Chrisan van der Merwe Physiotherapist

Chrisan van der Merwe Physiotherapist I specialize in orthopaedic problems and sport injuries, but also treat alot of respiratory and surgical patients.

"Guidelines for Safe Shockwave Therapy”
09/09/2025

"Guidelines for Safe Shockwave Therapy”

📱 Hoekom voel jou nek so seer na lang ure op jou foon?Jou kop weeg gemiddeld sowat 5 kg in ’n regop posisie. Maar hoe ve...
09/09/2025

📱 Hoekom voel jou nek so seer na lang ure op jou foon?
Jou kop weeg gemiddeld sowat 5 kg in ’n regop posisie. Maar hoe verder jy vorentoe buig, hoe swaarder word die las op jou nek:

• 15° = 12 kg
• 30° = 18 kg
• 45° = 22 kg
• 60° = 27 kg

Dit beteken ure se foon- of skermtyd kan jou nekspiere en ruggraat onnodig belas en pyn veroorsaak.

✅ Hou jou toestel op ooghoogte.
✅ Sit regop en neem gereeld breuke.

Klein aanpassings kan groot verskil maak vir jou postuur en welstand.

💥 Say goodbye to stubborn pain! 💥I’m thrilled to announce that I now offer Shockwave Therapy 🙌
05/09/2025

💥 Say goodbye to stubborn pain! 💥
I’m thrilled to announce that I now offer Shockwave Therapy 🙌

01/09/2025
26/08/2025
26/08/2025
06/08/2025

Send a message to learn more

17/07/2025
14/07/2025

📢 Just published

Individuals with Chronic Low Back Pain Have Reduced Myofascial Force Transmission Between Latissimus Dorsi and Contralateral Gluteus Maximus Muscles

🔃 The human body's myofascial system consists of connective tissues that enable mechanical force transmission not only within but also between muscles across joints and anatomical regions. Anatomical studies and cadaveric dissections have indicated potential myofascial continuity between the latissimus dorsi (LD) and contralateral gluteus maximus (GM) muscles via the thoracolumbar fascia (TLF), forming part of the so-called posterior oblique sling system [11,12].

📘 Previous research suggested this interconnected system may facilitate force transmission across the trunk and pelvis and contribute to load transfer during gait and dynamic movement [1,7]. However, whether these transmission pathways are functionally relevant in vivo—particularly in pathological populations—remained unclear. Chronic low back pain (CLBP), which affects approximately 23% of the global population at some point in life [2], has been associated with impaired neuromuscular control and myofascial alterations [3,4,8]. Therefore, a brand-new study by Procópio and colleagues investigated whether myofascial force transmission between the LD and contralateral GM differs between individuals with CLBP and healthy controls (https://pubmed.ncbi.nlm.nih.gov/40616971/).

🧪 Methods

A total of 40 participants were included: 20 with clinically diagnosed chronic low back pain (CLBP group) and 20 age- and sex-matched healthy controls. Using ultrasound-based shear wave elastography (SWE), the researchers assessed passive tissue stiffness in the contralateral GM muscle during an isometric contraction of the LD muscle.

Each subject lay prone while performing submaximal shoulder extension (activating the LD), and SWE was used to detect changes in the stiffness of the contralateral GM muscle, representing a proxy for myofascial force transmission (s. figure in comments). The primary outcome was the percent change in stiffness of the contralateral GM during LD contraction, compared between groups.

📊 Results

▶️ In healthy controls, contraction of the LD muscle led to a significant increase in stiffness of the contralateral GM (mean increase: 12.7%, p < 0.001), indicating effective force transmission through the thoracolumbar fascial chain.

▶️ In contrast, CLBP patients showed no significant change in contralateral GM stiffness (mean increase: 1.5%, p = 0.421).

▶️ The between-group comparison revealed a statistically significant reduction in stiffness increase in the CLBP group compared to controls (p < 0.001).

💬 Discussion

The results support the functional existence of a myofascial connection between the LD and contralateral GM via the TLF in healthy individuals, consistent with prior anatomical and modeling studies [5,11]. The observed impairment in the CLBP group aligns with research showing altered neuromuscular coordination, reduced fascial mobility, and increased connective tissue stiffness in individuals with chronic back pain [3,4,8].

These findings suggest that CLBP may disrupt long-range myofascial force chains, which could have implications for trunk and pelvic force transfer and locomotion efficiency. Such dysfunction may contribute to persistent motor control deficits and compensatory strategies commonly reported in CLBP populations [7,9,10].

Importantly, this study provides the first in vivo functional evidence—using shear wave elastography—of altered intermuscular force transmission in a chronic pain population. It strengthens the notion that the thoracolumbar fascia acts not just as a passive structure but as an active participant in force modulation and transmission across regions.

However, we do not know whether this reduced myofascial force transmission is a cause, a consequence or an epiphenomenon of CLBP. Furthermore, there is no data to show which intervention is best suited to rehabilitate this reduced force transmission.

✅ Conclusion

This study demonstrates that chronic low back pain is associated with reduced myofascial force transmission between the latissimus dorsi and contralateral gluteus maximus muscles. Thus, potential factors such as greater weakness [12], and decreased GM cross-sectional area [13] commonly observed in this population, reduced fascial gliding (3), the presence of fibrosis and adhesions in the thoracolumbar fascia, and alterations in neuromuscular control (3,4,11) may all contribute to impaired MFT in the pathway investigated.

📘 Illustration: https://pubmed.ncbi.nlm.nih.gov/30616942/

📚 Key References (as cited in the study)

1. Barker, P. J., et al. (2007). Clinical Biomechanics, 22, 939–945.

2. Balagué, F., et al. (2012). Lancet, 379(9814), 482–491.

3. Langevin, H. M., et al. (2011). Spine, 36(13), E868–E876.

4. Langevin, H. M., & Sherman, K. J. (2007). Medical Hypotheses, 68(1), 74–80.

5. Vleeming, A., et al. (1995). Spine, 20(7), 753–760.

6. Willard, F. H., et al. (2012). Journal of Bodywork and Movement Therapies, 16(1), 66–73.

7. Wilke, J., et al. (2017). Journal of Anatomy, 231(6), 947–956.

8. Hodges, P. W., & Moseley, G. L. (2003). Manual Therapy, 8(4), 200–206.

9. Van Dieën, J. H., et al. (2003). Clinical Biomechanics, 18(7), 637–655.

10. Carvalhais, V. O. C., et al. (2013). Journal of Biomechanics 46 (5): 1003–7.

11. Huijing, P. A. (2009). European Journal of Applied Physiology, 108(3), 389–404.

12. Nadler, S.F., et al. (2000). Clin. J. Sport Med. 10, 89–97.

13. Amabile, A.H., et al. (2017). PLoS One 12 (7).

09/07/2025

Front (top) and cut-away (bottom) views of the knee joint demonstrating the location of the anterior cruciate ligament.

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Welkom
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