Comparison of Low Back Pain Recovery and Persistence

Abstract

Background Persistent low back pain is a significant problem worldwide. Early identification and treatment of individuals at high risk for persistent low back pain have been suggested as strategies to decrease the rate of disability associated with this condition. Purpose To examine and compare demographic, pain-related, psychological, and somatosensory characteristics in a cohort of participants with acute low back pain who later went on to experience persistent low back pain or whose pain resolved within the first 6 weeks after initial onset. Methods A descriptive study was conducted among men and women 18–50 years of age who had an acute episode of low back pain. Study questionnaires were administered to collect demographic information and measures of pain, coping, reactivity, mood, work history and satisfaction, and disability. A standardized protocol of quantitative sensory testing was performed on each participant at the painful area of their low back and at a remote site on their arm. Results The sample consisted of 48 participants, of whom 19 went on to develop persistent low back pain and 29 resolved. Compared to the resolved group, the persistent low back pain group was significantly older and had a lower level of educational attainment, a higher body mass index, and higher mean “least” pain score on the Brief Pain Inventory–Short Form. Significantly higher thermal detection thresholds at the painful and remote sites as well as signs of central sensitivity differentiated the persistent pain group from the resolved group during the acute stage of low back pain.

Circulating Lipids and Acute Pain Sensitization

“…Recruitment took place at primary healthcare clinics through advertisements. More detail is available in Starkweather, Lyon, et al (2016).…”

“…In a cohort of patients with acute low back pain, a standardized QST protocol was used to measure the threshold and tolerance of noxious mechanical and thermal stimuli at the painful site of the lower back and a remote site (dominant forearm) (Starkweather, Lyon, et al, 2016). Some of the participants manifested signs of peripheral and central sensitization to mechanical and thermal stimuli as evidenced by reduced thresholds at both the painful region of the low back and the remote site.…”

“…Some of the participants manifested signs of peripheral and central sensitization to mechanical and thermal stimuli as evidenced by reduced thresholds at both the painful region of the low back and the remote site. As a putative mechanism underlying sensitization, the levels of circulating lipid-based molecules in plasma were analyzed from the first 30 participants enrolled in the case-control observational study conducted by Starkweather, Lyon et al (2016). Our hypothesis was that pain sensitized and non-sensitized individuals with acute low back pain would have significantly different levels of lipid molecules.…”

Biological determinants of health: Genes, microbes, and metabolism exemplars of nursing science

“…Starkweather and colleagues simultaneously examined differences in peripheral and central sensitivity and expression levels of pain sensitivity genes at the onset of low back pain and over time in patients with an acute episode that either resolved or became chronic (Starkweather, Lyon, et al, 2016). Participants enrolled in the study during an acute phase of low back pain and categorized as either “recovered” if their pain resolved in the first six weeks after onset or as “persistent” if their pain continued for six months.…”

“…The team’s initial goal was to identify differential expression pain genes at the onset of acute low back pain. They found that participants with acute low back pain had significantly increased expression of prepro-nociceptin ( PNOC ), the precursor of nociceptin, chemokine (C-C motif) ligand 2 ( CCL2 ), and cannabinoid type-2 (CB2) receptor ( CNR2 ) compared to the healthy no-pain control group (Starkweather, Ramesh, et al, 2016). In addition, dysregulated expression of multiple genes involved in pain processing were identified at the onset of acute low back pain, including GCH1, CSF1, TRPV1, CALCA, PTGES, GDNF , and KCNQ2 .…”