Biological Issues Related to Emotional/Behavioral Disorders (continued)

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One construct that frequently emerges in discussions of the psychoneurological bases of emotional/behavioral disorders is executive function. Executive function regulates, integrates, and coordinates other cognitive functions, such as attention, memory, language, and visual-spatial skills, toward the successful completion of goals (Welsh, 1994). Executive functioning supports successful problem solving and strategizing. Any unique academic task that requires critical thinking, judgment, planning, or self-monitoring requires executive function skills.

Executive function has great implications for behavior. Welsh (1994), using the available vast research base, suggests that executive functioning skills are mediated in the prefrontal section of the brain. The symptoms demonstrated by adult patients who have received damage to the frontal lobe suggest that this part of the brain is uniquely dedicated to support the executive function activities of insight, anticipation, planning, self-evaluation, and goal directedness (Damasio, 1985; Fuster, 1980).

Attention Deficit Hyperactivity Disorder again provides a good example of the complexity of the impact of psychoneurological processes and behavior. Studies have demonstrated that in some learners with Attention Deficit Hyperactivity Disorder, the central nervous system is underaroused (Ferguson & Rappaport, 1983). In addition, decreased cerebral blood flow has been documented in the frontal lobe of these learners, and the use of a stimulant medication, Ritalin, increased the blood flow to this area of the brain (Lou, Henricksen, & Bruhn, 1984). Ritalin released stored dopamine, a neurotransmitter, from neurons, suggesting that the level of neurotransmitters also has an effect on executive function. In a later study, Lou, Henriksen, Bruhn, Borner, and Nielsen (1989) found more specifically that the locus of the diminished blood flow was the basal ganglia, the structure in the subcortex with many dopamine receptors that connects to the frontal lobe. Neurochemical research (Shaywitz, Cohen, & Bowers, 1983) has indicated that the depletion of dopamine may underly attention deficits; Ritalin releases stored dopamine, decreases motor activity, and supports increased attention in many learners with Attention Deficit Hyperactivity Disorder (Barkley, 1977).

Glucose utilization has been related to central nervous system underarousal and Attention Deficit Hyperactivity Disorder (Pennington, 1991). Among learners identified as emotionally/behaviorally disordered, glucose underutilization has been isolated in the right frontal lobe and increased utilization in posterior brain regions (Zametkin, Nordahl, Gross, King, Semple, Rumsey, Hammburger, & Cohen, 1991). So, at least in terms of Attention Deficit Hyperactivity Disorder, the psychoneurological bases of behavior may be a complex interaction of structure, blood flow, and neurotransmitter release,

The role of neurotransmitters in self-esteem and aggression has also been explored. The brain uses several dozen neurotransmitters and hormonal systems during information processes. Sylvester (1997) contends that fluctuations in serotonin, one of the neurotransmitters, plays an important role in regulating self-esteem and position in the social hierarchy. High levels of serotonin are related to high self-esteem and social status and low levels to low self-esteem and social status. High levels are related to smooth control, and low levels are related to impulsive, reckless, violent, or suicidal behavior.

Sylvester (1997) suggests that it is possible to stimulate serotonin when conditions are adverse and self-esteem and serotonin levels are low. Administering a medication such as Prosac is one way to increase serotonin levels that enhances self-esteem. Increased self-esteem enhances mood, leading to positive social feedback, allowing the natural system to take over in time. Alcohol, sometimes used by individuals to deal with depression, increases serotonin short-term, but eventually depletes the store of serotonin, even further decreasing impulse control.