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

TL;DR

This study demonstrates that damage to specific white matter bottlenecks in the left hemisphere, especially in the posterior temporal lobe, significantly contributes to language impairments after stroke, affecting multiple language functions.

Contribution

It provides direct evidence linking white matter bottleneck damage to language deficits, highlighting the importance of these regions in post-stroke aphasia recovery.

Findings

Damage to posterior temporal bottleneck predicts deficits in all language measures.

Damage to anterior bottleneck predicts deficits in category fluency.

White matter bottleneck damage is a key factor in chronic language deficits.

Abstract

Damage to the white matter underlying the left posterior temporal lobe leads to deficits in multiple language functions. The posterior temporal white matter may correspond to a bottleneck where both dorsal and ventral language pathways are vulnerable to simultaneous damage. Damage to a second putative white matter bottleneck in the left deep prefrontal white matter involving projections associated with ventral language pathways and thalamo-cortical projections has recently been proposed as a source of semantic deficits after stroke. However, the effects of damage to a priori identified white matter bottlenecks on language function have not been directly investigated. Here, we first used white matter atlases to identify the previously described white matter bottlenecks in the posterior temporal and deep prefrontal white matter. We then assessed the effects of damage to each region on measures of category fluency, picture naming, and auditory semantic decision-making in 43 patients with chronic aphasia. Damage to the posterior temporal bottleneck predicted deficits on all language measures, while damage to the anterior bottleneck only predicted deficits in category fluency. Importantly, the effects of damage to the bottleneck regions were not attributable to lesion volume, lesion loads on the tracts traversing the bottlenecks, or damage to nearby cortical language areas. Multivariate lesion-symptom mapping and fiber tracking analyses corroborated these findings. Together, our results provide strong support for the proposal that spatially specific white matter damage affecting white matter bottlenecks, particularly in the posterior temporal lobe, contribute to chronic language deficits after left hemispheric stroke. Our results suggest that damage to this area is likely to simultaneously disrupt signaling via the simultaneous disruption of dorsal and ventral language processing streams.