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While everybody to some extent, and at certain times, occasionally has trouble sitting still, paying attention, or controlling impulsive behaviour , many others experience impulsivity, hyperactivity, and inattention at such mal-adaptively high levels that their daily lives at home, at school, at work, and in social settings are disrupted to a considerable and sometimes disabling extent. These people may have a common neurobiological disorder called Attention Deficit Hyperactivity Disorder (ADHD). There is also a less common and more severe form of ADHD called Hyperkinetic Disorder.
Although ADHD is a neurobiological disorder, it is defined at a behavioural level. That means that the symptoms are based upon observations about how people behave: ‘impulsivity’ signifies premature and thoughtless actions; ‘hyperactivity’ a restless and shifting excess of movement; and ‘inattention’ is a disorganised style preventing sustained effort. These symptoms are shown by individuals to different extents, and are influenced by context as well as by the constitution of the individual. People with ADHD may also be clumsy, unable to sleep, have temper tantrums and mood swings and find it hard to socialise and make friends.
Until recently, it was believed that children outgrew ADHD in adolescence, because sometimes hyperactivity seems to lessen in teen years. It is now known, however, that many symptoms continue into adulthood and hyperactivity may instead be experienced as internal restlessness. Undiagnosed ADHD in adults may have severe consequences including academic failure, substance abuse, criminal activity, failed relationships, troubled work relationships, and emotional difficulties such as anxiety and depression.
While most people diagnosed with ADHD can recall having problems during childhood, there have been some accounts recently of people experiencing “late-onset ADHD” in that as adults they meet the diagnostic criteria but did not during their childhood. This raises the possibility that symptoms of ADHD might emerge at different developmental stages. Researchers offer the following possible explanations for late-onset ADHD.
“The traditional explanation for this is that children with high intelligence quotients (IQs) or well developed executive function skills, who are well supported by structured home and school settings, might make use of so-called external scaffolding that facilitates compensatory behavioural mechanisms. Once such external scaffolding is removed, when leaving home and school for example, the full syndrome could emerge. Interestingly, this account of later-onset ADHD shows the interdependence of the association between symptoms and impairments of the disorder. An alternative hypothesis suggests that ADHD symptom expression depends on the efficiency of executive control processes. Poor maturation of cortical control during the adolescent years might lead to later emerging ADHD in some cases. Findings suggest that a late-onset ADHD-like syndrome might emerge, even in the absence of substantial childhood symptoms, perhaps reflecting an acquired syndrome with a different set of causal risk factors” (Asherson, Buitelaar, Faraone & Rohde, 2016).
ADHD has a long history but in the interests of space this is a shortened listing of major events.
1. 450 to c. 350 BCE: The Hippocratic Corpus
There is a description of a condition that resembles an aspect of what we now know as ADHD in the chapter titled Regimen in Volume IV of Hippocrates.
The author of this section explains that those who want to treat their patients correctly must first acquire the knowledge and understanding of human nature and must have knowledge of its primary constituents (fire and water) and must understand how they interact with each other because this helps determine the correct regimen. In other words, the doctor cannot treat a patient correctly if he does not understand his patient’s mind. The author goes on to describe the various blends of fire and water and how these mixtures affects a man’s or woman’s robustness as well as the impact it has on their intelligence and mind.
One such blending of fire and water is described thus:
“But if the power of water be further mastered by the fire, the soul must be quicker, in proportion to its more rapid motion, and strike its sensations more rapidly, but be less constant than the souls discussed above, because it more rapidly passes judgment on the things presented to it, and on account of its speed rushes on to too many objects” [Hippocrates IV, p. 289].
The author suggests the following treatment for managing this condition:
“eat barley bread rather than wheaten, and fish rather than meat; . . . exercises should be as far as possible natural and there should be plenty of them; violent exercise should be sparingly used, and only when necessary; . . . such persons are also benefited if they eat a meal before they go about their duties, instead of doing them without food, as their soul is more stable when it is mixed with its appropriate nourishment than when it lacks nourishment“[Hippocrates IV, p. 289-291].
2. 1775: Der Philosophische Arzt by Dr Melchior Adam Weikard
In a chapter in this medical textbook, Dr Melchior Adam Weikard, described symptoms now associated with the inattentive aspects of ADHD. Dr’s Barkley and Peters provided the following English translation:
“An inattentive person won’t remark anything but will be shallow everywhere. He studies his matters only superficially; his judgements are erroneous and he misconceives the worth of things because he does not spend enough time and patience to search a matter individually or by the piece with the adequate accuracy. Such people only hear half of everything; they memorize or inform only half of it or do it in a messy manner. According to a proverb they generally know a little bit of all and nothing of the whole…. They are mostly reckless, often copious considering imprudent projects, but they are also most inconstant in execution. They treat everything in a light manner since they are not attentive enough to feel denigration or disadvantages“[Barkley & Peters, 2012]
Weikard recommended the following treatment:
“The inattentive person is to be separated from the noise or any other objects; he is to be kept solitary, in the dark, when he is too active. The easily agile fibres are to be fixated by rubbing, cold baths, steel powder, cinchona (a botanical remedy), mineral waters, horseback riding, and gymnastic exercises” [Barkley & Peters, 2012].
3. 1798: An Inquiry into the Nature and Origin of Mental Derangement by Sir Alexander Crichton
In Book II his text book, Sir Alexander Crichton included a chapter called “On Attention and is Diseases” and in this chapter, he wrote the following:
“The incapacity of attending with a necessary degree of constancy to any one object, almost always arises from an unnatural or morbid sensibility of the nerves, by which means this faculty is incessantly withdrawn from one impression to another. It may be either born with a person, or it may be the effect of accidental diseases. When born with a person it becomes evident at a very early period of life, and has a very bad effect, inasmuch as it renders him incapable of attending with constancy to any one object of education. But it seldom is in so great a degree as totally to impede all instruction; and what is very fortunate, it is generally diminished with age” [Crichton, page 271]
He also wrote:
“In this disease of attention, if it can with propriety be called so, every impression seems to agitate the person, and gives him or her an unnatural degree of mental restlessness. People walking up and down the room, a slight noise in the same, the moving of a table, the shutting a door suddenly, a slight excess of heat or of cold, too much light, or too little light, all destroy constant attention in such patients, inasmuch as it is easily excited by every impression. The barking of dogs, an ill-tuned organ, or the scolding of women, are sufficient to distract patients of this description to such a degree, as almost approaches to the nature of delirium” [Crichton, page 272].
And Sir Alexander added that people with this condition have a name for it “which is expressive enough of their feelings. They say they have the fidgets” [Crichton, page 272].
4. 1845: Lustige Geschichten und drollige Bilder mit 15 schön kolorierten Tafeln für Kinder von 3–6 Jahren (Funny Stories and Whimsical Pictures with 15 Beautifully Coloured Panels for Children Aged 3 to 6) by Dr Heinrich Hoffman
Let me see if Philip can/Be a little gentleman;/Let me see, if he is able/To sit still for once at table/Thus Papa bade Phil behave;/And Mamma look’d very grave./But fidgety Phil,/He won’t sit still;/He wriggles/And giggles,/And then, I declare,/Swings backwards and forwards/And tilts up his chair,/Just like any rocking horse; -/“Philip! I am getting cross!”/See the naughty restless child/Growing still more rude and wild,/Till his chair falls over quite . . . [Hoffman, pages 18-20].
5. 1902, March 4th, 6th, & 11th: Sir George Frederick Still gave three lectures for the Goulstonian Lectures called “Some Abnormal Psychical Conditions in Children.”
Sir George begins this series of lectures by saying the following:
“. . . there are other cases which cannot be included in this category—children who show a temporary or permanent defect of moral control such as to raise the question whether it may not be the manifestation of a morbid mental state, but who nevertheless pass for children of normal intellect; it is this condition in particular which seems to me to call for careful observation and inquiry. The importance of some more widespread knowledge of these morbid states, if such they be, is very great, and although some of them persist into adult life, at no other period are the opportunities for investigating them so favourable as in childhood; for in early years the influence of environment has not yet become so varied and complicated as to be altogether beyond our gauge, and it is possible to obtain a more or less accurate and detailed history of the whole life of the individual, a point of extreme importance when the question of a congenital deficiency arises, as it will do in connexion with these cases: moreover, if there be any question of a morbid failure in the development of a mental process it can best be studied in the child, who is still at the age when, as we shall see, such development should be in progress” [Still, page 3].
He then gave detailed descriptions of 43 cases of children with normal intellect who nevertheless had abnormal problems with sustained attention and emotional and behavioural dysregulation.
6. 1918-1919: Postencephalitic behaviour disorder
A worldwide influenza pandemic left survivors with encephalitis which caused neurological dysfunction. Some of the symptoms were like those of ADHD (emotional instability, cognitive deficits, hyperactivity, depression etc.) and this later led researchers to believe that some of the ADHD symptoms could be caused by an underlying brain damage [Lange, Reichl, Lange, 2010].
7. 1932: Hyperkinetic disease of infancy
In a report published in 1932, the German doctors gave descriptions of a condition they called a hyperkinetic disease of infancy. These descriptions match the current system of describing ADHD [Lange, Reichl, Lange, 2010].
8. 1937: The first treatment of hyperactivity with a stimulant
Dr Charles Bradley published a study of the use of Benzedrine to treat children who had been hospitalized with emotional, behavioural and learning problems. He had been attempting to treat them for headaches caused by neurological examinations but although the Benzedrine did not help with the children’s headaches, Dr Bradley noticed that some of the children experienced an big improvement in behaviour and school performance. Because of this, he started a trial of the medication with 30 children and found that they became more interested in their school work and performed better. Some children also had a decrease in motor activity and became more emotionally stable. He later found that the children who benefited the most from Benzedrine were those who had short attention spans, dyscalculia, mood lability, hyperactivity, impulsiveness, and poor memory. Dr Bradley wrote in his report that “portions of the higher levels of the central nervous system have inhibition as their function, and that stimulation of these portions might indeed produce the clinical picture of reduced activity through increased voluntary control.” Since Benzedrine is a stimulant, Dr Bradley’s discovery that it could help calm children down was revolutionary. But despite this his report had almost no influence on research for approximately 25 years. This was possibly due to the popularity of psychoanalysis as a treatment. [Lange, 2010]
9. 1930’s, 1940’s, 1950’s: Minimal brain damage
During this time, there was a growing belief that hyperactivity was caused by brain damage. This came out of the work by Sir George Still, a report by Dr A. F. Tredgold in 1908, as well as the reports from the encephalitis pandemic from 1917-1928. This was borne out by research into epilepsy, lead poisoning, birth trauma, head injuries, and damage caused by infections. Eventually researchers and doctors began accepting hyperactivity as a symptom of underlying brain damage even when that damage couldn’t be found. They just assumed it was present somewhere in the brain [Lange, Reichl, Lange, 2010]
10. 1960’s: Minimal brain dysfunction
Researchers began to question whether hyperactivity was caused by brain damage in all cases particularly in those children who had no history of infections or trauma. They began to hypothesize that the symptoms were the result of disturbances in the brain’s functioning rather than anatomical brain damage. As a result, in 1963 the term ‘minimal brain damage’ was changed to ‘minimal brain dysfunction’ and a national task force was created to work on terminology and identification of the dysfunction. The adoption of the new terminology shifted the focus from social (parents & families as suggested by psychoanalysts) and environmental causes for symptoms to neurological factors. As a result of this work, the three core symptoms of inattention, impulsivity, and hyperactivity became defined by the term ‘minimal brain dysfunction.’ In addition, the term included children who fell within the definition of dysfunction and were also within the normal ranges of intelligence but it did not include those children who had learning difficulties. [Lange, Reichl, Lange, 2010]
11. 1968: Hyperkinetic reaction of childhood
It wasn’t long before the term ‘minimal brain dysfunction’ was criticized for being too general, not definitive enough, and that it lacked evidence for its use. As a result, a definition of the concept of hyperactivity was included in the second edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-II), and it was labelled ‘Hyperkinetic Reaction of Childhood.’ Then in the 1970’s the focus shifted from hyperactivity to trying to understand attention deficits. [Lange, Reichl, Lange, 2010]
12. 1980: DSM III
The DSM-III is published by the American Psychiatric Association (APA) and it includes Attention Deficit Disorder (ADD) with 3 subtypes: ADD with Hyperactivity, ADD without Hyperactivity, and ADD Residual type.
13. 1987: DSM-III-R
The DSM-III-R is published changing the name from ADD to ADHD. The subtypes are not named.
14. 1990’s: Adults with ADHD
It was finally recognized during this time that ADHD did not always disappear with age as previously thought but instead remained as a persistent disorder into adulthood. Also, new neuroimaging techniques were revealing structural abnormalities in the brains of children with ADHD that supported the concept of dysfunction and further research also found a genetic component. [Lange, Reichl, Lange, 2010]
15. 1994: Workplace Difficulties
The American Psychiatric Association (APA) accredited the diagnosis of ADHD in adulthood by including examples of workplace difficulties in the description of symptoms. [Lange, Reichl, Lange, 2010]
16. 1999: MTA Study
The National Institute of Mental Health (NIMH) published the “Multimodal Treatment Study of ADHD (MTA Study)” which showed that medication alone was more effective than psychosocial treatments alone, but a combination of both was more effective.
17. 2000: DSM-IV-TR
The DSM-IV-TR is published which renames the 3 subtypes of ADHD as ADHD predominantly Hyperactive/Impulsive type, ADHD predominantly inattentive type, and ADHD combined type.
18. September 2008: CG72
In September 2008, the National Institute for Clinical Excellence (NICE) published the clinical guideline (CG72) titled “Attention Deficit Hyperactivity Disorder: diagnosis and management.” This guideline, which is evidence based and relevant for England and Wales, covers diagnosing and managing ADHD in children over 3 years, young people, and adults. It is designed to improve the diagnosis of ADHD as well as the quality of care and support for people with ADHD.
19. Current times:
It has now been well established that unrecognised and untreated ADHD in adults causes unnecessary distress & loneliness, can cause significant mental health problems, significant psychosocial impairments, and significant educational and occupational problems.
There has been an increase in the recognition and treatment of adults with ADHD, and some licensed drug treatments for adults are now available. But even though the guidelines were published 8 years ago, and despite the fact that (due to large advances in research) the diagnosis is no longer controversial, too many adults are still finding it difficult to access services for assessment and treatment and there are still too few psychological services. It is also disappointing to note that the growth in private psychiatric and psychological services has outstripped the growth in NHS mental health services; although we recognise that the latter is due in part to the Government’s lack of adequate funding for mental health services.
There is still work to be done!
ADHD is a common disorder. In the UK, surveys of children between the ages of 5 and 15 years found that 3.62% of boys and 0.85% of girls had ADHD. Hyperkinetic Disorder is less common and prevalence estimates are around 1.5% for boys in the primary school years. The worldwide prevalence for children with ADHD is 5% (Faraone, Sergeant, Gilberg & Biederman, 2003).
Also, a recent review of longitudinal follow-up studies of individuals diagnosed with ADHD as children found that by age 25 only 15% retained the full ADHD diagnosis. However, a much larger proportion (65%) fulfilled criteria for either ADHD or ADHD in partial remission, indicating the persistence of some symptoms associated with clinical impairments in the majority of cases. It is likely, therefore, that about 0.6–1.2% of adults retain the full diagnosis by age 25 years and a larger percentage (2–4%) have ADHD in partial remission. This is consistent with population surveys in adult populations that estimate prevalence of ADHD in adults to be between 3 and 4% (CG72 Full Version page 26-27).
When researchers are conducting studies, they typically use the same definitions of ADHD for both boys and girls, and usually find more boys than girls with ADHD (a ratio of about 3 to 1). The gender ratio for children attending ADHD clinics, however, is usually higher than in the research surveys, which raises the possibility that females with ADHD receive less recognition. Similarly, in adult life, the male-female ratio for ADHD appears to be approximately equal, which again suggests the possibility that the high gender ratios in childhood may be partly a result of under-identifying the problem in girls, or of a different presentation of symptoms in girls (CG72 Full Version pages 127-128).
Research has demonstrated that AD/HD has a very strong neurobiological basis. Although precise causes have not yet been identified, there is little question that heredity makes the largest contribution to the expression of the disorder in the population.
1. Hereditary Factors
Studies indicate that multiple genes contribute to a susceptibility to ADHD. Pharmacologic, neuroimaging, and animal-model findings suggested imbalances in monoaminergic (dopaminergic, serotonergic, and noradrenergic) neurotransmission in ADHD. Several studies examined monoaminergic candidate genes for possible genetic association with ADHD in the Irish population, focusing particularly on genes of the dopaminergic and serotonergic systems. Several of the genes were associated with ADHD, including DAT1, DBH, DRD4, DRD5, and 5HT1B (Online Mendelian Inheritance in Man). Also, twin studies suggest that around 75% of the variation in ADHD symptoms in the population are because of variable genetic factors. (CG72 Full Version pages 28-29)
2. Biological Factors
A range of factors may adversely affect brain development during perinatal life and early childhood. These include difficulties during pregnancy; fetal oxygen deprivation; maternal smoking, alcohol consumption, and heroin use during pregnancy; premature delivery; very low birth weight, exposure to high lead levels; a deficiency of zinc; and postnatal injury to the prefrontal regions of the brain. These may all lead to an increase in the risk of having ADHD. These risk factors, however, do not act alone, but may interact with the hereditary factors. For example, the risk of ADHD associated with maternal alcohol consumption in pregnancy may be stronger in those children with a dopamine transporter (DAT) susceptibility gene. Furthermore, there is increased risk of ADHD symptoms in epilepsy and of ADHD in genetic conditions such as neurofibromatosis type 1, and syndromes such as Angelman, Prader-Willi, Smith Magenis, velocardiofacial and fragile X. Secondary ADHD may follow traumatic brain injury. (CG72 Full Version pages 28-29)
3. Psychosocial Factors
ADHD has been associated with severe early psychosocial adversity, for instance, in children who have survived depriving institutional care. The mechanisms are not known but may include a failure to acquire cognitive and emotional control. Disrupted and discordant relationships are more common in the families of young people with ADHD. Discordant family relationships, however, may be as much a consequence of living with a child with ADHD as a risk for the disorder itself. In established ADHD, discordant relationships with a harsh parenting style are a risk factor for developing oppositional and conduct problems. Parents themselves may also have unrecognised and untreated ADHD, which may adversely affect their ability to manage a child with the disorder. (CG72 Full Version pages 28-29).
Excessive television viewing, poor child management by parents, or social and environmental factors such as poverty or family chaos have also been suggested by some as possible causes of ADHD, but while these may aggravate symptoms, the evidence for such circumstances is not strong enough to conclude that they are primary causes of ADHD. (CG72 Full Version pages 28-29)
4. Dietary Factors
The influence of dietary factors in ADHD has attracted much public attention: food additives, excessive intake of sugar, colourings and ‘E’ numbers are sometimes regarded as causes of ADHD, and elimination and supplementation diets are used, often without professional advice. But the evidence is not strong enough to indicate that these cause ADHD. Nevertheless, epidemiological research indicates a link between additives and preservatives in the diet and levels of hyperactivity amongst a small proportion of children with ADHD.
Reviews have also been conducted on the evidence on associations between ADHD and longchain polyunsaturated fatty acids (PUFA) and these have remarked upon the brain’s need throughout life for adequate supplies, on a relative lack of omega-3 PUFA, and a possibility that males may be more vulnerable because testosterone may impair PUFA synthesis. Scientific uncertainties remain, however, concerning the physiological significance of different measures of PUFA metabolism and they are not used in practice (CG72 Full Version pages 28-29).
1.A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder. The MTA Cooperative Group. Multimodal Treatment Study of Children with ADHD. Arch Gen Psychiatry. 1999 Dec;56(12):1073-86.
2. Asherson, P., Buitelaar, J., Faraone, S. V., & Rohde, L. A. (2016). Adult attention-deficit hyperactivity disorder: key conceptual issues. The Lancet Psychiatry, 3(6), 568-578.
3. Barkley, R. A., Peters, H. (2012). The Earliest Reference to ADHD in the Medical Literature? Melchior Adam Weikard’s Description in 1775 of “Attention Deficit” (Mangel der Aufmerksamkeit, Attentio Volubilis). Journal of Attention Disorders, 16 (8), 623-630.
4. Crichton, Sir Alexander. An Inquiry into the Nature and Origin of Mental Derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects. London: T. Cadell, Junior, and W. Davies, 1798.
5. Faraone, S. V., Sergeant, J., Gillberg, C., & Biederman, J. (2003). The worldwide prevalence of ADHD: Is it an American condition? World Psychiatry, 2, 104–113.
6. CG72: National Institute for Health and Clinical Excellence (2008) Attention deficit hyperactivity disorder: Diagnosis and management of ADHD in children, young people and adults. London: National Institute for Health and Clinical Excellence.
7. Hippocrates. Vol IV. Regimen I. Reprinted ed. Translated by W.H.S. Jones. Loeb Classical Library. London: William Heinemann Ltd, 1959.
8. Hoffman, H. The English Struwwelpeter or Pretty Stories and Funny Pictures. London: George Routledge & Sons Ltd., 1909.
9. Lange, K.W., Reichl, S., Lange, K.M. et al. ADHD Atten Def Hyp Disord (2010) 2: 241.
10. Palmer, E. D., Finger, S. (2001). An Early Description of ADHD (Inattentive Subtype): Dr Alexander Crichton and ‘Mental Restlessness’ (1798). Child Psychology and Psychiatry Review, 6(2), 66-73.
11. Still, G. F. The Goulstonian Lectures On Some Abnormal Psychical Conditions in Children. The Lancet, 159 (4104), 1163 – 1168
12. Tredgold, A.F. Mental Deficiency (Amentia). New York: William Wood & Company, 1908.
13. Von Economo, Constantin. Encephalitis Lethargica: its sequelae and treatment. Translator K.O. Newman. London: Oxford University Press, 1931.
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Review date: 14/03/2017
Next review due: 15/03/2020
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