Academic journal article Exceptional Children

Neurological Basis of Attention Deficit Hyperactivity Disorder

Academic journal article Exceptional Children

Neurological Basis of Attention Deficit Hyperactivity Disorder

Article excerpt

As described by McBurnett, Lahey, and Pfiffner (this issue), the conceptualization of attention deficit disorder (ADD) in the Diagnostic and Statistical Manual (DSM) of the American Psychiatric Association (1968,1980,1987) has changed over time. Concurrent with shifts in conceptualization and changes in diagnostic nomenclature, research related to the neurological basis of ADD has taken a variety of theoretical approaches (Hynd, Hem, Voeller, & Marshall, 1991).

One can study attentional mechanisms from a neuroanatomical, neurochemical, or neurophysiological perspective. The neuroanatomical approach focuses on the location of brain areas that subserve those systems thought to mediate the regulation of attention and inhibit motor activity. The neurochemical approach addresses the role of specific neurotransmitters that facilitate communication among the neuronal circuits implicated in this disorder. The neurophysiological perspective attempts to explain the dynamic interaction between the neurochemical and anatomical components that together form a functional system. Professionals who work with these children should have some understanding of these models, as well as the neurocognitive correlates. Although we will not attempt here to resolve the issues regarding the neurological basis of ADD, we will review the various models and supporting research. When feasible, we also will review the neurocognitive deficits associated with each model, along with associated research.

One of the problems facing researchers attempting to localize or identify the neurological basis of ADD is the inability to map behavioral descriptors onto relevant neurologic components. Swanson et al. (1991) have argued that presumed attentional deficits can be linked neither to specific cognitive operations nor to specific neural systems. Although researchers perceive attention as a unitary process, it appears to be subserved by a number of brain structures with a corresponding variety of symptoms and etiology related to attentional deficits (Colby, 1991). This is complicated by the lack of operationalized criteria for ADD and the heterogeneity of the clinical group identified as ADD (Goodyear & Hynd, 1992; Hynd, Semrud-Clikeman et al., 1991). Routine neurological examination of children with ADD is generally normal, and clinical evaluations with neuroimaging (computerized tomography [CT], magnetic resonance imaging, [MRI]) and electroencephalographic [EEG]) studies typically do not reveal specific lesions (Shaywitz, Shaywitz, Byrne, Cohen, & Rothman, 1983; Voeller, 1991). Despite these problems, however, the recent expansion of technology has led to adaptations in traditional imaging and electrophysiological methods, resulting in evidence of some structural/morphological differences in the brains of children with ADD as a group Voeller, 1991).

NEUROANATOMICAL BASIS OF ADD

Typically, these hypotheses propose the involvement of cortical (frontal) and subcortical structures (brain stem reticular activating system, thalamus, hypothalamus, and basal ganglia). These are identified in Figure 1. Parallels have been drawn between frontal lobe dysfunction and ADD, with the prefrontal region, in particular, posited as involved in ADD (Chelune, Ferguson, Koon, & Dickey, 1986; Gualtieri & Hicks, 1985; Hynd, Semrud-Clikeman, Lorys, Novey, & Eliopulos, 1990; Mattes, 1980; Voeller & Heilman, 1988). One possible explanation includes a developmental delay in the myelination of the prefrontal area (Mattes, 1980).

Support for frontal lobe involvement comes from positron emission tomographic (PET) scan studies with findings of reduced whole brain glucose utilization, particularly in the right frontal area, and specifically the posterior-medial orbital areas (Zametkin et al., 1990). Researchers have found, through regional cerebral blood flow comparisons of dysphasic, ADD, and control children, that the ADD children showed decreased metabolic activity in the frontal lobes and basal ganglia, with increased metabolic activity in the primary sensory and sensorimotor regions (Lou, Henriksen, & Bruhn, 1984; Lou, Henriksen, Bruhn, Borner, & Nielsen, 1989). …

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