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The present findings suggest that sleep deprivation produces hyperalgesic changes that cannot be explained by nonspecific alterations in somatosensory functions.

P atients with chronic pain syndromes often suffer from sleep disturbances (1). However, it is difficult to determine the direction of cause between pain and sleep disturbance. The usual perspective favours an arousal-augmenting function of pain, which prevents the initiation or the continuation of sleep. Alternatively, it is believed that the modulation of pain and sleep-wake regulation share common neurobiological systems, in particular the central serotoninergic one (2). Consequently, the association of pain and disturbed sleep might be a secondary phenomenon due to a common neurobiological dysfunction. Finally, a rather unusual perspective is that poor sleep can interfere with pain processing. With this latter direction of relation in mind, we have addressed the following issues by reviewing the literature with a clear focus on experimental studies. The following perspectives may help to integrate the reviewed findings. The relationship between sleep disturbances and pain assuggested by correlational data. The majority of studies on the relationship between sleep and pain were not based on an experimental design, but relied on correlations only. In this section, a brief summary of the clinical investigations is given, including their first clues concerning the influence of disturbed sleep on pain, and their limitation in deriving causal relations.2. Sleep deprivation as a methodological approach to mimic disturbed sleep and derive experimental evidence for algesic effects. A comprehensive review of animal and human studies, which used sleep deprivation as an independent variable and examined its influence on pain processing, is provided.3. Assumptions on the algesic mechanisms of sleep deprivation.Results from animals studies suggest various neurochemical changes during and after sleep deprivation, which seemed to be involved in the modulation of pain. With a focus on the serotoninergic system, sleep deprivation affects 5-hydroxytryptamine (5-HT) turnover (3), the firing rate of serotoninergic neurons in the dorsal nucleus raphé (4) and 5-HT receptor functions (5). Given the well-known pain inhibitory effects of 5-HT, these changes may be tentatively integrated into a serotoninergic model of hyperalgesic action of sleep deprivation. Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture. One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain. To fathom this direction of cause, experimental human and animal studies on the effects of sleep deprivation on pain processing were reviewed. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action.The heterogeneity of the human data and the exclusive interest in rapid eye movement sleep deprivation in animals so far do not allow us to draw firm conclusions as to wheth...

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Background Chronotype and insomnia have been related to the development and to an unfavourable course of depression. However, the mutual relationship of both risk factors is as yet unclear, especially in acute, clinically manifest depressive disorders. Aims The present study was carried out to elucidate the separate direct and indirect influence of chronotype and poor sleep quality on depression severity in patients hospitalized for depression. Methods Depression severity (BDI-II), chronotype (Morningness-Eveningness Questionnaire), and subjective sleep quality (Pittsburgh Sleep Quality Index total score) were assessed concurrently in inpatients with a depressive syndrome and insomnia during routine treatment. Correlations, multiple regression and bootstrapping methods for testing mediation models were applied to assess the independent direct and indirect effects of chronotype and sleep quality on depression severity, after adjusting for effects of age and gender. Results Data from 57 consecutively admitted patients (88% with major depression) were analyzed (68% women, mean age 41 ± 13 years). Significant correlations between morningness-eveningness (p <0.05) or sleep quality (p <0.01) and depression severity were found; in a multiple regression model comprising chronotype, sleep quality, age and gender, only chronotype (p <0.05) and sleep disturbances (p <0.01) remained as independent significant concurrent predictors of depression severity (R(2) = 0.184, p <0.01). Two mediation models revealed no significant results. Conclusions Eveningness and poor subjective sleep quality were independently and directly associated with higher depression severity in inpatients with depressive syndromes. Chronotype and sleep quality should be taken into account not only in risk assessment and prevention but also in hospitalized patients to develop and improve treatment options.

Background: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Methods: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Results: Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Conclusions: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.

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The individual's chronotype is regarded as rather stable trait with substantial heritability and normal distribution of the "morningness-eveningness" dimension in the general population. Eveningness has been related to the risk of developing affective, particularly depressive, disorders. However, age and other sociobiological factors may influence chronotypes. The present study investigated the distribution, stability, and clinical correlates of chronotype and morningness-eveningness in hospitalized patients with affective disorder. Chronotype was assessed with the morningness-eveningness questionnaire (MEQ) in 93 patients with nonseasonal depressive syndrome (85% major depression; 15% depressive adjustment disorder) after admission, and in 19 patients again before discharge. Distribution, stability and correlations of MEQ scores with clinical variables were calculated. Additionally, a literature analysis of chronotype distributions in samples of nondepressed persons and patients with nonseasonal depression was carried out. MEQ scores (mean 49 ± 11, range 23-75, higher scores indicate morningness) in 93 acutely depressed inpatients (age 41 ± 14 years, range 18-75 years; 63% women; hospitalization 48 ± 22 days; BDI-II 32 ± 11) were normally distributed (Shapiro-Wilk test; W = 0.993, p = 0.920) with 59.1% intermediate types, 19.4% evening types, and 21.5% morning types. MEQ change scores from admission to discharge were nonsignificant (-1.3 ± 5.0; paired t-test, t18 = -1.09; p = 0.29) despite significantly improved depression scores (-19.4 ± 7.6; paired t-test, t18 = 11.2, p < 0.001). Age (r = 0.24), and depression scores (r = -0.21) correlated significantly (p < 0.05) with MEQ scores; associations with sex and hospitalization duration were nonsignificant. The present study and literature findings revealed that the frequency of evening types is not clearly elevated in depression, but morning types are less frequent compared to healthy samples (p < 0.001). Morningness-eveningness scores were normally distributed and stable in depressive inpatients. In line with previous findings, but contrary to theoretical assumptions, evening types were not overrepresented in depressed patients. Additionally, relatively less morning types and more intermediate types were found in depressed patients. Future studies should focus on transitions from morning to intermediate types as a tentative risk or correlate of emerging depression.