Acta Neurol Belg DOI 10.1007/s13760-014-0321-z

LETTER TO THE EDITOR

Unilateral subarachnoid and intravitreous FLAIR hyperintensities after gadolinium-enhanced MRI Dimitri Renard • Christian Moesch • Jean Christophe Boyer • Cornelia Freitag Eric Thouvenot



Received: 9 May 2014 / Accepted: 4 June 2014 Ó Belgian Neurological Society 2014

Keywords Subarachnoid  Intravitreous  FLAIR  Hyperintensity  Gadolinium  MRI

Case report 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.

D. Renard (&)  E. Thouvenot Department of Neurology, CHU Nıˆmes, Hoˆpital Caremeau, Place du Pr Debre´, 30029 Nıˆmes Cedex 4, France e-mail: [email protected] C. Moesch Service de Pharmacologie, Toxicologie et Pharmacovigilance, CHU Limoges, 87042 Limoges Cedex, France J. C. Boyer Laboratoire de Biochimie, CHU Nıˆmes, Hoˆpital Caremeau, Nıˆmes, France C. Freitag Department of Radiology, CHU Nıˆmes, Hoˆpital Caremeau, Nıˆmes, France E. Thouvenot Institut de Ge´nomique Fonctionnelle, CNRS UMR 5203, INSERM U661, Universite´ Montpellier 1, Universite´ Montpellier 2, Montpellier, France

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 lg/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 lg/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.

Discussion Other causes of subarachnoid FLAIR hyperintensities without previous gadolinium-injection include subarachnoid hemorrhage, meningitis, venous thrombosis, and artefact-related causes (e.g. vascular pulsation, motion artefact, CSF flow, supplemental oxygen, metal-related artefact). Delayed gadolinium-enhancement on FLAIR, due to blood–brain barrier disruption, have been reported in patients after thrombolytic therapy, after revascularisation procedures (the so-called re- or hyperperfusion syndrome), after seizure, in nonketotic hyperglycemia, in migraine with aura, in renal failure, in transthyretin-related familial amyloid polyneuropathy, and sometimes in patients

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Acta Neurol Belg Fig. 1 Initial MRI showing multiple acute MCA infarctions on DWI (a, arrowheads), carotid stenosis on gadoliniuminjected MRA (b, arrowhead), and absence of FLAIR abnormalities (c). Four hours later, left-hemispheric subarachnoid FLAIR hyperintensities—showing a gravity-related intensity gradient (d–f, arrows)—are seen with a fluid–fluid level (d, arrowhead) and a probable (d–f), together with a left intravitreous FLAIR hyperintensities (f, arrowhead). These FLAIR abnormalities disappeared 5 days later (g–i). The infarctions are seen on g and h (arrowheads)

without any of these disorders [1]. Spontaneous intravitreous FLAIR hyperintensity is seen in intravitreous hemorrhage, and intravitreous FLAIR hyperintensities after gadolinium-injection have been reported in patients with various forms of retinopathy (e.g. retinitis, vitrectomy, retinal laser treatment), transthyretin-related familial amyloid polyneuropathy, or renal failure [2]. To the best of our knowledge, the association of unilateral subarachnoid and intravitreous FLAIR hyperintensities due to gadolinium-injection has never been described earlier. Conflict of interest

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We have no conflict of interest to declare.

References 1. Morris JM, Miller GM (2007) Increased signal in the subarachnoid space on fluid-attenuated inversion recovery imaging associated with the clearance dynamics of gadolinium chelate: a potential diagnostic pitfall. Am J Neuroradiol 28:1964–1967 2. Berkowitz BA, Wilson CA, Tofts PS, Peshock RM (1994) Effect of vitreous fluidity on the measurement of blood-retinal barrier permeability using contrast-enhanced MRI. Magn Reson Med 31:61–66

Unilateral subarachnoid and intravitreous FLAIR hyperintensities after gadolinium-enhanced MRI.

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