Abstract 150: Diffusion Abnormalities and Quality of Life Outcomes After Intracerebral Hemorrhage
Background: Diffusion weighted imaging (DWI) abnormalities, consistent with acute brain infarcts, occur in approximately one-quarter of patients with intracerebral hemorrhage (ICH). Prior studies have observed that DWI lesions remote from the hematoma predict long-term disability. Their impact on health-related quality of life (HRQOL) outcomes, however, has not been described. We tested the hypothesis that DWI lesions remote from the hematoma worsen HRQOL after ICH.
Methods: From a prospective registry of consecutive patients admitted to a single center with spontaneous ICH, we identified patients in whom DWI was performed within 1 week of admission, 1 or 3 month modified Rankin (mRS) and Neuro-QOL measures for upper extremity (UE) and lower extremity(LE) motor function were obtained. We excluded patients who underwent MRI after craniotomy or angiography. Two raters independently evaluated each MRI for DWI abnormalities remote from the hematoma blinded to outcome data. We assessed whether DWI lesions independently predicted outcomes using ordinal regression for mRS and linear regression of Neuro-QOL T-scores.
Results: Among 106 patients with ICH, 95 met inclusion criteria (mean age 61.6±14.6 years; 51.6% male; 58.9% white; median ICH score 1). DWI lesions remote from the hematoma were found in 23 (24.2%) patients. Poor outcome (mRS >2) was more common (61.9% vs. 36.1%, P=0.035) and T-scores were lower in those with versus without DWI lesions (UE: 31.7 vs. 40.5, P=0.011; LE: 32.4 vs. 41.0, P=0.021). Adjusted for ICH score and initial NIHSS score, DWI abnormality was an independent predictor of mRS (P=0.044) and UE (P=0.017) and LE T-scores (P=0.040).
Discussion: We confirm that DWI lesions remote from the hematoma are common after spontaneous ICH and predict disability at 3 months independent of the ICH score and stroke severity. In addition, DWI lesions worsen Neuro-QOL motor function scores. Further research is needed to understand mechanisms of secondary brain ischemia after ICH and targeted approaches to prevent its occurrence.
Author Disclosures: S. Kaskar: None. E. Liotta: None. M. Maas: None. M. Kim: None. F. Sorond: None. A. Naidech: None. S. Prabhakaran: None.
- © 2017 by American Heart Association, Inc.