TY - JOUR
T1 - Hyperacute injury marker (HARM) in primary hemorrhage
T2 - A distinct form of CNS barrier disruption
AU - Kidwell, C. S.
AU - Burgess, R.
AU - Menon, R.
AU - Warach, S.
AU - Latour, L. L.
N1 - Funding Information:
Study funding: Supported in part by the Division of Intramural Research, National Institute of Neurological Disorders and Stroke (NINDS).
Funding Information:
Dr. Kidwell serves on the editorial boards of Neurocritical Care, the Journal of Neuroimaging, and Stroke Research and Treatment; serves/served as a consultant for Embrella Cardiovascular, Inc., Inc. and Simcere Pharmaceutical Group; and receives research support from Baxter International Inc. and the NIH/NINDS. Dr. Burgess receives research support from the NIH/NINDS. Dr. Menon receives research support from the NIH (NINDS, NIMHD). Dr. Warach serves on the editorial boards of the Journal of Cerebral Blood Flow and Metabolism, Stroke, The Lancet Neurology, International Journal of Stroke, and Cerebrovascular Diseases; and receives research support from NINDS, Division of Intramural Research. Dr. Latour reports no disclosures.
PY - 2011/11/8
Y1 - 2011/11/8
N2 - Objective: The objective of the study was to characterize a previously unreported form of CNS barrier disruption in intracerebral hemorrhage (ICH): hyperacute injury marker (HARM). Methods: In this retrospective cohort analysis of patients presenting with primary ICH, precontrast and postcontrast MRI scans obtained within 5 days of symptom onset were analyzed. The presence of CNS barrier disruption was defined by 1) perihematomal or intrahematomal enhancement visualized on postcontrast T1-weighted MRI or 2) HARM: sulcal or ventricular hyperintensity visualized on postcontrast fluid-attenuated inversion recovery sequences (graded on a 5-point scale). Results: Forty-six patients were included in the analysis. Mean age was 65 years, median NIH Stroke Scale score was 7, and mean ICH volume was 12.2 mL (range 0.3-46.9 mL). HARM was visualized in 85% of patients, and this was moderate to severe in 50%. In all cases, the sulcal enhancement was noncontiguous with the hematoma. Of those patients with postcontrast T1- weighted imaging, perihematomal or intrahematomal contrast enhancement was visualized in 75% of patients. Conclusions: This study demonstrates that HARM occurs in intracerebral hemorrhage and that it likely represents a second type of CNS barrier disruption distinct from parenchymal postcontrast T1-weighted enhancement. Similar to T1 enhancement, this phenomenon may serve as a clinically useful biomarker to test therapies aimed at stabilizing acute ICH and CNS barrier disruption. Future studies are needed to further define the time course and prognostic implications of this finding.
AB - Objective: The objective of the study was to characterize a previously unreported form of CNS barrier disruption in intracerebral hemorrhage (ICH): hyperacute injury marker (HARM). Methods: In this retrospective cohort analysis of patients presenting with primary ICH, precontrast and postcontrast MRI scans obtained within 5 days of symptom onset were analyzed. The presence of CNS barrier disruption was defined by 1) perihematomal or intrahematomal enhancement visualized on postcontrast T1-weighted MRI or 2) HARM: sulcal or ventricular hyperintensity visualized on postcontrast fluid-attenuated inversion recovery sequences (graded on a 5-point scale). Results: Forty-six patients were included in the analysis. Mean age was 65 years, median NIH Stroke Scale score was 7, and mean ICH volume was 12.2 mL (range 0.3-46.9 mL). HARM was visualized in 85% of patients, and this was moderate to severe in 50%. In all cases, the sulcal enhancement was noncontiguous with the hematoma. Of those patients with postcontrast T1- weighted imaging, perihematomal or intrahematomal contrast enhancement was visualized in 75% of patients. Conclusions: This study demonstrates that HARM occurs in intracerebral hemorrhage and that it likely represents a second type of CNS barrier disruption distinct from parenchymal postcontrast T1-weighted enhancement. Similar to T1 enhancement, this phenomenon may serve as a clinically useful biomarker to test therapies aimed at stabilizing acute ICH and CNS barrier disruption. Future studies are needed to further define the time course and prognostic implications of this finding.
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U2 - 10.1212/WNL.0b013e318236ef46
DO - 10.1212/WNL.0b013e318236ef46
M3 - Article
C2 - 22031531
AN - SCOPUS:82955243955
SN - 0028-3878
VL - 77
SP - 1725
EP - 1728
JO - Neurology
JF - Neurology
IS - 19
ER -