The effects of gamma-hydroxybutyrate (GHB: 25 mg/kg h.s. and 3 h later) vs. placebo on objectively evaluated nighttime sleep and daytime sleepiness in narcolepsy were evaluated in a double-blind, counterbalanced crossover design. Twenty narcolepsy patients were given an overnight polysomnogram (PSG), followed by a daytime multiple sleep latency test (MSLT) at baseline and on the 1st and 29th days of GHB and placebo treatment. The overnight PSGs indicated that the narcolepsy patients had the following significant results during GHB versus placebo treatment: decreased stage 1 (p = 0.012), increased stage 3 (p = 0.008), increased delta (stage 3 and 4 combined) sleep (p = 0.049), fewer stage shifts (p = 0.002), and fewer awakenings (p = 0.006). Minutes of wakefulness were significantly increased only for the last 2 h of the 8 h sleep period on GHB versus placebo (p = 0.019), which is beyond the time of GHB's direct influence. The MSLTs indicated that the narcolepsy patients had a marginally increased sleep latency mean during GHB versus placebo treatment (p = 0.074) and significantly increased total stage 0 (wakefulness) on day 29 of GHB versus day 29 of placebo treatment (p = 0.038). Female narcolepsy patients had significantly fewer naps with REM sleep (REM naps) on day 29 of GHB vs. day 29 of placebo treatment (p = 0.020). The therapeutic effect of GHB in narcolepsy patients, i.e., decreases cataplexy, appears to be due to its improving nocturnal sleep quality, since its half-life is only 1.5 to 2 h. It is conjectured that GHB, an endogenous neurochemical, may be a sleep neurotransmitter or neuromodulator, since GHB rapidly induces sleep, and increases sleep continuity and delta sleep without suppressing REM sleep in both normals and narcolepsy patients.
This study directly tested the beneficial effect of isolated REM and isolated NREM sleep on the recall of narcoleptics. In a within subject design, 10 narcoleptics were instructed to sleep for a certain optimal duration and at a certain optimal time before each session, and were given 12–14 sessions, one a day, on different lists of a complex associative memory task and a minimally associative memory task. Following the 10‐min task, the subject either had 20 min of polygraphically recorded napping or card playing, followed by a free recall test. The results for the complex associative task indicated significant differences between the three conditions for free recall. Recall was significantly better after isolated REM than after isolated NREM sleep or wakefulness and was significantly better after NREM than after wakefulness. The results from the minimally associative task were inconclusive. The results are consistent with the proposed neuronal activity correlates (NAC) theory that REM sleep actively consolidates and/or integrates complex associative information and that NREM sleep passively prevents retroactive interference of recently acquired complex associative information.
The presence of anterior and posterior nasal packs in patients with epistaxis is known to be associated with cardiorespiratory problems and sometimes death, although the mechanism has not been well understood. To determine the incidence and severity of obstructive sleep apnea in patients with epistaxis treated with both anterior and posterior nasal packs, we obtained polysomnograms on twelve patients while the packs were in place. Ten of these patients demonstrated obstructive sleep apnea. The apnea index (apneas/hour sleep) ranged from 1 to 83, with a mean of 29; the hypopnea index (hypopneas/hour sleep) ranged from 9 to 33, with a mean of 20; and the lowest oxygen saturation (SaO2) ranged from 17% to 91%, with a mean of 77%. Ten patients returned for another polysomnogram after removal of the packs. These baseline studies showed improvement in the apnea index and in the lowest SaO2 in all patients, although four patients still demonstrated at least mild obstructive sleep apnea. This study demonstrates that nasal packs used for the treatment of epistaxis may induce obstructive sleep apnea or markedly exacerbate underlying obstructive sleep apnea and, therefore, contribute to the sudden deaths that have been reported in epistaxis patients.
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