Pulse radiofrequency has been recently described as a technique to apply a relatively high voltage near a nerve but without the usual effects of a rise in temperature or subsequent nerve injury. In this set of case reports, the effect of pulsed radiofrequency (PRF) is described in patients with neuropathic pain syndromes which have been poorly controlled with other oral and invasive treatments. Whilst anecdotal, the results have been remarkable and should encourage further research into this technique. Observations from the basic science tend to support the concept that PRF may induce some sort of long-term depression in the spinal cord.
The aims of this study were to investigate the occurrence of apoptotic cell death in the dorsal horn of the adult rat spinal cord following chronic constriction injury (CCI) to the sciatic nerve and to correlate this with behavioural responses. Six groups of six rats were used as follows: 1) CCI, 2) CCI, 3) MK801 + CCI, 4) axotomy, 5) sham, and 6) naive. Group 1 animals were behaviourally tested for thermal hyperalgesia 8 days following surgery and sacrificed and the spinal cords removed and frozen. The rest of the groups underwent the same procedure 14 days following surgery. The lumbar region of the spinal cord was cryosectioned and the incidence of apoptotic cells investigated using the TUNEL technique plus Hoechst double labelling. By 8 days post-CCI, hyperalgesia had developed in the ipsilateral paw, which was still present 14 days after the injury compared to the contralateral paw and naive and sham animals. Preemptive MK-801 prevented the onset of hyperalgesia. Significant numbers of apoptotic cells were present in the ipsilateral dorsal horn of the spinal cord 8 and 14 days following CCI compared to the contralateral side and to naive and sham animals. Preemptive treatment with MK-801 reduced the extent of apoptosis resulting from CCI to the level seen in control animals. This study demonstrates that cells undergo apoptosis as a result of CCI simultaneous with the occurrence of hyperalgesia. Furthermore, MK-801 prevents the onset of hyperalgesia and reduces the extent of apoptotic cell death, suggesting, perhaps, that apoptosis contributes to the initiation/maintenance of hyperalgesia.
We have attempted to define some of the patterns of expression of the IEG Fos in pain-related states. On one level, Fos may be used simply as marker of afferent stimulation and disease state, and in this respect Fos activation may be a useful tool after nociceptive stimulation to examine the effectiveness of different analgesic regimens. For example, certain analgesics such as opioids, alpha 2 agonists and local anaesthetics are more effective when given pre-emptively or early in the injury rather than later on. Furthermore, the persistent expression of Fos in the presence of high dose pre-emptive opioids is disturbing and yet it may explain variable success of studies attempting to show pre-emptive analgesia with opioid-based analgesic regimens. We suggest that Fos expression, as well as defining the magnitude and the duration of insult to the spinal cord seems also to signal the adaptive responses of the nervous system to nociceptive insult. Though we have focused on only one IEG, c-fos, and attempted to relate appearance to known functional changes within the spinal cord, there are in fact many more genes known to be upregulated with the same or slower kinetics (e.g. Fos B, FRA-1, FRA-2, Jun B, Jun D, NGFI-A). Increased understanding of the role of these genes is likely to lead to many novel targets in the search for normalization or restoration of spinal cord function in pain states and after nerve injury.
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