Tics and Tourette’s Disorder – 7% of children with ADHD have a tic disorder.
40 to 50% of those with Tourette’s disorder have ADHD
There are factors in infancy, such as difficult temperament, that appear to be early precursors of ADHD.
Initial development of ADHD is most often during the preschool years.
While there is often a decline in the level of hyperactivity and some improvement in attention and impulse control in adolescence, perhaps 80 % continue to be impaired by their symptoms and meet current diagnostic criteria.
A significant number of children with ADHD (probably over 50%) continue to display problems into the adult years.
Prognosis of ADHD
Outcome of ADHD in adolescents is highlighted by the results of a study by Barkley, Fischer, et al, (1990).
This study followed a large sample of ADHD (158) and normal children (81) prospectively for 8 years after diagnosis.
123 hyperactive children and 66 normals were located, interviewed and complete questionnaires.
In the hyperactive group 12 (9.7%) were female and 111 were male. In the normal group 4 of the subjects were female and 62 were male.
Prognosis In Adolescence
The vast majority of the hyperactive subjects (71.5%) met DSM III-R criteria for ADHD at follow up.
More than 59% met criteria for Oppositional Defiant Disorder as compared to 11% of the controls.
Approximately 43 % of the hyperactive group could be diagnosed as CD as compared to 1.6% of the control group.
Hyperactive subjects were more likely to have had an auto accident , to have had more automobile accidents , to have had more bodily injuries in accidents, and to be at fault for accidents more often than did controls.
Adolescents in the hyperactive group were also more likely to have received traffic citations , especially for speeding
Cigarette and alcohol use were the only categories of substance use that differentiated hyperactives and normals.
When the the hyperactive sample was separated into groups (purely ADHD and ADHD + CD) purely ADHD subjects showed no greater use of cigarettes, alcohol, or marijuana than did normal controls.
Mixed hyperactive/Conduct disordered children displayed two to five times the rate of substance use as did pure hyperactives or normals .
Three times as many hyperactives had failed a grade (29.3% versus 10%), had been suspended (46.3% versus 15.2%) or had been expelled (10.6% versus 1.5%).
Results indicated that hyperactivity alone increases the risk of suspension (30.6% vs 15.2%), and dropping out
(4.8% vs 0% ) as compared to controls
However, the added diagnosis of CD greatly increases the risk (67% suspended, 13% dropped out).
The presence of CD accounted almost entirely for the > risk of expulsion within the hyperactive group
Prognosis In Adulthood
As many as 67% of children diagnosed with ADHD will display symptoms in adulthood serious enough to interfere with academic, vocational or social functioning.
There are indications that the type of ADHD that persists into adulthood is more highly genetic than the type that remits in childhood.
ADHD in adults is sometimes considered a “hidden disorder” as symptoms are often obscured by other problems.
Prevalence is thought to be 2 – 4% with sex ratio of 2 – 1 or lower ).
Maternal cigarette use
Maternal alcohol use
Unusually long or short labor
Birth during the month of September.
Minor physical anomalies
Etiology - Genetics
Between 10 and 35 per-cent of the immediate family members of children with ADHD also display this disorder.
Risk for siblings of children with disorder is approximately 32%
If a parent has ADHD the risk to offspring is on the order of 50+%
Twin studies suggest concordance rates for monozygotic twins is around 80% with concordance rates of approximately 30% for dizygotic twins.
Overall, twin studies suggest an average heritability of .80
Etiology: Molecular Genetics
Molecular genetics has begun to identify specific genes related to ADHD.
A “dopamine type 2 gene” has been found to be related to ADHD as well as Tourette’s and alcoholism.
More recently a "dopamine transporter gene" and a “dopamine repeater gene” have been identified.
This gene, found to be related to ADHD in multiple studies, seems to be related to post-synaptic sensitivity in the frontal and prefrontal cortical regions and to be associated with executive functions.
Genetic Contributions (cont.)
With developments in molecular genetics occurring at an increasingly rapid rate (due to the Human Genome Project), in the near future, we may have genetic tests that can provide early screening for ADHD and possibly associated comorbidities .
Genetic factors are clearly strongly implicated in the development of this disorder.
Hereditary is one of the most well supported etiological factors in the development of ADHD
Etiology – Neurological Insult
Multiple factors that can result in brain damage are associated with ADHD.
For example, anoxia, is associated with increased frequencies of hyperactivity and attentional problems.
ADHD occurs more often in children with seizure disorders, who are presumed to have neurological involvement
As was noted earlier, diseases such as encephalitis can also result in symptoms of ADHD as can various types of infections.
Etiology: Brain Damage
These findings suggest that neurological insult can result in an increased probability of developing ADHD.
However, most children with ADHD do not have a significant history of brain injury .
Indeed, such injuries are unlikely to account for ADHD in most children.
In fact probably 95% of hyperactive children show no evidence of documentable neurological impairment .
This does not mean, however, that neurological factors are not involved.
Neuropsychological Test Findings
Results from research involving neuropsychological testing has often suggested that children with ADHD have problems;
in inhibiting behavioral responses,
with working memory,
with planning and organization,
with verbal fluency,
In motor sequencing,
with other frontal lobe functions.
Research with Neuropsychological Testing (Cont.)
Not only do children with ADHD show executive functioning deficits but siblings of ADHD children who do not have ADHD , have milder yet significant impairments of the same type .
This suggests a possible genetic risk for executive function deficits in families.
Cerebral Blood Flow
Studies of cerebral blood flow in ADHD and normal children have consistently shown decreased blood flow to the prefrontal regions and pathways connecting these regions to the limbic system via the striatum and specifically its anterior region (the Caudate Nucleus)
Studies using PET scans to assess cerebral glucose metabolism in the frontal regions have found diminished metabolism in, adults and adolescent females with ADHD.
Cerebral Blood Flow Continued
Significant correlation's between diminished metabolic activity in the left anterior frontal region and severity of symptoms in adolescents with ADHD have also been demonstrated
This demonstration of a relationship between decreased metabolic activity of certain brain regions and severity of ADHD symptoms is crucial to documenting the importance of the link between brain activation and behaviors associated with ADHD
Early studies found differences in the Corpus Callosum, with this structure being smaller in children with ADHD. – Not always replicated .
Other MRI studies have found children with ADHD to have a smaller left caudate nucleus than did normal children. These findings are interesting in light of the results of earlier blood flow studies suggesting lower levels of activation in this specific area in children with ADHD.
Several more recent MRI studies, with larger samples, have replicated these early results by finding that ADHD children had significantly smaller anterior right frontal regions, a smaller caudate nucleus, and smaller golbus pallidus regions that normals.
Research has also found decreased cerebellar volume in ADHD children.
Work in this area suggests that abnormalities in the development of the frontal-striatal regions may well underlie the development of ADHD.
The possibility of a neurotransmitter dysfunction in children with ADHD has been suggested for many years.
This notion seemed to originate from observations of the response of children with ADHD to different type of stimulant drugs.
The fact that stimulant drugs have an impact on ADHD and that they increase dopamine has contributed to the neurotransmitter dysfunction hypothesis.
There is more direct evidence of neurotransmitter deficiencies from studies of cerebral spinal fluid in ADHD and normal children which suggests decreased dopamine levels in ADHD children
There is also some evidence of a deficiency in the availability of norepinephrine in children with ADHD.
This is of interest given that a very new non-stimulant ADHD medication, Straterra, is thought to act on norepinephrine levels.
Etiology: Psychosocial Factors
There is little evidence for the role of psychosocial factors in the development of ADHD, although factors such as parent-child conflict may exacerbate problems in a child with ADHD.
Psychosocial factors may also contribute to the development of certain comorbid disorders that may complicate the clinical picture.
In reviewing the literature on the etiology of ADHD, Barkley suggests …
“ It should be evident from the research…that neurological and genetic factors make a substantial contribution to symptoms of ADHD and the occurrence of this disorder.
A variety of genetic and neurological etiologies (e.g., pregnancy and birth complications, acquired brain damage, toxins, infections, and genetic effects) can give rise to the disorder through some disturbance in a final common pathway in the nervous system.
That final common pathway appears to be the integrity of the prefrontal cortical-striatal network.
It now appears that hereditary factors play the largest role in the occurrence of ADHD symptoms in children.
It may be that what is transmitted genetically is a tendency toward a smaller and less active prefrontal-striatal network.
The condition can also be caused or exacerbated by pregnancy complications, exposure to toxins, or neurological disease
Social factors alone cannot be supported as causal in this disorder, but such factors may exacerbate the condition, contribute to its persistence, and more likely, contribute to the forms of comorbid disorders associated with ADHD.
Cases of ADHD can arise without genetic predisposition if the child is exposed to a significant disruption or neurological injury to this final common neurological pathway, but this would seem to account for only a small minority of ADHD children. “
Treatment of ADHD
Commonly Used Stimulant Medications
Between 70 and 80 % of children with ADHD respond positively to stimulant drugs.
Stimulant drugs represent an empirically supported treatment for core symptoms of ADHD.
Side Effects of Stimulants
Common side effects can include: loss of appetite, weight loss, sleeping problems, irritability,