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Investigation of the Gradual Increase of Lesion Size in the Chronic Stage of Stroke

Poster C29 in Poster Session C, Friday, October 7, 10:15 am - 12:00 pm EDT, Millennium Hall
Also presenting in Poster Slam C, Friday, October 7, 10:00 - 10:15 am EDT, Regency Ballroom

Lisa Johnson¹, Roger Newman-Norlund¹, Chris Rorden¹, Natalie Busby¹, Alex Teghipco¹, Argye Hillis², Leonardo Bonilha³, Julius Fridriksson¹; ¹University of South Carolina, ²Johns Hopkins University, ³Emory University

Introduction: Stroke is a leading cause of death and disability worldwide and affects nearly 800,000 people in the United States each year. With great advances in treatment of acute stroke in the hospital setting, the rate of stroke-related deaths has declined leaving stroke survivors with long-withstanding chronic deficits. The pathophysiology and neuronal recovery patterns during the acute stage have been well defined, leaving such efforts in chronic stage unexplored. Some investigation in subacute and early chronic stroke recovery have shown evidence of necrotic tissue and edema remaining in perilesional regions. This inflammation likely dysfunction may explain the high rates of stroke-related dementia in the years following a stroke event and could explain the inherent unreliability in treatment response to post-stroke therapy. For these reasons, better understanding of chronic stroke pathophysiology is very much needed and could shed light on long-term recovery patterns in these patients. Methods: This was a retrospective study in which 102 stroke survivors with at least 2 structural MRI scans (k=259 observations) more than 6-months between scans were included. Lesion masks were created using automated lesion segmentation software LINDA and lesion volumes at each timepoint were subsequently calculated. A paired sample t-test was conducted between initial and final follow-up lesion sizes. To investigate factors that predict lesion size changes over time, a linear mixed effects model (LME) was conducted with lesion volume at each time point as the dependent variable and the following independent variables: months post-stroke at scan, sex, years of education, age at stroke, and NIH stroke scale (NIHSS). Results: A paired t-test between initial and final follow-up scan indicated lesion size at final follow-up scan (M=106.4, SD=70.1) was significantly larger compared to the initial time point (M=96.5, SD=65.1) after controlling for time between scans (t=-7.13; df=101; p<.0001). The results from the mixed effects model suggest that months post stroke onset (p<.0001), sex (p=.04), age at stroke (p=.003), and initial rating on the NIHSS (p<.0001) are significant predictors of lesion growth in the chronic stage. The model suggests that with every month post-stroke, the lesion expands by approximately .2cm3 voxels. Men appear to have a greater rate of lesion growth, increasing by ab out 24.9cm3 voxels compared to females. With every year increase of stroke age, lesion size tends to decrease by 1.6cm3 voxels. Finally, initial NIHSS (taken in the chronic stage of recovery), significantly predicted growth of lesion size by 8.9cm3 voxels with every increased point on the NIHSS (higher score indicates greater severity). Summary: Results from the present study provide evidence that the lesion size the chronic stage of stroke recovery (>6 months post-stroke) can change over time. Demographic and behavioral variables such as age at stroke, months post-stroke, sex, and NIHSS are significant predictors of lesion size changes. We suggest that further investigation of the pathophysiology of the stroke lesion in the chronic stages of stroke is merited, particularly in identifying any association between lesion growth and persistent stroke-related deficits.

Topic Areas: Disorders: Acquired, Language Therapy