Efficacy of Pulsed Radiofrequency to Cervical Nerve Root for Postherpetic Neuralgia in Upper Extremity

A study is carried out of the spatial distribution and time dependence of electric and thermal fields in the tissue around a radiofrequency (RF) electrode used in pain therapy. Finite-element calculation of the fields is performed, and results are compared with ex vivo tissue data. Field predictions are made for continuous and for pulsed RF applications. A special RF cannula electrode is constructed with both macro and micro thermocouple sensors to measure both average and rapid, transitory temperature effects. Temperatures and impedances are recorded in liver and egg-white models using signal outputs from a commercially available RF lesion generator. These data are compared with the results of finite-element calculations using electric field equations and the bio-heat equation. Average and pulsatory temperatures at the RF electrode are measured. Rapid temperature spikes during pulsed RF bursts are observed. These data compared well with theoretical calculations using known electrical and thermal tissue parameters. Continuous RF lesioning causes heat destruction of neurons. Pulsed RF lesioning (PRFL) produces heat bursts with temperatures in the range associated with destructive heat lesions. PRFL also produces very high electric fields that may be capable of disrupting neuronal membranes and function. Finite-element calculations agree substantially with the measured data, giving confidence to their predictions of fields around the RF electrode.

Pulsed radiofrequency (PRF) fields applied by an electrode to neural structures, such as the peripheral sensory nociceptor axons and dorsal root ganglion, are clinically effective in reducing pain and other neuropathic syndromes. However, a full understanding of the underlying mechanisms by which this occurs has not yet been clarified. In this study, PRF is applied to the afferent axons of the sciatic nerves of rats. A standard radiofrequency (RF) electrode and RF generator is used to apply the RF signal output to the sciatic nerve using standard PRF parameters that have been successfully used in clinical practice. The ultrastructure of the treated axons is observed after 10 days by electron microscopy. A control, sham application is simultaneously applied to the contralateral sciatic nerve to provide a statistical differential comparison. It is found that the internal ultrastructural components of the axons show microscopic damage after PRF exposure, including: abnormal membranes and morphology of mitochondria, and disruption and disorganization of microfilaments and microtubules. The damage appears to be more pronounced for C-fibers than for A-delta and A-beta fibers. The results are discussed in terms of internal electric field strengths and thermodynamic parameters.

Application of pulsed radiofrequency (RF) currents to the dorsal ganglion has been reported to produce long-term relief of spinal pain without causing thermal ablation. The present study was undertaken to identify spinal cord neurons activated by exposure of the dorsal ganglion to pulsed RF currents in rats. Left-sided hemilaminectomy was performed in adult Sprague-Dawley rats to expose the C6 dorsal root ganglion. An RF electrode (0.5 mm diameter) with a thermocouple for temperature monitoring was positioned on the exposed ganglion, and rats were assigned to one of three treatment groups: pulsed RF treatment (20 ms of 500-kHz RF pulses delivered at a rate of 2 Hz for 120 s to produce tissue heated to 38 degrees C), continuous RF (continuous RF currents for 120 s to produce tissue heated to 38 degrees C), or sham treatment (no RF current; electrode maintained in contact with ganglion for 120 s). Treatment with pulsed RF but not continuous RF was associated with a significant increase in the number of cFOS-immunoreactive neurons in the superficial laminae of the dorsal horn as observed 3 hours after treatment. Exposure of the dorsal ganglion to pulsed RF currents activates pain-processing neurons in the dorsal horn. This effect is not mediated by tissue heating.