Abstract
Data on the efficacy of radiofrequency lesioning of dorsal root ganglia in the treatment of chronic spinal pain are contradictory. Following a review of the available clinical trials, we will discuss physical effects of radiofrequency and hyperthermia, pathophysiological mechanisms associated with radiofrequency and hyperthermia, mechanisms of hyperthermic cell modulation and cell killing, and a possible parallel of radiofrequency lesioning of dorsal root ganglia with lesioning of the trigeminal ganglion. Next, various hypotheses on the mode of action of radiofrequency lesioning are critically reviewed. Finally, a model is presented based on recent advances in hyperthermia, molecular biology and neurobiology, which improves our insight into the impact of heat on a dorsal root ganglion. Radiofrequency lesioning of a dorsal root ganglion is followed by: (i) direct heat damage of axons and perikarya in a small central necrotic area; (ii) ischemia in a surrounding zone by damage to vascular endothelial cells, inducing Wallerian degeneration; (iii) gene activation and expression of stress proteins in neurons and supportive cells, induced by temperatures of around 43°C in a larger outer surrounding zone.
In conclusion, since a therapeutic effect of radiofrequency lesioning of the dorsal root ganglion is more appropriately explained by moderate (42-43°C) than by high (65°C) heat, treatment of the whole dorsal root ganglion at 42-43°C may be a key to neuromodulation of certain chronic pain syndromes.