PT  - JOURNAL ARTICLE
AU  - Moon, Won-Jin
AU  - Na, Dong Gyu
AU  - Kim, Sam Soo
AU  - Ryoo, Jae Wook
AU  - Chung, Eun Chul
TI  - Diffusion Abnormality of Deep Gray Matter in External Capsular Hemorrhage
DP  - 2005 Feb 01
TA  - American Journal of Neuroradiology
PG  - 229--235
VI  - 26
IP  - 2
4099  - http://www.ajnr.org/content/26/2/229.short
4100  - http://www.ajnr.org/content/26/2/229.full
SO  - Am. J. Neuroradiol.2005 Feb 01; 26
AB  - BACKGROUND AND PURPOSE: To our knowledge, diffusion abnormality of the unaffected deep gray matter during striatocapsular hemorrhage has not been previously described in the literature. We report the presence of the diffusion abnormality separated from hematoma in patients with external capsular (lateral striatocapsular) hemorrhage and suggest the plausible mechanisms of diffusion signal intensity change.METHODS: We retrospectively reviewed MR images in 28 consecutive patients with spontaneous striatocapsular hemorrhage and evaluated signal intensity changes at sites separated from the hemorrhage and the lesions on diffusion-weighted (DW) images. Apparent diffusion coefficients (ADCs) of the lesions were measured, and volume changes in the deep gray matter were assessed at follow-up.RESULTS: On DW images, hyperintensity of deep gray matter was found in nine patients (25%). In all patients with DW imaging abnormality, the hemorrhage was located in the external capsule, and the interval from hemorrhagic ictus to MR imaging study was 8–54 days. Hyperintensity of the deep gray matter was seen in the caudate (n = 8), putamen (n = 7), thalamus (n = 5), and substantia nigra (n = 2). Mean relative ADC ratios of the diffusion abnormality were 0.76 ± 0.10 in the caudate, 0.79 ± 0.07 in the putamen, and 0.85 ± 0.11 in the thalamus. DW imaging abnormality disappeared with mild atrophy in two patients who underwent follow-up imaging.CONCLUSION: External capsular hemorrhage may be uncommonly accompanied by diffusion abnormality in the striatum or thalamus at follow-up, and the lesion should not be misdiagnosed as new-onset infarction. Secondary neuronal degeneration may play an important role in the development of diffusion abnormality.