Rest-activity Disturbance Research Articles

Rest-activity disturbances and light exposure in myotonic dystrophy type 1 patients with apathy: An exploratory study using actigraphy

BackgroundRest-activity rhythm disturbances have been reported in myotonic dystrophy type 1 (DM1) but no study has assessed its relationship with apathy and light exposure using actigraphy. MethodsThirty-three DM1 patients wore an actigraph for two consecutive weeks. The Lille Apathy Rating Scale was used to assess apathy. Actigraphy was used to characterize sleep, activity, and light exposure and nonparametric analysis was performed to characterize intraday variability (IV), interday stability (IS), least active five-hour period (L5), most active ten-hour period (M10), and relative amplitude (RA). ResultsApathy was found in 42.4% of patients. Patients with apathy have a larger number of CTG repeat than those without (774 vs 381, p<0.01) Also, patients with apathy had higher IV values (0.98 vs 0.69, p<0.001) as well as lower IS (0.34 vs 0.47, p<0.05), RA (0.65 vs 0.83, p<0.05), and M10 (182.6 vs 493.8, p<0.001) values compared to patients without apathy. In addition, DM1 patients with apathy were exposed to less bright light (≥1000 lux) (41.4 vs 141.2 minutes p<0.01) than patients without. No difference was observed relatively to sleep quality and quantity. ConclusionsDaytime activity levels and bright light exposure were significantly lower in DM1 patients with apathy versus those without. The more fragmented, less stable, and lower amplitude rest-activity rhythm of DM1 patients with apathy, as revealed by non parametric analysis, can be partly ascribed to reduced daylight exposure. The use of bright light therapy as well as physical activity interventions should be explored to help prevent or reduce apathy levels in DM1.

Rest-Activity Disturbances in Children with Septo-Optic Dysplasia Characterized by Actigraphy and 24-Hour Plasma Melatonin Profiles

A trial of melatonin treatment in children with septo-optic dysplasia (SOD) and sleep disruption is accepted clinical practice in many centers. However, no objective measurements of sleep/activity patterns with 24-h melatonin profiles have been published for these individuals, and the pathophysiological basis underlying sleep disorders in SOD remains largely unknown. We studied six children with rest-activity disturbances and SOD. All wore an Actiwatch-Mini (a noninvasive method of detecting and recording movement intensity) for 2 wk and were admitted to hospital for a 24-h period during which hourly measurements of serum melatonin were taken. Sleep data were analyzed in conjunction with a detailed sleep diary. Ethical approval was obtained for these studies. Two children produced virtually no melatonin throughout the 24-h period of measurement and had fragmented sleep patterns with no evidence of a non-24-h sleep-wake disorder or delayed sleep-phase disorder. One child had a normal melatonin profile despite actigraphy showing an arrhythmic sleep pattern. The remaining three children had fragmented sleep, with two having normal melatonin profiles and one having a modest increase in daytime melatonin concentrations, making the timing of dim-light melatonin onset difficult to discern. There is considerable variation in timing and amount of melatonin secretion in these children. Surprisingly, none of the children had either actigraphic or melatonin profile evidence of a non-24-h sleep-wake disorder or delayed sleep-phase disorder. Understanding the heterogeneous nature of underlying sleep disorders in this group of children is important and has implications for their management.