Psychiatric Manifestations of Attention Deficit Hyperactivity Disorder
- Author: Stephen Soreff, MD; Chief Editor: Eduardo Dunayevich, MD more...
Background
Attention deficit hyperactivity disorder (ADHD) is a developmental condition of inattention and distractibility, with or without accompanying hyperactivity. In the past, various terms were used to describe this condition, including hyperactive syndrome and, from the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III), "minimal brain dysfunction." In the revised DSM-III, this condition was renamed ADHD. In the DSM-IV-TR, adults or children must have had an onset of symptoms before age 7 years that caused significant social or academic impairment. More recently, attention has focused on adult forms of ADHD, which probably have been underdiagnosed.
Case study
The parents of a 7-year-old boy take him to the family practitioner because they have become increasingly concerned about his behavior not only in school but also a home. In the first grade, he has been bored, disruptive, fighting with classmates, and rude to his teacher. At home he cannot sit still and meals have been very unpleasant. The lad himself wonders why he is there. The parents have 2 older daughters who say their brother is a “pain” and spoiled. There were no pregnancy or birth problems and the child is on no medications. He has had all his scheduled shots.
The doctor decides more information is required before any treatment is indicated. She wants careful observations of the child both at home and in school. She wishes to talk with his teacher and suggests psychological testing. She also wants some time to see the patient alone. Careful investigation and thorough observations must be done before any intervention. Both the physician and the parents are concerned about overuse of medications and the value for behavioral interventions.
Pathophysiology
The pathology of ADHD is not clear. Psychostimulants (which facilitate dopamine release) and noradrenergic tricyclics used to treat this condition have led to speculation that certain brain areas related to attention are deficient in neural transmission. PET scan imaging indicates that methylphenidate acts to increase dopamine.[1] The neurotransmitters dopamine and norepinephrine have been associated with ADHD.
The underlying brain regions predominantly thought to be involved are frontal and prefrontal; the parietal lobe and cerebellum may also be involved. In one functional MRI study, children with ADHD who performed response-inhibition tasks were reported to have differing activation in frontostriatal areas compared with healthy controls. A 2010 study again indicated the presence of frontostriatal malfunctioning in the etiology of ADHD.[2] Although ADHD has been associated with structural and functional alterations in the frontostriatal circuitry, recent studies have further demonstrated changes just outside that region and more specifically in the cerebellum and the parietal lobes.[3] Another study using proton magnetic spectroscopy demonstrated right prefrontal neurochemical changes in adolescents with ADHD.[4]
Work by Sobel et al has demonstrated deformations in the basal ganglia nuclei (caudate, putamen, globus pallidus) in children with ADHD. The more prominent the deformations, the greater the severity of symptoms. Furthermore, Sobel et al have shown that stimulants may normalize the deformations.[5]
Adults with ADHD also have been reported to have deficits in anterior cingulate activation while performing similar tasks.
In a longitudinal analysis, Shaw et al used 389 neuroanatomic MRI images to compare 193 typically developing children with varying levels of symptoms of hyperactivity and impulsivity (measured with the Conners' Parent Rating Scale) with 197 children with ADHD (using 337 imaging scans).[6] Children with higher levels of hyperactivity/impulsivity had a slower rate of cortical thinning. This was most notable in prefrontal cortical regions, bilaterally in the middle frontal/premotor gyri, extending down the medial prefrontal wall to the anterior cingulate. It was also noted in the orbitofrontal cortex and the right inferior frontal gyrus. Slower cortical thinning during adolescence is characteristic of ADHD and provides neurobiological evidence for dimensionality.
A PET scan study by Volkow et al revealed that in adults with ADHD, depressed dopamine activity in caudate and preliminary evidence in limbic regions was associated with inattention and enhanced reinforcing responses to intravenous methylphenidate. This concludes that dopamine dysfunction may be involved with symptoms of inattention but may also contribute to substance abuse comorbidity.[7]
Individuals with ADHD have inhibition impairment, which is difficulty stopping their responses.[8]
Epidemiology
Frequency
United States
Incidence in school-age children is estimated to be 3-7%.
International
In Great Britain, incidence is reported to be less than 1%. The differences between the US and British reported frequencies may be cultural ("environmental expectations") and due to the heterogeneity of ADHD (ie, the many etiological paths to get to inattention/distractibility/hyperactivity). Furthermore, the International Classification of Diseases, 10th Revision (ICD-10) criteria for ADHD used in Great Britain may be considered stricter than the DSM-IV-TR criteria. However, other studies suggest that the worldwide prevalence of ADHD is between 8% and 12%.
Mortality/Morbidity
No clear correlation with mortality exists in ADHD. However, studies suggest that childhood ADHD is a risk factor for subsequent conduct and substance abuse problems, which can carry significant mortality and morbidity.
ADHD may lead to difficulties with academics or employment and social difficulties that can profoundly affect normal development. However, exact morbidity has not been established.
Sex
In children, ADHD is 3-5 times more common in boys than in girls. Some studies report an incidence ratio of as high as 5:1. The predominantly inattentive type of ADHD is found more commonly in girls than in boys.
In adults, the sex ratio is closer to even.
Age
ADHD is a developmental disorder that requires an onset of symptoms before age 7 years. After childhood, symptoms may persist into adolescence and adulthood, or they may ameliorate or disappear.
The percentages in each group are not well established, but at least an estimated 15-20% of children with ADHD maintain the full diagnosis into adulthood. As many as 65% of these children will have ADHD or some residual symptoms of ADHD as adults.
The prevalence rate in adults has been estimated at 2-7%. The prevalence rate of ADHD in the adult general population is 4-5%.[9]
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