Musculoskeletal Physiotherapy

MSc/PGDip/PGCert MSK physiotherapy: University of Brighton


Are Nerve Sliders and Tensioners Effective for Sciatica? (Part 2)

Seeing the Wood for the Trees

What is ‘Sciatica’?!

‘Sciatica’ is used to describe a host of back-related leg pain presentations of different causes; Bogduk (2009) argues that ‘sciatica’ is outdated, and as pain physiology has evolved so should nomenclature. It is well established (Genevay et al., 2017; Ostelo, 2020; Schmid, Fundaun and Tampin, 2020) that mislabelling of symptoms is a significant hinderance in research and may confuse clinicians, leading to mismanagement of patients. So, what is ‘sciatica’?

Categorising low back-related leg pain

Low back-related leg pain can be divided into 3 main categories (see Fig.1), with sciatica categorised by popular consensus (Bogduk, 2009; Genevay et al., 2017; Ostelo, 2020) as radicular pain, or painful radiculopathy.

These categories originate from seminal experiments where healthy subjects received pain-stimulating procedures and had their pain documented (see Fig.2 & 3 ). It is important the clinician differentiates somatic referred from radicular pain/painful radiculopathy, as in the former neural mobilisations are not indicated (Coppieters and Nee, 2015). This important factor may reduce treatment effect in research that has not excluded this population, and may have influenced literature in part 1, especially as more than one presentation can exist concurrently (Schmid, 2015). Both radicular pain & painful radiculopathies are defined as entrapment neuropathies (Schmid, Fundaun and Tampin, 2020). Below I have outlined the current relevant factors which may influence clinical management.

Entrapment Neuropathy

The aetiology of entrapment neuropathy is multifactorial and not fully understood; the key feature is focal demyelination and appears to be caused by a complex interaction of mechanical compression and/or ischemia (Schmid, 2015). This leads to various pathophysiological changes, resulting in pain, dysfunction and eventually nerve damage (See Fig. 4) (Schmid, 2015). The intricacy of entrapment neuropathies is beyond the scope of this blog (for comprehensive review see Schmid, 2015), below is outlined the influence neural mobilisations may have.


Intraneural Ischemia & Oedema

Intraneural ischemia occurs when relatively small pressure-changes alter the sensitive nerve-blood interface in the presence of extra-neural pressure, and may eventually cause intraneural oedema (Schmid, Fundaun and Tampin, 2020). Nerve sliding techniques may aid reversal of this process and improve nerve function; Schmid et al. (2012) appeared to show positive influence on intraneural oedema on imaging versus wait-and-see approach in carpal tunnel syndrome. Although the observed signal changes may have been from unwanted intraneural blood-flow there were no reported adverse effects, suggesting this was not the case. Nerve tensioning techniques may also influence sciatic intraneural oedema – Gilbert et al.’s 2014 in vitro study reported tensioners dispersed intraneural dye further longitudinally than no movement. However, this was a small study on dead tissue and so we should not assume the same would be true on living tissue, it may warrant further investigation.

Fibrosis & Demyelination

Prolonged oedema may lead to intraneural and extraneural fibrotic changes which can impair the sliding ability of nerves (Ellis et al., 2017), and in combination with prolonged mechanical pressure can cause demyelination and associated abnormal impulse generating sites (Schmid, 2015). As sliders have been shown in vivo (Coppieters, Hough and Dilley, 2009; Coppieters et al., 2015) to create up to 5 times greater excursion properties in sciatic nerve with less neural strain then tensioners, it would seem logical that clinical application to this population would be beneficial. I was unable to find any literature on expected timeframe for changes to occur, but they may present clinically as sudden/random electric shock pain (Coppieters and Nee, 2015) and reduced range of movement of a positive neurodynamic test, but as previously mentioned neurodynamic testing is only indicative of heightened neural mechanosensitivity (which itself may be caused by further physiological changes we will cover).

Neurogenic inflammation

Neurogenic inflammation appears to be pivotal in the generation and maintenance of neuropathic pain (Schmid, 2015). Continuing from ‘ischemia & oedema’, when the nerve-blood interface is compromised various inflammatory mediators are released initiating an immune cell response which causes local swelling and further sensitivity. This can spread to other injured and uninjured neurones and target tissue (Schmid, Fundaun and Tampin, 2020). In mild chronic nerve trunk compression (Schmid et al., 2013) and nerve root compromise (Otoshi et al., 2010; Albrecht et al., 2018) this series of events spreads beyond local injury to remote sites, including the dorsal root ganglion. Both Schmid et al. (2013) and Otoshi et al. (2010) were experimental studies with obvious limitations, but importantly both replicate events occurring in human population accurately meaning results may be more transferable than animal studies observing severe acute injuries. This information is relevant in the context of this blog as the remote spread of NI may explain extraterritorial symptoms which are reportedly as high as 64-70% in radicular pain (Schmid, 2015), and may further aid clinical management of sciatica.

Interestingly, sciatic tensioners reduced pain behaviour, glial cell activation and brain-secreted nerve growth factor in experimental chronic compression injury against several control groups (Giardini et al., 2017), whilst ankle mobilisations yielded very similar results for Dilley and Bove (2008) in sciatic crush injury. Schmid (2015) reminds us that these injuries are more severe than typical human entrapment neuropathies, with studies yet to observe such widespread immune response within human population. However, I feel they demonstrate perfectly how the central and peripheral nervous systems are one continuous structure, and the influence we may have on both with reasoned interventions. This remains of upmost clinical importance in the management of such complex presentations.

Heightened Neural Mechanosensitivity

Heightened neural mechanosensitivity is a painful response to mechanical stimulation of nerve fibres which can pose problems to clinicians trying to diagnose symptoms, as it can occur in the absence of nerve lesion and in combination with other low back-related leg pain presentations (Schmid, 2015). Schmid (2015) explains how neurogenic inflammation within the neural connective tissue of the epineurium may sensitise the nervi nervorum as it travels throughout the peripheral trunk, which may in turn activate nociceptive axons and cause spontaneous ectopic discharges. At this point the clinician should be reminded of Schafer et al.’s (2011) study showing heightened neural mechanosensitivity as most the responsive subgroup to neural mobilisations when applied frequently, and short of symptom provocation.


Writing these blogs has helped me to understand the underpinning pathophysiology of sciatica and made me appreciate the heterogenic limitations that investigating this population will always have.

There seems to be a reasonable body of mostly low-quality evidence to support the use of nerve sliders and tensioners in the clinical management of sciatica (and other nerve related MSK conditions), but we are yet to establish the optimal application and target group.

Despite considerable research the precise impact of any therapeutic intervention on sciatica remains unknown, and as such it may be sensible assume natural progression may ultimately be heavily influenced by other factors such as genetic predisposition, BMI & comorbidities (Schmid, 2015), not to mention psychosocial drivers (which undoubtedly affect this population but remain largely unexplored).

I now have a greater appreciation for what nerve sliders and tensioners do, and what I am targeting. Perhaps more importantly, I now appreciate that clinical reasoning should extend far beyond biomechanical properties alone.

Thank you for joining me on this journey, I hope you found it useful.


Albrecht, D.S., Ahmed, S.U., Kettner, N.W., Borra, R.J.H., Cohen-Adad, J., Deng, H., Houle, T.T., Opalacz, A., Roth, S.A., Melo, M.F.V., Chen, L., Mao, J., Hooker, J.M., Loggia, M.L. and Zhang, Y. (2018). Neuroinflammation of the spinal cord and nerve roots in chronic radicular pain patients. PAIN, 159(5), pp.968–977.

Bogduk, N (2009). On the definitions and physiology of back pain, referred pain, and radicular pain. PAIN, 147 pp. 17–19

Coppieters, M.W., Hough, A.D. and Dilley, A. (2009). Different Nerve-Gliding Exercises Induce Different Magnitudes of Median Nerve Longitudinal Excursion: An In Vivo Study Using Dynamic Ultrasound Imaging. Journal of Orthopaedic & Sports Physical Therapy, 39(3), pp.164–171.

Coppieters, M. and Nee, R. (2015). Neurodynamic Management of the Peripheral Nervous System. In: Jull, G.A., Moore, A., Falla, D., Lewis, J., McCarthy, C. and Sterling, M. eds. Grieve’s modern musculoskeletal physiotherapy. 4th ed. Edinburgh: Elsevier, pp 287-294.

Coppieters, M.W., Andersen, L.S., Johansen, R., Giskegjerde, P.K., Høivik, M., Vestre, S. and Nee, R.J. (2015a). Excursion of the Sciatic Nerve During Nerve Mobilization Exercises: An In Vivo Cross-sectional Study Using Dynamic Ultrasound Imaging. The Journal of orthopaedic and sports physical therapy, [online] 45(10), pp.731–7.

Dilley, A. and Bove, G.M. (2008). Disruption of axoplasmic transport induces mechanical sensitivity in intact rat C-fibre nociceptor axons. The Journal of Physiology, 586(2), pp.593–604.

Ellis, R., Blyth, R., Arnold, N. and Miner-Williams, W. (2017). Is there a relationship between impaired median nerve excursion and carpal tunnel syndrome? A systematic review. Journal of Hand Therapy, 30(1), pp.3–12.

Genevay, S., Courvoisier, D.S., Konstantinou, K., Kovacs, F.M., Marty, M., Rainville, J., Norberg, M., Kaux, J.-F., Cha, T.D., Katz, J.N. and Atlas, S.J. (2017). Clinical classification criteria for radicular pain caused by lumbar disc herniation: the radicular pain caused by disc herniation (RAPIDH) criteria. The Spine Journal, 17(10), pp.1464–1471.

Giardini, A.C., Santos, F.M. dos, da Silva, J.T., de Oliveira, M.E., Martins, D.O. and Chacur, M. (2017). Neural Mobilization Treatment Decreases Glial Cells and Brain-Derived Neurotrophic Factor Expression in the Central Nervous System in Rats with Neuropathic Pain Induced by CCI in Rats. Pain Research and Management, 2017, pp.1–9.

‌Gilbert, K.K., Roger James, C., Apte, G., Brown, C., Sizer, P.S., Brismée, J.-M. and Smith, M.P. (2014). Effects of simulated neural mobilization on fluid movement in cadaveric peripheral nerve sections: implications for the treatment of neuropathic pain and dysfunction. Journal of Manual & Manipulative Therapy, 23(4), pp.219–225.

Jesson, T. (2018). Tom-final.pdf. [online] Google Docs. Available at:

Ostelo, R.W. (2020). Physiotherapy management of sciatica. Journal of Physiotherapy, 66(2), pp.83–88.

‌Otoshi, K., Kikuchi, S., Konno, S. and Sekiguchi, M. (2010). The Reactions of Glial Cells and Endoneurial Macrophages in the Dorsal Root Ganglion and Their Contribution to Pain-Related Behavior After Application of Nucleus Pulposus Onto the Nerve Root in Rats. Spine, 35(1), pp.10–17.

Schäfer, A., Hall, T., Müller, G. and Briffa, K. (2010). Outcomes differ between subgroups of patients with low back and leg pain following neural manual therapy: a prospective cohort study. European Spine Journal, 20(3), pp.482–490.

Schmid, A.B., Elliott, J.M., Strudwick, M.W., Little, M. and Coppieters, M.W. (2012). Effect of splinting and exercise on intraneural edema of the median nerve in carpal tunnel syndrome–an MRI study to reveal therapeutic mechanisms. Journal of Orthopaedic Research: Official Publication of the Orthopaedic Research Society, [online] 30(8), pp.1343–1350. Available at: [Accessed 14 Oct. 2020].

Schmid, A.B., Coppieters, M.W., Ruitenberg, M.J. and McLachlan, E.M. (2013). Local and Remote Immune-Mediated Inflammation After Mild Peripheral Nerve Compression in Rats. Journal of Neuropathology & Experimental Neurology, 72(7), pp.662–680.

‌Schmid, A.B. (2015). The Peripheral Nervous System and it’s Compromise in Entrapment Neuropathies. In: Jull, G.A., Moore, A., Falla, D., Lewis, J., McCarthy, C. and Sterling, M. eds. Grieve’s modern musculoskeletal physiotherapy. 4th ed. Edinburgh: Elsevier, pp 78-92.

Schmid, A.B., Fundaun, J. and Tampin, B. (2020). Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management. PAIN Reports, 5(4), p.e829.

Ross Tippett • July 30, 2021

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  1. HealthTimes October 19, 2021 - 5:38 am Reply

    Great article source to read. Thank you for sharing this info.

    • Clair Hebron October 19, 2021 - 9:16 am Reply

      Thank you Jason

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