Abstract
White matter hyperintensities of presumed vascular origin (WMH) are a prevalent form of cerebral small-vessel disease and an important risk factor for post-stroke cognitive dysfunction. Despite this prevalence, it is not well understood how WMH contributes to post-stroke cognitive dysfunction. Preliminary findings suggest that increasing WMH volume is associated with total hippocampal volume in chronic stroke patients. The hippocampus, however, is a complex structure with distinct subfields that have varying roles in the function of the hippocampal circuitry and unique anatomical projections to different brain regions. For these reasons, an investigation into the relationship between WMH and hippocampal subfield volume may further delineate how WMH predispose to post-stroke cognitive dysfunction. In a prospective study of acute ischemic stroke patients with moderate/severe WMH burden, we assessed the relationship between quantitative WMH burden and hippocampal subfield volumes. Patients underwent a 3T MRI brain within 2–5 days of stroke onset. Total WMH volume was calculated in a semi-automated manner. Mean cortical thickness and hippocampal volumes were measured in the contralesional hemisphere. Total and subfield hippocampal volumes were measured using an automated, high-resolution, ex vivo computational atlas. Linear regression analyses were performed for predictors of total and subfield hippocampal volumes. Forty patients with acute ischemic stroke and moderate/severe white matter hyperintensity burden were included in this analysis. Median WMH volume was 9.0 cm3. Adjusting for intracranial volume and stroke laterality, age (β = −3.7, P < 0.001), hypertension (β = −44.7, P = 0.04), WMH volume (β = −0.89, P = 0.049), and mean cortical thickness (β = 286.2, P = 0.006) were associated with total hippocampal volume. In multivariable analysis, age (β = −3.3, P < 0.001) and cortical thickness (β = 205.2, P = 0.028) remained independently associated with total hippocampal volume. In linear regression for predictors of hippocampal subfield volume, increasing WMH volume was associated with decreased hippocampal-amygdala transition area volume (β = −0.04, P = 0.001). These finding suggest that in ischemic stroke patients, increased WMH burden is associated with selective hippocampal subfield degeneration in the hippocampal-amygdala transition area.
Highlights
Post-stroke cognitive impairment/dysfunction (PSCID) is highly prevalent and associated with poor global outcomes [1,2,3]
In univariable linear regression for predictors of total hippocampal volume, increasing age, hypertension, and WMH volume (WMHv) were associated with decreased hippocampal volume, while cortical thickness showed a positive association (Table 2)
In a cohort of AIS patients with moderate to severe WMH burden and no prestroke dementia, we show that WMHv is a negative predictor of total hippocampal volume and selectively associated with volume of the Hippocampal Amygdala Transition Area (HATA) subfield
Summary
Post-stroke cognitive impairment/dysfunction (PSCID) is highly prevalent and associated with poor global outcomes [1,2,3]. Recognition of the factors that predispose to PSCID is clinically important, as early identification of vulnerable patients could guide individualized therapies focused on PSCID prevention and rehabilitation Along these lines, identifying clinically relevant biomarkers that identify patients at risk for poor stroke outcomes is of major clinical interest [4]. In a comparison of patients with minor stroke, the addition of other markers of small-vessel disease to WMH volume did not improve prediction accuracy of PSCID [9] While these observations exemplify the clinical relevance of WMH as a biomarker to identify patients at high risk for poor functional and cognitive outcomes after stroke, it remains unclear how increasing WMH burden predisposes to PSCID
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