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However, when these children were investigated in two other "smell" categories, which included discrimination between different smells, and the actual identification of particular agents causing the smell, they should no advantages over their non-ADHD peers. Similar studies have also been done on adults with ADHD, and have shown little to no effect between ADHD and sense of smell. These findings seem to agree with another recent report on olfactory impairments in children with ADHD. This study found that children with ADHD were worse at identifying the nature of particular odors than non-ADHD children. It appears that these deficits are tied to a specific brain region called the orbitofrontal region, the outer section which is approximated by the green region in the diagram below (original file source can be found here). Note that this region has numerous implications with regards to the disorder of ADHD.

To throw another wrinkle into the mix, it appears that stimulant medication treatments for ADHD may negate these olfactory advantages (with regards to the increased ability of ADHD children to detect minute levels of odors better than their peers). The Romanos study also investigated another group of similar age and gendered individuals with ADHD who were on the medication methylphenidate (Ritalin, Concerta, Daytrana, etc.). Like the non-medicated ADHD children, this group all had the combined subtype of ADHD (meaning that both hyperactive/impulsive as well as inattentive symptoms were present to a large extent). They found that the medicated children did not have the improved smell sensitivity that their non-medicated ADHD peers did, but rather had an odor detectability level similar to that of the non-ADHD group. In other words, it appeared that methylphenidate (as well as other ADHD stimulant medications, potentially), may offset any improvements in smell detection in ADHD individuals.

It is believed that the dopamine system and pathways play a critical role in smell differences between ADHD children and their peers. Keep in mind that methylphenidate and most other stimulants for ADHD work by increasing the concentration of the neurotransmitter dopamine in the areas between neuronal cells, by reducing the transport of this important brain chemical into the cells themselves (individuals with ADHD often have an imbalance between the dopamine levels inside and outside of these neurons, and often have insufficient dopamine levels in the surrounding areas outside the neuron cells). Dopamine levels have been shown to have a protective effect on olfactory neurons (neurons related to smell). Chemical alterations of dopamine levels, such as those introduced by methylphenidate or other ADHD stimulants may therefore interfere with odor sensitivities in key regions of smell such as the olfactory bulb region of the brain.

On a final note, the findings by Romanos and coworkers are of potential interest because of the fact that many neuropsychiatric disorders are accompanied by a sharp decrease in odor detection and sense of smell. These include Parkinsons Disease, obsessive-compulsive disorder (OCD), schizophrenia, autism, and depression. Because of this, it may be possible to use odor sensitivity tests to help differentiate between ADHD and other neuropsychiatric disorders, at least in children. Although we have seen that there is some conflicting evidence surrounding studies, it appears that we could, at least in theory, administer some type of smell test of trace levels of specific odorous chemical agents that are undetectable to the majority of the child population and see whether the potential ADHD candidate could detect these minute traces. Furthermore, it would be interesting to see whether other stimulant medications besides methylphenidate have the same effects on curbing the increased odor sensitivities exhibited in ADHD children.