Another perspective on AUD relapse risk derives from the sleep literature. Sleep disturbances are highly prevalent in AUD (for review, Colrain et al., 2014; Jia et al., 2007) and may be associated with relapse (Conroy, 2015). The thalamus, a key region of arousal modulation, is responsible for producing sleep-specific electroencephalogram (EEG) phenomena such as sleep spindles (Steriade, 1993), which are compromised in AUD (Colrain et al., 2014). Another study, using tissue from the lateral geniculate nucleus of the thalamus of monkey model of chronic alcohol drinking by self-administration, found reduced calcium currents in thalamic relay cells known to contribute to normal sleep patterns (Carden et al., 2006). In humans, an MRI study reported that AUD subjects with smaller thalamic volumes at treatment entry tended to resume heavy alcohol consumption at 6-month follow-up (Segobin et al., 2014).
