{{Short description|Impairment in the clarity of consciousness}} {{Redirect-distinguish|Brain fog|Brain fag|Mild cognitive impairment}} '''Clouding of consciousness''', also called '''brain fog''' or '''mental fog''',<ref name="Schildkrout">{{cite book |first=Barbara|last=Schildkrout |title= Unmasking Psychological Symptoms |publisher=John Wiley & Sons |year=2011 |pages=183–184 |url=https://books.google.com/books?id=xIL8VHItTp4C&q=%22clouding+of+consciousness%22+%22mental+fog%22&pg=PA184 |isbn=978-0-470-63907-8 }}</ref><ref name="Basa">{{cite book |first=M.|last=Basavanna |title=Dictionary of Psychology |publisher=Allied Publishers |year=2000 |page=65 |url=https://books.google.com/books?id=sXgbdsaGDKYC&q=%22clouding+of+consciousness%22+%22mental+fog%22&pg=PA65 |isbn=81-7764-030-5}}</ref> occurs when a person is conscious but slightly less wakeful or aware than normal.<ref name="Plum5">{{cite book |url=https://books.google.com/books?id=eDcWsh3FCFQC&q=clouding&pg=PT20 |title=Plum and Posner's diagnosis of stupor and coma |publisher=Oxford University Press |year=2007 |isbn=978-0-19-988653-1 |pages=5–6}}</ref> The term "brain fog" is used to represent a subjective condition of perceived cognitive impairment. A 2023 review article defined brain fog as "a phenomenon of fluctuating states of perceived cognitive dysfunction that could have implications in the functional application of cognitive skills in people's participation in daily activities".<ref name=":0">{{Cite journal |last1=Dass |first1=Ronessa |last2=Kalia |first2=Mohini |last3=Harris |first3=Jocelyn |last4=Packham |first4=Tara |date=2023-12-31 |title=Understanding the Experience and Impacts of Brain Fog in Chronic Pain: A Scoping Review |journal=Canadian Journal of Pain |language=en |volume=7 |issue=1 |doi=10.1080/24740527.2023.2217865 |issn=2474-0527 |pmc=10334862 |pmid=37441085 |article-number=2217865}}</ref> Sufferers may be less aware of time and their surroundings, and find it difficult to pay attention.<ref name="Plum5" /> People describe this subjective sensation as their mind being "foggy".<ref name="Grassi82">{{cite book |author1=Augusto Caraceni |author2=Luigi Grassi |title=Delirium: Acute Confusional States in Palliative Medicine |publisher=Oxford University Press |year=2011 |page=82 |url=https://books.google.com/books?id=qiUfHyoC_zUC&q=foggy+clouding&pg=PA81 |isbn=978-0-19-957205-2}}</ref>
==Background== Clouding of consciousness denotes a less severe state of cognitive impairment than outright delirium. As more abject alteration of consciousness is recognized, physicians may describe patients as in a "confusional state" or delirious, "obtunded", "stuporous", or, in the severest cases, "comatose".<ref name=":32">{{Cite journal |last1=Anastasian |first1=Zirka H. |last2=Ornstein |first2=Eugene |last3=Heyer |first3=Eric J. |date=2009-09-01 |title=Delayed Arousal |journal=Anesthesiology Clinics |series=Problems with Geriatric Anesthesia Patients |volume=27 |issue=3 |pages=429–450 |doi=10.1016/j.anclin.2009.07.007 |pmid=19825485 |pmc=3036001 |issn=1932-2275}}</ref>
=== Feature of delirium === The term ''clouding of consciousness'' has always denoted the main pathogenetic feature of delirium since physician Georg Greiner<ref name="Verdunkelung">{{cite book |author=Georg Friedrich Christoph Greiner|title=Der Traum und das fieberhafte Irreseyn: ein physiologisch-psychologischer Versuch|publisher=F. A Brockhaus|year=1817|oclc=695736431|url=https://books.google.com/books?id=RcIAAAAAcAAJ&pg=PP5}}</ref> pioneered the term (''{{lang|de|Verdunkelung des Bewusstseins}}'') in 1817.<ref name="Grassi2">{{cite book |author1=Augusto Caraceni |author2=Luigi Grassi |title=Delirium: Acute Confusional States in Palliative Medicine |publisher=Oxford University Press |year=2011 |page=2 |url=https://books.google.com/books?id=qiUfHyoC_zUC&q=Verdunkelung+des+Bewusstseins&pg=PA2 |isbn=978-0-19-957205-2}}</ref> The ''Diagnostic and Statistical Manual of Mental Disorders'' (DSM) has historically used the term in its definition of delirium.<ref>{{cite book |author1=George Stein |author2=Greg Wilkinson |title=Seminars in General Adult Psychiatry |publisher=RCPsych Publications|date=2007 |page=490|url=https://books.google.com/books?id=6PGzHFuS1xkC&q=%22clouding+of+consciousness%22&pg=PA490 |isbn=978-1-904671-44-2}}</ref> The DSM-III-R and the DSM-IV replaced "clouding of consciousness" with "disturbance of consciousness" to make it easier to operationalize, but it is still fundamentally the same thing.<ref name="Blazer">{{cite journal |author1=Dan G. Blazer |author2=Adrienne O. van Nieuwenhuizen |journal=Curr Opin Psychiatry |volume=25 |issue=3 |title=Evidence for the Diagnostic Criteria of Delirium |year=2012 |pages=239–243 | url=http://www.medscape.com/viewarticle/761823_2 |doi=10.1097/yco.0b013e3283523ce8|pmid=22449764 |s2cid=39516431 |url-access=subscription }}</ref> Clouding of consciousness may be less severe than delirium on a spectrum of abnormal consciousness.<ref name="Plum5" /><ref>{{cite book |author1=Anthony David |author2=Simon Fleminger |author3=Michael Kopelman |author4=Simon Lovestone |author5=John Mellers |title=Lishman's Organic Psychiatry: A Textbook of Neuropsychiatry |publisher=John Wiley & Sons |date=April 2012 |page=5 |url=https://books.google.com/books?id=ohG6I1C_NeAC&q=%22clouding+of+consciousness+denotes+the+mildest+stage%22&pg=PA5 |isbn=978-0-470-67507-6}}</ref><ref>{{cite book |author=Fang Gao Smith|title=Core Topics in Critical Care Medicine|publisher=Cambridge University Press|year= 2010 |page=312 |url=https://books.google.com/books?id=7ruHkxLgIQ8C&q=%22clouding+of+consciousness+very+mild+form+of+mental+status%22&pg=PA312 |isbn=978-1-139-48968-3 }}</ref> Clouding of consciousness may be synonymous with ''subsyndromal delirium''.<ref name="Ouimet">{{cite journal |author=Sébastien Ouimet |journal=Intensive Care Med |volume=33 |title=Subsyndromal delirium in the ICU: evidence for a disease spectrum |year=2007 |pages=1007–1013 |doi=10.1007/s00134-007-0618-y |pmid=17404704 |last2=Riker |first2=R |last3=Bergeron |first3=N |last4=Cossette |first4=M |last5=Kavanagh |first5=B |last6=Skrobik |first6=Y |issue=6 |s2cid=20565946 |display-authors=etal}}</ref>
Subsyndromal delirium differs from normal delirium by being overall less severe, lacking acuteness in onset and duration, having a relatively stable sleep-wake cycle, and having relatively stable motor alterations.<ref name="Meagher">{{cite journal |author=David Meagher|journal=The British Journal of Psychiatry|volume=200|doi=10.1192/bjp.bp.111.095273|title=Features of subsyndromal and persistent delirium |year=2012 |pages=37–44|last2=Adamis |first2=D. |last3=Trzepacz |first3=P. |last4=Leonard |first4=M. |pmid=22075650 |issue=1|display-authors=etal|doi-access=free }}</ref> Subsyndromal delirium's significant clinical features are inattention, thought process abnormalities, comprehension abnormalities, and language abnormalities.<ref name="Meagher"/> Delirium's full clinical manifestations may never be reached.<ref name="Ouimet"/> Among intensive care unit patients, subsyndromal subjects were as likely to survive as patients with a Delirium Screening Checklist score of 0, but required extended care at rates greater than 0-scoring patients (although lower rates than those with full ICU delirium)<ref name="Ouimet"/> and had a decreased post-discharge level of functional independence compared to the general population.<ref name="Meagher"/>
In clinical practice, no standard test is exclusive and specific; therefore, diagnosis depends on the physician's subjective impression. The DSM-IV-TR instructs clinicians to code subsyndromal delirium presentations under the miscellaneous category "cognitive disorder not otherwise specified".<ref name="Grassi11">{{cite book |author1=Augusto Caraceni |author2=Luigi Grassi |title=Delirium: Acute Confusional States in Palliative Medicine |publisher=Oxford University Press |year=2011 |page=11 |url=https://books.google.com/books?id=qiUfHyoC_zUC&q=%22subsyndromal+presentations+need+to+be+carefully+assessed%22&pg=PA11 |isbn=978-0-19-957205-2}}</ref>
==Psychopathology== {{Expand section|* *Elaboration of ascending reticular activating system *Explanation of pedunculopontine neurons and motor/cognitive disinhibition|date=December 2025}} The cerebral cortex and the hippocampus are known to play a critical role in the presentation of brain fog in specific settings. The cerebral cortex, the brain's outermost layer, attached to the cerebrum, is responsible for more advanced processes, such as thought, information recall, maintained wakefulness, and consciousness. The hippocampus, deep within the brain's temporal lobe, organizes, stores, and retrieves information within it, converting memory from short-term to long. It plays a crucial role in enhancing spatial and verbal memory. The cerebral cortex and hippocampus work together to organize and add timing to multiple unconscious brain processes, turning them into a continuous and coherent flow of conscious experience.<ref>{{cite journal |last1=Friedman |first1=Garrett |title=The Current of Consciousness: Neural Correlates and Clinical Aspects |journal=Current Neurology and Neuroscience Reports |date=12 June 2023 |volume=23 |doi=10.1007/s11910-023-01276-0 |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC10287796/pdf/11910_2023_Article_1276.pdf |access-date=6 Dec 2025}}</ref>
Disrupting circadian regulation interferes with neural activation and hippocampus memory processing, reducing thought clarity and alertness and causing confusion. Dysfunction in the hippocampus may limit awareness and make forming cohesive thoughts difficult, resulting in cognitive lapses. These irregularities collectively cause what is known as "brain fog" or clouded consciousness.{{Citation needed|date=December 2025|reason=It's good to have a citation at least once every paragraph for clarity}}
The prefrontal cortex (PFC), in the anterior part of the frontal lobe, helps to regulate thought, feeling, and objective-based behavior. It is the final{{Clarify|reason=Final in what context?|date=December 2025}} brain region that undergoes myelination, a mechanism by which insulating myelin sheaths form surrounding axons to improve the rapidity and efficacy of communication between neurons via brain networks.{{Clarify|reason=Might want to simplify to preserve comprehension. It gets fairly technical here, which is necessary, but may confuse readers unfamiliar with the topic|date=December 2025}}{{Citation needed|date=December 2025|reason=I presume the citation is the one used in the next paragraph over, but if you could confirm that it would be appreciated}}
Research has found that higher cognitive function requires coordinated interaction between the PFC and posterior cortical regions. These posterior areas provide the sensory and perceptual content of conscious experience, whereas the PFC facilitates the executive processes that organize, regulate, and keep that content in awareness. The specific aspects of consciousness correspond to precise patterns of activation within posterior cortical regions, while the PFC helps structure and integrate those activations into coherent thought.<ref>{{cite journal |last1=Frith |first1=Chris |title=The role of the prefrontal cortex in higher cognitive functions |journal=Cognitive Brain Research |volume=5 |page=180 |doi=10.1016/S0926-6410(96)00054-7 }}</ref>
=== Wake–sleep regulation and neuronal disinhibition === Consciousness was historically believed to be a product of the whole of activity in the cerebral hemispheres. But the conscious state is not altered by injury to one hemisphere, "except if the size of [a brain lesion] affects other cortical areas or the diencephalon" or if the lesion is exceptionally large.<ref name=":32" /><ref>{{Citation |last=Tindall |first=Suzie C. |title=Level of Consciousness |date=1990 |work=Clinical Methods: The History, Physical, and Laboratory Examinations |editor-last=Walker |editor-first=H. Kenneth |url=http://www.ncbi.nlm.nih.gov/books/NBK380/ |access-date=2025-11-25 |edition=3rd |place=Boston |publisher=Butterworths |isbn=978-0-409-90077-4 |pmid=21250221 |editor2-last=Hall |editor2-first=W. Dallas |editor3-last=Hurst |editor3-first=J. Willis}}</ref> 1916 research by Romanian-Viennese neurologist Constantin von Economo found that specific regions of the brain (the midbrain and diencephalon) targeted by encephalitis lethargica (sleeping sickness) produced alterations in wake-sleep regulation.<ref name=":32" /><ref name=":33">{{Cite journal |last1=Saper |first1=Clifford B. |last2=Scammell |first2=Thomas E. |last3=Lu |first3=Jun |date=2005-10-26 |title=Hypothalamic regulation of sleep and circadian rhythms |url=https://www.nature.com/articles/nature04284 |journal=Nature |language=en |volume=437 |issue=7063 |pages=1257–1263 |doi=10.1038/nature04284 |pmid=16251950 |bibcode=2005Natur.437.1257S |issn=1476-4687|url-access=subscription }}</ref> He identified a site at the junction of the brainstem and forebrain where lesions produced prolonged sleepiness, as well as a site that included the anterior hypothalamus where, conversely, lesions produced prolonged insomnia.<ref name=":33" /> Based on his observation of patients experiencing lethargy who all had lesions at the junction between these two regions (an area that included the posterior lateral hypothalamus), Von Economo proposed "an ascending arousal system originating in the brainstem that kept the forebrain awake", suggesting that narcolepsy was caused by its dysfunction.<ref name=":33" /> This supports the modern notion that distinct segments of the central nervous system are critical for consciousness.<ref name=":32" />
The conceptual model of clouding of consciousness in psychopathology is that of a part of the brain regulating the "overall level" of consciousness, which is responsible for awareness of oneself and of the environment.<ref name="Plum5" /><ref name="Grassi20">{{cite book |author1=Augusto Caraceni |author2=Luigi Grassi |title=Delirium: Acute Confusional States in Palliative Medicine |publisher=Oxford University Press |year=2011 |pages=19–21 |url=https://books.google.com/books?id=qiUfHyoC_zUC&q=%22level+of+consciousness+and+the+content+of+consciousness%22&pg=PA19 |isbn=978-0-19-957205-2}}</ref> Various etiologies disturb this regulating part of the brain, which in turn disturbs the "overall level" of consciousness.<ref name="Stuart477">{{cite book |author=Yudofsky & Hales |title=The American Psychiatric Publishing textbook of neuropsychiatry and behavioral neurosciences |publisher=American Psychiatric Pub |year=2008 |page=477 |url=https://books.google.com/books?id=f5BEk-6yO_4C&q=%22funnel+into+a+final+common+neural+pathway%22&pg=PA477 |isbn=978-1-58562-239-9}}</ref> This system of a sort of general activation of consciousness is called "arousal" or "wakefulness".<ref name="Grassi20" />
=== Altered cognition === Clouding of consciousness is not necessarily accompanied by drowsiness.<ref name="RogerMacKinnon">{{cite book |author1=Roger A. MacKinnon |author2=Robert Michels |author3=Peter J. Buckley |title=The Psychiatric Interview in Clinical Practice |edition =2nd|publisher=American Psychiatric Publishing, Inc. |year=2006 |pages=462–464 }}</ref> Patients may not be sleepy yet still have clouded consciousness (disorder of wakefulness).<ref name="Plum8">{{cite book |title=Plum and Posner's diagnosis of stupor and coma |publisher=Oxford University Press |year=2007 |page=8 |url=https://books.google.com/books?id=Otivdh2ZoVwC&q=%22However%2C+when+awakened%2C+consciousness+is+clearly+clouded%22&pg=PA8 |isbn=978-0-19-804336-2 }}</ref> Paradoxically, affected individuals say they are "awake but, in another way, not".<ref name="Duppils">{{cite journal |author1=G Sorensen Duppils |author2=K Wikblad |journal=Journal of Clinical Nursing |volume=16|issue=5|title=Patients' experiences of being delirious|date=May 2007|pages=810–818 |doi=10.1111/j.1365-2702.2006.01806.x|pmid=17462032}}</ref> Lipowski points out that decreased "wakefulness" as used here is not exactly synonymous with drowsiness. One is a stage on the way to coma, the other on the way to sleep, which is very different.<ref>{{cite journal |author=Lipowski ZJ.|journal=Journal of Nervous and Mental Disease |volume=145 |issue=3 |title=Delirium, clouding of consciousness and confusion|year=1967|pages=227–255 |doi=10.1097/00005053-196709000-00006 |pmid=4863989}}</ref><ref>{{cite book |title=Organic Psychiatry: The Psychological Consequences of Cerebral Disorder|author=William Alwyn Lishman |publisher=John Wiley & Sons |year=1998 |page=4 }}</ref>
The affected person has a sensation of mental clouding described in the patient's own words as "foggy".<ref name="Grassi82"/> One patient said, "I thought it became like misty, in some way... the outlines were sort of fuzzy".<ref name="Duppils"/> Others may describe a "spaced-out" feeling.<ref>{{cite book |author=Fred Ovsiew, M.D.|title=Neuropsychiatry and Mental Health Services |publisher=American Psychiatric Press, Inc. |year=1999 |page=170|url=https://books.google.com/books?id=l6giB-cCvl0C&q=%22level+of+consciousness+that+may+range+from+a+%22spaced+out%22+feeling%22&pg=PA170 |isbn=0-88048-730-5 }}</ref> Affected people compare their overall experience to that of a dream, because, as in a dream, consciousness, attention, orientation to time and place, perception, and awareness are disturbed.<ref>{{cite journal | title= Remembering delirium | author = Simon Fleminger | journal= The British Journal of Psychiatry | volume= 180 | pages= 4–5 | year= 2002 | doi= 10.1192/bjp.180.1.4 | pmid= 11772842 | issue=1| doi-access= free }}</ref> Barbara Schildkrout, a clinical instructor in psychiatry at the Harvard Medical School, described her subjective experience of clouding of consciousness, which she also called "mental fog", after taking a single dose of chlorpheniramine (an antihistamine for her allergy to cottonwood) on a cross-country road trip. She described feeling "out of it" and being in a "dreamy state". She described a sense of not trusting her own judgment and a dulled awareness, not knowing how much time had passed.<ref name="Schildkrout"/> Clouding of consciousness is not the same thing as ''depersonalization'', though people affected by both compare their experience to that of a dream. Psychometric tests produce little evidence of a relationship between clouding of consciousness and depersonalization.<ref>{{cite journal |last1=Sedman |first1=G. |title=Theories of Depersonalization: A Re-appraisal |journal=British Journal of Psychiatry |date=July 1970 |volume=117 |issue=536 |pages=1–14 |doi=10.1192/s0007125000192104 |pmid=4920886 |s2cid=246610704 }}</ref>
Brain fog may affect performance on virtually any cognitive task.<ref name="Schildkrout"/> As one author put it, "It should be apparent that cognition is not possible without a reasonable degree of arousal."<ref name="Plum5"/> Cognition includes perception, memory, learning, executive functions, language, constructive abilities, voluntary motor control, attention, and mental speed. Brain fog's most significant clinical features are inattention, thought process abnormalities, comprehension abnormalities, and language abnormalities.<ref name="Meagher"/> The extent of the impairment is variable because inattention may impair several cognitive functions. Affected people may complain of forgetfulness, being "confused",<ref name="JohnNoble"/> or being "unable to think straight".<ref name="JohnNoble">{{cite book |author1=John Noble |author2=Harry L. Greene |title=Textbook of Primary Care Medicine |publisher=Mosby|year=1996|page=1325}}</ref> Despite the similarities, subsyndromal delirium is not the same thing as ''mild cognitive impairment''; the fundamental difference is that mild cognitive impairment is a dementia-like impairment, which does not involve a disturbance in arousal (wakefulness).<ref name="Plum7">{{cite book |title=Plum and Posner's diagnosis of stupor and coma |publisher=Oxford University Press |year=2007 |page=7 |url=https://books.google.com/books?id=eDcWsh3FCFQC&q=%22not+usually+accompanied+by+a+reduction+in+arousal%22&pg=PT23 |isbn=978-0-19-988653-1}}</ref>
== Drug use and withdrawal == Use of and withdrawal from certain recreational and prescription drugs has been shown to alter brain cognition and contribute to memory loss, impaired recall, emotional volatility, mood instability, and altered behavior.<ref>{{Cite web |title=Brain recovery after alcohol and other drug use - Alcohol and Drug Foundation |url=https://adf.org.au/insights/brain-recovery-after-aod/ |access-date=2025-09-28 |website=adf.org.au |language=en}}</ref> It can also heighten stress, dysregulate pleasure and the basal ganglia's reward system, and limit executive control function by disrupting normal function of the prefrontal cortex, leading to difficulty concentrating, "organiz[ing] thoughts and activities, prioritiz[ing] tasks, manag[ing] time, and mak[ing] decisions".<ref name=":16">{{Citation |last1=Administration (US) |first1=Substance Abuse and Mental Health Services |title=THE NEUROBIOLOGY OF SUBSTANCE USE, MISUSE, AND ADDICTION |date=November 2016 |work=Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health [Internet] |url=https://www.ncbi.nlm.nih.gov/books/NBK424849/ |access-date=2025-11-19 |publisher=US Department of Health and Human Services |language=en |last2=General (US) |first2=Office of the Surgeon}}</ref>
People may misuse substances as a means of self-medication for psychological/neuro-cognitive difficulties, masking symptoms during use periods but leading to a rebound or exacerbation of symptoms in the immediate post-abstinence period.<ref name=":16" /><ref name=":5">{{Cite journal |last1=Starzer |first1=Marie Stefanie Kejser |last2=Nordentoft |first2=Merete |last3=Hjorthøj |first3=Carsten |date=April 2018 |title=Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis |url=https://psychiatryonline.org/doi/10.1176/appi.ajp.2017.17020223 |journal=American Journal of Psychiatry |volume=175 |issue=4 |pages=343–350 |doi=10.1176/appi.ajp.2017.17020223 |pmid=29179576 |issn=0002-953X}}</ref> This may result from the users' dependency on and subsequent restriction from the substance in question, or from neurocognitive impairment / neurodegeneration resulting from use.<ref name=":16" />
=== Dopamine dysregulation === As addictive behaviors persist, dopamine is depleted at a faster pace, and its receptors increasingly dulled by oversaturation, leading to a reduced sensitivity to dopamine produced naturally by the body over time.<ref name=":19">{{Cite web |date=2024-11-17 |title=Dopamine: Function, Relation With Addiction, Dysregulation Effect, And Recovery |url=https://whitelightbh.com/resources/dopamine/ |access-date=2025-11-19 |website=White Light Behavioral Health |language=en-US}}</ref> It has been consistently shown that addicts present with both lower responsiveness to dopamine, particularly in D2 receptors, and lower dopamine production overall.<ref name=":16" /><ref>{{Cite journal |last1=Volkow |first1=N. D. |last2=Wang |first2=G.-J. |last3=Fowler |first3=J. S. |last4=Logan |first4=J. |last5=Gatley |first5=S. J. |last6=Hitzemann |first6=R. |last7=Chen |first7=A. D. |last8=Dewey |first8=S. L. |last9=Pappas |first9=N. |date=1997-04-24 |title=Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects |url=https://www.nature.com/articles/386830a0 |journal=Nature |language=en |volume=386 |issue=6627 |pages=830–833 |doi=10.1038/386830a0 |pmid=9126741 |bibcode=1997Natur.386..830V |issn=1476-4687 |url-access=subscription }}</ref><ref>{{Cite journal |last1=Volkow |first1=N. D. |last2=Tomasi |first2=D. |last3=Wang |first3=G.-J. |last4=Logan |first4=J. |last5=Alexoff |first5=D. L. |last6=Jayne |first6=M. |last7=Fowler |first7=J. S. |last8=Wong |first8=C. |last9=Yin |first9=P. |last10=Du |first10=C. |date=2014-06-10 |title=Stimulant-induced dopamine increases are markedly blunted in active cocaine abusers |journal=Molecular Psychiatry |volume=19 |issue=9 |pages=1037–1043 |doi=10.1038/mp.2014.58 |issn=1476-5578 |pmc=4827430 |pmid=24912491}}</ref> This, in turn, dysregulates the brain's natural reward mechanisms, leading to decreased motivation, anxiety, difficulty thinking and concentrating, impulsivity, fatigue, emotional blunting, short-term memory disruptions, forgetfulness, disorganization, loss of coordination and balance, and social withdrawal.<ref name=":19" /><ref>{{Cite web |title=Dopamine Deficiency: Symptoms, Causes & Treatment |url=https://my.clevelandclinic.org/health/articles/22588-dopamine-deficiency |archive-url=https://web.archive.org/web/20250819211309/https://my.clevelandclinic.org/health/articles/22588-dopamine-deficiency |archive-date=2025-08-19 |access-date=2025-11-19 |website=Cleveland Clinic |language=en}}</ref>
This self-reinforcing process is often reversed with restriction from the substance in question. Initial acute impacts are pronounced, but dopamine levels begin to stabilize during the withdrawal period, albeit slowly, and eventually return to a healthy baseline.<ref name=":19" />
=== By substance === {{Expand section|* * Expand cannabis use section * Expand alcohol use section to include: Elaboration of alcoholism without complication; explanation of consequences of acute alcohol withdrawal; expansion to include other alcohol-related cognitive effects * Explanation of consequences of use for: Cocaine; Methamphetamines; Nitrous; Heroin and Opiates; Psychedelics; Sedatives; Whippets|date=November 2025}}
==== Alcohol ==== {{See also|Alcohol-related brain damage}}
Heavy, progressive, and persistent alcohol abuse (alcohol use disorder (AUD)) lasting more than several years has been shown to lead to brain damage.<ref>{{Cite web |title=Alcohol-related brain damage (ARBD): what is it and who gets it? {{!}} Alzheimer's Society |url=https://www.alzheimers.org.uk/about-dementia/types-dementia/alcohol-related-brain-damage-arbd |access-date=2025-11-26 |website=www.alzheimers.org.uk |language=en}}</ref> Cognitive difficulties related to alcohol use that do not progress into more severe illness are called alcohol-related brain damage (ARBD).<ref name=":34">{{Cite journal |last1=Zahr |first1=Natalie M. |last2=Kaufman |first2=Kimberley L. |last3=Harper |first3=Clive G. |date=2011-04-12 |title=Clinical and pathological features of alcohol-related brain damage |journal=Nature Reviews. Neurology |volume=7 |issue=5 |pages=284–294 |doi=10.1038/nrneurol.2011.42 |issn=1759-4766 |pmc=8121189 |pmid=21487421}}</ref> Symptoms include mild executive dysfunction as well as deficits in memory, coordination, motor control, and visuospatial skills.<ref name=":34" /><ref>{{Cite journal |last1=van Holst |first1=Ruth Janke |last2=Schilt |first2=Thelma |date=March 2011 |title=Drug-related decrease in neuropsychological functions of abstinent drug users |journal=Current Drug Abuse Reviews |volume=4 |issue=1 |pages=42–56 |doi=10.2174/1874473711104010042 |issn=1874-4745 |pmid=21466500}}</ref> Cognitive deficits differ significantly between patients, suggesting "that the functions affected by chronic alcohol consumption are dissociable and supported by different neural systems".<ref name=":34" />
===== Wernicke-Korsakoff Syndrome ===== {{Main|Wernicke–Korsakoff syndrome}}
Persistent alcohol use disorder lasting several years or more can contribute to severe malnutrition.<ref name=":34" /> Alcohol abuse hinders the gut's ability to properly absorb critical nutrients, and the brain's ability to phosphorylate them.<ref name=":34" /><ref name=":35">{{Cite journal |last1=Oudman |first1=Erik |last2=Van der Stigchel |first2=Stefan |last3=Postma |first3=Albert |last4=Wijnia |first4=Jan W. |last5=Nijboer |first5=Tanja C. W. |date=2014-05-27 |title=A Case of Chronic Wernicke's Encephalopathy: A Neuropsychological Study |journal=Frontiers in Psychiatry |volume=5 |page=59 |doi=10.3389/fpsyt.2014.00059 |doi-access=free |issn=1664-0640 |pmc=4034510 |pmid=24904442}}</ref> Chief among these deficiencies is thiamine (Vitamin B-1). With an incidence rate as high as 12.5% in patients with alcoholism, such a deficiency can lead to Wernicke encephalopathy (WE), though this is reversible through rapid therapeutic treatment with thiamine and glucose.<ref name=":34" /><ref name=":35" /><ref name=":36">{{Cite web |title=Wernicke-Korsakoff Syndrome {{!}} National Institute on Alcohol Abuse and Alcoholism (NIAAA) |url=https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/wernicke-korsakoff-syndrome |access-date=2025-11-26 |website=www.niaaa.nih.gov |language=en}}</ref> This stage is characterized by confusion (of a more severe degree than brain fog), incoherence, motor impairments, loss of coordination and balance, and impairments in the visual domain.<ref name=":36" /> The mortality rate for patients at this stage is around 20%. Roughly 12% of patients experience disease improvement, with chronic brain damage potentially being avoided with treatment, though not all cognitive effects are reversible.<ref name=":35" /><ref name=":36" />
WE, if left untreated, can progress to Korsakoff syndrome (as is the case in roughly 68-80% of cases), an irreversible form of chronic amnesia. This stage is characterized by relief from severe confusion, less incoherence, and clear consciousness over the course of the day, but, in the longer term, severe anterograde memory impairments (both memory formation (anterograde amnesia) and recall), confabulation, hallucination, repetitive speech and action, severe executive dysfunction, lack of motivation, and emotional apathy.<ref name=":34" /><ref name=":35" /><ref name=":36" /> Additionally, patients may experience symptoms more reminiscent of brain fog, including "deficits on tests of problem solving, working memory, cognitive flexibility, perseverative responding, and self-regulation."<ref name=":34" /> Memory rehabilitation therapy may help to relieve symptoms; severe cases often require institutionalization.<ref name=":36" /><ref>{{Cite journal |last1=THOMSON |first1=ALLAN D. |last2=MARSHALL |first2=E. JANE |date=2005-12-29 |title=The Natural History and Pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis |url=https://academic.oup.com/alcalc/article/41/2/151/134954 |journal=Alcohol and Alcoholism |language=en |volume=41 |issue=2 |pages=151–158 |doi=10.1093/alcalc/agh249 |pmid=16384871 |issn=1464-3502 |archive-url=https://web.archive.org/web/20230320223021/https://academic.oup.com/alcalc/article/41/2/151/134954 |archive-date=2023-03-20|url-access=subscription }}</ref>
==== Cannabis ==== The effects of cannabis on neurological function have become better known in recent years, with the overwhelming majority of research finding that cannabis impairs cognitive function. The duration and frequency of use and quantity and concentration of product consumed correlates with the degree and duration of impairment.<ref name=":6">{{Cite web |last1=Hill |first1=Kevin |last2=Hsu |first2=Michael|date=2022-06-14 |title=Cognitive effects in midlife of long-term cannabis use |url=https://www.health.harvard.edu/blog/cognitive-effects-of-long-term-cannabis-use-in-midlife-202206142760 |access-date=2025-09-29 |website=Harvard Health |language=en}}</ref><ref name=":7">{{Cite journal |last1=Bourque |first1=Josiane |last2=Potvin |first2=Stéphane |date=2021-06-10 |title=Cannabis and Cognitive Functioning: From Acute to Residual Effects, From Randomized Controlled Trials to Prospective Designs |journal=Frontiers in Psychiatry |language=English |volume=12 |article-number=596601 |doi=10.3389/fpsyt.2021.596601 |pmid=34177633 |pmc=8222623 |doi-access=free |issn=1664-0640}}</ref><ref name=":8">{{Cite web |date=2025-05-12 |title=THC Content in Cannabis Has Surged: Here's What You Need to Know |url=https://www.bu.edu/articles/2025/thc-content-in-cannabis-has-surged/ |access-date=2025-09-29 |website=Boston University |language=en}}</ref> The immediate short-term effects of cannabis use can include "impaired short-term memory and motor coordination, altered judgment, paranoia, and psychosis".<ref name=":15">{{Cite journal |last1=Bahji |first1=Anees |last2=Stephenson |first2=Callum |last3=Tyo |first3=Richard |last4=Hawken |first4=Emily R. |last5=Seitz |first5=Dallas |date=2020-04-09 |title=Prevalence of Cannabis Withdrawal Symptoms Among People With Regular or Dependent Use of Cannabinoids: A Systematic Review and Meta-analysis |journal=JAMA Network Open |volume=3 |issue=4 |pages=e202370 |doi=10.1001/jamanetworkopen.2020.2370 |pmid=32271390 |pmc=7146100 }}</ref> Long-term use can lead to "altered brain development, poor educational outcomes, cognitive impairment, diminished quality of life", and increased risk of suicide.<ref name=":15" />
The rapid increase in the THC concentration of cannabis products in recent years has led to concern among physicians that it may contribute to adverse health effects among the general population, particularly adolescents and young adults.<ref name=":7" /><ref name=":8" /><ref>{{Cite web |last=Mallenbaum |first=Carly |date=2025-04-18 |title=THC in pot is way more potent than it was decades ago |url=https://www.axios.com/local/san-francisco/2025/04/18/cannabis-thc-high-levels-potency-chart |access-date=2025-09-29 |website=Axios |language=en}}</ref><ref>{{Cite journal |last1=ElSohly |first1=Mahmoud A. |last2=Chandra |first2=Suman |last3=Radwan |first3=Mohammed |last4=Majumdar |first4=Chandrani Gon |last5=Church |first5=James C. |date=June 2021 |title=A Comprehensive Review of Cannabis Potency in the United States in the Last Decade |journal=Biological Psychiatry. Cognitive Neuroscience and Neuroimaging |volume=6 |issue=6 |pages=603–606 |doi=10.1016/j.bpsc.2020.12.016 |issn=2451-9030 |pmid=33508497}}</ref><ref>{{Cite journal |last1=Li |first1=Ruixuan |last2=Tao |first2=Feng |title=Effects of Cannabis Exposure on Adolescent Health and Development: A Narrative Review |url=https://www.eurekaselect.com/article/137374 |journal=Current Drug Research Reviews |date=2025 |language=en |volume=17 |issue=2 |pages=160–169 |doi=10.2174/0125899775273727231224185028 |pmid=40761110 |pmc=12376134 }}</ref><ref name=":11">{{Cite journal |last1=Testai |first1=Fernando D. |last2=Gorelick |first2=Philip B. |last3=Aparicio |first3=Hugo J. |last4=Filbey |first4=Francesca M. |last5=Gonzalez |first5=Raul |last6=Gottesman |first6=Rebecca F. |last7=Melis |first7=Miriam |last8=Piano |first8=Mariann R. |last9=Rubino |first9=Tiziana |last10=Song |first10=Sarah Y. |others=On behalf of the American Heart Association Stroke Brain Health Science Subcommittee of the Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; and Council on Peripheral Vascular Disease |date=2022-02-10 |title=Use of Marijuana: Effect on Brain Health: A Scientific Statement From the American Heart Association |url=https://www.ahajournals.org/doi/10.1161/STR.0000000000000396 |journal=Stroke |volume=53 |issue=4 |pages=e176–e187 |doi=10.1161/STR.0000000000000396 |pmid=35142225 |hdl=11584/344803 |hdl-access=free }}</ref>
===== Cannabis use disorder ===== {{Main|Cannabis use disorder}}
A 40-year-long study in New Zealand followed roughly 1,000 people from age 3 to 45 to measure the impacts of cannabis usage on brain function and functional IQ. It found that long-term cannabis users (those who reported consistent or dependent usage of the drug at age 45 and at least one previous period of sustained heavy usage){{efn|Weekly or more (as reported at ages 18, 21, 26, 32, 38, and 45)<ref name=":6" /><ref name=":9"/>}} experienced a mean 5.5-point drop in IQ from childhood to adulthood.<ref name=":6"/><ref name=":9">{{Cite journal |last1=Meier |first1=Madeline H. |last2=Caspi |first2=Avshalom |last3=Knodt |first3=Annchen R. |last4=Hall |first4=Wayne |last5=Ambler |first5=Antony |last6=Harrington |first6=HonaLee |last7=Hogan |first7=Sean |last8=M. Houts |first8=Renate |last9=Poulton |first9=Richie |last10=Ramrakha |first10=Sandhya |last11=Hariri |first11=Ahmad R. |last12=Moffitt |first12=Terrie E. |date=2022-03-08 |title=Long-Term Cannabis Use and Cognitive Reserves and Hippocampal Volume in Midlife |journal=American Journal of Psychiatry |volume=179 |issue=5 |pages=362–374 |doi=10.1176/appi.ajp.2021.21060664 |issn=0002-953X |pmc=9426660 |pmid=35255711}}</ref> These cognitive deficits "could not be explained by persistent tobacco, alcohol, or other illicit drug use, childhood socioeconomic status, low childhood self-control, or family history of substance dependence." Comparative groups fared significantly better; non-users of all substances were the only group to experience a positive change in IQ over the length of the study. Cannabis quitters (those with at least one previous instance of diagnosed cannabis dependency who reported no usage at the conclusion of the study) and recreational midlife users (those reporting use between 6 and 51 days per year in their 30s and 40s, with no history of weekly or dependent usage) experienced a smaller but nevertheless comparatively significant drop in IQ. Long-term users were the only group whose performance worsened on every cognitive benchmark assessment administered at the end of the study period.<ref name=":9" />
===== Presentation in psychotic disorders ===== Numerous studies have shown that heavy cannabis users face a markedly higher risk of schizophrenia, bipolar disorder, and transient psychotic episodes than the general population, with up to 50% of those who experienced cannabis-induced psychosis going on to develop schizophrenia.<ref name=":5" /><ref name=":10">{{Cite journal |last1=Seddon |first1=Jennifer L. |last2=Birchwood |first2=Max |last3=Copello |first3=Alex |last4=Everard |first4=Linda |last5=Jones |first5=Peter B. |last6=Fowler |first6=David |last7=Amos |first7=Tim |last8=Freemantle |first8=Nick |last9=Sharma |first9=Vimal |last10=Marshall |first10=Max |last11=Singh |first11=Swaran P. |date=May 2016 |title=Cannabis Use Is Associated With Increased Psychotic Symptoms and Poorer Psychosocial Functioning in First-Episode Psychosis: A Report From the UK National EDEN Study |journal=Schizophrenia Bulletin |volume=42 |issue=3 |pages=619–625 |doi=10.1093/schbul/sbv154 |issn=1745-1701 |pmc=4838086 |pmid=26536902}}</ref><ref>{{Cite journal |last1=Rognli |first1=Eline B. |last2=Heiberg |first2=Ina H. |last3=Jacobsen |first3=Bjarne K. |last4=Høye |first4=Anne |last5=Bramness |first5=Jørgen G. |date=2023-05-03 |title=Transition From Substance-Induced Psychosis to Schizophrenia Spectrum Disorder or Bipolar Disorder |url=https://psychiatryonline.org/ajp/doi/10.1176/appi.ajp.22010076 |journal=American Journal of Psychiatry |volume=180 |issue=6 |pages=437–444 |doi=10.1176/appi.ajp.22010076 |pmid=37132221 |hdl=10037/32997 |issn=0002-953X|hdl-access=free }}</ref> But a 2010 meta-analysis of previous research in the ''Schizophrenia Bulletin'' showed evidence that those same people have a paradoxically lower risk of neurocognitive difficulties; use of the substance substantially increased the prevalence of positive symptoms, but was simultaneously associated with reduced neurocognitive deficits or, in some cases, boosted cognitive performance (e.g., visual memory, working memory, and executive function).<ref name=":10" /><ref>{{Cite journal |last1=Yücel |first1=Murat |last2=Bora |first2=Emre |last3=Lubman |first3=Dan I. |last4=Solowij |first4=Nadia |last5=Brewer |first5=Warrick J. |last6=Cotton |first6=Sue M. |last7=Conus |first7=Philippe |last8=Takagi |first8=Michael J. |last9=Fornito |first9=Alex |last10=Wood |first10=Stephen J. |last11=McGorry |first11=Patrick D. |last12=Pantelis |first12=Christos |date=March 2012 |title=The impact of cannabis use on cognitive functioning in patients with schizophrenia: a meta-analysis of existing findings and new data in a first-episode sample |journal=Schizophrenia Bulletin |volume=38 |issue=2 |pages=316–330 |doi=10.1093/schbul/sbq079 |issn=1745-1701 |pmc=3283159 |pmid=20660494}}</ref>
===== Heart health and cerebrovascular deficits ===== Studies published over the past decade have shown that cannabis use (particularly in cases of heavy use or dosage) is associated with significantly increased risk of cardiovascular deficits and/or coronary events in people under age 50, particularly ischemic strokes and myocardial infarctions (heart attacks).<ref>{{Cite journal |last1=Jouanjus |first1=Emilie |last2=Raymond |first2=Valentin |last3=Lapeyre-Mestre |first3=Maryse |last4=Wolff |first4=Valérie |date=2017-04-21 |title=What is the Current Knowledge About the Cardiovascular Risk for Users of Cannabis-Based Products? A Systematic Review |journal=Current Atherosclerosis Reports |language=en |volume=19 |issue=6 |page=26 |doi=10.1007/s11883-017-0663-0 |pmid=28432636 |issn=1534-6242}}</ref><ref>{{Cite journal |last1=Kamel |first1=Ibrahim |last2=Mahmoud |first2=Ahmed K. |last3=Twayana |first3=Anu Radha |last4=Younes |first4=Ahmed M. |last5=Horn |first5=Benjamin |last6=Dietzius |first6=Harold |date=May 2025 |title=Myocardial Infarction and Cardiovascular Risks Associated With Cannabis Use |journal=JACC: Advances |volume=4 |issue=5 |article-number=101698 |doi=10.1016/j.jacadv.2025.101698 |pmc=12235408 |pmid=40104933}}</ref><ref>{{Cite web |title=Cannabis Use Substantially Increases Risk of Heart Attack |url=https://www.acc.org/Latest-in-Cardiology/Journal-Scans/2025/03/24/13/52/http%3a%2f%2fwww.acc.org%2fLatest-in-Cardiology%2fJournal-Scans%2f2025%2f03%2f24%2f13%2f52%2fCannabis-Use-Substantially-Increases-Risk-of-Heart-Attack-acc-2025 |access-date=2025-09-28 |website=American College of Cardiology}}</ref> This effect is especially pronounced in young children.<ref>{{Cite news |last=Lehman |first=Charles |date=2024-07-03 |title=The Real Problem With Legal Weed |url=https://www.nytimes.com/2024/07/03/magazine/marijuana-legalization-new-york.html |access-date=2025-09-28 |work=New York Times Magazine |language=en}}</ref><ref>{{Cite journal |last1=Tweet |first1=Marit |last2=Nemanich |first2=Antonia |last3=Wahl |first3=Michael |date=2023-02-01 |title=Pediatric Edible Cannabis Exposures and Acute Toxicity: 2017–2021 |url=https://publications.aap.org/pediatrics/article/151/2/e2022057761/190427/Pediatric-Edible-Cannabis-Exposures-and-Acute?autologincheck=redirected |journal=Pediatrics |language=English |volume=151 |issue=2 |article-number=e2022057761 |doi=10.1542/peds.2022-057761 |pmid=36594224 |issn=0031-4005 |archive-url=https://web.archive.org/web/20250806051623/https://publications.aap.org/pediatrics/article/151/2/e2022057761/190427/Pediatric-Edible-Cannabis-Exposures-and-Acute?autologincheck=redirected |archive-date=2025-08-06|url-access=subscription }}</ref> Despite having an immediate short-term impact of lowering blood pressure, cannabis has been associated with hypertension in regular and heavy users.<ref name=":11" /> This, in turn, can restrict the flow of oxygen to the brain, leading to "forgetfulness, trouble with learning, memory and comprehension".<ref>{{Cite web |last=Mittal |first=Sanjay |title=6 Signs and Symptoms of Hypertension (High BP) {{!}} Medanta |url=https://www.medanta.org/patient-education-blog/6-signs-of-high-blood-pressure |access-date=2025-09-29 |website=Medanta |language=en}}</ref> Continued restriction can lead to cerebral small and large vessel disease later in life, which significantly increases the likelihood of dementia onset.<ref>{{Cite journal |last1=Gąsecki |first1=Dariusz |last2=Kwarciany |first2=Mariusz |last3=Nyka |first3=Walenty |last4=Narkiewicz |first4=Krzysztof |date=2013-10-23 |title=Hypertension, brain damage and cognitive decline |journal=Current Hypertension Reports |volume=15 |issue=6 |pages=547–558 |doi=10.1007/s11906-013-0398-4 |issn=1534-3111 |pmc=3838597 |pmid=24146223}}</ref>
== Disease and health complications == {{Expand section|date=November 2025}}
=== Anxiety / general anxiety disorder (GAD) === {{Main|Anxiety|General anxiety disorder|Anxiety disorder}}
=== Anaemia === {{Main|Anaemia}}
=== Attention deficit hyperactivity disorder (ADHD) === {{Main|Attention deficit hyperactivity disorder}}
Brain fog has been shown to be a primary symptom of ADHD, though it can also be due to associated co-morbidities. In adults, ADHD typically presents as difficulties with memory and attention, as opposed to the hyperactivity typically observed in children.<ref>{{Cite web |date=2018-11-01 |title=Is that brain fog really adult ADHD? |url=https://www.health.harvard.edu/diseases-and-conditions/is-that-brain-fog-really-adult-adhd |access-date=2025-11-23 |website=Harvard Health |language=en}}</ref>
=== Autism === {{Main|Autism|Autistic burnout}}
=== Cancer and chemotherapy === {{Expand section|* *Explanation of chemotherapeutic treatments' effect on bodily processes which may influence overall cognition. *Elaboration of debate over cognitive deficits resulting from chemotherapy or cancer itself|date=November 2025}}{{See also|Chemotherapy|Post-chemotherapy cognitive impairment}} Patients undergoing chemotherapy often present with brain fog (often called "chemo brain", "chemo fog", or chemotherapy-induced cognitive impairment (CICI)), a complication of the all-encompassing damage done to the brain and body over the course of treatment.<ref name=":17" /> Patients often report experiencing fatigue and difficulty with memory, language use, visuo-spatial skills, immediate and delayed recall, processing speed, and executive function.<ref name=":28">{{Cite journal |last1=Bernstein |first1=Lori J. |last2=McCreath |first2=Graham A. |last3=Komeylian |first3=Zahra |last4=Rich |first4=Jill B. |date=2017-12-01 |title=Cognitive impairment in breast cancer survivors treated with chemotherapy depends on control group type and cognitive domains assessed: A multilevel meta-analysis |url=https://www.sciencedirect.com/science/article/pii/S0149763417301355 |journal=Neuroscience & Biobehavioral Reviews |volume=83 |pages=417–428 |doi=10.1016/j.neubiorev.2017.10.028 |pmid=29092778 |issn=0149-7634|url-access=subscription }}</ref><ref name=":29">{{Cite journal |last1=Mounier |first1=Noha M. |last2=Abdel-Maged |first2=Amany El-Shahawy |last3=Wahdan |first3=Sara A. |last4=Gad |first4=Amany M. |last5=Azab |first5=Samar S. |date=2020-10-01 |title=Chemotherapy-induced cognitive impairment (CICI): An overview of etiology and pathogenesis |url=https://www.sciencedirect.com/science/article/pii/S0024320520308225 |journal=Life Sciences |volume=258 |article-number=118071 |doi=10.1016/j.lfs.2020.118071 |pmid=32673664 |issn=0024-3205 |via=Elsevier Science Direct|url-access=subscription }}</ref> Such difficulties can surface both during and after treatment, with cognitive deficits being reported as much as 21 years after treatment.<ref name=":28" /> But some studies have found that neuro-cognitive deficits were present in some patients before beginning treatment.<ref name=":28" /> Hypotheses for the cause of these symptoms include "direct neurotoxicity, [[Blood–brain barrier disruption|[blood–brain barrier] disruption]], decreased hippocampal neurogenesis, white matter abnormalities, secondary neuro-inflammatory response and increased oxidative stress".<ref name=":29" />
Symptoms can be exacerbated by additional side effects of treatment, including sleep cycle impairmen<nowiki/>t, dietary issues, fatigue, and imbalanced mood.<ref name=":18">{{Cite web |last=Dietrich |first=Jorg |date=2019-11-20 |title=Suffering from "chemo brain"? There's hope and many things you can do |url=https://www.health.harvard.edu/blog/suffering-from-chemo-brain-theres-hope-and-many-things-you-can-do-2019112018403 |access-date=2025-11-19 |website=Harvard Health |language=en}}</ref> Though therapeutic treatments are not yet widely available, common recommendations for accelerating neuro-regeneration include regular physical exercise, proper sleep and nutrition, stress reduction, and engagement in pleasurable activity.<ref name=":18" />
==== Criticism and counterarguments ==== Research published in 2017 in Neuroscience & Biobehavioral Reviews criticized the results of earlier meta-analyses and studies for their inconsistent assessment and control methods and for being broadly cross-sectional: there was no real means by which age, cancer severity, or prior treatment could be accounted for in determining the degree to which the effects of chemotherapy on cognitive function were real. That same meta-analysis found no significant difference in magnitude between the reported neurocognitive impairment of cancer survivors who underwent chemotherapy and those who did not.<ref name=":28" /> Additionally, little difference was shown between the moderating effect of time on cognitive impairment between those two groups, though statistical complications that may have affected such determination were acknowledged.<ref name=":28" />
=== Chronic fatigue === {{Main|Myalgic encephalomyelitis/chronic fatigue syndrome}}
In chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis, the CDC's recommended criteria for diagnosis<ref name="CDCsym2020">{{cite web |title=Symptoms of ME/CFS {{!}} Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) |url=https://www.cdc.gov/me-cfs/symptoms-diagnosis/symptoms.html |website=CDC |date=9 February 2021 }}</ref> include that one of the following symptoms must be present:<ref name="CDCsym2020" /> * Problems with thinking and memory (cognitive dysfunction, sometimes described as "brain fog")<!-- <ref name=CDCsym2020/> --> * While standing or sitting upright, lightheadedness, dizziness, weakness, fainting, or vision changes may occur (orthostatic intolerance)<!-- <ref name=CDCsym2020/> --> Patients diagnosed with CFS have been shown to experience reduced activation of the basal ganglia, responsible for the brain's reward system, and a primary center for inflammation therein. Treatment thus centers upon increasing dopaminergic activity/receptivity in the brain and/or preventing inflammation.<ref name=":17">{{Cite web |last=Loftus |first=Mary |date=Summer 2023 |title=Lost in a Brain Fog |url=https://news.emory.edu/features/2023/07/emag-brain-fog-13-07-23/index.html |access-date=2025-11-19 |website=news.emory.edu |language=en}}</ref>
=== Chronic pain === Brain fog is a common symptom in many illnesses where chronic pain is a major component.<ref name=":0" /> Brain fog affects 15% to 40% of those with chronic pain as their major illness.<ref>{{Cite journal |last1=Kucyi |first1=Aaron |last2=Davis |first2=Karen D. |date=2015 |title=The dynamic pain connectome |url=https://linkinghub.elsevier.com/retrieve/pii/S0166223614002173 |journal=Trends in Neurosciences |language=en |volume=38 |issue=2 |pages=86–95 |doi=10.1016/j.tins.2014.11.006 |pmid=25541287 |s2cid=745129 |url-access=subscription}}</ref> In such illnesses, pain processing may use up resources, decreasing the brain's ability to think effectively.<ref name=":0" />
=== Chronic sleep deprivation === {{Main|Chronic sleep deprivation}}
=== Chronic stress === {{Main|Chronic stress}}
=== Chronic traumatic encephalopothy === {{Main|Chronic traumatic encephalopathy}}
=== Cognitive disengagement syndrome === Cognitive disengagement syndrome was implicated in the expression of brain fog symptoms.<ref name=":3">{{cite book |last1=Barkley |first1=Russell A. |url=https://books.google.com/books?id=BSLF7yueqoUC&pg=PA150 |title=Taking Charge of ADHD: The Complete, Authoritative Guide for Parents |date=2013 |publisher=Guilford Publications |isbn=978-1-4625-0789-4 |page=150}}</ref>
=== Depression === {{Main|Biology of depression|Major depressive disorder}}
=== Encephalitis === {{Main|Encephalitis}}
=== Fibromyalgia === Many people with fibromyalgia experience cognitive problems<ref name="p17092441">{{cite journal |last1=Glass |first1=Jennifer M. |date=November 2006 |title=Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: New trends and future directions |journal=Current Rheumatology Reports |volume=8 |issue=6 |pages=425–429 |doi=10.1007/s11926-006-0036-0 |pmid=17092441 |s2cid=27103590}}</ref> (often called "fibrofog"), which may involve impaired concentration,<ref name=":20">{{cite journal |last1=Arnold |first1=Lesley M. |last2=Bennett |first2=Robert M. |last3=Crofford |first3=Leslie J. |last4=Dean |first4=Linda E. |last5=Clauw |first5=Daniel J. |last6=Goldenberg |first6=Don L. |last7=Fitzcharles |first7=Mary-Ann |last8=Paiva |first8=Eduardo S. |last9=Staud |first9=Roland |last10=Sarzi-Puttini |first10=Piercarlo |last11=Buskila |first11=Dan |last12=Macfarlane |first12=Gary J. |date=June 2019 |title=AAPT Diagnostic Criteria for Fibromyalgia |journal=The Journal of Pain |volume=20 |issue=6 |pages=611–628 |doi=10.1016/j.jpain.2018.10.008 |hdl=2434/632765 |pmid=30453109 |s2cid=53872511 |doi-access=free |hdl-access=free}}</ref><ref name=":21">{{cite journal |last1=Williams |first1=David A |last2=Clauw |first2=Daniel J |last3=Glass |first3=Jennifer M |date=April 2011 |title=Perceived Cognitive Dysfunction in Fibromyalgia Syndrome |journal=Journal of Musculoskeletal Pain |volume=19 |issue=2 |pages=66–75 |doi=10.3109/10582452.2011.558989 |s2cid=144893303}}</ref>{{MEDRS|date=March 2022}}<ref name="pmid17041327">{{MEDRS|date=March 2022}} {{cite journal |last1=Leavitt |first1=Frank |last2=Katz |first2=Robert S. |last3=Mills |first3=Megan |last4=Heard |first4=Amy R. |date=April 2002 |title=Cognitive and Dissociative Manifestations in Fibromyalgia |journal=JCR: Journal of Clinical Rheumatology |volume=8 |issue=2 |pages=77–84 |doi=10.1097/00124743-200204000-00003 |pmid=17041327 |s2cid=12352666}}</ref> problems with short-<ref name="pmid17894922">{{cite journal |last1=Buskila |first1=Dan |last2=Cohen |first2=Hagit |date=October 2007 |title=Comorbidity of fibromyalgia and psychiatric disorders |journal=Current Pain and Headache Reports |volume=11 |issue=5 |pages=333–338 |doi=10.1007/s11916-007-0214-4 |pmid=17894922 |s2cid=28038437}}</ref> and long-term memory, short-term memory consolidation,<ref name="pmid17894922" /> working memory,<ref name=":22">{{cite journal |last1=Mercado |first1=Francisco |last2=Ferrera |first2=David |last3=Fernandes-Magalhaes |first3=Roberto |last4=Peláez |first4=Irene |last5=Barjola |first5=Paloma |date=2 March 2022 |title=Altered Subprocesses of Working Memory in Patients with Fibromyalgia: An Event-Related Potential Study Using N -Back Task |journal=Pain Medicine |volume=23 |issue=3 |pages=475–487 |doi=10.1093/pm/pnab190 |pmid=34145889}}</ref> impaired speed of performance,<ref name="pmid17894922" /> inability to multitask, cognitive overload,<ref name="pmid17894922" /> and diminished attention span. About 75% of fibromyalgia patients report significant problems with concentration, memory, and multitasking.<ref name="Bell2018">{{cite journal |last1=Bell |first1=Tyler |last2=Trost |first2=Zina |last3=Buelow |first3=Melissa T. |last4=Clay |first4=Olivio |last5=Younger |first5=Jarred |last6=Moore |first6=David |last7=Crowe |first7=Michael |date=9 August 2018 |title=Meta-analysis of cognitive performance in fibromyalgia |journal=Journal of Clinical and Experimental Neuropsychology |volume=40 |issue=7 |pages=698–714 |doi=10.1080/13803395.2017.1422699 |pmc=6151134 |pmid=29388512}}</ref> A 2018 meta-analysis found that the largest differences between fibromyalgia patients and healthy subjects were in inhibitory control, memory, and processing speed.<ref name="Bell2018" /> Many of these are also common symptoms of ADHD, and studies have linked the two conditions, to the point that a fibromyalgia diagnosis has been proposed as an indication to screen for ADHD.<ref name=":23">{{cite journal |last1=Bou Khalil |first1=Rami |last2=Khoury |first2=Elie |last3=Richa |first3=Sami |date=1 September 2018 |title=The Comorbidity of Fibromyalgia Syndrome and Attention Deficit and Hyperactivity Disorder from a Pathogenic Perspective |journal=Pain Medicine |volume=19 |issue=9 |pages=1705–1709 |doi=10.1093/pm/pny142 |pmid=30053155 |doi-access=free}}</ref><ref name=":24">{{cite journal |last1=Yilmaz |first1=Ertan |last2=Tamam |first2=Lut |date=24 July 2018 |title=Attention-deficit hyperactivity disorder and impulsivity in female patients with fibromyalgia |journal=Neuropsychiatric Disease and Treatment |volume=14 |pages=1883–1889 |doi=10.2147/NDT.S159312 |pmc=6063452 |pmid=30100723 |doi-access=free}}</ref><ref name=":25">{{cite web |date=28 December 2017 |title=Study Suggests Screening Patients with Fibromyalgia Syndrome for ADHD |url=https://www.ajmc.com/view/study-suggests-screening-patients-with-fibromyalgia-syndrome-for-adhd-}}</ref> It is alternatively hypothesized that increased pain compromises attention systems, resulting in cognitive problems.<ref name="Bell2018" />
=== Hypersomnia === {{Main|Hypersomnia|Idiopathic hypersomnia}}
=== Hypoglycemia and diabetes === {{Main|Hypoglycemia}}
=== Hypothyroidism === Brain fog and additional neuro-cognitive difficulties are a common symptom of hypothyroidism.<ref>{{Cite journal |last1=Wekking |first1=Ellie M. |last2=Appelhof |first2=Bente C. |last3=Fliers |first3=Eric |last4=Schene |first4=Aart H. |last5=Huyser |first5=Jochanan |last6=Tijssen |first6=Jan G. P. |last7=Wiersinga |first7=Wilmar M. |date=December 2005 |title=Cognitive functioning and well-being in euthyroid patients on thyroxine replacement therapy for primary hypothyroidism |journal=European Journal of Endocrinology |volume=153 |issue=6 |pages=747–753 |doi=10.1530/eje.1.02025 |issn=0804-4643 |pmid=16322379}}</ref><ref name=":26" /><ref name=":27">{{Cite journal |last=Ebner |first=Susana|date=May 2022 |title=Hypothyroid patients described what brain fog feels like |url=https://www.thyroid.org/wp-content/uploads/publications/ctfp/ct_public_v155.pdf |journal=Clinical Thyroidology for the Public - American Thyroid Association |volume=15 |issue=5 |pages=3–4 |via=thyroid.org}}</ref> Symptoms often include "fatigue, depressed mood, and cognitive difficulties, including problems with memory and word-finding".<ref name=":30">{{Cite journal |last1=Samuels |first1=Mary H. |last2=Bernstein |first2=Lori J. |date=July 2022 |title=Brain Fog in Hypothyroidism: What Is It, How Is It Measured, and What Can Be Done About It |journal=Thyroid|volume=32 |issue=7 |pages=752–763 |doi=10.1089/thy.2022.0139 |issn=1557-9077 |pmc=9469742 |pmid=35414261}}</ref> In some cases, this may result from insufficient treatment of thyroid deficiencies, or additional, untreated co-morbidities, such as "depression, sleep apnea, or vitamin B12 deficiency".<ref name=":26" /> A 2022 survey showed that 79.2% of those with the condition reported experiencing brain fog to some extent, selecting the options "frequently" or "all the time".<ref name=":26">{{cite journal |last1=Ettleson |first1=Matthew D. |last2=Raine |first2=Ava |last3=Batistuzzo |first3=Alice |last4=Batista |first4=Samuel P. |last5=McAninch |first5=Elizabeth |last6=Teixeira |first6=Maria Cristina T.V. |last7=Jonklaas |first7=Jacqueline |last8=Laiteerapong |first8=Neda |last9=Ribeiro |first9=Miriam O. |last10=Bianco |first10=Antonio C. |date=March 2022 |title=Brain Fog in Hypothyroidism: Understanding the Patient's Perspective |journal=Endocrine Practice |volume=28 |issue=3 |pages=257–264 |doi=10.1016/j.eprac.2021.12.003 |pmc=8901556 |pmid=34890786}}</ref> One American Thyroid Association study found that among a cohort of 5,000 patients presenting with hypothyroidism, more than 95% of those experiencing brain fog (a majority of study participants) reported experiencing "fatigue, forgetfulness, sleepiness and difficulty focusing".
It is unclear how hypothyroidism leads to brain fog, but levothyroxine has been shown to reduce cognitive impairment in some patients.<ref>{{cite journal |last1=Smith |first1=Jeremy W. |last2=Evans |first2=A Tudor |last3=Costall |first3=B |last4=Smythe |first4=James W. |date=January 2002 |title=Thyroid hormones, brain function and cognition: a brief review |journal=Neuroscience & Biobehavioral Reviews |volume=26 |issue=1 |pages=045–60 |doi=10.1016/s0149-7634(01)00037-9 |pmid=11835983}}</ref> However, roughly 10-15% of those receiving such treatment experience persistent cognitive deficits and reduced quality of life, with some believing this demonstrates persistent hypothyroidism at the cellular level despite tests showing TSH results in the normal range.<ref name=":31">{{Cite journal |last1=Saravanan |first1=P. |last2=Chau |first2=W.-F. |last3=Roberts |first3=N. |last4=Vedhara |first4=K. |last5=Greenwood |first5=R. |last6=Dayan |first6=C. M. |date=2002 |title=Psychological well-being in patients on 'adequate' doses of l-thyroxine: results of a large, controlled community-based questionnaire study |url=https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2265.2002.01654.x |journal=Clinical Endocrinology |language=en |volume=57 |issue=5 |pages=577–585 |doi=10.1046/j.1365-2265.2002.01654.x |pmid=12390330 |issn=1365-2265|url-access=subscription }}</ref> This may lead patients to seek higher dosage, which doctors often dismiss, or alternative therapies, such as desiccated thyroid extract (DTE), despite the lack of evidence supporting its use.<ref name=":30" /><ref name=":31" /> Some patients, more commonly those over age 50, reported improvement with the addition of liothyronine (L-T3) to their treatment regimen, though some researchers question its efficacy .<ref name=":27" /><ref name=":30" /> Rest and exercise have also been shown to help alleviate symptoms.<ref name=":26" /><ref name=":27" />
=== Lupus === {{Main|Lupus}}
=== Lyme disease === Lyme disease's neurologic syndrome, called Lyme encephalopathy, is associated with subtle memory and cognitive difficulties, among other issues.<ref name="MayoClin2008">{{cite journal |last1=Bratton |first1=Robert L. |last2=Whiteside |first2=John W. |last3=Hovan |first3=Michael J. |last4=Engle |first4=Richard L. |last5=Edwards |first5=Frederick D. |date=May 2008 |title=Diagnosis and Treatment of Lyme Disease |journal=Mayo Clinic Proceedings |volume=83 |issue=5 |pages=566–571 |doi=10.4065/83.5.566 |pmid=18452688 |doi-access=free}}</ref> Lyme can Count, L. S., Count, L. L., Growth, H., Dandruff, H., & Foods, H. (2020). Brain fog. Brain. a chronic encephalomyelitis that resembles multiple sclerosis. It may be progressive and can involve cognitive impairment, migraines, balance problems, and other symptoms.{{citation needed|date=June 2022}}
=== Menopause === {{Expand section|Explanation of progesterone and estrogen fluctuations on cognitive performance (specific) and bodily processes which may influence cognitive function|date=November 2025}}{{Main|Menopause}}
Menopause, officially described as the end of menstruation and reproductive hormone production in those assigned female at birth who still possess primary female sexual characteristics, can be characterized in all stages by deficits in cognitive performance (sometimes referred to as "meno-fog").<ref name=":37">{{Cite web |title=What Is Menopause? |url=https://my.clevelandclinic.org/health/diseases/21841-menopause |archive-url=https://web.archive.org/web/20251004081242/https://my.clevelandclinic.org/health/diseases/21841-menopause |archive-date=2025-10-04 |access-date=2025-11-27 |website=Cleveland Clinic |language=en}}</ref><ref>{{Cite web |last=GenderGP |date=2021-10-21 |title=Inclusive Language and the Menopause |url=https://www.gendergp.com/blog-menopause-inclusivity/ |access-date=2025-11-27 |website=GenderGP |language=en-GB}}</ref><ref name=":38">{{Cite web |last=Salamon |first=Maureen |date=2022-06-01 |title=Menopause and brain fog: What's the link? |url=https://www.health.harvard.edu/womens-health/menopause-and-brain-fog-whats-the-link |access-date=2025-11-27 |website=Harvard Health |language=en}}</ref><ref name=":39">{{Cite report |url=https://www.rand.org/pubs/commentary/2025/04/understanding-meno-fog-navigating-brain-fog-during.html |title=Understanding Meno-Fog: Navigating Brain Fog During Menopause |last=Troxel |first=Wendy M. |date=2025-04-02 |language=en |via=RAND Corporation}}</ref> Though symptoms vary significantly between patients depending on factors such as genetics, ethnicity, and preexisting conditions, brain fog has been shown to be exceptionally common, with up to 80% of people experiencing it at some point over the course of transition.<ref name=":37" /><ref name=":39" /><ref name=":40">{{Cite web |last=Petridis |first=Eileen |date=2022-01-12 |title=Severity of Menopause Symptoms Can Affect a Woman's Cognitive Performance |url=https://menopause.org/wp-content/uploads/press-release/cognitive-performance-affected-by-severity-of-menopausal-symptoms.pdf |website=The North American Menopause Society}}</ref> Cognitive dysfunction is most prevalent in the perimenopausal period, particularly in the domains of informational acquisition, concentration, and memory; anecdotal evidence suggests that absent-mindedness and confusion are common in several stages. But these symptoms are often temporary, and begin to relieve as the postmenopausal period progresses.<ref name=":37" /><ref name=":38" /><ref name=":39" /><ref name=":42">{{Cite journal |last1=Shanmugan |first1=Sheila |last2=Epperson |first2=C. Neill |date=2012-12-14 |title=Estrogen and the prefrontal cortex: towards a new understanding of estrogen's effects on executive functions in the menopause transition |journal=Human Brain Mapping |volume=35 |issue=3 |pages=847–865 |doi=10.1002/hbm.22218 |issn=1097-0193 |pmc=4104582 |pmid=23238908}}</ref>
A 2022 study published in ''Menopause'' analyzed a group of 404 women from rural India between the ages of 40 and 65, assessing the severity of their menopausal symptoms (on the Greene Climacteric Scale) and cognitive performance (scoring orientation, registration, attention, recall, and language and visuospatial skills by means of the Hindi Mini-Mental State Examination).<ref name=":40" /><ref name=":41">{{Cite journal |last1=Kaur |first1=Mankamal |last2=Kaur |first2=Maninder |date=2022-01-10 |title=Is cognitive performance of women sensitive to the severity of menopausal symptoms? |url=https://journals.lww.com/menopausejournal/abstract/2022/02000/is_cognitive_performance_of_women_sensitive_to_the.9.aspx |journal=Menopause |language=en-US |volume=29 |issue=2 |pages=170–177 |doi=10.1097/GME.0000000000001910 |pmid=35013054 |issn=1530-0374 |archive-url=https://web.archive.org/web/20250507231136/https://journals.lww.com/menopausejournal/abstract/2022/02000/is_cognitive_performance_of_women_sensitive_to_the.9.aspx |archive-date=2025-05-07|url-access=subscription }}</ref> Women with severe menopausal symptoms presented with significantly lower mean performance across all cognitive domains.<ref name=":41" /> The study additionally found evidence that common menopause symptoms, particularly severe depression and greater sexual dysfunction, were closely linked to cognitive difficulties, though it failed to establish a causal relationship between them, meaning there was little indication whether one preceded the other.<ref name=":38" /><ref name=":40" /><ref name=":41" /> Symptoms of "depression, total psychological, sexual, and somatic dysfunction" were most severe for late postmenopausal women (those whose periods had ceased more than 5 years before the time of the study); anxiety and hot flashes were found to be most common among those in early postmenopause (whose periods had ceased less than 5 years earlier).<ref name=":38" /><ref>{{Cite web |last=Gallagher |first=Ashley |date=2025-11-27 |title=Severity of menopause symptoms can affect cognitive performance {{!}} Contemporary OB/GYN |url=https://www.contemporaryobgyn.net/view/severity-of-menopause-symptoms-can-affect-cognitive-performance |access-date=2025-11-27 |website=www.contemporaryobgyn.net |language=en}}</ref> The study found no relationship between the severity of vasomotor symptoms (hot flashes) and cognitive performance.<ref name=":40" />
Cognitive deficits are believed to result in part from the sudden drop in estrogen across "virtually every organ", contributing in turn to hormonal imbalances that disrupt the brain's and body's natural processes.<ref name=":38" /><ref name=":42" /> It is believed that estrogen plays a crucial role for people of all genders in the function of the prefrontal cortex, the proper functioning of which is critical to executive processes such as "inhibiting distracting information and stimuli, planning, evaluating consequences when making decisions, and working memory."<ref name=":42" /> The transition affects serotonergic and dopaminergic expression, contributing to imbalances in cognition and mood.<ref name=":39" /> Additionally, elevated stress and a subsequent increase in cortisol may contribute to memory and processing difficulties.<ref name=":39" /><ref>{{Cite journal |last1=Greendale |first1=Gail A. |last2=Wight |first2=Richard G. |last3=Huang |first3=Mei-Hua |last4=Avis |first4=Nancy |last5=Gold |first5=Ellen B. |last6=Joffe |first6=Hadine |last7=Seeman |first7=Teresa |last8=Vuge |first8=Marike |last9=Karlamangla |first9=Arun S. |date=2010-06-01 |title=Menopause-associated symptoms and cognitive performance: results from the study of women's health across the nation |journal=American Journal of Epidemiology |volume=171 |issue=11 |pages=1214–1224 |doi=10.1093/aje/kwq067 |issn=1476-6256 |pmc=2915492 |pmid=20442205}}</ref>
Prescriptions depend upon determination of the cause of cognitive dysfunction. Reducing stress, challenging oneself intellectually, maintaining proper fitness and nutrition, adequate hydration, sleep (known to be particularly dysfunctional amid menopause), sun exposure, and social support are generally known to assist in improving cognition.<ref name=":37" /><ref name=":38" /><ref name=":39" /> Hormone replacement therapy is thought to help relieve cognitive and broader symptoms in some patients.<ref name=":39" />
=== Menstruation === {{Main|Premenstrual syndrome|Menstruation cycle|Menstruation}}
=== Migraine disorders === {{Main|Migraine}}
=== Mold exposure === Brain fog and other neurological symptoms may also result from mold exposure.<ref name="pmid19854819">{{cite journal | vauthors = Empting LD | title = Neurologic and neuropsychiatric syndrome features of mold and mycotoxin exposure | journal = Toxicol Ind Health | volume = 25 | issue = 9–10 | pages = 577–581 | date = 2009 | pmid = 19854819 | doi = 10.1177/0748233709348393 | bibcode = 2009ToxIH..25..577E | s2cid = 27769836 | url = }}</ref><ref name="pmid28848553">{{cite journal | vauthors = Valtonen V | title = Clinical Diagnosis of the Dampness and Mold Hypersensitivity Syndrome: Review of the Literature and Suggested Diagnostic Criteria | journal = Front Immunol | volume = 8 | issue = | article-number = 951 | date = 2017 | pmid = 28848553 | pmc = 5554125 | doi = 10.3389/fimmu.2017.00951 | url = | doi-access = free }}</ref><ref name="pmid36638914">{{cite journal | vauthors = Harding CF, Liao D, Persaud R, DeStefano RA, Page KG, Stalbow LL, Roa T, Ford JC, Goman KD, Pytte CL | title = Differential effects of exposure to toxic or nontoxic mold spores on brain inflammation and Morris water maze performance | journal = Behav Brain Res | volume = 442 | issue = | article-number = 114294 | date = March 2023 | pmid = 36638914 | doi = 10.1016/j.bbr.2023.114294 | pmc = 10460635 | url = }}</ref><ref name="pmid29880330">{{cite journal | vauthors = Ratnaseelan AM, Tsilioni I, Theoharides TC | title = Effects of Mycotoxins on Neuropsychiatric Symptoms and Immune Processes | journal = Clin Ther | volume = 40 | issue = 6 | pages = 903–917 | date = June 2018 | pmid = 29880330 | doi = 10.1016/j.clinthera.2018.05.004 | url = | doi-access = free }}</ref><ref name="pmid31751617">{{cite journal | vauthors = Harding CF, Pytte CL, Page KG, Ryberg KJ, Normand E, Remigio GJ, DeStefano RA, Morris DB, Voronina J, Lopez A, Stalbow LA, Williams EP, Abreu N | title = Mold inhalation causes innate immune activation, neural, cognitive and emotional dysfunction | journal = Brain Behav Immun | volume = 87 | issue = | pages = 218–228 | date = July 2020 | pmid = 31751617 | pmc = 7231651 | doi = 10.1016/j.bbi.2019.11.006 | url = }}</ref> This may be due to mycotoxin exposure and consequent innate immune system activation and inflammation, including in the central nervous system.<ref name="ViljoenClaassen2023">{{cite journal | last1 = Viljoen | first1 = Margaretha | last2 = Claassen | first2 = Nicolaas | title = Pathophysiological aspects of exposure to dampness-associated indoor mould and mycotoxins: A mini-overview | journal = Journal of Hazardous Materials Advances | date = February 2023 | volume = 9 | article-number = 100228 | issn = 2772-4166 | doi = 10.1016/j.hazadv.2022.100228 | pmid = | url = | doi-access = free | bibcode = 2023JHzMA...900228V | hdl = 2263/95331 | hdl-access = free }}</ref><ref name="pmid19854819" /><ref name="pmid28848553" /><ref name="pmid36638914" /><ref name="pmid29880330" /><ref name="pmid31751617" /> But adverse neurological health effects of mold exposure are controversial due to inadequate research and data, and more research is needed in this area.<ref name="ViljoenClaassen2023" /><ref name="pmid28453304">{{cite journal | vauthors = Rudert A, Portnoy J | title = Mold allergy: is it real and what do we do about it? | journal = Expert Rev Clin Immunol | volume = 13 | issue = 8 | pages = 823–835 | date = August 2017 | pmid = 28453304 | doi = 10.1080/1744666X.2017.1324298 | s2cid = 4755858 | url = }}</ref><ref name="pmid28299723">{{cite journal | vauthors = Borchers AT, Chang C, Eric Gershwin M | title = Mold and Human Health: a Reality Check | journal = Clin Rev Allergy Immunol | volume = 52 | issue = 3 | pages = 305–322 | date = June 2017 | pmid = 28299723 | doi = 10.1007/s12016-017-8601-z | s2cid = 25709697 | url = }}</ref><ref name="pmid19854819" /><ref name="pmid36638914" /><ref name="pmid31751617" />
=== Obsessive–compulsive disorder (OCD) === {{Main|Obsessive–compulsive disorder}}
=== Oophorectomy and ovariectomy (OVX) === {{Main|Oophorectomy|Ovariectomy}}
=== Pregnancy === {{Main|Prenatal stress|Postpartum depression|Postpartum period}}
=== Psychotic disorders === {{Main|Schizophrenia|Schizoaffective disorder|Bipolar disorder|Postpartum psychosis|Psychosis}}
==See also== {{Portal|Psychiatry|Psychology|Medicine}} <!-- Please keep entries in alphabetical order & add a short description WP:SEEALSO --> {{div col}} * Altered level of consciousness * Brain fag syndrome * Cannabis use disorder * Cognitive orthotics * Depersonalization-derealization disorder * Excessive daytime sleepiness * Four boxes test * Idiopathic hypersomnia * Insomnia * Mental confusion * Mild cognitive impairment * Obtundation * Postural orthostatic tachycardia syndrome (POTS) * Post-chemotherapy cognitive impairment * Pumphead syndrome * Reactive hypoglycemia * Sleep inertia * Slow-wave sleep * Somnolence * Stupor {{div col end}}
==Notes== {{notelist}}
==References== {{reflist}}
{{Medical resources | ICD11 = {{ICD11|MB20.2}} }}
Category:Symptoms and signs of mental disorders Category:Symptoms and signs: Nervous system Category:Cognitive disorders Category:Psychopathological syndromes Category:Symptoms, signs or clinical findings involving consciousness