SLEEP

kryger, Meir, H.

doi: 10.1093/sleep/17.5.405pmid: N/A

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Chambers, Mark, J.;Hauri, Peter, J.;Wisbey,, Joyce

doi: 10.1093/sleep/17.5.408pmid: N/A

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Phillips, Barbara, A.;Berry, David T., R.;Schmitt, Frederick, A.;Harbison,, Lynn;Lipke-Molby,, Tanja

doi: 10.1093/sleep/17.5.411pmid: 7991951

Summary: We report the results of a study of the effects of sleep-disordered breathing in a cohort of healthy elderly subjects followed longitudinally for 3 years. In a comprehensive evaluation of daytime functioning, including medical history and physical examination, pulmonary function testing and neuropsychiatric testing, we found very little difference in the neuropsychiatric or medical sequelae between those subjects with moderate [apnea + hypopnea index (AHI) ≥ 5] and low (AHI < 5) levels of sleep-disordered breathing at baseline. Although there were no differences in the electrocardiogram, pulse rate or cardiac history data, a mild association was found between indices of sleep-disordered breathing and pulmonary function. We conclude that moderate levels of sleep-disordered breathing in an otherwise asymptomatic healthy geriatric patient should probably not be considered pathologic in the short term. Sleep-disordered breathing, Elderly, Pulmonary function This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

Javaheri,, Shahrokh;Colangelo,, Gregory;Lacey,, William;Gartside, Peter, S.

doi: 10.1093/sleep/17.5.416pmid: 7991952

Summary: In order to determine the relationship between chronic hypercapnia and anthropomorphic data, pulmonary function tests and slopes of ventilatory responses to hypercapnia (HVCR) and hypoxia (HVR), we studied 55 patients with sleep apnea-hypopnea syndrome (SAHS). Patients were divided into hypercapnic, PaCO2 ≥ 45 mm Hg (Group I, n = 23, PaO2 = 61 ± 10 and PaCO2 = 50 ± 5 mm Hg, and [HCO−3] = 30 ± 4 mEq/l [means ± SD]) and normocapnic (or eucapnic), PaCO2 < 45 mm Hg (Group II, n = 32, PaO2 = 76 ± 10 and PaCO2 = 39 ± 4 mm Hg and [HCO−3] = 25 ± 3 mEq/l [means ± SD]) groups. When compared to the normocapnic group, hypercapnic patients were significantly heavier (with greater body surface area) and had significantly more severe restrictive and obstructive defects and impaired HVR and HCVR. The means (±SD) of some of the data follow (* indicates p < 0.05 when Group I is compared to Group II): Grp . Age (y) . Wt (kg) . BSA (m2) . FEV1 (L/sec) . FVC (L) . TLC (L) . MVV (L/min) . SHVR (L/min/SaO2) . SHCVR (L/min mm Hg) . I 55 128* 2.39* 2.0* 2.6* 5.0* 75* −0.6* 1.1* ±8 ±34 ±2.9 ±1.0 ±1.1 ±1.6 ±31 ±0.8 ±0.7 II 55 112 2.24 2.8 3.6 5.8 108 −1.6 2.3 ±10 ±22 ±0.22 ±0.7 ±1.1 ±1.0 ±33 ±1.2 ±1.3 Grp . Age (y) . Wt (kg) . BSA (m2) . FEV1 (L/sec) . FVC (L) . TLC (L) . MVV (L/min) . SHVR (L/min/SaO2) . SHCVR (L/min mm Hg) . I 55 128* 2.39* 2.0* 2.6* 5.0* 75* −0.6* 1.1* ±8 ±34 ±2.9 ±1.0 ±1.1 ±1.6 ±31 ±0.8 ±0.7 II 55 112 2.24 2.8 3.6 5.8 108 −1.6 2.3 ±10 ±22 ±0.22 ±0.7 ±1.1 ±1.0 ±33 ±1.2 ±1.3 When subgroups of hypercapnic and eucapnic patients with similar lung functions were compared, the subgroups differed significantly in their weights; conversely, in subgroups with comparable weights, lung function tests differed significantly. These data suggest that the mechanisms of chronic hypercapnia are multifactorial, and we hypothesize that, in the face of repetitive apneas and hypopneas, increased weight and abnormal lung function tests interact and contribute to the generation and maintenance of hypercapnia. This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

Reid, Malcolm, S.;Tafti,, Mehdi;Nishino,, Seiji;Siegel, Jerome, M.;Dement, William, C.;Mignot,, Emmanuel

doi: 10.1093/sleep/17.5.424pmid: N/A

Summary: Both rapid eye movement sleep and cataplexy in the narcoleptic canine have been shown to increase after both systemic and local administration of cholinergic agonists in the pontine reticular formation. Furthermore, binding studies indicate an increase in the number of M2 muscarinic receptors in the pontine reticular formation of narcoleptic canines. In the present study we have investigated the receptor subtypes involved in mediating the cholinergic stimulation of cataplexy, as defined by brief periods of hypotonia induced by emotions, within the pontine reticular formation of narcoleptic canines. Specific cholinergic and monoaminergic agonists and antagonists, and excitatory or inhibitory amino-acid neurotransmitter receptor agonists, were perfused through microdialysis probes implanted bilaterally in the pontine reticular formation of narcoleptic canines, and cataplexy was monitored using the Food-Elicited Cataplexy Test and recordings of electroencephalogram, electrooculogram and electromyo-gram. In narcoleptic canines, bilateral perfusion with oxotremorine (M2 muscarinic) (10−5−10−3 M) in the pontine reticular formation produced a dose-dependent increase in cataplexy, which reached complete muscle atonia (status cataplecticus) during the highest concentration. In control canines bilateral perfusion with oxotremorine (10−5−10−3 M) did not produce any cataplectic attacks, but did produce muscle atonia after the highest concentration. Bilateral perfusion with either McN-A-343 (Ml muscarinic) or nicotine (both 10−5−10−3 M) did not have any effect on cataplexy in either narcoleptic or control canines. The increase in cataplexy in narcoleptic canines produced by local perfusion with carbachol (10−4 M) followed by equimolar perfusion with a muscarinic antagonist was rapidly reversed by atropine (muscarinic) and gallamine (M2 muscarinic), partially reversed by 4-DAMP (M3/M1 muscarinic) and completely unaffected by pirenzepine (M1 muscarinic). Bilateral perfusion with excitatory, glutamatergic receptor agonists N-methyl-D-aspartate, AMPA (both at 10−4−10−3 M) and kainic acid (10−5−10−4 M) did not have any effect on cataplexy, whereas bilateral perfusion with the inhibitory GABAergic receptor agonist muscimol (10−4− 10−3 M) produced a moderate increase in cataplexy in the narcoleptic canines. Bilateral perfusion with numerous monoaminergic compounds, BHT-920 (alpha-2 agonist), yohimbine (alpha-2 antagonist), propranolol (beta antagonist) and prazosin (alpha-1 antagonist), did not have any effect on cataplexy. These findings demonstrate that cholinergic regulation of cataplexy in the narcoleptic canine at the level of the pontine reticular formation is mediated by M2, and possibly M3, muscarinic receptors. The effects of muscimol indicate that the stimulation of cataplexy might be elicited by local neuronal inhibition. Narcolepsy, Cataplexy, Oxotremorine, Muscimol This content is only available as a PDF.

Mignot,, E.;Nishino,, S.;Guilleminault,, C.;Dement, W., C.

doi: 10.1093/sleep/17.5.436pmid: 7991954

Article PDF first page preview Close This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

Roehrs,, Timothy;Merlotti,, Lori;Petrucelli,, Nancie;Stepanski,, Edward;Roth,, Thomas

doi: 10.1093/sleep/17.5.438pmid: 7991955

Summary: Thirty-six healthy young men and women (age range 21–35 years) were studied in an experimental model of sleep fragmentation. On 2 nights sleep was disrupted by presenting tones to produce brief electroencephalogram (EEG) arousals (without shortening sleep time) and daytime function was assessed the following day with the Multiple Sleep Latency Test and a divided attention performance test. The fragmentation of sleep produced significant disruption of nocturnal sleep and reduced daytime alertness. Adaptation in EEG-defined arousals occurred from the 1st to the 2nd night of fragmentation. Threshold (measured indirectly) characteristics of EEG-defined arousals were somewhat different than those of previous studies requiring behavioral awakening. The percent of tone series producing arousal, number of tones necessary for arousal and duration of the arousal all reflected heightened thresholds in stage 3/4 and rapid eye movement (REM) sleep compared to stage 1 and stage 2 sleep. In the last 3 hours of sleep versus the first 3 hours, arousals occurred less frequently, required more tones to produce, resulted in shorter durations and in fewer sleep stage changes, except for REM sleep where the converse was the case. Sleep fragmentation, Brief arousals, Daytime sleepiness/alertness, Multiple Sleep Latency Test This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

Lauerma,, H.;Kaartinen,, J.;Polo,, O.;Sallinen,, M.;Lyytinen,, H.

doi: 10.1093/sleep/17.5.444pmid: 7991956

Summary: Previous studies have demonstrated that motor activity during sleep is lateralized to the nondominant hand. There are two basic theories concerning this phenomenon: 1) The nondominant hemisphere is nonspecifically more alert or responsive than the dominant one, and 2) the lateralization to the nondominant side is task specific, reflecting the spatially oriented mode of information processing that is responsible for movements during sleep. We examined the motor responses to auditory stimuli during waking and sleep of 10 right-handed healthy subjects, who were instructed to switch off a tone stimulus by pressing a transducer that was attached to each hand. Sleep stage scoring was performed according to Rechtschaffen and Kales's criteria. During wakefulness and in all stages of sleep, with and without alpha activity occurring after stimulus onset, the dominant hand was used more, but during nonrapid eye movement Sl sleep the difference was not statistically significant. When alpha activity was present in the electroencephalogram after stimulus onset, the responses were significantly more lateralized to the right hand than when there was no alpha activity. During an actimetric home recording of both wrists of the subjects, there was an excess of left-sided movements during sleep as compared to waking. The results do not support the idea that the right hemisphere is generally more responsive than the left during sleep. They are, however, in accordance with the hypothesis that spatial information processing is a crucial factor in the nondominant lateralization of spontaneous sleep movements. The findings leave open the possibility that during the sleep onset process the nondominant side might be relatively more responsive to auditory stimuli than during either waking or sleep. Cerebral laterality, Movement monitoring, Motor response, Sleep, Hand This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

Bové,, Antonio;Culebras,, Antonio;Moore, James, T.;Westlake, Robert, E.

doi: 10.1093/sleep/17.5.449pmid: 7991957

Summary: Sleep spindles (SS) and K complexes constitute the physiological markers of stage 2 sleep. Because sleep allows a spontaneous thalamic manifestation in the form of SS, one could hypothesize that there is some kind of relationship between SS and the complaint of hypersomnia. To investigate this possible relationship we compared nonhypersomnolent subjects with hypersomnolent patients who carried a diagnosis of narcolepsy or idiopathic hypersomnia. SS were counted in well-defined nocturnal stage 2 sleep segments, and the average SS density (number of SS in stage 2/minute stage 2) was tabulated for the entire night. Agreement between two independent scorers was higher than 95%. The results show that the average SS density is higher in both cerebral hemispheres in the hypersomnolent group, especially in the idiopathic hypersomnia patients. At the beginning and at the end of the nocturnal sleep time, SS density is increased in this group compared with the normal one. These findings support the complaint of hypersomnia, mainly in idiopathic hypersomnia patients. This is in agreement with the notion that SS are generated by thalamic structures that serve a gatekeeping function during nonrapid eye movement sleep, and further suggests that their relative abundance expresses the power of that control. Sleep spindle-Narcolepsy, Idiopathic hypersomnia, Thalamus This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society

McCarren,, Madeline;Goldberg,, Jack;Ramakrishnan,, Viswanathan;Fabsitz,, Richard

doi: 10.1093/sleep/17.5.456pmid: 7991958

Summary: Genetic and environmental influences on insomnia were studied in 2,825 pairs of Vietnam era veteran male twins. The self-reported sleep problems studied included trouble falling asleep, trouble staying asleep, waking often, waking tired and a composite sleep scale. Twin correlations for each of the sleep problems were larger in monozygotic than in dizygotic pairs, with heritability estimates ranging from 0.21 to 0.42. There was no effect of common familial environment. Phenotypic correlations for combat experience and sleep problems were small, ranging from 0.00 to 0.09, with no differences seen in monozygotic and dizygotic twins. When the effects of genes and combat exposure were evaluated simultaneously, there was a significant genetic contribution to all sleep measures, but combat exposure was significantly associated only with overall sleep quality, waking often and having trouble staying asleep. Genetics, Sleep, Twins, Combat, Insomnia This content is only available as a PDF. © 1994 American Sleep Disorders Association and Sleep Research Society