ADHD is now accepted as a difference in brain structure and chemistry that is primarily genetic. But the understanding of the condition has changed immensely over the past hundred and twenty years, since it was first studied as a unique condition in western medical history. Read on to understand more about the history of ADHD - from its name, to its presumed causes, to the evolution of research on the emotional regulation aspects of ADHD.

In short:

• The name ADHD has only been around and used in diagnostic settings since 1987. The two previous official names were ADD and hyperkinetic reaction of childhood, which were used in the DSM in 1980 and 1968 respectively.
• The understanding that ADHD is genetic started being developed by Dr. Paul Wender in the early 1970 by showing how ADHD runs in families.
• Neuroimaging studies that show that ADHD brains are different structurally than other brains has fully disproved the claim that ADHD is behavioural or environmental.
• Despite widespread misconceptions, there are both stimulant and non-stimulant options for ADHD medication. Both have very diverse impacts on individuals, but can be extremely effective treatment options.
• Emotional dysregulation traits of ADHD are important, although currently less understood and prioritized in diagnosis. Hopefully this will be an area of future progress within treatment and diagnosis.
• Want to learn more about the basics of ADHD - like common traits, diagnosis & the science behind the brain difference? Check out our article on What is ADHD?

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What’s in a name?

ADHD has only been considered a unique condition in written western medical history consistently (with some sporadic earlier mentions) since around the turn of the 20th century with the work of Sir George Frederick Still and Sir Thomas Smith Clouston. That being said, the traits of inattention, hyperactivity, and impulsiveness have been studied together for much longer - with some references to something that could potentially have been ADHD as early as 493BC in the writing of the Greek physician Hyppocrites. ADHD isn’t something that is new and it’s not cultural, despite pervasive myths and misconceptions. It’s conceptualization in western medicine, however, does have a relatively short and tumultuous history.

Through the first half of the 20th century, ADHD was identified as a unique set of traits by a few physicians, but did not have a unified name. The cause of the traits was hypothesized by Sir George Frederick Still to be the result of a brain difference, unrelated to home environment and intelligence, while other physicians of the early 1900s argued that the traits were likely the result of brain damage (Rodden 2019).

It wasn’t until the 1960s that this changed definitively and ADHD was added to the DSM. In 1968, ‘the second edition of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, the DSM-II lists the disorder, but under the name “hyperkinetic reaction of childhood.”(CHADD 2020).

At that time, ‘it was thought to cause restlessness and distractibility in children, but believed to go away or lessen by adolescence’ (CHADD 2020).

A key moment in ADHD research came in 1972 when Dr. Paul Wender was able to link ADHD to a person's genetics by showing that ADHD runs in families (Charach et al. 2011). As Rodden (2019) points out, this is what ultimately spurred future genetic research into ADHD.

The name ADD was finally written into the DSM-III in 1980. The specific diagnosis of ADHD has only been around since 1987, when it first appeared in the revised third edition of the DSM (Rodden 2019). The DSM IV, in 1994, refined the diagnosis to include the three subtypes - inattentive type, hyperactive/impulsive type, and combined type.The current DSM updated these to be called ‘presentations’ and not types - affirming that someone’s presentation can change over time.

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Stimulant medication & controversy

Public controversy around the use of stimulant medication as treatment for people with ADHD has been rampant throughout the century, despite improvements in wellbeing for many people with ADHD who take stimulant medication.

The first stimulant medications given to children with ‘emotional problems’ were tested in 1937 by the psychiatrist Dr. Charles Bradley, at which point they had the unexpected side effect of improving interest in school (Rodden 2019).

Through the 1950s there was broad experimentation with using stimulants to treat various mental illnesses, which ended up being a part of developing improved medications for ADHD over time (but recall: ADHD was still called hyperkinetic reaction of childhood until 1980! So at the time this would not have been a known outcome or goal of the research into stimulants). Ritalin was approved by the FDA in 1955.

Through the 1970s there was significant backlash to treating children with stimulants (Mayes et al 2008). The Amphetamine epidemic (and subsequent classification of Amphetamines as schedule III then schedule II substances) meant growing public scepticism for treating mental health conditions with stimulants, as well as difficulty accessing stimulant medication (Rodden 2019).

There needs to be more research on optimizing ADHD medication dosages for individual patients, as well as de-stigmatizing the use of stimulants, which can be extremely effective for supporting attentional and emotional regulation for some people with ADHD

There are currently two stimulant medications that are approved in the US to treat ADHD: methylphenidate and amphetamine, along with three non-stimulant medications. ADHD medications are available in different forms and dosage, which significantly impact that effectiveness of medication. There needs to be more research on optimizing ADHD medication dosages for individual patients, as well as de-stigmatizing the use of stimulants, which can be extremely effective for supporting attentional and emotional regulation for some people with ADHD.

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Neuroimaging and recent developments in the understanding of ADHD

In the early 20th Century (and onwards), there was debate over whether ADHD was primarily behavioural and/or the result of certain environments, or it was genetic. This question has been more definitively answered since studies using neuroimaging have revealed differences in brain structure between people with ADHD and people without ADHD.

In the words of Dr. Oren Mason and Dr. Tamara Rosier ‘Neuroimaging studies have revealed the structural differences in the ADHD brain. Several studies have pointed to a smaller prefrontal cortex and basal ganglia, and decreased volume of the posterior inferior vermis of the cerebellum — all of which play important roles in focus and attention.’ (2020)

This change in perspective about ADHD that is aligned with the neurodiversity paradigm - that brain differences are a natural and valuable part of human diversity

What neuroimaging clearly showed is what many ADHD researchers and people with ADHD have been saying all along: that ADHD is not a set of behavioural problems and it is not primarily environmental. Instead, ADHD is the result of a difference in brain structure and chemistry that affects a person’s perceptions and experiences throughout environments over time.

Dr. Daniel Amen writes that ‘In my opinion, imaging completely changes the discussion around mental health. After looking at their scans, patients often see that their problems are medical, not moral.’ This change in perspective about ADHD that is aligned with the neurodiversity paradigm - that brain differences are a natural and valuable part of human diversity - is also the most scientifically accurate conceptualization.