Increased signal in the subarachnoid space on fluid-attenuated inversion recovery imaging associated with the clearance dynamics of gadolinium chelate: a potential diagnostic pitfall

J M Morris, G M Miller
AJNR. American Journal of Neuroradiology 2007, 28 (10): 1964-7

BACKGROUND AND PURPOSE: Hyperintense CSF in the subarachnoid space (SAS) on fluid-attenuated inversion recovery (FLAIR) imaging has been reported in numerous pathologic conditions, including subarachnoid hemorrhage, meningitis, meningeal carcinomatosis, superior sagittal thrombosis, adjacent tumors, status epilepticus, and stroke. It has also been reported in otherwise healthy patients undergoing anesthesia with supplemental oxygen. We present a series of 11 patients with hyperintense CSF signal intensity in the SAS on FLAIR imaging after previous administration of gadolinium chelate.

MATERIALS AND METHODS: Head MR images of patients who had a prior gadolinium-enhanced body, spine, or brain MR imaging and who had increased signal intensity in the SAS on FLAIR images were prospectively and retrospectively reviewed. Correlation was made with the clinical and laboratory findings.

RESULTS: Eight of the 11 patients had negative findings on lumbar punctures. Seven patients had either chronic renal insufficiency or acute renal failure, but the remaining 4 had normal renal function. Nine patients had no other significant intracranial abnormalities, and 2 patients had acute infarcts remote from the CSF hyperintensity. One patient had follow-up studies at 24 and 48 hours, documenting resolution of the CSF hyperintensities.

CONCLUSION: Given the sharp rise in volume of contrast-enhanced MR imaging studies, it is inevitable that some patients will have undergone a contrast-enhanced MR imaging 24-48 hours before an MR imaging of the brain. The neuroradiologist should be aware that previous administration of gadolinium chelate can cause increased signal intensity in the SAS on FLAIR imaging in patients with or without a history of renal insufficiency and without abnormalities known to disrupt the blood-brain barrier.

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