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Introduction By maintaining sufficient cerebral blood flow and oxygenation, the goal of cardiopulmonary resuscitation (CPR) is to preserve the pre-arrest neurological state. To date, cerebral monitoring abilities during CPR have been limited. Therefore, we investigated the time-course of cerebral oxygen saturation values (rSO2) during advanced life support in out-of-hospital cardiac arrest. Our primary aim was to compare rSO2 values during advanced life support from patients with return of spontaneous circulation (ROSC) to patients who did not achieve ROSC. Methods We performed an observational study to measure rSO2 using Equanox™ (Nonin, Plymouth, MI) from the start of advanced life support in the pre-hospital setting. Results rSO2 of 49 consecutive out-of-hospital cardiac arrest patients were analyzed. The total increase from initial rSO2 value until two minutes before ROSC or end of advanced life support efforts was significantly larger in the group with ROSC 16% (9 to 36) compared to the patients without ROSC 10% (4 to 15) (P = 0.02). Mean rSO2 from the start of measurement until two minutes before ROSC or until termination of advanced life support was higher in patients with ROSC than in those without, namely 39% ± 7 and 31% ± 4 (P = 0.05) respectively. Conclusions During pre-hospital advanced life support, higher increases in rSO2 are observed in patients attaining ROSC, even before ROSC was clinically determined. Our findings suggest that rSO2 could be used in the future to guide patient tailored treatment during cardiac arrest and could therefore be a surrogate marker of the systemic oxygenation state of the patient.

Standard clinical practice in patients with elevated intracranial pressure (ICP) is to keep cerebral perfusion pressure (CPP) at (or above) 60 mmHg: we performed this retrospective study to analyze whether induction of barbiturate coma impedes compliance to this target CPP value. It has been repetitively shown that, although proven as an efficient therapy for refractory elevated ICP, barbiturate coma may cause a decrease in mean arterial pressure (MAP) and CPP [1].

Cerebral oximetry, using near-infrared spectroscopy to measure cerebral tissue oxygen saturation (SctO2), is being increasingly used in the ICU. We hypothesized that if a patient becomes brain dead in the ICU, this must be reflected in SctO2 values. This might help in the timing of invasive procedures such as angiography, sometimes necessary in the confirmation of brain death.

Since catecholamines have been shown to modulate various immunological functions, the goal of this work was to investigate their effects on staurosporin-induced apoptosis of Jurkat T cells, a well-established model for human T lymphocytes.

Elevated levels of neuron-specific proteins, such as neuron-specific enolase (NSE) and/or neuromodulin in serum or cerebrospinal fluid (CSF) of brain trauma patients are of prognostic value for the patients' outcome. Recently tau, a neuron-specific microtubule-associated protein, has been found to be elevated in CSF of Alzheimer patients. This elevation is at least partially due to loss of neuronal cells. Until now tau has not been detected in serum. Therefore, we investigated whether tau in serum or CSF can be used as a marker for neuronal loss in patients with various forms of acute cerebral injury.