Comparison of Spinal Cord Stimulation Outcomes Between Preoperative Opioid Users and Nonusers: A Cohort Study of 467 Patients

ObjectivesSpinal cord stimulation (SCS) is a surgical treatment modality reserved for a subset of patients with neuropathic pain in which conventional pharmacologic treatment has proven insufficient. Previous studies have suggested a possible negative relationship between opioid use at referral and subsequent success of SCS therapy. The aim of this cohort study was to investigate whether preoperative opioid use was associated with inferior SCS outcomes.Materials and MethodsData were obtained from the Danish Neurizon Neuromodulation Database and comprised preoperative registrations of analgesic use, postoperative Patients’ Global Impression of Change (PGIC) ratings, pre- and postoperative pain intensity scores (Numeric Rating Scale), and detailed surgical data. Patients were dichotomized according to preoperative opioid use (users vs nonusers) with subsequent assessment of the latest PGIC rating, reduction in pain intensity, and current treatment status (implanted/explanted). In addition, daily preoperative opioid dosages were quantified in oral morphine equivalents (OME) and correlated to the treatment outcomes.ResultsA total of 467 patients were included; 296 consumed opioids before SCS implantation (median 80 OME/d). Preoperative opioid use was not associated with the latest PGIC rating, reduction in pain intensity (30% or 50%), or risk of undergoing explantation (median follow-up = 3.0 years). Likewise, preoperative median OME per day of opioid users was not correlated with any of the defined outcomes.ConclusionsPreoperative opioid usage did not predict the outcome of SCS therapy in a large cohort of patients permanently implanted with an SCS system. The results do not support withholding otherwise well-indicated SCS therapy in patients with chronic neuropathic pain conditions based merely on preoperative opioid usage.     

Pain and somatosensory findings in patients 3 years after total hip arthroplasty

Background: Chronic hip pain after total hip arthroplasty (THA) is a significant problem, but the aetiology remains unclear. Aims: To determine sensory function in patients with chronic hip pain 3 years after THA. Patients without hip pain after THA served as controls. Methods: Eighteen patients with chronic hip pain and 18 controls without chronic hip pain were recruited from a previous questionnaire study about hip pain after total hip arthroplasty. All participants answered questions about pain and mental vulnerability and underwent clinical examination followed by quantitative sensory testing (brush‐evoked allodynia, pinprick hyperalgesia, mechanical and thermal thresholds). Results: Brush‐evoked allodynia was present in 4 patients with hip pain (P=0.1) and pinprick hyperalgesia (P=0.02) was more frequent in patients with chronic hip pain. Mechanical and thermal thresholds were similar in patients and controls. Patients with chronic hip pain had higher scores on the mental vulnerability scale (P<0.001). Chronic hip pain was significantly associated with low back pain (P=0.002). Conclusions: We found signs of hypersensitivity on the operated side, which was more prominent in patients with pain. Pain referred from the back or deeper structures in the hip seems to play a role for the pain in subgroups of patients. In addition, chronic hip pain was associated with mental vulnerability.     

Acute postoperative pain as a risk factor for chronic pain after surgery

Chronic postoperative pain is a major clinical problem. Several risk factors, including younger age, female gender, psychological, and genetic factors, have been identified. Surgery itself is the most important risk factor. Preoperative pain and severe acute postoperative pain are also very consistent risk factors for the development of chronic postoperative pain. Theoretically, a reduction of postoperative pain should reduce the risk of developing chronic postoperative pain. The present article will summarize the epidemiology of chronic pain after various surgical procedures. The emphasis will be on the relation between acute postoperative pain and chronic postoperative pain. Preventive measures will be discussed.     

Validation of the Nordic flow cytometry standard for CD34+ cell enumeration in blood and autografts: report from the third workshop. Nordic Stem Cell Laboratory Group

Following two workshops on standardization of enumeration of CD34+ cells in blood and leukapheresis products, the Nordic Stem Cell Laboratory Group (NSCL-G) evaluated the Milan/Mulhouse/Nordic standard in clinical practice during the third workshop (WS-III). This report documents an acceptable interlaboratory variation in the most clinically active laboratories, with a coefficient of variation (CV) below 0.19 in 7 of 8 analyses performed. The introduction of a pan-CD45 antibody in the analysis did not improve the CV. Comparison of two different CD34 class II antibodies on a total of 99 samples and procedures with and without washing on a total of 96 samples revealed a significant correlation (r2 >0.99) for all analyses. Finally, subset analysis of uncommitted and lineage-specific progenitors revealed major gating difficulties, indicating that further improvements are necessary. In an analysis of more than 600 patients undergoing mobilization and harvest of blood progenitors, with about 500 patients autografted, we found a significant correlation between blood levels of CD34+ cells and recovery of CD34+ cells from each harvest as well as between CD34+ cell number reinfused and time to neutrophil and platelet recovery. This report documents for the first time that the very simple Milan/Mulhouse method (termed The Nordic Standard) can be used by a group of laboratories to obtain important clinical information. Consequently, we consider this method as the conventional method in quality assessment of autografts, which should provide a benchmark for development of second-generation improvements.     

Pain perception is altered by a nucleotide polymorphism in SCN9A

The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele (P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation (P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype.