Insomnia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Insomnia is a sleep disorder characterized by an inability to sleep and/or inability to remain asleep for a reasonable period. It might occur as a standalone condition or along with existing physical or mental comorbidities.
Pathophysiology
Genetics
A gene is reported to be responsible for insomnia, called human circadian clock gene CRY1 .
Pathogenesis
- Although sleep is influenced by a myriad of conditions, both physical and environmental, most sleep patterns follow a circadian rhythm which is in turn regulated by a number of compounds in the body.[1]
- These compounds are broadly divided into either sleep-promoting or wake-promoting.[2]
- Examples of sleep-promoting compounds are melatonin, adenosine, serotonin, etc.
- Wake-promoting compounds include catecholamines, histamine, etc.
- Although all cases of insomnia cannot be explained by an imbalance between sleep-promoting and wake-promoting compounds, an imbalance or an excess of either points to sleep-wake disorder of some kind.
- Comorbid conditions like GERD, restless leg syndrome, anxiety disorder can result in chronic insomnia.
- Local sleep theory proposed by Krueger et al, defines sleep as a "fundamental emergent property of highly interconnected neurons"[3]. This theory states that in insomnia, compounds which regulate sleep act locally at the site of neurons and influence sleep-wake regulation.
References
- ↑ Ban HJ, Kim SC, Seo J, Kang HB, Choi JK (2011). "Genetic and metabolic characterization of insomnia". PLoS One. 6 (4): e18455. doi:10.1371/journal.pone.0018455. PMC 3071826. PMID 21494683.
- ↑ Griffith LC (2013). "Neuromodulatory control of sleep in Drosophila melanogaster: integration of competing and complementary behaviors". Curr Opin Neurobiol. 23 (5): 819–23. doi:10.1016/j.conb.2013.05.003. PMC 3783581. PMID 23743247.
- ↑ Krueger JM, Rector DM, Roy S, Van Dongen HP, Belenky G, Panksepp J (2008). "Sleep as a fundamental property of neuronal assemblies". Nat Rev Neurosci. 9 (12): 910–9. doi:10.1038/nrn2521. PMC 2586424. PMID 18985047.