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Manual scoring of polysomnography data is labor-intensive and time-consuming, and most existing software does not account for subjective differences and user variability. Therefore, we evaluated a supervised machine learning algorithm, SomnivoreTM, for automated wake–sleep stage classification. We designed an algorithm that extracts features from various input channels, following a brief session of manual scoring, and provides automated wake-sleep stage classification for each recording. For algorithm validation, polysomnography data was obtained from independent laboratories, and include normal, cognitively-impaired, and alcohol-treated human subjects (total n = 52), narcoleptic mice and drug-treated rats (total n = 56), and pigeons (n = 5). Training and testing sets for validation were previously scored manually by 1–2 trained sleep technologists from each laboratory. F-measure was used to assess precision and sensitivity for statistical analysis of classifier output and human scorer agreement. The algorithm gave high concordance with manual visual scoring across all human data (wake 0.91 ± 0.01; N1 0.57 ± 0.01; N2 0.81 ± 0.01; N3 0.86 ± 0.01; REM 0.87 ± 0.01), which was comparable to manual inter-scorer agreement on all stages. Similarly, high concordance was observed across all rodent (wake 0.95 ± 0.01; NREM 0.94 ± 0.01; REM 0.91 ± 0.01) and pigeon (wake 0.96 ± 0.006; NREM 0.97 ± 0.01; REM 0.86 ± 0.02) data. Effects of classifier learning from single signal inputs, simple stage reclassification, automated removal of transition epochs, and training set size were also examined. In summary, we have developed a polysomnography analysis program for automated sleep-stage classification of data from diverse species. Somnivore enables flexible, accurate, and high-throughput analysis of experimental and clinical sleep studies.

Torpor is a peculiar mammalian behaviour, characterized by the active reduction of metabolic rate, followed by a drop in body temperature. To enter torpor, the activation of all thermogenic organs that could potentially defend body temperature must be prevented. Most of these organs, such as the brown adipose tissue, are controlled by the key thermoregulatory region of the Raphe Pallidus (RPa). Currently, it is not known which brain areas mediate the entrance into torpor. To identify these areas, the expression of the early gene c-Fos at torpor onset was assessed in different brain regions in mice injected with a retrograde tracer (Cholera Toxin subunit b, CTb) into the RPa region. The results show a network of hypothalamic neurons that are specifically activated at torpor onset and a direct torpor-specific projection from the Dorsomedial Hypothalamus to the RPa that could putatively mediate the suppression of thermogenesis during torpor.

Cerebral blood flow measurements during sleep are reviewed and discussed in relation to the different techniques utilized (Positron Emission Tomography, functional Magnetic Resonance Imaging, Flowmeters, Radioactive Microspheres, Brain Temperature Recordings, Spectrophotometry) since these methodological approaches aim at diverse features of circulation changes in the spatial or temporal domain. The regulation of cerebral circulation during sleep reveals no specific state-dependent features, flow-activity coupling being the prevailing mechanism, with O2, as the primary candidate for the metabolic side of the link. On a general level, the latest data on brain circulation are compatible with the classical hypothesis of a "restorative" function of sleep processes. © 2002 Elsevier Science Ltd. All rights reserved.

Cerebral vessels are extensively innervated by sympathetic nerves arising from superior cervical ganglia, and these nerves might play a protective role during the large arterial pressure surges of active sleep (AS). We studied lambs (n = 10) undergoing spontaneous sleep-wake cycles before and after bilateral removal of the superior cervical ganglia (SCGx, n = 5) or sham ganglionectomy (n = 5). Lambs were instrumented to record cerebral blood flow (CBF, flow probe on the superior sagittal sinus), carotid arterial pressure (Pca), intra-cranial pressure (Pic), cerebral perfusion pressure (P cp = Pca-Pic) and cerebral vascular resistance (CVR). Prior to SCGx, CBF (mL min-1) was significantly higher in AS than in Quiet Sleep (QS) and Quiet Wakefulness (QW) (17 +/- 2, 13 +/- 3, and 14 +/- 3 respectively, mean +/- SD, P < 0.05). Following SCGx, baseline CBF increased by 34, 31, and 29% respectively (P < 0.05). CVR also decreased in all states by ~25% (P < 0.05). During phasic AS, surges of Pca were associated with transient increases in Pcp, Pic and CBF. Following SCGx, peak CBF and Pic during surges became higher and more prolonged (P < 0.05). Our study is the first to reveal that tonic sympathetic nerve activity (SNA) constricts the cerebral circulation and restrains baseline CBF in sleep. SNA is further incremented during arterial pressure surges of AS, limiting rises in CBF and Pic, possibly by opposing vascular distension as well as by constricting resistance vessels. Thus, SNA may protect cerebral micro vessels from excessive distension during AS, when large arterial blood pressure surges are common. © 2005 European Sleep Research Society.

Cerebral blood flow measurements during sleep are reviewed and discussed in relation to the different techniques utilized (Positron Emission Tomography, functional Magnetic Resonance Imaging, Flowmeters, Radioactive Microspheres, Brain Temperature Recordings, Spectrophotometry) since these methodological approaches aim at diverse features of circulation changes in the spatial or temporal domain. The regulation of cerebral circulation during sleep reveals no specific state-dependent features, flow-activity coupling being the prevailing mechanism, with O2, as the primary candidate for the metabolic side of the link. On a general level, the latest data on brain circulation are compatible with the classical hypothesis of a "restorative" function of sleep processes. © 2002 Elsevier Science Ltd. All rights reserved.

Cerebral vessels are extensively innervated by sympathetic nerves arising from superior cervical ganglia, and these nerves might play a protective role during the large arterial pressure surges of active sleep (AS). We studied lambs (n = 10) undergoing spontaneous sleep-wake cycles before and after bilateral removal of the superior cervical ganglia (SCGx, n = 5) or sham ganglionectomy (n = 5). Lambs were instrumented to record cerebral blood flow (CBF, flow probe on the superior sagittal sinus), carotid arterial pressure (Pca), intra-cranial pressure (Pic), cerebral perfusion pressure (P cp = Pca-Pic) and cerebral vascular resistance (CVR). Prior to SCGx, CBF (mL min-1) was significantly higher in AS than in Quiet Sleep (QS) and Quiet Wakefulness (QW) (17 +/- 2, 13 +/- 3, and 14 +/- 3 respectively, mean +/- SD, P < 0.05). Following SCGx, baseline CBF increased by 34, 31, and 29% respectively (P < 0.05). CVR also decreased in all states by ~25% (P < 0.05). During phasic AS, surges of Pca were associated with transient increases in Pcp, Pic and CBF. Following SCGx, peak CBF and Pic during surges became higher and more prolonged (P < 0.05). Our study is the first to reveal that tonic sympathetic nerve activity (SNA) constricts the cerebral circulation and restrains baseline CBF in sleep. SNA is further incremented during arterial pressure surges of AS, limiting rises in CBF and Pic, possibly by opposing vascular distension as well as by constricting resistance vessels. Thus, SNA may protect cerebral micro vessels from excessive distension during AS, when large arterial blood pressure surges are common. © 2005 European Sleep Research Society.