Etiology Of ADHD

The etiology of ADHD is unclear and there are various factors that may contribute to the ADHD, pre-natal and peri-natal complications, genetic Mendelian inheritance and^[33][34]epigenetic inheritance. Research on children with ADHD has shown a general reduction of brain volume, but with a proportionally greater reduction in the volume of the left-sided prefrontal cortex. These findings suggest that the core ADHD features of inattention, hyperactivity, and impulsivity may reflect frontal lobe dysfunction, but other brain regions particularly the cerebellum have also been implicated. Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research not diagnostic purposes.A review of published studies involving neuroimaging, neuropsychological genetics, and neurochemistry found evidence to suggest that four connected frontostriatal regions play a role in the pathophysiology of ADHD: The lateral prefrontal cortex, dorsal anterior cingulate cortex, caudate, and putamen.

Neuroimaging studies conducted by the National Institute of Mental Health showed a delay in subjects with ADHD in "attaining peak thickness throughout most of the cerebrum: The delay was most prominent in prefrontal regions important for control of cognitive processes including attention and motor planning". In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterizes ADHD.

Maturation of the brain, as reflected in the age at which a cortex area attains peak thickness, in ADHD (above) and normal development (below). Lighter areas are thinner, darker areas thicker. Light blue in the ADHD sequence corresponds to the same thickness as light purple in the normal development sequence. The darkest areas in the lower part of the brain, which are not associated with ADHD, had either already peaked in thickness by the start of the study, or, for statistical reasons, were not amenable to defining an age of peak cortex thickness. Source: NIMH Child Psychiatry Branch

Stimulant medication may itself affect growth factors of the central nervous system.^[42]

The same laboratory had previously found involvement of the "7-repeat" variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement.

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity), and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce dopamine itself. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to "childhood learning problems" in healthy subjects as well. One interpretation of dopamine pathway tracers is that the biochemical "reward" mechanism works for those with ADHD only when the task performed is inherently motivating; low levels of dopamine raise the threshold at which someone can maintain focus on a task which is otherwise boring.

A 1990 PET scan study by Alan J. Zametkin et al. found that global cerebral glucose metabolism was 8% lower in medication-naive adults who had been hyperactive since childhood. Further studies found that chronic stimulant treatment had little effect on global glucose metabolism, a 1993 study in girls failed to find a decreased global glucose metabolism, but found significant differences in glucose metabolism in 6 specific regions of the brains of ADHD girls as compared to control subjects. The study also found that differences in one specific region of the frontal lobe were statistically correlated with symptom severity. A further study in 1997 also failed to find global differences in glucose metabolism, but similarly found differences in glucose normalization in specific regions of the brain. The 1997 study also noted that their findings were somewhat different than those in the 1993 study, and concluded that sexual maturation may have played a role in this discrepancy^. The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results.

dikutip dari : http://en.wikipedia.org/wiki/Attention-deficit_hyperactivity_disorder