Introduction and History

Radiofrequency (RF) currents have been used clinically to create predictable and quantifiable thermal lesions since the 1950s and have been used in the treatment of pain since the early 1970s.¹ During conventional RF (CRF) application for the treatment of pain, the RF currents are passed through an electrode that is placed in the vicinity of a nociceptive pathway. Consequently, the electrical energy imparted to the tissues immediately surrounding the active electrode tip creates a thermal lesion, likely interrupting the nociceptive impulses.² Because tissue temperatures above 45° C are known to be neurodestructive,³ tissue temperatures are characteristically raised to well above the neurodestructive range but below the point of gas formation—80° C to 90° C. Although selective destruction of unmyelinated C and A-δ fibers by CRF thermal lesioning has been suggested,⁴ further studies showed indiscriminate destruction of all nerve fiber types during thermal CRF lesioning.⁵ Because of the possible risk of injury to the motor nerve fibers, local neuritis, loss of sensation, and deafferentation pain, the clinical use of CRF has generally been limited to facet denervation.⁶ Observation that low temperature non–tissue-destructive CRF application had results similar to high temperature tissue-destructive CRF generated immense interest. It was theorized that electrical currents rather than temperature determined the outcomes of CRF application.⁷ During pulsed RF (PRF), an attempt is made to maximize the delivery of electrical currents to the tissues by using higher voltage RF currents, and the risk of thermal tissue injury is minimized by maintaining the tissue temperatures below the neurodestructive range. These contradictory goals are achieved by applying the RF currents in a pulsatile manner to allow the heat to dissipate in between the RF pulses.⁸

Mechanism of Effect

Sluijter et al ⁸ in their first description of PRF use described its possible mechanism of action. These authors assumed that by maintaining the electrode temperatures below the thermal destructive range that thermal tissue injury was obviated and the sustained high-density electrical fields that were generated stressed the biomolecules and caused cellular dysfunction and death. However, later investigators observed the slow response time of the temperature-measuring devices used during PRF application and concluded that the generation of brief high-temperature spikes could not be excluded, suggesting a combined role of electrical and thermal tissue injury.^9,¹⁰ In laboratory studies, evidence of neuronal activation,^11,¹² cellular stress,¹³ and damage to cellular substructure⁹ have been demonstrated after PRF application. Conversely, other experimental studies showed that the observed PRF effects are predominantly a function of the set temperature and undermined the role of electrical currents.^14,¹⁵ Among other postulated mechanisms, neuromodulation as a possible mechanism of PRF effect has also been suggested.¹⁶ The exact mechanism of the clinical effects of PRF is therefore unclear, and no evidence currently exists of nociceptive pathway interruption in response to PRF application.