SPD-SWG Participants

Stein, Barry E., PhD

Title: Professor and Chair
Department: Department of Neurobiology and Anatomy
Institution: Wake Forest University School of Medicine
Mailing Address: Medical Center Boulevard, Winston-Salem, NC 27157-1010
Phone: (336) 716-4386
Website: http://www1.wfubmc.edu/Nba/Faculty/stein.htm

Research Interests

Barry Stein has led a broad range of studies documenting the organization, development and plasticity of multisensory integration in the midbrain and in the cerebral cortex. He and his colleagues have been specifically interested in how the brain is able to synthesize information from different senses to guide overt behavior and the principles underlying this capability can be used in therapeutic settings.

SPD Research Summary

Overall Objective: To Understand the Processes Underlying the Normal and Abnormal Development of Multisensory Integration

Sensory Processing Disorder (SPD) involves anomalies in processing and properly responding to tactile, auditory and/or visual stimuli. SPD is manifested in disturbances in overt attentive/orientation (or withdrawal) behavior to innocuous sensory (tactile, auditory, visual) stimuli. The fundamental question we are asking is: How does the brain normally integrate these multisensory stimuli to properly initiate and control these attentive/orientation (or withdrawal) behaviors? How are the underlying computations different than those involved in integrating unisensory stimuli? And – what developmental disruptions in the underlying neural circuit could help explain why sensory anomalies like those in SPD are occurring, so we can develop effective strategies for ameliorating them?

The neural circuit responsible for the integration of tactile, auditory and visual cues to initiate and control attentive/orientation behavior has been identified and well characterized in an animal model (i.e., cat).

We hypothesize that the overt sensory anomalies observed in SPD involve miscommunication between cortex and midbrain (i.e., SC). Early experience- based adaptations allow the brain to best deal with the environment in which it finds itself.

We predict that if the association cortex is rendered temporally inactive during early life when SC multisensory capabilities are being formed, these multi- sensory integrative capabilities will not develop; however unisensory integration will be unaffected.

We also have preliminary evidence that SC neurons fail to develop normal multisensory integration when animals do not have early experience with cross- modal cues and, of special interest in this context, when association cortex cannot acquire early cross-modal sensory experience. The data indicate that the development of multisensory integration is highly dependent on early experience acquired by association areas of cortex; thus, abnormal experience produces developmental disorders by disrupting maturation of the cortico-SC axis. Currently we are evaluating the reliability of these data, and understanding how a number of variations in early experience are encoded in cortex and expressed physiologically and behaviorally via the cortical-SC axis. This will help us understand how changes in the brain mediate these physiological and behavioral processes and provide insight into the neural processes underlying the sensory anomalies apparent in individuals with SPD.

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