Figure 1.

Illustrated mechanism of central neuropathic pain associated with spinal cord injury (SCI). These mechanisms include transient receptor potential vanilloid type 1 (TRPV1) overexpression in dorsal root ganglion (DRG) neurons, glial cell activation, dendritic spine remodeling, glutamate receptor activation and loss of GABAergic interneuron in the spinal dorsal horn, and spontaneous firing of neurons in the thalamus and primary somatosensory cortex. It has been suggested that the antinociceptive mechanism of botulinum toxins (BTXs) applied to the nerve endings not only affects the primary afferent neurons but also acts on the DRG and spinal dorsal horn through retrograde axonal transport.