***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Introduction Subarachnoid haemorrhage ( SAH ) may damage the hypothalamo-pituitary-adrenal gl and ( HPA ) axis and disturb cortisol metabolism . There are no available data that relates to the response of the HPA axis in the acute phase of SAH . We aim ed to characterise the behavior of serum adrenocorticotropic hormone ( ACTH ) , total cortisol , stimulated total cortisol and free cortisol concentrations in acute aneurysmal SAH . Methods A prospect i ve cohort study was conducted of patients with acute aneurysmal SAH ( n = 30 ) admitted to a tertiary university hospital . Patients admitted for elective aneurysmal surgery ( n = 16 ) served as the control group . An ACTH stimulation test was performed twice during the first week and at three months . The main outcome measure was description of the ACTH-cortisol response by calculating serum free cortisol and measuring total cortisol and ACTH concentrations . A mixed models method was used for testing between the groups , allowing heterogeneity between the groups . Results Patients with SAH had higher initial serum total cortisol ( mean + /- SD ; 793 + /- 312 nmol/L ) and free cortisol concentrations ( 83 + /- 55 nmol/L ) than control patients ( 535 + /- 193 nmol/L , p = 0.001 and 33 + /- 18 nmol/L , p < 0.001 , respectively ) . Thereafter , there were no differences in this respect . Serum free and total cortisol concentrations correlated but were unaffected by the severity of SAH . ACTH concentrations were comparable between SAH and control groups . Patients with Hunt-Hess grade s IV to V had higher ACTH concentrations at day one ( 10.7 + /- 7.1 pmol/l/L ) and day five ( 8.2 + /- 7.7 pmol/L ) than patients with grade I-III ( day one : 3.8 + /- 2.0 pmol/L , p = 0.002 ; day five : 4.7 + /- 1.8 pmol/L , p = 0.04 ) . Conclusions Calculation of serum free cortisol concentration was not helpful in identifying patients with potential hypocortisolism . SAH severity did not affect cortisol concentrations , possibly indicating relative pituitary-adrenal insufficiency in patients with more severe bleeding . Trial registration Clinical Trials.gov Identifier NCT00614887 Background Neuroendocrine changes have been reported after ischemic stroke , subarachnoid hemorrhage , and brain trauma . As there are no corresponding data in patients with intracerebral hemorrhage ( ICH ) we analyzed various neuroendocrine parameters to investigate possible alterations in hormone profiles of patients with ICH . Methods Twenty patients with ICH were prospect ively enrolled in the study . Patients were a priori parted into two groups : Ten non-ventilated patients treated on the stroke-unit ( hemorrhage volumes < 20 ml , “ small ICH ” ) , and 10 ventilated patients treated on the neurocritical care unit ( hematoma volumes > 20 ml with possible additional ventricular involvement ( “ large ICH ” ) . Neuroendocrine parameters were compared between both groups referring to reference values . The following parameters were obtained over a period of 9 days in 20 patients with spontaneous supratentorial ICH : thyrotropin , free thiiodothyronine and thyroxine , human growth hormone , insulin-like growth factor 1 , luteinizing hormone , follicle-stimulating hormone , testosterone , prolactin , adrenocorticotropic hormone , and cortisol . Results Small ICH patients were in a median 71 ( 54–88 ) years old and had a mean ICH volume of 9.5 ± 6.5 ml , whereas large ICH patients were 65 ( 47–80 ) years old and showed a mean volume of 56 ± 30.2 ml . None of the patients revealed pathological alterations for thyrotropin , free thiiodothyronine , thyroxine , human growth hormone , insulin-like growth factor 1 , and testosterone . There was only a mild decrease of adrenocorticotropic hormone and cortisol on day 3 in large ICH patients . Small ICH patients showed pathologically elevated levels of luteinizing and follicle-stimulating hormone throughout the observation period . Large ICH patients showed a marked increase of prolactin that developed during the course . Conclusions Overall , neuroendocrine changes in ICH patients are not as profound as reported for ischemic stroke or subarachnoid hemorrhage . The clinical significance of increased LH and FSH levels in small ICH is unclear , whereas elevation of prolactin in large ICH was anticipated . Future r and omized controlled trials should also focus on neuroendocrine parameters to clarify the impact of possible hormonal alterations on functional outcome Background and Purpose — & agr;-Melanocyte stimulating hormone ( & agr;-MSH ) is an endogenously produced neuropeptide derived from the same precursor as adrenocorticotropic hormone . & agr;-MSH has profound immunomodulatory properties and may also be neuroprotective . Nothing is known about & agr;-MSH and changes in its plasma concentrations in patients with acute ischemic stroke . Methods — In this prospect i ve observational study , plasma concentrations of & agr;-MSH , adrenocorticotropic hormone , cortisol , and interleukin 6 were assessed longitudinally over the course of 1 year after stroke onset in 111 patients .  Logistic regression was used to the effect of initial plasma & agr;-MSH , adrenocorticotropic hormone , cortisol , and interleukin 6 on long-term outcome . Results — There was an early decrease in plasma & agr;-MSH in patients with severe stroke ( National Institutes of Health Stroke Scale ≥17 ) that normalized over the course of the year ; these same patients evidence d elevations in plasma cortisol and interleukin 6 . Higher initial plasma & agr;-MSH , but not adrenocorticotropic hormone , cortisol , or interleukin 6 , was independently predictive of good long-term outcome . Conclusions — This research is the first to study endogenous changes in plasma & agr;-MSH after stroke . The independent effect of early plasma & agr;-MSH on stroke outcome , as well as a growing body of experimental data demonstrating improved stroke outcome with exogenous & agr;-MSH administration , suggests a potential therapeutic role for & agr;-MSH in the treatment of stroke Altered hypothalamo-pituitary-adrenal axis was reported in stroke patients ; however , mechanisms responsible for this phenomenon are barely understood . Acute cerebral ischemia triggers interleukin-6 ( IL-6 ) release into blood . Circulating IL-6 can stimulate hypothalamo-pituitary-adrenal axis . The goal of our study was to assess a relationship between serum IL-6 and cortisol in acute ischemic stroke . Twenty two patients with ischemic stroke and 17 controls were included . Serum sample s were collected on the 2nd day of stroke at 6:00 , 10:00 18:00 , 22:00 h and at the same time points in control group . Cytokines and cortisol levels were measured using ELISA method .  Serum IL-6 and cortisol levels were higher in stroke patients than in controls . Cortisol displayed diurnal variations in both stroke patients and controls . In contrast with control subjects , serum IL-6 levels did not display diurnal variations in stroke patients . In stroke patients , but not in controls , IL-6 level correlated significantly with cortisol level and morning serum IL-6 level independently predicted evening/night cortisol level . In conclusion , brain ischemia could stimulate IL-6 release in blood and in this way modulate hypothalamo-pituitary-adrenal axis Background and Purpose : Experimental and clinical data suggest that overactivation of the sympathetic nerve system ( SNS ) is an essential mediator of stroke-induced immunodepression , which in turn increases susceptibility to post-stroke infections . In a post hoc analysis of the PANTHERIS ( Preventive Antibacterial Treatment in Acute Stroke ) trial , we investigated the impact of distinct lesion patterns on SNS activation , immunodepression , and frequency of post-stroke infections . Methods : Stroke volume , stress hormone levels , and immune function were determined on day 1 after stroke onset . Stroke localization was grade d using the Alberta Stroke Programme Early CT score ( ASPECTS ) . In univariate analysis , we investigated the impact of clinical ( National Institutes of Health Stroke Scale , NIHSS ) and imaging stroke characteristics ( lesion volume , lateralization , localization grading ) on autonomous nervous system activity ( norepinephrine , cortisol ) , immune competence ( monocytic HLA-DR expression ) , and the frequency of post-stroke infections . In a logistic regression model , we tested for independent factors that might increase susceptibility to post-stroke infections . Results : In a single-factor analysis , large stroke volume , lesions affecting distinct regions of the MCA cortex , and SNS activation ( elevated norepinephrine levels ) were associated with an impaired immune function ( reduced mHLA-DR expression ) and a higher susceptibility to post-stroke infections . Multivariate analysis identified increased levels of norepinephrine and infa rct ion of the anterior MCA cortex as independent risk factors of post-stroke infections . Neither stroke severity nor stroke volume was independently associated with post-stroke infections . Conclusions : Apart from sympathetic activation , our data suggest that ischemic lesion in the anterior MCA cortex may be a major determinant of stroke-associated infection . This finding has to be confirmed in larger prospect i ve studies Assessment s of mood disturbance and “ vegetative ” ( appetite or sleep ) disturbance as well as a single‐dose dexamethasone suppression test ( DST ) were carried out in 25 r and omly selected stroke patients and in 13 nonstroke control patients hosptalized in a rehabilitation center .  Prevalence rates of moderate‐to‐sever depression of mood and vegetative disturbance were significantly higher in stroke patients than controls ( 48 % and 52 % versus 0 % and 8 % , respectively ) , as was the prevalence of abnormal DST results ( 52 % versus 8 % ) . Abnormal DST  results were associated with the occurrence of moderate to severe mood , appetite , and sleep disturbances among all patients . In 2 stroke patients , repeated DST results paralleled the clinical course . The DST may be useful as an adjunct to the diagnosis and in monitoring the progress of the common and potentially reversible mood and vegetative disturbances occurring after stroke Background / Aim : The cause of elevated blood pressure ( BP ) in acute stroke is unknown . Stress is often suggested as a main contributing factor . We aim ed to investigate the relationship between BP and stress in patients with acute stroke . Methods : 58 patients with clinical symptoms of stroke were recruited prospect ively after exclusion of haemorrhage by CT scan within 14 h and 15 min ( mean ) after symptom onset ( range 2 h and 45 min–23 h and 40 min ) . The mean age of the patients was 66 years ( range 39–86 years ) , and the mean National Institute of Health Stroke Scale score was 7 ( range 1–26 ) . BP and pulse rate were recorded by non-invasive automatic monitoring hourly for 24 h. Stress was evaluated by testing the level of  salivary cortisol .  Four sample s of saliva were obtained at inclusion , on the evening of the inclusion day ( 20.00–22.00 h ) , on the morning of the next day ( 7.00–9.00 h ) and on the afternoon of the inclusion day/next day ( 15.00–17.00 h ) within 24 h after inclusion in the study . Logarithmic transformation was done for cortisol levels . Results : The 24-hour mean cortisol level ( geometric mean 13.6 nmol/l ) was related to 24-hour mean systolic BP [ SBP ; r = 0.36 , p = 0.01 , multivariate p = 0.02 ] , mean night-time ( 22.00–6.00 h ) SBP ( r = 0.43 , p = 0.001 , multivariate p < 0.005 ) and mean night-time diastolic BP ( r = 0.31 , p = 0.02 , multivariate p = 0.02 ) . Cortisol levels at inclusion ( r = 0.31 , p = 0.02 , multivariate p = 0.05 for 24-hour SBP ) and in the evening were also statistically significantly related to the above BP variables . The morning cortisol ( r = 0.28 , p = 0.04 , multivariate p = 0.04 ) was related to night-time SBP . Conclusions : Salivary cortisol was positively correlated with 24-hour SBP and night-time BP , suggesting that stress is a contributing factor for high BP in acute stroke BACKGROUND Hippocampal volume reduction , declarative memory deficits , and cortisol elevations are reported in persons with major depressive disorder ; however , data linking cortisol elevations with hippocampal atrophy are lacking . Prescription corticosteroid-treated patients offer an opportunity to examine corticosteroid effects on hippocampal volume and biochemistry and memory in humans . METHODS Seventeen patients on long-term pres 
    Output:
    
Cortisol levels are high for at least 7 days after stroke .
Elevated cortisol after stroke is associated with dependency , morbidity , and mortality ; however , there is insufficient evidence to conclude that these relationships are independent of stroke severity