Gadolinium-enhanced MR imaging of infarction of the anterior spinal cord.

A 42-year-old previously healthy man experienced paresthesias in both hands 5 min after he had flexed his neck extremely far when trying to creep under a barbed wire. Three hours later he was unable to turn a key with his right hand. Twelve hours later he could not sit up in his bed. At admission, neurologic examination showed a complete flaccid paralysis in the C7-T1 myotomes on both sides. Moderate paresis of the upper motor neuron type was present in the left leg. Pain and temperature sensations were lost in the C4-T8 dermatomes; proprioceptive sensation was spared. Plain radiographs of the cervical spine, CT scans of the cervical spinal cord, and duplex sonograms of the vertebrraland carotid arteries were normal. An MR study of the spine was performed within 24 hr of the injury. T2weighted, 2000/22, 90/2 (TRITE/excitations), and T1-weighted spinecho images, 500/20/3, obtained before and after IV administration of Gd-DOT A were normal. During the following days, motor loss in the arms and legs gradually disappeared. The dissociated sensory loss persisted in the C4-T8 dermatomes. Sagittal T1-weighted images obtained 1 week after the injury were normal, but a highintensity lesion was seen anteriorly in the cervical cord at the C5 level on the sagittal T2-weighted images (Fig. 1 A). The presence of pulsation artifacts made it difficult to evaluate the caudal extension of the lesion on these images. However, postcontrast images showed enhancement anteriorly in the cervical cord at levels C4 to C7 (Fig. 1 B). The diagnosis of anterior spinal artery syndrome was confirmed, and the MR-based diagnosis of ischemia or infarction was made. A cervicothoracic spinal angiogram excluded an arteriovenous fistula. MR images obtained 3 months later showed cystic lesions anteriorly in the cervical cord from C5 down to C7 (Fig. 1 C). Mild paresis of both hands and loss of the sensations of pain and temperature in the C6-T8 dermatomes persisted.