Interhemispheric effects of simulated lesions in a neural model of letter identification

Experimental studies have produced conflicting results about the extent to which the intact, nonlesioned cerebral hemisphere is responsible for recovery from cognitive deficits following focal brain damage such as a stroke. To obtain a better theoretical understanding of interhemispheric interactions during recovery, we examined the effects of simulated lesions to a bihemispheric neural model of letter identification under various assumptions about hemispheric asymmetries, corpus callosum influence, and lesion size. Among other results, the model demonstrates that the intact hemispheric region's participation in the recovery process is a function of preexisting lateralization and lesion size, indicating that interpretation of experimental work should take these factors into account.