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.