title: Identification of brain tissue necrosis by MRI: validation by histomorphometry.
abstract: The volume of an experimental necrotic lesion of the cortex expands up to 400% of its initial size within the first 24 h after the insult. Lesion expansion, a clinically well known phenomenon, is often accompanied by perifocal brain edema and consequently difficult to image and to analyze by magnetic resonance imaging (MRI). Therefore we aimed to validate a T(2)-weighted spin echo sequence upon its ability to distinguish necrotic from edematous brain tissue. Male Sprague-Dawley rats (n = 5 per group) were subjected to a cortical freezing lesion leading to immediate tissue necrosis with subsequent perifocal vasogenic brain edema. Immediately and 4, 12, and 24 h after the lesion the maximal area of necrosis was quantified longitudinally by coronal T(2)-weighted spin echo MRI-scans. After the last scan, animals were sacrificed for direct comparison of the lesion area obtained by MRI and histomorphometry. In parallel groups of animals, lesion expansion was quantified by histology. The acquired T(2)-maps clearly distinguish the cortical necrosis from perifocal edema and healthy brain. Focal freezing led to a cortical lesion of 5.24 +/- 0.36 mm(2) immediately after trauma (0 h; 100%) which expanded progressively to a maximum of 6.82 +/- 0.34 mm(2) after 24 h (131%; *p < 0.01 vs. 0 h). Lesion expansion quantified by histology was almost identical (132% within 24 h). Histological assessment resulted in smaller absolute lesion areas compared to MRI, most likely due to shrinking during tissue processing (4.72 +/- 0.26 mm(2) vs. 6.82 +/- 0.34 mm(2), p < 0.01). The current study shows that necrotic brain tissue can be distinguished from surrounding brain edema by T(2)-mapping. The technique is sensitive enough to detect small changes in necrosis expansion in vivo as validated by histology. The presented technique may be a useful future tool for the non-invasive identification of necrotic brain tissue following brain injury (e. g., from trauma or ischemia).
authors.affiliation: Department of Neurosurgery, Rheinische Friedrich-Wilhelms-University, Bonn, Germany. michael.stoffel@ukb.uni-bonn.de
authors.forename: Michael
authors.initials: M
authors.lastname: Stoffel
authors.forename: Cornelia
authors.initials: C
authors.lastname: Blau
authors.forename: Herbert
authors.initials: H
authors.lastname: Reinl
authors.forename: Jörg
authors.initials: J
authors.lastname: Breidt
authors.forename: Klaus
authors.initials: K
authors.lastname: Gersonde
authors.forename: Alexander
authors.initials: A
authors.lastname: Baethmann
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Plesnila
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D001929:Brain Edema / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D003080:Cold Temperature; D003937:Diagnosis, Differential; D017352:Echo-Planar Imaging; D005240:Feasibility Studies; D008297:Male; D009336:Necrosis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors