Contrast spinal enhancement

However, presynaptic NMDA autoreceptors may also mediate opposite effects, i.e., a reduction of glutamate release. At parallel fiber Purkinje cell synapses, activation of presynaptic NMDA receptors caused significant reductions in excitatory postsynaptic currents (Casado et al. 2002). Likewise, spontaneous and evoked glutamate release from the nerve endings of primary afferents in the spinal cord was reduced when presynaptic NMDA receptors were activated (Bardoni et al. 2004). In contrast to this, substance P release at such synapses was shown to be enhanced by the activation of presynaptic NMDA receptors (Liu et al. 1997). 

Fig. 17.1a,b. Contrast-enhanced spinal MR angiography, sagittal views, a First phase the segmental arteries are visible (arrowhead), note the bright enhancement of the aorta, b Second phase the accompanying veins arise (arrow)... 

Fig. 17.5. Normal anterior and posterior median spinal veins of the thoracolumbar cord. Sagittal contrast-enhanced Tl-weighted MR images (right side, subtraction image). The large anterior median vein (arrows) continues with the filum terminale...

In most cases of the thoracolumbar infarction, the swollen cord shows peripheral enhancement of the central gray matter. The concomitant enhancement of the cauda equina was reported first by Friedman and Flanders in 1992 (Fig. 17.8). This phenomenon is a characteristic finding in the course of spinal cord ischemia which might involve the cord itself and the ventral cauda equina as well, which is composed of motor fibre bundles (Amano et al. 1998). It indicates disruption of the blood-cord barrier as well as reactive hyperemia (Friedman and Flanders 1992 Amano et al. 1998). The differential diagnosis of contrast enhancement of the cauda equina includes transverse myelitis, bacterial or viral meningitis, and spinal metastasis. 

Fig. 17.13a-c. First-pass contrast-enhanced MR angiography, a Normal finding, b Thoracic SDAVF (T7 left, arrow), c Thoracolumbar spinal AVM (arrows)... 

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