Decreased modulation of segregated SEEKING and selective attention systems in chronic insomnia

摘要

Sleep-related attentional bias and instinctual craving-sleep status may be associated with value-driven selective attention network and SEEKING system. We hypothesized that the two networks might be important components and underlie etiology of inability to initiate or/and maintain sleep in patients with chronic insomnia (PIs). Our aim is to investigate whether frequency-frequency couplings(temporal and spatial coupling, and differences of a set of imaging parameters) could elevate the sensibility to characterize the two insomnia-related networks in studying their relationships with sleep parameters and post-insomnia emotions. Forty-eight PIs and 48 status-matched good sleepers were requested to complete sleep and emotion-related questionnaires. Receiver operating characteristic curve was used to calculate the discriminatory power of a set of parameters. Granger causality and mediating causality analysis were used to address the causal relationships between the two networks and sleep/emotion-related parameters. Frequency-frequency couplings could characterize the two networks with high discriminatory power (AUC, 0.951; sensitivity, 87.5%; specificity, 95.8%), which suggested that the frequency-frequency couplings could be served as a useful biomarker to address the insomnia-related brain networks. Functional deficits of the SEEKING system played decreased mediator acting in post-insomnia negative emotions (decreased frequency-frequency coupling). Functional hyperarousal of the value-driven attention network played decreased mediator acting in sleep regulation (increased frequency-frequency coupling). Granger causality analysis showed decreased causal effect connectivity between and within the two networks. The between-network causal effect connectivity segregation played decreased mediator acting in sleep regulation (decreased connectivity). These findings suggest that the functional deficits and segregation of the two systems may underlie etiology of PIs.