[FIRES Syndrome in a Preschool Child]. / Sindrom FIRES u doshkol'nika.

Severe epileptic syndromes of childhood are an urgent problem for pediatric neurologists and neuroresuscitators. The article presents a clinical observation of FIRES syndrome in a pediatric patient, which is a form of severe drug-resistant epilepsy in children of preschool and school age, the development of which is caused by hyperthermia, probably associated with herpesvirus (human herpesvirus type 6) infection. The features of the progressive course and the difficulties of diagnostic search are reflected. An empirical approach to etiotropic therapy is described, since the disease manifested itself with respiratory manifestations and fever. The tactic of pathogenetic treatment is described, in which drugs of polyfunctional action, such as Cytoflavin, have a priority, many years of experience in the use of which allows the authors to recommend it as a starting intensive therapy.

[Clinical-etiological and MRI parallels of encephalitis in children]. / Kliniko-etiologicheskie i MRT paralleli entsefalitov u detei.

OBJECTIVE: Improving the diagnosis of encephalitis (EF) in children by establishing clinical, etiological and MRI parallels. MATERIAL AND METHODS: 364 children aged from 1 month to 17 years with EF were examined. MRI of the brain and spinal cord, blood and CSF examination for herpes viruses type 1-6 (HHV), enteroviruses (EV), tick-borne encephalitis viruses (TBEV), Borrelia burgdorferi (BB), varicella zoster (VVZ), herpes simplex (HSV1) and Epstein-Barr (EBV) were performed. RESULTS: The etiological structure was dominated by HHV types 1-6, tick-borne infections (19%), EV (14.6%), and other agents (6%). Clinical and topical variants of EF: leukoencephalitis (leukoePH) - 68.4%, polyoencephalitis (polioePH) - 22.8% and panencephalitis (panePH) - 8.8%. LEUKOEPH was more often caused by VVZ, EBV and BB, foci in the white matter of the large hemispheres, sensitive, cerebellar and pyramidal symptoms, acute course followed by complete recovery (65.8%), the risk of exacerbations and progression with the development of multiple sclerosis in 6% were observed in 80.7%. POLIO in 71.1% were caused by TBEV or EV, lesions were located in the thalamus, basal ganglia, cortex, manifested by deep depression of consciousness, epilepsy, central paralysis and speech disorders, in 83.1% there was a chronic course with the development of brain atrophy. PanEF was caused by cytomegalovirus in more than 1/2 of cases, with subtotal-total white matter damage, in 1/3 of cases - with the involvement of other structures, there was a chronic course with polymorphism of neurological symptoms, rare complete recovery (15.6%). The cerebellar form of EF in 88.7% was associated with VZV, subcortical and stem - with TBEV and EV, cortical and limbic - with HSV-1 and 2 and HHV-6. The outcomes of EF depend both on the timeliness of etiological and neuroimaging diagnostics, and on the adequacy of early therapy already with EF, including the use of acyclovir in combination with recombinant interferons alpha-2-ß with antioxidants, and the immediate appointment of Cytoflavin infusions upon admission to the hospital. CONCLUSIONS: Clinical and topical variants and forms of EF in children are associated with etiology, have different rates of complications, the nature of the course and outcomes, the knowledge of which makes it possible to optimize the diagnostic process.