Causes
Unlike ADHD, the general causes of SCT symptoms are unknown, though some studies of twins suggest that the condition appears to be as heritable or genetic in nature as ADHD. That is to say that the majority of differences among individuals in these traits in the population may be due mostly to variation in their genes. For instance, in ADHD, the genetic contribution to individual differences in ADHD traits typically averages between 75 and 80% and may even be as high as 90%+ in some studies. Far less is known about this group having SCT yet the impairments seem to indicate that the posterior attention networks may be more involved in the disorder than the prefrontal cortex region of the brain and difficulties with working memory so prominent in ADHD. While the 7-repeat allele polymorphism of the DRD4 gene is also linked more strongly as those with ADHD-PI group as those with ADHD/C subgroups, there are no studies of molecular genetics that specifically evaluated individuals having SCT.
Although ADHD appears to be linked to problems with the availability of or sensitivity to variations dopamine and norepinephrine, and/or the efficiency of the large chemical structures of the specific receptors and re-uptake receptors, the neurotransmitters that may be linked to SCT are unknown.
A recent study found a link between thyroid functioning and SCT, but effects were small and suggests that thyroid dysfunction is not the cause of SCT. SCT symptoms were also observed in pediatric survivors of acute lymphoblastic leukemia, where they were associated with cognitive late effects. Another study found high rates of SCT in children who had suffered prenatal alcohol exosure. However, since as much as 5% of the population may have SCT, these causes may not account for the majority of cases.
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