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Attention-Deficit/Hyperactivity Disorder - Brain Regions and their Dysfunctions



ADHD: Attention-Deficit/Hyperactivity Disorder

"We hypothesize that impaired PFC and ACC function in ADHD reduces the ability to optimally recruit subsidiary brain regions and strategies to perform cognitive tasks. (...) individuals with ADHD may be less able to engage higher order executive systems to flexibly recruit brain regions to match given task demands. This may result in greater reliance on neuroanatomy that is associated with visual, spatial, and motoric processing rather than verbal strategies. The authors speculate that this impaired flexibility in recruiting brain regions and associated strategies limits adaptation to new cognitive demands as they present and may require more effortful processing." S

"From a pathophysiological point of view, the most striking functional differences between healthy adolescents and ADHD patients were in the ACC and SPL. We suggest that increased SPL activation in ADHD reflected attentional compensation for low ACC activation during the encoding of neutral pictures. The higher salience of emotional stimuli, in contrast, regulated the interplay between ACC and SPL in conjunction with improving memory to the level of healthy adolescents." S

"Relative to controls, ADHD adults had significantly smaller overall cortical gray matter, prefrontal and ACC volumes." S
Affected Region Dysfunctions
Prefrontal Cortex Impaired PFC and ACC function reduces the ability to optimally recruit subsidiary brain regions and strategies to perform cognitive tasks. S
Superior parietal lobule ACC dysfunction leads to a failure to predict the likelihood that an error occurs in a given context; the performance limitations in ADHD may be caused by a specific deficit in monitoring ongoing behaviour, rather than insufficient strategic adjustments S

Functional differences in the SPL: increased SPL activation reflects attentional compensation for low ACC activation during the encoding of neutral pictures S

"The right ACC was significantly smaller for the ADHD-treatment na´ve group compared to the ADHD-treated and control group." S
Medial temporal lobe Diminished MTL-ACC response pattern: "deficits in higher-level functions might be secondary to disruptions in earlier limbic processes." S
Anterior cingulate cortex ACC dysfunction leads to a failure to predict the likelihood that an error occurs in a given context; the performance limitations in ADHD may be caused by a specific deficit in monitoring ongoing behaviour, rather than insufficient strategic adjustments S

ACC is functionally different in adolescent ADHD patients: low ACC activation during the encoding of neutral pictures S
Basal ganglia, Striatum "These preliminary results suggest that the DAT1 gene (dopamine transporter gene) effects in the striatum are involved in translating the genetic risk of ADHD into a neurobiological substrate." S

" Dysfunction of basal ganglia is a consistent finding in childhood and adulthood ADHD, reflecting dysregulation of fronto-striatal circuitry." S
Caudate nucleus "There were significant differences bilaterally on caudate volume for both ADHD groups (ADHD-treatment na´ve group compared to the ADHD-treated) vs controls, with no difference between the ADHD groups on either side." S
Superior colliculus "It is proposed that in ADHD, the colliculus is hyper-responsive, leading to the core symptom of increased distractibility." S
Cerebellum "The cerebellum, and its role in affect and cognition, is also persistently implicated in the pathology of ADHD." S

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