Faculty Bibliography

BACKGROUND: Trigger point (TrPs) identification has become the mainstay of diagnosis for the treatment of Myofascial Pain Syndrome; however, manual pressure (MP) to identify TrPs by determining low-pressure pain threshold has low interrater reliability and may lack validity since it is done on inactive muscles. To elicit contractions and mimic an active muscle or movement that 'causes' pain, a Muscle Pain Detection Device (MPDD) has been developed. A selected muscle is stimulated and painful muscles are precisely detected, allowing distinctions between primary and referred muscle pain as well as distinguishing other functional muscle pain thought to cause MPS. METHODS: An IRB approved randomized controlled study is presented of MP (20 patients) control vs MPDD (20 patients) to identify which muscle(s) was the source of pain in subjects presenting to the NYU Pain Management Center with a minimum 3 months history of back pain. Patients were unaware of their diagnostic method. Subjects were injected in 1-3 sites identified via MP or MPDD by a separate, blinded physician. Prior to, and following treatment at one week and one month, the patients were administered Oswestry and visual analog scale pain questionnaires by a blinded evaluator, and their range of motion was measured by a blinded physical therapist. RESULTS: The MPDD group reported significantly larger improvements in pain, mood and Oswestry scores compared with the control (P < 0.05). Moreover, the MPDD group reported 82.5% pain relief at 1 month, compared with 53.2% in the control (P < 0.001). The range of motion measurements failed to reveal any significant difference between the groups. CONCLUSIONS: Using the MPDD appears to be more valid and potentially more reliable than palpation to identify muscles causing regional pain that could benefit from injections

BACKGROUND: In 2006, the authors observed a cluster of three deaths, which circumstances suggested were opioid-related, within 1 day after placement of intrathecal opioid pumps for noncancer pain. Further investigation suggested that mortality among such patients was higher than previously appreciated. The authors performed investigations to quantify that mortality and compare the results to control populations, including spinal cord stimulation and low back surgery. METHODS: After analyzing nine index cases--three sentinel cases and six identified by a prospective strategy--the authors used epidemiological methods to investigate whether mortality rates reflected patient- or therapy-related differences. Mortality rates after intrathecal opioid therapy and spinal cord stimulation were derived by correlating Medtronic device registration data with de-identified data from the Social Security Death Master File. Aggregate demographic and comorbidity data were obtained from Medicare and United Healthcare population databases to examine the influence of demographics and comorbidities on mortality. RESULTS: Device registration and Social Security analyses revealed an intrathecal opioid therapy mortality rate of 0.088% at 3 days after implantation, 0.39% at 1 month, and 3.89% at 1 yr-a higher mortality than after spinal cord stimulation implants or after lumbar diskectomy in community hospitals. Demographic, illness profile, and mortality analyses of large databases suggest, despite limitations, that excess mortality was related to intrathecal opioid therapy, and could not be fully explained by other factors. These findings were consistent with the nine index cases that revealed that respiratory arrest caused or contributed to death in all patients. No device malfunctions associated with overinfusion were identified among cases where data were available. CONCLUSIONS: Patients with noncancer pain treated with intrathecal opioid therapy experience increased mortality compared to similar patients treated by using other therapies. Respiratory depression as a consequence of intrathecal drug overdosage or mixed intrathecal and systemic drug interactions is one plausible, but hypothetical mechanism. The exact causes for patient deaths and the proportion of those deaths attributable to intrathecal opioid therapy remain to be determined. These findings, although based on incomplete information, suggest that it may be possible to reduce mortality in noncancer intrathecal opioid therapy patients

Introduction: Manual pressure (MP) to identify Trigger Points (TrPs) by determining low pressure pain threshold has low inter-rater reliability and may lack validity since it is done on inactive muscles. Muscle pain is generally experienced with activity. To elicit a muscle contraction and mimic movement that causes pain, a Muscle Pain Detection Device (MPDD) has been developed. A selected muscle is stimulated and painful muscles are precisely detected, allowing distinctions between primary and referred muscle pain [in our nomenclature, Muscle Pain Amenable to Injection vs. TrPs] as well as distinguishing other functional muscle pain thought to cause myofascial pain syndrome. MPDD could provide a valid, reliable assessment of muscle pain which is frequently ignored/mistreated. Methods: An IRB approved doubleblind, randomized controlled study of the MPDD (20 patients) vs. MP (20 patients) control to identify which muscle(s) was the source of pain in 40 subjects presenting to the NYU Pain Management Center with a minimum 3 month history of back pain. Patients were unaware of their diagnostic group. Subjects were injected in 1-3 sites identified via MP or MPDD by a separate physician blinded from the method of detection. Prior to, and following treatment at one week and one month, the patients are given a physical exam and administered Oswestry and VAS pain questionnaires by a blinded evaluator. Results: The MPDD group reported statistically significant improvement in pain, mood and Oswestry scores at 1 week and one month (P < 0.004 - 0.001). The control reported no statistical improvements except for the Oswestry scores at 1 week. Moreover, the MPDD group reported 82.5% pain relief at 1 month, compared to 53.2% in the control (P < 0.001). Conclusion: Using the MPDD appears to be more valid and reliable than palpation to identify muscles causing regional pain that could benefit from muscle injections

OBJECTIVE: The purpose of this series was to explore a 12.5:1 fixed-dose ratio of an intravenous nalbuphine and naloxone mixture (NNM) for use in patients following gynecologic surgery. DESIGN AND PATIENTS: Open-label, nonrandomized case series. The first series was a dose-ranging investigation for 12 patients following elective total abdominal hysterectomy or myomectomy. In this series, fentanyl was used for intraoperative analgesia, and patients were assigned to a lower NNM (2.5 mg/0.2 mg) or to a higher NNM (5 mg/0.4 mg) dose group. The second series evaluated the fixed dose of 5 mg nalbuphine/0.4 mg naloxone for four patients undergoing ambulatory gynecologic procedures. In the second series, no opioid agents were administered intraoperatively to eliminate the possibility of mu-opioid reversal by naloxone postoperatively. OUTCOME MEASURES: Pain control was assessed using a Verbal Pain Scale (0-10). Vital signs, side effects, and adverse events were recorded to determine drug safety. RESULTS: In the first series, there were no adverse events; however, each patient required rescue medication (either morphine or fentanyl). In the second series, two of the four patients reported a reduction in pain following drug administration and did not require any further analgesic agents in the 3-hour postoperative period. One patient had an asymptomatic lowering of heart rate after receiving the drug. CONCLUSION: Additional research of the unique combination therapy of nalbuphine and naloxone is warranted to further determine its potential clinical efficacy and safety

Immense progress in pain research in the last 40 years has led to improved diagnosis and treatment of pain patients. Since Melzak and Wall's landmark gate theory published in 1965, overwhelming evidence, from both basic science research and clinical investigation, has replaced the simplistic 'wire concept' of pain transmission with new and more subtle pathophysiologic mechanisms. One of the main findings has been that, whereas acute pain can be related to tissue injury, and pain is usually a symptom of this injury, lasting chronic pain has been shown to represent a different condition which is not related to peripheral nociceptive input but represents a disease state of its own. This disease state is created by neural plastic changes of the nervous system usually referred to as 'sensitization.' Because it is a disease involving the nervous system, it is not surprising that chronic pain may be associated with significant psychological effects leading to psychopathology.