OBJECTIVES: The S100B protein subgroup is a thermolabile acidic calcium-binding protein. S100B protein was first described in the central nervous system. Destruction of the nerve tissue results in S100B protein release from astrocytic glial cells and elevation of its levels in the cerebrospinal fluid. If the blood-brain barrier is also damaged, S100B gets into the systemic circulation and elevated blood levels of S100B are detected. Higher S100B serum levels in patients with head injury are predictive of possible development of secondary brain injury and the extent of permanent injury to the CNS. MATHERIAL AND METHODS: The authors present their results obtained in the group of 39 children aged 0 (newborns) to 17 years with isolated craniocerebral injury. RESULTS: Our group included 39 children aged 0-17 years. Excellent results (GOS - Glasgow outcome scale 4-5) were observed in 33 patients already at the time of transfer from our ICU to the neurological department. There was no death and the poor outcome group included only 6 children. Second GOS evaluation was performed 6 months later, when 36 children were in the GOS 4-5 group and only 3 children in the GOS 2-3 group. CONCLUSIONS: Due to high variability in S100B protein serum levels in children depending on age and gender, no correlation between...

Abstract Head injury is the leading cause of death and disability in trauma patients, and alcohol misuse is often associated with such injuries. Despite modern diagnostic facilities, the extent of traumatic brain injury (TBI) is difficult to assess and supplementary diagnostic tools are warranted. The contribution of alcohol misuse to traumas also needs to be elucidated, as the role of different patterns of alcohol drinking in particular has received less attention. We investigated the clinical utility of a novel serum marker of brain damage, protein S100B, as a tool for assessing TBI in patients with trauma. We also investigated the patterns of alcohol drinking among trauma patients and the trauma mechanisms in relation to blood alcohol concentration (BAC), with special emphasis on head traumas. Finally, we studied the early identification of hazardous drinkers among trauma patients. Serum protein S100B was found to be a feasible supplementary method for assessing TBI, as the latter was shown to elevate its levels significantly, the highest values being found in patients with severe injuries. S100B was also found to be elevated in patients with mild head injury, where it was associated with an increased risk of developing post-concussion symptoms (PCSs). Extracranial injuries also increased S100B values in patients with multitrauma. Accordingly, S100B was not specific to TBI. The more severe the extracranial injury, the higher the S100B value that was found. Binge drinking was found to be the predominant pattern in trauma patients. Alcohol intoxication on admission and hazardous drinking patterns were more often present in patients with head injury than in those with other types of trauma. The risk of sustaining a head trauma significantly increased with increasing BAC. The results also demonstrated that BAC on admission is the best marker of alcohol misuse in trauma patients. The BAC test depicts hazardous alcohol drinking better than conventional biochemical markers of alcohol misuse such as gamma-glutamyl transpeptidase (GGT), aspartate aminotransferase (AST), carbohydrate-deficient transferrin (CDT), or mean corpuscular volume (MCV) of erythrocytes. The findings support the use of S100B as a supplementary method for assessing TBI and the use of BAC as a marker of alcohol misuse in trauma patients.

Die vorliegende Arbeit setzt sich mit den funktionellen und strukturellen Veränderungen im Zentralnervensystem im Zusammenhang mit angeborenen Vitien und deren chirurgischer Behandlung mit Hilfe der extrakorporalen Zirkulation (EKZ) sowohl klinisch als auch tierexperimentell auseinander mit dem Ziel, neuroprotektive Strategien zu entwickeln. Wir haben mit den verfügbaren Methoden der Neuroüberwachung die charakteristischen Verläufe definiert und beschrieben. Zusätzlich wurden diese nicht-invasiven Methoden wie die Nahinfrarot-Spektroskopie sowohl klinisch als auch tierexperimentell validisiert. Es konnte jedoch gezeigt werden, dass diese Methoden eine zuverlässig signifikante globale Alteration in der Oxygenation und Perfusion anzeigen. Durch das Erarbeiten und die Charakterisierung des Verlaufs der Serumwerte des astroglialen Proteins S-100B wurde die klinische Wertigkeit genauer definiert. Es konnte klinisch und tierexperimentell gezeigt werden, dass die abnorm erhöhten Werte des S-100B im Serum von einem signifikanten diagnostischen Wert sind. Im Gegensatz dazu wurde die untergeordnete Rolle der Bestimmung von neuronalen Marker im Serum bestätigt. Durch die tierexperimentellen Arbeiten wurde gezeigt, dass die überwiegenden morphologischen Veränderungen nach EKZ im Gehirn in den Astrozyten und Gliazelen zu finden sind. Die neuronale Zelldegeneration war nach dem tiefhypothermen Kreislaufstillstand überwiegend in Form von hypoxischer Zellnekrose. Die apoptotische Zelldegeneration trat zellspezifisch im Gyrus Dentatus des Hippocampus auf. Vor allem konnte die bedeutende protektive Rolle der Hypothermie und der hypothermen Perfusion der EKZ demonstriert werden. Bei einer effektiven systemischen Kühlung an der EKZ könnte ein Kreislaufstillstand ohne signifikante neuronale Schädigungen überstanden werden. Die EKZ und der tiefhypotherme Kreislaufstillstand stellen an sich für das unreife Gehirn eine grobe nicht-physiologische Situation dar. Im Tiermodel könnte histologisch gezeigt werden, das die systemische Vorbehandlung mit Methylprednisolone keine protektive Wirkung hat. Obwohl eine signifikante Neuroprotektion durch Gabe von FK506 und Cyclosporin unter extremen Bedingungen der EKZ und tiefhypothermem Kreislaufstillstand erzielt wurde, bedarf es vor einer klinischen Anwendung weiterer tierexperimenteller und klinischer Überprüfungen. / The aim of our clinical and experimental studies was to evaluate functional and structural changes in the brain during corrective cardiac surgery using cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) in order to develop neuroprotective strategies. Using the available neurmonitoring methods such as the transcranial Doppler and near infrared spectroscopy (NIRS) characteristic changes in cerebral perfusion and oxygenation were defined and described according to the changes in hemodynamic parameters such perfusion pressure, temperature and flow rate. The diagnostic value of the astrocytic cell protein S100B was evaluated by measurement of the serum concentrations in infants and children with and without neurological complications. Additionally, the normal and abnormal release patterns were evaluated in experimental setting using an animal model of CPB and DHCA. According to the neuropathological assessment of the brain initial morphological changes were found predominantly in the astroglial cells. Systemic hypothermic perfusion on CPB before the induction of circulatory arrest period of 60 minutes was significantly protective. Ischemic neuronal injury in form of cell nekrosis was found in different brain region particularly after the prolongation of circulatory arrest time in deep hypothermia. The apoptotic cell death was found predominantly in the hippocampal region of the dentate gyrus. The routinely prophylactic systemic use steroid during cardiac surgery is not protective against ischemia and has been found to induce apoptosis in the hippocampus. In the same model the systemic pre-treatment with single high dose of Cyclosporin and FK506 decreased significantly the ischemic neuronal cell injury in different brain region. However, before clinical use further studies are necessary to optimise the dose and mode of application.