The use of erythtropoietin in cerebral diseases.

Global and focal cerebral ischemia is followed by a secondary damage characterized by oxidative stress, excitotoxicity, inflammation and apoptosis. Erythropoietin (EPO) exerts antiapoptotic, anti-inflammatory, antioxidative, angiogenetic and neurotrophic properties. Its potential therapeutic role has been demonstrated in several animal models of cerebral ischemia and also in a clinical trial of ischemic stroke, so it could be considered an ideal compound for neuroprotection in ischemic stroke and in cardiac arrest. Intracerebral hemorrhage (ICH) is the least treatable form of stroke; the mechanisms involved in the secondary brain injury include hematoma mass effect, neuronal apoptosis and necrosis, inflammation. It has been demonstrated in an experimental ICH that EPO intervenes in the inflammatory process, reduces brain water content, hemorrhage volume and hemispheric atrophy, promotes cell survival, preserves cerebral blood flow, has antiapoptotic protective function against oxidative stress and excitotoxic damage. EPO can attenuate acute vasoconstriction and prevent brain ischemic damage in subarachnoid hemorrhage. The neuroprotective function of EPO has been studied also in traumatic brain injury: it reduces the inflammation and improves cognitive and motor deficits. The authors review some of the physiological actions of EPO in the physiopathology of ischemic and hemorrhagic stroke, subarachnoid hemorrhage and brain trauma, and its potential usefulness in the brain injured patient management.

Elevated S100B levels do not correlate with the severity of encephalopathy during sepsis.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is defined as a diffuse cerebral dysfunction induced by the systemic response to infection without any clinical or laboratory evidence of direct infectious involvement of the central nervous system. The astroglial protein S100B has been used as a marker of severity of brain injury and as a prognostic index in trauma patients and cardiac arrest survivors. We measured S100B serum levels in patients with severe sepsis to investigate if the severity of SAE correlated with an increase in S100B levels. METHODS: Twenty-one patients, with a diagnosis of severe sepsis, were included in this study. S100B levels were measured at intensive care unit (ICU) admission, 72 h and 7 days after admission. Their association with markers of brain dysfunction such as Glasgow coma scale (GCS), and EEG, and with sepsis-related organ failure assessment score (SOFA) and ICU mortality was investigated. RESULTS: Fourteen patients had elevated S100B levels. The levels did not correlate with GCS at admission, EEG pattern, or SOFA scores. Also, S100B levels did not differ between patients who recovered neurologically and those who did not (P = 0.62). CONCLUSIONS: In severe sepsis, an increase in S100B does not allow the physicians to distinguish patients with severe impairment of consciousness from those with milder derangements or to prognosticate neurological recovery.

S100B is not a reliable prognostic index in paediatric TBI.

BACKGROUND: As far as paediatric traumatic brain injury is concerned, it is difficult to quantify the extent of the primary insult, to monitor secondary changes and to predict neurological outcomes by means of the currently used diagnostic tools: physical examination, Glasgow Coma Scale (GCS) score and computed tomography. For this reason, several papers focused on the use of biochemical markers (S100B, neuron-specific enolase) to detect and define the severity of brain damage and predict outcome after traumatic head injury or cardiac arrest. OBJECTIVE: The aim of this paper is measuring the range of S100B serum concentrations in children affected by traumatic brain injury and describing the possible roles of this protein in the reaction to trauma. METHODS: Fifteen children aged 1-15 years were included in the study. Traumatic brain injury severity was defined by paediatric GCS score as mild (9 patients), moderate (2 patients) or severe (4 patients). Blood samples for S100B serum measurement were taken at emergency department admission and after 48 h. RESULTS: The serum S100B concentration was higher in the group of severe trauma patients, who scored the lowest on the GCS at admission, and among them, the highest values were reported by the children with concomitant peripheral lesions. CONCLUSIONS: The role of S100B in paediatric traumatic brain injury has not been clarified yet, and the interpretation of its increase when the head trauma is associated with other injuries needs the understanding of the physiopathological mechanisms that rule its release in the systemic circulation. The levels of S100B in serum after a brain injury could be related to the mechanical discharge from a destroyed blood-brain barrier, or they could be due to the active expression by the brain, as a part of its involvement in the systemic inflammatory reaction. Early increase of this protein is not a reliable prognostic index of neurological outcome after pediatric traumatic brain injury, since even very elevated values are compatible with a complete neurological recovery.

S100B is a sensitive but not specific prognostic index in comatose patients after cardiac arrest.

AIM: The aim of this study was to compare serum S100B levels and EEG findings as prognostic indexes in comatose (GCS<8) patients after cardiac arrest. METHODS: S100B serum levels were assessed 12 h after the event and EEG findings were recorded within 24 h in comatose cardiac arrest survivors. At hospital discharge, patients were divided into groups according the Glasgow-outcome scale (GOS): group 1 with bad neurological outcome and group 2 with good neurological outcome (GOS 4-5). S100B levels and EEG findings were retrospectively tested about their predictive value. RESULTS: S100B has a very low specificity (37.5%) while S100B sensitivity is 100%. EEG findings specificity is 75% and sensitivity 50%. S100B was not significantly lower in patients who recovered consciousness (10 patients) and there was no significant difference in EEGs findings between group 1 and 2. CONCLUSIONS: The association of serum S100B levels with EEG might be helpful when used together to formulate outcome in comatose patients within 24 h after cardiac arrest. However, increased levels of S100B 12 h after a cardiac arrest might be expression of a still amendable brain damage.