Is It the Muscle — or the Nerve?

Understanding Mechanosensitivity and Neurodynamics

Why your range of motion assessments may be missing a crucial piece of the picture

You have a client in front of you. They cannot touch their toes. Their straight leg raise is restricted. Their shoulder won't move past 90 degrees of abduction without pain radiating down the arm. You assess the muscle, find it tight, and prescribe stretching. Six weeks later, nothing has changed.

There is a good chance the limiting factor was never the muscle in the first place.

The nervous system runs continuously from the brain to the fingertips and toes — a vast, integrated network that must move, bend, glide and accommodate every position the body adopts. When it cannot do so freely, or when it has become hypersensitive to mechanical load, the result can look exactly like muscle tightness, restricted range of motion or joint stiffness. But stretching a muscle when the problem lies in the nerve's ability to move within its mechanical interface is not just ineffective — it can make things worse.

This is the domain of neurodynamics, and it is one of the most consistently overlooked dimensions of musculoskeletal assessment in everyday clinical practice.

What Is Mechanosensitivity?

Every tissue in the body has mechanosensitivity — a degree of responsiveness to mechanical forces such as pressure, stretch, tension and compression. Nerves are no exception. Under normal circumstances, neural tissue has a baseline level of mechanosensitivity that allows it to detect and respond to mechanical stimuli without generating pain or restriction.

When a nerve becomes injured, compressed, inflamed or poorly perfused, its mechanosensitivity increases. The threshold for generating a nociceptive response drops — less force is now required to provoke symptoms. As researchers in the field have described it: the more mechanosensitive the nerve, the less force is needed to elicit activity, and the more intense the response.

This heightened mechanosensitivity can arise from a number of sources: direct compression of a nerve root (such as in disc herniation), peripheral entrapment (such as in carpal tunnel syndrome), inflammatory processes in surrounding tissues, ischaemia from compromised blood supply to the nerve, or cumulative mechanical stress from repetitive movement patterns. Crucially, it can also arise without any demonstrable structural pathology at all — a fact that has important clinical implications, because it means mechanosensitivity can be present and clinically significant even when scans and neurological examination appear normal.

The Nervous System in Motion — Neurodynamics

To understand mechanosensitivity clinically, you need to understand how the nervous system moves. This is the domain of neurodynamics — a term and framework developed and refined primarily by two physiotherapists: David Butler and Michael Shacklock.

Neurodynamics, as defined by Shacklock, is the clinical application of the mechanics and physiology of the nervous system as they relate to each other and are integrated with musculoskeletal function. It describes how the nervous system responds to mechanical forces during movement — not just at the site of the nerve itself, but throughout the entire mechanical interface it travels through.

The nervous system does not simply sit passively in the body. It glides, slides, accommodates tension and compression, and changes shape with every movement the body makes. When you bend your elbow, the ulnar nerve must lengthen and slide proximally to accommodate that change. When you flex your hip with your knee extended, the sciatic nerve and its associated dural structures are placed under longitudinal tension all the way from the lumbar spine to the foot. When you flex the neck, tension is transmitted down the spinal cord and out into the peripheral nerves of the upper limb.

This continuity is one of the most important features of the nervous system from a clinical perspective. It means that a problem anywhere along the neural pathway can manifest as symptoms at a distant location — and that movements of body parts apparently unconnected to the area of complaint can reproduce or relieve those symptoms. This is the principle that underpins neurodynamic testing.

Neurodynamic Tests — What They Assess and How They Work

Neurodynamic tests are structured sequences of body movements designed to progressively load specific neural pathways. By adding and removing components of the test in a deliberate sequence, the clinician can determine whether symptoms are arising from neural tissue rather than from adjacent muscles, joints or other structures. This process is called structural differentiation.

The key principle of structural differentiation is straightforward: if a component of movement that has no direct mechanical link to the symptomatic area except through the nervous system changes the client's symptoms, then the nervous system is implicated in those symptoms.

The main neurodynamic tests used in clinical practice include:

The Straight Leg Raise (SLR) — the most widely recognised, testing primarily the sciatic nerve and the lumbosacral neural tract. With the patient supine, the leg is passively raised with the knee extended. Normal range is typically considered above 70–80 degrees of hip flexion. Structural differentiation is achieved by adding ankle dorsiflexion (which increases neural tension distally) or cervical flexion (which increases tension proximally through the spinal canal). If symptoms change with these additions, neural involvement is suggested.

The Slump Test — a more comprehensive test of the entire posterior neurological tract from the brain to the foot. The patient sits at the edge of the plinth, slumps the thoracolumbar spine into flexion, adds cervical flexion, then extends the knee and dorsiflexes the ankle. The critical structural differentiation component is cervical extension — releasing the neck should reduce symptoms if the nervous system is the source, because it reduces the longitudinal tension in the neural canal.

Upper Limb Neurodynamic Tests (ULNTs) — also known as upper limb tension tests, these assess the mechanosensitivity of the brachial plexus and its peripheral branches (median, radial and ulnar nerves) in the upper limb. Each test involves a specific sequence of shoulder, elbow, wrist and finger positions combined with contralateral cervical lateral flexion as the structural differentiation component.

The Femoral Nerve Test — assesses the femoral nerve and upper lumbar neural structures, performed in prone or side lying with hip extension and knee flexion.

What Makes a Test Positive — and Why This Matters

This is where clinical judgment becomes critical, and where many practitioners get into difficulty.

A neurodynamic test is not simply positive because it reproduces discomfort. Many entirely healthy people will feel some degree of posterior thigh pulling, forearm tingling or calf heaviness during these tests — these are normal neurodynamic responses that reflect the mechanical load being placed on neural tissue. Reporting discomfort during a straight leg raise does not, on its own, mean anything pathological.

According to David Butler, a test should be considered positive when four criteria are met: it reproduces the client's familiar symptoms; structural differentiation supports a neurogenic source (symptoms change when a remote body part is moved); there are differences left to right and compared to known normal responses; and there is supporting evidence from the history, symptom location and any relevant investigations.

Shacklock additionally distinguishes between normal neurodynamic responses and abnormal (overt) neurodynamic responses — the former being expected neural sensations that occur during testing, the latter being the reproduction of the specific symptoms that the patient is actually presenting with. This distinction is crucial. The test is not a measure of sensitivity per se — it is a measure of whether the nervous system is mechanically contributing to the patient's clinical presentation.

Where This Gets Missed: Neural Tension and Range of Motion

Here is the clinical problem that the neurodynamics literature highlights repeatedly, and that everyday practice consistently overlooks.

When a client presents with restricted range of motion — limited straight leg raise, reduced knee extension, restricted shoulder abduction or reduced cervical lateral flexion — the default assumption is almost always that the limiting structure is a shortened or tight muscle. Treatment follows accordingly: stretch the hamstrings, mobilise the glenohumeral joint, work on the cervical muscles.

But the nervous system is a major contributor to range of motion. Decreased hamstring flexibility, as evidenced by limited range in the passive straight leg raise test, could be due to altered neurodynamics affecting the sciatic, tibial and common fibular nerves. When these neural structures have increased mechanosensitivity, the body's protective response can limit the range to which a joint can move — not because the muscle is short, but because the nervous system is limiting movement to protect itself from mechanical load.

Kuilart and colleagues found that subjects who perceived they had tight hamstrings were unlikely to have reduced hamstring length or extensibility. It was postulated that neural mechanosensitivity may play a significant role in explaining perceived hamstring tightness.

This matters because the treatment implications are completely different. Aggressively stretching a muscle that is actually protecting a sensitised nerve can increase that sensitivity and worsen the problem. Understanding whether you are dealing with true hamstring tightness or neural tension is crucial, as aggressively stretching neural structures can lead to irritation, sensitisation and long-term dysfunction.

The hamstring example is the most widely studied, but the same principle applies throughout the body. Restricted shoulder range that is attributed to posterior capsule tightness may reflect upper limb neural tension. Reduced cervical rotation that appears to be muscular may have a neurodynamic component. Ankle dorsiflexion restriction may involve the sural or tibial nerve. In each case, the range restriction will not respond to muscular treatment, and the oversight delays recovery.

How Neurodynamic Testing Differs From Standard Clinical Testing

Most standard clinical testing is designed to identify the end range of motion — how far does a joint or limb move before restriction occurs? Neurodynamic testing is fundamentally different in both what it measures and how it is interpreted.

Standard range of motion testing asks: how far does the limb move?

Neurodynamic testing asks: what is producing the limitation, and where is that structure located?

The structural differentiation process — systematically adding and removing distant components of the test to see whether symptoms change — is the key differentiating feature. This is not done in standard flexibility or joint range assessment. When you passively raise someone's leg in a standard assessment, you are measuring the combined mechanical resistance of all structures in the posterior chain simultaneously: hamstrings, sciatic nerve, lumbosacral roots, dura, hip joint capsule and posterior fascial structures. You cannot determine from that test alone which structure is limiting the movement.

Neurodynamic testing resolves this by using the continuous nature of the nervous system as a diagnostic tool. Adding ankle dorsiflexion to a straight leg raise increases tension on the neural tract but adds no additional load to the hamstring muscles. If this addition significantly changes symptoms or range, the nervous system is implicated. If it makes no difference, the hamstrings (or other non-neural structures) are more likely the primary limiting factor.

This distinction between what limits range and how much range is available is one of the most clinically significant things neurodynamic assessment adds to standard musculoskeletal practice — and it is largely absent from most therapy training curricula.

Sliders and Tensioners — Treatment Approaches

Once neural mechanosensitivity has been identified, treatment approaches are also meaningfully different from those used for muscular restriction.

Neural mobilisation techniques fall into two main categories, as described by Coppieters and Butler:

Neural sliders involve increasing tension at one end of the nerve while simultaneously releasing tension at the other. For example, in a sciatic slider the patient alternates between hip flexion with knee flexion and hip extension with knee extension. This creates a sliding movement of the nerve through its mechanical interface rather than a sustained stretch. Sliders are generally used when the nerve is highly sensitive and cannot tolerate sustained tension.

Neural tensioners involve increasing tension simultaneously at both ends of the nerve. They produce greater longitudinal force through the neural tract and are used when sensitivity has reduced and the goal is to improve load tolerance. They require more caution and are not appropriate in the acute or highly sensitised phase.

Both approaches are fundamentally different from static stretching in their mechanism. The goal is not to lengthen the nerve but to restore its ability to glide freely within its mechanical interface, reduce intraneural pressure, and improve blood supply to the nerve — all of which contribute to reducing mechanosensitivity over time.

Clinical Take-Home Tips

1. Add structural differentiation to your straight leg raise. Before concluding that a restricted SLR is a hamstring problem, add ankle dorsiflexion and note whether symptoms change. Then release the ankle and flex the cervical spine. Changes in either direction suggest neural involvement. This takes 30 seconds and changes your entire treatment approach.

2. Use the slump test routinely in low back pain and posterior thigh complaints. The cervical extension release is the most important component. If releasing the neck reduces symptoms during knee extension, the nervous system is a primary driver. This is not a hamstring problem.

3. Distinguish between the quality of the sensation and the quantity of range. Neural mechanosensitivity typically produces a different quality of sensation to muscular stretch — often more electric, burning, radiating or sharp, and often distributed along a neurological pathway rather than localised to a muscle belly. Ask your clients to describe not just where they feel the restriction but what it feels like.

4. Side-to-side comparison is essential. Asymmetry in range of motion, symptom quality or resistance to movement during neurodynamic testing is more diagnostically meaningful than absolute values. One leg raising to 70 degrees with neural symptoms is more significant if the other reaches 85 degrees symptom-free.

5. Do not stretch a sensitised nerve. If neurodynamic testing is positive and the client is symptomatic, start with slider techniques rather than tensioners, and avoid sustained end-range stretching of the neural pathway. Increasing tension in a sensitised nerve will increase its sensitivity, not reduce it.

6. Consider the mechanical interface, not just the nerve. The nerve travels through and between muscles, under fascial bands, around joints and through tunnels. Restriction can arise from any of these interfaces. A tight piriformis can compress the sciatic nerve. A thickened carpal tunnel ligament can compress the median nerve. Thoracic hypomobility can contribute to upper limb neural tension. Treating the interface can reduce neural load without directly mobilising the nerve.

7. Think about the whole neural pathway. The slump test changes symptoms in the foot because the nervous system is continuous. A client presenting with plantar fascia symptoms may have a neural contribution from the lumbar spine. A client with lateral epicondylagia may have a radial nerve involvement at the cervical spine. When treatment directed at the local area is not working, look upstream and downstream along the neural pathway.

8. Neural mechanosensitivity does not require structural pathology. Normal nerve conduction studies, negative MRI and absent neurological signs do not rule out clinically significant neural mechanosensitivity. The tests assess sensitivity, not structural damage. Many clients with ongoing symptoms that have defied structural explanation have a neurodynamic component that has simply never been assessed.

Further Reading

For practitioners who want to explore this area in depth, the two foundational texts are David Butler's Mobilisation of the Nervous System (1991) and Michael Shacklock's Clinical Neurodynamics (2005). Both remain essential reading and provide the theoretical and practical foundation for everything described in this post. Butler's Explain Pain (co-authored with Lorimer Moseley) also provides an accessible framework for understanding how central and peripheral sensitisation interact in clinical practice.

Sources:

Boyd BS et al. Mechanosensitivity of the lower extremity nervous system during straight-leg raise neurodynamic testing in healthy individuals. JOSPT, 2009.

Butler DS. Mobilisation of the Nervous System. Churchill Livingstone, 1991.

Butler DS, Moseley GL. Explain Pain. NOI Group, 2003. Coppieters MW, Butler DS. Do sliders slide and tensioners tension? An analysis of neurodynamic techniques. Manual Therapy, 2008.

Hall T et al. Between-session reliability and within-session repeatability of the slump neurodynamic test. Manual Therapy, 2006.

Shacklock M. Clinical Neurodynamics: A New System of Musculoskeletal Treatment. Elsevier, 2005.

This post is written for qualified sports massage therapists and allied health professionals and is intended to support evidence-informed clinical practice.