Biological Issues Related to Emotional/Behavioral Disorders
The consideration of biological issues related to emotional/behavioral disorders is the basis of the biophysical perspective. This view of the individual emphasizes neurologic and other organic factors as the cause of behavior. If the cause of behavior is organic, then it would folllow that the ways of dealing with emotional/behavioral disorders would include nutrition, medication, and other medical interventions.
Recent work in three areas has made significant contributions to the biophysical perspective. First, an analysis of risk factors has suggested a significant relationship between physical and mental health. Second, studies of families with histories of alcoholism and depression have raised questions of genetic predisposition. Finally, medical technology has provided far greater insight into psychoneurology and various brain functions.
The prevention of placing children at risk for physical and mental health problems begins at the onset of pregnancy (Slavin, 1989). Physical problems, such as lead poisoning and poor nutrition, have been related to children's behavioral problems in school. The last decade has seen significant reversals in the general health indicators that affect children. Studies by Baumeister, Kupstas, and Klindworth (1990) suggested that without specific prevention efforts, a "biological underclass" of children, whose problems are related to poverty, a lack of prenatal care, and the prevalence of chronic illnesses such as AIDS and Hepatitis B, will emerge.
The risks to children of poverty have been described by Parker, Greer, and Zuckerman (1988) as "double jeopardy." The interaction of both biological factors and poor social support puts children at serious risk for emotional/behavioral disorders. Children living in poverty are biologically vulnerable due to prematurity, maternal depression, temperamental passivity, and inadequate early stimulation.
The term genetic predisposition is used to describe the likelihood that a particular characteristic present in the parents will be present in their child. Although the particular gene responsible for the trait (characteristic) has not been identified, its likelihood suggests that some emotional/behavioral disorders may be inherited, or, "run in families." For example, it is estimated that 30% of fathers and 20% of mothers of children with attention deficit hyperactivity disorder have the disorder themselves (Copps, 1992). Alcoholism and drug abuse may also be linked to genetic predisposition (Crabbe, MccSwigan, & Kelknap, 1985). The occurrence of schizophrenia, a very low-incidence disorder, has been studied in families. According to Paul (1980), the children of schizophrenic individuals are far more likely to have schizophrenia, and among identical twins, even those raised apart, there is the same incidence of schizophrenia.
Using the case of Attention Deficit Hyperactivity Disorder, Copps (1992) describes the evolution of our understanding of the psychoneurological bases of some emotional/behavioral disorders.
Copps relates the history of Attention Deficit Hyperactivity Disorder as beginning in 1845, when Henrich Hoffman described "fidgety Phil," the boy who never sat still, as being naughty, rude, and wile (cunning). In 1902, George Still indicated that such children had a "deficit in moral control." However, he described a biologic deficit in "inhibitory volition" because these children often had competent parents who would not typically have had such "morally defective" children.
Following an outbreak of encephalitis in the 1 940s, there were reports of children becoming disruptive, inattentive, and hyperactive as a result of being afflicted with this neurologic disease. These children were referred to as "brain damaged" or "behavior disordered"; children who did not have a physically detectable neurologic deficit were said to have "minimal brain damage." Despite intensive study of children who demonstrated these behaviors, direct evidence could not be found for minimal brain damage. Because no evidence of damage was detected, and also because the term itself was considered distasteful, the name of this condition was changed to "minimal brain dysfunction."
As the symptoms of Attention Deficit Hyperactivity Disorder became increasingly accepted as a dysfunction, rather than a damage, and as a result of a resurgence of a belief in the idea that nurture, rather than nature, determined a child's behavior, poor parenting emerged as a probable cause of this disorder. The response to medication, however, increasingly cast doubt on ineffective parenting and supported a biological cause.
With increased technology, it became possible to measure the functioning of the brain and levels of neurotransmitters, which are chemicals in the brain that affect the efficiency with which the brain functions. It became apparent that individuals with Attention Deficit Hyperactivity Disorder show a deficiency or imbalance in the chemical elements catecholamine, dopamine, and norepinephrine. Although it is not yet clear whether there is a decrease in production or excessive absorption of these neurotransmitters, a significant body of evidence indicates that inefficient transmission of neurological impulses affects the entire attention system of the brain, including attention, inhibition, and motor planning. Viewing Attention Deficit Hyperactivity Disorder in this way, children with this disorder have a deficiency in executive control, which governs the inhibition and monitoring of behavior. These students then neurologically have difficulty selecting and maintaining goals, anticipating, planning, completing tasks, and adapting plans.
Similar evolutionary paths are apparent in our understanding of pervasive developmental disorders, including autism, which was once thought to be a consequence of inadequate parenting, but is now thought, by some, to be a complex neurological disorder; Tourette's disorder; borderline personality disorder; and obsessive compulsive disorder. These disorders, with the exception of autism, will be discussed in more detail in another section of this chapter.
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.
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