Treatment of Chronic Axial Back Pain with 60‐day Percutaneous Medial Branch PNS: Primary Endpoint Results from a Prospective, Multicenter Study

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

<div class="section"> <a class="named-anchor" id="papr13055-sec-0100">  </a> <h5 class="section-title" id="d5442832e527">Background</h5> <p id="d5442832e529">The objective of this prospective, multicenter study is to characterize responses to percutaneous medial branch peripheral nerve stimulation (PNS) to determine if results from earlier, smaller single‐center studies and reports were generalizable when performed at a larger number and wider variety of centers in patients recalcitrant to nonsurgical treatments. </p> </div><div class="section"> <a class="named-anchor" id="papr13055-sec-0101">  </a> <h5 class="section-title" id="d5442832e532">Materials & Methods</h5> <p id="d5442832e534">Participants with chronic axial low back pain (LBP) were implanted with percutaneous PNS leads targeting the lumbar medial branch nerves for up to 60 days, after which the leads were removed. Participants were followed long‐term for 12 months after the 2‐month PNS treatment. Data collection is complete for visits through end of treatment with PNS (primary end point) and 6 months after lead removal (8 months after start of treatment), with some participant follow‐up visits thereafter in progress. </p> </div><div class="section"> <a class="named-anchor" id="papr13055-sec-0102">  </a> <h5 class="section-title" id="d5442832e537">Results</h5> <p id="d5442832e539">Clinically and statistically significant reductions in pain intensity, disability, and pain interference were reported by a majority of participants. Seventy‐three percent of participants were successes for the primary end point, reporting clinically significant (≥30%) reductions in back pain intensity after the 2‐month percutaneous PNS treatment ( <i>n</i> = 54/74). Whereas prospective follow‐up is ongoing, among those who had already completed the long‐term follow‐up visits ( <i>n</i> = 51), reductions in pain intensity, disability, and pain interference were sustained in a majority of participants through 14 months after the start of treatment. </p> </div><div class="section"> <a class="named-anchor" id="papr13055-sec-0103">  </a> <h5 class="section-title" id="d5442832e548">Conclusion</h5> <p id="d5442832e550">Given the minimally invasive, nondestructive nature of percutaneous PNS and the significant benefits experienced by participants who were recalcitrant to nonsurgical treatments, percutaneous PNS may provide a promising first‐line neurostimulation treatment option for patients with chronic axial back pain. </p> </div>

Related collections

Most cited references 63

Record: found
Abstract: found
Article: not found

Non-specific low back pain.

Rachelle Buchbinder, Martin Underwood, Chris Maher (2017)

Non-specific low back pain affects people of all ages and is a leading contributor to disease burden worldwide. Management guidelines endorse triage to identify the rare cases of low back pain that are caused by medically serious pathology, and so require diagnostic work-up or specialist referral, or both. Because non-specific low back pain does not have a known pathoanatomical cause, treatment focuses on reducing pain and its consequences. Management consists of education and reassurance, analgesic medicines, non-pharmacological therapies, and timely review. The clinical course of low back pain is often favourable, thus many patients require little if any formal medical care. Two treatment strategies are currently used, a stepped approach beginning with more simple care that is progressed if the patient does not respond, and the use of simple risk prediction methods to individualise the amount and type of care provided. The overuse of imaging, opioids, and surgery remains a widespread problem.

0 comments Cited 770 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Central sensitization: a generator of pain hypersensitivity by central neural plasticity.

Alban Latremoliere, Clifford Woolf (2009)

Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.

0 comments Cited 526 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function.

David Seminowicz, Timothy Wideman, Lina Naso … (2011)

Chronic pain is associated with reduced brain gray matter and impaired cognitive ability. In this longitudinal study, we assessed whether neuroanatomical and functional abnormalities were reversible and dependent on treatment outcomes. We acquired MRI scans from chronic low back pain (CLBP) patients before (n = 18) and 6 months after (spine surgery or facet joint injections; n = 14) treatment. In addition, we scanned 16 healthy controls, 10 of which returned 6 months after the first visit. We performed cortical thickness analysis on structural MRI scans, and subjects performed a cognitive task during the functional MRI. We compared patients and controls, as well as patients before versus after treatment. After treatment, patients had increased cortical thickness in the left dorsolateral prefrontal cortex (DLPFC), which was thinner before treatment compared with controls. Increased DLPFC thickness correlated with the reduction of both pain and physical disability. Additionally, increased thickness in primary motor cortex was associated specifically with reduced physical disability, and right anterior insula was associated specifically with reduced pain. Left DLPFC activity during an attention-demanding cognitive task was abnormal before treatment, but normalized following treatment. These data indicate that functional and structural brain abnormalities-specifically in the left DLPFC-are reversible, suggesting that treating chronic pain can restore normal brain function in humans.