Skip to main content

Advertisement

We’d like to understand how you use our websites in order to improve them. Register your interest.
Download PDF

Comparison of MRI cross-sectional area and functions of core muscles among asymptomatic individuals with and without lumbar intervertebral disc degeneration

BMC Musculoskeletal Disorders volume 20, Article number: 576 (2019) Cite this article

Abstract

Background

Previous studies suggested that patients with symptomatic intervertebral disc degeneration (IDD) of lumbar spine have reduced cross-sectional area (CSA) and functions of core muscles. However, reduced CSA and functions of core muscles have been observed not only in patients with symptomatic IDD but also in patients with other subgroups of low back pain (LBP). Thus, it is uncertain whether reduced CSA and functions of core muscles lead to IDD and LBP, or pain leads to reduced CSA and functions of core muscles in patients with symptomatic IDD. Therefore, this study aimed to compare the CSA and functions of core muscles between asymptomatic participants with and without IDD in magnetic resonance imaging (MRI).

Methods

Twenty asymptomatic participants (12 men and 8 women) participated in this study. Ten participants had asymptomatic IDD at L4–5. The others were healthy controls (without IDD at all levels of lumbar spine). The CSA of core muscles was measured using MRI. Maximal isometric trunk flexor strength and side bridge strength were measured by a Smart KEMA strength sensor. Trunk flexor endurance test, side bridge endurance test and plank endurance test were used to measure core endurance. Double legs loading test was used to measure core stability. Mann-Whitney U test was used to compare the differences between two groups.

Results

There were no significant differences in core muscle functions between the two groups (p > 0.05). Moreover, there was no significant difference in CSA between the two groups (p > 0.05).

Conclusions

There was no significant difference in CSA and core muscle functions between asymptomatic participants with and without IDD. These findings indicate that a degenerative or bulging disc in asymptomatic individuals has little effect on CSA and functions of core muscles, especially in young age. Therefore, the general core endurance test or strength test could not differentiate asymptomatic people with and without IDD of lumbar spine.

Trial registration number

Clinical Research information Service. KCT0004061. Registered 13 June 2019. retrospectively registered.

Peer Review reports

Background

Intervertebral disc degeneration (IDD) of the lumbar spine is an underlying factor of low back pain (LBP) [1]. Magnetic resonance imaging (MRI) is the most widely used method for clinical assessment of IDD of the lumbar spine [2, 3]. Loss of water content, proteoglycans, and collagens that occur in IDD can be visualized on MRI under T2 weighting with a hypointense signal [2]. With the loss of proteoglycans, the osmotic pressure of the disc falls, and the disc cannot maintain hydration under load [4]. Consequently, IDD alters disc height and the mechanics of the rest of the spinal column, possibly adversely affecting the behavior of other spinal structures such as muscles and ligaments [5].

Biomechanical studies suggested that buckling failure of the lumbar spine, devoid of muscle, occurs with compressive loading of as little as 90 N [6, 7]. Thus, muscle activity is required to stiffen intervertebral joints, and muscle functions (strength and endurance) are required to meet the demands of control [6, 7]. Core muscles comprise a muscular box with the abdominals (rectus abdominis, external oblique, internal oblique, transversus abdominis) in the front, para-spinal muscles (erector spinae, multifidus, quadratus lumborum, psoas major) in the back, diaphragm as the roof, and pelvic floor musculature as the bottom around the spine [8]. Core muscles serve as a muscular corset that stabilizes the body and spine [9]. Therefore, isometric core muscle endurance tests, plank endurance test and double-leg loading test have been used to measure the core muscle functions in clinical and field setting [10,11,12,13,14]. The cross-sectional area (CSA) of core muscles has been associated with the capacity of muscles to generate force [15], as reduced CSA of the core muscles could lead to muscle force imbalance [16]. Muscle force imbalance may lead to kinetic instability of the spine, a possible reason for LBP [16].

Previous studies investigating the differences between patients with symptomatic IDD of lumbar spine and healthy controls showed that these patients have reduced CSA of paraspinal muscles [17,18,19,20,21,22], which is supported by laboratory studies [23,24,25]. Experimentally induced disc or nerve injury in animals showed rapid atrophy of paraspinal muscles [23,24,25]. However, reduced CSA of the paraspinal muscles and functions of core muscles have been observed not only in patients with symptomatic IDD but also in patients with other subgroups of LBP [16, 26, 27]. In patients with LBP, pain could be responsible for the reduced CSA and core muscle function [27], causing disuse atrophy [28] and reflexive inhibition [26]. Induced pain on paraspinal muscles after hypertonic saline injections could cause reduced muscle activity [24, 25]. Thus, it is uncertain whether reduced CSA and functions of core muscles lead to IDD and LBP, or pain leads to reduced CSA and functions of core muscles in patients with symptomatic IDD. Therefore, this study aimed to compare the CSA and functions of core muscles between asymptomatic participants with and without IDD in MRI.

Methods

Participants

Fifty asymptomatic participants (25 men and 25 women) recruited to the study. Twenty two of fifty participants had asymptomatic IDD (at the level of L3–4 in 1 participant, at L4–5 in 10 participants, at L5-S1 in 11 participants). Twenty of fifty asymptomatic participants (12 men and 8 women) participated in this study (Fig. 1). Of asymptomatic participants with IDD, only those who had asymptomatic IDD at L4–5 level were participated in this study (n = 10) due to limitation of analytical methods. The others were healthy matched controls for age, sex and weight (without IDD at all levels of lumbar spine). Participants were included if they did not have current LBP or a history of back pain in the last 12 months, previous spinal surgery or spinal fracture, neurological or orthopedic disease, or open abdominal surgery [29]. Participants were excluded if they had contraindications to MRI such as metallic implants, cardiac pacemakers, or claustrophobia [30]. Before the study, all participants received explanations about all procedures of the study and signed an informed consent form approved by the Institutional Review Board of Yonsei University Wonju Institutional Review Board (1041849–201,904-BM-053-01).

Fig. 1
figure1

Flowchart showing a schematic summary of participants recruitment and data analysis in this study

Full size image

Magnetic resonance imaging assessment

MR scans were obtained using a 1.5 T Magnetom Avanto (Siemens, Erlangen, Germany). T2 axial MR scans were obtained using repetition time (TR)/echo time (TE) = 2100 ms/91 ms, 256 × 156 matrix, field of view (FOV) 400 × 325 mm, and slice thickness 5 mm. Participants were required to hold their breath during the MR scan to prevent movement artifacts. MR scans were analyzed using the PACSPLUS Viewer (Medical Standard, Seongnam, Korea). Based on the Pfirrmann classification, the discs were then divided into two groups: without IDD at all levels of lumbar spine (Pfirrmann ≤2) and with IDD at L4–5 level (Pfirrmann ≥3) [31]. The CSA of abdominal muscles (rectus abdominis, lateral abdominal wall) and paraspinal muscles (erector spinae, multifidus, quadratus lumborum, psoas major) were measured by free-hand drawing using the PACSPLUS Viewer in both groups. The CSA of abdominal muscles and paraspinal muscles, except for the multifidus, was measured using the MR images centered on L3–4 (Fig. 2). Considering nerve innervation of the multifidus, the CSA of multifidus was measured using the MR images centered on the L4 lower vertebral endplate (Fig. 3) [32]. All data analysis was conducted by one assessor for consistency.

Fig. 2
figure2

Magnetic resonance imaging of abdominal muscles and paraspinal muscles at L3–4 level. RA = Rectus abdominis; LAW = Lateral abdominal wall; QL = Quadratus lumborum; PM = Psoas major

Full size image
Fig. 3
figure3

Magnetic resonance imaging of erector spinae and multifidus muscles at L4 vertebral endplate. ES = Erector spinae; MF = Multifidus

Full size image

Measurement of maximal isometric trunk flexor and side bridge strength

Maximal isometric trunk flexor strength and side bridge strength were measured by a Smart KEMA strength sensor (KOREATECH, Inc., Seoul, Korea) [33, 34]. Data measured using the sensor were transferred to a tablet PC (Galaxy Tab A6 10.1; Samsung, Inc., Seoul, Korea) via bluetooth network and analyzed using the Smart KEMA application (KOREATECH, Inc., Seoul, Korea). To measure maximal isometric trunk flexor strength [35], participants laid in hook lying position on a table with their feet fixed to the table with an adjustable belt to stabilize the lower limbs during trunk flexion. A belt was connected to the sensor placed on the middle of the sternum. Participants were instructed to sit up and pull the belt with maximum efforts. While participants performed trunk flexion maximally, the sensor measured the maximal isometric strength as both sides of the sensor were pulled by the belts (Fig. 4). To measure maximal isometric side bridge strength [36], the participants laid on their sides with their legs extended. A belt connected to the strength sensor was placed between the top of the iliac crest and the greater trochanter. Participants were instructed to lift their hips off the table and to rest on one elbow and their feet with maximum effort. While participants performed the side bridge task, the sensor measured the maximal isometric strength (Fig. 4). The initial tension value for measuring maximal isometric strength was set to 2 kgf in the start position to control the tension [34]. Both sides were measured and the sum value of both sides was used for data analysis. Participants were asked to maintain maximal isometric strength for 5 s to reach the maximal strength plateau [37], and the average value was calculated from the middle 3 s to eliminate the effect of insufficient muscle recruitment during first 1 s and the effect of muscle fatigue during last 1 s. The mean values of two trials were used for data analyses. There was a 30-s rest after each trial and a 5-min rest between conditions to prevent muscle fatigue.

Fig. 4
figure4

Core muscles function test

Full size image

Measurement of core muscle endurance

To test the trunk flexor endurance, the participants held a sit-up posture with their back resting against back supports angled 55° away from the table (Fig. 4) [10, 13]. Both knees and hips were flexed to 90°. The arms were folded across their chest with their hands placed on the opposite shoulders, and their feet were placed under feet straps. The participants were instructed to maintain the body position while the back supports were pulled back 10 cm to begin the test according to previous reported methods [10, 13]. Failure is determined to occur when any part of the person’s back touched the back supports, or the participant requested to stop, or if they were unable to preserve form after one verbal warning. To test the lateral musculature endurance, the side bridge endurance test was performed (Fig. 4) [10, 13]. The participants lay on their sides with the legs extended. The top foot was placed in front of the lower foot for support. Participants were instructed to maintain support on one elbow and on their feet while lifting their hips off the floor to maintain a straight line over their body length. The uninvolved arm was held across the chest with the hand placed on the opposite shoulder. The test ended when the participants lost the straight-back posture and the hip returned to the ground, the participants requested to stop, or they were unable to preserve form after one verbal warning. Both sides were measured, and the positive value of both sides was used for data analysis. For the plank endurance test (Fig. 4) [12, 38], participants lay prone with the elbows in contact with the ground, such that the humerus formed a perpendicular line with the horizontal plane, directly beneath the shoulders. The elbows were spaced shoulder-width apart in a neutral position, and the feet were set with a narrow base, but not touching. The participants were then instructed to raise their pelvis from the floor so that only the forearms and toes were in contact with the floor while maintaining their shoulders, hips, and ankles in a straight line. The test ended when the straight line was no longer be maintained, and the hips dropped toward the floor, or the participants requested to stop, or they were unable to preserve form after one verbal warning. During the endurance tests, participants were reminded to maintain the position for as long as possible. To avoid muscle fatigue, participants rested for 5 min between conditions.

Measurement of lumbopelvic control ability (modified double legs loading test)

To test the ability to control the spine, the modified double legs loading test was performed by maintaining abdominal pressure during movements of the lower limbs (Fig. 4) [14, 39]. The participants were in the supine with their hip and knee flexed to 90°. A Smart KEMA pressure sensor (KOREATECH, Inc.) was set to 40 mmHg and placed below the lordotic curvature of the spine between S1 and L1 with the hip and knee in 90° flexion. A strap with a Smart KEMA motion sensor (KOREATECH, Inc.) was placed on the lateral thigh between the greater trochanter and knee joint. Participants were instructed to maintain the 40 mmHg pressure while extending both legs. The angle of both legs lowering (hip extension) was measured with a motion sensor was defined as lumbopelvic control ability and when pressure changed more than 10 mmHg during both-legs lowering. The mean values of two trials were used for data analyses for both legs lowering. To avoid muscle fatigue, participants rested for 5 min between tests.

Statistical analyses

SPSS ver. 25.0 (SPSS, Inc., Chicago, IL, USA) was used for statistical analysis. The ICC (3, 1) model was used to test intra-rater reliability of measurements. Data normality was examined using the Shapiro-Wilk test. Medians and interquartile ranges (25th–75th percentile) were used for descriptive analyses of quantitative variables due to significance of some variables. Therefore, non-parametric tests were deemed more adequate for statistical analysis. Comparisons were performed using the Mann-Whitney U test. The level of statistical significance was set at α = 0.05. The software G*Power 3.1.9.2 was used to estimate the sample size needed for the study. A power analysis based on the mean and standard deviation from the study by Abdelraouf and Abdel-Aziem [40] demonstrated that at least 8 participants were required in each group with 80% power and alpha value of 0.05.

Results

The general characteristics of participants are listed in Table 1. There were no significant differences in age, height, or body weight between the two groups. Among 10 cases of IDD, 9 were grade 3 and 1 was grade 4. There were no significant differences in core muscle functions between the two groups (p > 0.05) (Table 2). The ICC (3, 1) for measuring trunk flexor strength was 0.967 [95% CI 0.918–0.987], for side bridge strength was 0.959 [95% CI 0.901–0.984], and for the modified double legs loading test was 0.981 [95% CI 0.952–0.992]. Moreover, there was no significant difference in CSA between the two groups (p > 0.05) (Table 3).

Table 1 Characteristics of study participants
Full size table
Table 2 Comparison of functions of core muscles between two groups
Full size table
Table 3 Comparison of cross-sectional area of core muscles between two groups
Full size table

Discussion

Patients with LBP or symptomatic IDD of lumbar spine have reduced CSA of paraspinal muscles and core muscle function compared to healthy controls [17,18,19,20,21,22]. However, in this study, we investigated the difference in CSA and core muscle functions between asymptomatic participants with and without IDD. There was no difference in CSA and core muscle function between the two groups. There are possible reasons for the lack of differences between the two groups.

In previous studies [17,18,19,20,21,22], because participants were patients with LBP or symptomatic IDD of lumbar spine, pain could be responsible for the reduced CSA and core muscle functions [27]. The effect of pain on muscle function, reducing the ability to contract, was demonstrated experimentally using a model of induced pain [25, 41]. Similarly, patients with LBP reportedly have a reduction in the ability to voluntarily contract the multifidus muscle [27]. In addition to muscle inhibition caused by pain, disuse and deconditioning due to pain could induce disuse muscle atrophy [42]. Because the CSA of muscles has been associated with the muscle’s capacity to generate force, reduced CSA of core muscles could decrease the function of core muscles [42]. In this study, participants were asymptomatic with and without IDD of the lumbar spine. It would be one possible reason why there was no significant difference in CSA and functions of core muscles between the groups.

The compression caused by the herniated disc on the dorsal and/or the ventral nerve roots is believed to cause LBP, sciatica, muscle spasms, and restriction of trunk movement [17]. Ploumis et al. reported ipsilateral atrophy of the paraspinal muscles in patients with unilateral back pain with monosegmental degenerative disc disease [21]. The mechanism of reduced CSA of ipsilateral paraspinal muscles may not be generalized disuse atrophy or spinal reflex inhibition [43]. Experimentally induced disc or nerve injury in animals showed rapid atrophy (3 days postinjury) of the paraspinal muscles [23,24,25]. IDD and atrophy of the multifidus muscles may be positively correlated at the L3-L4 disc level in patients with symptomatic IDD [19]. Additionally, there was more severe atrophy of the multifidus muscles compared to patients with non-specific LBP in the study [19]. In this study, participants with IDD of the lumbar spine were rated from grade 1–5 using the Pfirrmann classification [44]. Nine participants were grade III, and one participant was grade IV IDD. Grade III IDD showed an intermediate gray signal intensity with a normal or slightly decreased disc height [44]. Disc bulging reportedly increases with the severity of disc degeneration [45]. In this study, considering that most participants with IDD were asymptomatic and grade III IDD, there might be little effect of nerve compression. A high prevalence (20–76%) of lumbar disc abnormalities has also been detected in asymptomatic individuals by MRI [46,47,48]. A bulging disc is also often observed in asymptomatic individuals [49]. Furthermore, the cohort studies showed that the findings on MRI were not predictive of the development or duration of LBP [50, 51]. Therefore, mere disc displacement does not appear to directly account for the pain [52]. Without pain, the effect of only IDD of the lumbar spine, not herniated, might be little on CSA and core muscle functions. This was another reason for the lack of differences between the groups.

Previous studies showed that high prevalence of IDD in young adults [47, 53,54,55]. Alyas et al. reported that 39.4% incidence of disc degeneration in 33 asymptomatic elite adolescent tennis players [54]. Elliott et al. reported a 21% incidence of disc degeneration or herniation in 24 male fast bowlers in cricket, who were bowling competitively freely, with a mean age of 13.7 years at a school and club level [53]. There was also no difference in the number of sit-up scores in 60 s between young fast bowlers with and without IDD in the study, showing 40 ± 7.5 and 34.5 ± 7 sit-ups scores, respectively [53]. These study results were consistent with those of our study. The results of our study showed that there was no difference in CSA and core muscle functions between young asymptomatic participants with and without IDD. This might be because there were no functional limitations and participation restrictions in young age [53,54,55]. Also, CSA and core muscle functions did not appear to be a causative factor of asymptomatic IDD in the lumbar spine. Therefore, clinically CSA and core muscle functions are not critical factors for evaluation or differentiation between asymptomatic individuals with and without IDD in young age. Thus, other etiological factors should be considered in young participants with asymptomatic IDD rather than CSA and core muscle function such as genetics [56], spinal alignment [31], and high mechanical stress [57].

Several limitations to the current study exist. First, the sample size is small. Thus, further study is needed to generalize the experimental results. Second, only young participants were recruited. Third, while CSA of the core muscles was measured, consistency changes in the muscle (fatty deposits or fibrous/connective tissue infiltration) were not assessed. Future research will need to investigate other morphologic and functional factors of the core muscles in symptomatic and asymptomatic participants with IDD of various ages.

Conclusion

There was no significant difference in CSA and core muscle functions between asymptomatic participants with and without IDD. These findings indicate that a degenerative or bulging disc in asymptomatic individuals has little effect on CSA and functions of core muscles, especially in young participants. Therefore, the general core endurance test or strength test could not differentiate asymptomatic people with and without IDD of lumbar spine.

Availability of data and materials

The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.

Abbreviations

CSA:

Cross-sectional area

IDD:

Intervertebral disc degeneration

LBP:

Low back pain

MRI:

Magnetic resonance imaging

References

  1. 1.

    Luoma K, Riihimäki H, Luukkonen R, Raininko R, Viikari-Juntura E, Lamminen A. Low back pain in relation to lumbar disc degeneration. Spine (Phila Pa 1976). 2000;25:487–92. doi:https://doi.org/10.1097/00007632-200002150-00016.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  2. 2.

    Qian W-W, Yin G-Y, Ren Y-X, Hu Z-Y, Yu L-P. MRI assessment of lumbar intervertebral disc degeneration with lumbar degenerative disease using the Pfirrmann grading systems. PLoS One. 2012;7:e48074.

    PubMed  PubMed Central  Article  CAS  Google Scholar 

  3. 3.

    Griffith JF, Wang YXJ, Antonio GE, Choi KC, Yu A, Ahuja AT, et al. Modified Pfirrmann grading system for lumbar intervertebral disc degeneration. Spine (Phila Pa 1976). 2007;32.

    PubMed  Article  PubMed Central  Google Scholar 

  4. 4.

    Raj PP. Intervertebral disc : anatomy-physiology-pathophysiology-treatment. Pain Pract. 2008;8:18–44.

    PubMed  Article  PubMed Central  Google Scholar 

  5. 5.

    Urban JPG, Roberts S. Degeneration of the intervertebral disc. Arthritis Res Ther. 2003;5:120.

    PubMed  PubMed Central  Article  Google Scholar 

  6. 6.

    Panjabi MM. The stabilizing system of the spine. Part I. function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992;5:383.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  7. 7.

    Cholewicki J, Juluru K, McGill SM. Intra-abdominal pressure mechanism for stabilizing the lumbar spine. J Biomech. 1999;32:13–7.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  8. 8.

    Hibbs AE, Thompson KG, French D, Wrigley A, Spears I. Optimizing performance by improving Core stability and strength. Sport Med. 2008;38:995–1008.

    Article  Google Scholar 

  9. 9.

    Akuthota V, Nadler SF. Core strengthening1. Arch Phys Med Rehabil. 2004;85:86–92.

    Article  Google Scholar 

  10. 10.

    McGill SM, Childs A, Liebenson C. Endurance times for low back stabilization exercises: clinical targets for testing and training from a normal database. Arch Phys Med Rehabil. 1999;80:941–4.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  11. 11.

    Peterson DD. Proposed performance standards for the plank for inclusion consideration into the navy’s physical readiness test. Strength Cond J. 2013;35:22–6.

    Article  Google Scholar 

  12. 12.

    Tong TK, Wu S, Nie J. Sport-specific endurance plank test for evaluation of global core muscle function. Phys Ther Sport. 2014;15:58–63.

    PubMed  Article  PubMed Central  Google Scholar 

  13. 13.

    McGill S, Belore M, Crosby I, Russell C. Clinical tools to quantify torso flexion endurance: normative data from student and firefighter populations. Occup Ergon. 2010;9:55–61.

    Google Scholar 

  14. 14.

    Sahrmann S. Diagnosis and treatment of movement impairment syndromes. Elsevier Health Sciences; 2002.

    Google Scholar 

  15. 15.

    Honkanen T, Mäntysaari M, Leino T, Avela J, Kerttula L, Haapamäki V, et al. Cross-sectional area of the paraspinal muscles and its association with muscle strength among fighter pilots: a 5-year follow-up. BMC Musculoskelet Disord. 2019;20:1–8.

    Article  Google Scholar 

  16. 16.

    Wan Q, Lin C, Li X, Zeng W, Ma C. MRI assessment of paraspinal muscles in patients with acute and chronic unilateral low back pain. Br J Radiol. 2015;88:20140546.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  17. 17.

    Zhao WP, Kawaguchi Y, Matsui H, Kanamori M, Kimura T. Histochemistry and morphology of the multifidus muscle in lumbar disc herniation: Comparative study between diseased and normal sides. Spine (Phila Pa 1976). 2000;25:2191–9.

    CAS  Article  Google Scholar 

  18. 18.

    Kalichman L, Hodges P, Li L. Changes in paraspinal muscles and their association with low back pain and spinal degeneration : CT study Changes in paraspinal muscles and their association with low back pain and spinal degeneration : CT Study. 2010; July.

  19. 19.

    Sun D, Liu P, Cheng J, Ma Z, Liu J, Qin T. Correlation between intervertebral disc degeneration, paraspinal muscle atrophy, and lumbar facet joints degeneration in patients with lumbar disc herniation. BMC Musculoskelet Disord. 2017;18:1–7.

    Article  Google Scholar 

  20. 20.

    Mengiardi B, Schmid MR, Boos N, Pfirrmann CWA, Brunner F, Elfering A, et al. Fat content of lumbar paraspinal muscles in patients with chronic low back pain and in asymptomatic volunteers: quantification with MR spectroscopy. Radiol. 2006;240:786–92.

    Article  Google Scholar 

  21. 21.

    Ploumis A, Michailidis N, Christodoulou P, Kalaitzoglou I, Gouvas G, Beris A. Ipsilateral atrophy of paraspinal and psoas muscle in unilateral back pain patients with monosegmental degenerative disc disease. Br J Radiol. 2011;84:709–13.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  22. 22.

    Varga PP, Fortin M, Lazáry À, Battié MC, McCall I. Paraspinal muscle asymmetry and fat infiltration in patients with symptomatic disc herniation. Eur Spine J. 2016;25:1452–9.

    PubMed  Article  PubMed Central  Google Scholar 

  23. 23.

    Hodges P, Holm AK, Hansson T, Holm S. Rapid atrophy of the lumbar multifidus follows experimental disc or nerve root injury. Spine (Phila Pa 1976). 2006;31:2926–33.

    Article  Google Scholar 

  24. 24.

    Dickx N, Cagnie B, Achten E, Vandemaele P, Parlevliet T, Danneels L. Changes in Lumbar Muscle Activity Because of Induced Muscle Pain Evaluated by Muscle Functional Magnetic Resonance Imaging. Spine (Phila Pa 1976). 2008;33:E983–9. https://doi.org/10.1097/BRS.0b013e31818917d0.

    Article  Google Scholar 

  25. 25.

    Dickx N, Cagnie B, Parlevliet T, Lavens A, Danneels L. The effect of unilateral muscle pain on recruitment of the lumbar multifidus during automatic contraction. An experimental pain study. Man Ther. 2010;15:364–9. https://doi.org/10.1016/j.math.2010.02.002.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  26. 26.

    Beneck GJ, Kulig K. Multifidus atrophy is localized and bilateral in active persons with chronic unilateral low back pain. Arch Phys Med Rehabil. 2012;93:300–6. https://doi.org/10.1016/j.apmr.2011.09.017.

    Article  PubMed  PubMed Central  Google Scholar 

  27. 27.

    Wallwork TL, Stanton WR, Freke M, Hides JA. The effect of chronic low back pain on size and contraction of the lumbar multifidus muscle q. Man Ther. 2009;14:496–500. https://doi.org/10.1016/j.math.2008.09.006.

    Article  PubMed  PubMed Central  Google Scholar 

  28. 28.

    Parkkola R, Rytökoski U, Kormano M. Magnetic resonance imaging of the discs and trunk muscles in patients with chronic low back pain and healthy control subjects. Spine (Phila Pa 1976). 1993;18:830–6.

    CAS  Article  Google Scholar 

  29. 29.

    Valentin S, Licka T, Elliott J. Age and side-related morphometric MRI evaluation of trunk muscles in people without back pain. Man Ther. 2015;20:90–5. https://doi.org/10.1016/j.math.2014.07.007.

    Article  PubMed  PubMed Central  Google Scholar 

  30. 30.

    Dill T. Contraindications to magnetic resonance imaging. Heart. 2008;94:943–8.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  31. 31.

    Nogueira-Barbosa MH, Defino HLA, Dalto VF, Bonugli GP, da Silva Herrero CFP, Menezes-Reis R. Association Between Lumbar Spine Sagittal Alignment and L4-L5 Disc Degeneration Among Asymptomatic Young Adults. Spine (Phila Pa 1976). 2016;41:E1081–7.

    Article  Google Scholar 

  32. 32.

    Freeman MD, Woodham MA, Woodham AW. The role of the lumbar Multifidus in chronic low Back pain: a review. PM R. 2010;2:142–6. https://doi.org/10.1016/j.pmrj.2009.11.006.

    Article  PubMed  PubMed Central  Google Scholar 

  33. 33.

    Kim HA, Hwang UJ, Jung SH, Ahn SH, Kim JH, Kwon OY. Comparison of shoulder strength in males with and without myofascial trigger points in the upper trapezius. Clin Biomech. 2017;49 September:134–138. doi:https://doi.org/10.1016/j.clinbiomech.2017.09.001.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  34. 34.

    Jung S Hoon, Hwang U Jae, Kim J Hee, Gwak GT, Kwon O Yun. Effects of horizontal shoulder abduction and adduction on the activity and strength of the scapular protractors. J Electromyogr Kinesiol. 2017;37 October:155–159. doi:https://doi.org/10.1016/j.jelekin.2017.10.011.

    PubMed  Article  PubMed Central  Google Scholar 

  35. 35.

    Maeo S, Takahashi T, Takai Y, Kanehisa H. Trunk muscle activities during abdominal bracing: comparison among muscles and exercises. J Sports Sci Med. 2013;12:467–74 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772590/.

    PubMed  PubMed Central  Google Scholar 

  36. 36.

    Stickler L, Finley M, Gulgin H. Relationship between hip and core strength and frontal plane alignment during a single leg squat. Phys Ther Sport. 2015;16:66–71. doi:https://doi.org/https://doi.org/10.1016/j.ptsp.2014.05.002.

  37. 37.

    Stoll T, Huber E, Seifert B, Michel BA, Stucki G. Maximal Isometric Muscle Strength: Normative Values and Gender-Specific Relation to Age. Clin Rheumatol. 2000:19:105–13.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  38. 38.

    Schellenberg KL, Lang JM, Chan KM, Burnham RS. A clinical tool for office assessment of lumbar spine stabilization endurance: prone and supine bridge maneuvers. Am J Phys Med Rehabil. 2007;86:380–6.

    PubMed  Article  PubMed Central  Google Scholar 

  39. 39.

    Stanton R, Reaburn PR, Humphries B. The effect of short-term swiss ball training on core stability and running economy. J Strength Cond Res. 2004;18:522–8.

    PubMed  PubMed Central  Google Scholar 

  40. 40.

    Abdelraouf OR, Abdel-aziem AA. The relationship between core endurance and back dysfunction in collegiate male athletes with and without NSLBP. Int J Sports Phys Ther. 2016;11:337–44.

    PubMed  PubMed Central  Google Scholar 

  41. 41.

    Kiesel KB, Uhl T, Underwood FB, Nitz AJ. Rehabilitative ultrasound measurement of select trunk muscle activation during induced pain. Man Ther. 2008;13:132–8.

    PubMed  Article  Google Scholar 

  42. 42.

    Seelen HA, Heijden GJ, Heuts PH, Verbunt JA, Vlaeyen JW, Knottnerus JA, et al. Disuse and deconditioning in chronic low back pain: concepts and hypotheses on contributing mechanisms. Eur J Pain. 2003;7:9–21.

    PubMed  Article  PubMed Central  Google Scholar 

  43. 43.

    Danneels LA, Vanderstraeten GG, Cambier DC, Witvrouw EE, De Cuyper HJ. CT imaging of trunk muscles in chronic low back pain patients and healthy control subjects. Eur Spine J. 2000;9:266–72. https://doi.org/10.1007/s005860000190.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  44. 44.

    Pfirrmann CWA, Metzdorf A, Zanetti M, Hodler J, Boos N. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine (Phila Pa 1976). 2001;26:1873–8.

    CAS  Article  Google Scholar 

  45. 45.

    Zou J, Yang H, Miyazaki M, Morishita Y, Wei F, McGovern S, et al. Dynamic bulging of intervertebral discs in the degenerative lumbar spine. Spine (Phila Pa 1976). 2009;34:2545–50.

    Article  Google Scholar 

  46. 46.

    Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994;331:69–73.

    CAS  PubMed  Article  PubMed Central  Google Scholar 

  47. 47.

    Takatalo J, Karppinen J, Niinimäki J, Taimela S, Näyhä S, Järvelin M-R, et al. Prevalence of degenerative imaging findings in lumbar magnetic resonance imaging among young adults. Spine (Phila Pa 1976). 2009;34:1716–21.

    Article  Google Scholar 

  48. 48.

    Boos N, Semmer N, Elfering A, Schade V, Gal I, Zanetti M, et al. Natural History of Individuals With Asymptomatic Disc Abnormalities in Magnetic Resonance Imaging: Predictors of Low Back Pain–Related Medical Consultation and Work Incapacity. Spine (Phila Pa 1976). 2000;25:1484–92. https://doi.org/10.1097/00007632-200006150-00006.

    CAS  Article  Google Scholar 

  49. 49.

    Farshad-Amacker NA, Farshad M, Winklehner A, Andreisek G. MR imaging of degenerative disc disease. Eur J Radiol. 2015;84:1768–76. https://doi.org/10.1016/j.ejrad.2015.04.002.

    Article  PubMed  PubMed Central  Google Scholar 

  50. 50.

    Borenstein DG, O’Mara J, Boden SD, Lauerman WC, Jacobson A, Platenberg C, et al. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: a seven-year follow-up study. J Bone Jt Surg - Ser A. 2001;83:1306–11.

    CAS  Article  Google Scholar 

  51. 51.

    Jarvik JG, Hollingworth W, Heagerty PJ, Haynor DR, Boyko EJ, Deyo R, Jarvik JG, Hollingworth W, Heagerty PJ, Haynor DR, Boyko EJ, et al. Three-year incidence of low back pain in an initially asymptomatic cohort: clinical and imaging risk factors. Spine (Phila Pa 1976). 2005;30:1541–8 discussion 1549.

    Article  Google Scholar 

  52. 52.

    Delgado-López PD, Rodríguez-Salazar A, Martin-Alonso J, Martín-Velasco V. Lumbar disc herniation: Natural history, role of physical examination, timing of surgery, treatment options and conflicts of interests. Neurocir (English Ed). 2017;28:124–34.

    Article  Google Scholar 

  53. 53.

    Elliott BC, Davis JW, Khangure MS, Hardcastle P, Foster D. Disc degeneration and the young fast bowler in cricket. Clin Biomech. 1993;8:227–34.

    CAS  Article  Google Scholar 

  54. 54.

    Alyas F, Turner M, Connell D. MRI findings in the lumbar spines of asymptomatic, adolescent, elite tennis players. Br J Sports Med. 2007;41:836–41.

    CAS  PubMed  PubMed Central  Article  Google Scholar 

  55. 55.

    Vadalà G, Russo F, Battisti S, Stellato L, Martina F, Del Vescovo R, et al. Early intervertebral disc degeneration changes in asymptomatic weightlifters assessed by t1ρ-magnetic resonance imaging. Spine (Phila Pa 1976). 2014;39:1881.

    Article  Google Scholar 

  56. 56.

    Battié MC, Videman T, Levalahti E, Gill K, Kaprio J. Heritability of low back pain and the role of disc degeneration. Pain. 2007;131:272–80.

    PubMed  Article  PubMed Central  Google Scholar 

  57. 57.

    Stokes IAF, Iatridis JC. Mechanical conditions that accelerate intervertebral disc degeneration: Overload versus immobilization. Spine (Phila Pa 1976). 2004;29:2724–32.

    Article  Google Scholar 

Download references

Acknowledgements

We acknowledge support by “Brain Korea 21 PLUS Project (Grant NO. 2016-51-0009)” sponsored by the Korean Research Foundation for Department of Physical Therapy in Graduate School, Yonsei University within the funding programme Open Access Publishing.

Funding

This study was supported by "Brain Korea 21 PLUS Project (Grant NO. 2016-51-0009)" sponsored by the Korean Research Foundation for Department of Physical Therapy in Graduate School, Yonsei University. The funder had no role in the design of the study and in writing the manuscript.

Author information

Affiliations

  1. Department of Physical Therapy, Graduate School, Yonsei University, Wonju, Republic of Korea
    • Gyeong-tae Gwak
    • , Ui-jae Hwang
    • , Sung-hoon Jung
    • , Hyun-a Kim
    •  & Jun-hee Kim
  2. Department of Physical Therapy, College of Health Science, Laboratory of Kinetic Ergocise Based on Movement Analysis, Yonsei University, Wonju, Republic of Korea
    • Oh-yun Kwon
Authors
  1. Gyeong-tae Gwak
    View author publications
    You can also search for this author in
  2. Ui-jae Hwang
    View author publications
    You can also search for this author in
  3. Sung-hoon Jung
    View author publications
    You can also search for this author in
  4. Hyun-a Kim
    View author publications
    You can also search for this author in
  5. Jun-hee Kim
    View author publications
    You can also search for this author in
  6. Oh-yun Kwon
    View author publications
    You can also search for this author in

Contributions

GTG took part in all elements of the study and drafted the manuscript as a first author of the manuscript. UJH, SHJ, HAK and JHK contributed to study design, analysis and revision of manuscript. OYK contributed to study design, interpretation, drafting, revision and final approval and supervised the research as a corresponding author of the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Oh-yun Kwon.

Ethics declarations

Ethics approval and consent to participate

The experimental protocol was established according to the ethical guidelines of the Helsinki Declaration and was approved by the Institutional Review Board of Yonsei University Wonju Institutional Review Board. Written informed consent was obtained from all participants.

Consent for publication

The authors have received written consent from participants to publish individual data.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Gwak, G., Hwang, U., Jung, S. et al. Comparison of MRI cross-sectional area and functions of core muscles among asymptomatic individuals with and without lumbar intervertebral disc degeneration. BMC Musculoskelet Disord 20, 576 (2019). https://doi.org/10.1186/s12891-019-2960-y

Download citation

Keywords

  • Asymptomatic diseases
  • Intervertebral disc degeneration
  • MRI
  • Cross-sectional area
  • Muscle functions
  • Core muscles

BMC Musculoskeletal Disorders

ISSN: 1471-2474

Contact us