Epidural spinal cord stimulation for neuropathic pain reduces blood pressure in patients with hypertension independent of pain relief: A retrospective study

Abstract

Evidence suggests that epidural spinal cord stimulation (SCS) reduces peripheral sympathetic outflow in patients treated for peripheral artery disease and neuropathic pain. However, the extent to which SCS reduces arterial blood pressure (BP) has received little attention. We tested the hypothesis that systolic BP (SBP) would be reduced in patients with hypertension (HTN) receiving surgically implanted SCS for management of neuropathic pain, and that SBP reduction would be independent of reduced neuropathic pain. Retrospective analysis of daytime SBP from patient medical records at the University of Iowa was performed from 2008 to 2018, and event‐triggered averaging was used to determine 2‐year SBP averages prior to SCS implant (pre‐SCS) and 2‐year SBP averages after SCS implant (SCS) in stage 1 HTN (n=170) and stage 2 HTN (n=141) patients. SCS SBP was significantly lower compared with pre‐SCS SBP (Pre‐SCS: 140±1 vs. SCS: 134±1 mmHg, P<0.001), and the reduction was greater in stage 2 HTN compared with stage 1 HTN (Stage 2: −11±1 vs. Stage 1: −2±1 mmHg, P<0.001), while reduction in neuropathic pain (scale 1–10) was not significantly different between groups (Stage 2: −1.4±0.3 vs. Stage 1: −1.1±0.2, P=0.37). Reduction in SBP following SCS was significantly greater in HTN patients on anti‐HTN medications compared with no anti‐HTN medications (Meds: −9±2 vs. No meds: −5±1 mmHg, P=0.036). The reduction in SBP following SCS was significantly correlated with higher Pre‐SCS SBP after controlling for sex, age, number of anti‐HTN medications, and reduction in neuropathic pain (R=−0.42, P<0.001). These findings suggest that SCS treatment for neuropathic pain in patients with HTN reduces BP independent of reductions in pain, and that the reduction in BP may be potentiated by anti‐HTN medications.Support or Funding InformationAHA (17POST33440101), T32 HL07121, NHLBI (P01HL014388), U54 TR001356 and AHA (13DG143400012)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.