Abstract

Objective: To evaluate, within a clinical research setting, the proposed percutaneous neuromodulation therapy (PNT) mechanism of action hypothesizing that patients with centrally facilitated pain benefit more from PNT than do other patients. Design: Analysis of pooled data collected during 3 prospective clinical trials. Setting: Outpatient pain treatment centers. Participants: 119 patients enrolled in clinical trials of PNT for subacute and chronic spinal pain (lumbar or cervical) with radiating pain. Patients were clinically grouped as having probable primary: (1) nociceptive pain due to a recurrent structural source such as disk protrusion, (2) centrally facilitated pain in absence of a defined structural problem such as fibromyalgia or myofascial pain, or (3) pain from a combination of both categories (recurrent structural plus centrally facilitated). Interventions: Patients received ≥4 PNT treatments and were followed approximately 1 week after completion of the last treatment. Main Outcome Measures: Pain ratings on a 10-cm visual analog scale (VAS). Results: A multivariate analysis of variance suggested that decrease in VAS scores was dependent on pain categorization ( P=.008). Patients with centrally facilitated pain had the greatest VAS decrease and patients with recurrent structural pain had the least. Similar baseline VAS scores were noted between the groups (centrally facilitated, 5.9±1.9; recurrent structural, 6.0±1.7; recurrent structural + centrally facilitated, 6.2±1.4). Compared with recurrent structural patients, centrally facilitated patients reported lower VAS ratings ( P=.05) after their last treatment (centrally facilitated, 3.2±2.1; recurrent structural, 4.5±2.5; recurrent structural + centrally facilitated, 4.1±2.4), and marginally significant greater decrease in VAS (baseline to last treatment; P=.08). Conclusions: Patients with centrally mediated pain had the greatest drop in VAS scores. In contrast to patients with nociceptive pain due to a recurrent structural source, PNT potentially reversed the pain centralization process, resulting in activation of pain-signaling pathways only in the presence of noxious stimulation.

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