In psychology and neuroscience, executive dysfunction, or executive function deficit, is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control.

Executive dysfunction is not the same as dysexecutive syndrome, a term coined by Alan Baddeley to describe a common pattern of dysfunction in executive functions, such as deficiencies in planning, abstract thinking, flexibility and behavioural control. This group of symptoms, usually resulting from brain damage, tend to occur together. However, the existence of dysexecutive syndrome is controversial.

Symptoms of DES fall into three broad categories: cognitive, emotional and behavioural. Many of the symptoms can be seen as a direct result of impairment to the central executive component of working memory, which is responsible for attentional control and inhibition. Although many of the symptoms regularly co-occur, it is common to encounter patients who have several, but not all symptoms. The accumulated effects of the symptoms have a large impact on daily life.

The emotional symptoms that individuals with DES experience may be quite extreme and can cause extensive problems. They may have difficulty inhibiting many types of emotions such as anger, excitement, sadness, or frustration. Due to multiple impairments of cognitive functioning, there can be much more frustration when expressing certain feelings and understanding how to interpret every day situations. Individuals with DES may have higher levels of aggression or anger because they lack abilities that are related to behavioural control. They can also have difficulty understanding others' points of view, which can lead to anger and frustration.

Delirium develops rapidly over a short period of time and is characterized by a disturbance in cognition, manifested by confusion, excitement, disorientation, and a clouding of consciousness. Hallucinations and illusions are common, and some individuals may experience acute onset change of consciousness. It is a disorder that makes situational awareness and processing new information very difficult for those diagnosed. It usually has a high rate of onset ranging from minutes to hours and sometimes days, but it does not last for very long, only a few hours to weeks. Delirium can also be accompanied by a shift in attention, mood swings, violent or unordinary behaviors, and hallucinations. It can be caused by a preexisting medical condition. Delirium during a hospital stay can result in a longer stay and more risk of complications and long terms stays.

Cognitive deficit or cognitive impairment is an inclusive term to describe any characteristic that acts as a barrier to the cognition process.

The term may describe

- deficits in overall intelligence (as with intellectual disabilities),

- specific and restricted deficits in cognitive abilities (such as in learning disorders like dyslexia),

- neuropsychological deficits (such as in attention, working memory or executive function),

- or it may describe drug-induced impairment in cognition and memory (such as that seen with alcohol, glucocorticoids, and the benzodiazepines.)

It usually refers to a durable characteristic, as opposed to altered level of consciousness, which may be acute and reversible. Cognitive deficits may be inborn or caused by environmental factors such as brain injuries, neurological disorders, or mental illness.

Mild and major neurocognitive disorders are usually associated with but not restricted to the elderly. Unlike delirium, conditions under these disorders develop slowly and are characterized by memory loss. In addition to memory loss and cognitive impairment, other symptoms include aphasia, apraxia, agnosia, loss of abstract thought, behavioral/personality changes, and impaired judgment. There may also be behavioral disturbances including psychosis, mood, and agitation.

Mild and major neurocognitive disorders are differentiated based on the severity of their symptoms. Previously known as dementia, major neurocognitive disorder is characterized by significant cognitive decline and interference with independence, while mild neurocognitive disorder is characterized by moderate cognitive decline and does not interfere with independence. To be diagnosed, it must not be due to delirium or other mental disorder. They are also usually accompanied by another cognitive dysfunction. For non-reversible causes of dementia such as age, the slow decline of memory and cognition is lifelong. It can be diagnosed by screening tests such as the Mini Mental State Examination (MMSE).

The CCAS has been described in both adults and children. The precise manifestations may vary on an individual basis, likely reflecting the precise location of the injury in the cerebellum. These investigators subsequently elaborated on the affective component of the CCAS, i.e., the neuropsychiatric phenomena. They reported that patients with injury isolated to the cerebellum may demonstrate distractibility, hyperactivity, impulsiveness, disinhibition, anxiety, ritualistic and stereotypical behaviors, illogical thought and lack of empathy, aggression, irritability, ruminative and obsessive behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, childlike behavior, and inability to comprehend social boundaries and assign ulterior motives.

The CCAS can be recognized by the pattern of deficits involving executive function, visual-spatial cognition, linguistic performance and changes in emotion and personality. Underdiagnosis may reflect lack of familiarity of this syndrome in the scientific and medical community. The nature and variety of the symptoms may also prove challenging. Levels of depression, anxiety, lack of emotion, and affect deregulation can vary between patients. The symptoms of CCAS are often moderately severe following acute injury in adults and children, but tend to lessen with time. This supports the view that the cerebellum is involved with the regulation of cognitive processes.

Older people with cognitive impairment appear to improve somewhat with light therapy.

The causes of CCAS lead to variations in symptoms, but a common core of symptoms can be seen regardless of etiology. Causes of CCAS include cerebellar agenesis, dysplasia and hypoplasia, cerebellar stroke, tumor, cerebellitis, trauma, and neurodegenerative diseases. CCAS can also be seen in children with prenatal, early postnatal, or developmental lesions. In these cases there are lesions of the cerebellum resulting in cognitive and affect deficits. The severity of CCAS varies depending on the site and extent of the lesion. In the original report that described this syndrome, patients with bihemispheric infarction, pancerebellar disease, or large unilateral posterior inferior cerebellar artery (PICA) infarcts had more cognitive deficits than patients with small right PICA infarcts, small right anterior interior cerebellar artery infarcts or superior cerebellar artery (SCA) territory. Overall, patients with damage to either the posterior lobe of the cerebellum or with bilateral lesions had the greatest severity of symptoms, whereas patients with lesions in the anterior lobe had less severe symptoms. In children, it was found that those with astrocytoma performed better than those with medulloblastoma on neuropsychological tests. When diagnosing a patient with CCAS, medical professionals must remember that CCAS has many different causes.

Additionally, requirements for a proposed diagnosis such as the number and duration of symptoms and the impact on functioning are continuing to be investigated. But there is no doubt that both ADHD and SCT are found in children and adults and are linked to significant impairment and a diminished quality of life (QoL). The research by Barkley suggests that this is especially true if ADHD and SCT occur together: In adults, those comorbid cases were more likely to be unmarried and to be out of work on disability compared to cases with ADHD alone. But SCT alone is also present in the population and can be quite impairing in educational and occupational settings, even if it is not as pervasively impairing as ADHD.

Mind-blindness is a cognitive disorder where an individual is unable to attribute mental states to others. As a result of this kind of social and empathetic cognitive deficit, the individual is incapable in putting himself "into someone else's shoes" and cannot conceptualize, understand or predict knowledge, thoughts and beliefs, emotions, feelings and desires, behaviour, actions and intentions of another person. Such an ability to develop a mental awareness of what is in the other minds is known as the theory of mind (ToM), and the "Mind-blindness" Theory asserts that children who delay in this development often are or will be autistic and Asperger's syndrome (AS) patients. In addition to autism and AS, ToM and mind-blindness research has recently been extended to other disorders such as schizophrenia, dementia, bipolar disorders, antisocial personality disorders as well as normal aging.

In many ways, those who have an SCT profile have some of the opposite symptoms of those with classic ADHD: instead of being hyperactive, extroverted, obtrusive, excessively energetic and risk takers, those with SCT are drifting, absent-minded, listless, introspective and daydreamy. They feel as if "in the fog" and seem "out of it".

The comorbid psychiatric problems often associated with SCT are more often of the internalizing types, such as anxiety, unhappiness or depression. Most consistent across studies was a pattern of reticence and social withdrawal in interactions with peers. Their typically shy nature and slow response time has often been misinterpreted as aloofness or disinterest by others. In social group interactions, those with SCT may be ignored. People with classic ADHD are more likely to be rejected in these situations, because of their social intrusiveness or aggressive behavior. Compared to children with SCT, they are also much more likely to show antisocial behaviours like substance abuse, oppositional-defiant disorder or conduct disorder (frequent lying, stealing, fighting etc.). Fittingly, in terms of personality, ADHD seems to be associated with sensitivity to reward and fun seeking while SCT may be associated with punishment sensitivity.

The cause of executive dysfunction is heterogeneous, as many neurocognitive processes are involved in the executive system and each may be compromised by a range of genetic and environmental factors. Learning and development of long-term memory play a role in the severity of executive dysfunction through dynamic interaction with neurological characteristics. Studies in cognitive neuroscience suggest that executive functions are widely distributed throughout the brain, though a few areas have been isolated as primary contributors. Executive dysfunction is studied extensively in clinical neuropsychology as well, allowing correlations to be drawn between such dysexecutive symptoms and their neurological correlates.

Executive processes are closely integrated with memory retrieval capabilities for overall cognitive control; in particular, goal/task-information is stored in both short-term and long-term memory, and effective performance requires effective storage and retrieval of this information.

Executive dysfunction characterizes many of the symptoms observed in numerous clinical populations. In the case of acquired brain injury and neurodegenerative diseases there is a clear neurological etiology producing dysexecutive symptoms. Conversely, syndromes and disorders are defined and diagnosed based on their symptomatology rather than etiology. Thus, while Parkinson's disease, a neurodegenerative condition, causes executive dysfunction, a disorder such as attention-deficit/hyperactivity disorder is a classification given to a set of subjectively-determined symptoms implicating executive dysfunction – current models indicate that such clinical symptoms are caused by executive dysfunction.

Inattention, hyperactivity (restlessness in adults), disruptive behavior, and impulsivity are common in ADHD. Academic difficulties are frequent as are problems with relationships. The symptoms can be difficult to define as it is hard to draw a line at where normal levels of inattention, hyperactivity, and impulsivity end and significant levels requiring interventions begin.

According to the DSM-5, symptoms must be present for six months or more to a degree that is much greater than others of the same age and they must cause significant problems functioning in at least two settings (e.g., social, school/work, or home). The full criteria must have been met prior to age 12 in order to receive a diagnosis of ADHD.

ADHD is divided into three subtypes: predominantly inattentive (ADHD-PI or ADHD-I), predominantly hyperactive-impulsive (ADHD-PH or ADHD-HI), and combined type (ADHD-C).

A child with ADHD inattentive type has most or all of following symptoms, excluding situations where these symptoms are better explained by another psychiatric or medical condition:

- Be easily distracted, miss details, forget things, and frequently switch from one activity to another

- Have difficulty maintaining focus on one task

- Become bored with a task after only a few minutes, unless doing something enjoyable

- Have difficulty focusing attention on organizing and completing a task or learning something new

- Have trouble completing or turning in homework assignments, often losing things (e.g., pencils, toys, assignments) needed to complete tasks or activities

- Seem to not be listening when spoken to

- Daydream, become easily confused, and move slowly

- Have difficulty processing information as quickly and accurately as others

- Struggle to follow instructions

- Have trouble understanding minute details

A child with ADHD hyperactive-impulsive type has most or all of the following symptoms, excluding situations where these symptoms are better explained by another psychiatric or medical condition:

- Fidget and squirm in their seats

- Talk nonstop

- Dash around, touching or playing with anything and everything in sight

- Have trouble sitting still during dinner, school, doing homework, and story time

- Be constantly in motion

- Have difficulty doing quiet tasks or activities

- Be very impatient

- Blurt out inappropriate comments, show their emotions without restraint, and act without regard for consequences

- Have difficulty waiting for things they want or waiting their turn in games

- Often interrupt conversations or others' activities

Girls tend to have less hyperactivity, inattention, and impulsivity but more intellectual problems. Symptoms of hyperactivity tend to go away with age and turn into "inner restlessness" in teens and adults with ADHD.

People with ADHD of all ages are more likely to have problems with social skills, such as social interaction and forming and maintaining friendships. This is true for all subtypes. About half of children and adolescents with ADHD experience social rejection by their peers compared to 10–15% of non-ADHD children and adolescents. People with attention deficits are prone to having difficulty processing verbal and nonverbal language which can negatively affect social interaction. They also may drift off during conversations, miss social cues, and have trouble learning social skills.

Difficulties managing anger are more common in children with ADHD as are poor handwriting and delays in speech, language and motor development. Although it causes significant impairment, particularly in modern society, many children with ADHD have a good attention span for tasks they find interesting.

Overall, studies have shown that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests. The significance of this is controversial due to the differences between people with ADHD and the difficulty determining the influence of symptoms, such as distractibility, on lower scores rather than intellectual capacity. In studies of ADHD, higher IQs may be over represented because many studies exclude individuals who have lower IQs despite those with ADHD scoring on average 9 points lower on standardized intelligence measures.

People with schizophrenia also show deficits associated with mind-blindness. However, there is an ongoing debate as to whether individuals with schizophrenia have an impaired ToM leading to mind-blindness or display an exaggerated ToM. Unlike autism or AS, schizophrenia is a late onset condition. It is speculated that this difference in the condition may account for differences seen in the ToM abilities. Brain lesion studies show that there are differences seen in the laterality of brain that account for mind-blindness. It is unknown whether the ToM in schizophrenia deteriorates in the affected person as the condition progresses.

The cognitive impairment linked to mind-blindness is best explained by a modular theory; the domain specific capabilities that account for mindreading and mentalization are lost in schizophrenia. Furthermore, Frith has predicted that the extent of mind-blindness depends on whether the objective/behavioural or subjective symptoms of ToM abilities prevail. Patients with the behavioural symptoms perform the poorest in ToM tasks, similar to autistic subjects, while patients displaying subjective/experiential symptoms have a ToM. However, these patients are impaired in using contextual information to infer what these mental states are.

Although many researchers believe dyscalculia to be a persistent disorder, evidence on the persistence of dyscalculia remains mixed. For instance, in a study done by Mazzocco and Myers (2003), researchers evaluated children on a slew of measures and selected their most consistent measure as their best diagnostic criterion: a stringent 10th-percentile cut-off on the TEMA-2. Even with their best criterion, they found dyscalculia diagnoses for children longitudinally did not persist; only 65% of students who were ever diagnosed over the course of four years were diagnosed for at least two years. The percentage of children who were diagnosed in two consecutive years was further reduced. It is unclear whether this was the result of misdiagnosed children improving in mathematics and spatial awareness as they progressed as normal, or that the subjects who showed improvement were accurately diagnosed, but exhibited signs of a non-persistent learning disability.

Cognitive symptoms from steroids appear within the first few weeks of treatment, appear to be dose dependent, and may or may not be accompanied by steroid psychosis or other Cushing's-type symptoms.

The symptoms include deficits in

- verbal and non-verbal memory

- working memory

- attention

- sustained concentration

- executive function

- psychomotor speed

- academic or occupational performance.

These symptoms have been shown to improve within months to a year after discontinuing glucocorticoid medication, but residual impairments following prolonged steroid use can remain.

Deficits in any area of information processing can manifest in a variety of specific learning disabilities. It is possible for an individual to have more than one of these difficulties. This is referred to as comorbidity or co-occurrence of learning disabilities. In the UK, the term "dual diagnosis" is often used to refer to co-occurrence of learning difficulties.

The Fregoli delusion, or the delusion of doubles, is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know.

The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras delusion, psychiatrists believe it is related to a breakdown in normal face perception.

Research on subtypes of dyscalculia has begun without consensus; preliminary research has focused on comorbid learning disorders as subtyping candidates. The most common comorbidity in individuals with dyscalculia is dyslexia. Most studies done with comorbid samples versus dyscalculic-only samples have shown different mechanisms at work and additive effects of comorbidity, indicating that such subtyping may not be helpful in diagnosing dyscalculia. But there is variability in results at present.

Due to high comorbidity with other disabilities such as dyslexia and ADHD, some researchers have suggested the possibility of subtypes of mathematical disabilities with different underlying profiles and causes. Whether a particular subtype is specifically termed "dyscalculia" as opposed to a more general mathematical learning disability is somewhat under debate in the scientific literature.

- Semantic memory: This subtype often coexists with reading disabilities such as dyslexia and is characterized by poor representation and retrieval from long-term memory. These processes share a common neural pathway in the left angular gyrus, which has been shown to be selective in arithmetic fact retrieval strategies and symbolic magnitude judgments. This region also shows low functional connectivity with language-related areas during phonological processing in adults with dyslexia. Thus, disruption to the left angular gyrus can cause both reading impairments and difficulties in calculation. This has been observed in individuals with Gerstmann syndrome, of which dyscalculia is one of constellation of symptoms.

- Procedural concepts: Research by Geary has shown that in addition to increased problems with fact retrieval, children with math disabilities may rely on immature computational strategies. Specifically, children with mathematical disabilities showed poor command of counting strategies unrelated to their ability to retrieve numeric facts. This research notes that it is difficult to discern whether poor conceptual knowledge is indicative of a qualitative deficit in number processing or simply a delay in typical mathematical development.

- Working memory: Studies have found that children with dyscalculia showed impaired performance on working memory tasks compared to neurotypical children. Furthermore, research has shown that children with dyscalculia have weaker activation of the intraparietal sulcus during visuospatial working memory tasks. Brain activity in this region during such tasks has been linked to overall arithmetic performance, indicating that numerical and working memory functions may converge in the intraparietal sulcus. However, working memory problems are confounded with domain-general learning difficulties, thus these deficits may not be specific to dyscalculia but rather may reflect a greater learning deficit. Dysfunction in prefrontal regions may also lead to deficits in working memory and other executive function, accounting for comorbidity with ADHD.

Studies have also shown indications of causes due to congenital or hereditary disorders, but evidence of this is not yet concrete.

Agnosia is the inability to recognize certain objects, persons or sounds. Agnosia is typically caused by damage to the brain (most commonly in the occipital or parietal lobes) or from a neurological disorder. Treatments vary depending on the location and cause of the damage. Recovery is possible depending on the severity of the disorder and the severity of the damage to the brain. Many more specific types of agnosia diagnoses exist, including: associative visual agnosia, astereognosis, auditory agnosia, auditory verbal agnosia, prosopagnosia, simultanagnosia, topographical disorientation, visual agnosia etc.

Signs and symptoms of Fregoli's:

- delusions

- visual memory deficit

- deficit in self-monitoring

- deficit in self-awareness

- hallucinations

- deficit in executive functions

- deficit in cognitive flexibility

- history of seizure activity

- epileptogenic activity

Sensory dysfunction disorder is a reported neurological disorder of information processing, characterized by difficulty in understanding and responding appropriately to sensory inputs. Sensory dysfunction disorder is not recognized by the American Medical Association. "Sensory processing (SP) difficulties have been reported in as many as 95% of children with autism, however, empirical research examining the existence of specific patterns of SP difficulties within this population is scarce."

The brain receives messages from the body's sensory systems, which informs the brain of what is going on around and to a person's body. If one or more of these systems become overstimulated, it may result in what is known as Sensory Dysfunction Disorder. An example of a response to overstimulation is expressed by A. Jean Ayres, in "Sensory Integration and the Child: Understanding Hidden Sensory Challenges". She writes, "When the flow of sensations is disorganized, life can be like a rush-hour traffic jam” (p. 289). The following sensory systems are broken down into individual categories to better understand the impact a sensitivity can have on an individual.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.