Cerebral small vessel disease is an independent determinant of dysphagia after acute stroke.

BACKGROUND

The high incidence of dysphagia after acute stroke is likely the result of cumulative effects of the stroke and pre-stroke brain health. While cerebral small vessel disease (cSVD) is recognized as a marker of compromised brain health, it's unclear which neuroanatomical pathologies of cSVD impact post-stroke dysphagia. We assessed the relation between cSVD pathologies, i.e., brain atrophy, white matter hyperintensities (WMH), perivascular spaces, as markers for brain integrity at the time of the stroke, and acute post-stroke dysphagia measured with the Modified Barium Swallow Study (MBSS).

METHODS

We conducted a retrospective, observational study of 40 individuals with an acute first-ever ischemic stroke. We segmented T1-weighted images into gray matter, white matter, and cerebrospinal fluid (CSF) to derive brain atrophy estimates. We scored the presence and severity of periventricular and deep WMH using the Fazekas scale and counted perivascular spaces in the basal ganglia following standard guidelines. Swallow impairments were determined with the Modified Barium Swallow Impairment Profile (MBSImP), Penetration-Aspiration Scale, and timing measures (oral (OTT), and pharyngeal transit times (PTT)). We performed regression to assess the relation between cSVD pathologies and swallowing while controlling for the stroke overlap with the right and left corticobulbar tracts, stroke volume, and the number of days between the MRI and MBSS.

RESULTS

Worse brain atrophy and more severe periventricular WMH were related to more severe MBSImP pharyngeal total scores, and worse deep WMH were related to aspiration events. More severe perivascular spaces in the basal ganglia were related to longer OTT and PTT, with a high explanatory value (27.5% and 25.1%, respectively), even when controlling for chronological age.

CONCLUSIONS

Our results suggest that several aspects of pre-stroke brain health impact dysphagia severity after acute stroke independent of the stroke site and size. These findings contribute to our understanding of mechanisms underlying the variability of post-stroke dysphagia and emphasize the importance of brain structural integrity before the stroke. Future larger studies are warranted.