A case of posterior spinal cord syndrome in which magnetic resonance images showed predominant T2 hyperintense signal in the adjacent vertebral body is reported.
To present the case for abnormal bone marrow magnetic resonance signal in the radiologic diagnosis of posterior spinal cord syndrome and to review its significance.
Infarction in the region of posterior spinal arteries has been rarely described. This is attributable not only to the infrequent occurrence of infarction of posterior spinal arteries, but also to a lack of well-established diagnostic procedures. It is of clinical value to define diagnostic images of posterior spinal cord syndrome, especially early in the course of the disease.
The subject was a 52-year-old man who was presented with acute nontraumatic myelopathy. Magnetic resonance imaging, performed serially after onset of the disorder from 5 hours to 11 months, was evaluated in comparison with neurologic findings. The literature was reviewed to discuss the magnetic resonance images of spinal cord infarction.
The neurologic findings were consistent with posterior spinal cord syndrome. A magnetic resonance image taken at 5 hours after onset of the syndrome showed T2 hyperintense signal in the T12 vertebral body. At 3 days after onset, T2 hyperintense signal became obvious in the posterior portion of the spinal cord at T9–T12 vertebral levels. Follow-up magnetic resonance imaging at 41 days, 8 months, and 11 months showed a decrease in the size and intensity of the T2 signal change in the spinal cord and T12 vertebral body. In the literature, T2 hyperintense bone marrow signal was defined in one case of posterior spinal cord syndrome and seven cases of anterior spinal cord syndrome.
Associated bone marrow abnormalities likely reflect the underlying pathology of the blood supply to the vertebral body, and may be an additional key sign for radiologic diagnosis of posterior spinal cord syndrome.
From the *Department of Orthopaedic Surgery and the
†Division of Rehabilitation, Sapporo Medical University School of Medicine, and the
‡Department of Orthopaedic Surgery, Takikawa Municipal Hospital, Japan.
Acknowledgment date: December 5, 2002.
First revision date: January 9, 2003.
Second revision date:.
Acceptance date: January 21, 2003.
The submitted manuscript does not contain information about medical devices or drugs.
No funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this article.
Address correspondence and reprint requests to Satoshi Kawaguchi, MD, Department of Orthopaedic Surgery, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo 060-8543, Japan; E-mail: email@example.com