Abstract
This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior. I begin with a general review of CC development, connectivity, and function, followed by discussion of the research methods typically utilized to study the callosum. The bulk of the review concentrates on specific developmental disorders, beginning with agenesis of the corpus callosum (AgCC)—the only condition diagnosed exclusively by callosal anatomy. This is followed by a review of several genetic disorders that commonly result in social impairments and/or psychopathology similar to AgCC (neurofibromatosis-1, Turner syndrome, 22q11.2 deletion syndrome, Williams yndrome, and fragile X) and two forms of prenatal injury (premature birth, fetal alcohol syndrome) known to impact callosal development. Finally, I examine callosal involvement in several common developmental disorders defined exclusively by behavioral patterns (developmental language delay, dyslexia, attention-deficit hyperactive disorder, autism spectrum disorders, and Tourette syndrome).
Highlights
This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior
Several recent studies have used diffusion-weighted magnetic resonance imaging (dMRI) and tract-tracing statistics to segment callosal regions according to the cortical areas they connect in an individual subject (Cascio et al 2006; Huang et al 2005; Dougherty et al 2007)
These studies indicate that compensatory pathways for interhemispheric transfer (IHT) in agenesis of the corpus callosum (AgCC) are limited, resulting in a fairly consistent pattern of impairment in complex behaviors that rely upon rapid information processing between hemispheres such as problem solving, nonliteral language, and social communication
Summary
The corpus callosum (CC) is unique to placental mammals and comprised of approximately ∼190 million axons that connect the left and right hemispheres. In the late 1960s, callosal transection was introduced as treatment for intractible epilepsy (Bogen 1985; Gordon and Sperry 1969; Milner et al 1968; Sperry et al 1974) and provided a radical foundation for exploring callosal functions in humans. Following surgery, these patients manifest a “disconnection syndrome” including absent callosal transfer of sensory information and deficits in bimanually coordinated motor activity. Understanding the contribution of the CC to developmental disorders requires considerations of its development, rather than consequences resulting from transection in adults
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
