Biopsy samples from the erector spinae of persons with nonspecific chronic low back pain display a decrease in glycolytic muscle fibers

Agten, Anouk; Stevens, Sjoerd; Verbrugghe, Jonas; Timmermans, Annick; Vandenabeele, Frank

doi:10.1016/j.spinee.2019.09.023

Cited by 26 publications

(50 citation statements)

References 46 publications

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“… 32 In contrast, results have also shown a greater proportion of type I relative to type IIa and IIx fibers in multifidus biopsies from male patients (but not female patients) undergoing surgery for IVD degeneration (compared to cadaver controls), 102 as well as when comparing the affected vs nonaffected side multifidus in IVD herniation patients. 98 Further, Agten et al, 101 using anthropometrically matched subjects, found that the erector spinae in patients with nonspecific CLBP had a greater proportion of type I (slow oxidative) and a lower proportion of type IIx (fast twitch glycolytic) fibers when compared to healthy controls; no significant difference was found in their multifidus samples. However, not all studies have found differences in fiber type characteristics in either LBP patients compared to healthy subjects 106 or IVD herniation patients compared to cadavers.…”

Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

“…However, others 36,102 have shown that the muscle fibers from IVD herniation patients had larger multifidus fiber CSAs (ie, hypertrophy) compared to controls (young individuals who died suddenly with no signs of neuromuscular disorder) 102 and literature norms for healthy multifidus fibers, 36 suggesting muscle fiber atrophy may not be the primary factor accounting for muscle loss and degeneration in LBPD patients. Further, a recent article by Agten et al 101 suggests there are no differences in multifidus and erector spinae muscle fiber CSAs in patients with nonspecific CLBP compared to healthy aged‐matched controls. Likewise, Ford et al 100 demonstrated that patients undergoing surgery for an acute IVD postero‐lateral protrusion demonstrated no differences in paraspinal muscle fiber CSAs compared to the less‐affected side (note that, the definition of acute was not reported in this article).…”

Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

“…Histological investigations of paraspinal muscle atrophy in patients with LBPDs are also inconsistent, with atrophic, 17,97–99 nonatrophic, 100,101 or even hypertrophic 36,102 findings reported across various LBPD populations. The predominate spine pathology investigated using histological techniques is lumbar IVD herniation, which largely suggests that atrophy is present in paraspinal muscle fibers 17,98,99 .…”

Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

See 2 more Smart Citations

Paraspinal muscle pathophysiology associated with low back pain and spine degenerative disorders

Noonan

Brown

2021

JOR Spine

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Low back pain disorders affect more than 80% of adults in their lifetime and are the leading cause of global disability. The muscles attaching to the spine (ie, paraspinal muscles) are critical for proper spine health and play a crucial role in the functioning of the spine and whole body; however, reports of muscle dysfunction and insufficiency in chronic LBP (CLBP) patients are common. This article presents a review of the current understanding of the relationship between paraspinal muscle pathophysiology and spine‐related disorders. Human literature demonstrates a clear association between altered muscle structure/function, most notably fatty infiltration and fibrosis, and low back pain disorders; other associations, including muscle cell atrophy and fiber type changes, are less clear. Animal literature then provides some mechanistic insight into the complex relationships, including initiating factors and time courses, between the spine and spine muscles under pathological conditions. It is apparent that spine pathology can directly lead to changes in the paraspinal muscle structure, function, and biology. It also appears that changes to the muscle structure and function can directly lead to changes in the spine (eg, deformity); however, this relationship is less well studied. Future work must focus on providing insight into possible mechanisms that regulate spine and paraspinal muscle health, as well as probing how muscle degeneration/dysfunction might be an initiating factor in the progression of spine pathology.

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Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

Section: Muscle Pathology In Lbpdsmentioning

confidence: 99%

See 1 more Smart Citation

Paraspinal muscle pathophysiology associated with low back pain and spine degenerative disorders

Noonan

Brown

2021

JOR Spine

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“… 58 , 59 Interestingly, there are also reports of the non-specific chronic low back pain (NSCLBP) patients, harboring paraspinal muscles with a larger number of type I fibers and lower number of type IIx glycolytic fibers, thereby increasing their oxidative potential. 60 This may be due to the increased mechanical load on the paraspinal muscle due to a shift in gait in NSCLBP patients.…”

Section: Peripheral Pathological Mechanism Of Clbpmentioning

confidence: 99%

Peripheral and Central Pathological Mechanisms of Chronic Low Back Pain: A Narrative Review

Li¹,

Gong²,

Liu³

et al. 2021

JPR

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Chronic low back pain (CLBP), lasting >3 months, is the end result of multiple pathogenic factors. Unfortunately, little is known about CLBP pathogenesis, which limits its advancements in clinical therapy and disease management. This paper summarizes the known pathological axes of CLBP, involving both peripheral and central systems. In particular, this paper details injurious nerve stimulation, inflammation-induced peripheral pathway, and central sensitization. Lumbar components, such as intervertebral disc (IVD), facet joints, muscles, fascia, ligaments, and joint capsules, contain pain receptors called nociceptors. Degeneration of the aforementioned lumbar components activates inflammatory pathways, which can directly damage nerves, lower nociceptor threshold to fire action potentials (AP), and cause pain. Additionally, damaged lumbar IVDs and endplates can also lead to the pathologic invasion of nerve growth and innervation, followed by the compression of herniated IVDs on nerve roots, thereby causing traumatic neuropathic pain. The central mechanism of CLBP involves alteration of the sensory processing of the brain and malfunction of the descending pain modulatory system, which facilitates pain amplification in the center nervous system (CNS). Lastly, abnormalities in the brain biochemical metabolism, activation of glial cells, and subsequent inflammation also play important roles in CLBP development. Taken together, inflammation plays an important role in both peripheral and central sensitization of CLBP. Due to the heterogeneity of CLBP, its pathological mechanism remains complex and difficult to understand. Therefore, it is a worthy field for future research into the subcomponents of CLBP pathogenesis, in order to distinguish the specific form of the disease, identify its origins, and develop corresponding highly effective comprehensive therapy against CLBP.

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“…However, very few treatments have proved effective. Among the 291 diseases studied, lower back pain in Western Europe was ranked as the highest disability burden, according to the Agten et al's study [51]. Rahmani et al's study showed that pain intensity and disability index were significantly correlated with muscle size, and the multifidus muscle size of 15-18 years old male adolescents with low back pain was lower than that of healthy people [37].…”

Section: Lumbar Degenerative Diseasementioning

confidence: 99%

Research Progress on the Mechanism of Lumbarmultifidus Injury and Degeneration

Wang

Jia

et al. 2021

Oxidative Medicine and Cellular Longevity

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This review summarizes recent research progress in the clinical features, image manifestations, and pathological mechanism of multifidus injury. After a brief introduction to the fiber classification, innervation, blood supply, and multifidus function, some factors of multifidus injury, consisting of denervation, intraoperative incision selection and traction, and lumbar degenerative disease are overviewed. In addition, the clinical index of multifidus injury including myoglobin, creatine kinase, IL-6, C-reactive protein, the cross-sectional area of multifidus, the degree of fat infiltration, and intraoperative biopsy are summarized. Furthermore, we recommend that patients with chronic low back pain should take the long-term exercise of lumbodorsal muscles. Finally, some remaining issues, including external fixation and the imaging quantitative evaluation criteria of multifidus, need to be further explored in the future.

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Biopsy samples from the erector spinae of persons with nonspecific chronic low back pain display a decrease in glycolytic muscle fibers

Cited by 26 publications

References 46 publications

Paraspinal muscle pathophysiology associated with low back pain and spine degenerative disorders

Paraspinal muscle pathophysiology associated with low back pain and spine degenerative disorders

Peripheral and Central Pathological Mechanisms of Chronic Low Back Pain: A Narrative Review

Research Progress on the Mechanism of Lumbarmultifidus Injury and Degeneration

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