Clouding of consciousness

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". Feature of delirium The term clouding of consciousness has always denoted the main pathogenetic feature of delirium since physician Georg Greiner pioneered the term ('') in 1817. The Diagnostic and Statistical Manual of Mental Disorders (DSM) has historically used the term in its definition of delirium. 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. Clouding of consciousness may be less severe than delirium on a spectrum of abnormal consciousness. Clouding of consciousness may be synonymous with subsyndromal delirium''. 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. Subsyndromal delirium's significant clinical features are inattention, thought process abnormalities, comprehension abnormalities, and language abnormalities. ==Psychopathology==

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. 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. 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 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. 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. 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. 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. 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. Various etiologies disturb this regulating part of the brain, which in turn disturbs the "overall level" of consciousness. This system of a sort of general activation of consciousness is called "arousal" or "wakefulness". Patients may not be sleepy yet still have clouded consciousness (disorder of wakefulness). Paradoxically, affected individuals say they are "awake but, in another way, not". 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. The affected person has a sensation of mental clouding described in the patient's own words as "foggy". 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. 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. Brain fog may affect performance on virtually any cognitive task. 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). == 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. 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". 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. This may result from the users' dependency on and subsequent restriction from the substance in question, or from neurocognitive impairment / neurodegeneration resulting from use. It has been consistently shown that addicts present with both lower responsiveness to dopamine, particularly in D2 receptors, and lower dopamine production overall. 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. 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. Cognitive difficulties related to alcohol use that do not progress into more severe illness are called alcohol-related brain damage (ARBD). Symptoms include mild executive dysfunction as well as deficits in memory, coordination, motor control, and visuospatial skills. Cognitive deficits differ significantly between patients, suggesting "that the functions affected by chronic alcohol consumption are dissociable and supported by different neural systems". 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. 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. 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. The immediate short-term effects of cannabis use can include "impaired short-term memory and motor coordination, altered judgment, paranoia, and psychosis". Long-term use can lead to "altered brain development, poor educational outcomes, cognitive impairment, diminished quality of life", and increased risk of suicide. 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) experienced a mean 5.5-point drop in IQ from childhood to adulthood. 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. 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). 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). This effect is especially pronounced in young children. Despite having an immediate short-term impact of lowering blood pressure, cannabis has been associated with hypertension in regular and heavy users. Continued restriction can lead to cerebral small and large vessel disease later in life, which significantly increases the likelihood of dementia onset. == Disease and health complications ==

Anxiety / general anxiety disorder (GAD) Anaemia Attention deficit hyperactivity disorder (ADHD) 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. Autism Cancer and chemotherapy 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. Such difficulties can surface both during and after treatment, with cognitive deficits being reported as much as 21 years after treatment. 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. include that one of the following symptoms must be present: Chronic pain Brain fog is a common symptom in many illnesses where chronic pain is a major component. In such illnesses, pain processing may use up resources, decreasing the brain's ability to think effectively. Depression Encephalitis Fibromyalgia Many people with fibromyalgia experience cognitive problems (often called "fibrofog"), which may involve impaired concentration, problems with short- and long-term memory, short-term memory consolidation, impaired speed of performance, A 2018 meta-analysis found that the largest differences between fibromyalgia patients and healthy subjects were in inhibitory control, memory, and processing speed. It is alternatively hypothesized that increased pain compromises attention systems, resulting in cognitive problems. Symptoms often include "fatigue, depressed mood, and cognitive difficulties, including problems with memory and word-finding". 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". 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. 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. 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. 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. 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"). 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. 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. 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). Women with severe menopausal symptoms presented with significantly lower mean performance across all cognitive domains. The study found no relationship between the severity of vasomotor symptoms (hot flashes) and cognitive performance. 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. This may be due to mycotoxin exposure and consequent innate immune system activation and inflammation, including in the central nervous system. Obsessive–compulsive disorder (OCD) Oophorectomy and ovariectomy (OVX) Pregnancy Psychotic disorders ==See also==