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  • Updated 02.13.2024
  • Released 11.28.1994
  • Expires For CME 02.13.2027

Attention deficit hyperactivity disorder



Attention deficit hyperactivity disorder (ADHD) is one of the most common conditions seen by child neurologists and psychiatrists. It is a neurobehavioral syndrome that is defined by its behavioral phenotype and frequently coexists with other cognitive and behavioral disorders. ADHD is a lifelong disorder. Although the diagnosis of ADHD is independent of any specific etiology, a strong familial component to ADHD exists. Genetic studies show a number of statistically significant relationships that are of small effect size. Converging data from a number of sources implicate frontal-striatal-cerebellar dysfunction as a possible mechanism for ADHD. These sources, however, fail to identify a single explanation for ADHD. Psychostimulant medications remain the mainstay of therapy, but several nonstimulant medications have been shown to be effective agents. An improvement in function in response to psychostimulants is not diagnostic of ADHD. Psychostimulants can have a beneficial effect on performance in children with no underlying attentional problems (coffee is as popular as it is for a reason).

Key points

• ADHD is a neurologic disorder that is defined by its behavioral characteristics.

• ADHD is frequently associated with comorbidities, such as disorders in motor, language, or academic functions.

• ADHD may persist into adulthood, and although the hyperactivity becomes attenuated, distractibility, impulsivity, and pathological disorganization may persist.

• Stimulants are the mainstay of therapy and have a wide therapeutic margin.

Historical note and terminology

Still and Tredgold are credited with the first modern descriptions of what is today known as "attention deficit hyperactivity disorder," or ADHD (17). They highlighted relevant features of ADHD and hypothesized a neurologic etiology. In the same era, other physicians were linking behavioral pathology to brain injuries.

In the 1930s, Strauss and colleagues described hyperactivity, distractibility, emotional lability, and perseveration in a group of survivors of encephalitis lethargica (283). These behaviors were posited to be de facto evidence of brain injury, and it was suggested that children who demonstrated these behaviors were brain damaged, even in the absence of any history of injury (282). The minimal brain damage concept persisted until the 1960s, despite the circularity of the reasoning that led to its existence. The minimal brain damage concept gave way to the minimal brain dysfunction concept.

Ultimately, the focus shifted to the symptoms rather than etiology or mechanism. The hyperactive child syndrome was included in the Diagnostic and Statistical Manual of Mental Disorders as the hyperkinetic reaction of childhood. Inattention became the predominant feature in DSM-III; attention deficit disorder was said to exist with or without hyperactivity. The core symptoms of inattention, hyperactivity, and impulsivity were not considered three independent variables, and they were merged into a single syndrome that required inattention and hyperactivity-impulsivity in DSM-III-R. DSM-IV reflects the covariation of hyperactivity with impulsivity and independence of inattention. Consequently, three major syndromes evolved: (1) inattention and hyperactivity-impulsivity, (2) inattention alone, and (3) hyperactivity-impulsivity alone.

DSM-5 modified the diagnostic criteria when applied to older adolescents and adults, recognizing that symptoms of inattention and hyperactivity may be less prominent in older adolescents and adults, and decreased the number of symptoms that define inattention or hyperactivity from six to five. However, cutoff scores of 4 for current symptoms of inattention and hyperactivity-impulsivity are sufficient to identify a college student as distinct from the norm (124).

Some people have questioned the specificity of inattention (118). Barkley presented a model of ADHD that posits poor behavioral inhibition as the central deficit (18; 19); this results in the disturbance in four neuropsychologic functions: (1) nonverbal working memory, (2) internalized self-speech, (3) self-regulation of affect-motivation-arousal, and (4) behavioral analysis and synthesis (reconstitution). Other models of ADHD have been put forth: Executive Dysfunction, State Regulation, Delay Aversion, and Dynamic Developmental (139). Working memory deficits have received increased attention as a model for inattentive ADHD (05). Impulsivity has been related to deficits in temporal processing (243). The Scandinavians maintain a broader view of the disorder and combine deficits of attention, motor control, and perception as the acronym "DAMP" (164).

It has been argued that the underlying deficit in ADHD with hyperactivity is distinct from attention deficit without hyperactivity (73), with the former representing a primary deficit in response inhibition and the latter representing a core deficit in working memory. This would have implications for the expected comorbidities as well as the type of intervention in the two groups.

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