Mozhlvo, deyakі from them mali "anticoagulant vovchak", anticardіolіpіnovі antitіla. The presence of anticoagulant volvchak is recommended to coat with a high partial thromboplastin hour, a hypo-positive VDRL test and a low number of platelets. The presence of anticardial antibodies in the diagnosis of the syndrome is not clear. About thromboembolic strokes occurred in ailments with infectious endocarditis, who suffer from marasmus, or nonbacterial endocarditis with thromboembolic syndrome, which can be associated with Kapos sarcoma. The association between thrombocytopenic purpura and SNID is not included. On the basis of the pentad of symptoms of thrombocytopenic purpura (in patients with SNID, all 5 symptoms are not required): thrombocytopenia, microangiopathic hemolytic anemia, pathology of pathology, fever, progression.

    Herpes virus infection. Herpesviruses infest CMV, herpes zoster virus (HZV) and herpes simplex virus type 1 and 2. Tsі viruses can be the cause of sickness both in the parenchyma of the brain, as well as in the shell. If the stench develops among ailments on VIL-infection, it is tricky to talk about "secondary viral encephalomyelomeningite." About іnhіh, non-hepatic virus infections, associated with immunodeficiency, such bovine yak, іnterіnіy encephalitis, enterіrusnі mіositis, with CHIDі is not common.

    CMV-Infectious Disease is able to control the manifestation of VIL-Infectious Diseases. Retinitis is known in 20-25% of ailments on SNID. Most of the time! Picking up the scent of the field in the sympathetic hemorrhagic exudate of the court region. Nadnikovykh zvichna for ailments with CMV-infectious diseases. CMV-encephalitis can contradict vognischevny, multifocal or generalized neurological symptoms. CTG and MRI can be normal. Four ailments on SNID have histological signs that can confirm the manifestation of CMV infection: neuronal necrosis, eosinophilic inclusion in the nuclei. CMV can also be considered important for polyradiculopathy. CMV-positive bacterial (cytomegal) cells are found in subpial, subendimal areas and nerve roots. The CMV can also be used to declare polyradiulopathy.

    Herpes zoster develop є inherited reactivation of latent infections and develop on the older stages of VIL. Ailments on SNID often cause herpes desemination and postherpetic neurological syndrome, as well as multifocal leukoencephalitis with intermediate abnormal lateralized neurological symptoms, signs of hidrocephalus on CTG. CSF can be normal. Pathological anatomical visualization of ventriculitis, focal necrosis with internal clutches in nependymal cells and glia. Cerebral granulomatous angiitis, as the inheritance of herpetic infection, manifests itself as fever, impaired symptoms, ischemic insults. Nareshty, the ailments may have malit, HZV victories.

    Ailments on SNID often cause a great fever of the disease, herpes simplex virus (HSV, herpes simplex virus - HSV). In tsyom vypadu duzhe high rhizik HSV-encephalitis. HSV-2 is used to develop perirectal and genetic changes, as well as management and communication.

    Div. Tab. 2-5.

    For the sickness, it is necessary to use non-steroidal anti-flue gas. If the stench does not help, it is possible to indicate amitriptyline, carbamazepin or phenytoin.

    Entrapment of cerebral sheaths

    Cryptococosis and other fungal infections. It is most common to become ill at the stage of VIL-infection. Meningiti, wiklikany Сrurtocossus peofоrtans, 5-10% of ailments are diagnosed on SNID, most often - among internal drug addicts and vasniks of birds. Іnshi fungal infections are more common in ailments on SNID. Dissemination of gastroplasmosis, coccidiomycosis is often more common in residents of endemic regions. іnshі fungal disease The disease can develop in ailments on SNID, including aspergiliasis, candidiasis and mucoromycosis.

    In ailments, cryptococcal menіngitis is sick є fever (65%), headache or discomfort in the head (75%), rigidity of the muscles (22%), syndrome of impaired dysfunction (28%) and neuropsychiatric symptoms (< 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.

    Necessary additional secondary chemoprophylaxis; for all, you can vikoristovuvati fluconazole, 200 mg all in the middle 1 time for doba; an alternative drug for additional secondary chemotherapy is іraconazole, 200 mg every other day, once in a while.

    There is still no concrete evidence of coryliness in the continuation of the prevention of the immune system function (CD4> 200 in 1 μl).

    In case of patients who are eligible for a substitute methadone therapy, it is necessary to remember about the use of fluconazole and methadone.

    Lymphatic meningitis. Ailments on SNID often develop non-Hodgkin's lymphocytes with B-lymphocyte markers. Puffy cells morphologically inflict primordial lymphocytes of the central nervous system, revenge the EBV genome and be encoded in the cells. Cancer is most often extranodal; the sheaths of the brain are drawn into the pathological process in 10-30% of cases. Paraspinal localization with the development of symptoms of spinal cord compression occurs in 10% of patients. With the meningeal form, there is a manifestation of parallel cranial nerves, radiculopathy and headache. In spinal cord ridges, pleocytosis occurs, due to the concentration of blood cells, in some cases - hypoglycorrhiza. Diagnosis primed on cytological preliminaries CMP. Lіkuvannya polyaga in combination of chemotherapy and radiootherapy.

    Dissemination of tuberculosis. VIL-confirmed with a positive test for cleansing a blood derivative may cause a high risk of development of deseminated tuberculosis (TB) and guilty of eliminating isoniazide with the help of prophylaxis. 2% of HIV-infected patients have active tuberculosis. You can actively become ill at any stage of HIV infection, and most often, if not expected, as a result of activation of latent infection. In ailments, meningeal symptoms can occur (fever, headache, rigidity of the disease). Also, there may be symptoms of spinal cord compression due to infection. I had a history of myelopathy symptoms with the appearance of mycobacteria in spinal cord biopsy. Nareshti, in ailments with tuberculosis deseminations, signs of supra-nirkova deficiency can be found.

    Shkirny test is negative in 70% of patients with SNID with active tuberculosis. radiography breast cancer often pathology occurs, with a lot of snakes localized in the lower and middle particles, and not in the upper, as it will develop in tuberculosis. Pukhlinopodibneosvita in the brain (tuberculoma) can be detected with CTG. In spinal cord ridges, mononuclear cytosis appears, as well as an increase in blood pressure and hypochondriasis. With microscopic CSF, acidic bacilli appear in 37% of cases, and vyavity in 45-90% (1-2 months are required at the price). New viprobation has been developed for the rapid detection of mycobacterium antigen.

    The excess of tuberculosis in VIL-infected patients is more severe, the disease is more foldable, and the frequency of side effects is higher. Three reasons for all ailments with active tuberculosis are guilty of being tested for HIV. VIL-diagnostics of ailments with acidic bacilli in a smear or biopsy are guilty of eliminating anti-tuberculous therapy for an hour, while the bacteriological period is being carried out, it is not necessary to stay in the middle of a sickness Mucobacterium avium intracellulare, but not M. tuberculosis.

    For VIL-informed patients with infections M.tuberculosis To promote a high risk of development of active TB, it is necessary to carry out prophylactic treatment with izoniazide at a dose of 5 mg / kg (or not more than 300 mg / dob) 1 time for dob, a course of 6 months.

    Syphilis. Є Suvorі epіdemiological regularities between syphilis and SNIDom. This means that all ailments with syphilis are guilty of being tested for HIV. Symptoms of syphilis can be detected in any stage of VIL-infection. Syphilis of the nervous system can be manifested by ischemic insult, meningitis, Bell's parallels, neuritis of the healthy nerve, polyradiulopathy and dementia. Oscillations greater than 25% VIL-related with neurosyphilis may be negative "nonspecific" anti-treponemal tests (VDRL, RPR). Insult types of tests are used to identify circulating anti-treponemal antibodies in the blood. More for everything, with VIL, the number of positive and positively negative results is higher, less when testing for syphilis of non-inferred VIL. The VDRL test can be successfully used to monitor the effectiveness of syphilis therapy in VIL-infected patients. Vikoristovuvati was taken for the diagnosis of neurosyphilis routinely and VDRL-testing of spinal cord ridin. An offense to the test is given in VIL-informed people with a greater number of positive and positive negative results.

    Neurosyphilis is subject to the introduction of large doses of penicilin G (24 million OD intradermally for 4 years and for 10-14 days). VIL-information with FTA-abs - positively responding and positive VDRL-test with CSF guilty of eliminating the drug in the designated mode. It is indicated for the introduction of high doses of penicillin internally with syphilis is not clear. Є occasionally about not too long stasis prolonged penicillin, which is introduced internally, in case of secondary syphilis elimination in VIL -inflicted.

    Spinal cord injury

    Vacuola myelopathy. Tse zhvoryuvannya develop viciously among the patients with SNID, about 20% of the ailments are hostile. If myelopathy is often associated with ADC, ailments can be diagnosed in patients with SNID and without dementia. Incidentally, it is impaired to walk in a combination with spastic paraparesis and sensory ataxia. With neurological obesity, hyperreflexia, spasticity, impaired responsiveness in the legs and instability in Romberg's position appear. Through a circle of visions or months, the non-triviality of the battle will come. The pre-treatment of the spinal cord is not informative. Wicked rumors and good health potential in the norm. Depend on the universesal coverage of vicious somatosensory potentials of the great posterior nerve. Tse can come back to the mainstream manifestation of becoming ill. Differential diagnostics includes spinal cord compression with lymphoma or as a result of tuberculosis, infectious myelitis, for example, in IL-seroconversion, herpes infection and HTLV-1, myelitis. In case of pathomorphological preliminaries, there is a demilinization and vacuolization of the white speech of the back and bone cords and a small number of macrophages with fatty inclusions. During electronic microscopy, it is necessary to stand up, but vacuoles are the result of internal microscopic filling. HIV antigens are rarely given as isolation from the tissue of the spinal cord in patients with vacuolar myelopathy. Naybіlsh important changes appear in the thoracic cavity of the spinal cord.

    Cranial nerve neuropathy. Neuropathy of the cranial nerves (most often - in an isolated one-sided paresis of the facial nerve) occurs in 10% of VIL -inflicted patients with a stretch of all entrapment in a second or In addition, puffy-like orbital (for example, lymphoma) may suffer from early oculomotor parallax. Parallich of the lower motoneuron of the facial nerve invoke to start in the middle phase of Bell's infection and nagadu parallich. Zazvychay sposterіgaєtsya oduzhannya without zhodnyy lіkuvannya.

    Nervous-myazovy

    Approximately 30% of ailments on SNID have a nervous malady. Deficiency of cobalamin, a-tocopherol, syphilis, thyroid dysfunction, side effects of such drugs, such as zidovudine, vincristine, disulfiram, can lead to symptoms of neuro-muscular disease.

    In patients with SNID, five neuropathic syndromes have been described: Gina - Barre, chronic demilinizing polyneuropathy, multiple mononeuritis, distal sensory peripheral neuropathy, state polyradiulopathy.

    Gin-Barre Syndrome. Tsey Sind-rum is to be found in the main in the early and middle phase of infection. In case of Gin-Barré syndrome, it is not until VIL-infec- When it is delayed, weakness, areflexia appears with normal sensitivity. The appearance of the surface antigen of hepatitis B and pathological "pechinks" tests are very susceptible. At the spinal cord rіdinі there is a high rіven bіlka. In bagatokh, albeit not in all ailments in the spinal cord, pleocytosis begins, which can be very strong VIL-infection. Evidence of pleocytosis in ailments with Gin-Barre syndrome Nerve conductivity can be normal or relied on for a depressive or a block of conductivity. Symptoms of denervation appear when neuromography is detected in the process of axons. In case of biopsies of peripheral nerves, the changes do not appear, but rather segmental demiєlіnіzatsiya is introduced. Perineural cells can be vacuolated. The stage of firing can be varied. Moss CMV-infection of Schwann cells, is especially viral in the area of ​​proximal roots. Retaliation monitoring of vital functions in cich illnesses є constipation of successful therapy for Hyun-Barre syndrome. Decrease of life of a lot Leggings less than 1 liter please є are shown for piece ventilation. I want a part of the ailments to insist on spontaneously harnessing, likewise substituting plasmas of a sick donor by the method of vibor.

    Chronic ignition demyelinating polyneuropathy (CIDP). The whole syndrome develops even in the middle stage of infection, if you want to develop in sick people on SNID. A bad turbine is progressively slower and it is intermittently weak. Afterwards, there is weakness in the proximal and distal muscle groups, normal (or rather normal) sensitivity and areflexia. The most frequent is the weakness in the meat of an individual. In spinal cord infections, proteinerachia and pleocytosis occur, which is most often the result of no HIV infection. It is not possible to achieve an exact differentiation of CVDP in case of VIL as an idiopathic type in view of the manifestation of pleocytosis, if it is possible to allow VIL infection. In a third of the ailments, the concentration of the basic myelin protein increases in the spinal cord. The correct diagnosis is based on the results of the HIV test. Pre-treatment of nerve conductivity in the presence of a decrease in the block of conductivity and depression, which indicates segmental demyelination. Electromyography in the process of receiving axons in the process of demining. With bio-PZII nerves, demyelination is evident, macrophage infiltration, perivascular and endoneural inflammation. Vacuolization of perineural cells can be found in a single cell. HIV antigens in the biopsy of nerves cannot be given. HVDP foldably differentiates from the Hyun-Barre syndrome, lymphocytic infiltration of nerve roots and toxic neuropathies, vicikanovy drugs (such as vinkristin, disulfiramide, disonin With corticosteroids elimination and plasmapheresis, CIDP regresses. In the case of the vipadkas, spontaneity is infused. Polishing can be correlated with normalization of the number of cells in the spinal cord. The causes of the CIDP are unavailable.

    Multiple mononeuropathy. Nayridkisnish ​​form of neuropathy. It is characterized by the raptus development of the great izolovannyh nerve stovburiv. The process can get started cranial nerves... For the reason, beep є gostre flamed or damaged bloodletting nerves. The whole syndrome is clinically important in the development of compression neuropathy, progressive polyradiculopathy, and if it is possible to reach a lot of nerves, it is in the CIDP.

    Progressive polyradiulopathy. In case of this syndrome, it is possible to develop into the development of the stage of VIL, the state of the stomach or of the progressive sensorimotor deficiency and reflexion, which is localized on the lumbosacral function of the intestinal spinal cord from the development of the spinal cord Ailments do not grow on their own, they have a lot of problems.

    With this syndrome, death is most often infused with a stretch of decilkoh months. In half of the diseases in the spinal cord, pleocytosis appears, a high level of glucose and a decrease in glucose. In half of the ailments, the virological method from the spinal cord is given CMV. Elektromyogram viyavlyak gostru denervation Differential diagnostics includes hypertension of the spinal cord, meningeal lymphomatosis and neurosyphilis. In case of virological pre-diagnosis of sectional material, CMV infection of endoneural cells of the back cortex of the spinal cord and endothelial cells is injected into the bag. An early sign of gancicloviru to produce ailments in children with ailments to the development of ailments.

    Breakdown of the autonomic nervous system (ANS)

    Dissection of the VNS, turn around the world, develop in the middle of the stage of infection and manifest orthostatic hypotension. Become struck by a cute, so parasympathetic viddil VNS. Є nasty correlation with other neurological manifestations of VIL. It is also possible to develop supra-nirkovy vines.


    List of Literature

    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 Ophthalmolo-gy. - 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.