in the previous issue of critical care , chen and colleagues investigate whether hydrocortisone influences the neurological outcome and mortality in a rat model of traumatic brain injury ( tbi)-induced critical illness - related corticosteroid insufficiency ( circi ) . up to 30 to 80% of tbi patients circi has been studied in sepsis but received much less attention after tbi , despite the fact that its incidence seems high . the authors postulated that early recognition of circi after tbi and treatment with corticosteroids may improve neurological outcome . this may prove important since bombardier and colleagues have shown that 51.3% of patients met the criteria for major depressive disorders during the first year after tbi . in the present study , chen and colleagues nicely demonstrate in a rat model of tbi that treating circi with hydrocortisone improves neurological recovery by blocking neuronal apoptosis , and reducing damage of the tight junction . interestingly , the authors also show that a synthetic glucocorticoid ( methylprednisolone ) did not alter neurological outcomes or mortality . hyponatremia is frequent after tbi , and recent evidence showed that mild hypernatremia could decrease the intracranial pressure , improving the cerebral perfusion pressure . second , after initial tbi , the exaggerated inflammatory response may cause circi by altering the function of the hypothalamic  pituitary  adrenal axis . tumour necrosis factor and interleukin ( il)-6 are increased in tbi or septic shock associated with circi . in particular , hoen and colleagues have shown that blood il-6 was significantly higher in severe trauma patients with circi as compared with patients without circi . it is well known that hydrocortisone decreases the production of these inflammatory cytokines , but recent evidence permits a reappraisal of the properties of hydrocortisone regarding the inflammatory response . in septic patients , hydrocortisone decreased the blood level of the anti - inflammatory cytokines ( il-10 ) and increased the blood levels of il-12 ( cytokine - enhancing immune response against bacterial infection ) without inducing immunosuppression . these data suggest that hydrocortisone is able to restore a balanced inflammatory response rather than inducing immunosuppression . third , corticosteroids are believed to be potent inducers of apoptosis mainly by a shutdown of the inflammatory response through inhibition of the nf-b pathway , which promotes survival of cells generally . these data were provided mainly with a high dose of synthetic glucocorticoids in patients with cancer or solid organ transplantation , but few data were published with hydrocortisone . chen and colleagues show that hydrocortisone prevents neuronal apoptosis even if the exact mechanism for this novel property of the drug remains largely unknown . the authors also demonstrate that hydrocortisone but not methylprednisolone improves neurological outcomes and prevents mortality in tbi rats . however , the benefit of corticosteroids in tbi patients remains controversial . in the crash study , a high dose of methylprednisolone worsened mortality as compared with placebo , and it was also speculated that hydrocortisone might increase the rate of secondary infections . in a recent cochrane systematic review , a stress dose of hydrocortisone ( 200 to 300  mg / day ) did not increase the rate of infection as compared with placebo in septic shock patients . in the hypolyte study involving severe trauma patients , including 65% tbi patients , the results obtained with hydrocortisone were spectacular in circi patients , whereas in the a priori planned subgroup analysis the treatment was particularly efficient in the tbi patients . answering the question of whether we should use hydrocortisone in tbi patients remains a subject of hard debate . detecting circi to select patients eligible for hydrocortisone treatment shows promise . the results of a large randomized multicenter study ( corti - tc ) will provide valuable data on the effects of hydrocortisone in severe tbi patients . circi : critical illness - related corticosteroid insufficiency ; il : interleukin ; tbi : traumatic brain injury .
data suggest that treatment of critical illness - related corticosteroid insufficiency after traumatic brain injury ( tbi ) with a stress dose of hydrocortisone may improve the neurological outcome and the mortality rate . 
 the mineralocorticoid properties of hydrocortisone may reduce the rate of hyponatremia and of brain swelling . 
 the exaggerated inflammatory response may cause critical illness - related corticosteroid insufficiency by altering the function of the hypothalamic  pituitary  adrenal axis , and hydrocortisone is able to restore a balanced inflammatory response rather than inducing immunosuppression . 
 hydrocortisone could also prevent neuronal apoptosis . 
 considering side effects , corticosteroids are not equal ; when a high dose of synthetic corticosteroids seems detrimental , a strategy using a stress dose of hydrocortisone seems attractive . 
 finally , results from a large multicenter study are needed to close the debate regarding the use of hydrocortisone in tbi patients .