Hindlimb pain models developed in rats have been transposed to mice, but assumed sciatic nerve neuroanatomic similarities have not been examined. We compared sciatic nerve structural organization in mouse strains (C57BL/6J, DBA/2J, and B6129PF2/J) and rat strains (Wistar, Brown Norway, and Sprague-Dawley). Dissection and retrograde labeling showed mouse sciatic nerve origins predominantly from the third lumbar (L3) and L4 spinal nerves, unlike the L4 and L5 in rats. Proportionate contributions by each level differed significantly between strains in both mice and rats. Whereas all rats had six lumbar vertebrae, variable patterns in mice included mostly five vertebrae in DBA/2J, mostly six vertebrae in C57BL/6J, and a mix in B6129PF2/J. Mice with a short lumbar vertebral column showed a rostral shift in relative contributions to the sciatic nerve by L3 and L4. Ligation of the mouse L4 nerve created hyperalgesia similar to that in rats after L5 ligation, and motor changes were similar after mouse L4 and rat L5 ligation (foot cupping) and after mouse L3 and rat L4 ligation (flexion weakness). Thus, mouse L3 and L4 neural segments are anatomically and functionally homologous with rat L4 and L5 segments. Neuronal changes after distal injury or inflammation should be sought in the mouse L3 and L4 ganglia, and the spinal nerve ligation model in mice should involve ligation of the L4 nerve while L3 remains intact. Strain-dependent variability in segmental contributions to the sciatic nerve may account in part for genetic differences in pain behavior after spinal nerve ligation.

The clinical benefit and increased application of opioid rotation has focused attention on efficacy differences between opioids and their respective equianalgesic dose ratios. Understanding the differences between the opioids is critical to understanding their equianalgesic dose ratios and for adjusting therapy following rotation to a new analgesic. The purpose of this article is to describe controversies regarding the relative potencies of these agents as presented in current equianalgesic charts and to provide pharmacologic information to assist the clinician with opioid rotation.

On the basis of the published material reviewed above, we conclude that there are many limitations that weaken the theoretic basis for neural blockade as a diagnostic or prognostic tool. In addition, these procedures in general lack thorough documentation of clinical usefulness. Reasonable employment of diagnostic neural blockade, therefore, requires not only care in technique and confirmation of effects, but also caution in interpretation and application of the results. This critical evaluation needs to be tempered, however, by two further observations. Experienced and observant clinicians have found these procedures may, on certain occasions, provide information that is helpful in guiding subsequent therapy, so we should not be in haste to dismiss the accumulated judgment of practitioners. Finally, the confusion and complexity that typifies diagnosis in chronic pain may justify the selective use of diagnostic blocks that make anatomic and physiologic sense, even if their validity is incompletely proved.

In both intact and nerve-injured animals, fluorescein accumulates freely in the DRG after intravenous, epidural, or paravertebral injection. The sciatic nerve is relatively impermeable to fluorescein, but access by either systemic or regional injection is enhanced after nerve injury.

Painful SNL nerve injury depresses resting [Ca]c in sensory neurons. This is most marked in axotomized neurons, especially the large and capsaicin-insensitive neurons presumed to transmit non-nociceptive sensory information.