Ilana S. Hairston

A test of the bidirectional association between sleep and mood in bipolar disorder and insomnia.

The present study investigates sleep, mood, and the proposed bidirectional relationship between the two in psychiatric disorders. Participants with interepisode bipolar disorder (n = 49), insomnia (n = 34), and no psychiatric history (n = 52) completed seven consecutive days of sleep diaries and mood measures. The interepisode bipolar and insomnia participants exhibited greater sleep disturbance than the healthy control individuals. Negative mood was equally heightened in both interepisode bipolar disorder and insomnia, and there were no differences between the three groups in positive mood. Total wake time was associated with next morning negative mood in bipolar disorder, whereas evening negative mood was associated with subsequent total wake time in both bipolar disorder and insomnia. Additionally, positive mood was associated with subsequent total wake time for the insomnia group. Results support the theory that disruptions in nighttime sleep and daytime mood may be mutually maintaining and suggest the potential importance of transdiagnostic or universal processes.

The Effect of Mood on Sleep Onset Latency and REM Sleep in Interepisode Bipolar Disorder

The present study investigates whether interepisode mood regulation impairment contributes to disturbances in sleep onset latency (SOL) and rapid eye movement (REM) sleep. Individuals with interepisode bipolar disorder (n = 28) and healthy controls (n = 28) slept in the laboratory for 2 baseline nights, a happy mood induction night, and a sad mood induction night. There was a significant interaction whereby on the happy mood induction night the bipolar group exhibited significantly longer SOL than did the control group, while there was no difference on the baseline nights. In addition, control participants exhibited shorter SOL on the happy mood induction night compared to the baseline nights, a finding that was not observed in the bipolar group. On the sad mood induction night, participants in both groups had shorter SOL and increased REM density when compared to the baseline nights. Bipolar participants exhibited heightened REM density compared to control participants on both nights. These results raise the possibility that regulation of positive stimuli may be a contributor to difficulties with SOL, while hyperactivity may be characteristic of REM sleep.

Sleep deprivation elevates plasma corticosterone levels in neonatal rats.

Plasma corticosterone (CORT) levels were measured after short periods of sleep deprivation in rats at postnatal days 12, 16, 20, and 24. There was an age-dependent increase in basal CORT levels and sleep deprivation significantly elevated CORT at all ages compared to non-sleep deprived controls. The levels of CORT after sleep deprivation in P16, P20 and P24 animals were similar, resulting in an age-dependent decrease of the magnitude of the response. Sleep deprived P12 animals had lower levels of CORT. However, the observed response to sleep deprivation suggests that sleep loss is a significant stressor at this age. These observations suggest that younger animals are more sensitive to the effects of mild sleep deprivation than older ones.

Sensory gating in primary insomnia.

Although previous research indicates that sleep architecture is largely intact in primary insomnia (PI), the spectral content of the sleeping electroencephalographic trace and measures of brain metabolism suggest that individuals with PI are physiologically more aroused than good sleepers. Such observations imply that individuals with PI may not experience the full deactivation of sensory and cognitive processing, resulting in reduced filtering of external sensory information during sleep. To test this hypothesis, gating of sensory information during sleep was tested in participants with primary insomnia (n = 18) and good sleepers (n = 20). Sensory gating was operationally defined as (i) the difference in magnitude of evoked response potentials elicited by pairs of clicks presented during Wake and Stage II sleep, and (ii) the number of K complexes evoked by the same auditory stimulus. During wake the groups did not differ in magnitude of sensory gating. During sleep, sensory gating of the N350 component was attenuated and completely diminished in participants with insomnia. P450, which occurred only during sleep, was strongly gated in good sleepers, and less so in participants with insomnia. Additionally, participants with insomnia showed no stimulus‐related increase in K complexes. Thus, PI is potentially associated with impaired capacity to filter out external sensory information, especially during sleep. The potential of using stimulus‐evoked K complexes as a biomarker for primary insomnia is discussed.

Neural Mechanisms of the Time-order Error: An MEG Study

The time-order error (TOE) refers to the influence of presentation order on performance accuracy in a discrimination task. Despite it being a well-documented perceptual bias, the underlying mechanisms have not been studied. In this study, observers were trained on a two-interval forced-choice procedure. The stimuli presented for discrimination were a standard, consisting of four tones presented at a 5-Hz rate, and targets, consisting of various rates higher than 5 Hz. Psychometric functions were measured for discrimination of the trained standard and targets, a novel standard of 13 Hz with higher target rates; and the trained 5 Hz standard with novel targets with rates below 5 Hz. Discrimination did not improve with training; in fact, accuracy declined when standard was presented in the first interval during the session, resulting in a TOE. The TOE was specific to the 5-Hz standard generalizing to the novel targets slower than 5 Hz, but not to the 13-Hz STANDARD. Analysis of the event-related magnetic field responses (ERFs) revealed a waveform to the whole stimulus, rather than to each tone in the train. Although ERFs in the second interval were attenuated independent of stimulus type, the M300 component in the second interval was attenuated only when the standard was first, but remained of equivalent magnitude when the standard was second. This was observed only in the two 5-Hz conditions. Combined, these results suggest that the TOE reflects the emergence of an internal representation of the standard, and that the M300 is potentially a neural correlate of plasticity.

Odors enhance slow-wave activity in non-rapid eye movement sleep

Most forms of suprathreshold sensory stimulation perturb sleep. In contrast, presentation of pure olfactory or mild trigeminal odorants does not lead to behavioral or physiological arousal. In fact, some odors promote objective and subjective measures of sleep quality in humans and rodents. The brain mechanisms underlying these sleep-protective properties of olfaction remain unclear. Slow oscillations in the electroencephalogram (EEG) are a marker of deep sleep, and K complexes (KCs) are an EEG marker of cortical response to sensory interference. We therefore hypothesized that odorants presented during sleep will increase power in slow EEG oscillations. Moreover, given that odorants do not drive sleep interruption, we hypothesized that unlike other sensory stimuli odorants would not drive KCs. To test these hypotheses we used polysomnography to measure sleep in 34 healthy subjects (19 women, 15 men; mean age 26.5 ± 2.5 yr) who were repeatedly presented with odor stimuli via a computer-controlled air-dilution olfactometer over the course of a single night. Each participant was exposed to one of four odorants, lavender oil (n = 13), vetiver oil (n = 5), vanillin (n = 12), or ammonium sulfide (n = 4), for durations of 5, 10, and 20 s every 9-15 min. Consistent with our hypotheses, we found that odor presentation during sleep enhanced the power of delta (0.5-4 Hz) and slow spindle (9-12 Hz) frequencies during non-rapid eye movement sleep. The increase was proportionate to odor duration. In addition, odor presentation did not modulate the occurrence of KCs. These findings imply a sleep-promoting olfactory mechanism that may deepen sleep through driving increased slow-frequency oscillations.

You'll feel better in the morning: slow wave activity and overnight mood regulation in interepisode bipolar disorder

BACKGROUND Sleep disturbances are prominent correlates of acute mood episodes and inadequate recovery in bipolar disorder (BD), yet the mechanistic relationship between sleep physiology and mood remains poorly understood. Using a series of pre-sleep mood inductions and overnight sleep recording, this study examined the relationship between overnight mood regulation and a marker of sleep intensity (non-rapid eye movement sleep slow wave activity; NREM SWA) during the interepisode phase of BD. METHODS Adults with interepisode BD type 1 (BD; n = 20) and healthy adult controls (CTL; n = 23) slept in the laboratory for a screening night, a neutral mood induction night (baseline), a happy mood induction night, and a sad mood induction night. NREM SWA (0.75-4.75 Hz) was derived from overnight sleep EEG recordings. Overnight mood regulation was evaluated using an affect grid pleasantness rating post-mood induction (pre-sleep) and the next morning. RESULTS Overnight mood regulation did not differ between groups following the sad or happy inductions. SWA did not significantly change for either group on the sad induction night compared with baseline. In BD only, SWA on the sad night was related to impaired overnight negative mood regulation. On the happy induction night, SWA increased relative to baseline in both groups, though SWA was not related to overnight mood regulation for either group. CONCLUSIONS These findings indicate that SWA disruption may play a role in sustaining negative mood state from the previous night in interepisode BD. However, positive mood state could enhance SWA in bipolar patients and healthy adults.

Olfaction and Sleep

As far as I know, the only reason we need to sleep that is really, really solid is because we get sleepy. Coming from William C. Dement, one of the pioneers of contemporary sleep research, this statement depicts sleep as a neurobiological black box. One of the best ways to probe such black boxes is through exceptions, and olfaction stands out as such an exceptional sensory system during sleep. Specifically, whereas sensory stimuli presented during sleep typically wake, this is not the case with odors. In fact, odors may promote sleep. In turn, they remain processed by the sleeping brain, and provide a telling window onto sleeping brain capabilities. Here, we briefly review the foundations of sleep, and then extensively detail the literature on olfaction in sleep, concentrating on studies in humans. We speculate that the unique interplay of sleep and smell whereby odors are processed in sleep without causing wake reflects unique aspects of olfactory neurophysiology, particularly the direct projections from periphery to cortex without a thalamic relay. Finally, although the mechanisms allowing odor processing during sleep without arousal remain unclear, this phenomenon lends itself to using olfaction as a window onto sleep mentation. This approach has uncovered several aspects of learning and memory during sleep. We review these efforts, and conclude with detailing their potential application in the treatment of disease.