ADHD drugs enhance human focus by expanding the levels of neurotransmitters from the prefrontal cortex of the brain which coordinate attention and behavior: norepinephrine and dopamine. Psychostimulants like methylphenidate (Ritalin) amphetamines (Adderall) encourage focus and attention, both in ADHD-diagnosed and non-ADHD-diagnosed people, regardless of one’s initial intellectual baseline.
Thus, giving stimulants to a person with a learning disability is like giving more time on a test: an advantage that might help anybody, but assists especially the ones in need (rather than fixing their brains).
In spite of the positive evidence, stimulant users do report different subjective realities: while ones get anxiety, others remain calm and relaxed. From a psychological point of view, it is assumed that part of the problem in ADHD is that the patient’s environment doesn’t stimulate their brains enough as it does in people without the disorder. As a result, ADHD-sufferers feel constantly bored and hence look for various ways to stimulate themselves by rapidly shifting their attention to something new. Therefore, in theory, by providing the missing excitement to the brain, these medicines allow ADHD people calm down and stay focused in a single activity.
Despite this highly plausible explanation, the neurological mechanism by which psychostimulants act as calming agents in humans with attention-deficit hyperactivity disorder or hyperkinetic disorder is currently unknown. Mice lacking the gene encoding the plasma membrane dopamine transporter (DAT) have elevated dopaminergic tone and are hyperactive, particularly when facing a novel environment. Furthermore, these mice are appreciably impaired in spatial cognitive function, and they display a decrease in locomotion in response to psychostimulants. The behavioural resemblance between the DAT knockout mice and individuals with ADHD bring to mind that common mechanisms may underlie some of their conducts and responses to psychostimulants, and that dopamine D4 receptor gene might be abnormal on these individuals.
“In contrast to the classical dopamine transporter (DAT)-dependent enhancement of the dopaminergic signal observed at concentrations of cocaine lower than 3 μM, the inhibitory effect of cocaine was found at concentrations higher than 3 μM. The paradoxical inhibitory effect of cocaine and methylphenidate was associated with a decrease in synapsin phosphorylation […] Interestingly, a cocaine-induced depression of DA release was only present in cocaine-insensitive animals (DAT-CI). Similar effects of cocaine were produced by methylphenidate in both wild-type and DAT-CI mice. On the other hand, nomifensine only enhanced the dopaminergic signal either in wild-type or in DAT-CI mice. Overall, these results indicate that cocaine and methylphenidate can increase or decrease DA neurotransmission by blocking reuptake and reducing the exocytotic release, respectively. The biphasic reshaping of DA neurotransmission could contribute to different behavioural effects of psychostimulants, including the calming ones, in attention deficit hyperactivity disorder”.
Thus, SUNY’s researcher David Erlij and his group of researchers sustain to have recognized a network of nerve terminals where stimulation of dopamine D4 receptors exhaust motor activity. This network seem to be localized deep in the brain, in the basal ganglia and the thalamus and its responses may explain the reduction in motor activity caused by psychostimulants. In this way, these results suggest that enhancing dopamine D4 transmission in the basal ganglia and the thalamus is likely part of the mechanism of the therapeutic effects of psychostimulants on ADHD patients.
In conclusion, because of genetic anomalies, people with ADHD might encounter stimulants antagonistically. While further research is required to clear up the mechanisms behind the cognitive enhancement itself (why does it also works for the healthy ones then?) at a neurological level, taking into account the subjective outcome of the individual -calm vs. nervous- becomes significant when choosing a treatment.
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