Кома — разлика између измена
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{{Infobox |
{{Infobox medical condition (new) |
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| name = Кома |
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| field = [[Neurology]], [[psychiatry]] |
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| symptoms = Unconsciousness |
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| complications = [[Persistent vegetative state]], [[death]] |
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| duration = Can vary from a few days to several years (longest recorded is 42 years) |
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'''Кома''' је потпуно одсуство [[свест]]и које личи на дубок [[сан]]. Одликује се губитком реакције на подражаје и губитком спонтаних [[Нервни систем|нервних активности]], што је обично повезано с церебралним повредама метаболичког или физичког порекла, напада [[епилепсија|епилепсије]], инфективних [[болест]]и и сл.<ref name="RR">{{Cite book|last=Weyhenmyeye|first=James A.|last2=Gallman|first2=Eve A.|title=Rapid Review Neuroscience 1st Ed|url=https://archive.org/details/neuroscience0000weyh|publisher=Mosby Elsevier|year=2007 |isbn=978-0-323-02261-3|pages=[https://archive.org/details/neuroscience0000weyh/page/177 177]-9 }}</ref><ref>{{РСР}}</ref> |
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'''Кома''' је потпуно одсуство [[свест]]и које личи на дубок [[сан]]. Одликује се губитком реакције на подражаје и губитком спонтаних [[Нервни систем|нервних активности]], што је обично повезано с церебралним повредама метаболичког или физичког порекла, напада [[епилепсија|епилепсије]], инфективних [[болест]]и и сл.<ref name=RR>{{cite book |author1=Weyhenmyeye, James A. |author2=Eve A. Gallman | title=Rapid Review Neuroscience 1st Ed | publisher=Mosby Elsevier | year=2007 | pages=177–9 | isbn=978-0-323-02261-3}}</ref><ref>{{РСР}}</ref> Coma patients exhibit a complete absence of wakefulness and are unable to consciously feel, speak or move.<ref name=":0">{{cite journal|last=Bordini|first=A.L.|author2=Luiz, T.F.|author3=Fernandes, M.|author4=Arruda, W. O.|author5=Teive, H. A.|year=2010|title=Coma scales: a historical review|journal=Arquivos de Neuro-Psiquiatria|volume=68|issue=6|pages=930–937|doi=10.1590/S0004-282X2010000600019|pmid=21243255|doi-access=free}}</ref><ref>{{Cite journal |last=Cooksley |first=Tim |last2=Holland |first2=Mark |date=2017-02-01 |title=The management of coma |url=https://www.medicinejournal.co.uk/article/S1357-3039(16)30257-2/abstract |journal=Medicine |language=English |volume=45 |issue=2 |pages=115–119 |doi=10.1016/j.mpmed.2016.12.001 |issn=1357-3039}}</ref> Comas can be derived by natural causes, or can be [[Induced coma|medically induced]].<ref>{{Cite web |author1=Marc Lallanilla |date=2013-09-06 |title=What Is a Medically Induced Coma? |url=https://www.livescience.com/39483-what-is-a-medically-induced-coma.html |access-date=2022-04-23 |website=livescience.com |language=en}}</ref> |
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Clinically, a coma can be defined as the inability consistently to follow a one-step command.<ref>{{Cite web|url=https://www.glasgowcomascale.org/|title=The Glasgow structured approach to assessment of the Glasgow Coma Scale|website=www.glasgowcomascale.org|access-date=2019-03-06}}</ref> <ref>{{Cite web |title=Coma - an overview {{!}} ScienceDirect Topics |url=https://www.sciencedirect.com/topics/neuroscience/coma |access-date=2022-04-28 |website=www.sciencedirect.com}}</ref>It can also be defined as a score of ≤ 8 on the [[Glasgow Coma Scale]] (GCS) lasting ≥ 6 hours.<ref>{{Cite web |title=Glasgow Coma Scale - an overview {{!}} ScienceDirect Topics |url=https://www.sciencedirect.com/topics/neuroscience/glasgow-coma-scale |access-date=2022-04-23 |website=www.sciencedirect.com}}</ref> For a patient to maintain consciousness, the components of ''wakefulness'' and ''awareness'' must be maintained. [[Wakefulness]] describes the quantitative degree of [[consciousness]], whereas [[awareness]] relates to the qualitative aspects of the functions mediated by the cortex, including cognitive abilities such as attention, sensory perception, explicit memory, language, the execution of tasks, temporal and spatial orientation and reality judgment.<ref name=":0" /><ref>{{Cite journal|last1=Laureys|last2=Boly|last3=Moonen|last4=Maquet|date=2009|title=Coma|url=http://www.coma.ulg.ac.be/papers/vs/EncConsc_coma_2009.pdf|journal=Encyclopedia of Neuroscience|volume=2|pages=1133–1142|doi=10.1016/B978-008045046-9.01770-8|isbn=9780080450469}}</ref> From a neurological perspective, consciousness is maintained by the activation of the [[cerebral cortex]]—the [[gray matter]] that forms the outer layer of the brain—and by the [[reticular activating system]] (RAS), a structure located within the [[brainstem]].<ref name=med>{{cite book |author=Hannaman, Robert A.|title=MedStudy Internal Medicine Review Core Curriculum: Neurology 11th Ed|publisher=MedStudy| year=2005 |pages=(11–1) to (11–2) |isbn=1-932703-01-2}}</ref><ref>{{cite journal|title=Persistent vegetative state: A medical minefield|journal=[[New Scientist]]|date=July 7, 2007|pages=40–3|url=https://www.newscientist.com/article/mg19526111.800-persistent-vegetative-state-a-medical-minefield.html?full=true}} See [https://www.newscientist.com/data/images/archive/2611/26111801.jpg diagram] {{Webarchive|url=https://web.archive.org/web/20170826032542/https://www.newscientist.com/data/images/archive/2611/26111801.jpg |date=2017-08-26 }}.</ref> |
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== Етимологија == |
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The term 'coma', from the Greek {{lang|grc|κῶμα}} ''koma'', meaning deep sleep, had already been used in the [[Hippocratic Corpus|Hippocratic corpus]] (''Epidemica'') and later by [[Galen]] (second century AD). Subsequently, it was hardly used in the known literature up to the middle of the 17th century. The term is found again in [[Thomas Willis]]' (1621–1675) influential ''De anima brutorum'' (1672), where [[lethargy]] (pathological sleep), 'coma' (heavy sleeping), ''carus'' (deprivation of the senses) and [[apoplexy]] (into which ''carus'' could turn and which he localized in the [[white matter]]) are mentioned. The term ''carus'' is also derived from Greek, where it can be found in the roots of several words meaning soporific or sleepy. It can still be found in the root of the term 'carotid'. [[Thomas Sydenham]] (1624–89) mentioned the term 'coma' in several cases of fever (Sydenham, 1685).<ref>{{cite dictionary|url=http://www.etymonline.com/index.php?term=coma&allowed_in_frame=0|title=''Coma'' Origin|dictionary=[[Online Etymology Dictionary]]|access-date=14 August 2015}}</ref><ref>{{Cite journal|last1=Wijdicks|first1=Eelco F. M.|last2=Koehler|first2=Peter J.|date=2008-03-01|title=Historical study of coma: looking back through medical and neurological texts|journal=Brain|volume=131|issue=3|pages=877–889|doi=10.1093/brain/awm332|pmid=18208847|issn=0006-8950|doi-access=free}}</ref> |
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== Знаци и симптоми == |
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General symptoms of a person in a comatose state are: |
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* Inability to voluntarily open the eyes |
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* A non-existent sleep-wake cycle |
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* Lack of response to physical (painful) or verbal stimuli |
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* Depressed brainstem reflexes, such as pupils not responding to light |
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* Irregular breathing |
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* Scores between 3 and 8<ref>{{cite web|title=Glasgow Coma Scale|author=Russ Rowlett|publisher=University of North Carolina at Chapel Hill|url=http://www.unc.edu/~rowlett/units/scales/glasgow.htm|access-date=2010-12-07|archive-date=2018-06-04|archive-url=https://web.archive.org/web/20180604074017/http://www.unc.edu/~rowlett/units/scales/glasgow.htm|url-status=dead}}</ref> on the [[Glasgow Coma Scale]]<ref name="RR" /> |
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== Узроци == |
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Many types of problems can cause a coma. Forty percent of comatose states result from [[drug poisoning]].<ref name="Liversedge 2010 337–339">{{cite journal|last1=Liversedge|first1=Timothy|last2=Hirsch|first2=Nicholas|year=2010|title=Coma|journal=Anaesthesia & Intensive Care Medicine|volume=11|issue=9|pages=337–339|doi=10.1016/j.mpaic.2010.05.008}}</ref> Certain drug use under certain conditions can damage or weaken the [[Synaptic vesicle|synaptic]] functioning in the [[Reticular formation|ascending reticular activating system]] (ARAS) and keep the system from properly functioning to arouse the brain.<ref name="Young 2009 32–47">{{cite journal|last=Young|first=G.B.|year=2009|title=Coma|journal=Ann. N. Y. Acad. Sci.|volume=1157|issue=1|pages=32–47|bibcode=2009NYASA1157...32Y|doi=10.1111/j.1749-6632.2009.04471.x|pmid=19351354|s2cid=222086047}}</ref> Secondary effects of drugs, which include abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly harm the functioning of the ARAS and lead to a coma. Given that drug poisoning is the cause for a large portion of patients in a coma, hospitals first test all comatose patients by observing pupil size and eye movement, through the [[Vestibulo–ocular reflex|vestibular-ocular reflex]]. (See ''Diagnosis'' below.)<ref name="Young 2009 32–47" /> |
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The second most common cause of coma, which makes up about 25% of cases, is lack of oxygen, generally resulting from [[cardiac arrest]].<ref name="Liversedge 2010 337–339" /> The [[Central nervous system|Central Nervous System (CNS)]] requires a great deal of oxygen for its [[neurons]]. Oxygen deprivation in the [[Human brain|brain]], also known as [[Cerebral hypoxia|hypoxia]], causes sodium and calcium from outside of the [[neuron]]s to decrease and intracellular calcium to increase, which harms neuron communication.<ref>{{cite journal|last=Busl|first=K. M.|author2=Greer, D. M.|year=2010|title=Hypoxic-ischemic brain injury: Pathophysiology, neuropathology and mechanisms|journal=NeuroRehabilitation|volume=26|issue=1|pages=5–13|doi=10.3233/NRE-2010-0531|pmid=20130351|doi-access=free}}</ref> Lack of oxygen in the brain also causes [[Adenosine triphosphate|ATP]] exhaustion and cellular breakdown from cytoskeleton damage and [[nitric oxide]] production. |
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Twenty percent of comatose states result from the side effects of a stroke.<ref name="Liversedge 2010 337–339" /> During a stroke, blood flow to part of the brain is restricted or blocked. An [[ischemic stroke]], [[Intracerebral hemorrhage|brain hemorrhage]], or tumor may cause restriction of blood flow. Lack of blood to cells in the brain prevents oxygen from getting to the neurons, and consequently causes cells to become disrupted and die. As brain cells die, brain tissue continues to deteriorate, which may affect the functioning of the ARAS. |
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The remaining 15% of comatose cases result from trauma, excessive [[blood loss]], [[malnutrition]], [[hypothermia]], [[hyperthermia]], abnormal glucose levels, and many other biological disorders. Furthermore, studies show that 1 out of 8 patients with traumatic brain injury experience a comatose state.<ref>{{Cite journal|last1=Lombardi|first1=Francesco FL|last2=Taricco|first2=Mariangela|last3=De Tanti|first3=Antonio|last4=Telaro|first4=Elena|last5=Liberati|first5=Alessandro|date=2002-04-22|title=Sensory stimulation for brain injured individuals in coma or vegetative state|journal=Cochrane Database of Systematic Reviews|issue=2|pages=CD001427|doi=10.1002/14651858.cd001427|pmid=12076410|issn=1465-1858 }}</ref> |
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== Патофизиологија == |
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Injury to either or both of the [[cerebral cortex]] or the [[reticular activating system]] (RAS) is sufficient to cause a person to enter coma.<ref>{{Cite web |title=Coma - an overview {{!}} ScienceDirect Topics |url=https://www.sciencedirect.com/topics/neuroscience/coma |access-date=2022-04-23 |website=www.sciencedirect.com}}</ref> |
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The [[cerebral cortex]] is the outer layer of [[neural tissue]] of the [[cerebrum]] of the [[brain]].<ref>{{Cite book|title=Human anatomy|last=S.|first=Saladin, Kenneth|date=2011|publisher=McGraw-Hill|isbn=9780073525600|edition= 3rd|location=New York|oclc=318191613}}</ref> The cerebral cortex is composed of [[Grey matter|gray matter]] which consists of the [[Nucleus (neuroanatomy)|nuclei]] of [[neuron]]s, whereas the inner portion of the [[cerebrum]] is composed of [[white matter]] and is composed of the [[axon]]s of [[neuron]].<ref>{{Citation |last1=Mercadante |first1=Anthony A. |title=Neuroanatomy, Gray Matter |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK553239/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31990494 |access-date=2022-04-23 |last2=Tadi |first2=Prasanna}}</ref> White matter is responsible for [[perception]], relay of the sensory input via the thalamic pathway, and many other neurological functions, including complex thinking. |
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The RAS, on the other hand, is a more primitive structure in the [[brainstem]] which includes the [[reticular formation]] (RF).<ref name="StatPearls Publishing">{{Citation |last1=Arguinchona |first1=Joseph H. |title=Neuroanatomy, Reticular Activating System |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK549835/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31751025 |access-date=2022-04-23 |last2=Tadi |first2=Prasanna}}</ref> The RAS has two tracts, the ascending and descending tract. The ascending track, or ascending reticular activating system (ARAS), is made up of a system of acetylcholine-producing neurons, and works to arouse and wake up the brain.<ref>{{Cite web |title=Ascending Reticular Activating System - an overview {{!}} ScienceDirect Topics |url=https://www.sciencedirect.com/topics/neuroscience/ascending-reticular-activating-system |access-date=2022-04-23 |website=www.sciencedirect.com}}</ref> Arousal of the brain begins from the RF, through the [[thalamus]], and then finally to the cerebral cortex.<ref name="Young 2009 32–47" /> Any impairment in ARAS functioning, a neuronal dysfunction, along the arousal pathway stated directly above, prevents the body from being aware of its surroundings.<ref name="StatPearls Publishing"/> Without the arousal and consciousness centers, the body cannot awaken, remaining in a comatose state.<ref name="Traub 2016 777–793">{{Cite journal|last1=Traub|first1=Stephen J.|last2=Wijdicks|first2=Eelco F.|date=2016|title=Initial Diagnosis and Management of Coma|journal=Emergency Medicine Clinics of North America|volume=34|issue=4|pages=777–793|doi=10.1016/j.emc.2016.06.017|issn=1558-0539|pmid=27741988}}</ref> |
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The severity and mode of onset of coma depends on the underlying cause. There are two main subdivisions of a coma: structural and diffuse neuronal.<ref>{{Citation |last1=Huff |first1=J. Stephen |title=Coma |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK430722/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28613473 |access-date=2022-04-23 |last2=Tadi |first2=Prasanna}}</ref> A structural cause, for example, is brought upon by a mechanical force that brings about cellular damage, such as physical pressure or a blockage in neural transmission.<ref>{{Cite journal |last1=Miller |first1=Margaret A. |last2=Zachary |first2=James F. |date=2017 |title=Mechanisms and Morphology of Cellular Injury, Adaptation, and Death |journal=Pathologic Basis of Veterinary Disease |pages=2–43.e19 |doi=10.1016/B978-0-323-35775-3.00001-1 |isbn=9780323357753 }}</ref> While a diffuse cause is limited to aberrations of cellular function, that fall under a metabolic or toxic subgroup. Toxin-induced comas are caused by extrinsic substances, whereas metabolic-induced comas are caused by intrinsic processes, such as body thermoregulation or ionic imbalances(e.g. sodium).<ref name="Traub 2016 777–793"/> For instance, severe [[hypoglycemia]] (low blood sugar) or [[hypercapnia]] (increased [[carbon dioxide]] levels in the blood) are examples of a metabolic diffuse neuronal dysfunction. Hypoglycemia or hypercapnia initially cause mild agitation and confusion, but progress to [[obtundation]], stupor, and finally, complete [[unconsciousness]].<ref>{{Citation |title=Obtundation, stupor and coma Peter Dickinson |date=2012-03-15 |url=http://dx.doi.org/10.1201/b15214-12 |work=Small Animal Neurological Emergencies |pages=140–155 |publisher=CRC Press |doi=10.1201/b15214-12 |isbn=978-0-429-15897-1 |access-date=2022-04-23}}</ref> In contrast, coma resulting from a severe [[traumatic brain injury]] or [[subarachnoid hemorrhage]] can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.<ref name="RR" /> |
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Structural and diffuse causes of coma are not isolated from one another, as one can lead to the other in some situations. For instance, coma induced by a diffuse metabolic process, such as hypoglycemia, can result in a structural coma if it is not resolved. Another example is if cerebral edema, a diffuse dysfunction, leads to ischemia of the brainstem, a structural issue, due to the blockage of the circulation in the brain.<ref name="Traub 2016 777–793"/> |
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== Референце == |
== Референце == |
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== Литература == |
== Литература == |
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{{refbegin|}} |
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* {{Cite book|ref=harv|last=Weyhenmyeye|first= James A.; Eve A. Gallman |title=Rapid Review Neuroscience 1st Ed|url=https://archive.org/details/neuroscience0000weyh|publisher=Mosby Elsevier|year=2007 |isbn=978-0-323-02261-3|pages=[https://archive.org/details/neuroscience0000weyh/page/177 177]-9 }} |
* {{Cite book|ref=harv|last=Weyhenmyeye|first= James A.; Eve A. Gallman |title=Rapid Review Neuroscience 1st Ed|url=https://archive.org/details/neuroscience0000weyh|publisher=Mosby Elsevier|year=2007 |isbn=978-0-323-02261-3|pages=[https://archive.org/details/neuroscience0000weyh/page/177 177]-9 }} |
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{{refend}} |
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== Спољашње везе == |
== Спољашње везе == |
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{{Medical resources |
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* [https://web.archive.org/web/20090206233657/http://psihoterapija.rs/koma.html „Корак” о коми] |
* [https://web.archive.org/web/20090206233657/http://psihoterapija.rs/koma.html „Корак” о коми] |
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* [http://www.blic.rs/Vesti/Svet/359485/Umrla-posle-42-godine-u-komi-hiljade-verovale-da-ima-isceliteljske-moci Умрла после 42 године у коми („Блиц“, 25. децембар 2012)] |
* [http://www.blic.rs/Vesti/Svet/359485/Umrla-posle-42-godine-u-komi-hiljade-verovale-da-ima-isceliteljske-moci Умрла после 42 године у коми („Блиц“, 25. децембар 2012)] |
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Верзија на датум 9. мај 2022. у 01:33
 | Један корисник управо ради на овом чланку. Молимо остале кориснике да му допусте да заврши са радом. Ако имате коментаре и питања у вези са чланком, користите страницу за разговор.
Хвала на стрпљењу. Када радови буду завршени, овај шаблон ће бити уклоњен. Напомене
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| Кома | |
|---|---|
| Специјалности | Neurology, psychiatry |
| Симптоми | Unconsciousness |
| Компликације | Persistent vegetative state, death |
| Трајање | Can vary from a few days to several years (longest recorded is 42 years) |
Кома је потпуно одсуство свести које личи на дубок сан. Одликује се губитком реакције на подражаје и губитком спонтаних нервних активности, што је обично повезано с церебралним повредама метаболичког или физичког порекла, напада епилепсије, инфективних болести и сл.[1][2] Coma patients exhibit a complete absence of wakefulness and are unable to consciously feel, speak or move.[3][4] Comas can be derived by natural causes, or can be medically induced.[5]
Clinically, a coma can be defined as the inability consistently to follow a one-step command.[6] [7]It can also be defined as a score of ≤ 8 on the Glasgow Coma Scale (GCS) lasting ≥ 6 hours.[8] For a patient to maintain consciousness, the components of wakefulness and awareness must be maintained. Wakefulness describes the quantitative degree of consciousness, whereas awareness relates to the qualitative aspects of the functions mediated by the cortex, including cognitive abilities such as attention, sensory perception, explicit memory, language, the execution of tasks, temporal and spatial orientation and reality judgment.[3][9] From a neurological perspective, consciousness is maintained by the activation of the cerebral cortex—the gray matter that forms the outer layer of the brain—and by the reticular activating system (RAS), a structure located within the brainstem.[10][11]
Етимологија
The term 'coma', from the Greek κῶμα koma, meaning deep sleep, had already been used in the Hippocratic corpus (Epidemica) and later by Galen (second century AD). Subsequently, it was hardly used in the known literature up to the middle of the 17th century. The term is found again in Thomas Willis' (1621–1675) influential De anima brutorum (1672), where lethargy (pathological sleep), 'coma' (heavy sleeping), carus (deprivation of the senses) and apoplexy (into which carus could turn and which he localized in the white matter) are mentioned. The term carus is also derived from Greek, where it can be found in the roots of several words meaning soporific or sleepy. It can still be found in the root of the term 'carotid'. Thomas Sydenham (1624–89) mentioned the term 'coma' in several cases of fever (Sydenham, 1685).[12][13]
Знаци и симптоми
General symptoms of a person in a comatose state are:
- Inability to voluntarily open the eyes
- A non-existent sleep-wake cycle
- Lack of response to physical (painful) or verbal stimuli
- Depressed brainstem reflexes, such as pupils not responding to light
- Irregular breathing
- Scores between 3 and 8[14] on the Glasgow Coma Scale[1]
Узроци
Many types of problems can cause a coma. Forty percent of comatose states result from drug poisoning.[15] Certain drug use under certain conditions can damage or weaken the synaptic functioning in the ascending reticular activating system (ARAS) and keep the system from properly functioning to arouse the brain.[16] Secondary effects of drugs, which include abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly harm the functioning of the ARAS and lead to a coma. Given that drug poisoning is the cause for a large portion of patients in a coma, hospitals first test all comatose patients by observing pupil size and eye movement, through the vestibular-ocular reflex. (See Diagnosis below.)[16]
The second most common cause of coma, which makes up about 25% of cases, is lack of oxygen, generally resulting from cardiac arrest.[15] The Central Nervous System (CNS) requires a great deal of oxygen for its neurons. Oxygen deprivation in the brain, also known as hypoxia, causes sodium and calcium from outside of the neurons to decrease and intracellular calcium to increase, which harms neuron communication.[17] Lack of oxygen in the brain also causes ATP exhaustion and cellular breakdown from cytoskeleton damage and nitric oxide production.
Twenty percent of comatose states result from the side effects of a stroke.[15] During a stroke, blood flow to part of the brain is restricted or blocked. An ischemic stroke, brain hemorrhage, or tumor may cause restriction of blood flow. Lack of blood to cells in the brain prevents oxygen from getting to the neurons, and consequently causes cells to become disrupted and die. As brain cells die, brain tissue continues to deteriorate, which may affect the functioning of the ARAS.
The remaining 15% of comatose cases result from trauma, excessive blood loss, malnutrition, hypothermia, hyperthermia, abnormal glucose levels, and many other biological disorders. Furthermore, studies show that 1 out of 8 patients with traumatic brain injury experience a comatose state.[18]
Патофизиологија
Injury to either or both of the cerebral cortex or the reticular activating system (RAS) is sufficient to cause a person to enter coma.[19]
The cerebral cortex is the outer layer of neural tissue of the cerebrum of the brain.[20] The cerebral cortex is composed of gray matter which consists of the nuclei of neurons, whereas the inner portion of the cerebrum is composed of white matter and is composed of the axons of neuron.[21] White matter is responsible for perception, relay of the sensory input via the thalamic pathway, and many other neurological functions, including complex thinking.
The RAS, on the other hand, is a more primitive structure in the brainstem which includes the reticular formation (RF).[22] The RAS has two tracts, the ascending and descending tract. The ascending track, or ascending reticular activating system (ARAS), is made up of a system of acetylcholine-producing neurons, and works to arouse and wake up the brain.[23] Arousal of the brain begins from the RF, through the thalamus, and then finally to the cerebral cortex.[16] Any impairment in ARAS functioning, a neuronal dysfunction, along the arousal pathway stated directly above, prevents the body from being aware of its surroundings.[22] Without the arousal and consciousness centers, the body cannot awaken, remaining in a comatose state.[24]
The severity and mode of onset of coma depends on the underlying cause. There are two main subdivisions of a coma: structural and diffuse neuronal.[25] A structural cause, for example, is brought upon by a mechanical force that brings about cellular damage, such as physical pressure or a blockage in neural transmission.[26] While a diffuse cause is limited to aberrations of cellular function, that fall under a metabolic or toxic subgroup. Toxin-induced comas are caused by extrinsic substances, whereas metabolic-induced comas are caused by intrinsic processes, such as body thermoregulation or ionic imbalances(e.g. sodium).[24] For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) are examples of a metabolic diffuse neuronal dysfunction. Hypoglycemia or hypercapnia initially cause mild agitation and confusion, but progress to obtundation, stupor, and finally, complete unconsciousness.[27] In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.[1]
Structural and diffuse causes of coma are not isolated from one another, as one can lead to the other in some situations. For instance, coma induced by a diffuse metabolic process, such as hypoglycemia, can result in a structural coma if it is not resolved. Another example is if cerebral edema, a diffuse dysfunction, leads to ischemia of the brainstem, a structural issue, due to the blockage of the circulation in the brain.[24]
Референце
- ^ а б в Weyhenmyeye, James A.; Eve A. Gallman (2007). Rapid Review Neuroscience 1st Ed. Mosby Elsevier. стр. 177—9. ISBN 978-0-323-02261-3.
- ^ Овај чланак или његов део изворно је преузет из Речника социјалног рада Ивана Видановића уз одобрење аутора.
- ^ а б Bordini, A.L.; Luiz, T.F.; Fernandes, M.; Arruda, W. O.; Teive, H. A. (2010). „Coma scales: a historical review”. Arquivos de Neuro-Psiquiatria. 68 (6): 930—937. PMID 21243255. doi:10.1590/S0004-282X2010000600019
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- ^ Cooksley, Tim; Holland, Mark (2017-02-01). „The management of coma”. Medicine (на језику: енглески). 45 (2): 115—119. ISSN 1357-3039. doi:10.1016/j.mpmed.2016.12.001.
- ^ Marc Lallanilla (2013-09-06). „What Is a Medically Induced Coma?”. livescience.com (на језику: енглески). Приступљено 2022-04-23.
- ^ „The Glasgow structured approach to assessment of the Glasgow Coma Scale”. www.glasgowcomascale.org. Приступљено 2019-03-06.
- ^ „Coma - an overview | ScienceDirect Topics”. www.sciencedirect.com. Приступљено 2022-04-28.
- ^ „Glasgow Coma Scale - an overview | ScienceDirect Topics”. www.sciencedirect.com. Приступљено 2022-04-23.
- ^ Laureys; Boly; Moonen; Maquet (2009). „Coma” (PDF). Encyclopedia of Neuroscience. 2: 1133—1142. ISBN 9780080450469. doi:10.1016/B978-008045046-9.01770-8.
- ^ Hannaman, Robert A. (2005). MedStudy Internal Medicine Review Core Curriculum: Neurology 11th Ed. MedStudy. стр. (11—1) to (11—2). ISBN 1-932703-01-2.
- ^ „Persistent vegetative state: A medical minefield”. New Scientist: 40—3. 7. 7. 2007. See diagram Архивирано 2017-08-26 на сајту Wayback Machine.
- ^ „Coma Origin”. Online Etymology Dictionary. Приступљено 14. 8. 2015.
- ^ Wijdicks, Eelco F. M.; Koehler, Peter J. (2008-03-01). „Historical study of coma: looking back through medical and neurological texts”. Brain. 131 (3): 877—889. ISSN 0006-8950. PMID 18208847. doi:10.1093/brain/awm332 .
- ^ Russ Rowlett. „Glasgow Coma Scale”. University of North Carolina at Chapel Hill. Архивирано из оригинала 2018-06-04. г. Приступљено 2010-12-07.
- ^ а б в Liversedge, Timothy; Hirsch, Nicholas (2010). „Coma”. Anaesthesia & Intensive Care Medicine. 11 (9): 337—339. doi:10.1016/j.mpaic.2010.05.008.
- ^ а б в Young, G.B. (2009). „Coma”. Ann. N. Y. Acad. Sci. 1157 (1): 32—47. Bibcode:2009NYASA1157...32Y. PMID 19351354. S2CID 222086047. doi:10.1111/j.1749-6632.2009.04471.x.
- ^ Busl, K. M.; Greer, D. M. (2010). „Hypoxic-ischemic brain injury: Pathophysiology, neuropathology and mechanisms”. NeuroRehabilitation. 26 (1): 5—13. PMID 20130351. doi:10.3233/NRE-2010-0531 .
- ^ Lombardi, Francesco FL; Taricco, Mariangela; De Tanti, Antonio; Telaro, Elena; Liberati, Alessandro (2002-04-22). „Sensory stimulation for brain injured individuals in coma or vegetative state”. Cochrane Database of Systematic Reviews (2): CD001427. ISSN 1465-1858. PMID 12076410. doi:10.1002/14651858.cd001427.
- ^ „Coma - an overview | ScienceDirect Topics”. www.sciencedirect.com. Приступљено 2022-04-23.
- ^ S., Saladin, Kenneth (2011). Human anatomy (3rd изд.). New York: McGraw-Hill. ISBN 9780073525600. OCLC 318191613.
- ^ Mercadante, Anthony A.; Tadi, Prasanna (2022), „Neuroanatomy, Gray Matter”, StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31990494, Приступљено 2022-04-23
- ^ а б Arguinchona, Joseph H.; Tadi, Prasanna (2022), „Neuroanatomy, Reticular Activating System”, StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31751025, Приступљено 2022-04-23
- ^ „Ascending Reticular Activating System - an overview | ScienceDirect Topics”. www.sciencedirect.com. Приступљено 2022-04-23.
- ^ а б в Traub, Stephen J.; Wijdicks, Eelco F. (2016). „Initial Diagnosis and Management of Coma”. Emergency Medicine Clinics of North America. 34 (4): 777—793. ISSN 1558-0539. PMID 27741988. doi:10.1016/j.emc.2016.06.017.
- ^ Huff, J. Stephen; Tadi, Prasanna (2022), „Coma”, StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 28613473, Приступљено 2022-04-23
- ^ Miller, Margaret A.; Zachary, James F. (2017). „Mechanisms and Morphology of Cellular Injury, Adaptation, and Death”. Pathologic Basis of Veterinary Disease: 2—43.e19. ISBN 9780323357753. doi:10.1016/B978-0-323-35775-3.00001-1.
- ^ „Obtundation, stupor and coma Peter Dickinson”, Small Animal Neurological Emergencies, CRC Press, стр. 140—155, 2012-03-15, ISBN 978-0-429-15897-1, doi:10.1201/b15214-12, Приступљено 2022-04-23
Литература
- Weyhenmyeye, James A.; Eve A. Gallman (2007). Rapid Review Neuroscience 1st Ed. Mosby Elsevier. стр. 177-9. ISBN 978-0-323-02261-3.
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