Editing Coma (section)

==Pathophysiology==
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 book |doi=10.1016/B978-0-12-374168-4.00011-3 |chapter=Coma |title=The Neurology of Consciousness |date=2009 |last1=Young |first1=G. Bryan |pages=137–150 |isbn=978-0-12-374168-4 }}</ref>

The [[cerebral cortex]] is the outer layer of [[neural tissue]] of the [[cerebrum]] of the [[brain]].<ref>{{cite book |last1=Saladin |first1=Kenneth S. |title=Human Anatomy |date=2011 |publisher=McGraw-Hill |isbn=978-0-07-352560-0 |oclc=318191613 }}{{pn|date=December 2024}}</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>{{cite book |last1=Mercadante |first1=Anthony A. |last2=Tadi |first2=Prasanna |title=StatPearls |date=2024 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK553239/ |chapter=Neuroanatomy, Gray Matter |pmid=31990494 }}</ref> 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).<ref name="Arguinchona Neuroanatomy">{{cite book |last1=Arguinchona |first1=Joseph H. |last2=Tadi |first2=Prasanna |title=StatPearls |date=2024 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK549835/ |chapter=Neuroanatomy, Reticular Activating System |pmid=31751025 }}</ref> The RAS has two tracts, the ascending and descending tract. The ascending tract, 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 book |doi=10.1016/B978-0-08-045396-5.00229-3 |chapter=Neuropsychology of Sleep |title=Encyclopedia of Behavioral Neuroscience |date=2010 |last1=Pace-Schott |first1=E.F. |pages=448–455 |isbn=978-0-08-045396-5 }}</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="Arguinchona Neuroanatomy"/> 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. |title=Initial Diagnosis and Management of Coma |journal=Emergency Medicine Clinics of North America |date=November 2016 |volume=34 |issue=4 |pages=777–793 |doi=10.1016/j.emc.2016.06.017 |pmid=27741988 }}</ref>

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 name="Huff Tadi Coma"/> 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 book |doi=10.1016/B978-0-323-35775-3.00001-1 |chapter=Mechanisms and Morphology of Cellular Injury, Adaptation, and Death |title=Pathologic Basis of Veterinary Disease |date=2017 |last1=Miller |first1=Margaret A. |last2=Zachary |first2=James F. |pages=2–43.e19 |isbn=978-0-323-35775-3 }}</ref> By contrast, a diffuse cause is limited to aberrations of cellular function which 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>{{cite book |doi=10.1201/b15214-12 |chapter=Obtundation, stupor and coma Peter Dickinson |title=Small Animal Neurological Emergencies |date=2012 |pages=140–155 |isbn=978-0-429-15897-1 }}</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" />

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"/>