Encephalitis — inflammatory damage of substance of a brain which is caused by viruses, more rare other infectious agents (for example, a mycoplasma or rickettsiae). Allocate primary encephalitis connected with direct penetration of the infectious agent possessing property of a neyrotropnost through a blood-brain barrier, and secondary encephalitis arising after an infection or vaccination, usually in connection with development of autoimmune process. At primary encephalitis (for example, at herpetic or tick-borne encephalitis) gray matter of a brain more is surprised (polioencephalitis), at secondary encephalitis — white matter (leukoencephalitis). When at the same time are surprised gray and white matter of a brain, speak about a panencephalitis. Pathological process at encephalitis can be focal (for example, it can be limited only to a brainstem or even its small part), but it is more often happens multifocal (multifocal) or diffusion. On a current allocate acute, subacute and chronic encephalitis. The clinical picture of encephalitis consists of all-infectious, meningeal, all-brain and focal neurologic manifestations. Against fever, a headache, nausea, vomiting, rigidities of cervical muscles and other meningeal signs at encephalitis are found signs of defeat of a parenchyma of a brain: confusion or oppression of consciousness, disorientation, psychotic frustration, epileptic seizures. Symptoms of focal defeat of a nervous system (gemi-or tetraparesis, damages of cranial nerves, aphasia, an ataxy, sensitivity disturbances) which can meet in the most various combination join. At research TsSZh in case of viral encephalitis usually find supertension, moderate increase in a cytosis (to several tens or hundreds of cells), mainly at the expense of lymphocytes, and also moderate increase of protein content and normal content of glucose. Identification of a normal cytosis, though does not exclude the diagnosis of viral encephalitis, has to stimulate search of noninfectious pathology (for example, a vasculitis, intoxication, a brain tumor). Apply virologic or serological methods to establishment of an etiology of encephalitis, however their results become known only several weeks later after the beginning of a disease. In recent years more and more wide circulation gets a definition method in the virus TsSZh DNA by means of the polimerazny chain reaction (PCR) allowing to establish an encephalitis etiology in the first days of a disease.
Etiology and pathogeny.
The causative agent of herpetic encephalitis is the herpes simplex virus like I which also causes herpetic rashes on a mucous membrane of an oral cavity. Herpetic encephalitis meets evenly during the whole year, affecting people of all age. In most cases it develops at persons without strong indications of an immunodeficiency. The virus of herpes is capable is long to persistirovat in a human body, mainly in neurons sensitive gangliyev, including a trifacial ganglion, becoming more active in certain conditions. Approximately in 1\3 cases encephalitis is result of new infection with a virus (usually at persons till 18 flyings), and in the remained cases — result of local reactivation of latent infection in brain cells. Originally the temporal share on the one hand is involved in process, and then defeat extends also to other party, leading to emergence of the multiple centers of a hemorrhagic necrosis.
The disease usually begins sharply, with fever, a headache, the general weakness, nausea, vomiting. Sometimes these symptoms are preceded by symptoms of an upper respiratory tract infection (cold, cough). The neurologic symptomatology can develop sharply or gradually. The clinical originality of herpetic encephalitis depends on preferential localization of the centers in temporal or frontal shares which signs of defeat are aphasia, olfactory or flavoring hallucinations, an anosmia, changes of behavior, memory disturbance, vegetative frustration, epileptic seizures. Quite often also other focal syndromes develop: hemiparesis, damages of cranial nerves. At most of patients meningeal symptoms come to light. It is necessary to emphasize that herpes labialis is absent at most of patients with herpetic encephalitis, but can appear at any feverish disease. The heavy current is characteristic of herpetic encephalitis. For lack of treatment the state continues to worsen for several days or weeks, the coma develops and in 50 — 70% of cases there comes the lethal outcome. But even at use of an acyclovir not less than at a half of patients rough neurologic and mental disorders develop (amnesia, aphasia, dementia, changes of the personality, epilepsy, paresis).
At research TsSZh reveal increase of pressure, a lymphocytic pleocytosis (on average 50 — 100 cells in 1 mkl), moderate increase of concentration of protein, normal content of glucose, sometimes erythrocytes and a xanthochromia that reflects hemorrhagic nature of defeat. At EEG focal changes in front departments of a brain (frontotemporal area) in the form of medlennovolnovy activity or epileptiform categories are registered. Focal changes in substance of a brain can be revealed by means of a computer or magnetic and resonant tomography. In this regard crucial importance in diagnosis of herpetic encephalitis belongs to virologic and serological methods. But the fastest and reliable diagnostic method of herpetic encephalitis is PTsR defining existence of DNA of a virus in TsSZh now. Polimerazny chain reaction becomes positive in the first days after emergence of neurologic symptomatology.
Patients with herpetic encephalitis of a nekontagiozna also do not demand isolation. In most cases they are placed in an intensive care unit. Treatment is carried out by antiviral drug the acyclovir suppressing synthesis of DNA of viruses of herpes and tearing off their reproduction. The drug is administered intravenously kapelno in a single dose of 10 mg/kg by 3 times a day within 10 — 14 days. Introduction of an acyclovir allowed to reduce more than twice lethality level at herpetic encephalitis. But drug is effective only on condition of earlier initiation of treatment (at least before development of a coma). Therefore it is accepted to appoint it at the slightest clinical suspicion to herpetic encephalitis. Also pathogenetic and symptomatic therapy directed to maintenance of functions of breath and cardiovascular activity, water and electrolytic balance, cerebral decompression, prevention and treatment of secondary bacterial and trophic complications (aspiration pneumonia, decubituses, an uric infection, etc.), a shin deep vein thrombosis is important. At epileptic seizures appoint antiepileptic means. Early rehabilitation therapy also allows to improve a disease outcome.