Objective:  Functional decline is experienced by up to 50% of older hospitalised patients and is associated with increased institutionalisation, mortality and length of stay (LOS). We aimed to determine the effectiveness of an exercise program in reducing functional decline and health service utilisation in older inpatients. Methods:  A single‐blinded randomised controlled trial was conducted in a tertiary metropolitan hospital involving 180 acute general medical patients aged ≥ 65 years. In addition to usual physiotherapy care, the intervention group performed an exercise program for 30 minutes, twice daily, with supervision and assistance. Change in physical function was measured by the modified Barthel index (mBI). Analysis was done on an intention‐to‐treat basis. Results:  When admission mBI scores were low, there was a greater improvement in mBI scores in the intervention group compared with the control group. The intervention group had a shorter total LOS (Hazard ratio (HR) 1.46 (95%CI 1.04–2.05); P = 0.026).

Skeletal muscle function was studied in 10 malnourished patients with various gastrointestinal disorders and in 22 normal subjects. The function of the adductor pollicis muscle was assessed by electrical stimulation of the ulnar nerve. The objective parameters of muscle function measured were: 1) Force of contraction expressed as a percentage of the maximal force obtained with electrical stimulation at 10, 20, 30, 50 and 100 Hz. 2) Maximal relaxation rate expressed as percentage force loss/!10 ms. 3) Endurance expressed as percentage force loss/30 s. The force of contraction at 10 Hz was higher in malnourished patients compared with normal subjects, with a mean +/- SEM (n) of 43.0 +/- 4.2% (n = 10) and 28.8 +/- 1.2% (n = 22), respectively, (p less than 0.001). The maximal relaxation rate was slower in patients compared with normals with a mean +/- SEM (n) of 7.2 +/- 0.4% (n = 9) ad 9.6 +/- 0.2% (n = 22), respectively, (p less than 0.001). Muscle endurance testing showed an increased force loss with prolonged tetanic stimulation in patients compared with normals, with a mean +/- SEM (n) of 29.1 +/- 4.0% (n = 7) and 3.5 +/- 0.8% (n = 22), respectively, (p less than 0.001). Four patients were restudied after a 4-wk period of total parenteral nutrition, with a significant improvement in muscle function parameters. Malnutrition results in both increased muscle fatiguability and an altered pattern of muscle contraction and relaxation which are reversible by nutritional supplementation. This technique promises to be valuable in assessing the functional effects of malnutrition and the response to nutritional support.

No abstract

Skeletal muscle function, body composition (total body nitrogen and total body potassium) and standard parameters of nutritional assessment were measured in six severely depleted patients with primary anorexia nervosa, both on admission and during oral refeeding. The function of the adductor pollicis muscle was assessed by electrical stimulation of the ulnar nerve. On admission muscle function was markedly abnormal in the patients with anorexia nervosa (n = 6) compared with normal subjects (n = 22), with a significant increase in the force of contraction at 10 Hz, with a mean +/- SEM of 48.0 +/- 3.7% and 28.8 +/- 1.2%, respectively (p less than 0.001). There was slowing of the maximal relaxation rate, 6.6 +/- 0.6% and 9.6 +/- 0.2%, respectively (p less than 0.001) and increased muscle fatigue 18.6 +/- 5.9% and 3.5 +/- 0.8%, respectively (p less than 0.01). Initially, the mean serum albumin was normal (4.0 +/- 0.1 g/dl), although there was evidence of severe depletion of somatic protein stores, with a low total body nitrogen and creatinine-height index. Within 4 wk of oral refeeding, maximal relaxation rate and muscle fatigability were restored to normal, and within 8 wk all parameters of muscle function were normal. During the study total body nitrogen increased by only 13% and was still 19.4% below the predicted normal total body nitrogen, whereas total body potassium increased by 32% and body fat by 46%. Normalization of muscle function may be related to restoration of muscle electrolytes rather than repletion of body nitrogen.

Skeletal muscle function and standard nutritional assessment parameters were measured in six obese patients. Base-line measurements were made on a weight-maintaining diet, and further measurements after 2 wk of a 400-cal diet, followed by 2 wk of fasting and then after 2 wk of refeeding. The function of the adductor pollicis muscle was assessed by electrical stimulation of the ulnar nerve. The objective parameters of muscle function measured were: 1) force of contraction expressed as a percentage of the maximal force obtained with electrical stimulation at 10, 20, 30, 50, and 100 Hz. 2) Maximal relaxation rate expressed as percentage force loss/10 ms. 3) Endurance expressed as percentage force loss/30 s. Standard nutritional assessment parameters (serum albumin and transferrin, creatinine height index, anthropometry and total body nitrogen and potassium) were also measured. There was a significant increase in the force of contraction at 10 Hz from a base-line of 29.6 +/- 1.0% to 49.0 +/- 2.8% (mean +/- SEM) after 2 wk of a 400-cal diet (p less than 0.01). These was a significant slowing of the maximal relaxation rate from a base-line of 9.8 +/- 0.03% force loss/10 ms to 8.2 +/0 0.3% force loss/10 ms (mean +/- SEM) (p less than 0.01) after 2 wk of a 400-cal diet. After a further 2 wk of fasting these abnormalities in muscle function persisted. There was a significant increase in muscle force loss from a base-line of 3.9 +/- 0.8% force loss/30 s to 13.7 +/- 3.4% force loss/30 s (mean +/- SEM) after fasting (P less than 0.01). After 2 wk of refeeding all aspects of muscle function measured were normal. During the study the standard nutritional assessment parameters did not change significantly.

The use of instrumental examinations in headache patients varies widely. In order to evaluate their usefulness, the most common instrumental procedures were evaluated, on the basis of evidence from the literature, by an EFNS Task Force (TF) on neurophysiological tests and imaging procedures in non‐acute headache patients. The conclusions of the TF regarding each technique are expressed in the following guidelines for clinical use. Interictal electroencephalography (EEG) is not routinely indicated in the diagnostic evaluation of headache patients. Interictal EEG is, however, indicated if the clinical history suggests a possible diagnosis of epilepsy (differential diagnosis). Ictal EEG could be useful in certain patients suffering from hemiplegic and basilar migraine. Recording of evoked potentials is not recommended for the diagnosis of headache disorders. There is no evidence to justify the recommendation of autonomic tests for the routine clinical examination of headache patients. Manual palpation of pericranial muscles, with standardized palpation pressure, can be recommended for subdividing patient groups but not for diagnosis. Pressure algometry and electromyography (EMG) cannot be recommended as clinical diagnostic tests. In adult and paediatric patients with migraine, with no recent change in attack pattern, no history of seizures, and no other focal neurological signs or symptoms, the routine use of neuroimaging is not warranted. In patients with atypical headache patterns, a history of seizures and/or focal neurological signs or symptoms, magnetic resonance imaging (MRI) may be indicated. If attacks can be fully accounted for by the standard headache classification [International Headache Society (IHS)], a positron emission tomography (PET) or single‐photon emission computerized tomography (SPECT) and scan will generally be of no further diagnostic value. Nuclear medicine examinations of the cerebral circulation and metabolism can be carried out in subgroups of headache patients for diagnosis and evaluation of complications, when patients experience unusually severe attacks, or when the quality or severity of attacks has changed. Transcranial Doppler examination is not helpful in headache diagnosis. Although many of the examinations described are of little or no value in the clinical setting, most of the tools have a vast potential for further exploring the pathophysiology of headaches and the effects of pharmacological treatment.

; for the ESO-KSU session participants* Abstract About the meeting: The purpose of the European Stroke Organisation (ESO)-Karolinska Stroke Update Conference is to provide updates on recent stroke therapy research and to give an opportunity for the participants to discuss how these results may be implemented into clinical routine. Several scientific sessions discussed in the meeting and each session produced consensus statements. The meeting started 20 years ago as Karolinska Stroke Update, but since 2014, it is a joint conference with ESO. Importantly, it provides a platform for discussion on the ESO guidelines process and on recommendations to the ESO guidelines committee on specific topics. By this, it adds a direct influence from stroke professionals otherwise not involved in committees and work groups on the guidelines procedure. The discussions at the conference may also inspire new guidelines when motivated. The topics raised at the meeting are selected by the scientific programme committee mainly based on recent important scientific publications. The ESO-Karolinska Stroke Update consensus statement and recommendations will be published every 2 years and it will work as implementation of ESO-guidelines Background: This year's ESO-Karolinska Stroke Update Meeting was held in Stockholm on 13-15 November 2016. There were 10 scientific sessions discussed in the meeting and each session produced a consensus statement (Full version with background, issues, conclusions and references are published as web-material and at http://www.eso-karolinska.org/2016 and http://eso-stroke.org) and recommendations which were prepared by a writing committee consisting of session chair(s), secretary and speakers and presented to the 312 participants of the meeting. In the open meeting, general participants commented on the consensus statement and recommendations and the final document were adjusted based on the discussion from the general participants. Recommendations (grade of evidence) were graded according to the 1998 Karolinska Stroke Update meeting with regard to the strength of evidence. Grade A Evidence: Strong support from randomised controlled trials and statistical reviews (at least one randomised controlled trial plus one statistical review). Grade B Evidence: Support from randomised controlled trials and statistical reviews (one randomised controlled trial or one statistical review). Grade C Evidence: No reasonable support from randomised controlled trials, recommendations based on small randomised and/or non-randomised controlled trials evidence.

OBJECTIVE To investigate if early electronic identification and bedside management of inpatients with diabetes improves glycemic control in noncritical care. RESEARCH DESIGN AND METHODS We investigated a proactive or early intervention model of care (whereby an inpatient diabetes team electronically identified individuals with diabetes and aimed to provide bedside management within 24 h of admission) compared with usual care (a referral-based consultation service). We conducted a cluster randomized trial on eight wards, consisting of a 10-week baseline period (all clusters received usual care) followed by a 12-week active period (clusters randomized to early intervention or usual care). Outcomes were adverse glycemic days (AGDs) (patient-days with glucose <4 or >15 mmol/L [<72 or >270 mg/dL]) and adverse patient outcomes. RESULTS We included 1,002 consecutive adult inpatients with diabetes or new hyperglycemia. More patients received specialist diabetes management (92% vs. 15%, P < 0.001) and new insulin treatment (57% vs. 34%, P = 0.001) with early intervention. At the cluster level, incidence of AGDs decreased by 24% from 243 to 186 per 1,000 patient-days in the intervention arm (P < 0.001), with no change in the control arm. At the individual level, adjusted number of AGDs per person decreased from a mean 1.4 (SD 1.6) to 1.0 (0.9) days (−28% change [95% CI −45 to −11], P = 0.001) in the intervention arm but did not change in the control arm (1.8 [2.0] to 1.5 [1.8], −9% change [−25 to 6], P = 0.23). Early intervention reduced overt hyperglycemia (55% decrease in patient-days with mean glucose >15 mmol/L, P < 0.001) and hospital-acquired infections (odds ratio 0.20 [95% CI 0.07–0.58], P = 0.003). CONCLUSIONS Early identification and management of inpatients with diabetes decreased hyperglycemia and hospital-acquired infections.