S100B is not a reliable prognostic index in paediatric TBI.

Pediatr Neurosurg. 2007;43(4):258-64

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

Sepsis associated encephalopathy studied by MRI and cerebral spinal fluid S100B measurement.

he pathogenesis of sepsis associated encephalopathy (SAE) is not yet clear: the blood-brain barrier (BBB) disruption has been indicated among the possible causative mechanisms. S100B, a calcium binding protein, originates in the central nervous system but it can be also produced by extra-cerebral sources; it is passively released from damaged glial cells and neurons; it has limited passage through the BBB. We aimed to demonstrate BBB damage as part of the pathogenesis of SAE by cerebral spinal fluid (CSF) and serum S100B measurements and by magnetic resonance imaging (MRI). This paper describes four septic patients in whom SAE was clinically evident, who underwent MRI and S100B measurement. We have not found any evidence of CSF-S100B increase. Serum S100B increase was found in three out of four patients. MRI did not identify images attributable to BBB disruption but vasogenic edema, probably caused by an alteration of autoregulation, was diagnosed. S100B does not increase in CSF of septic patients; S100B increase in serum may be due to extracerebral sources and does not prove any injury of BBB. MRI can exclude other cerebral pathologies causing brain dysfunction but is not specific of SAE. BBB damage may be numbered among the contributors of SAE, which aetiology is certainly multifactorial: an interplay between the toxic mediators involved in sepsis and the indirect effects of hyperthermia, hypossia and hypoperfusion