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.

Stimulants are typically formulated in fast and slow-acting as well as short and long-acting formulations. The fast-acting amphetamine mixed salts (Adderall) and its derivatives, with short and long-acting formulations bind to the trace amine associated receptor and triggers the release of dopamine into the synaptic cleft. They may have a better cardiovascular disease profile than methylphenidate and potentially better tolerated.

The fast-acting methylphenidate (Ritalin), is a dopamine reuptake inhibitor. In the short term, methylphenidate is well tolerated. However, long term studies have not been conducted in adults and concerns about increases in blood pressure have not been established.

The slow and long-acting nonstimulant atomoxetine (Strattera), is primarily a norepinephrine reuptake inhibitor and, to a lesser extent, a dopamine reuptake inhibitor. It may be more effective for those with predominantly inattentive concentration. It is sometimes prescribed in adults who do not get enough vigilant concentration response from mixed amphetamine salts (Adderall) or get too many side effects. It is also approved for ADHD by the US Food and Drug Administration.

The use of cholinergic adjunctive medications is uncommon and their clinical effects are poorly researched; consequently, cholinergics such as galantamine or varenicline would be off label use for ADHD. New nicotinic cholinergic medications in development for ADHD are pozanicline, ABT-418, and .

Cognitive-behavioural therapy (CBT) is a frequently suggested treatment for executive dysfunction, but has shown limited effectiveness. However, a study of CBT in a group rehabilitation setting showed a significant increase in positive treatment outcome compared with individual therapy. Patients' self-reported symptoms on 16 different ADHD/executive-related items were reduced following the treatment period.

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.

Although ADHD has most often been treated with medication, medications do not cure ADHD. They are used solely to treat the symptoms associated with this disorder and the symptoms will come back once the medication stops.

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.

There is no cure for the condition. Management is through therapy.

The current treatments for CCAS focus on relieving the symptoms. One treatment is a cognitive-behavioral therapy (CBT) technique that involves making the patient aware of his or hers cognitive problems. For example, many CCAS patients struggle with multitasking. With CBT, the patient would have to be aware of this problem and focus on just one task at a time. This technique is also used to relieve some motor symptoms. In a case study with a patient who had a stroke and developed CCAS, improvements in mental function and attention were achieved through reality orientation therapy and attention process training. Reality orientation therapy consists of continually exposing the patient to stimuli of past events, such as photos. Attention process training consists of visual and auditory tasks that have been shown to improve attention. The patient struggled in applying these skills to “real-life” situations. It was the help of his family at home that significantly helped him regain his ability to perform activities of daily living. The family would motivate the patient to perform basic tasks and made a regular schedule for him to follow.

Transcranial magnetic stimulation (TMS) has also been proposed to be a possible treatment of psychiatric disorders of the cerebellum. One study used TMS on the vermis of patients with schizophrenia. After stimulation, the patients showed increased happiness, alertness and energy, and decreased sadness. Neuropsychological testing post-stimulation showed improvements in working memory, attention, and visual spatial skill. Another possible method of treatment for CCAS is doing exercises that are used to relieve the motor symptoms. These physical exercises have been shown to also help with the cognitive symptoms.

Medications that help relieve deficits in traumatic brain injuries in adults have been proposed as candidates to treat CCAS. Bromocriptine, a direct D2 agonist, has been shown to help with deficits in executive function and spatial learning abilities. Methylphendiate has been shown to help with deficits in attention and inhibition. Neither of these drugs has yet been tested on a CCAS population. It may also be that some of the symptoms of CCAS improve over time without any formal treatment. In the original report of CCAS, four patients with CCAS were re-examined one to nine months after their initial neuropsychological evaluation. Three of the patients showed improvement in deficits without any kind of formal treatment, though executive function was still found to be one standard deviation below average. In one patient, the deficits worsened over time. This patient had cerebellar atrophy and worsened in visual spatial abilities, concept formation, and verbal memory. It should be noted that none of these treatments were tested on a large enough sample to determine if they would help with the general CCAS population. Further research needs to be done on treatments for CCAS.

No medications directly treat the core symptoms of AS. Although research into the efficacy of pharmaceutical intervention for AS is limited, it is essential to diagnose and treat comorbid conditions. Deficits in self-identifying emotions or in observing effects of one's behavior on others can make it difficult for individuals with AS to see why medication may be appropriate. Medication can be effective in combination with behavioral interventions and environmental accommodations in treating comorbid symptoms such as anxiety disorder, major depressive disorder, inattention and aggression. The atypical antipsychotic medications risperidone and olanzapine have been shown to reduce the associated symptoms of AS; risperidone can reduce repetitive and self-injurious behaviors, aggressive outbursts and impulsivity, and improve stereotypical patterns of behavior and social relatedness. The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine, and sertraline have been effective in treating restricted and repetitive interests and behaviors.

Care must be taken with medications, as side effects may be more common and harder to evaluate in individuals with AS, and tests of drugs' effectiveness against comorbid conditions routinely exclude individuals from the autism spectrum. Abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications, along with serious long-term neurological side effects. SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression, and sleep disturbance. Weight gain and fatigue are commonly reported side effects of risperidone, which may also lead to increased risk for extrapyramidal symptoms such as restlessness and dystonia and increased serum prolactin levels. Sedation and weight gain are more common with olanzapine, which has also been linked with diabetes. Sedative side-effects in school-age children have ramifications for classroom learning. Individuals with AS may be unable to identify and communicate their internal moods and emotions or to tolerate side effects that for most people would not be problematic.

Reactive strategies include:

- Redirection: distracting the person by offering another activity, or changing the topic of conversation. Offer the person a choice of 2 or 3 things, but no more than 3, because this can be overwhelming. In offering a choice, make sure to pause to allow the person time to process the information and give a response.

- Talking to the person and finding out what the problem is

- Working out what the person's behaviour is trying to communicate

- Crisis management

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.

Positive Behaviour Support (PBS) is a treatment approach that looks at the best way to work with each individual with disabilities. A behavioural therapist conducts a functional analysis of behaviour which helps to determine ways to improve the quality of life for the person and does not just deal with problem behaviour.

PBS also acknowledges the needs of support staff and includes strategies to manage crises when they arise. The following model is a brief guide to staff to remind them of key things to think about when planning support for a person with disabilities. There are two main objectives: reacting situationally when the behaviour occurs, and then acting proactively to prevent the behaviour from occurring.

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

Some of these treatments (for example, sensorimotor handling) have a questionable rationale and no empirical evidence. Other treatments (for example, prism lenses, physical exercise, and auditory integration training) have had studies with small positive outcomes, but few conclusions can be made about them due to methodological problems with the studies.

Although replicable treatments have been described and valid outcome measures are known, gaps exist in knowledge related to sensory integration dysfunction and therapy.

Empirical support is limited, therefore systematic evaluation is needed if these interventions are used.

Children with hypo-reactivity may be exposed to strong sensations such as stroking with a brush, vibrations or rubbing. Play may involve a range of materials to stimulate the senses such as play dough or finger painting.

Children with hyper-reactivity may be exposed to peaceful activities including quiet music and gentle rocking in a softly lit room. Treats and rewards may be used to encourage children to tolerate activities they would normally avoid.

While occupational therapists using a sensory integration frame of reference work on increasing a child's ability to adequately process sensory input, other OTs may focus on environmental accommodations that parents and school staff can use to enhance the child's function at home, school, and in the community. These may include selecting soft, tag-free clothing, avoiding fluorescent lighting, and providing ear plugs for "emergency" use (such as for fire drills).

Dietary modifications may be of benefit to a small proportion of children with ADHD. A 2013 meta-analysis found less than a third of children with ADHD see some improvement in symptoms with free fatty acid supplementation or decreased eating of artificial food coloring. These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications. This review also found that evidence does not support removing other foods from the diet to treat ADHD. A 2014 review found that an elimination diet results in a small overall benefit. A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is discouraged. Iron, magnesium and iodine may also have an effect on ADHD symptoms. There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD. In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD. However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD. There is evidence of a modest benefit of omega 3 fatty acid supplementation, but it is not recommended in place of traditional medication.

There is no cure for neurocognitive disorder or the diseases that cause it. Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to maintain a better quality of life for everyone involved. Speech therapy has been shown to help with language impairment.

Studies suggest that diets with high Omega 3 content, low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such a newly developed “computerized brain training programs” can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence, the ability to adapt and deal with new problems or challenges the first time encountered, and in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information. If it is caused by an underlying cause such as Alzheimer's disease or infections, the cause may be treated but the amnesia may not be.

The ideal treatment for AS coordinates therapies that address core symptoms of the disorder, including poor communication skills and obsessive or repetitive routines. While most professionals agree that the earlier the intervention, the better, there is no single best treatment package. AS treatment resembles that of other high-functioning ASDs, except that it takes into account the linguistic capabilities, verbal strengths, and nonverbal vulnerabilities of individuals with AS. A typical program generally includes:

- A positive behavior support procedure includes training and support of parents and school faculty in behavior management strategies to use in the home and school;

- An applied behavior analysis (ABA) technique called social skills training for more effective interpersonal interactions;

- Cognitive behavioral therapy to improve stress management relating to anxiety or explosive emotions and to cut back on obsessive interests and repetitive routines;

- Medication, for coexisting conditions such as major depressive disorder and anxiety disorder;

- Occupational or physical therapy to assist with poor sensory processing and motor coordination;

- Social communication intervention, which is specialized speech therapy to help with the pragmatics of the give and take of normal conversation.

Of the many studies on behavior-based early intervention programs, most are case reports of up to five participants and typically examine a few problem behaviors such as self-injury, aggression, noncompliance, stereotypies, or spontaneous language; unintended side effects are largely ignored. Despite the popularity of social skills training, its effectiveness is not firmly established. A randomized controlled study of a model for training parents in problem behaviors in their children with AS showed that parents attending a one-day workshop or six individual lessons reported fewer behavioral problems, while parents receiving the individual lessons reported less intense behavioral problems in their AS children. Vocational training is important to teach job interview etiquette and workplace behavior to older children and adults with AS, and organization software and personal data assistants can improve the work and life management of people with AS.

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.

Stimulant medications are the pharmaceutical treatment of choice. They have at least some effect on symptoms in the short term in about 80% of people. Methylphenidate appears to improve symptoms as reported by teachers and parents. Stimulants may also reduce the risk of unintentional injuries in children with ADHD.

There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives, or added to stimulant therapy. There are no good studies comparing the various medications; however, they appear more or less equal with respect to side effects. Stimulants appear to improve academic performance while atomoxetine does not. Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use. There is little evidence on the effects of medication on social behaviors. , the long-term effects of ADHD medication have yet to be fully determined. Magnetic resonance imaging studies suggest that long-term treatment with amphetamine or methylphenidate decreases abnormalities in brain structure and function found in subjects with ADHD.

Guidelines on when to use medications vary by country, with the United Kingdom's National Institute for Health and Care Excellence recommending use for children only in severe cases, though for adults medication is a first-line treatment, while most United States guidelines recommend medications in most age groups. Medications are not recommended for preschool children. Underdosing of stimulants may occur and result in a lack of response or later loss of effectiveness. This is particularly common in adolescents and adults as approved dosing is based on school-aged children, causing some practitioners to use weight based or benefit based off-label dosing instead.

While stimulants and atomoxetine are usually safe, there are side-effects and contraindications to their use. A large overdose on ADHD stimulants is commonly associated with symptoms such as stimulant psychosis and mania; although very rare, at therapeutic doses these events appear to occur in approximately 0.1% of individuals within the first several weeks after starting amphetamine or methylphenidate therapy. Administration of an antipsychotic medication has been found to effectively resolve the symptoms of acute amphetamine psychosis. Regular monitoring has been recommended in those on long-term treatment. Stimulant therapy should be stopped periodically to assess continuing need for medication, decrease possible growth delay, and reduce tolerance. Long-term misuse of stimulant medications at doses above the therapeutic range for ADHD treatment is associated with addiction and dependence. Untreated ADHD, however, is also associated with elevated risk of substance use disorders and conduct disorders. The use of stimulants appears to either reduce this risk or have no effect on it. The safety of these medications in pregnancy is unclear.

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.

Glucocorticoid medications have been known to be associated with significant side effects involving behavior and mood, regardless of previous psychiatric or cognitive condition, since the early 1950s. But cognitive side effects of steroid medications involving memory and attention are not as widely publicized and may be misdiagnosed as separate conditions, such as attention deficit disorder (ADHD or ADD) in children or early Alzheimer's disease in elderly patients.

Since the underlying cause of the disorder is damage to the brain, at present ideational apraxia is not reversible. However, Occupational or Physical Therapy may be able to slow the progression and help patients regain some functional control, with the treatment approach being the same as that of ideomotor apraxia. Some recovery may occur in younger patients after stroke, because brain plasticity may allow the functions of these damaged regions to be remapped. As patients develop new behaviors to cope with their apraxia, their brain's functioning neurons may take on some of the functions of the dead or damaged regions.

In the context of dementia, apraxia is a major cause of morbidity, and progresses with the underlying disease sometimes to the extent that patients may be unable to feed themselves or use simple utensils. Patients often become highly dependent or require nursing home placement because of their inability to properly use objects.

Brain imaging techniques such as fMRI, EEG, and PET scans may help in understanding the neuroanatomical and computational basis of ideational apraxia. Understanding these mechanisms is likely to be crucial in developing new modes of therapy to help patients cope with their disorder.

Aside from discontinuation of glucocorticoid medication, potential treatments discussed in the research literature include:

- anti-glucocorticoids

- psychoactive drugs that up-regulate the GRII glucocorticoid receptor:

- tricyclic antidepressants: Desipramine, Imipramine, and Amitriptyline (SSRIs do not )

- serotonin antagonists: Ketanserin

- mood stabilizers: Lithium

- corticotropin-releasing hormone (CRH) antagonists

- glutamate antagonists

- dehydroepiandrosterone (DHEA)

- small molecule brain-derived neurotrophic factor (BDNF) analogs

- stress reduction therapies and exercise.

LBLD can be an enduring problem. Some people might experience overlapping learning disabilities that make improvement problematic. Others with single disabilities often show more improvement. Most subjects can achieve literacy via coping mechanisms and education.

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.