Possible etiologies of ADHD
(10-31-13)

Neurological factor explanations

Brain Damage: structural damage due to harmful influence

Brain injury, especially hypoxic/anoxic insults, have been associated with attention deficits and hyperactivity.

ADHD symptoms appear to be over represented in children with a history of seizure disorders.

However, recall that brain injury acts as a "nonspecific risk factor" in children, and ADHD symptoms are neither exceptionally common or uniquely associated with these injuries.

Reviews have suggested that <5% of children diagnosed with ADHD have any hard neurological findings indicative of actual brain damage.

Conclusion: minor contributor, explains only a few cases.

Delayed Brain Maturation: brain is "normal", just developing slowly

Immature social behavior, neuromaturational delay on neurological examinations, and similarity of deficits in attention, impulse control, and self-regulation to younger normal children have been interpreted as possibly indicating a developmental delay in CNS maturation.

This position was more tenable when it was believed that many/most children eventually "outgrew" ADHD. With accumulating evidence that symptoms often persist into adulthood this explanation has become less attractive.

Also, there was never any direct evidence of the perported "delay in maturation."

Conclusion: jury still out, but unlikely a significant factor.

Brain Dysfunction: brain is not functioning in same manner as "normal" children

Several lines of evidence suggest abnormalities in brain functioning in populations of children diagnosed with ADHD, when compared with normal control populations:

Neurotransmitter dysfunction or imbalances, especially selective deficiency in dopamine availability has been reported.

Cerebral flood flow studies suggest diminished perfusion to the striatum & orbital prefrontal regions, with possibly more involvement of the right hemisphere.

BEAM (Brain Electrical Activity Monitoring) studies have shown less electrical activation in prefrontal and frontal-limbic regions, possibly more involvement of right hemisphere.

Neuropsychological studies has reported disinhibition of behavioral responses, suggesting possible orbital-frontal and orbital-limbic impairments.

Conclusion: Brain dysfunction (not brain damage) appears to be a major etiological factor in ADHD.

Genetic factor explanations

20% to 32% of parents and siblings of children diagnosed with ADHD also show the disorder. Siblings of probands are 6 times as likely as controls to show ADHD; children of proband parent may have as high as 50% probability of diagnosis (Barkley, 1998)

51% to 66% concordance for ADHD in monozygotic twins; 28% to 33% concordance for dizygotic twins (Goodman & Stevenson, 1989; Sherman, Iacono, & McGue, 1997); heritability factor is estimated at approximately 0.80 (possibly up to 80% of the differences in attention, overactivity, and impulsivity between individuals with and without a diagnosis of ADHD can be accounted for genetically)

approximately 1 in 4 diagnosed children has a biological parent diagnosed with ADHD (Zametkin, 1995)

several studies suggest dysfunction in the dopamine system and/or underactivity of the prefrontal-striatal-limbic system; or imbalance of deopamine and serotonin; or dopomine transporter or receptor genes on several chromosomes (esp. chromosome 5, 11), (genetic heterogeneity is suggested by the high rates of comorbidity; also, ADD [as opposed to ADHD] may reflect dysfunction of posterior parietal activity, more right than left, rather than dysfunction of anterior, frontal activity [Bradshaw, 2001]). (life is not simple)

Conclusion: Genetic (presumably hereditary) transmission appears to be a major etiological factor in ADHD.

Environmental Toxins explanations

Food Additives

Controlled studies have suggested that a very small number of children diagnosed with ADHD (probably in range of .5 to 1%) respond very positively to diets free of color and preservative agents.

Sugar

Controlled studies have suggested no role for refined sugar in producing ADHD symptoms (but a very large role for "expectancy effects"/placebo effects if anyone involved knows when the child is getting the real sugar).

Lead

Usually lead poisoning leads to mental retardation and learning problems, but occasionally to ADHD like syndromes. This would fall into the Brain Damage group discussed above.

Maternal cigarette smoking during pregnancy

Possibly a minor etiological factor, it is unclear what aspect of exposure (tars, nicotine alkaloids, reduced oxygen saturation, and/or other/unknown factors) produces the risk.

interaction of a version of the Dopomine Transporter Gene in a male fetus and maternal smoking during pregnancy may increase risk of ADHD

Prenatal exposure to alcohol

ADHD is associated with Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Effects (FAE), and one of the symptoms is increased risk of ADHD. This would fall into the Brain Damage group discussed above.

Fluorescent lighting

Controlled studies have suggested no role for exposure to fluorescent lights in producing ADHD symptoms.

Anticonvulsants

Some seizure medications, especially Phenobarbital and Dilantin, have been reported to cause ADHD like syndromes in children. Symptoms typically remit if the anticonvulsants are discontinued. The majority of children diagnosed with ADHD have not history of seizures and have never been treated with anticonvulsant medications.

theophylline

Controlled studies have suggest no increased risk of ADHD symptoms in children using theophylline derivatives for treatment of asthma and other respiratory difficulties.

Conclusion: Environmental toxins appears to be a very minor etiological factor in ADHD.

Environmental & Psychosocial Factors

Overly critical, commanding, and negative behavior has been observed in mother of children diagnosed with ADHD in informal situations and dyadic test situations. These behavioral differences, however, are not necessarily seen in the mothers' interactions with their non-ADHD children. The suggestion is often made that these behavior differences are the result of interacting with a child showing ADHD characteristics, rather than being a cause of the difficulty.

Some authors, however, believe that poor parenting skills and expectations for appropriate child behavior has contributed to the increased prevalence of ADHD reported by some studies.

Conclusion: The possible role of parental and family learning influences on the initiation of ADHD symptoms is still debated. There is some consensus that families can influence these behavior, and that certain patterns of parental behavior can contribute to improvements in the children. There is much less agreement that psychosocial factors have any primary etiological role. The actions of parents can almost certainly make the child's behavior better and worse, but probably did not "cause" it.

The big winners: neurological dysfunction involving the neurotransmitter systems and genetic transmission are the major etiological factors supported by available empirical research. These may be two facets of the same effect -- what is being inherited may be problems in neurotrasport (production/release/reuptake/inhibition/metabolism) of neurotransmitters, especially those associated with frontal brain systems and the subcortical circuits associated with the frontal lobe, but this attractive hypothesis has, as yet, no direct or conclusive empirical support.