Neurologic displays of HIV infection (neuroaIDS) — the generalized clinical concept including the diverse primary and secondary syndromes and diseases of nervous system caused by HIV. As displays of neuroaIDS the encephalomeningitis, a polyneuropathy, entsefalo-and a miyelopatiya, opportunistic neuroinfections, TsNS tumors, cerebral vascular disorders, etc. can act. NeuroaIDS is diagnosed by comparison of results of analyses on HIV, data of neurologic survey, neuropsychological testing, likvorologichesky and tomographic researches, EFI of the neuromuscular device. Treatment of neuroaIDS is performed within therapy of HIV infection with purpose of specific and symptomatic therapy of the available neurologic manifestations.
It is well-known that at development of AIDS pathological changes in a varying degree affect practically all vitals and systems. In this regard AIDS is recognized as multidisciplinary pathology. However main "blow" is the share of immune and nervous systems. Clinical neurologic displays of HIV infection are observed at 30-40% of patients with AIDS, and on autopsy these or those changes in nervous system come to light in 90-100% of cases. According to various data, from 20% to 30% of cases of AIDS demonstrate various neurologic symptoms. At the same time neuroaIDS has very variable clinical manifestations that significantly complicates its diagnostics by experts in the field of neurology, especially in cases when neurologic frustration are the first display of a disease. If neuroaIDS arises at the established diagnosis of HIV infection, its diagnostics often is complicated by the fact that patients prefer to hide the HIV status.
Causes of neuroaIDS
Despite general recognition of a neyrotropnost of HIV, concrete pathogenetic mechanisms of its impact on the nervous system (NS) are up to the end not clear. It is supposed that neuroaIDS is caused as the straight lines which were so mediated by impact of a virus on NANOSECOND. Direct influence is connected with a HIV tropnost to CD4 receptors which are available not only in a membrane of lymphocytes, but also in glial cells of brain fabric.
Penetration of a virus through a hematoencephalic barrier (GEB) is explained with increase in permeability of the last against the background of a viral infection and existence in cages an endoteliya of GEB of the same CD4 receptors. According to other hypothesis, the virus can be transferred to brain fabrics together with macrophages who freely pass GEB. It is known that at neuroaIDS only glial cages are surprised; the neurons which do not have CD4 receptors remain intaktna. However, as cages of a glia carry out a role of "service" of neurons, at their defeat normal functioning of the last is also broken.
The mediated influence of HIV is implemented by several ways. First, this development of opportunistic infections and tumoral processes due to sharp decrease in the immune status of an organism. Secondly, assume existence of the autoimmune mechanisms (for example, in development of aseptic meningitis and a polyneuropathy at neuroaIDS) connected with synthesis of antibodies to the nervous cages having the built-in HIV - the anti-gen. There is also a hypothesis of neurotoxic action of the produced HIV of chemicals. Besides, development of neuroaIDS is possible owing to the damage an endoteliya of brain vessels pro-inflammatory tsitokina leading to disorder of the microcirculation and a hypoxia causing death of neurons.
It should be noted that lack of full clarity in an etiopatogeneza of HIV infection and neuroaIDS in particular, existence of essential number of false positive reactions to HIV at its laboratory diagnosis, and also complexity with allocation of a virus was led to emergence among physicians and experts in the field of immunology of the persons considering unauthorized the concept HIV infection. At the same time supporters of HIV denial recognize existence of a syndrome of immunodeficiency per se, but are afraid that with introduction of the concepts HIV infection and neuroaIDS under these diagnoses patients with various other diseases in large quantities get.
Classification of neuroaIDS
According to the direct or mediated impact of HIV on nervous system it is accepted to distinguish primary and secondary neuroaIDS. Carry to basic clinical forms which are included by primary neuroaIDS: sharp aseptic meningitis, HIV encephalopathy (AIDS dementia), VICh-miyelopatiyu (vakuolyarny miyelopatiya), vascular neuroaIDS, defeats of peripheral NANOSECOND (disteel symmetric neuropathy, syndrome to Giyena-Barra, multiple mononeuropathy, chronic inflammatory demiyeliniziruyushchy polyneuropathy, syndrome of a horse tail), damage of muscles (myopathy).
Secondary neuroaIDS includes opportunistic neuroinfections and tumors. The first differ in big variety: the cerebral toxoplasmosis, kriptokokkovy meningitis, a gerpesvirusny neuroinfection (surrounding herpes, Cytomegaloviral and gerpesvirusny encephalitis, a Cytomegaloviral poliradikulopatiya gerpesvirusny miyelit also ganglionevrita), the progressing multifocal leykoentsefalopatiya, tubercular defeats of NANOSECOND, neurosyphilis. The most often found tumors of the central NANOSECOND at neuroaIDS are: primary lymphoma of a brain, Berkitt's lymphoma, glioneyroblastoma, disseminirovanny sarcoma of Kaposha.
Primary neuroaIDS often has an asymptomatic subclinical current. In 10-20% of cases neurologic symptoms are debuted in the first 2-6 weeks from HIV infection (the serokonversiya period). During this period against the background of a febrilitet, a limfadenopatiya and skin rashes at a part of patients demonstrate symptoms of aseptic meningitis and a sharp radikulonevropatiya. Other clinical forms of primary neuroaIDS (HIV encephalopathy, VICh-miyelopatiya) arise mainly in the developed HIV infection stage against the background of system manifestations and the expressed immunosupression. Secondary neuroaIDS develops in a phase of simptomny chronic HIV infection (a stage of secondary diseases) which comes during from 2 to 15 years from the moment of the first clinical manifestations. Separate neurologic symptoms (a headache, a polyneuropathy, sleep disorders, an adynamy, a depression, a myopathy) can be caused by toxic anti-retrovirus therapy.
Aseptic meningitis is observed at 5-10% of patients with HIV. The clinical picture corresponds to sharp serous meningitis. Distinctive feature is increase in tserebrospinalny liquid of level of CD8 lymphocytes whereas at viral meningitis of other etiology the quantity of CD4 lymphocytes increases. More rare and severe form is the sharp encephalomeningitis demonstrating mental disorders, tranzitorny violations of consciousness (up to a coma) and epipristupam.
The sharp radikulonevropatiya is connected with a sharp inflammatory demiyelinization of backs of spinal and cranial nerves. Sluggish tetraparesis, polinevritichesky type of violations of sensitivity, a radicular syndrome, defeat front (is more rare than glazodvigatelny) nerves, bulbarny frustration are characteristic. The phase of increase of symptoms can last from several days to one month, then after 2-4 weeks of a stable state regress of symptomatology begins. At 70% of patients with this neuroaIDS form the complete recovery, at 15% - the expressed residual paresis is noted.
HIV encephalopathy is the most frequent display of primary neuroaIDS. Includes cognitive, behavioural and motive frustration. The last are presented by a cerebellar ataxy, a tremor, pyramidal insufficiency, secondary parkinsonism, giperkineza. Separate symptoms and moderate cognitive deficiency are noted approximately at 75% of patients with AIDS. At 3-5% of patients encephalopathy acts as an initial syndrome of neuroaIDS. A morphological substratum is multifocal gigantokletochny encephalitis with defeat of mainly frontal and temporal lobes, subcrustal structures, the bridge and a cerebellum.
VICh-miyelopatiya it is shown by the lower spastic paraparesis and pelvic frustration. Also the calla differs in a slow current and variability of weight of clinical symptoms from slight paresis to a rough plegiya with an incontience of urine. This display of neuroaIDS is noted at 20% of patients with HIV. Morphologically the vakuolization of white spinal substance which is most expressed in chest segments comes to light. However on change backbone MRT often are not fixed.
Vascular neuroaIDS is caused vaskulity cerebral vessels and often leads to development of an ischemic stroke which distinctive feature is the wavy current and frequent transformation in a hemorrhagic stroke. TIA preceding a stroke, and also repeated strokes, owing to multifocal defeat of vessels are characteristic.
Diagnosis of neuroaIDS
Considering frequent occurrence of neuroaIDS, consultation of the neurologist is recommended to all sick with HIV infection. Because as the first symptoms of HIV encephalopathy cognitive violations often act, it is expedient to supplement a research of the neurologic status with neuropsychological inspection. Among practical neurologists there has to be a certain vigilance concerning for the first time the addressed patients from risk groups as neurologic manifestations at them can be symptoms of primary neuroaIDS. In such cases it is necessary to pay attention to presence at the patient of signs of immunosupression and system symptoms (decrease in body weight, a limfadenopatiya, a hair loss, etc.).
Along with obligatory blood tests in diagnosis of HIV infection by IFA, an immunoblotting and definition of virus loading by means of PTsR, in diagnosis of neuroaIDS electrophysiological, tomographic and likvorologichesky methods are widely used. If necessary consultations of the psychiatrist, neurosurgeon, etc. experts are held. Diagnostics and the analysis of results of treatment of defeats of peripheral NANOSECOND at neuroaIDS are performed mainly by means of EFI of neuromuscular system (EMG, ENMG, research VP).
For the purpose of diagnostics of defeats of the central NANOSECOND at neuroaIDS, for the analysis of their current and efficiency of the carried-out therapy methods of a computer tomography and a magnetic and resonant tomography widely are used. KT of a brain is especially informative in diagnostics of secondary volume processes of cerebral localization. Brain MRT visualizes diffusion and melkoochagovy changes (sites of an atrophy and demiyelinization) located in deep departments of a brain the pathological centers more effectively. However results of autopsy show that modern methods of neurovisualization are capable to display not all morphological changes happening in brain fabric at neuroaIDS.
Important value in diagnosis of neuroaIDS has a research of the tserebrospinalny liquid received at a lyumbalny puncture. At seropozitivny patients even in the absence of neurologic symptomatology in a likvor it is often observed moderated , increase in level of protein and decrease in concentration of glucose. In the presence of neurologic manifestation these changes, along with decrease in level of CD4 lymphocytes, speak about possible development of neuroaIDS. Immunological researches of a likvor, as a rule, reveal the increased maintenance of IgG.
Treatment of neuroaIDS
The basis of therapy and prevention of development of neuroaIDS is made by treatment of HIV infection. Effective anti-retrovirus therapy (ART) the pharmaceuticals capable to pass through GEB, allows to block replication of HIV, to stop increase of an immunodeficiency and thus to reduce weight of clinical displays of neuroaIDS, to reduce risk of developing of opportunistic neuroinfections and to increase efficiency of their therapy. Treat the most approved means applied at neuroaIDS a zidovudine, , . Considering toxicity of the majority of anti-retrovirus medicines, the ART is appointed according to individually picked up scheme only in the presence of indications and with the consent of the patient.
About the ART specific and symptomatic therapy of the arisen neuroaIDS clinical form is performed. So, at HIV encephalopathy apply it is well-cared and soft nootropa (, , piracetam, feninut), at a stroke — anticoagulants and , at a polyneuropathy — , the combined medicines of vitamins of group B, at sharp mental violations — antipsychotic means (clozapine). At defeats of peripheral NANOSECOND efficiency of a plasma exchange is noted. In treatment of myopathies use a plasma exchange and kortikosteroidny therapy.
At opportunistic neuroinfections apply etiotropny medicines: at kriptokokovy meningitis — with amfoteritsiny, toksoplazmenny encephalitis — , , , at herpetic defeats — an acyclovir, , , , . Treatment of the tumors arising as display of secondary neuroaIDS can demand surgical intervention. The question of need of operation is considered together with the neurosurgeon.