DAMP—deficits in attention, motor control and perception—is a controversial psychiatric concept conceived by Christopher Gillberg.

DAMP is similar to minimal brain dysfunction (MBD), a concept that was formulated in the 1960s. Both concepts are related to certain psychiatric conditions, such as hyperactivity. The concept of MBD was strongly criticized by Sir Michael Rutter [Gillberg, 2003, p. 904] and several other researchers, and this led to its abandonment in the 1980s. At the same time, research showed that something similar was needed. One alternative concept was ADHD (Attention-Deficit Hyperactivity Disorder). Gillberg proposed another alternative: DAMP. Gillberg's concept was formulated in the early 1980s, and the term itself was introduced in a paper that Gillberg published in 1986 (see Gillberg [1986]). (DAMP is essentially MBD without the etiological assumptions.)

The concept of DAMP met with considerable criticism. For example, Sir Michael Rutter stated that the concept of DAMP (unlike ADHD) was "muddled" and "lacks both internal coherence and external discriminative validity ... it has no demonstrated treatment or prognostic implications"; he concluded that the concept should be abandoned. Another example is the criticism of Per-Anders Rydelius, Professor of Child Psychiatry at the Karolinska Institute, who argued that the definition of DAMP was too vague: "the borderline between DAMP and conduct disorders [is] unclear ... the borderline between DAMP and ADHD [is] unclear"; he concluded that "the concept is in need of revision". And in 2000, Eva Kärfve, a sociologist at the University of Lund, published a book which argued that Gillberg's work on DAMP should be rejected.

Perhaps the strongest criticism of DAMP is that Gillberg and his co-workers in Gothenburg are almost the only people doing research on DAMP. Indeed, in a review of DAMP published by Gillberg in 2003, it was noted that there were only "about 50" research papers that had been published on DAMP and that the "vast majority of these have either originated in the author's own clinical and research setting or have been supervised and/or co-authored by him" [Gillberg, 2003, p. 904]. This is in contrast to ADHD, on which "several thousand papers" had been published [Gillberg, 2003, p. 905]. As far as clinical practice goes, DAMP has been primarily accepted only in Gillberg's native Sweden and in Denmark [Gillberg, 2003, p. 904], and even in those countries acceptance is mixed.

In 2003, Gillberg revised his definition of DAMP. The new definition is as follows:

1. ADHD as defined in DSM-IV;

2. Developmental Coordination Disorder (DCD) as defined in DSM-IV;

3. condition not better accounted for by cerebral palsy; and

4. IQ should be higher than about 50 [Gillberg, 2003: box 1]. (In the WHO system, this would be a hyperkinetic disorder combined with a developmental disorder of motor function.) About half of children with ADHD are believed to also have DCD [Gillberg, 2003; Martin et al., 2006].

Strong criticism of DAMP, however, has continued. In particular, it has been observed that "the validity and utility of DAMP will remain unclear until stronger evidence of the special status of the overlap between its constituent disorders is provided".

In 2005, there was an hour-long television program broadcast on Swedish TV, questioning why Sweden, almost alone in the world, would accept the DAMP construct. The program featured critical commentary from Sir Michael Rutter. It also considered some of the controversies over Gillberg's Gothenburg study.

The concept of DAMP (deficits in attention, motor control, and perception) has been in clinical use in Scandinavia for about 20 years. DAMP is diagnosed on the basis of concomitant attention deficit/hyperactivity disorder and developmental coordination disorder in children who do not have severe learning disability or cerebral palsy. In clinically severe form it affects about 1.5% of the general population of school age children; another few per cent are affected by more moderate variants. Boys are overrepresented; girls are currently probably underdiagnosed. There are many comorbid problems/overlapping conditions, including conduct disorder, depression/anxiety, and academic failure. There is a strong link with autism spectrum disorders in severe DAMP. Familial factors and pre- and perinatal risk factors account for much of the variance. Psychosocial risk factors appear to increase the risk of marked psychiatric abnormality in DAMP. Outcome in early adult age was psychosocially poor in one study in almost 60% of unmedicated cases. There are effective interventions available for many of the problems encountered in DAMP.

Developmental coordination disorder is a lifelong neurological condition that is more common in males than in females, with a ratio of approximately four males to every female. The exact proportion of people with the disorder is unknown since the disorder can be difficult to detect due to a lack of specific laboratory tests, thus making diagnosis of the condition one of elimination of all other possible causes/diseases. Approximately 5–6% of children are affected by this condition.

It is estimated that up to 16.5% of elementary school aged children present elevated SOR behaviors in the tactile or auditory modalities. However, this figure might represent an underestimation of Sensory Over Responsivity prevalence, since this study did not include children with developmental disorders or those delivered preterm, who are more likely to present it.

This figure is, nonetheless, larger than what previous studies with smaller samples had shown: an estimate of 5–13% of elementary school aged children.

Incidence for the remaining subtypes is currently unknown.

In some cases, children who enjoy learning may develop a sense of fear when faced with structured or planned work, especially long or group-based assignments that require extended focus, even if they thoroughly understand the topic. Children with ADHD may be at greater risk of academic failures and early withdrawal from school. Teachers and parents may make incorrect assumptions about the behaviours and attitudes of a child with ADHD-PI, and may provide them with frequent and erroneous negative feedback (e.g. "careless", "you're irresponsible", "you're immature", "you're lazy", "you don't care/show any effort", "you just aren't trying", etc.).

The inattentive children may realize on some level that they are somehow different internally from their peers. However, they are also likely to accept and internalize the continuous negative feedback, creating a negative self-image that becomes self-reinforcing. If these children progress into adulthood undiagnosed or untreated, their inattentiveness, ongoing frustrations, and poor self-image frequently create numerous and severe problems maintaining healthy relationships, succeeding in postsecondary schooling, or succeeding in the workplace. These problems can compound frustrations and low self-esteem, and will often lead to the development of secondary pathologies including anxiety disorders, mood disorders, and substance abuse.

It has been suggested that some of the symptoms of ADHD present in childhood appear to be less overt in adulthood. This is likely due to an adult's ability to make cognitive adjustments and develop compensating or coping skills to minimize the impact of inattentive or hyperactive symptoms. However, the core problems of ADHD do not disappear with age. Some researchers have suggested that individuals with reduced or less overt hyperactivity symptoms should receive the ADHD-combined diagnosis. Hallowell and Ratey (2005) suggest that the manifestation of hyperactivity simply changes with adolescence and adulthood, becoming a more generalized restlessness or tendency to fidget.

Because comorbid conditions are common with sensory integration issues, a person may have other conditions as well. People who receive the diagnosis of sensory processing disorder may also have signs of anxiety problems, ADHD, food intolerances, behavioral disorders and other disorders.

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.

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.

Neurodevelopmental disorders are in their multitude associated with widely varying degrees of difficulty, depending on which there are different degrees of mental, emotional, physical, and economic consequences for individuals, and in turn families, groups and society.

There is some evidence that children with AS may see a lessening of symptoms; up to 20% of children may no longer meet the diagnostic criteria as adults, although social and communication difficulties may persist. As of 2006, no studies addressing the long-term outcome of individuals with Asperger syndrome are available and there are no systematic long-term follow-up studies of children with AS. Individuals with AS appear to have normal life expectancy, but have an increased prevalence of comorbid psychiatric conditions, such as major depressive disorder and anxiety disorder that may significantly affect prognosis. Although social impairment may be lifelong, the outcome is generally more positive than with individuals with lower functioning autism spectrum disorders; for example, ASD symptoms are more likely to diminish with time in children with AS or HFA. Most students with AS/HFA have average mathematical ability and test slightly worse in mathematics than in general intelligence, but some are gifted in mathematics. AS has potentially been linked to some accomplishments, such as Vernon L. Smith winning the Nobel Memorial Prize in Economic Sciences; however, Smith is self-diagnosed.

Although many attend regular education classes, some children with AS may utilize special education services because of their social and behavioral difficulties. Adolescents with AS may exhibit ongoing difficulty with self care or organization, and disturbances in social and romantic relationships. Despite high cognitive potential, most young adults with AS remain at home, yet some do marry and work independently. The "different-ness" adolescents experience can be traumatic. Anxiety may stem from preoccupation over possible violations of routines and rituals, from being placed in a situation without a clear schedule or expectations, or from concern with failing in social encounters; the resulting stress may manifest as inattention, withdrawal, reliance on obsessions, hyperactivity, or aggressive or oppositional behavior. Depression is often the result of chronic frustration from repeated failure to engage others socially, and mood disorders requiring treatment may develop. Clinical experience suggests the rate of suicide may be higher among those with AS, but this has not been confirmed by systematic empirical studies.

Education of families is critical in developing strategies for understanding strengths and weaknesses; helping the family to cope improves outcomes in children. Prognosis may be improved by diagnosis at a younger age that allows for early interventions, while interventions in adulthood are valuable but less beneficial. There are legal implications for individuals with AS as they run the risk of exploitation by others and may be unable to comprehend the societal implications of their actions.

In addition to genetics, some environmental factors might play a role in causing ADHD. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.

Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71). There is an association between long term but not short term use of acetaminophen during pregnancy and ADHD. At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage.

Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms but the evidence is weak and may only apply to children with food sensitivities. The United Kingdom and the European Union have put in place regulatory measures based on these concerns. In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.

Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.

Most ADHD cases are of unknown causes. It is believed to involve interactions between genetics, the environment, and social factors. Certain cases are related to previous infection of or trauma to the brain.

Neurocognitive disorders can have numerous causes: genetics, brain trauma, stroke, and heart issues. The main causes are neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease because they affect or deteriorate brain functions. Other diseases and conditions that cause NDCs include vascular dementia, frontotemporal degeneration, Lewy body disease, prion disease, normal pressure hydrocephalus, and dementia/neurocognitive issues due to HIV infection. They may also include dementia due to substance abuse or exposure to toxins.

Neurocongnitive disorder may also be caused by brain trauma, including concussions and Traumatic Brain Injuries, as well as post-traumatic stress and alcoholism. This is referred to as amnesia, and is characterized by damage to major memory encoding parts of the brain such as the hippocampus. Difficulty creating recent term memories is called anterograde amnesia and is caused by damage to the hippocampus part of the brain, which is a major part of the memory process. Retrograde amnesia is also caused by damage to the hippocampus, but the memories that were encoded or in the process of being encoded in long term memory are erased

Developmental coordination disorder is classified (by doctors) in the fifth revision of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5) as a motor disorder, in the category of neurodevelopmental disorders.

Systemic infections can result in neurodevelopmental consequences, when they occur in infancy and childhood of humans, but would not be called a primary neurodevelopmental disorder per se, as for example HIV Infections of the head and brain, like brain abscesses, meningitis or encephalitis have a high risk of causing neurodevelopmental problems and eventually a disorder. For example, measles can progress to subacute sclerosing panencephalitis.

A number of infectious diseases can be transmitted either congenitally (before or at birth), and can cause serious neurodevelopmental problems, as for example the viruses HSV, CMV, rubella (congenital rubella syndrome), Zika virus, or bacteria like "Treponema pallidum" in congenital syphilis, which may progress to neurosyphilis if it remains untreated. Protozoa like "Plasmodium" or "Toxoplasma" which can cause congenital toxoplasmosis with multiple cysts in the brain and other organs, leading to a variety of neurological deficits.

Some cases of schizophrenia may be related to congenital infections though the majority are of unknown causes.

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.

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.

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

Frequency estimates vary enormously. In 2015 it was estimated that 37.2 million people globally are affected. A 2003 review of epidemiological studies of children found autism rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1; combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000. Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari "et al.", and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria. Females with autism spectrum disorders may be underdiagnosed.

Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%. Reports have associated AS with medical conditions such as aminoaciduria and ligamentous laxity, but these have been case reports or small studies and no factors have been associated with AS across studies. One study of males with AS found an increased rate of epilepsy and a high rate (51%) of nonverbal learning disorder. AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive–compulsive disorder and obsessive–compulsive personality disorder. However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common.

Cerebellar cognitive affective syndrome (CCAS), also called "Schmahmann's syndrome" is a condition that follows from lesions (damage) to the cerebellum of the brain. This syndrome, described by Dr. Jeremy Schmahmann and his colleagues refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

Language delays are the most frequent developmental delays, and can occur for many reasons. A delay can be due to being a “late bloomer,” or a more serious problem. The most common causes of speech delay include

- Hearing loss

- Slow development

- Intellectual Disability

Such delays can occur in conjunction with a lack of mirroring of facial responses, unresponsiveness or unawareness of certain noises, a lack of interest in playing with other children or toys, or no pain response to stimuli.

Other causes include:

- Psychosocial deprivation - The child doesn't spend enough time talking with adults. Research on early brain development shows that babies and toddlers have a critical need for direct interactions with parents and other significant care givers for healthy brain growth and the development of appropriate social, emotional, and cognitive skills.

- Television viewing is associated with delayed language development. Children who watched television alone were 8.47 times more likely to have language delay when compared to children who interacted with their caregivers during television viewing. As recommended by the American Academy of Pediatrics (AAP), children under the age of 2 should watch no television at all, and after age 2 watch no more than one to two hours of quality programming a day. Therefore, exposing such young children to television programs should be discouraged. Parents should engage children in more conversational activities to avoid television-related delays to their children language development, which could impair their intellectual performance.

- Stress during pregnancy is associated with language delay.

- Being a twin

- Attention deficit hyperactivity disorder

- Autism (a developmental disorder) - There is strong evidence that autism is commonly associated with language delay. Asperger syndrome, which is on the autistic spectrum, however, is not associated with language delay.

- Selective mutism (the child just doesn't want to talk)

- Cerebral palsy (a movement disorder caused by brain damage)

- Genetic abnormalities - In 2005, researchers found a connection between expressive language delay and a genetic abnormality: a duplicate set of the same genes that are missing in sufferers of Williams-Beuren syndrome. Also so called XYY syndrome can often cause speech delay.

- Correlation with male sex, previous family history, and maternal education has been demonstrated.

Delirium can be caused by the worsening of previous medical conditions, substance abuse or withdrawal, mental illness, severe pain, immobilization, sleep deprivation and hypnosis.

Other common causes that may increase the risk of delirium include infections of urinary tract, skin and stomach, pneumonia, old age, and poor nutrition.

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.

Studies have failed to find clear evidence that language delay can be prevented by training or educating health care professionals in the subject. Overall, some of the reviews show positive results regarding interventions in language delay, but are not curative. (Commentary - Early Identification of Language Delays, 2005)

Ideational apraxia (IA) is a neurological disorder which explains the loss of ability to conceptualize, plan, and execute the complex sequences of motor actions involved in the use of tools or otherwise interacting with objects in everyday life. Ideational apraxia is a condition in which an individual is unable to plan movements related to interaction with objects, because he has lost the perception of the object's purpose. Characteristics of this disorder include a disturbance in the concept of the sequential organization of voluntary actions. The patient appears to have lost the knowledge or thought of what an object represents. This disorder was first seen 100 years ago by Doctor Arnold Pick, who described a patient who appeared to have lost their ability to use objects. The patient would make errors such as combing their hair with the wrong side of the comb or placing a pistol in his mouth. From that point on, several other

researchers and doctors have stumbled upon this unique disorder. IA has been described under several names such as, agnosia of utilization, conceptual apraxia or loss of knowledge about the use of tools, or semantic amnesia of tool usage. The term apraxia was first created by Steinthal in 1871 and was then applied by Gogol, Kusmaul, Star, and Pick to patients who failed to pantomime the use of tools. It was not until the 1900s, when Liepmann refined the definition, that it specifically described disorders that involved motor planning, rather than disturbances in the patient’s visual perception, language, or symbolism.