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.

An 8-year follow up of children diagnosed with ADHD (combined type) found that they often have difficulties in adolescence, regardless of treatment or lack thereof. In the USA, fewer than 5% of individuals with ADHD get a college degree, compared to 28% of the general population aged 25 years and older. The proportion of children meeting criteria for ADHD drops by about half in the three years following the diagnosis and this occurs regardless of treatments used. ADHD persists into adulthood in about 30–50% of cases. Those affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms. Children with ADHD have a higher risk of unintentional injuries, and greater mortality rates.

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.

The rate in school age children is thought to be about 1.5%, compared with an estimated 5.3% for ADHD.

The prognosis of SCT is unknown. In contrast, much is known about the adolescent and adult outcomes of children having ADHD. Those with SCT symptoms typically show a later onset of their symptoms than do those with ADHD, perhaps by as much as a year or two later on average. They have as much or more difficulty with academic tasks and far fewer social difficulties than do people having ADHD. They do not have the same risks for oppositional defiant disorder, conduct disorder, or social aggression and thus may have different life course outcomes compared to children with ADHD-HI and Combined subtypes who have far higher risks for these other "externalizing" disorders.

However, unlike ADHD, there are no longitudinal studies of children with SCT that can shed light on the developmental course and adolescent or adult outcomes of these individuals.

Hyperkinetic disorder is a psychiatric neurodevelopmental condition emerging in early childhood that features an enduring pattern of severe, developmentally inappropriate symptoms, namely inattention, hyperactivity, and impulsivity across different settings (e.g., home and school) that significantly impair academic, social and work performance. The disorder, which appears in the World Health Organization's ICD-10, is roughly similiar to the "combined presentation" of attention deficit hyperactivity disorder in the American Psychiatric Association's DSM-V.

Hyperkinetic people display disorganized, poorly controlled and excessive activity; they lack perseverance in tasks involving thought and attention, and tend to move from one activity to the next without completing any. They are frequently accident-prone, reckless and impulsive, and may thoughtlessly (rather than defiantly) break rules. Cognitive impairment and delayed language and motor development are more common in this group than in the general population; and they may experience low self-esteem and engage in dissocial behavior as a consequence of the disorder.

While hyperkinetic children are commonly incautious and unreserved with adults, they might be isolated and unpopular with other children.

Unlike ADHD, the general causes of SCT symptoms are almost unknown, though one recent study of twins suggested that the condition appears to be nearly as heritable or genetically influenced in nature as ADHD. That is to say that the majority of differences among individuals in these traits in the population may be due mostly to variation in their genes. The heritability of SCT symptoms in that study was only slightly lower than that for ADHD symptoms with a somewhat greater share of trait variation being due to unique environmental events. For instance, in ADHD, the genetic contribution to individual differences in ADHD traits typically averages between 75 and 80% and may even be as high as 90%+ in some studies. That for SCT may be 50–60%.

Far less is known about SCT yet the symptoms seem to indicate that the posterior attention networks may be more involved in the disorder than the prefrontal cortex region of the brain and difficulties with working memory so prominent in ADHD. This hypothesis gained greater support following a 2015 fMRI-study comparing Inattentive ADHD and SCT-diagnosed patients, which found that the left superior parietal lobule (SPL) showed remarkably decreased activity in SCT-cohorts.

Unlike ADHD in which there exist hundreds of studies on molecular genetics identifying candidate genes that may contribute to the disorder, there are no studies of molecular genetics that specifically evaluated individuals having SCT. Although ADHD appears to be linked to problems with the availability of or sensitivity to dopamine and norepinephrine and the efficiency of the large chemical structures of the specific receptors and re-uptake receptors, the neurotransmitters that may be linked to SCT are unknown.

Recently a study showed a small link between thyroid functioning and SCT symptoms suggesting that thyroid dysfunction is not the cause of SCT. High rates of SCT were observed in children who had suffered prenatal alcohol exposure and in survivors of acute lymphoblastic leukemia, where they were associated with cognitive late effects.

ADHD often precedes the onset of ODD, and approximately half of children with ADHD, Combined Type also have ODD. ODD is a risk factor for CD and frequently precedes the onset of CD symptoms. Children with an early onset of CD symptoms, with at least one symptom before age 10 years, are at risk for more severe and persistent antisocial behavior continuing into adulthood. Youth with early-onset conduct problems are particularly at risk for ASPD (note that an onset of CD prior to age 15 is part of the diagnostic criteria for ASPD), whereas CD is typically limited to adolescence when youth's CD symptoms begin during adolescence.

Externalizing disorders are frequently comorbid or co-occurring with other disorders. Individuals who have the co-occurrence of more than one externalizing disorder have homotypic comorbidity, whereas individuals who have co-occurring externalizing and Internalizing disorders have heterotypic comorbidity. It is not uncommon for children with early externalizing problems to develop both internalizing and further externalizing problems across the lifespan.

The affective spectrum is a spectrum of affective disorders (mood disorders). It is a grouping of related psychiatric and medical disorders which may accompany bipolar, unipolar, and schizoaffective disorders at statistically higher rates than would normally be expected. These disorders are identified by a common positive response to the same types of pharmacologic treatments. They also aggregate strongly in families and may therefore share common heritable underlying physiologic anomalies.

Affective spectrum disorders include:

- Attention deficit hyperactivity disorder

- Bipolar disorder

- Body dysmorphic disorder

- Bulimia nervosa and other eating disorders

- Cataplexy

- Dysthymia

- Generalized anxiety disorder

- Hypersexuality

- Irritable bowel syndrome

- Impulse-control disorders

- Kleptomania

- Migraine

- Major depressive disorder

- Obsessive-compulsive disorder

- Oppositional defiant disorder

- Panic disorder

- Posttraumatic stress disorder

- Premenstrual dysphoric disorder

- Social anxiety disorder

- Fibromyalgia

The following may also be part of the spectrum accompanying affective disorders.

- Chronic pain

- Intermittent explosive disorder

- Pathological gambling

- Personality disorder

- Pyromania

- Substance abuse and addiction (includes alcoholism)

- Trichotillomania

Also, there are now studies linking heart disease.

Many of the terms above overlap. The American Psychiatric Association's definitions of these terms can be found in the "Diagnostic and Statistical Manual of Mental Disorders" (DSM).

Attention deficit hyperactivity disorder is a neurodevelopmental disorder that is characterised by significant levels of hyperactivity, inattentiveness, and impulsiveness. There are three subtypes of ADHD: predominantly inattentive, predominantly hyperactive, and combined (which presents as both hyperactive and inattentive subtypes).

Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the U.S. population. Most people suffering from anxiety disorder report some form of racing thoughts symptom

The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reportings, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.

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.

The scientific study of the causes of developmental disorders involves many different theories. Some of the major differences between these theories involves whether or not environment disrupts normal development, or if abnormalities are pre-determined.

Normal development occurs with a combination of contributions from both the environment and genetics. The theories vary in the part each factor has to play in normal development, thus affecting how the abnormalities are caused.

One theory that supports environmental causes of developmental disorders involves stress in early childhood. Researcher and child psychiatrist Bruce D. Perry, M.D., Ph.D, theorizes that developmental disorders can be caused by early childhood traumatization. In his works he compares developmental disorders in traumatized children to adults with post-traumatic stress disorder, linking extreme environmental stress to the cause of developmental difficulties. Other stress theories suggest that even small stresses can accumulate to result in emotional, behavioral, or social disorders in children.

A 2017 study tested all 20,000 genes in about 4,300 families with children with rare developmental difficulties in the UK and Ireland in order to identify if these difficulties had a genetic cause.They found 14 new developmental disorders caused by spontaneous genetic mutations not found in either parent (such as a fault in the CDK13 gene). They estimated that about one in 300 children are born with spontaneous genetic mutations associated with rare developmental disorders.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

Emotional and behavioral disorders (EBD; sometimes called emotional disturbance or serious emotional disturbance) refer to a disability classification used in educational settings that allows educational institutions to provide special education and related services to students that have poor social or academic adjustment that cannot be better explained by biological abnormalities or a developmental disability.

The classification is often given to students that need individualized behavior supports to receive a free and appropriate public education, but would not be eligible for an individualized education program under another disability category of the Individuals with Disabilities Education Act (IDEA).

PBA is one of the most frequently reported post-stroke behavioral syndromes, with a range of reported prevalence rates from 28% to 52%. The higher prevalence rates tend to be reported in stroke patients who are older and/or who have a history of prior stroke. The relationship between post-stroke depression and PBA is complicated, because the depressive syndrome also occurs with high frequency in stroke survivors. Post-stroke patients with PBA are more depressed than poststroke patients without PBA, and the presence of a depressive syndrome may exacerbate the weeping side of PBA symptoms.

The exact cause of cyclothymia is unknown. It is known that major depression, bipolar disorder, and cyclothymia often occur together within families. There may be a genetic component to cyclothymia: In one study, it was found that an individual is 2–3 times more likely to have the disorder if an identical twin is affected.

It is also believed that a person suffering with PTSD may experience similar shifts in mood based on how many flashbacks they've been dealing with.

Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes. While racing thoughts are most commonly described in people with bipolar disorder and sleep apnea, they are also common with anxiety disorders, OCD, and other psychiatric disorders such as attention deficit hyperactivity disorder. Racing thoughts are also associated with sleep deprivation, hyperthyroidism. and the use of amphetamines.

Prevalence estimates place the number of people with PBA between 1.5 and 2 million in the United States alone, which would be less than 1% of the U.S. population even at the high end of the estimate. Some argue that the number is probably higher and that clinicians underdiagnose PBA. However, the prevalence estimate of 2 million is based on an online survey. Self-selected computer-savvy patients in at-risk groups evaluated their own symptoms and submitted their self-diagnoses. No doctor or clinic confirmed the data. Motivation to participate could have been influenced by the presence of symptoms, which would have skewed the results. The actual prevalence could very well be quite a bit lower than estimated.

Bipolar I disorder (BD-I; pronounced "type one bipolar disorder") is a bipolar spectrum disorder characterized by the occurrence of at least one manic or mixed episode. Most patients also, at other times, have one or more depressive episodes, and all experience a hypomanic stage before progressing to full mania.

It is a type of bipolar disorder, and conforms to the classic concept of manic-depressive illness, which can include psychosis during mood episodes. The difference with bipolar II disorder is that the latter requires that the individual must never have experienced a full manic or mixed-manic episode - only less severe hypomanic episode(s).

Emotional dysregulation (ED) is a term used in the mental health community to refer to an emotional response that is poorly modulated, and does not fall within the conventionally accepted range of emotive response.

Possible manifestations of emotional dysregulation include angry outbursts or behavior outbursts such as destroying or throwing objects, aggression towards self or others, and threats to kill oneself. These variations usually occur in seconds to minutes or hours. Emotional dysregulation can lead to behavioral problems and can interfere with a person's social interactions and relationships at home, in school, or at place of employment.

Emotional dysregulation can be associated with an experience of early psychological trauma, brain injury, or chronic maltreatment (such as child abuse, child neglect, or institutional neglect/abuse), and associated disorders such as reactive attachment disorder. Emotional dysregulation may present in people with psychiatric disorders such as attention deficit hyperactivity disorder, bipolar disorder, borderline personality disorder, narcissistic personality disorder, and complex post-traumatic stress disorder. ED is also found among those with autism spectrum disorders. In such cases as borderline personality disorder, hypersensitivity to emotional stimuli causes a slower return to a normal emotional state. This is manifested biologically by deficits in the frontal cortices of the brain.

The IDEA requires that a student must exhibit one or more of the following characteristics over a long duration, and to a marked degree that adversely affects their educational performance, to receive an EBD classification:

- Difficulty to learn that cannot be explained by intellectual, sensory, or health factors.

- Difficulty to build or maintain satisfactory interpersonal relationships with peers and teachers.

- Inappropriate types of behavior (acting out against self or others) or feelings (expresses the need to harm self or others, low self-worth, etc.) under normal circumstances.

- A general pervasive mood of unhappiness or depression.

- A tendency to develop physical symptoms or fears associated with personal or school problems.

The term "EBD" includes students diagnosed with schizophrenia, but does not apply to students who are "socially maladjusted", unless it is determined that they also meet the criteria for an EBD classification.

Pooled data suggest the incidence of NMS is between 0.2%–3.23%. However, more physician awareness coupled with increased use of atypical anti-psychotics have likely reduced the prevalence of NMS. Additionally, young males are particularly susceptible and the male:female ratio has been reported to be as high as 2:1.