M., Whiton, K., Albert, S.M. et al. (2015). National Sleep Foundation's sleep time duration recommendations: methodology and results summary. Sleep Health 1 (1): 40–43. https://doi.org/10.1016/j.sleh.2014.12.010.19 19 Rouse, W. and Smith, M. (1992). Lucretius: On the Nature of Things, 34. Cambridge, MA: Harvard University Press.
20 20 von Economo, C. (1930). Sleep as a problem of localization. J. Nerv. Ment. Dis. 71: 249–259.
21 21 Berger, H. (1930). Ueber das elektroenkephalogram des menschen. J. Psychol. Neurol. 40: 160–179.
22 22 Lee‐Chiong, T. (2012). Foreword: biology of sleep. Sleep Med. Clin. 3: xi–xii.
23 23 España, R.A. and Scammell, T.E. (2011). Sleep neurobiology from a clinical perspective. Sleep 34 (7): 845–858.
24 24 Eban‐Rothschild, A., Appelbaum, L., and de Lecea, L. (2018). Neuronal mechanisms for sleep/wake regulation and modulatory drive. Neuropsychopharmacology 43: 937–952.
25 25 Stahl, S.M. (2002). Brainstorms clinical neuroscience update. J. Clin. Psychiatry 63 (6): 467–468.
26 26 Saper, C.B., Chou, T.C., and Scammell, T.E. (2001). The sleep switch: hypothalamic control of sleep and wakedfullness. Trends Neurosci. 24 (12): 726–731.
27 27 Theibert, A.B. (2020). Chapter 9: neurotransmitter systems II: monoamines, purines, neuropeptides, & unconventional neurotransmitters. In: Essentials of Modern Neuroscience, 159–176. McGraw Hill.
28 28 Wisor, J.M., Nishino, S., Sora, I. et al. (2001). Dopaminergic role in stimulant‐induced wakefulness. J. Neurosci. 21 (5): 1787–1794.
29 29 Fried, I., Wilson, C.L., Morrow, J.W. et al. (2001). Increased dopamine release in the human amygdala during performance of cognitive tasks. Nat. Neurosci. 4 (2): 201–206.
30 30 Steriade, M. and Hobson, J. (1976). Neuronal activity during the sleep‐waking cycle. Prog. Neurobiol. 6: 155–376.
31 31 Ursin R. Serotonin and sleep. Sleep Med. Rev. 2002; 6(1):57–69. doi:https://doi.org/10.1053/smrv.2001.0174
32 32 McCormick, D.A. (1992). Neurotransmitter actions in the thalamus and cerebral cortex. J. Clin. Neurophysiol. 9: 212–223.
33 33 Haas, H.L., Sergeeva, O.A., and Selbach, O. (2008). Histamine in the nervous system. Physiol. Rev. 88: 1183–1241.
34 34 Kanbayashi, T., Kodama, T., Kondo, H. et al. (2009). CSF histamine contents in narcolepsy, idiopathic hypersomnia and obstructive sleep apnea syndrome. Sleep 32 (2): 181–187.
35 35 Scammell, TE, Jackson AC, Franks NP, Wisden W, Dauvilliers Y. Histamine: neural circuits and new medications. Sleep 2019; 42(1):1–8. doi: https://doi.org/10.1093/sleep/zsy183
36 36 de Lecea, L., Kilduff, T.S., Peyron, C. et al. (1998). The hypocretins: hypothalamus specific peptides with neuroexcitatory activity. Proc. Natl. Acad. Sci. USA 95: 322–327.
37 37 Kryger, M.H., Roth, T., and Dement, W.C. (2017). Normal human sleep. An overview. In: Principles and Practice of Sleep Medicine. Elsevier Saunders.
38 38 Watson, C.J. and Baghdoyan, H.A. (2012). Neuropharmacology of sleep and wakefullness: 2012 update. Sleep Med. Clin. 7: 469–486.
39 39 Ghiciuc, C.M., Dima Cozma, L.C., Bercea, R.M. et al. (2013). Restoring the salivary cortisol awakening response through nasdal continuous positive airway pressure therapy in obstructive sleep apnea. Chronobiol. Int. 30 (8): 1024–1031. https://doi.org/10.3109/07420528.2013.795155.
40 40 Porkka‐Heiskanen, T., Strecker, R.E., Thakkar, M. et al. (1997). Adenosine: a mediator of the sleep‐inducing effects of prolonged wakefulness. Science 276 (5316): 1265–1268.
41 41 Gandhi, A.V., Mosser, E.A., Oikonomou, G., and Prober, D.A. (2015). Melatonin is required for the circadian regulation of sleep. Neuron 85: 1193–1199. https://doi.org/10.1016/j.neuron.2015.02.016.
42 42 Lüthi, A. (2016). Sleep: switching off the off‐switch. Curr. Biol. 26: R756–R777.
43 43 Farré, N., Farré, R., and Gozal, D. (2018). Sleep apnea morbidity a consequence of microbial‐immune cross‐talk? Chest 154 (4): 754–759.
44 44 Smith, R.P., Easson, C., Lyle, S.M. et al. (2019). Gut microbiome diversity is associated with sleep physiology in humans. PLoS ONE 14 (10): e0222394. https://doi.org/10.1371/journal.pone.0222394.
45 45 Vitetta, L., Vitetta, G., and Hall, S. (2018). Commentary: the brain–intestinal mucosa–appendix–microbiome–brain loop. Diseases 6 (23): 1–9.
3 Pathophysiology of Sleep‐Related Breathing Disorders
Conceptual Overview
The origin and cause of sleep‐related breathing disorders (SRBDs) are ongoing areas of study and interest, as well as the many contributing factors. The pathophysiology of SRBD is multifactorial, involving the anatomy, the function of the airway physiologically and other contributing factors such as the control of respiration neurologically, age, sex, weight and other sleep disorders. In addition, SRBDs are often times progressive. This may begin simply as chronic mouth breathing, especially during sleep, and progress to snoring and then to obstructive sleep apnea (OSA) [1]. In addition, there may be neurogenic changes that can impact the sensory and motor activity of the upper airway related to vibration, inflammation, and even hypoxia [2]. There may also be a developmental aspect to the evolution of SRBD in the human. This involves the loss of the eppiglottic‐soft palatal lock‐up that in other primates prevents the tongue from collapsing into the airway during sleep. This has been attributed to the acquisition of speech, associated with the descent of the larynx, termed the great leap forward [3] (Figure 3.1).
Insomnia also needs to be considered and may be associated with painful conditions, psychological issues such as anxiety or depression, and may be residual to adequately managed SRBD. This association was first reported in 1973 [4]. It has been reported that about 50% of patients presented with both the SRBD and insomnia, and it was termed sleep breathing disorder plus [5] also referred to as complex insomnia [6].
Normal Respiration
A brief discussion and review of respiration needs to be addressed. Under normal circumstances respiration is mostly considered to be involuntary. It is primarily under the control of the diaphragm that is innervated by the phrenic nerve, composed primarily of muscle fibers that cause contraction. The phrenic nerve is derived from the cervical nerves at the C‐3 to C‐5 level. During passive breathing the diaphragm contracts and moves downward causing an increase in the negative pressure within the lungs and the alveoli. This negative pressure causes air to enter the lungs to fill them. In addition, this action may be impacted by the action of the intercostal muscles as well as the scalenes. Expiration during quiet breathing is passive and there is no active muscle activity. The process is related to the elastic recoil of the lungs and the rib cage.
Forced
