# Structural correlates of aphasia severity, cognitive impairment, and outcome after stroke

**Authors:** Célise Haldin, Hélène Lœvenbruck, Céline Piscicelli, Valérie Marcon, Shenhao Dai, Olivier Detante, Dominic Pérennou, Monica Baciu

PMC · DOI: 10.1016/j.nicl.2026.103954 · 2026-01-19

## TL;DR

This study identifies brain structures linked to aphasia severity and cognitive issues after a stroke, focusing on language and executive function networks.

## Contribution

The study reveals how damage to specific white matter tracts correlates with aphasia severity and cognitive impairments after stroke.

## Key findings

- Damage to ventral and dorsal language pathways correlates with aphasia severity and naming deficits.
- Executive dysfunction is linked to disconnections in fronto-parietal and salience networks.
- White matter tracts in language streams shape cognitive phenotypes in post-stroke aphasia.

## Abstract

•Aphasia results from network disconnections.•Dorsal and ventral language streams shape post-stroke aphasia cognitive phenotypes.•Dorsal and ventral streams damage is linked to aphasia severity and naming deficits.•Damage to executive control networks is related to executive dysfunction.

Aphasia results from network disconnections.

Dorsal and ventral language streams shape post-stroke aphasia cognitive phenotypes.

Dorsal and ventral streams damage is linked to aphasia severity and naming deficits.

Damage to executive control networks is related to executive dysfunction.

In this study, we aimed to identify structural biomarkers linked to the severity and outcome of aphasia after a left-hemispheric stroke. We recruited 72 individuals with post-stroke aphasia and assessed their initial aphasia severity using the Aphasia Severity Rating Scale, alongside measures of naming ability and executive function. Aphasia outcome was determined for 56 out of 72 participants with available Aphasia Severity Rating Scale scores at discharge. We performed support-vector regression symptom mapping analyses at both cortical and white matter levels to examine the relationship between structural brain damage and our variables of interest (initial aphasia severity, naming, executive functions, and aphasia outcome). Our results revealed that (a) disconnections in white matter tracts within ventral and dorsal language pathways were associated with aphasia severity and naming deficits initially; and (b) disconnections in white matter tracts within executive networks (i.e., fronto-parietal, executive control, and salience networks) were related to executive dysfunction. This retrospective cohort study highlighted the crucial roles of white matter tracts within both dorsal (i.e., arcuate fasciculus, superior longitudinal fasciculus) and ventral (uncinate, inferior longitudinal, and middle longitudinal fasciculi) language streams in shaping the cognitive phenotypes of post-stroke aphasia patients, particularly concerning aphasia severity and naming impairment, by delineating distinct patterns of affected brain structures.

## Linked entities

- **Diseases:** aphasia (MONDO:0000598)

## Full-text entities

- **Genes:** CST12P (cystatin 12, pseudogene) [NCBI Gene 106478911] {aka Cst, Ctes4, E2}, ATR (ATR checkpoint kinase) [NCBI Gene 545] {aka FCTCS, FRP1, MEC1, SCKL, SCKL1}
- **Diseases:** Naming deficits (MESH:D009461), cortical lesions (MESH:D054220), post (MESH:D000094025), impairments in semantic memory (MESH:D008569), Damage to executive control networks (MESH:D007174), AF (MESH:D012607), Anomia (MESH:D000849), EF impairments (MESH:D003072), lesion (MESH:D009059), brain lesions (MESH:D001927), grey matter lesions (MESH:D055652), apraxia (MESH:D001072), behavioral deficits (MESH:D019958), fluent and non-fluent aphasia (MESH:D001041), mood disorders (MESH:D019964), naming impairment (MESH:D060825), Executive dysfunction (MESH:D006331), communication disorder (MESH:D003147), Stroke (MESH:D020521), gliomas (MESH:D005910), fluency (MESH:D013064), psychiatric (MESH:D001523), ischemic stroke (MESH:D002544), brain damage (MESH:D001925), language disorders (MESH:D007806), ventricular dilatation (MESH:C566255), infarct (MESH:D007238), malignant (MESH:D009369), speech handicaps (MESH:D009422), Aphasia (MESH:D001037), WM damage (MESH:D056784), dementia (MESH:D003704), subarachnoid haemorrhage (MESH:D013345), cerebral herniation (MESH:D004677), hydrocephalus (MESH:D006849), EF deficits (MESH:D001289), cerebral atrophy (MESH:D001284)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12874455/full.md

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Source: https://tomesphere.com/paper/PMC12874455