Distinct loci of lexical and semantic access deficits in aphasia: Evidence from voxel-based lesion-symptom mapping and diffusion tensor imaging

Abstract

Please cite this article as: Harvey DY, Schnur TT, Distinct loci of lexical and semantic access deficits in aphasia: Evidence from voxel-based lesion-symptom mapping and diffusion tensor imaging, CORTEX (2015), doi: 10.1016/j.cortex.2015.03.004. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Further, damage to the left inferior frontal gyrus (LIFG), a region implicated in cognitive control, results in increasing semantic interference when items repeat across cycles in both language production and comprehension (Jefferies, Baker, Doran, & Lambon Ralph, 2007). This generates the prediction that the LIFG via white matter connections supports resolution of semantic interference arising from different loci (lexical vs. semantic) in the temporal lobe. However, it remains unclear whether the cognitive and neural mechanisms that resolve semantic interference are the same across tasks. Thus, we examined which gray matter structures (using whole brain and region of interest approaches) and white matter connections (using deterministic tractography) when damaged impact semantic interference and its increase across cycles when repeatedly producing and understanding words in 15 speakers with varying lexical-semantic deficits from left hemisphere stroke. We found that damage to distinct brain regions, the posterior vs. anterior temporal lobe, was associated with semantic interference (collapsed across cycles) in naming and comprehension, respectively. Further, those with LIFG damage compared to those without exhibited marginally larger increases in semantic interference across cycles in naming but not comprehension. Lastly, the inferior fronto-occipital fasciculus, connecting the LIFG with posterior temporal lobe, related to semantic interference in naming, whereas the inferior longitudinal fasciculus, connecting posterior with anterior temporal regions related to semantic interference in comprehension. These neuroanatomical-behavioral findings have

Damage to white matter bottlenecks contributes to language impairments after left hemispheric stroke

“…4). This corroborates findings from previous studies that have implicated damage to the WM underlying the posterior temporal lobe in language deficits that span broad domains of language function (Baldo et al, 2013, Bonilha et al, 2015, Butler et al, 2014, Dronkers et al, 2004, Fridriksson, 2010, Fridriksson et al, 2013, Geva et al, 2012, Harvey and Schnur, 2015, Henseler et al, 2014, Ivanova et al, 2016). This region contains fibers associated with both dorsal (AF) and ventral (ILF and IFOF) language processing streams that support integrated sensorimotor language processing and the extraction of meaning from auditory language, respectively (Kümmerer et al, 2013, Saur et al, 2008).…”

“…Damage to the WM underlying the left posterior superior and middle temporal gyri (pSTG and pMTG) has been consistently implicated as a source of deficits in multiple language domains including comprehension (Dronkers et al, 2004, Geva et al, 2012, Henseler et al, 2014, Pustina et al, 2016, Yourganov et al, 2016), naming (Baldo et al, 2013, Harvey and Schnur, 2015, Henseler et al, 2014, Pustina et al, 2016, Yourganov et al, 2016), repetition (Butler et al, 2014, Henseler et al, 2014, Pustina et al, 2016, Yourganov et al, 2016), and phonology (Butler et al, 2014). The presence of lesions affecting the posterior temporal WM and disrupting posterior temporal connectivity also predicts poor responses to language therapies (Bonilha et al, 2015, Fridriksson, 2010).…”

Phonological and semantic processing during comprehension in Wernicke's aphasia: An N400 and Phonological Mapping Negativity Study

“…These findings support the phonological hypothesis and the long-standing theory of WA that language comprehension is impaired because poor quality phonological analysis of the speech stream has a downstream impact on semantic access and analysis (Luria, 1976;Luria & Hutton, 1977). Consistent with this hypothesis all the WA aphasia participants also displayed a lesion to the superior temporal sulcus, a region associated with phonological analysis (DeWitt & Rauschecker, 2012;Harvey & Schnur, 2015;Humphries, Binder et al, 2007;Indefrey & Levelt, 2004;Krieger-Redwood & Jefferies, 2014;Saur, Schelter et al, 2010). This hypothesis was further examined in the control population by artificially degrading the speech input using Saberi speech.…”

“…All WA participants displayed a lesion affecting the middle temporal gyrus, a region associated with semantic processing (DeWitt & Rauschecker, 2012;Harvey & Schnur, 2015;Humphries, Binder et al, 2007;Indefrey & Levelt, 2004;Krieger-Redwood & Jefferies, 2014;Saur, Schelter et al, 2010) and seen to be modulated by the same experimental features as the N400 in functional imaging experiments (Lau, Phillips et al, 2008). Supporting the semantic hypothesis, greater N400 effects were identified in the WA group when semantic incongruency judgments were easier.…”

Brain white matter fibre tracts: a review of functional neuro-oncological relevance

“…However, in terms of permanent deficits, because DES-elicited errors constitute the stopping point for oncological resections, any postoperative language deficits are typically transient and difficult to attribute uniquely to IFOF damage. Yet recently, a preliminary voxel-based lesion mapping study in stroke patients found semantic naming deficits to associate with IFOF damage 29. Neurological studies suggest that IFOF fibres may additionally contribute to aspects of face processing, although evidence of selective face recognition deficits associated with oncological damage is currently lacking.…”