Sleep structure in blindness is influenced by circadian desynchrony

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Visual deprivation, as in the case of total or partial blindness, induces structural and functional changes in visual cortical areas (Kupers and Ptito, 2014; Park et al., 2009; Ptito et al., 2008), and in other parts of the brain (Cecchetti et al., 2016; Chebat et al., 2007; Ptito et al., 2008; Tomaiuolo et al., 2014). Besides these changes, a number of electrophysiological changes have been reported. Particularly, resting‐state occipital alpha oscillations, when eyes are closed, are absent in blind individuals (Noebels et al., 1978). Various studies have shown these oscillations to be associated with activity of the visual cortex, thalamus and insula (Feige et al., 2005; Goldman et al., 2002; Larson et al., 1998; Sadato et al., 1998), although their nature and significance remain to be elucidated. Furthermore, reduced parieto‐occipital alpha power has been reported in blind individuals during cognitive tasks (Kober et al., 2014; Kriegseis et al., 2006; Schubert et al., 2015), possibly reflecting alterations in the thalamo‐cortical pathway (lateral geniculate nucleus and primary visual cortex; Cecchetti et al., 2016; Kupers and Ptito, 2014).
Given such severe anatomo‐physiological changes (Kupers and Ptito, 2014), sleep states may also be modulated by the absence of visual input. Indeed, blind individuals report more sleep disturbances than do normal‐sighted controls (Aubin et al., 2016; Leger et al., 1999; Tabandeh et al., 1998). In totally blind individuals, sleep disturbances may be partially explained by a free‐running circadian rhythm that results from the absence of entrainment by light (Flynn‐Evans et al., 2014; Uchiyama and Lockley, 2015). More specifically, sleep is mediated by two processes: a homeostatic drive for sleep and a circadian rhythm of wake (Borbély, 1982; Borbély et al., 2016). Disruptions of either process generate disturbances in sleep and its underlying structure. Thus, the incidence of free‐running circadian rhythms associated with blindness can account for some, but not all, of the sleep disturbances reported by blind individuals (Leger et al., 1999; Lockley et al., 1997; Moseley et al., 1996).
Nevertheless, relatively little is known about the structure of sleep and its electrophysiological correlates in blind individuals. In addition, the few published studies investigating sleep electroencephalogram (EEG) in the blind report inconsistent or contradictory results with respect to both rapid eye movement (REM) and non‐REM (NREM) sleep. Some early studies conducted in small cohorts (n = 5) of blind participants with varying degrees of light perception suggest that deep sleep (N3 or NREM stages 3 and 4 in earlier terminology), characterised by slow‐wave activity (SWA), may be reduced or absent in blindness (Hono et al., 1999; Krieger and Glick, 1971). This conclusion is corroborated by the results of a recent study in a larger group of 10 blind participants without conscious light perception (Ayala‐Guerrero and Mexicano, 2015). None of these studies, however, reported any differences between blind and normal‐sighted control groups for NREM sleep stage 2 (N2) or REM sleep. Leger et al. (2002) examined the structure of night‐time sleep in a large sample (n = 26) of totally blind individuals, with either congenital or acquired blindness, who all had free‐running circadian rhythms. Blind participants had reduced sleep duration and lower sleep efficiency than did their age‐ and sex‐matched sighted controls. Blind participants also had reduced REM sleep duration and increased REM sleep latency. The variations in timing and duration of REM sleep support the presence of free‐running circadian rhythms, as REM sleep is strongly dependent on circadian phase (Czeisler et al., 1979, 1980).
The current knowledge on the sleep structure of blind individuals is, however, limited by studies consisting of small sample sizes and the absence of a circadian marker.
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