- 1902 - the English pediatrician George Still described a condition analogous to ADHD. He regarded it as innate and not caused by the environment.
- The 1918–1919 influenza pandemic left many survivors with encephalitis,
affecting their neurological functions. Some of these exhibited immediate
behavioral problems which correspond to ADD. This caused many to believe
that the condition was the result of injury rather than genetics.
3.1937 - Dr. Bradley in Providence RI reported that a group of children with behavioral problems improved after being treated with stimulant medication. - 1957 - the stimulant Methylphenidate (Ritalin) became available.
- 1960 - Stella Chess described "Hyperactive Child Syndrome" introducing the concept of hyperactivity not being caused by brain damage.
- By 1966, following observations that the condition existed without any objectively observed pathological disorder or injury, researchers changed the terminology from Minimal Brain Damage to Minimal Brain Dysfunction. (Source: Oxford English Dictionary Online)
- 1970s - Canadian Virginia Douglas released various publications to promote the idea that attention deficit was of more significance than the hyperactivity, influencing the American Psychiatric Association.
- 1971 - the Church of Scientology set up the Citizen's Commission on Human Rights (CCHR), which lobbied using the media against psychiatric medication in general, and Ritalin in particular.
- 1973 - Dr Ben F. Feingold, once a Professor of Allergy in San Francisco, claimed that hyperactivity was increasing in proportion to the level of food additives.
- 1980 - the name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition.
- 1987 - the DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder."
- 1994 - DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.
- 1998 - the NIH developed and issued a Consensus Statement attesting to the existence of ADHD. A link is provided in the External Links section below.
Evidence for ADHD as an organic phenomenon
Brain imaging research using magnetic resonance imaging (MRI) has shown
that differences exist between the brains of children with and without
ADHD, though these differences have not been shown in any way to be pathological
in nature. Additionally PET studies have shown there might be a link between
a person's ability to pay continued attention to external directives and
the use of glucose - the body's major fuel - in the brain. In adults diagnosed
with ADHD, the brain areas that control attention use less glucose and
appear to be less active, suggesting that a lower level of activity in
some parts of the brain may cause inattention (Zametkin et al.). However,
there is no evidence that this low level of glucose in fact causes the
low level of attention to external direction; it could in fact be no more
than an indicator for low attention, or in the alternative, superior self-direction.
Also worth noting are the results of some studies using SPECT (Single Photon Emission Computed Tomography). One study (Lou et al. in Arch. Neurol. 46(1989) 48-52) found people labeled as ADHD have reduced blood circulation in the striatum. But even more significant may be the discovery that people with ADHD seem to have a significantly higher concentration of dopamine transporters in the striatum (Dougherty et al. in Lancet 354 (1999) 2132-2133; Dresel et al. in Eur.J.Nucl.Med. 25 (1998) 31-39). Researchers have also shown that individuals labeled as either bipolar or ADHD often have variant dopamine receptor alleles. Researchers have reported, for example, that DRD4 7 repeat alleles appear more frequently in certain aboriginal cultures with low population densities such as the Amazon, whereas DRD4 2 repeat alleles are especially common in higher population density regions, including the Orient.