Co-design of a walking activity intervention for stroke survivors.

Introduction: Stroke survivors may not maintain gains made in gait performance after task-oriented circuit training. Behavior change interventions may enhance the long-term adoption of physical activity. This study uses a co-design methodology to develop an intervention and tools to facilitate physical and exercise therapists in supporting an active lifestyle in stroke survivors, which is defined as a lifestyle that integrates daily walking performance with day-to-day activity. Objectives: (1) To describe the insights generated during the co-design process; and (2) To describe the tools that were developed during the co-design process. Methods: A multidisciplinary team consisting of staff members of the Royal Dutch Society for Physical Therapy, exercise and physical therapists specializing in neurorehabilitation and conducting task-oriented circuit class training in primary care settings or day therapy centers within residential care facilities, stroke survivors and their carers, experts in measuring movement behavior in stroke survivors, a company specializing in manufacturing sensors and related software, behavior change specialists, and co-designers all collaborated in a three-stage (define, develop, and deliver) co-design process. Results: In the design process, the team iteratively developed a prototype accelerometer system for measuring walking performance with a feedback function for stroke survivors and their therapists and a prototype toolbox for therapists to support the facilitation of behavior change in their stroke survivors. Discussion: This study shows how co-design can be applied to develop interventions for stroke survivors. Both the prototype system for measuring walking performance and the toolbox incorporate behavior change techniques to support a more physically active lifestyle in stroke survivors. Further research will investigate the feasibility of the intervention.

Extended steep ramp test normative values for 19-24-year-old healthy active young adults.

PURPOSE: To extend currently available sex and age-specific normative values in children and adolescents for the peak work rate (WRpeak) attained at the steep ramp test (SRT) to healthy active young adults. METHODS: Healthy male and female participants aged between 19 and 24 years were recruited. After screening and anthropometric measurements, participants performed a SRT on a cycle ergometer (increments of 25 W/10 s), monitoring and recording SRT-WRpeak, heart rate (HR), and blood pressure (BP) at rest and directly after peak exercise. RESULTS: Fifty-seven participants (31 males and 26 females; median age of 21.3 years) volunteered and were tested. Anthropometrics, resting BP and lung function were all within normal ranges. Ninety-three percent of the participants attained a peak HR (HRpeak) > 80% of predicted (mean HRpeak 87 ± 5% of predicted). No differences were found in resting and peak exercise variables between females and males, except for absolute SRT-WRpeak (350 W [Q1: 306; Q3: 371] and 487 W [Q1: 450; Q3: 517], respectively) and SRT-WRpeak normalized for body mass (relative SRT-WRpeak; 5.4 ± 0.5 and 6.2 ± 0.6 W/kg, respectively). Low-to-moderate correlations (ρ [0.02-0.71]) were observed between SRT-WRpeak and anthropometric variables for females and males separately. Extended reference curves (8-24-year-old subjects) for SRT performance show different trends between male and female subjects when modelled against age, body height, and body mass. CONCLUSIONS: The present study provides sex-, age-, body height-, and body mass-related normative values (presented as reference centiles) for absolute and relative SRT performance throughout childhood and early adulthood.

CSF hypocretin-1 levels in narcolepsy, Kleine-Levin syndrome, and other hypersomnias and neurological conditions.

OBJECTIVE: To determine the role of CSF hypocretin-1 in narcolepsy with and without cataplexy, Kleine-Levin syndrome (KLS), idiopathic and other hypersomnias, and several neurological conditions. PATIENTS: 26 narcoleptic patients with cataplexy, 9 narcoleptic patients without cataplexy, 2 patients with abnormal REM-sleep-associated hypersomnia, 7 patients with idiopathic hypersomnia, 2 patients with post-traumatic hypersomnia, 4 patients with KLS, and 88 patients with other neurological disorders. RESULTS: 23 patients with narcolepsy-cataplexy had low CSF hypocretin-1 levels, while one patient had a normal hypocretin level (HLA-DQB1*0602 negative) and the other two had intermediate levels (familial forms). One narcoleptic patient without cataplexy had a low hypocretin level. One patient affected with post-traumatic hypersomnia had intermediate hypocretin levels. The KLS patients had normal hypocretin levels while asymptomatic, but one KLS patient (also affected with Prader-Willi syndrome) showed a twofold decrease in hypocretin levels during a symptomatic episode. Among the patients without hypersomnia, two patients with normal pressure hydrocephalus and one with unclear central vertigo had intermediate levels. CONCLUSION: Low CSF hypocretin-1 is highly specific (99.1%) and sensitive (88.5%) for narcolepsy with cataplexy. Hypocretin ligand deficiency appears not to be the major cause for other hypersomnias, with a possible continuum in the pathophysiology of narcolepsy without cataplexy and idiopathic hypersomnia. However, partial hypocretin lesions without low CSF hypocretin-1 consequences cannot be definitely excluded in those disorders. The existence of normal hypocretin levels in narcoleptic patients and intermediate levels in other rare aetiologies needs further investigation, especially for KLS, to establish the functional significance of hypocretin neurotransmission alterations.