Editing Catecholamine (section)

===Modality===
Two catecholamines, [[norepinephrine]] and [[dopamine]], act as [[neuromodulators]] in the [[central nervous system]] and as hormones in the blood circulation. The catecholamine [[norepinephrine]] is a neuromodulator of the peripheral sympathetic nervous system but is also present in the blood (mostly through "spillover" from the [[synapse]]s of the sympathetic system).{{citation needed|date=January 2021}}

High catecholamine levels in blood are associated with [[Stress (medicine)|stress]], which can be induced from psychological reactions or environmental stressors such as [[noise health effects|elevated sound levels]], [[light pollution|intense light]], or [[Hypoglycemia|low blood sugar levels]].<ref>{{Citation |last1=Chu |first1=Brianna |title=Physiology, Stress Reaction |date=2024 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK541120/ |access-date=2024-06-28 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31082164 |last2=Marwaha |first2=Komal |last3=Sanvictores |first3=Terrence |last4=Awosika |first4=Ayoola O. |last5=Ayers |first5=Derek}}</ref>

Extremely high levels of catecholamines (also known as catecholamine toxicity) can occur in [[central nervous system]] trauma due to stimulation or damage of [[nucleus (neuroanatomy)|nuclei]] in the [[brainstem]], in particular, those nuclei affecting the [[sympathetic nervous system]]. In [[emergency medicine]], this occurrence is widely known as a "catecholamine dump".

Extremely high levels of catecholamine can also be caused by [[neuroendocrine tumor]]s in the [[adrenal medulla]], a treatable condition known as [[pheochromocytoma]].

High levels of catecholamines can also be caused by [[monoamine oxidase A|monoamine oxidase A (MAO-A)]] deficiency, known as [[Brunner syndrome]]. As MAO-A is one of the enzymes responsible for degradation of these neurotransmitters, its deficiency increases the [[bioavailability]] of these neurotransmitters considerably. It occurs in the absence of [[pheochromocytoma]], [[neuroendocrine tumor]]s, and [[carcinoid syndrome]], but it looks similar to carcinoid syndrome with symptoms such as facial flushing and aggression.<ref>{{ cite journal | last1 = Manor | first1 = I. | last2 = Tyano | first2 = S. | last3 = Mel | first3 = E. | last4 = Eisenberg | first4 = J. | last5 = Bachner-Melman | first5 = R. | last6 = Kotler | first6 = M. | last7 = Ebstein | first7 = R. P. | title = Family-Based and Association Studies of Monoamine Oxidase A and Attention Deficit Hyperactivity Disorder (ADHD): Preferential Transmission of the Long Promoter-Region Repeat and its Association with Impaired Performance on a Continuous Performance Test (TOVA) | journal = Molecular Psychiatry | volume = 7 | issue = 6 | pages = 626–632 | year = 2002 | pmid = 12140786 | doi = 10.1038/sj.mp.4001037 | doi-access = free }}</ref><ref>{{ Cite book | author = Brunner, H. G. | chapter = MAOA Deficiency and Abnormal Behaviour: Perspectives on an Association | title = Genetics of Criminal and Antisocial Behaviour | series = Ciba Foundation Symposium | volume = 194 | pages = 155–167 | year = 1996 | pmid = 8862875 | doi = 10.1002/9780470514825.ch9 | publisher = Wiley| isbn = 978-0-470-51482-5 }}</ref>

Acute [[porphyria]] can cause elevated catecholamines.<ref>{{cite journal| last1=Stewart |first1=M. F. |last2=Croft |first2=J. |last3=Reed |first3=P. |last4=New |first4=J. P. | pmc= 1994495 | pmid=17660335 | doi=10.1136/jcp.2005.032722 | volume=60 |issue=8 | title=Acute intermittent porphyria and phaeochromocytoma: shared features | journal=Journal of Clinical Pathology | pages=935–936 | year=2006}}</ref>