Longitudinally extensive vasogenic edema following spinal cord infarction

Abstract

Although transient lesion expansion has been reported after spinal cord infarction, longitudinally extensive lesion expanding more than several vertebral segments is extremely rare. We report a 45‐year‐old man having spinal cord infarction with subsequent longitudinally extensive lesion expansion on magnetic resonance imaging (MRI) 10 days after the infarction. The length of T2 hyperintense lesion was four vertebral segments on initial MRI but enlarged to span 12 vertebral segments on subsequent MRI, with Lhermitte's sign, but otherwise without neurological deterioration. The expanded lesion extended beyond the anterior spinal artery region with high apparent diffusion coefficient value in the acute phase but improved within 10 days after starting cervical collar, suggesting that lesion expansion was due to vasogenic edema. This case illustrates that transient longitudinal lesion expansion accompanied by spinal cord infarction can reach lengths of up to 12 vertebral segments. Caution should be exercised while interpreting MRI findings to avoid excessive treatment or secondary damage.

Unilateral Posterior Spinal Cord Ischemia Due to a Floating Aortic Thrombus: A Case Report

“…A transient lesion expansion in MRI after SCI has been previously reported as pencil-shaped necrosis [10], with a length usually limited to several vertebral segments [11]. Actually, vasogenic edema in the spinal cord may occur from the acute phase, when a cervical cord compression due to cervical spondylosis causes secondary venous congestion [12]. Venous congestion is a known cause of longitudinally extensive spinal cord swelling, and may initially mimic a peripheral nerve disorder; however, the T2-hyperintense lesion is most often seen in the center of the spinal cord with peripheral sparing [12,13].…”

“…Actually, vasogenic edema in the spinal cord may occur from the acute phase, when a cervical cord compression due to cervical spondylosis causes secondary venous congestion [12]. Venous congestion is a known cause of longitudinally extensive spinal cord swelling, and may initially mimic a peripheral nerve disorder; however, the T2-hyperintense lesion is most often seen in the center of the spinal cord with peripheral sparing [12,13]. In our case, the marked hyperintensity in DWI was associated with decreased ADC (brightness), due to the T2-shine-through effect, which allowed us to differentiate between the cytotoxic edema due to the acute infarction and the vasogenic component of the edema, which most likely depended on the venous congestion.…”