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.

ADHD-PI is an attention-concentration deficit that has everything in common with other forms of ADHD except that it has fewer hyperactivity or impulsivity symptoms and has more directed attention fatigue symptoms.

Different countries have used different ways of diagnosing ADHD-PI. In the United Kingdom, diagnosis is based on quite a narrow set of symptoms, and about 0.5–1% of children are thought to have attention or hyperactivity problems.

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 DSM-5 allows for diagnosis of the "predominantly inattentive" presentations of ADHD (code 314.00) if the individual presents six or more (five for adults) of the following symptoms of inattention for at least six months to a point that is disruptive and inappropriate for developmental level:

- Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.

- Often has trouble keeping attention on tasks or play activities.

- Often does not seem to listen when spoken to directly.

- Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).

- Often has trouble organizing activities.

- Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period (such as schoolwork or homework).

- Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).

- Is often easily distracted.

- Is often forgetful in daily activities.

An ADHD diagnosis is contingent upon the symptoms of impairment presenting themselves in two or more settings (e.g., at school or work and at home). There must also be clear evidence of clinically significant impairment in social, academic, or occupational functioning. Lastly, the symptoms must not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder, and are not better accounted for by another mental disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, personality disorder).

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.

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.

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.

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).

In psychology, disinhibition is a lack of restraint manifested in disregard for social conventions, impulsivity, and poor risk assessment. Disinhibition affects motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms similar to the diagnostic criteria for mania. Hypersexuality, hyperphagia, and aggressive outbursts are indicative of disinhibited instinctual drives.

SAD is a type of major depressive disorder, and sufferers may exhibit any of the associated symptoms, such as feelings of hopelessness and worthlessness, thoughts of suicide, loss of interest in activities, withdrawal from social interaction, sleep and appetite problems, difficulty with concentrating and making decisions, decreased sex drive, a lack of energy, or agitation. Symptoms of winter SAD often include oversleeping or difficulty waking up in the morning, nausea, and a tendency to over eat, often with a craving for carbohydrates, which leads to weight gain. SAD is typically associated with winter depression, but springtime lethargy or other seasonal mood patterns are not uncommon. Although each individual case is different, in contrast to winter SAD, people who experience spring and summer depression may be more likely to show symptoms such as insomnia, decreased appetite and weight loss, and agitation or anxiety.

According to Grafman et al. "disinhibition" is a lack of restraint manifested in several ways, affecting motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms e.g. impulsivity, disregard for others and social norms, aggressive outbursts, misconduct and oppositional behaviors, disinhibited instinctual drives including risk taking behaviors and hypersexuality. Disinhibition is a common symptom following brain injury, or lesions, particularly to the frontal lobe and primarily to the orbitofrontal cortex. The neuropsychiatric sequelae following brain injuries could include diffuse cognitive impairment, with more prominent deficits in the rate of information processing, attention, memory, cognitive flexibility, and problem solving. Prominent impulsivity, affective instability, and disinhibition are seen frequently, secondary to injury to frontal, temporal, and limbic areas. In association with the typical cognitive deficits, these sequelae characterize the frequently noted "personality changes" in TBI (Traumatic Brain Injury) patients. Disinhibition syndromes, in brain injuries and insults including brain tumors, strokes and epilepsy range from mildly inappropriate social behavior, lack of control over one's behaviour to the full-blown mania, depending on the lesions to specific brain regions. Several studies in brain traumas and insults have demonstrated significant associations between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices, affecting visuospatial functions, somatosensation, and spatial memory, motoric, instinctive, affective, and intellectual behaviors.

Disinhibition syndromes have also been reported with mania-like manifestations in old age with lesions to the orbito-frontal and basotemporal cortex involving limbic and frontal connections (orbitofrontal circuit), especially in the right hemisphere. Behavioral disinhibition as a result of damage to frontal lobe could be seen as a result of consumption of alcohol and central nervous system depressants drugs, e.g. benzodiazepines that disinhibit the frontal cortex from self-regulation and control. It has also been argued that ADHD, hyperactive/impulsive subtype have a general behavioural disinhibition beyond impulsivity and many morbidities or complications of ADHD, e.g. conduct disorder, anti-social personality disorder. substance abuse and risk taking behaviours are all consequences of untreated behavioural disinhibition.

Seasonal affective disorder (SAD) is a mood disorder subset in which people who have normal mental health throughout most of the year exhibit depressive symptoms at the same time each year, most commonly in the winter. People may sleep too much or have little energy. The condition in the summer can include heightened anxiety.

In the "Diagnostic and Statistical Manual of Mental Disorders" DSM-IV and DSM-5, its status was changed. It is no longer classified as a unique mood disorder but is now a specifier, called "with seasonal pattern", for recurrent major depressive disorder that occurs at a specific time of the year and fully remits otherwise. Although experts were initially skeptical, this condition is now recognized as a common disorder. SAD's highlighting of the disparity in people's moods at different points in the year, and the differing climates in which these discrepancies are measured, therefore advocates the importance of perceiving climate change as an immediate threat to people's mental health, both psychologically and psycho-socially.

SAD in the United States affects from 1.4% in Florida to 9.9% in Alaska. SAD was formally described and named in 1984 by Norman E. Rosenthal and colleagues at the National Institute of Mental Health. The validity of SAD has been questioned by a 2016 analysis by the Center for Disease Control, in which no links were detected between depression and seasonality or sunlight exposure.

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.

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 the mental health field, schizophasia or word salad is language that is confused and often repetitious, symptomatic of various mental illnesses.

It is usually associated with a manic presentation of bipolar affective disorder and other symptoms of serious mental illnesses, such as psychosis, including schizophrenia. It is characterized by an apparently confused usage of words with no apparent meaning or relationship attached to them. In this context, it is considered to be a symptom of a formal thought disorder. In some cases schizophasia can be a sign of asymptomatic schizophrenia; e.g. the question "Why do people believe in God?" could elicit a response consisting of a series of words commonly associated with religion or prayer but strung together with no regard to language rules.

Schizophasia should be contrasted with another symptom of cognitive disruption and cognitive slippage involving certain idiosyncratic arrangements of words. With this symptom, the language may or may not be grammatically correct depending on the severity of the disease and the particular mechanisms which have been impacted by the disease.

The American diagnostic codes, from the "DSM-IV", do not specifically code for this disorder although they include it as a symptom under the diagnosis of schizophrenia.

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

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.

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.

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.

Premorbidity refers to the state of functionality prior to the onset of a disease or illness. It is most often used in relation to psychological function (e.g. premorbid personality or premorbid intelligence), but can also be used in relation to other medical conditions (e.g. premorbid lung function or premorbid heart rate).

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.

Genes are attributed about a third of general anxiety disorder's variance. Individuals with a genetic predisposition for GAD are more likely to develop GAD, especially in response to a life stressor.

Endogenous depression "(melancholia)" is an atypical sub-class of the mood disorder, major depressive disorder (clinical depression). Endogenous depression occurs due to the presence of an internal (cognitive, biological) stressor instead of an external (social, environmental) stressor. Endogenous depression includes patients with treatment-resistant, non-psychotic, major depressive disorder, characterized by abnormal behavior of the endogenous opioid system but not the monoaminergic system. Symptoms vary in severity, type, and frequency and can be attributed to cognitive, social, biological, or environmental factors that result in persistent feelings of sadness and distress. Since symptoms are due to a biological phenomenon, prevalence rates tend to be higher in older adults. Due to this fact, biological-focused treatment plans are often used in therapy to ensure the best prognosis.

The forefront indication a depressive episode is manifesting is the sudden loss of energy or motivation in daily routines. When this occurs, it is not uncommon for individuals to seek medical attention with excessive worrying or anxiety that a more severe, physiological disease may be the underlying issue. However, without an actual disease present, this neurotic thinking often results in severe anxiety, sleep disturbance, and mood swings which may hinder social relationships. Individuals with endogenous depression may experience inconsistencies in symptom severity which is often the reason for delayed treatment. If left untreated, symptoms may progress to a major depressive episode.