ADHD and adult brain function
Evidence of the link between childhood ADHD and adult brain function adds to the significance of understanding the underlying biological causes of ADHD. Research recently published in the journal Biological Psychiatry addresses one important aspect; the authors state:
"Timing abilities are critical to the successful management of everyday activities and personal safety, and timing abnormalities have been argued to be fundamental to impulsiveness, a core symptom of attention-deficit/hyperactivity disorder (ADHD)...The present study examined subsecond sensorimotor timing and its neural substrates in ADHD adults."
They used functional magnetic resonance imaging of the blood oxygenation level-dependent contrast response to quantify task-related neural activity in unmedicated adults with ADHD and 19 control subjects. What did the data show?
"The imaging results demonstrated that, relative to control subjects, ADHD adults showed less activity in a number of regions associated with sensorimotor timing, including prefrontal and precentral gyri, basal ganglia, cerebellum, inferior parietal lobule, superior temporal gyri, and insula."
The authors' conclusion articulates our concern about the continuity of childhood and adult brain dysfunction:
"Our findings show that subsecond timing abnormalities in ADHD youth persist into adulthood and suggest that abnormalities in the temporal structure of behavior observed in ADHD adults result from atypical function of corticocerebellar and corticostriatal timing systems."
We can see the link between childhood and adult brain in the genetic potential transmitted from parent to child in a study just published in the Archives of General Psychiatry. The authors investigated the link between parental impairments in serotonin production and ADHD in their offspring:
"Exposure to adverse events during prenatal and postnatal development, as well as serotonin deficiency, have been implicated in disturbances of mood and impulsivity...To investigate the long-term effects of an impaired serotonin synthesis on the developing human brain, we studied the effects of nonsynonymous mutations affecting tryptophan hydroxylase (TPH) enzymes responsible for serotonin production in maternal reproductive tissues (TPH1) and the brain (TPH2)."
They investigated for the relevant genetic mutations among 459 patients with ADHD and 187 controls along with 97 additional family members. This was correlated with psychiatric diagnoses and symptoms obtained from 606 controls, the 459 patients, and their relatives. Their data paint a compelling picture:
"Family analysis of 38 TPH1 mutation carriers and 41 of their offspring revealed that offspring of mothers carrying TPH1 mutations reported 1.5- to 2.5-times-higher ADHD scores and related symptoms during childhood and as adults than did controls or offspring of fathers with the corresponding TPH1 mutations."
Clinicians and parents should bear in mind that medications that attempt to convert the brain to 'run' on insufficient amounts of serotonin do not repair or support the brain's ability to produce it adequately (as in the functional approach to natural precursor therapy) when contemplating the authors' conclusion:
"Impaired maternal serotonin production may have long-term consequences for brain development and increase the risk of ADHD-related symptoms and behavior in offspring."