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This exaggerated response is phenotypically seen both in acute and chronic brain dysfunction after a systemic LPS challenge.
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A cortisol cut-off value of 232 nmol/L determined brain dysfunction after sedation withdrawal with a sensitivity 59% and a specificity 63%.
Cerebral microdialysis (CMD) has largely contributed to a better understanding of the pathophysiology of acute brain dysfunction after TBI and was introduced recently as an additional bedside neuromonitoring tool in this context.
A brain MRI should be considered in case of persistent brain dysfunction after control of sepsis and exclusion of major confounding factors.
The purpose of this review is to discuss recent developments in our understanding of the pathophysiologic mechanisms, prevention, and treatments that have been designed to ameliorate brain dysfunction after cardiac surgery.
Microglia activation is not only relevant to the acute phase of brain dysfunction after sepsis.
Nox2 is essential for glial cell activation and emphasize the critical role of oxidative damage and Nox2-derived ROS as central factors contributing to acute and long-term brain dysfunction after sepsis [128].
We did not assess our patients for minor brain dysfunction after hypoglycaemia.
Only difference in age was found with regard to brain dysfunction after sedation withdrawal.
One-half of patients who were generally called full recovery could not work as they did before because they had higher brain dysfunction after resuscitation.
Such evidence suggests that ALI might have implications on brain dysfunction after intensive care unit stay, but such involvement is as yet poorly understood.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com