Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions

Abstract

Background and purpose: Carbon monoxide intoxication has delayed effects on the cerebral white matter characterized by bilateral, confluent lesions that reflect diffuse demyelination. To increase our understanding of this process, we assessed the diffusion characteristics of these lesions.

Methods: Five consecutive patients with delayed encephalopathy of CO intoxication were examined with diffusion MR imaging. Diffusion-weighted images (DWIs) were obtained 25-95 days after their exposure to CO and during a relapse of neuropsychiatric symptoms, which occurred after an initial recovery. Imaging was performed at 1.5 T by using a spin-echo echo-planar sequence with diffusion gradients of 0, 500, and 1000 s/mm(2). DWIs and apparent diffusion coefficient (ADC) maps were visually evaluated, and mean ADCs were calculated from the periventricular white matter and the centrum semiovale, where confluent hyperintensity was seen on T2-weighted images. Findings were compared with those of normal-looking white matter.

Results: In all five patients, both T2-weighted images and DWIs showed the white matter lesions as bilateral, diffuse, confluent areas of hyperintensity in the periventricular white matter and centrum semiovale. On ADC maps, these lesions were isointense, with focal areas of hypointensity (n = 4) or diffuse hypointensity (n = 1). Mean ADC values of the white matter lesions were significantly lower than those of normal-looking white matter, regardless of their isointensity or hypointensity on ADC maps (P <.05).

Conclusion: Bilateral, confluent, white matter lesions in patients with delayed encephalopathy of CO intoxication show decreased diffusivity.

Fig 1.

Case 1. MR images obtained in a 54-year-old woman on day 25 after CO exposure. A and B, T2-weighted images (TR/TE/NEX, 4000/98/1) show bilateral, symmetric, confluent areas of high signal intensity in both the centrum semiovale (A) and periventricular white matter (B). The high intensity appears more prominent in the frontal lobes than elsewhere. C and D, ADC maps (calculated from DWIs [6500/98/1, b = 0 and 1000 s/mm²]) obtained at the same levels as in A and B, respectively, show focal areas of low signal intensity (decreased diffusion) in the bilateral frontal lobes. Most of the remaining centrum semiovale and periventricular white matter appears isointense. DWIs at the same levels showed confluent high signal intensity in the centrum semiovale and periventricular white matter. The appearance was similar to that on the T2-weighted images (not shown) and mainly resulted from a T2 shine-through effect.

Fig 2.

Case 2. MR images obtained in a 71- year-old man on day 41 after CO exposure. A, FLAIR image (TR/TE/TI/NEX, 9000/110/2200/1) shows asymmetric distribution of the high-intensity lesions in the periventricular white matter and corpus callosum. B, DWI (TR/TE/NEX, 6500/98/1; b = 1000 s/mm²) shows similar high signal intensity in the periventricular white matter and corpus callosum. The high intensity is more prominent in the right frontal lobe and on the right side of the genu of the corpus callosum than elsewhere. C, ADC map shows a focal area of subtle low signal intensity in the right frontal lobe (arrow). Other white matter lesions appear isointense.

Fig 3.

Case 4. MR images obtained in a 65-year-old woman on day 55 after CO exposure. A, FLAIR image (TR/TE/TI/NEX, 9000/110/2200/1) shows diffuse high-intensity lesions in the periventricular white matter. B, DWI (TR/TE/NEX, 6500/98/1; b = 1000 s/mm²) shows confluent high signal intensity in the same periventricular white matter. C, ADC map shows diffuse low signal intensity in the periventricular white matter.