Abstract

INTRODUCTION: Temporal lobe resections for epilepsy or neoplasms often result in significant confrontation naming decline. This can be socio-economically disabling and prevent patients from returning to independent functioning. While the exact substrates responsible are unknown, it was previously assumed that injury to the superior temporal gyrus or resection size predicts these declines. A clear understanding of the most critical constituents might influence surgical strategies to minimize language declines. METHODS: Data were obtained from 95 patients who underwent surgical resection in the dominant left temporal lobe for medication-resistant epilepsy. Patients underwent neuropsychological testing and MRI prior to and 6 months following surgery. Lesion masks were traced on postoperative MRIs and aligned to a normative space. The effects of preoperative scores and seizure outcomes were removed from postoperative scores via linear regression. VLSM using multivariate support vector regression was used to assess postoperative test scores. Beta maps were converted to p values and corrected using a permutation-based cluster level correction. Additionally, a surface-based mixed-effects multilevel analysis was used to estimate broadband gamma activity during picture naming across a subset of subjects with ECoG recordings, and results were integrated with VLSM. Lastly, fMRI (picture naming) was used to assess SNR in significant regions. RESULTS: VLSM analysis revealed that the loss of basal temporal regions was associated with a prominent decline in BNT scores (p < 0.005). Similarly, ECoG analysis showed a significant increase in activity in the mid fusiform gyrus (mFus) immediately preceding articulation. Many of these voxels were associated with low SNR on fMRI, perhaps explaining why this region has been under-appreciated as the locus responsible for postoperative deficits. CONCLUSION: The importance of the ventral temporal cortex in lexical access is shown using multivariate VLSM and supported with ECoG. While it has previously been assumed that mFus lesions do not cause pervasive impairment, our data and recent work (FATES study) argue against this and support the role of the mFus as a critical semantic access hub.

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