ADHD with Hyperactivity

ADD is much less common (possibly about 1%). It is likely to be an entity distinct from ADHD, perhaps more akin to a learning difficulty. ADD sufferers are mostly girls, characterized by anxiety, sluggishness and daydreaming. They are less aggressive, overactive or impulsive, better at making and keeping friendships and their academic performance is worse in tests that involve perceptual-motor speed. Because they do not display the degree of behavioural disturbance boys do, they do not get referred as often as they should. When they do, they are more likely to be misdiagnosed.

Current Aetiological Theories

No evidence exists to suggest that ADHD is caused by other than neurobiological malfunctioning. Although environmental factors may influence the course of the disorder over a lifetime, they do not bring the condition about. The significance of several anatomical and neurochemical abnormalities is still unclear. These include deficits in dopamine-decarboxylase in the anterior frontal cortex, leading to reduced dopamine availability and diminished focusing and attention; more symmetrical brains; smaller-sized brains in the area of the prefrontal cortex (caudate, globus pallidus); duplication polymorphism in the DRD4 and DAT genes.

The prevailing theory that tries to explain ADHD implicates the frontal cortex and its importance in response inhibition. ADHD sufferers have difficulty in suppressing impulse. Therefore, they respond to all impulses, being unable to exclude those that are unnecessary for the situation. Rather than failing to pay attention, they pay more attention to more cues than the average person, and are unable to stop the relentless flow of information. These people fail to pause, to consider the situation, options and consequences before exercising volition. Instead they act without thinking. They frequently report that they function best when caught 'in the thrill of it all' whatever the 'all' may be.

There is strong evidence for a genetic predisposition to ADHD with a concordance rate in monozygotic twins ranging from 75-91% (Goodman and Stevenson, 1989). One third of affected individuals have at least one parent who suffers from the same condition. Non-genetic factors that have been found to predispose people to developing ADHD are low birth weight (<1500g), environmental toxins, tobacco, alcohol and cocaine abuse during pregnancy (Milberger et al, 1996).

ADHD Across the Lifespan

Children with ADHD do not grow out of it. Between 70-80% carry the condition into their adult life to a varying degree (Klein and Mannuzza, 1991). Early identification and multimodal treatment reduces the risk of developing further complications such as antisocial behaviour, abuse of alcohol, tobacco and illicit substances, poor academic and social functioning, and further psychiatric morbidity.

About the author: Dr. Myttas is a Consultant Child and Adolescent Psychiatrist, Finchley Memorial Hospital, London.

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References

American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, 4th edn. APA, Washington DC.
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Goodman R, Stevenson JA (1989) Twin study of hyperactive II. The etiological role of genes, family relationships and prenatal adversity. J Child Psychol Psychiatry 5: 691
Klein RG, Mannuzza S (1991) Long-term outcome of hyperactive children: a review. J Am Acad Child Adolesc Psychiatry 30: 383-7
Mash EJ, Barkley RA (1998) Treatment of Childhood Disorders, 2nd edn. Guilford, New York
Milberger S, Biererman J, Faraone SV, Chen L, Jones J (1996) Is maternal smoking a risk factor for attention deficit hyperactivity disorder in children? Am J Psychiatry 153: 1138-42
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Tredgold AF (1908) Mental Deficiency (Amentia). W Wood, New York
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