Dysphagia is a common deficit after a stroke, and it is frequently associated with pneumonia, malnutrition, dehydration, and poor quality of life. It is not yet fully clear which brain regions are directly related to swallowing, and how lesions affect swallow physiology. This study aimed to assess the statistical relationship between acute stroke lesion locations and impairment of specific aspects of swallow physiology. We performed lesion symptom mapping with 68 retrospectively recruited, acute, first-ever ischemic stroke patients. Lesions were determined on diffusion weighted MRI scans. Post-stroke swallow physiology was determined using the Modified Barium Swallow Study Impairment Profile (MBSImP©™). The relationship between brain lesion location and 17 physiological aspects of swallowing were tested using voxel-based and region-based statistical associations corrected for multiple comparisons using permutation thresholding. We found that laryngeal elevation, anterior hyoid excursion, laryngeal vestibular closure, and pharyngeal residue were associated with lesioned voxels or regions of interests. All components showed distinct and overlapping lesion locations, mostly in the right hemisphere, and including cortical regions (inferior frontal gyrus, pre- and postcentral gyrus, supramarginal gyrus, angular gyrus, superior temporal gyrus, insula), subcortical regions (thalamus, amygdala) and white matter tracts (superior longitudinal fasciculus, corona radiata, internal capsule, external capsule, ansa lenticularis, lenticular fasciculus). Our findings indicate that different aspects of post-stroke swallow physiology are associated with distinct lesion locations, primarily in the right hemisphere, and primarily including sensory-motor integration areas and their corresponding white matter tracts. Future studies are needed to expand on our findings and thus, support the development of a neuroanatomical model of post-stroke swallow physiology and treatment approaches targeting the neurophysiological underpinnings of swallowing post stroke.

Purpose: Swallowing is a complex process, mediated by a broad bilateral neural network that spans from the brainstem to subcortical and cortical brain structures. Although the cortex's role in swallowing was historically neglected, we now understand, especially through clinical observations and research of patients with stroke, that it substantially contributes to swallowing control. Neuroimaging techniques (e.g., magnetic resonance imaging) have helped significantly to elucidate the role of cortical and subcortical brain areas, in general, and the importance of specific areas in swallowing control in healthy individuals and patients with stroke. We will review recent discoveries in cortical and subcortical neuroimaging research studies and their generalizability across patients to discuss their potential implications and translation to dysphagia diagnosis and treatment in clinical practice.Conclusions: Stroke lesion locations have been identified that are commonly associated across patients with the occurrence and recovery of dysphagia, suggesting that clinical brain scans provide useful information for improving the diagnosis and treatment of patients with stroke. However, individual differences in brain structure and function limit the generalizability of these relationships and emphasize that the extent of the motor and sensory pathology in swallowing, and how the patient recovers, also depends on a patient's individual brain constitution. The involvement of the damaged brain tissue in swallowing control before the stroke and the health of the residual, undamaged brain tissue are crucial factors that can differ between individuals.

We sought to determine the underlying pathophysiology relating white matter hyperintensities to chronic aphasia severity. We hypothesized that: (i) white matter hyperintensities are associated with damage to fibres of any length, but to a higher percentage of long-range compared to mid- and short-range intracerebral white matter fibres; and (ii) the number of long-range fibres mediates the relationship between white matter hyperintensities and chronic post-stroke aphasia severity. We measured the severity of periventricular and deep white matter hyperintensities and calculated the number and percentages of short-, mid- and long-range white matter fibres in 48 individuals with chronic post-stroke aphasia. Correlation and mediation analyses were performed to assess the relationship between white matter hyperintensities, connectome fibre-length measures and aphasia severity as measured with the aphasia quotient of the Western Aphasia Battery-Revised (WAB-AQ). We found that more severe periventricular and deep white matter hyperintensities correlated with a lower proportion of long-range fibres (r = −0.423, P = 0.003 and r = −0.315, P = 0.029, respectively), counterbalanced by a higher proportion of short-range fibres (r = 0.427, P = 0.002 and r = 0.285, P = 0.050, respectively). More severe periventricular white matter hyperintensities also correlated with a lower proportion of mid-range fibres (r = −0.334, P = 0.020), while deep white matter hyperintensities did not correlate with mid-range fibres (r = −0.169, P = 0.250). Mediation analyses revealed: (i) a significant total effect of periventricular white matter hyperintensities on WAB-AQ (standardized beta = −0.348, P = 0.008); (ii) a non-significant direct effect of periventricular white matter hyperintensities on WAB-AQ (P > 0.05); (iii) significant indirect effects of more severe periventricular white matter hyperintensities on worse aphasia severity mediated in parallel by fewer long-range fibres (effect = −6.23, bootstrapping: standard error = 2.64, 95%CI: −11.82 to −1.56) and more short-range fibres (effect = 4.50, bootstrapping: standard error = 2.59, 95%CI: 0.16 to 10.29). We conclude that small vessel brain disease seems to affect chronic aphasia severity through a change of the proportions of long- and short-range fibres. This observation provides insight into the pathophysiology of small vessel brain disease, and its relationship with brain health and chronic aphasia severity.

Purpose: We aimed to evaluate the construct validity of the Eating Assessment Tool (EAT-10) by determining its dimensionality, rating scale integrity, item-person match, precision and relationship with the degree of airway invasion and functional oral intake. Methods: We conducted a retrospective analysis of patients’ EAT-10 scores. We used the Rasch rating scale model. We investigated correlations between the EAT-10 and scores on the Penetration-Aspiration Scale (PAS) and Functional Oral Intake Scale (FOIS). Results: The median score of the EAT-10 from 127 patients was 16 of 40 (range 0–40). Confirmatory factor analysis supported unidimensionality. The 5-point rating scale categories met published criteria. Two items misfit the Rasch model and two other items displayed differential item functioning. Rasch person reliability was 0.79. Our patient cohort was divided into three person-strata. Correlations between the EAT-10 and the PAS and FOIS were weak to moderate in strength (respectively: r = 0.26, p = 0.0036; r = −0.27, p = 0.0027). Conclusions: Our analyses identified deficits in the construct validity of the EAT-10 suggestive of a need to improve the EAT-10 to support its frequent use in clinical practice and research.

Aphasia recovery after stroke depends on the condition of the remaining, extralesional brain network. Network control theory (NCT) provides a unique, quantitative approach to assess the interaction between brain networks. In this longitudinal, large-scale, whole-brain connectome study, we evaluated whether controllability measures of language-related regions are associated with treated aphasia recovery. Using probabilistic tractography and controlling for the effects of structural lesions, we reconstructed whole-brain diffusion tensor imaging (DTI) connectomes from 68 individuals (20 female, 48 male) with chronic poststroke aphasia who completed a three-week language therapy. Applying principles of NCT, we computed regional (1) average and (2) modal controllability, which decode the ability of a region to (1) spread control input through the brain network and (2) to facilitate brain state transitions. We tested the relationship between pretreatment controllability measures of 20 language-related left hemisphere regions and improvements in naming six months after language therapy using multiple linear regressions and a parsimonious elastic net regression model with cross-validation. Regional controllability of the inferior frontal gyrus (IFG) pars opercularis, pars orbitalis, and the anterior insula were associated with treatment outcomes independently of baseline aphasia severity, lesion volume, age, education, and network size. Modal controllability of the IFG pars opercularis was the strongest predictor of treated aphasia recovery with cross-validation and outperformed traditional graph theory, lesion load, and demographic measures. Regional NCT measures can reflect the status of the residual language network and its interaction with the remaining brain network, being able to predict language recovery after aphasia treatment.SIGNIFICANCE STATEMENTPredicting and understanding language recovery after brain injury remains a challenging, albeit a fundamental aspect of human neurology and neuroscience. In this study, we applied network control theory (NCT) to fully harness the concept of brain networks as dynamic systems and to evaluate their interaction. We studied 68 stroke survivors with aphasia who underwent imaging and longitudinal behavioral assessments coupled with language therapy. We found that the controllability of the inferior frontal regional network significantly predicted recovery in language production six months after treatment. Importantly, controllability outperformed traditional demographic, lesion, and graph-theoretical measures. Our findings shed light on the neurobiological basis of human language and can be translated into personalized rehabilitation approaches.