Clouding of consciousness, also called brain fog or mental fog, occurs when a person is conscious but slightly less wakeful or aware than normal. 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". Sufferers may be less aware of time and their surroundings, and find it difficult to pay attention. People describe this subjective sensation as their mind being "foggy".
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".
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. Delirium's full clinical manifestations may never be reached. 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) and had a decreased post-discharge level of functional independence compared to the general population.
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".
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. 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. This supports the modern notion that distinct segments of the central nervous system are critical for consciousness.
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. 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".
Altered cognition Clouding of consciousness is not necessarily accompanied by drowsiness. 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". One patient said, "I thought it became like misty, in some way... the outlines were sort of fuzzy". Others may describe a "spaced-out" feeling. 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. 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.
Brain fog may affect performance on virtually any cognitive task. As one author put it, "It should be apparent that cognition is not possible without a reasonable degree of arousal." 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. The extent of the impairment is variable because inattention may impair several cognitive functions. Affected people may complain of forgetfulness, being "confused", or being "unable to think straight". 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.
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. 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.
By substance
Alcohol
Heavy, progressive, and persistent alcohol abuse (alcohol use disorder (AUD)) lasting more than several years has been shown to lead to brain damage. 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".
Wernicke-Korsakoff Syndrome