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Although development of the full syndrome of kernicterus is relatively rare, neonatal jaundice continues to occur frequently. Controversy remains concerning whether or not infants with moderate elevations in bilirubin are at risk for neurodevelopmental disorders in later childhood. Sites of brain pathology associated with bilirubin neurotoxicity are identified and well established. Based on these regions of brain involvement, we apply neuroscientific principles of brain-behavior relationships to predict types of cognitive features that may accompany hyperbilirubinemia. We address a range of neurodevelopmental abnormalities that can arise as a function of elevated neonatal bilirubin levels affecting these brain regions, even in the absence of full kernicterus syndrome. Moreover, we explain the neuropathologic mechanisms that would drive these abnormalities. We thus attempt to establish a blueprint for future investigations of these conditions, to improve neurodevelopmental outcomes., (Copyright © 2013 Elsevier Inc. All rights reserved.)

This paper posits that the brain evolved for the control of action rather than for the development of cognition per se. We note that the terms commonly used to describe brain-behavior relationships define, and in many ways limit, how we conceptualize and investigate them and may therefore constrain the questions we ask and the utility of the "answers" we generate. Many constructs are so nonspecific and over-inclusive as to be scientifically meaningless. "Executive function" is one such term in common usage. As the construct is increasingly focal in neuroscience research, defining it clearly is critical. We propose a definition that places executive function within a model of continuous sensorimotor interaction with the environment. We posit that control of behavior is the essence of "executive function," and we explore the evolutionary advantage conferred by being able to anticipate and control behavior with both implicit and explicit mechanisms. We focus on the cerebellum's critical role in these control processes. We then hypothesize about the ways in which procedural (skill) learning contributes to the acquisition of declarative (semantic) knowledge. We hypothesize how these systems might interact in the process of grounding knowledge in sensorimotor anticipation, thereby directly linking movement to thought and "embodied cognition." We close with a discussion of ways in which the cerebellum instructs frontal systems how to think ahead by providing anticipatory control mechanisms, and we briefly review this model's potential applications.

Current models of cognition and behavioral diagnosis emphasize categorical classification over continuous considerations of function and promote the "differential diagnosis" of various conditions according to observational criteria. However, an overemphasis on a purely behavioral, categorical approach to understanding human function fails to address the comorbidity of different disorders and does not include a consideration of overlapping levels of function, from "pathological" through "normal," to "gifted" or exceptional. The frequent co-occurrence of "gifted" and "pathological" function is thus difficult to understand from a corticocentric and purely behavioral and observational point of view. This article reviews "giftedness" in relation to the diagnosis of attention-deficit hyperactivity disorder, coexistence of which is termed "twice exceptional." It additionally considers problems in assessing these functions using current neuropsychological tests and methodologies that are presumably based upon a corticocentric model of cognition.

This paper examines conditions that have variously been called sensory integration disorder, sensory processing disorder, and sensory modulation disorder (SID/SPD/SMD). As these conditions lack readily and consistently agreed-upon operational definitions, there has been confusion as to how these disorders are conceptualized. Rather than addressing various diagnostic controversies, we will instead focus upon explaining the symptoms that are believed to characterize these disorders. First, to clarify the overall context within which to view symptoms, we summarize a paradigm of adaptation characterized by continuous sensorimotor interaction with the environment. Next, we review a dual-tiered, integrated model of brain function in order to establish neuroanatomic underpinnings with which to conceptualize the symptom presentations. Generally accepted functions of the neocortex, basal ganglia, and cerebellum are described to illustrate how interactions between these brain regions generate both adaptive and pathological symptoms and behaviors. We then examine the symptoms of SID/SPD/SMD within this interactive model and in relation to their impact upon the development of inhibitory control, working memory, academic skill development, and behavioral automation. We present likely etiologies for these symptoms, not only as they drive neurodevelopmental pathologies but also as they can be understood as variations in the development of neural networks.

Current cortico-centric models of cognition lack a cohesive neuroanatomic framework that sufficiently considers overlapping levels of function, from "pathological" through "normal" to "gifted" or exceptional ability. While most cognitive theories presume an evolutionary context, few actively consider the process of adaptation, including concepts of neurodevelopment. Further, the frequent co-occurrence of "gifted" and "pathological" function is difficult to explain from a cortico-centric point of view. This comprehensive review paper proposes a framework that includes the brain's vertical organization and considers "giftedness" from an evolutionary and neurodevelopmental vantage point. We begin by discussing the current cortico-centric model of cognition and its relationship to intelligence. We then review an integrated, dual-tiered model of cognition that better explains the process of adaptation by simultaneously allowing for both stimulus-based processing and higher-order cognitive control. We consider the role of the basal ganglia within this model, particularly in relation to reward circuitry and instrumental learning. We review the important role of white matter tracts in relation to speed of adaptation and development of behavioral mastery. We examine the cerebellum's critical role in behavioral refinement and in cognitive and behavioral automation, particularly in relation to expertise and giftedness. We conclude this integrated model of brain function by considering the savant syndrome, which we believe is best understood within the context of a dual-tiered model of cognition that allows for automaticity in adaptation as well as higher-order executive control.