Insomnia pathophysiology: Difference between revisions
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===Pathogenesis=== | ===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.<ref name="pmid21494683">{{cite journal| author=Ban HJ, Kim SC, Seo J, Kang HB, Choi JK| title=Genetic and metabolic characterization of insomnia. | journal=PLoS One | year= 2011 | volume= 6 | issue= 4 | pages= e18455 | pmid=21494683 | doi=10.1371/journal.pone.0018455 | pmc=3071826 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21494683 }} </ref> | |||
*These compounds are broadly divided into either sleep-promoting or wake-promoting.<ref name="pmid23743247">{{cite journal| author=Griffith LC| title=Neuromodulatory control of sleep in Drosophila melanogaster: integration of competing and complementary behaviors. | journal=Curr Opin Neurobiol | year= 2013 | volume= 23 | issue= 5 | pages= 819-23 | pmid=23743247 | doi=10.1016/j.conb.2013.05.003 | pmc=3783581 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23743247 }} </ref> | |||
* 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"<ref name="pmid18985047">{{cite journal| author=Krueger JM, Rector DM, Roy S, Van Dongen HP, Belenky G, Panksepp J| title=Sleep as a fundamental property of neuronal assemblies. | journal=Nat Rev Neurosci | year= 2008 | volume= 9 | issue= 12 | pages= 910-9 | pmid=18985047 | doi=10.1038/nrn2521 | pmc=2586424 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18985047 }} </ref>. This theory states that in insomnia, compounds which regulate sleep act locally at the site of [[neuron]]s and influence sleep-wake regulation. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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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.