cognitive impairments seem associated with functional decline in hospitalised older people. Causality cannot be inferred, and limitations include low quality of studies and possible confounding.

No abstract

Objective In children with traumatic brain injury (TBI), 1) to describe the hospital discharge functional outcome and change from baseline function using the Functional Status Scale (FSS) and 2) to determine any associations between discharge FSS and age, injury mechanism, neurologic exam, imaging, and other predictors of outcome. Design Prospective observational cohort study, May 2013 to November 2015. Setting Two U.S. children's hospitals designated as American College of Surgeons level 1 Pediatric Trauma Centers. Patients Children < 18 years old admitted to an intensive care unit (ICU) with acute TBI and either a surgical or critical care intervention within the first 24 hours or in-hospital mortality. Interventions None Measurements and Main Results The primary outcome was hospital discharge FSS. Most, 133/196 (68%), had severe TBI (admission GCS 3–8). Overall hospital mortality was 14%; 20% among those with severe TBI. Hospital discharge FSS had an inverse relationship with GCS: for each increase in admission GCS by 1, the discharge FSS decreased by 0.5 (95% CI: 0.7 to 0.3). Baseline FSS was collected at one site, N = 75. At that site, nearly all (61/62) of the survivors had normal or near-normal (≤ 7) pre-injury FSS. More than one-third, 23/62 (37%), of survivors had new morbidity at hospital discharge (increase in FSS ≥ 3). Among children with severe TBI who had baseline FSS collected, 21/41 (51%) of survivors had new morbidity at hospital discharge. The mean change in FSS from baseline to hospital discharge was 3.9 ± 4.9 overall and 5.2 ± 5.4 in children with severe TBI. Conclusions More than one-third of survivors, and approximately half of survivors with severe TBI, will have new morbidity. Hospital discharge FSS, change from baseline FSS, and new morbidity acquisition can be used as outcome measures for hospital-based care process improvement initiatives and interventional studies of children with TBI.

Anorexia nervosa is associated with abnormalities in neuroendocrine function including sustained hypercortisolism, which has been shown elsewhere to be associated with impairment of function in learning, memory and attention. Cognitive impairment has also been observed in anorexia nervosa. These effects may be mediated in part through cortisol effects on the hippocampus, which is dense with glucocorticoid receptors. We investigated the association between cortisol levels and cognitive function in anorexia nervosa by measuring both 24-hour urinary cortisol counts and performance on tasks of learning, memory and attention in patients suffering from the disorder. Cortisol secretion was shown to be significantly higher in the patient group than in a matched control group and patients were also shown to be impaired in memory and attention. However, no correlations were found between the cognitive deficits and cortisol measures. It is suggested that more sensitive profiling of cortisol levels throughout the circadian cycle may be useful in future studies of cognitive function in anorexia nervosa.