16 Matching Annotations
  1. Feb 2019
    1. Sleep talking, formally known as somniloquy, is a sleep disorder defined as talking during sleep without being aware of it. Sleep talking can involve complicated dialogues or monologues, complete gibberish or mumbling.
  2. Jan 2019
    1. Clonidine is associated with diminished susceptibility to hypocapnic central apnoea without significant effect on ventilation or upper airway mechanics.

      In other words, clonidine elevates CO2. I'm not yet sure whether this is a good thing.

    1. ConclusionsThese findings suggest that in patients with HF, sodium intake plays a role in the pathogenesis of SA.

      The question remains, then, for the general population with SA.

    1. CONCLUSIONS: These findings suggest that pharyngeal edema contributes to sleep-disordered breathing in obese patients with severe OSA, hypertension, and diastolic heart failure. Upper airway edema may contribute to the frequent occurrence of OSA in patients with heart disease.

      I suspect it also plays a role in UARS. This study probably selected people with heart failure because the fluid retention leads to a more dramatic response. Hypertension was likely a neccesary ethical consideration. Hypotension is common in UARS; therefore, one is unlikely to find a study administering diuretics to UARS patients. That leaves correlation as the only tool available to confirm this suspicion.

    1. 50 mg naltrexone at bed-time.

      Interesting. Conventional doses of naltrexone appear effective for sleep apnea. I'll be interested in seeing if LDN fairs well.

    1. So if you are tired during the day, check that you’re giving yourself the opportunity to get 7 to 9 hours.

      This is super helpful. Bold

    2. So if you are tired during the day, check that you’re giving yourself the opportunity to get 7 to 9 hours.

      This is super helpful.

  3. Nov 2018
    1. Why, though, do we not romanticize our preservation? The same matter of chance, of the fleeting nature of fate exists on the other side of the coin. What would have happened if we were better rested, if our energy was better preserved, if we managed our time and said what we really mean? Rarely do we approach whether we get eight hours of sleep with the same guilt as we do whether or not we attended a party, even when, according to sleep expert Matthew Walker, sleep deprivation prevents the brain from remembering information, creating new memories, and sustaining emotional well-being.

      A great observation!

    1. CONCLUSION: This meta-analysis confirms a medium effect (SMD = 0.62) of sleep deprivation on pain perception. As this meta-analysis is based on experimental studies in healthy subjects, the clinical relevance should be clarified.

      I'll have to look at this meta-analysis more closely, but they are likely looking at total sleep deprivation for one night, or partial sleep deprivation for one or several nights. Partial sleep deprivation tends to deprive more REM sleep via early awaking. I'd expect the greatest effect from SWS deprivation.

  4. Oct 2018
    1. SWS was generally not affected. It is concluded that beta 1 neurotransmission is directly involved in the regulation of PS.

      Full text summary: Beta 1 but not beta 2 is involved in REM sleep generation. High dose propranolol (which is not selective) practically obliterated REM sleep. Selective beta 1 agonism restored REM, while selective beta 2 agonism did not.

    1. Low BP was more prevalent in subjects with upper airway resistance syndrome (UARS) (23%) than in subjects with obstructive sleep apnea syndrome (OSAS) (0.06%), parasomnia (0.7%), restless leg syndrome (0.9%), or psychological insomnia (0.9%).

      That's an extremely high rate of hypotension in UARS. This may be what I have. If UARS causes hypotension, then sleep apnea (SA) may be different because of its link to obesity.

  5. Sep 2018
    1. Ritanserin, 5 mg, produced a substantially larger increase in SWS (51.4%) than either ketanserin, 20 mg (17.2%) or ketanserin, 40 mg (24.4%). Ritanserin has a significantly higher affinity than ketanserin for 5-HT2C receptor binding sites in the human brain and, based on estimates of per cent occupancy by the two compounds at brain 5-HT2A and 5-HT2C receptors, we conclude that SWS in humans is primarily regulated by 5-HT2C receptors.

      This doesn't quite clarify the effect of 5HT2C antagonism in the absence of 5HT2A antagonism.

  6. Oct 2017
    1. Beta blockers have long been associated with sleep disturbances such as difficulty falling asleep, staying asleep, and insomnia. They have been shown to reduce the production of melatonin via specific inhibition of beta-1 adrenergic receptors. Melatonin is a hormone secreted by the pineal gland in the brain, and helps in maintaining normal circadian rhythms.6,20-21 People with hypertension already have a lower melatonin production rate than those with normal blood pressure.22

      The question becomes, then, do beta blockers impair sleep when exogenous melatonin is administered concurrently?

  7. Feb 2016
    1. To test this notion, a recent study investigated the consequences of perturbing slow wave activity. During sleep, EEG was used to record the ongoing brain activity. When slow wave activity increased above a certain threshold, a device started to play sounds. These sounds served to reduce the slow wave activity. After sleep the brain activation following the recall of memories recently acquired was tested. The study demonstrated that MTL activation probed by the memory recall was reduced following the slow wave intervention (Van Der Werf et al., 2009). Using this type of BSDS, it was concluded that slow wave sleep is causally related to memory formation.