Preliminary investigation of the relationships between sleep duration, reward circuitry function, and mood dysregulation in youth offspring of parents with bipolar disorder

Abstract

Background Altered reward circuitry function is observed in individuals with bipolar disorder (BD) and their unaffected offspring (OBP). While OBP are at elevated risk for BD, modifiable risk factors that may exacerbate neural vulnerabilities in OBP remain under-characterized. As sleep loss is strongly linked to mania in BD, this study tested associations between sleep duration, reward circuitry function, and mood dysregulation in OBP. Methods Two groups of youth unaffected with BD (9-17yr) completed a number-guessing fMRI reward paradigm: 25 OBP and 21 age-sex-IQ-matched offspring of control parents with non-BD psychopathology (OCP), to differentiate risk for BD from risk for psychopathology more broadly. Regressions tested effects of group status, self-reported past-week sleep duration, and their interaction on neural activity and bilateral ventral striatum(VS) functional connectivity to win>control. Correlations with parent-reported mood dysregulation were assessed. Results Group effects were observed for right posterior insula activity (OCP>OBP) and VS-left posterior insula connectivity (OBP>OCP). Group*sleep duration interactions were observed for left dorsal anterior-mid-cingulate(daMCC) activity and VS-left anterior insula/ventrolateral prefrontal cortex(VLPFC) connectivity. Specifically, sleep duration and daMCC activity were positively related in OBP, but negatively related in OCP and sleep duration and VS-left anterior insula/VLPFC connectivity were negatively related in OBP, but positively in OCP. Additionally, increased VS-left posterior insula connectivity and VS-left anterior insula/VLPFC connectivity were associated with greater mood dysregulation in OBP only. Limitations Cross-sectional design and small sample size. Conclusions Altered reward-related VS-insula connectivity could represent a neural pathway underpinning mood dysregulation in OBP, and may be modulated by shortened sleep duration.

The sleep and circadian modulation of neural reward pathways: a protocol for a pair of systematic reviews

“…Sleep and circadian function have been shown to be important in numerous reward-related disorders (e.g. bipolar disorder, depression, drug and alcohol use; [ 1 – 8 ]) but is also relevant for optimal functioning in healthy individuals [ 9 – 11 ]. Remarkably, no review to date has systematically examined existing brain imaging evidence for sleep or circadian modulation of the neural pathways of reward.…”

Treatment of Psychiatric Symptoms Among Offspring of Parents With Bipolar Disorder

“…Offspring of parents with Bipolar Disorder also have a number of sleep disturbance symptoms, including excessive daytime sleepiness, headaches after awakening, and nightmares compared to youth offspring of parents without Bipolar Disorder [36]; poor sleeping high-risk youth are more likely to develop Bipolar Disorder compared to good or variable sleepers [37], with a potentially negative impact of shortened sleep duration on ventral striatum-insula brain connectivity during reward processing [38]. These studies suggest that sleep is an important early target for intervention in high-risk youth, but no studies to date have evaluated a sleep intervention in youth offspring of parents with Bipolar Disorder.…”

Neural connectivity in youth at-risk for bipolar disorder: a review of functional magnetic resonance imaging studies

“…No additional article was found in the manual search. Most of the studies were conducted in adolescents [23][24][25][26][27][28][29][30] with only two studies conducted in young adults [31,32]. The samples of subjects at-risk for BD were comprised of healthy offspring of bipolar patients [25,28,29], healthy and symptomatic offspring of bipolar patients [24,26,27,30], symptomatic offspring of bipolar patients [23] and healthy and symptomatic offspring or siblings of bipolar patients [31,32].…”

“…The samples of subjects at-risk for BD were comprised of healthy offspring of bipolar patients [25,28,29], healthy and symptomatic offspring of bipolar patients [24,26,27,30], symptomatic offspring of bipolar patients [23] and healthy and symptomatic offspring or siblings of bipolar patients [31,32]. Some studies were conducted by the same research groups, with partially overlapping samples [23,26,27,30] The studies focused in 4 functional imaging domains: 2 studies employed an emotion processing task [23,26]; 2 studies employed a cognitive-affective task [25,31]; 3 studies employed a reward processing task [27,28,30] and 3 were resting state fMRI studies [24,29,32]. Table 1 resume the main methodological characteristics and results of the selected studies.…”

“…Using the same reward processing paradigm and the same method of functional connectivity analysis, Soehner and colleagues [30] compared the offspring of parents with BD with the offspring of non-bipolar parents and correlated the functional connectivity results with sleeping and mood dysregulation data obtained from psychometric instruments. The authors found that the offspring of parents with BD showed significantly more ventral striatum-left posterior insula connectivity than offspring of non-bipolar parents.…”