Date: October 10, 2008

Time: Noon to 1:00

Title: "Neurodevelopmental consequences of childhood chronic illness and its treatment: Implications for intervention and prevention"

Speaker: Daniel Armstrong, PhD
Leonard M. Miller School of Medicine
University of Miami

About the Talk:
Over the past 20 years, treatment of childhood chronic illness like cancer, sickle cell disease, and HIV  has improved to the point where most children are expected to be long-term survivors.  For selected subgroups of diagnoses, it is anticipated that a combination of treatments will result in cure long-term disease stability, but with long-term neurocognitive deficits that gradually emerge in the years after treatment.  There are multiple biologic mechanisms that may contribute to these late effects, including genetic risk factors, neural structural damage, vascular injury or obstruction, neurotransmitter abnormalities, metabolic abnormalities, neuroendocrine abnormalities, environmental factors such as poverty, malnutrition, or lack of adequate stimulation, and disruption in the development of neural structures and connections.  However, most late effects are associated with neural system development, characterized by interrupted myelination, calcification of microvascular structures, and failure of adequate white matter and connecting structure development.

We have described a neurodevelopmental model to guide research in this area.  First, the age of the child is a significant risk factor, with younger age at the time of treatment associated with more significant and global impairment.  Second, greater intensity of treatment is associated with more risk for neurocognitive impairment.  Third, specific functional neurocognitive deficits emerge over time, and greater degrees of impairment occur as time since treatment increases.  Fourth, specific treatments  increase risk of neurocognitive deficits.  Fifth, female gender is associated with greater risk for neurocognitive impairment. Finally, specific subgroups of children with chronic illness are at greater risk for neurocognitive impairment because of these factors. 

Specific patterns of neurocognitive late effects have been identified.  These include impairments in processing speed, visual and sequential memory, sustained attention and concentration, visual-motor integration skills, organizational and planning abilities, math calculation skills, and reading comprehension skills.  In general, abilities that were present prior to diagnosis and treatment are not impaired, while those that would developmentally emerge after treatment are at most risk for impairment. 

Over the past 5 years, several approaches to treatment have been evaluated.  These include cognitive rehabilitation, use of stimulants, and use of compensatory educational approaches using assistive technology and specific accommodations.  All of these approaches offer promising outcomes.  More recent proposals focus on early intervention and prevention strategies offered during treatment and prior to emergence of neurodevelopmental difficulties.  As more children reach young adulthood, new strategies for dealing with college, vocation, and other life experiences are being developed. 

Where:  John D. Wiley Conference Center
Room T216, Second Floor, North Tower

For Further Information: Contact Teresa Palumbo at 263-5837 or
palumbo@waisman.wisc.edu

This Seminar Series is partially funded by the John D. Wiley Conference Center Fund, the Friends of the Waisman Center and NIH grant P30 HD003352.