The complex neuropsychiatric condition known as Attention Deficit Hyperactivity Disorder (ADHD) is characterized by persistent, developmentally appropriate levels of impulsivity, inattention, and overactivity. Inattentive and hyperactive/impulsive behaviors are the two broad groups into which childhood ADHD symptoms fall. However, due to aging or changing circumstances with new behavioral restrictions, symptoms frequently lessen with time or become less noticeable. The causes of ADHD, which differ from person to person and include genetic, environmental, and neurological foundations, are exceedingly varied.
Neurotransmitters, which are released between the synapses of neurons to stimulate the following cell in the pathway, are used to convey information via neural circuits from one area of the brain to another. Neurotransmitter deficits are prevalent in many disorders including anxiety and obsessive-compulsive disorder (OCD). ADHD has been found to be linked with a deficiency of the norepinephrine neurotransmitter. Through the precursor molecule dopa, norepinephrine is also connected to dopamine, the transmitter related to the reward and pleasure center of the brain. The brain's reinforcement signal and the mechanisms of reinforcement learning have both been strongly linked to dopamine. The dopamine cell response to rewarding stimuli typically extends to earlier cues that predict reinforcement. Dopamine cell response to cue-predicting reinforcement fails to transfer in children with ADHD. Alterations in dopamine function may underline symptoms of ADHD related to altered reward processing.
In addition to neurotransmitter deficit, the ADHD brain has impaired activity in four functional regions of the brain: the frontal cortex, the limbic system, the basal ganglia, and the reticular activating system. Executive function is the neurocognitive process that organizes thoughts and activities, prioritizes tasks, manages time efficiently, and maintains an appropriate problem-solving set to attain a later goal. Norepinephrine insufficiency results in poor executive function, disarray, and inattentiveness. The limbic system controls emotions and attention. An imbalance in this area leads to agitation, inattention, or emotional instability. By sending information to the appropriate areas of the brain, the neural circuits of the basal ganglia control communication between brain regions. An information "short-circuit" caused by a weakness in this area could result in impulsivity or inattention. Inattention, impulsivity, or hyperactivity would come from a deficiency in the brain's principal relay system, the reticular activating system (RAS).
Neuroimaging has noted differential abnormalities and delineated gross anatomical changes in brain dimensions. Executive function, motivation, and vigilance-attention were the key areas where deficiencies occured, with a specific emphasis on altered processing of rewards and reinforcement. A decreased total brain volume has been observed, as well as smaller volumes in a number of subcortical (e.g. amygdala, thalamus, basal ganglia, cerebellum) and cortical (e.g. prefrontal, premotor, anterior cingulate, temporal, anterior insula, supplementary motor, primary sensorimotor). Noted anomalies include reduced volume, increased gray matter density, and increased cortical thickness in the same locations. Despite the fact that ADHD is a heterogeneous condition and symptoms vary from person to person, distinct abnormalities of the head and body of the caudate nucleus can explain inconsistencies.
Neuroimaging collections of biological measurements of the brain aims to increase our understanding of the biological underpinnings of ADHD to facilitate the application of findings in clinical diagnosis and treatment. Significant developments increase the understanding of the most commonly identified neuropsychological deficits on ADHD that can further inform the neuroanatomical study of ADHD.
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