The Neurological Basis of Attention Deficit Hyperactivity Disorder

Article excerpt

In the last decade, attention deficit hyperactivity disorder (ADHD) has received significant attention from the education and counseling communities, with some considering it a life disability (Silver, 1992). The problems encountered by an individual diagnosed with ADHD occur not only during the school years, but throughout the entire life span.

ADHD is found in 3-6% of the child population in the United States, or nearly 2 million children (Dulcan & Popper, 1991). Recent estimates indicate that close to 40% of children referred to mental health clinics show symptoms of ADHD. It is more likely to occur in males than females, with ratios as high as 9:1 in clinic populations. Since boys are usually more aggressive and thus more likely to be referred, ADHD in girls may go unrecognized and untreated (Barkley, 1981).

ADHD is a biological disorder (with heredity playing a role) that can be exacerbated by social factors. A person's ability to maintain attention, self-regulate impulsivity, and delay gratification are all symptoms and, correspondingly, are prefrontal brain functions. Symptoms of the disorder often appear in early childhood.

A number of explanations have been postulated as to why attention deficit children evidence undesirable behavioral, social, and learning characteristics. Goodman and Poillion (1991) have indicated that the majority of causes of ADHD are attributable to organic problems. Their research indicated that genetics is the only presumed cause of ADHD, sighted by 48% of the authors they investigated. However, no specific gene responsible for ADHD has yet been isolated. There is some evidence that ADHD-type behaviors tend to recur in families, especially in first- and second-degree relatives of ADHD children (Barkley, 1981). While ADHD behaviors may be precipitated by deleterious social factors, with the exception of head injury occurring at a young age, there is no evidence of a single environmental agent causing ADHD (Pennington, 1991).

Research involving neurological factors has provided insight into the brain that may relate to the attention deficit characteristics of children diagnosed with ADHD. Neuroanatomical studies have sought to explain ADHD in terms of brain areas that are considered important in the regulation of attention, while neurochemical studies have considered the role of neurotransmitter substances (Hynd, Kytja, Voeller, Hern, & Marshall, 1993). Neurophysiological research has investigated the interaction between neurochemical and anatomical components of the brain.

The brain consists of modules specialized for processing specific data. These modules are autonomous to a degree in both function and neural representation (Fodor, 1983). The outermost layer of the brain represents the cerebral cortex. The cortical (frontal) section of the brain is related to learning and thinking. The layer underneath, the subcortex, comprises a relay system that is involved in sending messages to the processing and memory parts of the brain. This subcortical system consists of the brain stem's reticular activating system, thalamus, hypothalamus, and basal ganglia. Recent research suggests that ADHD children generally have impaired functioning in the cortical, and subcortical areas (Garber, Garber, Spizman, 1990). In particular, frontal lobe and prefrontal lobe dysfunction have been suggested (Hynd et al., 1991). This is significant because the frontal and motor cortex play a role in attention, impulsivity, and motor activity. It has been proposed that within the prefrontal area, different sections specialize in certain representative functions. For instance, the dorsal convexity maintains spatial representations, while the orbital area maintains representations of rewards or motivators, including social rewards (Pennington, 1991). Positron emission tomography (PET) scan studies have shown reduced brain glucose utilization, particularly as related to the right frontal lobe, in ADHD children (Zametkin & Rapoport, 1987). …