ADHD is a common neurobehavioural disorder characterised by developmentally inappropriate levels of hyperactivity, impulsiveness and inattention. Typical symptoms include excessive running and climbing, squirming in seat, careless mistakes on assignments, difficulty awaiting turn, and excessive talking. These behaviours are evident in more than one setting. The prevalence of ADHD is between 3 and 5 percent of school children worldwide1(brown). It was recently estimated to occur in 5-10 percent of Irish children2(hadd).
Longitudinal studies have shown that children with ADHD are more prone to learning, behavioural and emotional problems during childhood and adolescence. Childhood ADHD pre-disposes to specific disadvantages such as less formal schooling (2 years less, on average)24. Children diagnosed with ADHD are more likely to fail academically in school despite scoring in the average to above average range on standardised ability tests25.
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People with ADHD are at increased risk of co-existing or associated psychiatric problems. Studies have shown that about 55% of children with ADHD also have oppositional defiant disorder (ODD), about 50% meet the criteria for conduct or mood disorder while 18% will experience depression and 25% have anxiety disorders. The person may have difficulty in various social settings, in particular where co-existing conditions are present5, 26. Children with ADHD are also more likely to have tics26, problems with motor co-ordination, psychosocial functioning and sleep27.
ADHD is not purely a childhood disorder. A significant number of children diagnosed with ADHD continue to display symptoms into adulthood. Although adults are typically better able to disguise the symptoms, ADHD may still present significant problems to the individual. Neuropsychological problems are characterised by impaired performance on verbal memory and concentration tasks as well as reduced motor processing speed.
Theories of Causation
No definitive cause has been established for ADHD. The disorder cannot be identified by any single genetic, environmental, or neurobiological factor. However, family, twin and adoption studies have indicated that ADHD has a strong genetic foundation. It has been firmly established that ADHD is not simply the result of a poor social environment; but there is a correlation between specific environmental factors and ADHD. Finally, neurobiological studies indicate that ADHD may be caused by alterations in neurological circuitry or specific structural changes in the brain. Ultimately, ADHD is most likely due to an interaction between these factors in genetically predisposed individuals.
Genetic Factors
For decades, research has shown that ADHD is primarily the result of genetic factors and is transmitted in families. ADHD occurs 5 to 7 times more frequently in family members with the disorder5. A recent longitudinal study showed that the parents of children with ADHD had significantly increased rates of ADHD as compared with the parents of children who did not have ADHD6. The child of an adult with ADHD has approximately a 25% chance of developing ADHD7. In agreement with these findings, studies found that adoptive relatives of children with ADHD are less likely than biological relatives to have the disorder or associated syndrome. A large scale study identified a 75 to 91 percent heritability across familial relationships (twin, sibling, and twin-sibling)8. This finding, along with numerous other studies, estimates the heritability to be 0.76 on average (Figure 1)9. A twin study reported a monozygotic probandwise concordance rate of 51 percent and dizygotic concordance rate of 33 percent10. Together, these studies provide compelling evidence that ADHD is a highly heritable disorder. Although no single genomic region is responsibility for ADHD, a number of genetic abnormalities have been associated with the disorder.
Genomic regions implicated by linkage studies do not show significant correlations and several different loci have been connected with ADHD. Given the absence of repeated results across the spectrum of studies to date, it is reasonable to speculate that genes with moderately large effect do not exist and that predisposition to ADHD is the result of a combination of genetic factors.
Meta-analyses have implicated polymorphisms in dopamine receptors DRD4, DRD5 and the dopamine transporter SLC6A3. DRD4 is also prevalent in the frontal-subcortical networks that are implicated in ADHD pathophysiology9. Imaging studies of adults with ADHD have demonstrated a reduction in dopamine-transporter binding9. Accordingly, the dopamine tranporter is a primary target of the most frequently prescribed pharmacological treatments, methylphenidate and amphetamine.
This figure demonstrates the correlation in data from heritability studies.
Environmental factors
There are multiple environmental factors which contribute to the risk of developing ADHD. The child is most vulnerable in utero where chronic exposure to certain toxins, including alcohol, nicotine and cocaine, is associated with an increased risk of ADHD. Delivery complications also increase the risk of ADHD. This includes foetal hypoxia, premature delivery and significantly low birth weight9, 13. Notably, the basal ganglia, which are associated with ADHD, are particularly sensitive to hypoxic insults9.
Postnatal environmental conditions have also been associated with ADHD. Rutter et al found that combinations of family environmental risk factors, rather than any one factor, contribute to the postnatal incidence of ADHD14. The risk factors include a large family size, maternal mental disorder, paternal criminality, severe marital discord, low social class and foster care placement15. It is not suggested that these risk factors cause ADHD, rather that there is a positive correlation between their presence and the presence of ADHD. Systematic studies discredit theories contending that particular foods or additives or excessive television viewing contribute to ADHD9. Despite being associated with ADHD, lead contamination is not found in most children with ADHD and many children with high lead exposure do not develop ADHD9.
Neurobiological models
There are two currently held neurobiological models to explain ADHD. The Neuro-Cognitive Model describes ADHD as an executive dysfunction caused by disturbances in the fronto-dorsal striatal circuit and associated dopaminergic branches (e.g. mesocortical pathway). A second account sites altered reward pathways (e.g. delay aversion). These implicate fronto-ventral striatal reward circuits and the meso-limbic branches that terminate in the ventral striatum, particularly the nucleus accumbens. Previously, these models were thought to be competing. However, they are now regarded as complementary accounts of two psycho-patho-physiological subtypes of ADHD with different developmental pathways, supported by different cortico-striatal circuits and modulated by alternative dopaminergic pathways16. Both models result in a reduction in attention-monitoring processes, inappropriate cognitive responses and behavioural impulsiveness. Many scientists now believe that cognitive disinhibition is the root cause of ADHD5, 17.
Electroencephalogram (EEG) studies show that over 90% of children diagnosed with ADHD demonstrate regulation disturbances in the prefrontal and sensorimotor cortices along with inhibited activity in all cortical areas. These children may be experiencing delayed maturation of the neural pathways because the regulation disturbances were seen in younger childrenaˆ™s brains (<8yrs). PET studies have shown that brain activity in adults with ADHD were significantly lower than control groups. The failure to adequately metabolise glucose was also implicated as a direct contributor to ADHD5. While these findings support the hypothesis that anatomical and physiological brain abnormalities are the basis of ADHD, no unique brain pattern has been identified. Slight variations of brain size and structure occur normally in the population. ADHD brains still have the same neurological and developmental features as the rest of the population.
Conclusion
ADHD is caused by a combination of genetic and environmental risk factors. These contribute approximately 75% and 25% respectively to ADHD susceptibility. The presence of certain genetic variations influences brain development in such a way that children with these configurations are more likely to develop inattention, hyperactivity and impulsivity. Environmental factors can exacerbate these behaviours. However, it is not yet known which environmental factor has the most prominent effect on each genetic continuum of ADHD.
Although the parameters of the disorder are vague and diagnosis can sometimes be difficult, it is very important to identify and treat people with ADHD. With the help of their medical practitioner, most people can find the treatment which is right for them. Successful treatment is paramount to allowing sufferers of ADHD to break free from the constraints of the disorder and fulfil their potential.
In the future, genetics may provide an avenue of very early diagnosis, even before the symptoms of the disorder present. However, more work is required before we can provide a new diagnostic approach for ADHD. Research continues to unravel the intricacies of ADHD and may provide scope for the introduction of early behavioural treatments in the future to tackle the disorder before its symptoms even present. A better appreciation of the genetics involved in ADHD susceptibility may allow for the selective use of medications which are more suited to the specific gene and neurobiological differences of each individual with ADHD.
Referenceaˆ™s
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