BackgroundPrimary insomnia (PI) is one of the most common sleep disorders. Diagnosis of insomnia is mainly based on subjective sleep difficulties, and it is still necessary to find objective neurobiological markers.PurposeTo investigate the functional connectivity (FC) of frontal hub regions important for PI.Material and MethodsWe enrolled 20 patients (5 men, 15 women) with PI and 20 controls (5 men, 15 women), matching age, sex. We used resting-state functional magnetic resonance imaging (fMRI) and voxel-mirrored homotopic connectivity (VMHC) to analyze the abnormal changes of FC in the frontal lobe of PI patients.ResultsCompared to controls, abnormal FC regions were mainly concentrated in the superior frontal gyrus (L/R), middle frontal gyrus (L/R), and inferior frontal gyrus (L) of the orbital region and the inferior frontal gyrus of the opercular region (L) (P < 0.05). The VMHC results showed abnormal FC in the middle frontal gyrus of the orbital region (GFR correction, voxel P < 0.01, cluster P < 0.025) in PI patients. The FC between the orbitofrontal gyrus and the inferior frontal gyrus of the opercular region with the frontal gyrus of the medial orbital region demonstrated a significant correlation with the clinical scale (p < 0.05).ConclusionOur study identified abnormal FC, which was mainly located in the orbitofrontal gyrus and the inferior frontal gyrus of the opercular region, in the frontal lobe of patients with insomnia using resting-state fMRI. This is helpful to understand the abnormal neural activity mechanism of insomnia in the frontal lobe and provide a relatively accurate brain region basis for future prevention, diagnosis, and treatment.

This study investigated the altered neural activation underlying cognitive control under emotional and sleep-related interference conditions and its role in subjective sleep disturbance in patients with chronic insomnia disorder. In total, 48 patients with chronic insomnia disorder, and 48 age-, sex- and body mass index-matched controls were included in this study. They completed self-reported questionnaires to assess subjective sleep and emotional distress. A sleep diary was used to evaluate subjective sleep parameters. All participants performed the emotional Stroop task (three blocks each of negative emotional, sleep-related, and neutral words) during functional magnetic resonance imaging assessments. We compared brain activation during the emotional Stroop task between the two groups. We also analysed the correlations between altered neural activation and sleep variables. Less neural activation was detected in the right anterior prefrontal cortex of patients with chronic insomnia disorder than in controls when performing the emotional Stroop task with negative emotional words. The decrease in neural activation was negatively correlated with scores on Pittsburgh Sleep Quality Index, Insomnia Severity Index, and Dysfunctional Beliefs and Attitudes about Sleep Scale. In contrast, they were positively correlated with subjective total sleep time and sleep efficiency as reported in sleep diaries. A decrease in right anterior prefrontal cortex activity under the negative emotional words condition of the emotional Stroop task in patients with chronic insomnia disorder suggests a failure of top-down inhibition of negative emotional stimuli. This failure induces disinhibition of cognitive hyperarousal, manifested as rumination or intrusive worries, and potentially causing subjective sleep disturbances.

Sleep deprivation is a prevalent issue that impacts cognitive function. Although numerous neuroimaging studies have explored the neural correlates of sleep loss, inconsistencies persist in the reported results, necessitating an investigation into the consistent brain functional changes resulting from sleep loss.

To establish the consistency of brain functional alterations associated with sleep deprivation through systematic searches of neuroimaging databases. Two meta-analytic methods, signed differential mapping (SDM) and activation likelihood estimation (ALE), were employed to analyze functional magnetic resonance imaging (fMRI) data.

A systematic search performed according to PRISMA guidelines was conducted across multiple databases through July 29, 2023. Studies that met specific inclu-sion criteria, focused on healthy subjects with acute sleep deprivation and reported whole-brain functional data in English were considered. A total of 21 studies were selected for SDM and ALE meta-analyses.

Twenty-one studies, including 23 experiments and 498 subjects, were included. Compared to pre-sleep deprivation, post-sleep deprivation brain function was associated with increased gray matter in the right corpus callosum and decreased activity in the left medial frontal gyrus and left inferior parietal lobule. SDM revealed increased brain functional activity in the left striatum and right central posterior gyrus and decreased activity in the right cerebellar gyrus, left middle frontal gyrus, corpus callosum, and right cuneus.

This meta-analysis consistently identified brain regions affected by sleep deprivation, notably the left medial frontal gyrus and corpus callosum, shedding light on the neuropathology of sleep deprivation and offering insights into its neurological impact.

Insomnia is one of the most common accompanying symptoms of depression, with both sharing highly overlapping molecular pathways. The same pathological changes can trigger comorbidity of insomnia and depression, which further forms a vicious cycle with the involvement of more mechanisms and disease progression. Thus, understanding the potential interaction mechanisms between insomnia and depression is critical for clinical diagnosis and treatment. Comorbidity genetic factors, the hypothalamic-pituitary-adrenal axis, along with circadian rhythms of cortisol and the brain reward mechanism, are important ways in contributing to the comorbidity occurrence and development. However, owing to lack of pertinent investigational data, intricate molecular mechanisms necessitate further elaboration. Synaptic plasticity is a solid foundation for neural homeostasis. Pathological alterations of depression and insomnia may perturb the production and release of neurotransmitter, dendritic spine remodeling and elimination, which converges and reflects in aberrant synaptic dynamics. Hence, the introduction of synaptic plasticity research route and the construction of a comprehensive model of depression and insomnia comorbidity can provide new ideas for clinical depression insomnia comorbidity treatment plans.