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Atrophy of gluteus maximus among women with a history of chronic low back pain.

ABSTRACT: Although the relationship between low back pain (LBP) and the size of certain trunk muscles has been extensively studied, the relationship between gluteus maximus (GM) size and LBP has been only minimally examined. Determining whether such a relationship exists would help improve our understanding of the etiology of LBP, and possibly provide a rationale for the use of therapeutic exercise interventions targeting GM with LBP patients. The objective of this study was to compare gluteus maximus cross-sectional area in individuals with chronic LBP, and in a group of individuals without LBP. Our hypothesis was that individuals with LBP would have greater atrophy in their gluteus maximus muscles than our control group.For this case-control study, we analyzed medical history and pelvic computed tomography (CT) scans for 36 female patients with a history of chronic LBP, and 32 female patients without a history of LBP. Muscle cross-sectional area of gluteus maximus was measured from axial CT scans using OsiriX MD software, then was normalized to patient height, and used to compare the two groups. The number of back pain-related medical visits was also correlated with gluteus maximus cross-sectional area.Mean normalized cross-sectional area was significantly smaller in the LBP group than in the control group, with t = 2.439 and P<0.05. The number of back pain-related visits was found to be significantly correlated with normalized cross-sectional area, with r = -0.270 and P<0.05. The atrophy seen in the present research may reflect incidental disuse atrophy seen with LBP, which is present in many muscle groups after prolonged immobilization or with a sedentary lifestyle.This research demonstrated a previously only minimally explored relationship between gluteus maximus cross-sectional area and LBP in women. Further research is indicated in individuals with varying age, sex, and LBP diagnoses.

SUBMITTER: Amabile AH

PROVIDER: S-EPMC5513394 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Project description:We recently showed that patients with different chronic pain conditions (such as chronic low back pain, fibromyalgia, migraine and Gulf War illness) demonstrated elevated brain and/or spinal cord levels of the glial marker 18-kDa translocator protein (TSPO), which suggests that neuroinflammation might be a pervasive phenomenon observable across multiple aetiologically heterogeneous pain disorders. Interestingly, the spatial distribution of this neuroinflammatory signal appears to exhibit a degree of disease specificity (e.g. with respect to the involvement of the primary somatosensory cortex), suggesting that different pain conditions may exhibit distinct 'neuroinflammatory signatures'. To explore this hypothesis further, we tested whether neuroinflammatory signal can characterize putative aetiological subtypes of chronic low back pain patients based on clinical presentation. Specifically, we explored neuroinflammation in patients whose chronic low back pain either did or did not radiate to the leg (i.e. 'radicular' versus 'axial' back pain). Fifty-four patients with chronic low back pain, 26 with axial back pain [43.7 ± 16.6 years old (mean ± SD)] and 28 with radicular back pain (48.3 ± 13.2 years old), underwent PET/MRI with 11C-PBR28, a second-generation radioligand for TSPO. 11C-PBR28 signal was quantified using standardized uptake values ratio (validated against volume of distribution ratio; n = 23). Functional MRI data were collected simultaneously to the 11C-PBR28 data (i) to functionally localize the primary somatosensory cortex back and leg subregions; and (ii) to perform functional connectivity analyses (in order to investigate possible neurophysiological correlations of the neuroinflammatory signal). PET and functional MRI measures were compared across groups, cross-correlated with one another and with the severity of 'fibromyalgianess' (i.e. the degree of pain centralization, or 'nociplastic pain'). Furthermore, statistical mediation models were used to explore possible causal relationships between these three variables. For the primary somatosensory cortex representation of back/leg, 11C-PBR28 PET signal and functional connectivity to the thalamus were: (i) higher in radicular compared to axial back pain patients; (ii) positively correlated with each other; (iii) positively correlated with fibromyalgianess scores, across groups; and finally (iv) fibromyalgianess mediated the association between 11C-PBR28 PET signal and primary somatosensory cortex-thalamus connectivity across groups. Our findings support the existence of 'neuroinflammatory signatures' that are accompanied by neurophysiological changes and correlate with clinical presentation (in particular, with the degree of nociplastic pain) in chronic pain patients. These signatures may contribute to the subtyping of distinct pain syndromes and also provide information about interindividual variability in neuroimmune brain signals, within diagnostic groups, that could eventually serve as targets for mechanism-based precision medicine approaches.

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Atrophy of gluteus maximus among women with a history of chronic low back pain.

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