Abstract
Despite the well-known clinical effects of spinal cord stimulation (SCS), the mechanisms of action have not yet been fully unraveled. The primary aim of this study was to measure whether electrochemical skin conductance, as a measure of peripheral sympathetic autonomic function, is altered by SCS. A second aim was to compare skin conductance levels of patients with failed back surgery syndrome (FBSS) with age- and sex-matched healthy controls. Twenty-three patients with FBSS treated with SCS participated in this study. Sudomotor function was measured with the SudoscanTM instrument on the hands and feet during SCS on and off states. Difference scores in skin conductance between patients and age- and sex-matched healthy controls were calculated. Normal sudomotor function at the painful lower limb was revealed for 61% of the patients when SCS was activated. Skin conductance levels were not altered between on and off states of SCS. Differences in scores between patients and healthy controls were significantly different from zero. This study showed that SCS does not influencing the sympathetic nervous system in patients with FBSS, as measured by skin conductance levels. Moreover, it suggested that there is no normalization of the functioning of the sympathetic nervous system, despite the effectiveness of SCS to reduce pain intensity.
Highlights
In many patients with failed back surgery syndrome (FBSS), the origin of the persisting element in the pain experience is still unknown, which makes targeted treatment difficult to deliver [1,2]
The goal of this study was to further unravel the mechanisms of action of Spinal cord stimulation (SCS) by evaluating whether SCS can influence the peripheral sympathetic nervous system; the first aim was to measure whether electrochemical skin conductance, as measured with the SudoscanTM, is altered by SCS in patients suffering from FBSS
The median duration that patients were implanted with SCS was 3 (Q1–Q3: 2–7) years
Summary
In many patients with failed back surgery syndrome (FBSS), the origin of the persisting element in the pain experience is still unknown, which makes targeted treatment difficult to deliver [1,2]. Since the late 1960s, with the introduction of the pain gate control theory [11], several complementary hypotheses based on spinal, segmental, and supraspinal elements have been proposed [12,13]. More recent research has pointed towards the involvement of glial cells [18,19], gene expression [20], and local tissue temperature increases [21]. Another hypothesis is the influence of the autonomic nervous system in chronic neuropathic pain and the possible target focus on this part of the nervous system by SCS [22]
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