In preschool, the main manifestation is hyperactivity. Inattention becomes more prom- inent during elementary school. During adolescence, signs of hyperactivity (e.g., running and climbing) are less common and may be confined to fidgetiness or an inner feeling of jitteriness, restlessness, or impatience. In adulthood, along with inattention and restless- ness, impulsivity may remain problematic even when hyperactivity has diminished.
Temperamental. ADHD is associated with reduced behavioral inhibition, effortful con- trol, or constraint; negative emotionality; and/ or elevated novelty seeking. These traits may predispose some children to ADHD but are not specific to the disorder.
Environmental. Very low birth weight (less than 1,500 grams) conveys a two- to three- fold risk for ADHD, but most children with low birth weight do not develop ADHD. Al- though ADHD is correlated with smoking during pregnancy, some of this association reﬂects common genetic risk. A minority of cases may be related to reactions to aspects of diet. There may be a history of child abuse, neglect, multiple foster placements, neurotoxin exposure (e.g., lead), infections (e.g., encephalitis), or alcohol exposure in utero. Exposure to environmental toxicants has been correlated with subsequent ADHD, but it is not known whether these associations are causal.
Genetic and physiological. ADHD is elevated in the first-degree biological relatives of individuals with ADHD. The heritability of ADHD is substantial. While specific genes have been correlated with ADHD, they are neither necessary nor sufficient causal factors.
Visual and hearing impairments, metabolic abnormalities, sleep disorders, nutritional de- ficiencies, and epilepsy should be considered as possible inﬂuences on ADHD symptoms.
ADHD is not associated with specific physical features, although rates of minor phys- ical anomalies (e.g., hypertelorism, highly arched palate, low-set ears) may be relatively elevated. Subtle motor delays and other neurological soft signs may occur. (Note that marked co-occurring clumsiness and motor delays should be coded separately [e.g., de- velopmental coordination disorder].)
Course modifiers. Family interaction patterns in early childhood are unlikely to cause
ADHD but may inﬂuence its course or contribute to secondary development of conduct problems.
Differences in ADHD prevalence rates across regions appear attributable mainly to differ- ent diagnostic and methodological practices. However, there also may be cultural varia- tion in attitudes toward or interpretations of children’s behaviors. Clinical identification rates in the United States for African American and Latino populations tend to be lower than for Caucasian populations. Informant symptom ratings may be inﬂuenced by cul- tural group of the child and the informant, suggesting that culturally appropriate practices are relevant in assessing ADHD.
ADHD is more frequent in males than in females in the general population, with a ratio of approximately 221 in children and 1.621 in adults. Females are more likely than males to present primarily with inattentive features.
ADHD is associated with reduced school performance and academic attainment, social re- jection, and, in adults, poorer occupational performance, attainment, attendance, and higher probability of unemployment as well as elevated interpersonal conﬂict. Children with ADHD are significantly more likely than their peers without ADHD to develop con- duct disorder in adolescence and antisocial personality disorder in adulthood, conse— quently increasing the likelihood for substance use disorders and incarceration. The risk of subsequent substance use disorders is elevated, especially when conduct disorder or an- tisocial personality disorder develops. Individuals with ADHD are more likely than peers to be injured. Traffic accidents and violations are more frequent in drivers with ADHD.
There may be an elevated likelihood of obesity among individuals with ADHD.