Diffusion-weighted MR imaging of global cerebral anoxia

Abstract

Background and purpose: Diffuse cerebral anoxia is a devastating event, and its acute findings, as revealed by conventional MR imaging and CT scanning, may be subtle. We analyzed diffusion-weighted and conventional MR images of patients with diffuse cerebral anoxia to determine their usefulness in establishing the diagnosis during the acute period and in determining the age of insult.

Methods: We reviewed 11 MR imaging studies of 10 patients who had experienced prolonged cardiac arrest. All of the patients underwent echo-planar diffusion-weighted imaging with low- and high-strength B values and multiplanar unenhanced MR imaging. We considered bright areas on the high-strength diffusion-weighted images to be abnormal when compared with low-strength images. Special attention was given to the cortex, basal ganglia, thalami, hippocampi, cerebellum, and white matter. Conventional MR studies also were reviewed, and abnormalities noted. The medical records of all of the patients were reviewed.

Results: Four patients who underwent imaging during the acute period (<24 hours) had bright basal ganglia (n = 2), bright cerebellum (n = 3), and bright cortex (n = 1) shown on their diffusion-weighted images. For these patients, conventional MR images showed questionable increased T2-weighted signal intensity in the basal ganglia (n = 1), and the results of two studies were judged to be normal. During the early subacute period (24 hours-13 days), four patients were studied, and were determined to have an abnormal cortex (n = 3) and basal ganglia (n = 2). For two of these patients, conventional MR images showed similar abnormalities, and the results of one study were normal. For two patients who underwent imaging during the late subacute period (14-20 days), diffusion-weighted images showed abnormalities mostly confined to white matter. Two patients who underwent imaging during the chronic phase (>21 days) had normal results of their diffusion-weighted imaging and one had evidence of laminar necrosis revealed by conventional MR imaging.

Conclusion: During the acute period, high-strength diffusion-weighted images showed the abnormal basal ganglia, cerebellum, and cortex to a better extent than did conventional MR images. During the early subacute period, gray matter abnormalities were seen on diffusion-weighted images. During the late subacute period, diffusion-weighted images showed mostly white matter abnormalities. During the chronic stage, the results of diffusion-weighted imaging were normal. Our findings suggest that diffusion-weighted images are helpful for evaluating and dating diffuse cerebral anoxia, and therefore aid in the determination of prognosis and management of these patients.

fig 1.

Bright cerebellum on diffusion-weighted images as the initial finding after cerebral anoxia. A, Axial T2-weighted image, 3300/105/1 (TR/TE/excitations), obtained within 3 hours of cardiac arrest, shows the cerebellum to be of normal appearance. B, Corresponding high-strength diffusion-weighted image, 0.8/123/1100 (TR/TE/B value), shows that the cerebellum (c) is diffusely bright when compared with the left occipital lobe (o). C, Follow-up image obtained 3 days after anoxic episode. Midsagittal T1-weighted image (570/15/1) shows swollen cerebellum with upward transtentorial and downward transforaminal herniations. The forth ventricle and brain stem are compressed. D, Axial T2-weighted image (3500/93/1), obtained at same time as the image shown in C, shows swollen and bright cortex, effaced cortical sulci, and bright basal ganglia. Because of technical problems, diffusion-weighted images were not obtained as part of the follow-up study. This patient died.

fig 2.

Sequential diffusion-weighted images show bright basal ganglia as the initial finding after anoxia. A, Axial high-strength diffusion-weighted image (0.8/123/1100), obtained less than 3 hours after cardiac arrest (because of electrocution), shows abnormal brightness in lentiform nuclei (arrows). Brightness in splenium of corpus callosum is normal because transverse white matter fibers are perpendicular to the plane (z) in which the diffusion gradient was applied. B, Axial T2-weighted image (4200/105/1), obtained 3 days after insult, shows increased signal intensity in basal ganglia and possibly in occipital cortices. C, High-strength diffusion-weighted image (0.8/123/1100), obtained at same time as the image shown in B, reveals abnormally bright basal ganglia and cortex in frontal, posterior temporal, and occipital lobes. D, High-strength diffusion-weighted image (0.8/123/1100), obtained at same time as the image shown in B, shows that the cortex in the frontal and parietal regions is abnormally bright. E, High-strength diffusion-weighted image (0.8/123/1100), obtained 14 days after insult and corresponding to the image shown in C, reveals decreasing signal intensity from gray matter structures and abnormal brightness in posterior limb of internal capsules. F, Axial high-strength diffusion-weighted image (0.8/123/1100), obtained at the same time as the image shown in E and at same level as the image shown in D, reveals decreasing signal intensity from the cortex and abnormal brightness in the centra semiovale. G, Corresponding conventional T2-weighted image (4500/105/1) shows normal results. This patient survived.

fig 3.

Bright basal ganglia and cortex on diffusion-weighted images obtained during the acute period (20 hours after insult). A, Axial T2-weighted image (4500/105/1) shows questionable increased signal intensity in basal ganglia. B, Corresponding low-strength diffusion-weighted image (0.8/123/30) shows no abnormality. C, Corresponding high-strength diffusion-weighted image (0.8/123/1100) shows abnormally bright basal ganglia, thalami, and cortex (particularly in medial-occipital regions). D, More cephalad axial low-strength diffusion-weighted image (0.8/123/30) shows no abnormality. E, Corresponding high-strength diffusion-weighted image (0.8/123/1100) shows abnormally bright cortex surrounding the central sulci. This patient survived.

fig 4.

Abnormally bright cortex in the early subacute period. A, Axial T2-weighted image (4500/105/1) initially was interpreted as normal. A careful retrospective analysis raised the possibility of increased signal intensity and thickening of the cortex. B, Corresponding high-strength diffusion-weighted image (0.8/123/1100) shows abnormal brightness preferentially involving the cortex. fig 5. Images of abnormal white matter obtained during the late subacute period (15–20 days). A, Axial T2-weighted image (3300/105/1) shows no definite abnormalities. There is subtle and nonspecific increased signal intensity in the white matter. B, Corresponding high-strength diffusion-weighted image (0.8/123/1100) shows abnormally bright white matter in centra semiovale and no definite cortical abnormalities. fig 6. Images of laminar necrosis obtained during the chronic period. A, Axial T1-weighted image (550/15/1) shows linear brightness along the superior frontal, pre-central, and central gyri corresponding to the sequelae of laminar necrosis 22 days after cardiac arrest. B, Axial high-strength diffusion-weighted image (0.8/123/1100), obtained inferior to the image shown in A (convexity diffusion images were degraded by magnetic susceptibility artifacts), shows normal results.