PT - JOURNAL ARTICLE AU - D R Enzmann AU - R H Britt AU - B E Lyons AU - J L Buxton AU - D A Wilson TI - Natural history of experimental intracerebral hemorrhage: sonography, computed tomography and neuropathology. DP - 1981 Nov 01 TA - American Journal of Neuroradiology PG - 517--526 VI - 2 IP - 6 4099 - http://www.ajnr.org/content/2/6/517.short 4100 - http://www.ajnr.org/content/2/6/517.full SO - Am. J. Neuroradiol.1981 Nov 01; 2 AB - The evolution of intracerebral hemorrhage was investigated in a canine model by high resolution sonography, computed tomography (CT), and neuropathologic examination. In 12 dogs, a parietal lobe hematoma was introduced by craniotomy. The sonographic appearance of acute hemorrhage was characteristic and consisted of a sharply circumscribed, homogeneous, highly echogenic lesion, the size and shape of which correlated closely to the area of increased density seen on the CT scan. This changed within 3-4 days to an echogenic rim surrounding a hypoechoic center. Histologically, this change corresponded to a loss of integrity of individual red blood cells. This occurred earliest in the hemorrhage center causing a hypoechoic center, while intact red blood cells at the periphery accounted for the echogenic rim. Shortly after the red blood cells lost their biconcave shape they began to lose their hemoglobin causing the hemorrhage to become isodense with surrounding brain on the CT scan. Faint contrast enhancement by CT was noted at this early stage and was related primarily to a mononuclear perivascular infiltrate at the edge of the hemorrhage. A collagen capsule formed around the hemorrhage over a 2 week period. This capsule slowly replaced intact red cells as the cause of the now shrinking echogenic rim. This capsule was also responsible for the increasing ring contrast enhancement around the resolving hemorrhage. The sequence of image changes seen on both CT and sonography in this experimental model closely resembled the findings seen in intracerebral hemorrhage in patients.