Clouding of consciousness

Clouding of consciousness, also called brain fog or mental fog,^[1][2] occurs when a person is conscious but slightly less wakeful or aware than normal.^[3] The term "brain fog" is used to represent a subjective condition of perceived cognitive impairment. It is defined 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] They are less aware of time and their surroundings, and find it difficult to pay attention.^[3] People describe this subjective sensation as their mind being "foggy".^[5]

"Brain fog" redirects here; not to be confused with Brain fag or Mild cognitive impairment.

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".^[6]

Feature of delirium

The term clouding of consciousness has always denoted the main pathogenetic feature of delirium since physician Georg Greiner^[7] pioneered the term (Verdunkelung des Bewusstseins) in 1817.^[8] The Diagnostic and Statistical Manual of Mental Disorders (DSM) has historically used the term in its definition of delirium.^[9] 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.^[10] Clouding of consciousness may be less severe than delirium on a spectrum of abnormal consciousness.^[3][11][12] Clouding of consciousness may be synonymous with subsyndromal delirium.^[13]

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.^[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] 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)^[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. The DSM-IV-TR instructs clinicians to code subsyndromal delirium presentations under the miscellaneous category "cognitive disorder not otherwise specified".^[15]

Psychopathology

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.^[6][16] 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.^[6][17] 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.^[17] 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.^[17] This supports the modern notion that distinct segments of the central nervous system are critical for consciousness.^[6]

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.^[3][18] Various etiologies disturb this regulating part of the brain, which in turn disturbs the "overall level" of consciousness.^[19] This system of a sort of general activation of consciousness is called "arousal" or "wakefulness".^[18]

Altered cognition

Clouding of consciousness is not necessarily accompanied by drowsiness.^[20] Patients may not be sleepy yet still have clouded consciousness (disorder of wakefulness).^[21] Paradoxically, affected individuals say they are "awake but, in another way, not".^[22] 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.^[23][24]

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".^[22] Others may describe a "spaced-out" feeling.^[25] 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.^[26] 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.^[1] 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.^[27]

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",^[28] or being "unable to think straight".^[28] 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).^[29]

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.^[30] 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".^[31]

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.^[31][32] This may result from the users' dependency on and subsequent restriction from the substance in question, or from neurocognitive impairment / neurodegeneration resulting from use.^[31]

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.^[33] It has been consistently shown that addicts present with both lower responsiveness to dopamine, particularly in D2 receptors, and lower dopamine production overall.^[31][34][35] 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.^[33][36]

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.^[33]

By substance

Alcohol

See also: Alcohol related brain damage

Heavy, progressive, and persistent alcohol abuse (referred to as alcohol use disorder (AUD)) lasting more than several years has been shown to lead to brain damage.^[37] Cognitive difficulties related to alcohol use that do not progress into more severe illness are referred to as Alcohol related brain damage (ARBD).^[38] Symptoms include mild executive dysfunction as well as deficits in memory, coordination, motor control, and visuospatial skills.^[38][39] Cognitive deficits differ significantly between patients, "[suggesting] that the functions affected by chronic alcohol consumption are dissociable and supported by different neural systems."^[38]

Wernicke-Korsakoff Syndrome

Main article: Wernicke–Korsakoff syndrome

Persistent alcohol use disorder lasting several years or more can contribute to severe malnutrition.^[38] Alcohol abuse hinders the gut's ability to properly absorb critical nutrients, and the brain's ability to phosphorylate them.^[38][40] 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.^[38][40][41] 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.^[41] 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.^[40][41]

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.^[38][40][41] 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."^[38] Memory rehabilitation therapy may help to relieve symptoms; severe cases often require institutionalization.^[41][42]

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.^[43][44][45] The immediate short-term effects of cannabis use can include "impaired short-term memory and motor coordination, altered judgment, paranoia, and psychosis".^[46] Long-term use can lead to "altered brain development, poor educational outcomes, cognitive impairment, diminished quality of life", and increased risk of suicide.^[46]

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.^{[44][45][47][48][49][50]}

Cannabis use disorder

Main article: 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)^[a] experienced a mean 5.5-point drop in IQ from childhood to adulthood.^[43][51] 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.^[51]

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.^[32][52][53] 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).^[52][54]

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).^[55][56][57] This effect is especially pronounced in young children.^[58][59] Despite having an immediate short-term impact of lowering blood pressure, cannabis has been associated with hypertension in regular and heavy users.^[50] This, in turn, can restrict the flow of oxygen to the brain, leading to "forgetfulness, trouble with learning, memory and comprehension".^[60] Continued restriction can lead to cerebral small and large vessel disease later in life, which significantly increases the likelihood of dementia onset.^[61]

Disease and health complications

Anxiety / general anxiety disorder (GAD)

Main articles: Anxiety, General anxiety disorder, and Anxiety disorder

Anaemia

Main article: Anaemia

Attention deficit hyperactivity disorder (ADHD)

Main article: 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.^[62]

Autism

Main articles: Autism and Autistic burnout

Cancer and chemotherapy

See also: Chemotherapy and 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.^[63] Patients often report experiencing fatigue and difficulty with memory, language use, visuo-spatial skills, immediate and delayed recall, processing speed, and executive function.^[64][65] Such difficulties can surface both during and after treatment, with cognitive deficits being reported as much as 21 years after treatment.^[64] But some studies have found that neuro-cognitive deficits were present in some patients before beginning treatment.^[64] Hypotheses for the cause of these symptoms include "direct neurotoxicity, [blood–brain barrier] disruption, decreased hippocampal neurogenesis, white matter abnormalities, secondary neuro-inflammatory response and increased oxidative stress".^[65]

Symptoms can be exacerbated by additional side effects of treatment, including sleep cycle impairment, dietary issues, fatigue, and imbalanced mood.^[66] 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.^[66]

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 that there was no significant difference in magnitude between the reported neurocognitive impairment of cancer survivors who underwent chemotherapy and those who did not.^[64] 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.^[64]

Chronic fatigue

Main article: Myalgic encephalomyelitis/chronic fatigue syndrome

In chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis, the CDC's recommended criteria for diagnosis^[67] include that one of the following symptoms must be present:^[67]

• Problems with thinking and memory (cognitive dysfunction, sometimes described as "brain fog")
• While standing or sitting upright, lightheadedness, dizziness, weakness, fainting, or vision changes may occur (orthostatic intolerance)

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.^[63]

Chronic pain

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.^[68] In such illnesses, pain processing may use up resources, decreasing the brain's ability to think effectively.^[4]

Chronic sleep deprivation

Main article: Chronic sleep deprivation

Chronic stress

Main article: Chronic stress

Chronic traumatic encephalopothy

Main article: Chronic traumatic encephalopathy

Cognitive disengagement syndrome

Cognitive disengagement syndrome was implicated in the expression of brain fog symptoms.^[69]

COVID-19

See also: COVID-19

Patients recovering from COVID-19 have reported experiencing brain fog, which can reflect a wide variety of neurological and psychological symptoms linked to COVID-19.^[70][71] Symptoms can persist for months, even years, and are often characterized by fatigue, difficulties with "attention...memory recall, language and executive functioning", as well as depression and anxiety.^[72][73][74] 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'".^[63]

COVID has also been shown to cause encephalopathy, though this is more common in elderly patients and those with preexisting chronic conditions.^[75] The Alpha and Delta variants of the virus were characterized by severe cognitive impairment at the time of infection, followed by slow recovery.^[72]

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".^[76]

Causes and treatment

Research from the UK 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 the limbic system, with evidence that the disruption of the olfactory 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] in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus", and markers of tissue damage in regions of the brain connected to the primary olfactory cortex.^[77] 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.^[75][78][79] COVID-19 patients also showed disrupted contact between different regions of the brain.^[75]

Individuals with long COVID are significantly more likely to experience gastrointestinal dysfunction, and have "reported worse anxiety, depression, and quality of life".^[80] 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.^[81] Studies of mice "[bio]-engineered to mimic long COVID in humans" showed that cognitive difficulties could be relieved through treatment with Prozac.^[82]

Initially, it was thought that the presentation of brain fog in long COVID shared molecular features with Alzheimer's disease.^[83] This was disproved in 2024 by researchers from Rutgers 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.^[84] Over two years, only half of patients involved in the study reported improvements in persistent cognitive difficulties.^[85][86] 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.^[85][84] Researchers believe that interferons, 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.^[86] Interferon-based therapies and antiviral drugs shown to be successful against the virus were found to be the best way to alleviate symptoms.^[85]

A 2025 study published in Nature found evidence that the SARS-CoV-2 virus was neuroinvasive, and could linger in the brain stem through slow replication regardless of the prevalence of infection in the body. Viral RNA and replicative virus were discovered in the brainstems of golden hamsters 80 days after initial infection. Subjects displayed signs of neurodegeneration, and "altered expression of genes involved in the dopaminergic and glutamatergic synapses, in energy metabolism, and in proteostasis."^[74]

Depression

Main articles: Biology of depression and Major depressive disorder

Encephalitis

Main article: Encephalitis

Fibromyalgia

Many people with fibromyalgia experience cognitive problems^[87] (often called "fibrofog"), which may involve impaired concentration,^{[88][89][unreliable medical source?][90]} problems with short-^[91] and long-term memory, short-term memory consolidation,^[91] working memory,^[92] impaired speed of performance,^[91] inability to multitask, cognitive overload,^[91] and diminished attention span. About 75% of fibromyalgia patients report significant problems with concentration, memory, and multitasking.^[93] A 2018 meta-analysis found that the largest differences between fibromyalgia patients and healthy subjects were in inhibitory control, memory, and processing speed.^[93] 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.^[94][95][96] It is alternatively hypothesized that increased pain compromises attention systems, resulting in cognitive problems.^[93]

Gut health

Main article: Gut–brain axis

The human digestive system is lined with a series of more than 100 million nerve cells, referred to as the enteric nervous system (ENS), which is primarily responsible for regulating gastrointestinal activity.^[97] The system is connected to the central nervous system by means of the gut-brain axis, a neurotransmission channel anchored by the vagus nerve.^[82] This system alongside the gut microbiome play a critical role in influencing cognitive function and controlling inflammatory response.^[98][99] 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 in interoception, and fatty acids; much of this is performed by means or with the help of immune cells located in and the microbiota of the gut.^{[82][100][98][101][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.^[100] Myriad cognitive and emotional challenges can, in turn, produce irritation in the gut, creating a positive feedback loop that can provoke further instability in both systems.^[100] Thus, "psychosocial factors influence the actual physiology of the gut, as well as symptoms".^[102] Individuals with irritable bowel syndrome (IBS) and other functional gastrointestinal disorders are known to experience psychiatric illness, depression, anxiety, anaemia, and fatigue at a higher rate than the general public.^{[97][100][103][104]} High stress and anxiety, depression, and psychiatric disorders have simultaneously been shown to produce higher-than-average rates of gastrointestinal disease, such as IBS, constipation, and diarrhea, and to influence the makeup of the gut microbiota, which can, in turn, heighten stress and worsen depression.^{[103][105][106]} 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.^[82][107]

Prescriptions

Certain antidepressant regimens and/or cognitive behavioral therapy (CBT) have been shown to relieve symptoms of functional gastrointestinal disorders in some patients, believed to be a result of their calming effect on the ENS.^[97] The vast majority of sources encourage improvement in one's diet as a means of promoting a healthy gut microbiome, recommending that they be plant-rich and fiber intensive.^[108] This includes the proper provisioning of prebiotics (proposed as a prerequisite to the proper development of an effective microbiome in the long term), reasonably significant quantities of soluble and insoluble fiber, probiotics (fermented foods), anti-oxidants, and anti-inflammatories.^{[82][100][101][104]} The controlled and limited use of antibiotics may be prescribed by doctors to clear persistent bacterial infection in the gastrointestinal tract.^[108][109]

Hypersomnia

Main articles: Hypersomnia and Idiopathic hypersomnia

Hypoglycemia and diabetes

Main article: Hypoglycemia

Hypothyroidism

Brain fog and additional neuro-cognitive difficulties are a common symptom of hypothyroidism.^{[110][111][112]} Symptoms often include "fatigue, depressed mood, and cognitive difficulties, including problems with memory and word-finding".^[113] 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".^[111] 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".^[111] 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.^[114] 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.^[115] 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.^[113][115] 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 .^[112][113] Rest and exercise have also been shown to help alleviate symptoms.^[111][112]

Lupus

Main article: Lupus

Lyme disease

Lyme disease's neurologic syndrome, called Lyme encephalopathy, is associated with subtle memory and cognitive difficulties, among other issues.^[116] Lyme can cause a chronic encephalomyelitis that resembles multiple sclerosis. It may be progressive and can involve cognitive impairment, migraines, balance problems, and other symptoms.^{[citation needed]}

Menopause

Main article: 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").^{[117][118][119][120]} Though symptoms vary significantly between patients depending on factors such as genetics, ethnicity, and pre-existing conditions, brain fog has been shown to be exceptionally common, with up to 80% of individuals experiencing it at some point over the course of transition.^{[117][120][121]} 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. These symptoms, however, are often temporary, and begin to relieve as the postmenopausal period progresses.^{[117][119][120][122]}

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).^[121][123] Women with severe menopausal symptoms presented with significantly lower mean performance across all cognitive domains.^[123] 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 cause-and-effect relationship between them, meaning there was little indication whether one preceded the other.^{[119][121][123]} 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).^[119][124] The study found no relationship between the severity of vasomotor symptoms (hot flashes) and cognitive performance.^[121]

Cognitive deficits are believed in part to result from the sudden drop in estrogen across "virtually every organ", contributing, in turn, to hormonal imbalances which disrupt the brain and body's natural processes.^[119][122] It's believed that estrogen plays a crucial role for both men and women 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."^[122] The transition affects serotonergic and dopaminergic expression, contributing to imbalances in cognition and mood.^[120] Additionally, elevated stress and a subsequent increase in cortisol may contribute to memory and processing difficulties.^[120][125]

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) and sun-exposure, and social support are generally known to assist in improving cognition.^{[117][119][120]} Hormone replacement therapy is thought to help relieve cognitive and broader symptoms in some patients.^[120]

Menstruation

Main articles: Premenstrual syndrome, Menstruation cycle, and Menstruation

Migraine disorders

Main article: Migraine

Mold exposure

Brain fog and other neurological symptoms may also result from mold exposure.^{[126][127][128][129][130]} This may be due to mycotoxin exposure and consequent innate immune system activation and inflammation, including in the central nervous system.^{[131][126][127][128][129][130]} But adverse neurological health effects of mold exposure are controversial due to inadequate research and data, and more research is needed in this area.^{[131][132][133][126][128][130]}

Obsessive-compulsive disorder (OCD)

Main article: Obsessive–compulsive disorder

Oophorectomy and ovariectomy (OVX)

Main articles: Oophorectomy and Ovariectomy

Pregnancy

Main articles: Prenatal stress, Postpartum depression, and Postpartum period

Psychotic disorders

Main articles: Schizophrenia, Schizoaffective disorder, Bipolar disorder, Postpartum psychosis, and Psychosis

See also

• Psychiatry portal
• Psychology portal
• Medicine portal

• 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

Notes

1. Weekly or more (as reported at ages 18, 21, 26, 32, 38, and 45)^[43][51]