Attention Deficit Hyperactivity Disorder

   (ADHD)

   Historically, a small group of children has always been seen as pathologically restive and unable to pay attention. In 1845, Heinrich Hoffmann (1809–1894), then a family doctor in Frankfurt am Main (later a psychiatrist), wrote an amusing little collection of children’s stories that featured, among other characters, "Struwwelpeter," a very bad boy who let his fingernails grow uncut for a whole year. Around 1900, Mark Twain translated the book (originally Der Struwwelpeter: oder lustige Geschichten und drollige Bilder für Kinder von 3-6 Jahren) as Slovenly Peter or Cheerful Stories and Funny Pictures for Good Little Folks. Struwwelpeter has always been considered a poster boy for hyperactivity, and here is Twain’s rendering of Hoffmann’s verse:

   See this frowsy ‘cratur’

   Pah! It’s Struwwelpeter

   On his fingers rusty,

   On his two-head musty,

   Scissors seldom come;

   Lets his talons grow a year

   Do any loathe him? Some!

   They hail him ‘Modern satyr-Disgusting Struwwelpeter.’

   (ADHD)

   ADHD: Diagnosis (from 1902). "Hyperactivity" in children was to become a familiar medical concept. In 1902, George F. Still (1868–1941), working at the Hospital for Sick Children in Great Ormond Street, London, and pioneer of the study of pediatrics as a discipline in England, described in the Lancet a group of children showing "a marked inability to concentrate and to sustain attention." One boy of 6 years was "unable to keep his attention even to a game for more than a very short time, and, as might be expected, the failure of attention was very noticeable at school. . . ." Still ascribed this syndrome, and numerous other "abnormal psychical conditions in children," to "defective moral control" (p. 1166).

   But it was only in the epidemic of encephalitis in Europe after the First World War that hyperactivity as a syndrome in children truly got on the medical radar, one of the symptoms of encephalitis often being hyperkinesis. There were subtler brain injuries than encephalitis also causing hyperactivity. The concept of children suffering behavioral consequences of real but scarcely detectable central nervous lesions was familiar even before Arnold Lucius Gesell (1880–1961), the Yale pediatrician, suggested in 1941 in his textbook, Developmental Disease, "minimal cerebral injury" as a cause of pathological behavior in children. Without making specific reference to hyperactivity, Gesell wrote: "It must be granted that a child may inherit motor weaknesses, motor eccentricities, even motor demeanors. But when these are highly atypical one is tempted to think of injury instead of inheritance" (p. 237).

   In the 1950s, various permutations of the phrases "minimal cerebral injury" or "minimal brain dysfunction" became associated with hyperactivity. In 1962, an Oxford conference organized by Ronald MacKeith (1908–1977), a pediatrician who was medical-education director of the Spastic Society and had an appointment at Guy’s Hospital in London, and Martin Bax (1933–), a psychiatrist also at Guy’s, recommended that "minimal brain dysfunction" replace "minimal brain damage." As for hyperactivity, the participants recommended: "In a child who has no history of a devastating cerebral illness, it cannot be stated with confidence that ‘brain damage’ is a necessary and constant precursor of hyperkinetic behaviour disorder" (Minimal Cerebral Dysfunction, p. 88).

   It was indeed the increasing implausibility—or social unacceptability—of the notion that the growing numbers of children with the diagnosis "MBD" had some kind of brain injury that led to the recasting of hyperactivity. In 1954, Maurice W. Laufer (1914–), Eric Denhoff (1913–), and Gerald Solomons at the Emma Pendleton Bradley Home in Riverside, Rhode Island, in a paper at a child psychiatry meeting in Toronto (and published in 1957 in Psychosomatic Medicine) proposed the "hyperkinetic impulse disorder" in children who were basically nonretarded but who could not sit still and manifested "short attention span and poor powers of concentration." The authors said, "It is necessary to emphasize that the hyperkinetic syndrome is a very specific entity. It does not account for the majority of children’s behavior disturbances" (p. 48).

   This language reappeared in DSM-II in 1968 as the "hyperkinetic reaction of childhood (or adolescence) . . . characterized by overactivity, restlessness, distractibility, and short attention span" (p. 50). In DSM-III (1980), the diagnosis became Attention Deficit Disorder (ADD), followed by the subcategory "with hyperactivity." And in Attention Deficit Hyperactivity Disorder (ADHD)

   DSM-III-R (1987)

   "ADHD" was born: The diagnosis became "Attention Deficit Hyperactivity Disorder."

   In 2003, Elizabeth R. Sowell (1965–), a member of the neurology department of the medical school of the University of California at Los Angeles (UCLA), and co-workers, using high-resolution magnetic resonance imaging (MRI), found in research published in the Lancet, that compared to controls, children with ADHD had smaller inferior dorsolateral aspects of the frontal cortices. There were other findings as well in regions that are "thought to form a broadly distributed action-attentional system that supports the maintenance of attentional focus and successful inhibitory control of unwanted impulses" (p. 1705). Although this study was not the first use of MRI in children with hyperactivity, it was the first worldwide, carried out at the UCLA Laboratory of Neuro Imaging, to computer-map the entire cortical surface.

   ADHD: Treatment (from 1937)

   Disruptive children have long been medicated: in the nineteenth century with opium and in the early twentieth century with barbiturates. Specific medication for hyperactivity, however, surfaced only with the amphetamines in the 1930s (Smith Kline & French introduced Benzedrine [racemic amphetamine sulfate] in 1936. See Antidepressant.) In 1937, Charles Bradley (1902–1979), a child psychiatrist who was medical director of the Emma Pendleton Bradley Home in Riverside (East Providence), Rhode Island, described the use of Benzedrine in nonretarded children who had "neurological and behavior disorders." "Fifteen of the 30 children responded to benzedrine by becoming distinctly subdued," he reported in the American Journal of Psychiatry (p. 579).

   In the days of the first psychiatric drug set of the 1950s, numerous antipsychotics such as chlorpromazine were indicated for children who presented "behavioral problems," in the absence of a specific psychiatric diagnosis. Yet, the definitive moment in the treatment of ADHD occurred in 1970 when the Ciba company began advertising its drug methylphenidate (Ritalin), a compound introduced in Europe in 1954 (in the United States in 1956) for depression, as effective for the " ‘hyperactive’ problem child." Although not an amphetamine, methylphenidate was chemically close to that drug class and similarly counted as a "stimulant." Stimulant medication went on to become the treatment of choice in ADHD.