Abstract
OBJECTIVE: To determine whether longitudinal progression of small vessel disease in chronic stroke survivors is associated with longitudinal worsening of chronic aphasia severity. DESIGN: A longitudinal retrospective study. Severity of white matter hyperintensities (WMHs) as a marker for small vessel disease was assessed on fluid-attenuated inversion recovery (FLAIR) scans using the Fazekas scale, with ratings for deep WMHs (DWMHs) and periventricular WMHs (PVHs). SETTING: University research laboratories. PARTICIPANTS: This study includes data from 49 chronic stroke survivors with aphasia (N=49; 15 women, 34 men, age range=32-81 years, >6 months post-stroke, stroke type: [46 ischemic, 3 hemorrhagic], community dwelling). All participants completed the Western Aphasia Battery-Revised (WAB) and had FLAIR scans at 2 timepoints (average years between timepoints: 1.87 years, SD=3.21 years). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Change in white matter hyperintensity severity (calculated using the Fazekas scale) and change in aphasia severity (difference in Western Aphasia Battery scores) were calculated between timepoints. Separate stepwise regression models were used to identify predictors of WMH severity change, with lesion volume, age, time between timepoints, body mass index (BMI), and presence of diabetes as independent variables. Additional stepwise regression models investigated predictors of change in aphasia severity, with PVH change, DWMH change, lesion volume, time between timepoints, and age as independent predictors. RESULTS: 22.5% of participants (11/49) had increased WMH severity. Increased BMI was associated with increases in PVH severity (P=.007), whereas the presence of diabetes was associated with increased DWMH severity (P=.002). Twenty-five percent of participants had increased aphasia severity which was significantly associated with increased severity of PVH (P<.001, 16.8% variance explained). CONCLUSION: Increased small vessel disease burden is associated with contributing to chronic changes in aphasia severity. These findings support the idea that good cardiovascular risk factor control may play an important role in the prevention of long-term worsening of aphasic symptoms.