Corinna Kloepfer

Does REM sleep contribute to subjective wake time in primary insomnia? A comparison of polysomnographic and subjective sleep in 100 patients

Primary insomnia (PI) is characterized by low subjective sleep quality which cannot always be verified using polysomnography (PSG). To shed light on this discrepancy, subjective estimates of sleep and PSG variables were compared in patients with PI and good sleeper controls (GSC). 100 patients with PI (age: 42.57 ± 12.50 years, medication free for at least 14 days) and 100 GSC (41.12 ± 13.99 years) with a sex distribution of 46 men and 54 women in each group were included. Both PSG and questionnaire variables showed clear impairments of sleep quality in PI compared with GSC. The arousal index within total sleep time was increased, which was mainly because of a strong increase within rapid eye movement (REM) sleep. Subjectively, more PI than GSC subjects estimated wake times longer than obtained from PSG. Linear modeling analysis of subjective wake time in terms of PSG parameters revealed that in addition to PSG defined wake time, REM sleep time contributed significantly to subjective wake time. This REM sleep contribution was larger for PI than for GSC subjects. The findings suggest that REM sleep‐related processes might contribute to subjectively disturbed sleep and the perception of waking time in patients with PI.

Sleep-related memory consolidation in primary insomnia.

It has been suggested that healthy sleep facilitates the consolidation of newly acquired memories and underlying brain plasticity. The authors tested the hypothesis that patients with primary insomnia (PI) would show deficits in sleep‐related memory consolidation compared to good sleeper controls (GSC). The study used a four‐group parallel design (n = 86) to investigate the effects of 12 h of night‐time, including polysomnographically monitored sleep (‘sleep condition’ in PI and GSC), versus 12 h of daytime wakefulness (‘wake condition’ in PI and GSC) on procedural (mirror tracing task) and declarative memory consolidation (visual and verbal learning task). Demographic characteristics and memory encoding did not differ between the groups at baseline. Polysomnography revealed a significantly disturbed sleep profile in PI compared to GSC in the sleep condition. Night‐time periods including sleep in GSC were associated with (i) a significantly enhanced procedural and declarative verbal memory consolidation compared to equal periods of daytime wakefulness in GSC and (ii) a significantly enhanced procedural memory consolidation compared to equal periods of daytime wakefulness and night‐time sleep in PI. Across retention intervals of daytime wakefulness, no differences between the experimental groups were observed. This pattern of results suggests that healthy sleep fosters the consolidation of new memories, and that this process is impaired for procedural memories in patients with PI. Future work is needed to investigate the impact of treatment on improving sleep and memory.

Functional and structural brain alterations in insomnia: implications for pathophysiology.

Insomnia is defined as the complaint of not being able to fall asleep or to maintain sleep, and/or nonrestorative sleep, accompanied by impaired daytime functioning on a social, emotional or professional level. Insomnia per se is a very frequent complaint and can be caused by environmental, medical, mental or psychosocial factors or the intake of drugs. Primary insomnia is an insomnia subtype characterized by the absence of a causative medical or psychiatric factor. From a pathophysiological point of view, persistent hyperarousal on autonomous, emotional, cognitive or neurobiological levels is thought to be the decisive factor for the development and persistence of chronic primary insomnia. This view is supported by studies confirming that patients with primary insomnia display heightened levels of fast frequencies of the sleep EEG, show increased production of cortisol and interleukin‐6, and demonstrate increased metabolism in several brain areas during sleep (as measured by positron emission tomography). Furthermore, primary insomnia is coupled with cognitive deficits during waking and with impairments of nocturnal memory consolidation. Just recently, reductions in hippocampal volume size have been reported in patients suffering from primary insomnia. In the light of neurobiological theories of sleep–wake regulation, primary insomnia may be conceptualised as the final common pathway of the interaction of a genetic vulnerability to an imbalance between arousing and sleep‐inducing brain centres (which is triggered by psychosocial and/or medical stressors) with perpetuating mechanisms such as maladaptive behaviours, learned sleep‐preventing associations and cognitive factors.

No persisting effect of partial sleep curtailment on cognitive performance and declarative memory recall in adolescents

Growing evidence indicates that sleep facilitates learning and memory processing. Sleep curtailment is increasingly common in adolescents. The aim of this study was to examine the effects of short‐term sleep curtailment on declarative memory consolidation in adolescents. A randomized, cross‐over study design was chosen. Twenty‐two healthy subjects, aged 14–16 years, spent three consecutive nights in the sleep laboratory with a bedtime of 9 h during the first night (adaptation), 4 h during the second (partial sleep curtailment) and 9 h during the third night (recovery). The control condition consisted of three consecutive nights with bedtimes of 9 h. Both experimental conditions were separated by at least 3 weeks. The acquisition phase for the declarative tests was between 16:00 and 18:00 hours before the second night. Memory performance was examined in the morning after the recovery night. Executive function, attention and concentration were also assessed to control for any possible effects of tiredness. During the 4‐h night, we observed a curtailment of 50% of non‐rapid eye movement (non‐REM), 5% of slow wave sleep (SWS) and 70% of REM sleep compared with the control night. Partial sleep curtailment of one night did not influence declarative memory retrieval significantly. Recall in the paired‐associate word list task was correlated positively with percentage of non‐REM sleep in the recovery night. Declarative memory consolidation does not appear to be influenced by short‐term sleep curtailment in adolescents. This may be explained by the high ability of adolescents to compensate for acute sleep loss. The correlation between non‐REM sleep and declarative memory performance supports earlier findings.

M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation

Preclinical studies have implicated cholinergic neurotransmission, specifically M1 muscarinic acetylcholine receptor (mAChR) activation, in sleep-associated memory consolidation. In the present study, we investigated the effects of administering the direct M1 mAChR agonist RS-86 on pre-post sleep memory consolidation. Twenty healthy human participants were tested in a declarative word-list task and a procedural mirror-tracing task. RS-86 significantly reduced rapid eye movement (REM) sleep latency and slow wave sleep (SWS) duration in comparison with placebo. Presleep acquisition and postsleep recall rates were within the expected ranges. However, recall rates in both tasks were almost identical for the RS-86 and placebo conditions. These results indicate that selective M1 mAChR activation in healthy humans has no clinically relevant effect on pre-post sleep consolidation of declarative or procedural memories at a dose that reduces REM sleep latency and SWS duration.

Impaired memory consolidation during sleep in patients with functional memory disorder

Functional memory disorder (FMD) is characterized by mnestic and attentional deficits without symptoms of mild cognitive impairment or dementia. FMD usually develops in subjects with high psychosocial stress level and is classified to the somatoform disorders. We assessed memory performance (procedural mirror tracing task, declarative visual and verbal memory task) and other cognitive functions before and after one night of sleep in 12 FMD patients (mean age: 51.7 yrs, 7 females) and 12 healthy subjects matched for age, gender and IQ. Memory performance and other neurocognitive tasks did not differ between the groups at baseline. After one night of sleep, FMD patients showed an impairment of declarative memory consolidation compared to healthy subjects (visual task: p=0.004; verbal task: p=0.039). Spectral analysis of sleep-EEG indicated an increased cortical excitation in FMD. We hypothesize that a hyperarousal state in FMD might contribute to sleep disturbance implicating negative effects on declarative memory consolidation.

Nicotine. Influence on sleep and its relevance for psychiatry and psychotherapy

BACKGROUND Nicotine, by its impact on several neurotransmitter systems, influences sleep. Sleep disturbance is a common symptom in different psychiatric disorders and there is a high prevalence of smoking in psychiatric patients. METHODS Systematic literature search. RESULTS Symptoms of insomnia are observed during nicotine consumption and its withdrawal. The effects of therapeutic nicotine substitution after smoking cessation on sleep are often masked by withdrawal symptoms. Depressive non-smokers experience an improvement of mood under nicotine administration and in turn, depressive symptoms and sleep impairment during nicotine withdrawal have a negative impact on abstinence rates. CONCLUSION Sleep disturbance is a comorbid risk factor influencing abstinence during smoking cessation. In depressive patients the complex relationship between affect, sleep, nicotine consumption and its withdrawal should be carefully monitored. In such subgroups of smokers willing to quit this has to be taken care of in therapeutic interventions.