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Neurological basis of attention deficit hyperactivity disorder.

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). Quantitative analysis of EEGs in boys with ADD revealed increased slow wave activity, predominantly in the frontal regions, and decreased beta activity in the temporal regions, compared to normal controls matched for age and sex (Mann, Lubar, Zimmerman, Miller, & Muenchen, 1992). This would indicate possible decreased cortical arousal in these children in those areas of the brain frequently associated with executive control and language. Hynd, Semrud-Clikeman, et al. (1990) used NMI to image the frontal lobes of children with ADD, dyslexia, and normal controls. Findings revealed decreased right frontal width measurements in children with ADD relative to normals, providing additional morphological evidence of frontal lobe involvement in ADD.

In conjunction with the frontal lobe, the caudate nucleus (within the basal ganglia on Figure 1) has also been implicated as involved in the neurological basis of ADD, partly because of the resemblance of ADD to the spectrum of behaviors associated with dysfunction in the caudate-frontal axis, a system in the brain known to be important in motor regulation and behavioral inhibition (Pontius, 1973; Zambelli, Stamm, Maitinsky, & Loiselle, 1977). Evidence to support possible dysfunction of the caudate includes cerebral blood flow studies, with findings of decreased metabolism in the caudate, particularly the right caudate (Lou et al., 1989).

Neuroimaging studies using MRI scans have revealed similar differences in the size of the right caudate, relative to the left, in children with ADD when compared to normal controls (Hynd, Hem, et al., in press). Specifically, as with the frontal lobes, the normal "right greater than left" asymmetry of the caudate appears to be absent in children with ADD compared to normal children. Further, inspection of MRI scans showed that children with ADD had a smaller corpus callosum in the region of the genu and the splenium and in the area just anterior to the splenium. Though subtle, the anatomical differences in these children may ultimately affect the cooperative, as well as individual, functioning of the hemispheres. This is because interhemispheric fibers (pathways) in these regions interconnect the two hemispheres of the brain, including the left and right frontal, occipital, parietal, and posterior temporal regions (Hynd, Semrud-Clikeman et al., 1991).

Whether the research focused on the frontal lobes or the basal ganglia, there is a tendency to implicate structures in question as located in the right hemisphere. Vallar and Perani (1986) have argued that the right hemisphere is specialized for attentional processes in adults; and Heilman, Voeller, and Nadeau (1991) have argued that this specialization occurs for the control of various aspects of motor response. For example, adult patients with right central-posterior lesions have shown less arousal when compared with patients with left hemisphere lesions (Heilman, Schwartz, & Watson, 1978). Further, other researchers have found a higher incidence of attentional deficits, problems in vigilance, distractibility, and difficulty performing intentional motor activities in children and adults with documented right hemisphere lesions (Heilman et al., 1991; Heilman Van Den Abell, 1980).

Some researchers have documented the relationship between the hyperactivity/impulsivity aspects of ADD and anterior or frontal lobe functioning, based on neurocognitive tasks (Chelune et al., 1986; Luria, 1980), whereas others have explored the relationship between the attentional aspects of ADD and right hemisphere parietal (posterior) lobe functioning (Ogden, 1985; Schaughency & Hynd, 1989). In view of these results, Schaughency and Hynd (1989) have posited that an anterior (frontal)-posterior (parietal) gradient may well exist in the differential effects (attention deficit disorder with hyperactivity vs. attention deficit disorder without hyperactivity) of these separate yet correlated systems. The relationship between these neuroanatomical/behavioral subtypes, however, have not been borne out by a study of group comparisons (Matazow Hynd, 1992a). Results of studies of frontal lobe functioning in children with ADD are equivocal, and Welsh and Pennington (1988) have cautioned against the interpretation of developmental alterations in prefrontal function as evidence of ADD. Not all studies focusing on the neurocognitive functioning of children with ADD have demonstrated significant frontal dysfunction for the group (Loge, Staton, & Beatty, 1990). Further, Benson (1991) has argued that the neurological basis of ADD cannot be limited to frontal immaturity or anomaly and that ADD appears to be related to more widespread dysfunction. Thus, while the frontal/prefrontal area has been consistently implicated, there continue to be dissenting opinions.

Research conducted on the neurobehavioral characteristics of children with evidence of right hemisphere dysfunction, based on neurological or neuropsychological measures, provides additional support for involvement of the right hemisphere in ADD (Heilman et al., 1991; Voeller & Heilman, 1988). In examining the behavioral, neurological, and neuropsychological characteristics of children with evidence of right-hemisphere dysfunction, Voeller (1986) found that 93% of the children met criteria for ADD. Results of a study comparing children with ADD with hyperactivity, children with ADD without hyperactivity, and children with learning disabilities on various neuropsychological measures of right and left hemisphere functioning, however, indicated that ADD is not simply attributable to right hemisphere dysfunction, but may involve a number of different brain systems, possibly implicating different functional systems in those children with or without the hyperactivity component (Matazow & Hynd, 1992b). In addition, results of a prospective study comparing children with right hemisphere dysfunction with children with left hemisphere dysfunction indicated that there were no significant group differences on rating scales sensitive to ADD. Group differences did emerge, however, on measures of impulsivity, with the right hemisphere dysfunction group evidencing significantly more errors of commission on a computerized continuous performance task (Branch, Cohen, & Hynd, 1992).

NEUROCHEMICAL BASIS OF ADD

The focus on the neurochemistry of ADD, and specifically the dopaminergic neurotransmitter system, has been reviewed in detail by Zametkin and Rapoport (1987). Researchers have generally accepted that the catecholamines (dopamine, norepinephrine) are implicated in ADD and appear to affect a wide variety of behaviors, including attention, inhibition and response of the motor system, and motivation (Clark, Geffen, & Geffen, 1987a, 1987b). Related to the focus on neurotransmitters, Mefford and Potter (1989) postulated that an imbalance in the formation of dopamine or norepinephrine resulted in the decreased stimulation of the locus coerulcus (brain stem reticular activating system in Figure 1). Some support for this conceptualization is provided from the efficacy of treatment with clonodine (Hunt, Minderra, & Cohen, 1985), as well as with psychostimulants (e.g., Ritalin) in some children with ADD (Pelham et al., 1990).

Further, researchers have suggested that attentional control involves two separate neural systems: (a) an activation system that is centered in the left hemisphere and specializes in analytic, sequential, and routinized cognitive operations, such as motor responses and is modulated by dopaminergic transmitters, and (b) an arousal system that is centered in the right hemisphere and is responsible for holistic, parallel, and novel cognitive functions, such as perceptual orienting responses and is modulated by norepinephrinergic neurotransmitters (Tucker, 1986; Tucker & Williamson, 1984). Heilman et al. (1991) have argued that evidence of frontal lobe dysfunction may be due to impairment of the mesocortical dopamine system. In a restatement of dopaminergic explanations of MBD, Levy (1991) suggested that the underlying dysfunction is a disorder of dopaminergic circuits between the prefrontal and striatal centers (basal ganglia). The impact includes disorders of planning and automatic instinctual motor programming. Related to the dopaminergic models, Posner, Inhoff, and Fredrich (1987) posited that the parietal lobe is involved in covert shifting of visual attention, whereas the frontal lobe is the attentional command system, and that both work together to regulate attentional processes as a complex functional system.

NEUROPHYSIOLOGICAL BASIS OF ADD

Although evidence has supported the role of both neurochemical and neuroanatomical perspectives of ADD, neither theory, taken individually, fully accounts for the myriad of behaviors associated with ADD (Voeller, 1991). Researchers have proposed that certain ascending/arousal and descending/inhibitory pathways (e.g., the loops that connect the frontal lobes, basal ganglia, and thalamus) constitute a system that activates/inactivates other brain regions. When this functional system is disrupted along the ascending/arousal loop, this component is no longer able to maintain an adequate level of arousal to the specifically targeted brain regions at the level of the cortex. Conversely, when this functional system is disrupted along the descending/inhibitory loop, an adequate level of inhibition/selective attention cannot be maintained (Eichler & Antelman, 1979; Magoun, 1952; Moruzzi & Magoun, 1949). Thus, as other researchers have hypothesized, interference at any level of this loop may lead to a cluster of clinically similar signs with diversity, depending on which level(s) are affected. Further, involvement of the subcortical limbic system (e.g., amygdala on Figure 1), along with the frontal lobe, might result in behavior disorders that occur comorbidly with ADD. This model, therefore, provides an explanation for "top-down" arousal (Watson, Valenstein, & Heilman, 1981), as well as accounting for the variability of behaviors and characteristics attributed to children with ADD.

Specifically, researchers have found that parietal, frontal, and limbic pathways terminate in the caudate (Goldman & Nauta, 1977; Selemon & Goldman-Rakic, 1990), with a similarly organized system between the somatosensory and premotor cortices to another component of the basal ganglia, the putamen (Alexander, DeLong, & Strick, 1986). Thus, the basal ganglia has emerged as a "hub" of influence over the thalamus and motor structures because of the number of crossing pathways that lead to and from the cortex (Selemon & Goldman-Rakic, 1990). In essence, this model incorporates the neurochemical as well as the neuroanatomical perspectives, without necessarily implicating or denying the importance of either hemisphere in particular. Voeller (1991) has suggested that this model provides the best explanation of the various clusters of behavior associated with ADD. However, though this theory has appeal for understanding the diverse characteristics associated with ADD, it lacks empirical support.

CONCLUSION

For the past century, researchers have presumed that ADD has an underlying neurological basis; the research reviewed here substantiates this presumption. This research provides evidence of morphological differences in this population, based on electrophysiological measures, cerebral blood flow, positron emission studies, and magnetic resonance imaging. Researchers have made limited progress, however, in characterizing definitive neurological mechanisms that account for the primary manifestations and associated characteristics of ADD. Some evidence implicates the frontal lobes, basal ganglia, and brain stem, as well as one of the major neurotransmitter systems; and some evidence points specifically to the right hemisphere as being selectively more involved in some children with ADD. Research findings, however, have not unequivocally supported any of this evidence. More recently, research has focused on the role of pathways between structures as a possible model for the neurological basis of ADD. Additional research, with more stringent methodological considerations, specific to this model as well as other models, is clearly needed to address the question of the neurological basis of ADD.

It is unlikely that the questions regarding the neurological basis of ADD will be answered unless a set of reliable criteria that are research-based can be established and consistently employed in the diagnosis of the disorder (Cohen & Gonzalez, 1992; Goodyear & Hynd, 1992; Riccio, Hynd, & Gonzalez, in press). In the absence of clear neurological evidence for diagnosis, clinicians will continue to make diagnoses based on behavioral observations. However, we must establish operationally defined behavioral criteria to make appropriate differential diagnosis and design an appropriate intervention program (Cohen & Gonzalez, 1992). Not only is it evident that we need differential diagnosis of ADD, learning disability, and conduct disorder, but the research relative to subtypes of ADD (with hyperactivity, without hyperactivity) indicates that a unidimensional perspective on the diagnosis of ADD is questionable (Goodyear & Hynd, 1992). It may be more appropriate to view ADD as a cluster of different behavioral deficits (attention, hyperactivity, and impulsivity), each with a specific neural substrate of varying severity, occurring in variable constellations, and sharing a common response to psychostimulants (Voeller, 1991). This type of multidimensional diagnosis may also be beneficial in addressing issues of comorbidity of ADD with learning disabilities and other behavior disorders.

Figure 1 [ILLUSTRATION OMITTED]

REFERENCES

Alexander, G. E., DeLong, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience, 9, 357-381. American Psychiatric Association. (1968). Diagnostic and statistical manual (2nd ed., DSM-II). Washington, DC: Author. American Psychiatric Association. (1980). Diagnostic and statistical manual (3rd ed., DSM-III). Washington, DC: Author. American Psychiatric Association. (1987). Diagnostic and statistical manual (3rd ed.-revised, DSM-III-R). Washington, DC: Author. Benson, D. F. (1991). The role of frontal dysfunction in attention deficit hyperactivity disorder. Journal of Child Neurology, 6, S, S9-S12. Branch, W. B., Cohen, M. J., & Hynd, G. W. (1992, February). Receptive prosody, academic achievement, and attention deficit/hyperactivity in left and right hemisphere learning disabled children. Paper presented at the 20th convention of the International Neuropsychological Society, San Diego. Chelune, G. J., Ferguson, W., Koon, R., & Dickey, T. O. (1986). Frontal lobe disinhibition in attention deficit disorder. Child Psychiatry and Human Development, 16, 221-234. Clark, C. R., Geffen, G. M., & Geffen, L. B. (1987a). Catecholamines and attention 1: Animal and clinical studies. Neuroscience and Biobehavioral Research, 11, 341-352. Clark, C. R., Geffen, G. M., & Geffen, L. B. (1987b). Catecholainines and attention II: Pharmacological studies in normal humans. Neuroscience and Biobehavioral Research, II, 353-364. Cohen, M. J., & Gonzalez, J. J. (1992, March). Prevalence of attention-deficit hyperactivity disorder in special education and clinic populations. Paper presented at the annual meeting of National Association of School Psychologists, Nashville, TN. Colby, C. L. (1991). The neuroanatomy and neurophysiology of attention. Journal of Child Neurology, 6, S, S88-S118. Eichler, A. J., & Antelman, S. M. (1979). Sensitization to amphetamine and stress may involve nucleus accumbens and medial frontal cortex. Brain Research, 176, 412-416. Goldman, P. S., & Nauta, W. J. H. (1977). An intricately patterned prefrontocaudate projection in the rhesus monkey. Journal of Comparative Neurology, 171, 369-386. Goodyear, P., & Hynd, G. W. (1992). Attention-deficit disorder with (ADD/H) hyperactivity and without ADD/WO) hyperactivity: Behavioral and neuropsychological differentiation. Journal of Clinical Child Psychology, 21, 273-305. Gualtieri, C. T., & Hicks, R. E. (1985). Neuropharmacology of methylphenidate and a neural substrate for childhood hyperactivity. Psychiatric Clinics of North America, 8, 875-892. Heilman, K. M., Schwartz, H. D., & Watson, R. T. (1978). Hypoarousalin patients with the neglect syndrome and emotional indifference. Neurology, 28, 229-232. Heilman, K. M.. & Van Den Abell, T. (1980). Right hemisphere dominance for attention: The mechanism underlying hemispheric asymmetries of inattention (neglect). Neurology, 30, 327-330. Heilman, K. M., Voeller, K. K. S., & Nadeau, S. E. (1991). A possible pathophysiological substrate of attention deficit hyperactivity disorder. Journal of Child Neurology, 6 S, S76-S81. Hunt, R. D., Minderra, R., & Cohen, D. J. (1985). Clonidine benefits children with attention deficit and hyperactivity. Journal of American Academy of Child and Adolescent Psychiatry, 24, 617-629. Hynd, G. W., Hem, K. L., Novey, E. S., Eliopolus, D., Marshall, R., Gonzalez, J. J., & Voeller, K. K. (in press). Attention-deficit hyperactivity disorder (ADHD) and asymmetry of the caudate nucleus. Journal of Child Neurology. Hynd, G. W., Hem, K. L., Voeller, K. K., & Marshall, R. M. (1991). Neurobiological basis of attention-deficit hyperactivity disorder (ADHD). School Psychology Review, 20, 174-186. Hynd, G. W., Semrud-Clikeman, M., Lorys, A. R., Novey, E. S., & Eliopulos, D. (1990). Brain morphology in developmental dyslexia and attention deficit disorder/hyperactivity. Archives of Neurology, 47,916-919. Hynd, G. W., Semrud-Clikeman, M., Lorys, A. R., Novey, E. S., Eliopulos, D., & Lyytinen, H. (1991). Corpus callosum morphology in attention-deficit hyperactivity disorder: Morphometric analysis of MRI. Journal of Learning Disabilities, 24, 141-155. Levy, F. (1991). The dopamine theory of attention deficit hyperactivity disorder (ADHD). Australian and New Zealand Journal of Psychiatry, 25, 277-283. Loge, D. V., Staton, R. D., & Beatty, W. W. (1990). Performance of children with ADHD on tests sensitive to frontal lobe dysfunction. Journal of the American Academy of Child & Adolescent Psychiatry, 29, 540-545. Lou, H. C., Henriksen, L., & Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology, 41, 825-829. Lou, H. C., Henriksen, L., Bruhn, P., Borner, H., & Nielsen, J. B. (1989). Striatal dysfunction in attention deficit and hyperkinetic disorder. Archives of Neurology, 46,48-52. Luria, A. (1980). Higher cortical functions in man. New York: Basic Books. Magoun, H. W. (1952). An ascending reticular activating system in the brain stem. Archives of Neurology and Psychiatry, 67, 145-154. Mann, C. A., Lubar, J. F., Zimmerman, A. W., Miller, C. A., & Muenchen, R. A. (1992). Quantitative analysis of EEG in boys with attention-deficit-hyperactivity disorder: Controlled study with clinical implications. Pediatric Neurology, 8, 30-36. Matazow, G. S., & Hynd, G. W. (1992a, February). Analysis of the anterior-posterior gradient hypothesis as applied to attention deficit disorder children. Paper presented at the 20th convention of the International Neuropsychological Society, San Diego. (ERIC Document Reproduction Service No. ED 344 374) Matazow, G. S., & Hynd, G. W. (1992b, February). Right hemisphere deficit syndrome: Similarities with subtypes of children with attention deficit disorder (ADD). Paper presented at the 20th convention of the International Neuropsychological Society, San Diego. Mattes, J. A. (1980). The role of frontal lobe dysfunction in childhood hyperkinesis. Comprehensive Psychiatry, 21, 358-369. Mefford, I. N., & Potter, W. Z. (1989). A neuroanatomical and biochemical basis for attention deficit disorder with hyperactivity in children: A defect in tonic adrenaline mediated inhibition of locus coeruleus stimulation. Medical Hypotheses, 29,33-42. Moruzzi, G., & Magoun, H. W. (1949). Brain stem reticular formation and activation of the EEG. Electroencephalography and Clinical Neuropsychology, 1, 455-473. Ogden, J. A. (1985). Anterior-posterior interhemispheric differences in the loci of lesions producing visual hemineglect. Brain and Cognition, 4, 59-75. Pelham, W. E., Greenslade, K. E., Vodde-Hamilton, M., Murphy, D. A., Greenstein, J. J., Gnagy, E. M., Guthrie, K. J., Hoover, M. D., & Dahl, R. E. (1990). Relative efficacy of long acting stimulants on children with attention deficit-hyperactivity disorder: A comparison of standard methylphenidate, sustained release methylphenidate, sustained release dextroamphetamine, and pemoline. Pediatrics, 86, 226-237. Pontius, A. A. (1973). Dysfunction patterns analogous to frontal lobe system and caudate nucleus syndromes in some groups of minimal brain dysfunction. Journal of American Medical Women's Association, 28, 285-292. Posner, M. I., Inhoff, A. W., & Fredrich, F. S. (1987). Isolating attentional systems: A cognitive-anatomical analysis. Psychobiology, 15, 107-121. Riccio, C. A., Hynd, G. W., & Gonzalez, J. J. (in press). Attention-deficit hyperactivity disorder (ADHD) and learning disabilities. Learning Disability Quarterly. Schaughency, E. A., & Hynd, G. W. (1989). Attentional control systems and the attention deficit disorders. Learning and Individual Differences, 14, 423-449. Selemon, L. D., & Goldman-Rakic, P. S. (1990). Topographic intermingling of striatonigral and striatopallidal neurons in the rhesus monkey. Journal of Comparative Neurology, 297, 359-376. Shaywitz, B. A., Shaywitz, S. E., Byrne, T., Cohen, D. J., & Rothman, S. (1983). Attention deficit disorder. Quantitative analysis of CT. Neurology, 33, 1500-1503. Swanson, J. M., Posner, M., Potkin, S., Bonforte, S., Youpa, D., Fiore, C., Cantwell, D., & Crinella, F. (1991). Activating tasks for the study of visual-spatial attention in ADHD children: A cognitive anatomic approach. Journal of Child Neurology, 6 S, S119-S127. Tucker, D. M. (1986). Hemisphere specialization: A mechanism for unifying anterior and posterior brain regions. In D. Ottoson (Ed.), Duality and unity of the brain: Unified functioning and specialization of the hemispheres. New York: Plenum Press. Tucker, D. M., & Williamson, P. A. (I 984). Asymmetric neural control systems in human self-regulation. Psychological Review, 91, 185-215. Vallar, G., & Perani, D. (1986). The anatomy of unilateral neglect after right-hemisphere stroke lesions: A clinical CT-scan correlation study in man. Neuropsychologia, 24. 609-622. Voeller, K. K. S. (1986). Right-hemisphere deficit syndrome in children. American Journal of Psychiatry, 143, 1004-1009. Voeller, K. K. S. (1991). Toward a neurobiologic nosology of attention deficit hyperactivity disorder. Journal of Clinical Neurology, 6 S, S2-S8. Voeller, K. K. S., & Heilman, K. M. (1988, September). Motor impersistence in children with attention deficit hyperactivity disorder: Evidence for right hemisphere dysfunction. Paper presented at the 17th annual meeting of the Child Neurology Society, Halifax, Nova Scotia. Watson, R. T., Valenstein, E., & Heilman, K. M. (198 1). Thalamic neglect, possible role of the medial thalamus and nucleus reticularis in behavior. Archives of Neurology, 38, 501-506. Welsh, M. C., & Pennington, B. F. (1988). Assessing frontal lobe functioning in children: Views from developmental psychology. Developmental Neuropsychology, 4, 199-230. Zambelli, A. J., Stamm, J. S., Maitinsky, S., & Loiselle, D. L. (1977). Auditory evoked polentials and selective attention in formerly hyperactive adolescent boys. American Journal of Psychiatry, 134, 742-747. Zametkin, A. J., Nordahl, T., Gross, M., King, A. C., Semple, W. E., Rumsey, J., Hamburger, S., & Cohen, R. M. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. New England Journal of Medicine, 323, 1361-1366. Zametkin, A. J., & Rapoport, J. L. (1987). Neurobiology of attention deficit disorder with hyperactivity: Where have we come in 50 years? American Academy of Child and Adolescent Psychiatry,26, 676-686.

ABOUT THE AUTHORS

CYNTHIA A. RICCIO, Post Doctoral Fellow, University of Georgia, Athens. GEORGE W. HYND, Director, Center for Clinical and Developmental Neuropsychology, University of Georgia, Athens, and Adjunct Faculty, Medical College of Georgia, Augusta. MORRIS J. COHEN, Pediatric Neuropsychologist and Director, Child Neuropsychology Service, Medical College of Georgia, Augusta, and Adjunct Faculty, University of Georgia, Athens. JOSE J. GONZALEZ (CEC # 637), Ph.D. student, University of Georgia, Athens.

Requests for reprints should be directed to George W. Hynd, Ed.D., Director, Center for Clinical and Developmental Neuropsychology, EXC 570 Aderhold Hall, University of Georgia, Athens, Georgia 30602.
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Author:Riccio, Cynthia A.; Hynd, George W.; Cohen, Morris J.; Gonzalez, Jose J.
Publication:Exceptional Children
Date:Oct 1, 1993
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