Magnetic Resonance Imaging and Histologic Findings of Acute and Subacute Stage of Experimental Cerebral Fat Embolism in Cats.
10.3348/jkrs.2002.46.4.301
- Author:
Hak Jin KIM
1
;
Chang Hun LEE
;
Suk Hong LEE
;
Byung Rae RARK
;
Sang Sik KIM
;
Yong Woo KIM
Author Information
1. The Department of Radiology, Pusan National University College of Medicine. hakjink@hyowon.pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Embolism, experimental;
Embolism, fat;
Magnetic resonance (MR), experimental;
Brain, MR
- MeSH:
Animals;
Blood-Brain Barrier;
Brain;
Carotid Arteries;
Cats*;
Demyelinating Diseases;
Edema;
Embolism, Fat*;
Magnetic Resonance Imaging*;
Natural History;
Necrosis;
Triolein;
Vacuoles
- From:Journal of the Korean Radiological Society
2002;46(4):301-308
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To determine the magnetic resonance imaging (MRI) findings and natural history of cerebral fat embolism in a cat model, and to correlate the MRI and histologic findings. MATERIALS AND METHODS: Using the femoral arterial approach, the internel carotid artery of 11 cats was injected with 0.1 ml of triolein. T2-weighted (T2WI), T1-weighted (T1WI) and Gd-enhanced T1-weighted (Gd-T1WI) images were obtained serially at 2 hours, 1 and 4 days and 1, 2 and 3 weeks after embolization. Any abnormal signal intensity (SI) was evaluated. After MR imaging at 3 weeks, brain tissue was obtained for light microscopic (LM) examination using hematoxylin-eosin and Luxol fast blue staining, and for electron microscopic (EM) examination. The histologic and MRI findings were correlated. RESULTS: At 2 hours, lesions showed high SI at T2WI, iso- or low SI at T1WI, and strong enhancement at Gd-T1WI. The high SI seen at T2WI decreased thereafter, and most lesions became iso-intense. At week 3, however, small focal areas of high SI were seen in the grey matter of eight cats and in the white matter of three. The low SI noted at acute-stage T1W1 subsequcntly became normal, though in the areas in which T2W1 had depicted high SI, focal areas of low SI remained. Lesion enhancement demonstrated by Gd-T1WI decreased continuously from day 1, and at week 3, weak enhancement was seen at the margin of the remained hypointense lesions in the gray matter in five cats. At LM examination with hematoxylin-eosin staining revealed normal histologic findings in the greater park of an embolized lesion. Cystic change was observed in the gray matter of eight cats, and in the gray and white matter of three of the eight. At LM examination, Luxol fast blue, staining demonstrated demyelination around the cystic change occurring in the white matter, and EM examination of the embolized cortex revealed sporadic intracapillary fat vacuoles (n=11) and disruption of the blood-brain barrier (n=4). Most lesions were normal, however, and perivascular interstitial edema and cellular swelling were mild compared with the control side. CONCLUSION: Experimental cerebral fat embolism was clearly demonstrated by T2WI and Gd-T1WI images obtained at all time points. The greater part of an embolized lesion showed reversible findings at MR and histologic examination; irreversible focal necrosis was, however, observed in gray and white matter at week 3.
