![]() At least one study has shown that there are not long-term changes in neurological anatomy5, although more follow-ups from RCTs should be conducted to determine the neurological changes potentially caused by long-term stimulant use.Įxploring the neuropsychology of intellectual disability: Multisystemic and dimensional views of intellectual and adaptive functioning However, while the short-term effects of stimulants on children with ADHD have been studied extensively, far less focus has been placed on the effects of long-term use on neurological development in children. It is hypothesized that stimulant medication reduces inattentive, hyperactive, and impulsive behaviors by increasing the binding of dopamine (and to a lessor extent, norepinephrine), either by antagonizing synaptic monoamine transporters (methylphenidate) or pre-synaptic vesicular monoamine transporters (amphetamine). Stimulants, including methylphenidate and amphetamine, have been shown to effectively reduce symptoms of Attention-Deficit/Hyperactivity Disorder (ADHD) and are strongly recommended by the American Academy of Pediatrics for the treatment of symptoms of ADHD in children 6 years and older.1,2 Positron emission tomography (PET) has been used to show that individuals with ADHD experience lower dopamine receptor binding in the nucleus accumbens compared to controls3, and diffusion tensor imaging (DTI) has shown reduced white matter projections between the nucleus accumbans and regions of the midbrain and cortex4. Stimulant use in ADHD: Pathways of activation, immediate effects, and long-term neurological changes ![]() Given that the microbiome influences reward processing, current research is investigating whether changes in the microbiome targeting the creation of these building blocks may be a feasible intervention for ADHD (Stevens et al., 2019). In the gut, monoamines, which are building blocks for neurotransmitters like dopamine, are formed (Aarts et al., 2017). One explanation for reward processing deficits is dysregulation of the reward neural network, particularly the uptake of dopamine (Aarts et al., 2017 Volkow et al., 2010). Attention-deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder defined by executive functioning deficits (Kasper, Alderson, & Hudec, 2012 Nigg, 2001), including aberrant reward processing (Aarts et al., 2017). Where the research stands on ADHD and the gut-brain axisĪ growing field of literature aims to understand the relationship between the brain and the microbiome of the gut, as well as its significance to mental health (Grenham, Clarke, Cryan, & Dinan, 2011 Sarkar et al., 2016).
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