Insomnia disorder, characterized by chronic sleep disruption, often co-occurs with maladaptive emotional memory processing. However, much remains unknown regarding the evolution of emotional memories and their neural representations over time among individuals with insomnia disorder.

We examined the electroencephalographic (EEG) activities during emotional memory encoding, post-encoding sleep, and multiple retrieval phases – including immediate post-encoding, post-sleep, and a 7-day delayed retrieval – among 34 participants with insomnia disorder and 35 healthy control participants.

Healthy controls exhibited adaptive dissipation of emotional memory: memory declined over time, accompanied by reduced subjective feelings toward negative memories. In contrast, participants with insomnia exhibited impaired dissipation: they retained both the emotional content and affective tone of the memories, with diminished time-dependent declines in memory and affect. Beyond behavioral performance, only participants with insomnia maintained stable neural representations of emotion over time, a pattern absent in healthy controls. Additionally, during the post-encoding sleep, slow-wave sleep (SWS), and rapid eye movement (REM) sleep durations predicted the adaptive dissipation of emotional memory over time, but only among healthy participants.

These findings highlight abnormalities in emotional memory processing among individuals with insomnia disorder and underscore the important function of SWS and REM sleep in facilitating adaptive emotional memory processing.

The heterogeneity of chronic post-COVID neuropsychiatric symptoms (PCNPS), especially after infection by the Omicron strain, has not been adequately explored.

To explore the clustering pattern of chronic PCNPS in a cohort of patients having their first COVID infection during the ‘Omicron wave’ and discover phenotypes of patients based on their symptoms’ patterns using a pre-registered protocol.

We assessed 1205 eligible subjects in Hong Kong using app-based questionnaires and cognitive tasks.

Partial network analysis of chronic PCNPS in this cohort produced two major symptom clusters (cognitive complaint–fatigue and anxiety–depression) and a minor headache–dizziness cluster, like our pre-Omicron cohort. Participants with high numbers of symptoms could be further grouped into two distinct phenotypes: a cognitive complaint–fatigue predominant phenotype and another with symptoms across multiple clusters. Multiple logistic regression showed that both phenotypes were predicted by the level of pre-infection deprivation (adjusted P-values of 0.025 and 0.0054, respectively). The severity of acute COVID (adjusted P = 0.023) and the number of pre-existing medical conditions predicted only the cognitive complaint–fatigue predominant phenotype (adjusted P = 0.003), and past suicidal ideas predicted only the symptoms across multiple clusters phenotype (adjusted P < 0.001). Pre-infection vaccination status did not predict either phenotype.

Our findings suggest that we should pursue a phenotype-driven approach with holistic biopsychosocial perspectives in disentangling the heterogeneity under the umbrella of chronic PCNPS. Management of patients complaining of chronic PCNPS should be stratified according to their phenotypes. Clinicians should recognise that depression and anxiety cannot explain all chronic post-COVID cognitive symptoms.