Diffusion-Weighted MRI in Severe Leukoaraiosis
To the Editor:
Recent articles1 2 have reported that diffusion-weighted MRI (DWI) is useful in both detecting very early ischemic lesions and identifying the responsible lesion in multiple subcortical lesions. Singer and colleagues1 described the very high accuracy of DWI for their 39 subjects with acute subcortical infarction. They reported that the sensitivity of DWI for acute subcortical infarction was 94.9% and the specificity was 94.1%. But they did not refer to its relation to the periventricular hyperintensity area (PVH).
We studied 18 cases (10 men and 8 women; mean age, 72±7.9 years) with serial acute cerebral infarction. They were consisted of 3 cases with cortical infarction and 15 cases with subcortical infarctions, including infratentorial regions. MRI was performed with a 1.5-T MR scanner with hardware for echo-planar imaging (Gyroscan ACS-NT, Philips). In all cases, the images were obtained during the same imaging session and at the same slice locations; 6-mm-thick sections without gap and 240-cm field of view were used for all scans. T1-weighted spin-echo (SE) used a 256×256 matrix, TR=360 ms, TE=14 ms, number of excitations=1, and acquisition time=2:16 (min:sec). T2-weighted fast-SE used an echo train length of 11, TR=2000, TE=140, number of excitations=1, and acquisition time=4:03. Fluid-attenuated inversion recovery (FLAIR) imaging was obtained with a fast-SE method with an echo train length of 19, TR=5500, TE=140, number of excitations=1, and acquisition time=3:40. DWI, used in Multishot, SE/echo-planar image sequence, was performed with diffusion sensitivity b=850 s/mm2, TR=857, TE=20, number of excitations=1, and acquisition time=1:36. Image analysis was performed by 3 examiners.
The time intervals of imaging relative to onset of ictus ranged from 2 hours to 10 days (mean, 71 hours). Of the 18 patients, 5 underwent imaging <24 hours after onset, 7 from 24 to 72 hours after onset, and 6 at up to 240 hours after onset. Of 5 patients who could be examined within 24 hours, the lesion could be identified in only 1 with T1WI, in 2 with T2WI, and in 3 with FLAIR. In contrast to these results, DWI revealed all responsible lesions. In patients with multiple subcortical lesions, in 6 of 7 cases the responsible lesion could not be correlated to neurological findings through routine MRI procedures. DWI revealed the responsible lesions in all cases. Furthermore, in all 5 cases of severe PVH (so-called Binswanger type), which could not be identified through routine MRI methods, the responsible lesions could be identified by DWI (Figure⇓).
White matter changes, including PVH, are often described as leukoaraiosis, which is defined as bilateral and either patchy or diffuse areas of hypodensity on CT or hyperdensity on T2-weighted MRI. The cause of leukoaraiosis is not fully understood. Clinically, severe leukoaraiosis is reported to relate to cognitive impairment, gait disturbances, and mood disorders.3 4 A pathological study of Binswanger’s disease revealed that these PVH included lacunar infarct, incomplete infarction, état criblé, perivascular degeneration, and gliosis.5 But its clinical course and pathophysiology are unclear, especially in subjects with multiple subcortical lesions and severe PVH.4 DWI may provide the information for formation and extension of PVH and elucidate the mechanism of white matter changes to Binswanger’s disease in vivo.
- Copyright © 1999 by American Heart Association
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