Unilateral subarachnoid and intravitreous FLAIR hyperintensities after gadolinium-enhanced MRI

Excerpt

A 73-year-old man, with a history of left-sided retinal detachment treated by vitrectomy 3 years earlier, presented with acute right arm weakness. MRI showed multiple acute left middle cerebral artery (MCA) infarctions, and an intracranial high-degree carotid stenosis at the level of the C4 cavernous segment (i.e. proximal of the branch of the ophthalmic artery) and a normal aspect of the MCA on gadolinium-injected (14 ml of gadoteric-acid 0.5 mmol/ml) MRA (Fig. 1). Immediately after MRI performance, a generalised tonic–clonic seizure occurred. Renal function was normal. Four hours later, a new MRI showed subarachnoid hyperintensity in the left hemisphere and the left vitreous body on FLAIR sequences (Fig. 1) while gradient-echo and perfusion-weighted imaging were normal. Eye fundus showed no hemorrhage. Lumbar puncture performed 15 h after the gadolinium-injection showed the presence of 5,177 µg/l of gadolinium in the CSF, using inductively coupled plasma mass spectrometry, without other abnormalities. Gadolinium CSF concentration in a healthy control patient without MRI performance using the same technique was <1 µg/l. Five days later, subarachnoid and intravitreous FLAIR hyperintensities disappeared (Fig. 1). FLAIR hyperintensities probably corresponded to the presence of gadolinium (administrated on initial MRI), related to the coexistence of the breakdown of the blood-retinal (related to ophthalmic artery ischemia and/or the history of retinal detachment) and the blood–brain (related to brain ischemia and/or seizure) barrier. The subarachnoid gadolinium might have caused the seizure.

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