Early cerebral hypoperfusion with small artery vasospasm and delayed development of cortical T2* hypointense lesions in contrast-induced encephalopathy

Abstract

Background: Contrast-induced encephalopathy (CIE) is a rare complication arising from neurotoxicity caused by iodinated contrast agents. Its clinical presentation closely resembles that of acute stroke, which can occur following endovascular procedures. Distinguishing these two conditions is essential for proper patient management but is challenging based on clinical symptoms alone. While characteristic computed tomography findings for CIE and magnetic resonance imaging (MRI) findings for acute stroke are well established, early MRI findings of CIE - particularly in magnetic resonance angiography (MRA) and perfusion imaging (MRP) - remain underrecognized. In addition, delayed cortical hypointensities on T2*-weighted imaging (T2*WI) in chronic-stage cases have not been previously reported.

Case description: A 78-year-old woman developed CIE immediately following endovascular coil embolization for an unruptured cerebral aneurysm. Small artery vasospasms and hypoperfusion were identified on MRA and MRP, respectively, in the affected hemisphere 6 h postprocedure and resolved a day before symptom improvement. Ten months later, asymptomatic, punctate, and short linear cortical hypointensities appeared on T2*WI, suggesting microhemorrhages.

Conclusion: Early transient small artery vasospasms and hypoperfusion on neuroimaging are indicative of CIE and likely contribute to the neurological symptoms of this condition. Persistent blood-brain barrier dysfunction may underlie the delayed development of cortical hypointensities on T2*WI, seen in chronic-stage CIE cases.

Keywords: Blood–brain barrier dysfunction; Contrast-induced encephalopathy; Hypoperfusion; Magnetic resonance imaging; Microhemorrhage; Vasospasm.

Figure 1:

Neuroimaging (MRI and MRA) on admission. (a) DWI, (b) FLAIR, (c) MRA. (a) No hyperintense lesions are observed on DWI. (b) Several small hyperintense lesions are visible in the cerebral white matter on FLAIR images. (c) Multiple small aneurysms are noted at the parasellar portion of the right internal carotid artery (ICA), the right A2–A3 bifurcation, and the left M1–M2 bifurcation (arrowheads). DWI: Diffusion-weighted imaging, FLAIR: Fluid-attenuated inversion recovery, ICA: Internal carotid artery, MRA: Magnetic resonance angiography, MRI: Magnetic resonance imaging.

Figure 2:

Neuroimaging (MRI and MRA) 1 h after the procedure. (a) DWI, (b) FLAIR, (c) MRA. (a and b) No new lesions are observed on MRI. (c) Delineation of the peripheral branches of the right MCA and ACA is slightly diminished on MRA. DWI: Diffusion-weighted imaging, FLAIR: Fluid-attenuated inversion recovery, MCA: Middle cerebral artery, ACA: Anterior cerebral artery, MRA: Magnetic resonance angiography, MRI: Magnetic resonance imaging.

Figure 3:

Neuroimaging (MRI, MRP, MRA, and CT) 6 h after the procedure. (a) DWI, (b) FLAIR, (c) MRP, (d) MRA, (e) CT. (a) DWI reveals multiple punctate cortical hyperintense lesions in the right MCA distribution (circles). (b) No additional hyperintense lesions are seen on FLAIR images. (c) MRP with ASL (PLD 1,525 ms) shows hypoperfusion in the right cerebral hemisphere. (d) MRA reveals small artery vasospasms in the peripheral branches of the right MCA (a circle) and ACA. (e) CT obtained 6.5 h postprocedure shows decreased gray/white matter contrast and diffuse increased attenuation in the right MCA and ACA territories, as well as in the right cerebral subarachnoid spaces. The CT values are as follows: right cerebral cortex, 39–40 HU; left cerebral cortex, 34 HU; right frontal white matter, 35 HU; left frontal white matter, 22 HU; right frontal subarachnoid space, 22 HU; left frontal subarachnoid space, 4 HU. ACA: Anterior cerebral artery, ASL: Arterial spin labeling, CT: Computed tomography, DWI: Diffusion-weighted imaging, FLAIR: Fluid-attenuated inversion recovery, HU: Hounsfield unit, MRA: Magnetic resonance angiography, MCA: Middle cerebral artery, MRP: Magnetic resonance perfusion imaging, PLD: Postlabeling delay.

Figure 4:

Neuroimaging (MRI, MRP, and MRA) on the day after the procedure. (a) DWI, (b) FLAIR, (c) MRP, (d) MRA. (a) Multiple punctate hyperintense lesions are detected in the right MCA territory on DWI (circles). (b) FLAIR images remain unchanged. (c) Hypoperfusion in the right cerebral hemisphere is resolved on the MRP with ASL (PLD 1,525 ms). (d) Small artery vasospasms in the right MCA and ACA are no longer visible on MRA. ASL: Arterial spin labeling, DWI: Diffusion-weighted imaging, FLAIR: Fluid-attenuated inversion recovery, MCA: Middle cerebral artery, MRA: Magnetic resonance angiography, MRP: Magnetic resonance perfusion imaging, MRI: Magnetic resonance imaging, PLD: Postlabeling delay.

Figure 5:

Neuroimaging (MRI and CT) 10 months after the procedure. (a) T2*WI, (b) CT with 1-mm slice thickness. (a) A few additional punctate and short linear hypointense lesions are observed in different regions of the right cerebral cortex compared to the previous hyperintense lesions on DWI (circles). No similar lesions are seen outside the right MCA territory. (b) No corresponding hyperattenuation is seen on CT, suggesting no deposition of iodinated contrast agent, calcification, or acute hemorrhage. CT: Computed tomography, DWI, Diffusion-weighted imaging, MCA: Middle cerebral artery, MRI: Magnetic resonance imaging, T2*WI: T2-star-weighted imaging.