Changes in brain, core and tail skin temperatures (Tbr, Tc and Tt) associated with transitions in the arousal states were recorded in rats throughout the 24-h diurnal cycle at 10 degrees C, 21 degrees C and 29 degrees C. Falling asleep was accompanied by decreases in both Tbr and Tc and vasodilation at 10 degrees C and 21 degrees C. At 29 degrees C, tail vessels were permanently dilated, and further dilation was not found on sleep onset. Tbr and Tc, however, continued to decrease during non-rapid-eye-movement sleep (NREMS); these changes are likely to result from reductions in heat production and increased conductive heat loss. The changes in Tbr, Tc and Tt on awakening mirrored those on falling asleep. It is suggested that the suppression of sleep in the cold and the enhancement of NREMS in the heat promote thermoregulation. Rapid-eye-movement sleep (REMS) was associated with sharp rises in Tbr. The rise in Tbr was the largest in the cold and was attenuated at 29 degrees C. Tc decreased and Tt increased in the cold, whereas Tc tended to increase and Tt to decrease in the heat. The paradoxical peripheral vasomotion during REMS supports previous suggestions on severe thermoregulatory impairment during REMS in other species.

The prevalence of insomnia is high in patients with chronic pain conditions, but the level of importance in relation to other symptoms for health aspects is low, and the associations with other important symptoms are relatively weak. One way to increase the effects of multimodal rehabilitation programs may be to provide interventions directed specifically at insomnia rather than focusing only on interventions that address pain, depression and anxiety. Implications for Rehabilitation The prevalence of insomnia is high in patients with complex chronic pain conditions. Relatively low correlations existed between insomnia and pain intensity, depression, anxiety and other psychological aspects. Pain intensity, anxiety and depression were more important for perceived health aspects than insomnia. One way to increase the effects of multimodal rehabilitation programs may be to also include interventions directed directly to insomnia.

Previously, it was suggested that a hypothalamic mechanism links somatotropin [growth hormone (GH)] secretion to sleep regulation, and this may explain the temporal correlation between GH release and nonrapid eye movement sleep (NREMS) on sleep onset. The purpose of these experiments was to study whether growth hormone-releasing factor (GRF), a hypothalamic peptide responsible for stimulation of GH secretion, also has the capacity to promote sleep in rats and rabbits. Artificial cerebrospinal fluid or GRF (human GRF-[1-40], 0.01, 0.1, and 1 nmol/kg) was intracerebroventricularly injected to rats at dark onset, and the electroencephalogram (EEG), brain temperature (Tbr), and motor activity were recorded for 24 h. Rabbits received the same doses of GRF during the light period, and sleep-wake activity was monitored for 6 h. GRF promoted NREMS and rapid eye movement sleep (REMS) and increased EEG slow-wave activity in both rats and rabbits. NREMS increased in postinjection hour 1 after low doses of GRF, whereas the effect was more prolonged after higher doses. REMS increased in response to the low and middle doses of GRF in postinjection hour 1 in rats and in hour 2 after each dose in rabbits. The diurnal rhythms of sleep-wake activity, motor activity, and Tbr were not affected in rats. Because GRF promotes sleep and also stimulates GH secretion, it is a likely candidate for linking GH secretion and sleep regulation.

Sleep states and power spectra of the electroencephalogram (EEG) were determined in freely moving young rats. Recordings during 24 h were obtained from the same animals at three different ages. Already at the age of 23 days waking predominated in the 12-h dark period. Rapid-eye-movement sleep (REMS) declined between the age of 23 and 40 days. Its 24-h maximum was situated in the dark period at 23 and 29 days of age and in the light period at 40 days. Slow-wave activity (SWA; 0.75-4.0 Hz) of the non-REMS (NREMS) EEG showed marked age-related changes: a declining trend in the 12-h light period was absent at 23 days, moderate at 29 days, and prominent at 40 days. At 23 days, SWA progressively declined within ultradian sleep episodes and at 24 days was massively increased after 2-h sleep deprivation (SD). At the age of 30 days, 6-h SD induced much smaller changes. The distinct 24-h pattern of high-frequency activity (10.25-25.0 Hz) was present at all ages and may represent an EEG correlate of a circadian process. We conclude that homeostatic mechanisms regulating NREMS intensity are already operative a few days after weaning.

Purpose: The remodeling of functional neuronal connectivity in chronic widespread pain (CWP) patients remains largely unexplored. This study aimed to investigate functional connectivity in CWP patients in brain networks related to chronic pain for changes related to pain sensitivity, psychological strain, and experienced pain. Patients and methods: Functional connectivity strength of the default mode network (DMN) and the salience network (SN) was assessed with functional magnetic resonance imaging. Between-group differences were investigated with an independent component analysis for altered connectivity within the whole DMN and SN. Then, changes in connectivity between nodes of the DMN and SN were investigated with the use of a seed-target analysis in relation to the covariates clinical pain intensity, pressure pain sensitivity, psychological strain, and as an effect of experienced experimental cuff-pressure pain. Results: CWP patients showed decreased connectivity in the inferior posterior cingulate cortex (PCC) in the DMN and increased connectivity in the left anterior insula/superior temporal gyrus in the SN when compared to controls. Moreover, higher pain sensitivity in CWP when compared to controls was related to increased connectivity within the SN (between left and right insula) and between SN and DMN (between right insula and left lateral parietal cortex). Conclusion: This study shows that connectivity within the DMN was decreased and connectivity within the SN was increased for CWP. Furthermore, we present a novel finding of interaction of pain sensitivity with SN and DMN-SN functional connectivity in CWP.

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

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Objective Insomnia is the most commonly diagnosed comorbidity disorder among patients with chronic pain. This circumstance requests brief and valid instruments for screening insomnia in epidemiological studies. The main object of this study was to assess the psychometric properties and factor structure of the Swedish version of the Insomnia Severity Index (ISI). The ISI is a short instrument designed to measure clinical insomnia and one of the most common used scales both in clinical and research practice. However there is no study in Sweden that guarantees neither its factor structure nor its feasibility in chronic pain patients. We further examined the measurement invariance property of the ISI across the two sexes. Methods The ISI was administered to 836 (269 men and 567 women) chronic pain patients from the Swedish Quality Registry for Pain Rehabilitation. This study used demographic data, the Hospital Anxiety and Depression Scale (HADS), the Mental Summary Component (MSC) of the Health Survey (SF-36) and the item 7 from Multidimensional Pain Inventory (MPI). The sample was divided into two random halves: exploratory factor analysis (EFA) was performed in the first sample (N1 = 334, 40%) and confirmatory factor analysis (CFA) in the second half of the sample (N2 = 502, 60%). The measurement and structural invariance of the proposed structure (4-item version) between the two sexes as well as reliability and validity indexes were further assessed. Results Exploratory factor analysis using the principal axis factoring method generated one global factor structure for the ISI, explaining 63.1% of the total variance. The one factor solution was stable between the two sexes. Principal component analysis was also applied and indicated almost identical results. The structure was further assessed by CFA, resulting in an adequate fit only after omitting three items. The difference on structural and measurement invariance in the loadings by participants' sex was not significant (Δχ2 = 10.6; df = 3; p = .69 and Δχ2 = 2.86; df = 3; p = 41 respectively). The shorter version four-item Insomnia Severity Index (ISI-4) was analysed further. The Chronbach's alpha for the global ISI-4 score was 0.88. The construct validity of the ISI-4 was also supported by the, Hospital Anxiety and Depression Scale, the Mental Summary Component of quality of life and quality of sleep data. Pain intensity was significantly associated with the ISI-4 score (beta = .29, p < 001) whereas no significant correlation between four-item Insomnia Severity Index score and age was observed (p > 05). Conclusions and implications Although short, the four-item Insomnia Severity Index (ISI-4) version seemed to effectively assess insomnia in chronic pain patients. An important clinical implication is that the four-item Swedish Insomnia Severity Index can be used in chronic pain cohorts when screening for insomnia problems. Its measurement and structural invariance property across the two sexes shows that the ISI-4 is a valid measure of the insomnia across groups ...