The Spine Journal 14 (2014) 3065–3066 Late-onset cauda equina contrast enhancement: a rare magnetic resonance imaging finding in subacute spinal cord infarction A 52-year-old woman with no relevant medical history was admitted to our emergency department for abrupt onset of flaccid paraplegia, sensory loss below L1 level, intense burning pain at both legs, and urinary retention. A magnetic resonance imaging (MRI) performed 3 hours after the onset of symptoms revealed a subtle T2-hyperintensity of the conus medullaris (Figure, Day 1). A follow-up MRI performed 3 days later documented more definite T2-hyperintensity, swelling, and water diffusivity restriction of the distal cord gray matter, indicative of an ischemic infarction (Figure, Day 3). In a further followup MRI examination performed on Day 14 (Figure, Day 14), postgadolinium T1-W images showed enhancement of the injured cord, indicating damage to the hematomyelic barrier, and of the right half of the Th12 vertebral body, indicating concomitant vertebral body infarction [1]. A diffuse enhancement of the cauda equina was also evident, indicating microvascular permeability changes in the nerve roots. Enhancement of the cauda equina nerve roots after gadolinium administration rarely occurs with subacute spinal cord infarction, with only a few cases being documented in the literature [2–4]. Consistently with the previous reports, this was a delayed finding that was not evident until several days after the onset of symptoms in our patient. The underlying pathophysiologic mechanisms have not been clarified. It has been hypothesized that neural transynaptic degeneration after ischemic injury may lead to the damage of the hematonervous barrier, whereas recruiting of collaterals may be responsible for delayed hyperemia [2–4]. Other conditions to be considered in the differential Figure. Day 1: Sagittal T2-W image shows subtle hyperintensity of the conus medullaris (arrow). Day 3: Swelling (arrowheads in A), gray matter T2hyperintensity (arrowheads in B), and water diffusivity restriction on diffusion-weighted images and corresponding apparent diffusion coefficient maps (arrowheads in C and D) of the distal spinal cord become apparent, indicating subacute ischemic infarction. Day 14: Sagittal (upper panel) and axial (lower panel) gadolinium-enhanced T1-W images with fat saturation reveal hematomyelic barrier breakdown (arrowheads), a coexistent infarction of Th12 vertebral body (empty arrows), and diffuse enhancement of the nerve roots of the cauda equina (thin arrows). http://dx.doi.org/10.1016/j.spinee.2014.08.003 1529-9430/Ó 2014 Elsevier Inc. All rights reserved. 3066 E. Pravata et al. / The Spine Journal 14 (2014) 3065–3066 diagnosis of cauda equina enhancement include GuillainBarre syndrome, infectious meningitis, leptomeningeal carcinomatosis, lymphoma, sarcoidosis, chronic inflammatory demyelinating polyneuropathy, and venous congestion from lumbosacral compression because of disc herniation and/or degenerative osteophytes [5]. References [1] Kastenbauer S, Br€ uning R, Pfister HW. Gadolinium enhancement of the cauda equina following ischemia of the lumbar cord. Nervenarzt 2005;76:479–81. [2] Amano Y, Machida T, Kumazaki T. Spinal cord infarcts with contrast enhancement of the cauda equina: two cases. Neuroradiology 1998;40:669–72. [3] Kawaguchi C, Niwa K, Hamano H, Haida M, Shinohara Y. Longterm gadolinium-enhancement of cauda equina on MRI in a case of spinal cord infarction after epidural anesthesia. Rinsho Shinkeigaku 1998;38:440–5. [4] Faig J, Busse O, Salbeck R. Vertebral body infarction as a confirmatory sign of spinal cord ischemic stroke report of three cases and review of the literature. Stroke 1998;29:239–43. [5] Marjelund S, Jaaskelainen S, Tikkakoski T, Tuisku S, Vapalahti O. Gadolinium enhancement of cauda equina: a new MR imaging finding in the radiculitic form of tick-borne encephalitis. AJNR Am J Neuroradiol 2006;27:995–7. Emanuele Pravata, MDa Carlo Cereda, MDb Alejandro Gabutti, MDa Daniela Distefano, MDa Alessandro Cianfoni, MDa a Department of Neuroradiology Neurocenter of Southern Switzerland via Tesserete 46, Lugano 6900, Switzerland b Department of Neurology Neurocenter of Southern Switzerland via Tesserete 46, Lugano 6900, Switzerland FDA device/drug status: Not applicable. Author disclosures: EP: Nothing to disclose. CC: Nothing to disclose. AG: Nothing to disclose. DD: Nothing to disclose. AC: Nothing to disclose.
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