SLEEP

Webster, Harry, H.;Friedman,, Lee;Jones, Barbara, E.

doi: 10.1093/sleep/9.1.1pmid: 3961365

Summary: A retractable wire knife was employed to transect the reticular formation at the pontomedullary junction in order to assess the respective importance of pontine and medullary reticular neurons and their pathways in paradoxical sleep. Thirteen cats were implanted with a standard array of electrodes for polygraphic recording of sleep-wakefulness states during 3 days in baseline condition and during 21 days after transections. Average electroencephalographic (EEG) amplitude, average electromyographic (EMG) amplitude, and ponto-geniculo-occipital (PGO) spike rate were measured per I-min epoch for each day. A trivariate computer graphics display of 1 day's data revealed three major clusters of points that corresponded to wakefulness, slow wave sleep, and paradoxical sleep in baseline. (a) After transections through the entire reticular formation at the pontomedullary junction, paradoxical sleep was no longer evident in the trivariate computer gr phics or polygraphic record, either by the presence of a high PGO spike rate or by that of muscle atonia in association with a low-amplitude EEG. These results indicated that the reticular fibers that pass through the pontomedullary junction and interconnect the pontine tegmentum and the medullary reticular formation are necessary for generating the cluster of electrographic variables that normally characterizes paradoxical sleep. (b) After transections through the dorsal half of the reticular formation, paradoxical sleep was still evident, though with a reduced PGO spike rate, and muscle atonia was normal. These results indicated that the descending noradrenaline locus coeruleus fibers and the “longitudinal catecholamine bundle,” which course through the dorsal tegmentum, are not necessary for the generation of muscle atonia or the state of paradoxical sleep. (c) After transections through the ventral half of the reticular formation, paradoxical sleep was still apparent by the association of a moderate, though reduced, rate of PGO spiking in association with low-amplitude EEG activity and a highamplitude EMG, indicating a loss of muscle atonia. The duration of the PS episodes, however, was greatly reduced. These results indicated that the descending “tegmentoreticular” and ascending reticulotegmental pathways, which course ventrally through the pontomedullary junction and interconnect the dorsolateral pontine tegmentum and the ventromedial medullary reticular formation, are essential for the muscle atonia of paradoxical sleep and important for the normal cyclic generation and maintenance of the state of paradoxical sleep. Paradoxical sleep, Sleep-wake cycle, Reticular formation, Catacholamine bundle, Transections This content is only available as a PDF. © 1986 Raven Press, New York

Gothe,, Barbara;Cherniack, Neil, S.;Williams,, Lin

doi: 10.1093/sleep/9.1.24pmid: 3083498

Summary: We examined the ventilatory response to CO2 at two levels of oxygenation during wakefulness and sleep in healthy young adults before and after the ingestion of a single dose of 30 mg flurazepam. Progressive hypercapnia was produced at two levels of arterial O2 saturation (>99 and 87%) by having subjects re-breathe from a tight-fitting face mask and a reservoir bag containing gas mixtures with two different O2 concentrations. Ventilation was measured with an inductive plethy mograph. O2 saturation was measured with an ear oximeter. Sleep was monitored using standard techniques by recording the electroencephalogram, eye movements, and chin electromyogram. During wakefulness, hypoxia increased the slope of the ventilatory response to CO2 and shifted the response slightly to the left. NREM sleep lowered the slope of the CO2 response under both hyperoxic and hypoxic conditions. The slope of the hyperoxic CO2 response curve was not affected by flurazepam during wakefulness or sleep. After administration of flurazepam to the subjects, the shift of the CO2 response curve to the left produced by hypoxia (additive effect) during NREM sleep was slightly less as compared to control, but hypoxia still increased the slope of the CO2 ventilatory response. During hypoxic hypercapnia, the PeO2 at arousal from sleep was significantly lower than during hyperoxic hypercapnia, but the level of ventilation at arousal during hypercapnia was similar in the control condition and after flurazepam. We conclude that (a) both natural and flurazepam-induced sleep depress ventilatory responses to hyperoxic and hypoxic hypercapnia and alter, in a complex fashion, the effects of hypoxia and hypercapnia on ventilation; and (b) hypoxia and hypercapnia interact as arousal stimuli in both natural and flurazepam-induced sleep. Sleep, Hypercapnia, Hypoxia, Benzodiazepines This content is only available as a PDF. © 1986 Raven Press, New York

Hauri,, Peter;Fisher,, Joan

doi: 10.1093/sleep/9.1.38pmid: 3961366

Summary: Persistent psychophysiologic (learned) insomnia (PPI) is an objectively verifiable sleep disturbance that develops secondary to chronic, somatized tension and negative conditioning. Twenty-two patients diagnosed as PPI were compared on sleep and psychological questionnaires to 22 normal subjects (Ns) and to 19 insomnia patients with dysthymic disorders (DD). PPI patients typically had difficulties initiating and maintaining sleep, as did the DDs, but showed normal sleep staging. While PPIs were similar to Ns on most psychological tests, they typically were repressors and sensation avoiders. Many PPI patients suffered from tension-related symptoms such as headaches. PPI patients and Ns revealed less psychopathology than DD patients on almost all psychological scales. Learned insomnia, Psychophysiologic insomnia, Dysthymic disorders This content is only available as a PDF. © 1986 Raven Press, New York

Jacobsen, John, H.;Rosenberg, Richard, S.;Huttenlocher, Peter, R.;Spire,, Jean-Paul

doi: 10.1093/sleep/9.1.54pmid: 3961367

Summary: A familial syndrome of painful nocturnal cramping and jerking in members of three generations is described. All-night polysomnograms demonstrated both myoclonic jerks and sustained muscular activity in three family members, a 4-year-old girl, who presented with frequent episodes of painful awakenings; her 7-year-old brother, who had similar but less severe symptoms; and the 28- year-old mother, who had suffered nocturnal cramping and awakenings for much of her life. To the authors' knowledge, this is the first description of a familial disorder characterized by exclusively nocturnal intermittent cramping and myoclonus of brainstem or spinal origin. Myoclonus, Familial disorders, Nocturnal cramping This content is only available as a PDF. © 1986 Raven Press, New York

Moldofsky,, H.;Musisi,, S.;Phillipson, E., A.

doi: 10.1093/sleep/9.1.61pmid: 3961368

Summary: We describe here the case of a 62-year-old man with advanced sleep phase syndrome who was treated successfully by phase advance chronotherapy. Advanced sleep phase syndrome, Chronotherapy This content is only available as a PDF. © 1986 Raven Press, New York

Spiegel,, René;Koberle,, Suse;Allen, Susan, R.

doi: 10.1093/sleep/9.1.66pmid: 3961369

Summary: Previous experimental observations, almost exclusively carried out with young healthy subjects, have been interpreted as showing a particular restorative role for human slow wave sleep (SWS). This article considers whether findings from polygraphic sleep studies in patients and elderly subjects lead to similar inferences about the meaning or “function” of SWS. The question was approached in three different ways: (a) by presenting results from a long-term study in elderly subjects whose SWS data were correlated with baseline medical and psychometric findings and with 5-year follow-up results; (b) by correlating nonmanipulated wake-time during days with parameters of SWS on subsequent nights in a group of 30 demented inpatients undergoing 72-h continuous sleepwake recording; (c) by reviewing and comparing published polygraphic sleep studies for a number of psychiatric conditions. None of these three approaches provided unequivocal evidence for a clinically significant role for SWS. Reasons for the different outcome of SWS studies in young experimental subjects and clinical populations are discussed. Slow wave sleep, Sleep stages, Sleep and old age, Dementia This content is only available as a PDF. © 1986 Raven Press, New York

Miller, Lyle, H.;Turnbull, Barry, A.;Kastin, Abba, J.;Coy, David, H.

doi: 10.1093/sleep/9.1.80pmid: 3754348

Summary: Delta sleep-inducing peptide (DSIP) significantly increases delta wave electrical activity in the brain of rats after intraperitoneal (i.p.) injection. Rats (n = 10) were peripherally injected with DSIP and [D-Ala4]DSIP-NH2 during the dark portion of a 12-h light/dark cycle prior to recording of epidural encephalographic (EEG) wave forms. Administration of [D-Ala4]DSIP-NH2, an analog that enters the brain after peripheral administration more readily than the parent DSIP molecule, resulted in significantly more delta waves than DSIP together with a highly significant amount of theta activity. DSIP was found to significantly increase EEG output in the delta range when compared with controls. In addition, the DSIP analog significantly decreased locomotor activity, whereas DSIP itself was without effect. These findings strongly support the controversial concepts that peripherally injected peptides can reach the brain and that DSIP compounds can increase sleep activity. Delta sleep-inducing peptide, peptide-[D-Ala4]Delta sleep-inducing peptide, Electroencephalography, Sleep-wave activity, Blood brain barrier This content is only available as a PDF. © 1986 Raven Press, New York

doi: 10.1093/sleep/9.1.99pmid: 3486444

Article PDF first page preview Close This content is only available as a PDF. © 1986 Raven Press, New York

Kilduff, Thomas, S.;Bowersox, S., Scott;Kaitin, Kenneth, I.;Baker, Theodore, L.;Ciaranello, Roland, D.;Dement, William, C.

doi: 10.1093/sleep/9.1.102pmid: 3704431

Summary: The role of the muscarinic cholinergic receptor in narcolepsy was examined using radioligand binding to various brain regions of normal and genetically narcoleptic Doberman pinschers. In this multi-litter study, a previous report of a proliferation of muscarinic cholinergic receptors in the brain stem was confirmed, and the concentration of the M2 receptor subtype, in particular, was elevated. This up-regulation of brainstem cholinergic receptors suggests a problem with release of acetylcholine, which, together with previous reports of an impairment of dopamine release, may be indicative of a fundamental membrane problem in narcolepsy. Narcoleps, Cataplexy, Sleep, Acetylcholine, Muscarinic receptor, Aminal model, Heredity This content is only available as a PDF. © 1986 Raven Press, New York

Faull, Kym, F.;Zeller-DeAmicis, Lori, C.;Radde,, Linda;Bowersox, S., Scott;Baker, Theodore, L.;Kilduff, Thomas, S.;Dement, William, C.

doi: 10.1093/sleep/9.1.107pmid: 3704432

Summary: Neuropharmacological data suggest involvement of the biogenic amines in narcolepsy. In humans, for example, drugs that increase biogenic amine concentrations in the synaptic cleft ameliorate symptoms of narcolepsy. Thus, agents that block monoamine reuptake (e.g., tricyclic antidepressants), potentiate monoamine release (e.g., methylphenidate), or inhibit monoamine oxidase possess therapeutic efficacy (1,2). Pharmacological experiments with genetic and nongenetic forms of the canine disease confirm these findings (3-5). In previous work, we compared monoamine metabolite concentrations in cisternal cerebrospinal fluid (CSF) collected from normal dogs and from adult miniature French poodles with a nongenetic but severe form of narcolepsy. Steady-state concentrations of dopamine and serotonin metabolites were lower in the CSF of the affected animals, and data collected with the use of the acid transport inhibitor probenecid suggested reduced turnover of serotonin and norepinephrine (6). These results suggested an abnormality in monoamine metabolism in the narcoleptic animals, and led us to undertake regional neurochemical studies in narcoleptic and normal animals. This content is only available as a PDF. © 1986 Raven Press, New York