Brainstem modulation of pain during sleep and waking

Foo, H.; Mason, Peggy

doi:10.1053/smrv.2002.0224

Cited by 126 publications

(86 citation statements)

References 66 publications

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“…Highly sensitive sleep phenomena may be altered by intrinsic and extrinsic factors (25). It is well known that sleep problems have a major impact on QOL (26).…”

Section: Discussionmentioning

confidence: 99%

Nocturnal Knee Pain Increases With the Severity of Knee Osteoarthritis, Disturbing Patient Sleep Quality

Sasaki

Tsuda

Yamamoto

et al. 2014

Arthritis Care & Research

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Objective. Sleep disturbances frequently accompany chronic pain from osteoarthritis (OA). Effective management of sleep disturbances may require successful treatment of chronic pain, a key factor in the clinical evaluation of knee OA. However, the relationship between the severity of knee OA and sleep quality is unclear. Our purpose was to correlate the prevalence of nocturnal knee pain with different OA severity levels and to determine its influence on sleep quality. Methods. Subjects included 1,214 local volunteers with mean ؎ SD age 58.1 ؎ 13.0 years. The existence and severity of knee OA were determined by the Kellgren/Lawrence (K/L) grade, and joint space widths were measured. The presence of nocturnal knee pain and Knee Injury and Osteoarthritis Outcome Scores (KOOS) were assessed by self-completed questionnaires. Sleep quality was evaluated by the Pittsburgh Sleep Quality Index. Knee-related factors affecting sleep quality were detected using statistical methods. Results. The prevalence of nocturnal knee pain was 3.6%, 6.9%, 19.4%, 32.7%, and 75.0% in K/L grades 0, 1, 2, 3, and 4, respectively. Also, prevalence significantly increased with OA severity (P < 0.001). Sleep problems also increased with K/L grade (P ‫؍‬ 0.038), and KOOS quality of life (QOL) was significantly lower in those with OA and sleep problems. Logistic regression showed that sleep problems were related to joint space narrowing (P ‫؍‬ 0.016) and nocturnal knee pain (P ‫؍‬ 0.039). Severe OA also disturbed onset and maintenance of sleep. Conclusion. The prevalence of nocturnal knee pain and sleep problems increased with the severity of OA, impacting QOL. These results suggest the necessity of appropriate nocturnal pain control.

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“…Highly sensitive sleep phenomena may be altered by intrinsic and extrinsic factors (25). It is well known that sleep problems have a major impact on QOL (26).…”

Section: Discussionmentioning

confidence: 99%

Nocturnal Knee Pain Increases With the Severity of Knee Osteoarthritis, Disturbing Patient Sleep Quality

Sasaki

Tsuda

Yamamoto

et al. 2014

Arthritis Care & Research

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“…In addition, high levels of 26RFa receptors have also been observed in various brain nuclei involved in the processing of pain such as the parafascicular thalamic nucleus (Weigel and Krauss, 2004), the locus coeruleus (Fukui et al, 2004;Imbe et al, 2004), the dorsal raphe nucleus (Foo and Mason, 2003;Cucchiaro et al, 2005), and the parabrachial nucleus (Cortelli and Pierangeli, 2003;Richard et al, 2005). The NPFF2 receptor has been previously reported also to be present in these nuclei (Elshourbagy et al, 2000;Zeng et al, 2003;Gouarderes et al, 2004), and the role of NPFF, one of the endogenous ligand of NPFF2 (Engström et al, 2003), in the modulation of pain transmission is now widely accepted (for review see Mollereau et al, 2005).…”

Section: Functional Considerationsmentioning

confidence: 98%

Distribution of 26RFa binding sites and GPR103 mRNA in the central nervous system of the rat

Bruzzone

Lectez

Dionne‐Laporte

et al. 2007

J of Comparative Neurology

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The novel RFamide peptide 26RFa, the endogenous ligand of the orphan receptor GPR103, affects food intake, locomotion, and activity of the gonadotropic axis. However, little is known regarding the localization of 26RFa receptors. The present report provides the first detailed mapping of 26RFa binding sites and GPR103 mRNA in the rat central nervous system (CNS). 26RFa binding sites were widely distributed in the brain and spinal cord, whereas the expression of GPR103 mRNA was more discrete, notably in the midbrain, the pons, and the medulla oblongata, suggesting that 26RFa can bind to a receptor(s) other than GPR103. Competition experiments confirmed that 26RFa interacts with an RFamide peptide receptor distinct from GPR103 that may be NPFF2. High densities of 26RFa binding sites were observed in olfactory, hypothalamic, and brainstem nuclei involved in the control of feeding behavior, including the piriform cortex, the ventromedial and dorsomedial hypothalamic nuclei, the paraventricular nucleus, the arcuate nucleus, the lateral hypothalamic area, and the nucleus of the solitary tract. The preoptic and anterior hypothalamic areas were also enriched with 26RFa recognition sites, supporting a physiological role of the neuropeptide in the regulation of the gonadotropic axis. A high density of 26RFa binding sites was detected in regions of the CNS involved in the processing of pain, such as the dorsal horn of the spinal cord and the parafascicular thalamic nucleus. The wide distribution of 26RFa binding sites suggests that 26RFa has multiple functions in the CNS that are mediated by at least two distinct receptors.

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“…However, it is quite diffi cult to prove which of these two factors (pain or sleep disturbances) causes the other. Both pain and sleep-wake cycles are regulated by common neurobiological systems, in particular the serotonergic system [66] . Thus, they might well be interrelated and augment each other in a vicious circle.…”

Section: Discussionmentioning

confidence: 99%

Insomnia in Somatoform Pain Disorder: Sleep Laboratory Studies on Differences to Controls and Acute Effects of Trazodone, Evaluated by the Somnolyzer 24 × 7 and the Siesta Database

et al. 2005

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Patients with chronic pain often suffer from sleep disturbances, specifically decreased deep sleep, and thus may get into a vicious circle which maintains their pain condition. Utilizing polysomnography and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients with nonorganic insomnia (F51.0) related to somatoform pain disorder (SPD; F45.4) as compared with age- and sex-matched healthy controls of the Siesta normative database. Patients demonstrated a markedly deteriorated Pittsburgh Sleep Quality Index, a decreased Quality of Life Index, slightly increased self-reported anxiety (Zung SAS) and depression scores (Zung SDS), as well as an increased Epworth Sleepiness Scale and International Restless Legs Syndrome Scale score. Subjective sleep and awakening quality was markedly reduced, while somatic complaints were increased. Polysomnographic evaluation by a recently developed automatic sleep classifier (Somnolyzer 24 × 7) based on the rules of Rechtschaffen and Kales demonstrated reduced slow-wave sleep (SWS), the target variable in the present study, a decreased stage shift index, increased SWS latency and stage 4 sleep (S4) latency and an increased frequency of shifts from S2 to wakefulness (W) in patients as compared with controls. Minimal oxygen saturation was found decreased, periodic leg movements (PLMs) were increased. In the morning, patients showed deteriorated well-being, drive, mood and wakefulness. There were no significant noopsychic or psychophysiological differences between patients and controls (except for a reduced numerical memory and a slightly increased morning diastolic blood pressure in patients). Subsequent evaluation of the acute effects of 100 mg of a controlled-release formulation of trazodone (Trittico^® retard) in the patients demonstrated an increase in the target variable SWS, accompanied by a reduction in the number of awakenings and stage shifts. It normalized the frequency of shifts from S2 to W and reduced the frequency of shifts from W to S1, from S1 to S2, as well as from any stage to S1 and S2. Trazodone, however, also significantly reduced the total sleep period and S2 and increased the latency to S1. Moreover, the drug increased the reduced minimal O₂saturation, reduced the arousal index and the PLMs-in-wake index and normalized the increased morning diastolic blood pressure. In conclusion, our study demonstrated that SPD induced significant changes in subjective and objective sleep and awakening quality, which were partially mitigated by trazodone therapy. The data on the target variable SWS support our hypothesis of a key-lock principle in the diagnosis and drug treatment of sleep disorders. Our study provided the first evidence on the usefulness of the Somnolyzer 24 × 7 and the Siesta database in clinical practice.

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Brainstem modulation of pain during sleep and waking

Cited by 126 publications

References 66 publications

Nocturnal Knee Pain Increases With the Severity of Knee Osteoarthritis, Disturbing Patient Sleep Quality

Nocturnal Knee Pain Increases With the Severity of Knee Osteoarthritis, Disturbing Patient Sleep Quality

Distribution of 26RFa binding sites and GPR103 mRNA in the central nervous system of the rat

Insomnia in Somatoform Pain Disorder: Sleep Laboratory Studies on Differences to Controls and Acute Effects of Trazodone, Evaluated by the Somnolyzer 24 × 7 and the Siesta Database

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