Abstract

BackgroundDuring normal semantic processing, the left hemisphere (LH) is suggested to restrict right hemisphere (RH) performance via interhemispheric suppression. However, a lesion in the LH or the use of concurrent tasks to overload the LH's attentional resource balance has been reported to result in RH disinhibition with subsequent improvements in RH performance. The current study examines variations in RH semantic processing in the context of unilateral LH lesions and the manipulation of the interhemispheric processing resource balance, in order to explore the relevance of RH disinhibition to hemispheric contributions to semantic processing following a unilateral LH lesion.MethodsRH disinhibition was examined for nine participants with a single LH lesion and 13 matched controls using the dual task paradigm. Hemispheric performance on a divided visual field lexical decision semantic priming task was compared over three verbal memory load conditions, of zero-, two- and six-words. Related stimuli consisted of categorically related, associatively related, and categorically and associatively related prime-target pairs. Response time and accuracy data were recorded and analyzed using linear mixed model analysis, and planned contrasts were performed to compare priming effects in both visual fields, for each of the memory load conditions.ResultsControl participants exhibited significant bilateral visual field priming for all related conditions (p < .05), and a LH advantage over all three memory load conditions. Participants with LH lesions exhibited an improvement in RH priming performance as memory load increased, with priming for the categorically related condition occurring only in the 2- and 6-word memory conditions. RH disinhibition was also reflected for the LH damage (LHD) group by the removal of the LH performance advantage following the introduction of the memory load conditions.ConclusionsThe results from the control group are consistent with suggestions of an age related hemispheric asymmetry reduction and indicate that in healthy aging compensatory bilateral activation may reduce the impact of inhibition. In comparison, the results for the LHD group indicate that following a LH lesion RH semantic processing can be manipulated and enhanced by the introduction of a verbal memory task designed to engage LH resources and allow disinhibition of RH processing.

Highlights

  • During normal semantic processing, the left hemisphere (LH) is suggested to restrict right hemisphere (RH) performance via interhemispheric suppression

  • Response time analysis Trials were excluded from response time (RT) analysis if responses were incorrect (LHD: 19.7%; Control: 10.8%), if eye movement was observed (LHD: 14.6%; Control: 12.4%), if RT deviated from the individuals conditional mean by more than two standard deviations, and if RT was extreme (> 2000 ms) and remained following removal of outliers, (LHD: 11.3%; Control: 5.5% of correct eye movement free trials)

  • The LH damage (LHD) group exhibited a different pattern with the 2-word condition (1038 ms) being significantly slower than both the 0-word (1002 ms) [p = .030] and 6-word (999 ms) [p = .037] conditions, which did not differ from each other [p > .1]

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Summary

Introduction

The left hemisphere (LH) is suggested to restrict right hemisphere (RH) performance via interhemispheric suppression. A lesion in the LH or the use of concurrent tasks to overload the LH’s attentional resource balance has been reported to result in RH disinhibition with subsequent improvements in RH performance. The current study examines variations in RH semantic processing in the context of unilateral LH lesions and the manipulation of the interhemispheric processing resource balance, in order to explore the relevance of RH disinhibition to hemispheric contributions to semantic processing following a unilateral LH lesion. The current study will reexamine hemispheric contributions to semantic processing following LH lesions under conditions designed to manipulate the degree of interhemispheric activation and inhibition

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