There are often challenges in the diagnosis of Idiopathic Hypersomnia (IH) in patients
with comorbid psychiatric disorders, mood disorders in particular, who often report
symptoms including excessive sleep duration and daytime somnolence. Further, 15-25% of
patients with IH report significant depressive symptoms. When comparing these patients
groups, studies have not found significant differences in depression scores, indicating
the severity of depression cannot be reliably used to support diagnostic distinctions.
These findings present significant challenges to the differential diagnosis of IH vs.
Hypersomnia Associated with a Psychiatric Disorder (HAPD). Indeed, the diagnostic
criteria of IH and HAPD overlap considerably, leaving clinicians to make the often
challenging distinction of whether hypersomnia symptoms are temporally related to the
course of the psychiatric disorder(s).
The difficulty in differentiating IH from HAPD has largely focused on subjective
sleepiness, but some studies have utilized objective measures of sleepiness, in
particular the MSLT, to compare these groups. Vgontzas and colleagues found that IH was
associated with faster sleep onset on daytime nap opportunities compared to HAPD.
Further, a systematic review and meta-analysis found that subjective hypersomnolence in
patients with mood disorders was not associated with faster sleep latency on the MSLT
compared to normative values, although there was significant heterogeneity. This
discrepancy between subjective and objective hypersomnia can logically be explained by
the presence of depressive symptoms. Depression is associated with cognitive distortions
that lead individuals to interpret events from a more negative perspective, which leads
to greater reporting of physical symptoms including pain and fatigue. An in-depth
investigation of depression in patients with IH and HAPD may shed light on fundamental
differences between these groups and improve diagnostic accuracy.
In understanding the relationship between depression and subjective hypersomnia it will
be critical to look beyond subjective depressive symptoms because there will be de facto
associations found due to the common use of self-report methods. Studies need to assess
the neurobiological domains that underlie depression, both to utilize more objective
methods and to understand the actual mechanisms driving these associations. A logical
target in this regard would be the reward system, which is activated by any pleasurable
stimuli and directs motivation to seek out these stimuli. Reward function is disrupted in
individuals with depression, leading to two core features of anhedonia, i.e reduced
capacity to experience pleasure and low motivation during waking hours. More
specifically, patients with MDD demonstrate deficits in areas of reward function, namely
reduced effort for rewards, discounting of monetary rewards, and impairments in reward
learning. It also seems totoo reasonable to expect that reward dysfunction is also
related to the experience of hypersomnia, although this has not been previously
investigated. Interestingly, investigations have recently begun to examine the ways in
which sleep disturbance may independently affect reward processes. Poor sleep at night
can contribute to impaired reward function the next day.
A second depression-related system to investigate would be the sleep/wake system.
Depression is known to be associated with abnormalities in sleep, in particular in slow
wave sleep, the most restorative type of sleep. More specifically, the quantity of slow
waves during sleep can be quantified as slow wave activity (SWA), with greater SWA
associated with greater perceptions of feeling rested the next day. Depression is
associated reduced SWA, which is thought the reflect deficient neuroplasticity. Patients
with depression and hypersomnia have been found to exhibit reduced SWA compared to those
without hypersomnia, suggesting a potential deficit in the restorative quality of sleep
in these individuals. This suggests that the SWA deficiencies may be specifically related
to subjective hypersomnia in depression. No studies have examined SWA dynamics in IH.
The overarching hypothesis is that greater severity of subjective, but not objective,
hypersomnia in patients with IH and HAPD is related to a combination of disruption in
slow wave sleep dynamics at night and deficits in reward processes. Demonstration of
these effects could improve understanding of the nature of subjective vs. objective
hypersomnia and lead to improve the differential diagnosis of hypersomnia disorders.
