Vertebral body infarction revealed by diffusion-weighted magnetic resonance imaging

Abstract

Vertebral body infarction (VBI) is infrequent, but evidence of VBI by magnetic resonance imaging (MRI) may serve as an indication of spinal cord ischemic stroke [1]. Diffusion-weighted MRI (DWI) is also useful, especially for early detection of spinal cord infarction (SCI) [2–4]; however, VBI manifestations on DWI have not been reported in detail. We describe a case of SCI accompanied by VBI that was detected and monitored by DWI. A 43-year-old woman noticed she could not move both legs properly the night before hospital examination; her condition worsened over the next 4 h until she could not walk unaided. The patient’s medical history included adultonset Still’s disease, dyslipidemia, hypertension, and allergies to cats and NSAIDs. On examination, we observed hypoalgesia of bilateral T8–T10 dermatomes, loss of proprioception and vibratory sense in lower limbs, and urinary retention. Brain CT was normal and CSF analysis revealed only mild elevation of total protein (48 mg/dl). Serum showed lupus anticoagulant positivity, but other blood tests were normal, including those for antinuclear antibodies, protein C activity, protein S activity, and anti-cardiolipin antibodies. A spinal DWI acquired 12 h after symptom onset revealed a slightly hyperintense lesion in the spinal cord at T6–T8 (Fig. 1a) with low signal on an apparent diffusion coefficient (ADC) map (Fig. 1b). In addition, a T2-weighted MR image revealed a hyperintensity in the dorsocaudal T8 vertebral body (Fig. 1c), which was also hyperintense on T1-weighted MR images and probably corresponded to fat deposition. These scans showed no evidence of aortic dissection. She was tentatively diagnosed with posterior spinal artery infarction and hospitalized. Intravenous steroid (methylprednisolone 1 g/day for 5 days) and antithrombotic therapy (argatroban 60 mg daily for the first 2 days and 20 mg per day for the next 5 days) was started. Despite treatment, she complained of occasional aggravated deep sensation and was assessed by follow-up MRI, 2 (Fig. 1d–f), 5 (Fig. 1g–j), and 18 days (Fig. 1k–m) after symptom onset. On DWI, the spinal cord lesion became more prominent after 2 days, and a new hyperintense lesion was observed in the dorsal T8 vertebral body after 5 days (Fig. 1g, arrow). The vertebral lesion was also high intensity on an ADC map (Fig. 1h, arrow) and on T2 (Fig. 1i, j, arrows), while the T1-weighted MR image revealed an isointensity signal. On T2 axial images, the spinal cord hyperintensity was located in the territory of the posterior spinal arteries (Fig. 1j). The clinical and MRI findings indicating spinal cord infarction made us consider that the new vertebral lesion was caused by the same etiology. After intravenous steroid and antithrombotic therapy, she was able to walk with a cane and was transferred to a rehabilitation center. The utility of DWI for early detection of SCI has been confirmed [2–4], but VBI manifestations on DWI have not been described in detail. VBI typically appears as a hyperintensity region on T2 and as an isoor low-intensity region on T1. The lesion contour may appear as characteristic triangles or take other various shapes, and the lesion is usually located at the same level or slightly below the SCI focus [1, 5–11]. In our case, VBI appeared as a T2 high-intensity and T1 iso-intensity lesion 5 days after symptom onset and was located near the lower end of SCI. VBI also appeared as a high-intensity area on DWI and an ADC map. The lesion had a higher ADC value (0.60 9 10 mm/s) than adjacent M. Kobayashi (&) T. Kanai Department of Neurology, Asahi General Hospital, 1326 I, Asahi, Chiba 289-2511, Japan e-mail: ma-ko@pg7.so-net.ne.jp