Clouding of consciousness, also calledbrain fog ormental fog,[1][2] occurs when a person isconscious but slightly lesswakeful oraware than normal.[3] 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".[4] Sufferers may be less aware of time and their surroundings, and find it difficult topay attention.[3] People describe thissubjective sensation as their mind being "foggy".[5]
Clouding of consciousness denotes a less severe state of cognitive impairment than outrightdelirium. 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".[6]
The termclouding of consciousness has always denoted the mainpathogenetic feature of delirium since physician Georg Greiner[7] pioneered the term (Verdunkelung des Bewusstseins) in 1817.[8]TheDiagnostic and Statistical Manual of Mental Disorders (DSM) has historically used the term in its definition of delirium.[9] TheDSM-III-R and theDSM-IV replaced "clouding of consciousness" with "disturbance of consciousness" to make it easier tooperationalize, but it is still fundamentally the same thing.[10] Clouding of consciousness may be less severe than delirium on a spectrum ofabnormal consciousness.[3][11][12] Clouding of consciousness may be synonymous withsubsyndromal delirium.[13]
Subsyndromal delirium differs from normal delirium by being overall less severe, lackingacuteness in onset and duration, having a relatively stablesleep-wake cycle, and having relatively stable motor alterations.[14] Subsyndromal delirium's significant clinical features are inattention, thought process abnormalities, comprehension abnormalities, and language abnormalities.[14] Delirium's full clinical manifestations may never be reached.[13] Amongintensive 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 fullICU delirium)[13] and had a decreased post-discharge level of functional independence compared to the general population.[14]
In clinical practice, no standard test is exclusive and specific; therefore, diagnosis depends on the physician's subjective impression. TheDSM-IV-TR instructs clinicians to code subsyndromal delirium presentations under the miscellaneous category "cognitive disorder not otherwise specified".[15]
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Thecerebral cortex and thehippocampus 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 thecerebrum, is responsible for more advanced processes, such asthought, information recall, maintainedwakefulness, andconsciousness. The hippocampus, deep within the brain'stemporal lobe, organizes, stores, and retrieves information within it, convertingmemory from short-term to long. It plays a crucial role in enhancingspatial andverbalmemory. 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.[16]
Disruptingcircadian regulation interferes with neural activation and hippocampus memory processing, reducing thought clarity andalertness 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]
Theprefrontal cortex (PFC), in the anterior part of thefrontal lobe, helps to regulate thought, feeling, and objective-based behavior. It is the final[clarification needed] brain region that undergoesmyelination, a mechanism by which insulatingmyelin sheaths form surroundingaxons to improve the rapidity and efficacy of communication between neurons via brain networks.[clarification needed][citation needed]
Research has found that higher cognitive function requires coordinated interaction between the PFC andposterior cortical regions. These posterior areas provide thesensory andperceptual 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.[17]
Consciousness was historically believed to be a product of the whole of activity in thecerebral hemispheres. But the conscious state is not altered by injury to one hemisphere, "except if the size of [abrain lesion] affects other cortical areas or thediencephalon" or if the lesion is exceptionally large.[6][18] 1916 research byRomanian-Viennese neurologistConstantin von Economo found that specific regions of the brain (themidbrain and diencephalon) targeted byencephalitis lethargica (sleeping sickness) produced alterations in wake-sleep regulation.[6][19] He identified a site at the junction of thebrainstem andforebrain where lesions produced prolongedsleepiness, as well as a site that included theanterior hypothalamus where, conversely, lesions produced prolongedinsomnia.[19] Based on his observation of patients experiencing lethargy who all had lesions at the junction between these two regions (an area that included the posteriorlateral hypothalamus), Von Economo proposed "anascending arousal system originating in the brainstem that kept the forebrain awake", suggesting thatnarcolepsy was caused by its dysfunction.[19] This supports the modern notion that distinct segments of the central nervous system are critical for consciousness.[6]
Theconceptual model of clouding of consciousness inpsychopathology 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.[3][20] Variousetiologies disturb this regulating part of the brain, which in turn disturbs the "overall level" of consciousness.[21] This system of a sort of general activation of consciousness is called "arousal" or "wakefulness".[20]
Clouding of consciousness is not necessarily accompanied bydrowsiness.[22] Patients may not be sleepy yet still have clouded consciousness (disorder of wakefulness).[23] Paradoxically, affected individuals say they are "awake but, in another way, not".[24] Lipowski points out that decreased "wakefulness" as used here is not exactly synonymous with drowsiness. One is a stage on the way tocoma, the other on the way to sleep, which is very different.[25][26]
The affected person has a sensation of mental clouding described in the patient's own words as "foggy".[5] One patient said, "I thought it became like misty, in some way... the outlines were sort of fuzzy".[24] Others may describe a "spaced-out" feeling.[27] 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.[28] 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 ofchlorpheniramine (anantihistamine 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.[1] Clouding of consciousness is not the same thing asdepersonalization, 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.[29]
Brain fog may affect performance on virtually any cognitive task.[1] As one author put it, "It should be apparent that cognition is not possible without a reasonable degree of arousal."[3] 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.[14] The extent of the impairment is variable because inattention may impair several cognitive functions. Affected people may complain of forgetfulness, being "confused",[30] or being "unable to think straight".[30] Despite the similarities, subsyndromal delirium is not the same thing asmild cognitive impairment; the fundamental difference is that mild cognitive impairment is adementia-like impairment, which does not involve a disturbance in arousal (wakefulness).[31]
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.[32] It can also heighten stress, dysregulate pleasure and thebasal ganglia's reward system, and limit executive control function by disrupting normal function of theprefrontal cortex, leading to difficulty concentrating, "organiz[ing] thoughts and activities, prioritiz[ing] tasks, manag[ing] time, and mak[ing] decisions".[33]
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.[33][34] This may result from the users' dependency on and subsequent restriction from the substance in question, or from neurocognitive impairment /neurodegeneration resulting from use.[33]
As addictive behaviors persist,dopamine is depleted at a faster pace, and itsreceptors increasingly dulled by oversaturation, leading to a reduced sensitivity to dopamine produced naturally by the body over time.[35] It has been consistently shown that addicts present with both lower responsiveness to dopamine, particularly inD2 receptors, and lower dopamine production overall.[33][36][37] This, in turn, dysregulates the brain's natural reward mechanisms, leading to decreasedmotivation, anxiety, difficulty thinking and concentrating,impulsivity,fatigue,emotional blunting,short-term memory disruptions,forgetfulness,disorganization, loss of coordination andbalance, andsocial withdrawal.[35][38]
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.[35]
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Heavy, progressive, and persistent alcohol abuse (alcohol use disorder (AUD)) lasting more than several years has been shown to lead to brain damage.[39] Cognitive difficulties related to alcohol use that do not progress into more severe illness are calledalcohol-related brain damage (ARBD).[40] Symptoms include mild executive dysfunction as well as deficits in memory, coordination, motor control, and visuospatial skills.[40][41] Cognitive deficits differ significantly between patients, suggesting "that the functions affected by chronic alcohol consumption are dissociable and supported by different neural systems".[40]
Persistent alcohol use disorder lasting several years or more can contribute to severe malnutrition.[40] Alcohol abuse hinders thegut's ability to properlyabsorb critical nutrients, and the brain's ability tophosphorylate them.[40][42] Chief among these deficiencies isthiamine (Vitamin B-1). With an incidence rate as high as 12.5% in patients with alcoholism, such a deficiency can lead toWernicke encephalopathy (WE), though this is reversible through rapid therapeutic treatment with thiamine andglucose.[40][42][43] 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.[43] 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.[42][43]
WE, if left untreated, can progress to Korsakoff syndrome (as is the case in roughly 68-80% of cases), an irreversible form of chronicamnesia. 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, severeexecutive dysfunction, lack of motivation, and emotional apathy.[40][42][43] 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."[40] Memory rehabilitation therapy may help to relieve symptoms; severe cases often require institutionalization.[43][44]
The effects ofcannabis onneurological 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.[45][46][47] The immediate short-term effects of cannabis use can include "impaired short-term memory and motor coordination, altered judgment, paranoia, and psychosis".[48] Long-term use can lead to "altered brain development, poor educational outcomes, cognitive impairment, diminished quality of life", and increased risk of suicide.[48]
The rapid increase in theTHC 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.[46][47][49][50][51][52]
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)[a] experienced a mean 5.5-point drop in IQ from childhood to adulthood.[45][53] 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.[53]
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.[34][54][55] But a 2010 meta-analysis of previous research in theSchizophrenia Bulletin showed evidence that those same people have a paradoxically lower risk of neurocognitive difficulties; use of the substance substantially increased the prevalence ofpositive 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).[54][56]
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, particularlyischemic strokes andmyocardial infarctions (heart attacks).[57][58][59] This effect is especially pronounced in young children.[60][61] Despite having an immediate short-term impact of lowering blood pressure, cannabis has been associated withhypertension in regular and heavy users.[52] This, in turn, can restrict the flow ofoxygen to the brain, leading to "forgetfulness, trouble with learning, memory and comprehension".[62] Continued restriction can lead tocerebral small and large vesseldisease later in life, which significantly increases the likelihood ofdementia onset.[63]
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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.[64]
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Patients undergoingchemotherapy often present with brain fog (often called "chemo brain", "chemo fog", orchemotherapy-induced cognitive impairment (CICI)), a complication of the all-encompassing damage done to the brain and body over the course of treatment.[65] Patients often report experiencing fatigue and difficulty with memory, language use, visuo-spatial skills, immediate and delayed recall, processing speed, and executive function.[66][67] Such difficulties can surface both during and after treatment, with cognitive deficits being reported as much as 21 years after treatment.[66] But some studies have found that neuro-cognitive deficits were present in some patients before beginning treatment.[66] Hypotheses for the cause of these symptoms include "directneurotoxicity,[blood–brain barrier] disruption, decreasedhippocampalneurogenesis, white matter abnormalities,secondary neuro-inflammatory response and increasedoxidative stress".[67]
Symptoms can be exacerbated by additional side effects of treatment, includingsleep cycle impairment,dietary issues, fatigue, and imbalanced mood.[68] Though therapeutic treatments are not yet widely available, common recommendations for accelerating neuro-regeneration include regularphysical exercise, proper sleep and nutrition,stress reduction, and engagement in pleasurable activity.[68]
Research published in 2017 inNeuroscience & Biobehavioral Reviews criticized the results of earlier meta-analyses and studies for their inconsistent assessment andcontrol methods and for being broadlycross-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 significantdifference in magnitude between the reported neurocognitive impairment of cancer survivors who underwent chemotherapy and those who did not.[66] 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.[66]
In chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis, theCDC's recommended criteria for diagnosis[69] include that one of the following symptoms must be present:[69]
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.[65]
Brain fog is a common symptom in many illnesses where chronic pain is a major component.[4] Brain fog affects 15% to 40% of those with chronic pain as their major illness.[70] In such illnesses, pain processing may use up resources, decreasing the brain's ability to think effectively.[4]
Cognitive disengagement syndrome was implicated in the expression of brain fog symptoms.[71]
| This sectionneeds expansion with: Recent advancements in understanding of relationship between Long Covid and reduction in serotonin, and subsequent physiological and cognitive effects. You can help byadding missing information.(November 2025) |
Patients recovering from COVID-19 have reported experiencing brain fog, which can reflect a wide variety ofneurological and psychological symptoms linked to COVID-19.[72][73] Symptoms can persist for months, even years, and are often characterized by fatigue, difficulties with "attention...memory recall, language andexecutive functioning", as well as depression and anxiety.[74][75][76] Descriptions are necessarily subjective, with some patients describing cognitive symptoms as "muddled or fuzzy thoughts", like "a bad wi-fi connection to a router", being "in slow motion", or "disappear[ing] like 'smoke' or a 'dream'".[65]
COVID has also been shown to causeencephalopathy, though this is more common in elderly patients and those with preexisting chronic conditions.[77] TheAlpha andDelta variants of the virus were characterized by severe cognitive impairment at the time of infection, followed by slow recovery.[74]
A 2025 Rutgers Health study highlighted the need for greater attention to long COVID symptoms in young children, given their necessarily lesser ability to accurately report and explain their symptoms. Infants and toddlers diagnosed with long COVID were found to experience greater "difficulty sleeping, fussiness, and poor appetite", alongside other physical symptoms, while preschoolers were more likely to experience "daytime tiredness and low energy".[78]
Research from theUK Biobank in 2022 showed comparative signs of neurodegeneration and cognitive decline amongst a group of 401 middle-aged and elderly COVID-19 patients (importantly, excluding 15 patients who had been hospitalized with the illness over that period) over roughly five months. The study focused mainly on imaging of thelimbic system, with evidence that the disruption of theolfactory system played a critical role in the disease's neurodegenerative effects. The researchers found that, in comparison with a control, there were decreases in total brain size, evidence of cognitive decline, "reduction[s] ingrey matter thickness and tissue contrast in theorbitofrontal cortex andparahippocampal gyrus", and markers of tissue damage in regions of the brain connected to theprimary olfactory cortex.[79] Over the observation period, those who had tested positive for COVID-19 lost 0.2% to 2% more brain matter than those who had not contracted the illness, the latter equivalent to 10 years worth of normal age-based degeneration.[77][80][81] COVID-19 patients also showed disrupted contact between different regions of the brain.[77]
People with long COVID are significantly more likely to experience gastrointestinal dysfunction and have "reported worse anxiety, depression, and quality of life".[82] COVID is thought to reduce the natural production of serotonin in the gut, which can disrupt normal cognitive processes and cause symptoms of brain fog.[83] Studies of mice "[bio]-engineered to mimic long COVID in humans" showed that cognitive difficulties could be relieved through treatment withProzac.[84]
Initially, it was thought that the presentation of brain fog inlong COVID shared molecular features withAlzheimer's disease.[85] This was disproved in 2024 by researchers fromRutgers University. 68% of COVID-19 patients who participated in their study had reported "a decline in thinking or memory", but comparison of cognitive testing scores between patients found similarities between the reported experiences of those with proven cognitive impairment and those whose experience was deemed subjective (i.e greater "fatigue, sleepiness, depression, and anxiety" than long COVID patients who reported no persistent neuro-intellectual symptoms), leading to uncertainty over the effects of long COVID on cognitive performance.[86] Over two years, only half of patients involved in the study reported improvements in persistent cognitive difficulties.[87][88] It was found that the persistence of symptoms was linked to auto-immune markers of viral infection, with the neurological changes associated with Alzheimer's not found in long COVID patients.[87][86] Researchers believe thatinterferons, markers of a strong autoimmune response to infection, were a key aspect of symptom relief, with those whose autoimmune response was lacking showing few signs of improvement.[88] Interferon-based therapies andantiviral drugs shown to be successful against the virus were found to be the best way to alleviate symptoms.[87]
A 2025 study published inNature found evidence that theSARS-CoV-2 virus was neuroinvasive, and could linger in the brain stem through slowreplication regardless of the prevalence of infection in the body. ViralRNA and replicative virus were discovered in thebrainstems ofgolden hamsters 80 days after initial infection. Subjects displayed signs of neurodegeneration, and "alteredexpression ofgenes involved in thedopaminergic andglutamatergicsynapses, in energymetabolism, and inproteostasis."[76]
Many people withfibromyalgia experience cognitive problems[89] (often called "fibrofog"), which may involve impaired concentration,[90][91][unreliable medical source?][92] problems withshort-[93] andlong-term memory, short-termmemory consolidation,[93] working memory,[94] impaired speed of performance,[93] inability to multitask, cognitive overload,[93] and diminished attention span. About 75% of fibromyalgia patients report significant problems with concentration, memory, and multitasking.[95] A 2018meta-analysis found that the largest differences between fibromyalgia patients and healthy subjects were ininhibitory control, memory, andprocessing speed.[95] 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.[96][97][98] It is alternatively hypothesized that increased pain compromises attention systems, resulting in cognitive problems.[95]
| This sectionneeds expansion with: Effects of endocrine signaling and autonomic disruption on cognitive function. You can help byadding missing information.(November 2025) |
Thehuman digestive system is lined with more than 100 millionnerve cells, referred to as theenteric nervous system (ENS), which is primarily responsible for regulating gastrointestinal activity.[99] The system is connected to thecentral nervous system by means of thegut-brain axis, a neurotransmission channel anchored by thevagus nerve.[84] This system and thegut microbiome play a critical role in influencing cognitive function and controlling inflammatory response.[100][101] More than 90% of the body's serotonin (which assists with memory and helps maintain calm and focus in the brain) is produced in the gut, alongside other key neurotransmitters, molecules implicated ininteroception, andfatty acids; much of this takes place by means or with the help of immune cells in and microbiota of the gut.[84][102][100][103][cleanup needed]
Dysregulation in either system can affect the other. Gut irritation can trigger stress and cognitive difficulties as well as changes in mood or behavior in the brain.[102] Myriad cognitive and emotional challenges can, in turn, produce irritation in the gut, creating apositive feedback loop that can provoke further instability in both systems.[102] "Psychosocial factors influence the actual physiology of the gut, as well as symptoms".[104] People withirritable bowel syndrome (IBS) and other functional gastrointestinal disorders are known to experiencepsychiatric illness, depression, anxiety,anaemia, and fatigue at a higher rate than the general public.[99][102][105][106] High stress and anxiety, depression, and psychiatric disorders have also shown to produce higher-than-average rates of gastrointestinal disease, such as IBS,constipation, anddiarrhea, and to influence the makeup of the gut microbiota, which can in turn heighten stress and worsen depression.[105][107][108] Fecal transplants from humans with depression to rats have shown that depressive and anxiogenic symptoms may be directly influenced by the makeup of the gut microbiome.[84][109]
Certain antidepressant regimens and/or cognitive behavioral therapy (CBT) have been shown to relieve symptoms of functional gastrointestinal disorders in some patients, which is believed to be a result of their calming effect on the ENS.[99] The vast majority of sources encourage improvement in one's diet as a means of promoting a healthy gut microbiome, recommending that they beplant-rich andfiber intensive.[110] This includes the proper provisioning ofprebiotics (proposed as a prerequisite to the proper development of an effective microbiome in the long term), reasonably significant quantities ofsoluble andinsoluble fiber,probiotics (fermented foods),anti-oxidants, andanti-inflammatories.[84][102][103][106][111] Thecontrolled andlimited use of antibiotics may beprescribed by doctors to clear persistentbacterial infection in the gastrointestinal tract.[110][112]
Brain fog and additional neuro-cognitive difficulties are a common symptom ofhypothyroidism.[113][114][115] Symptoms often include "fatigue, depressed mood, and cognitive difficulties, including problems with memory and word-finding".[116] 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".[114] 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".[114] OneAmerican 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, butlevothyroxine has been shown to reduce cognitive impairment in some patients.[117] 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 showingTSH results in the normal range.[118] This may lead patients to seek higher dosage, which doctors often dismiss, or alternative therapies, such asdesiccated thyroid extract (DTE), despite the lack of evidence supporting its use.[116][118] Some patients, more commonly those over age 50, reported improvement with the addition ofliothyronine (L-T3) to their treatment regimen, though some researchers question its efficacy .[115][116] Rest and exercise have also been shown to help alleviate symptoms.[114][115]
Lyme disease's neurologic syndrome, called Lyme encephalopathy, is associated with subtle memory and cognitive difficulties, among other issues.[119] Lyme can cause a chronicencephalomyelitis that resemblesmultiple sclerosis. It may be progressive and can involve cognitive impairment,migraines, balance problems, and other symptoms.[citation needed]
| This sectionneeds expansion with: Explanation of progesterone and estrogen fluctuations on cognitive performance (specific) and bodily processes which may influence cognitive function. You can help byadding missing information.(November 2025) |
Menopause, officially described as the end of menstruation andreproductive hormone production in thoseassigned female at birth who still possessprimary female sexual characteristics, can be characterized in all stages by deficits in cognitive performance (sometimes referred to as "meno-fog").[120][121][122][123] 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.[120][123][124] Cognitive dysfunction is most prevalent in theperimenopausal 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 thepostmenopausal period progresses.[120][122][123][125]
A 2022 study published inMenopause analyzed a group of 404 women from ruralIndia between the ages of 40 and 65, assessing the severity of their menopausal symptoms (on theGreene Climacteric Scale) and cognitive performance (scoringorientation, registration,attention,recall, and language andvisuospatial skills by means of theHindiMini-Mental State Examination).[124][126] Women with severe menopausal symptoms presented with significantly lower mean performance across all cognitive domains.[126] 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.[122][124][126] Symptoms of "depression, total psychological, sexual, andsomatic 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).[122][127] The study found no relationship between the severity ofvasomotor symptoms (hot flashes) and cognitive performance.[124]
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.[122][125] 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."[125] The transition affects serotonergic and dopaminergic expression, contributing to imbalances in cognition and mood.[123] Additionally, elevated stress and a subsequent increase in cortisol may contribute to memory and processing difficulties.[123][128]
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.[120][122][123]Hormone replacement therapy is thought to help relieve cognitive and broader symptoms in some patients.[123]
Brain fog and other neurological symptoms may also result from mold exposure.[129][130][131][132][133] This may be due tomycotoxin exposure and consequent innate immune system activation and inflammation, including in the central nervous system.[134][129][130][131][132][133] But adverse neurological health effects of mold exposure are controversial due to inadequate research and data, and more research is needed in this area.[134][135][136][129][131][133]
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