Orthopedics · Part Four · Seeing and Ruling Out
Lesson 37 / 44
Adverse Neural Tension: How Nerves Move, and What Happens When They Cannot
Nerves are built to move. When they cannot glide, they can become the pain generator themselves, and neurodynamic testing helps a clinician tell that story apart from a muscle or a joint.
Adverse neural tension is what happens when a nerve loses its ability to glide through the tissues around it. Nerves are built to move, and the movement is measurable. One median nerve gliding exercise produced 10.2 millimeters of longitudinal excursion in the upper arm, while a tensioning version produced 1.8. In people with chronic arm pain, that longitudinal movement fell by about 70 percent. The Unified Model of Tone reads neural tension as a regulated variable rather than a fixed length.
Cervical cord length from neutral posture to full flexion
up 10 percent behind, 6 percent in front
Rabbit tibial nerve held at 6 percent strain for one hour
action potential amplitude down 70 percent
Most responsive fibers in an inflamed nerve answered
3 percent stretch
Neural mobilization in chronic low back pain, disability
9.26 points of 50 on the Oswestry
Adverse neural tension
The clinical term for a nerve that has lost the freedom to lengthen and slide as a limb moves, and that now produces symptoms from motion it once tolerated. Neurodynamics is the study of that mechanics. Its tests load the nerve through a sequence of joint positions and then change one distant joint to see whether the symptom follows the nerve.
How a nerve accommodates motion
Nerve trunks lie in a bed of loose connective tissue and slide within it. Inside the trunk, wavy fiber bundles straighten before the whole nerve is stretched, which buys length before tension rises. When a region stops moving, that reserve is lost in two ways. Fibrosis inside the trunk binds the bundles to each other, and fibrosis outside it tethers the trunk to its bed.
01The moving nerve
A nerve is built to move, and the movement is measured in millimeters
Adverse neural tension describes what happens when a nerve loses its ability to glide. The question a patient carries is whether an arm or a leg symptom is coming from the nerve itself rather than from a muscle or a joint. Most examination concentrates on joints and muscles. Neural tissue has biomechanical properties of its own.
A nerve is not a passive cable. It is an elastic network of tiny conduits that telescopes in and out using internal undulations, with fiber bundles that slide past one another as a limb moves. Healthy nerves accommodate stretch easily. They glide between tissues, through bony tunnels and around bony prominences whenever a person moves.
Ultrasound has put numbers on that glide. Coppieters and colleagues imaged the median nerve in the upper arm of 15 asymptomatic volunteers during six nerve-gliding exercises (Coppieters 2009). A sliding technique, which lengthens the nerve bed at one joint while shortening it at another, produced 10.2 millimeters of longitudinal excursion. A tensioning technique, which lengthens the bed at both ends, produced 1.8.
The whole network answers a local pull
Kleinrensink and colleagues showed how far a local pull travels. Buckle force transducers were placed in six embalmed arms, and tension was introduced distally in the median, ulnar and radial nerves (Kleinrensink 2000). That tension was transmitted upward into the medial, lateral and posterior cords of the brachial plexus. Pull on one part of that network and the whole thing responds.
The nervous system behaves as one continuous unit, mechanically, electrically and chemically. Michael Shacklock built the field of neurodynamics on that continuity, treating neural tissue as a structure organized for movement. The historic dissection known as Harriet, prepared by Rufus Weaver MD in 1888, shows the shape of it: one branching structure lifted out whole.
02Findings
What the research shows
From a cadaver series, an imaging study of the cord, a rabbit stretch model, a rat neuritis model, two ultrasound studies and a meta-analysis.
03When glide is lost
Small strains change conduction, and inflammation makes stretch itself painful
Nerves tolerate very little sustained tension before their electrical behavior changes. Wall and colleagues stretched the tibial nerve in 24 rabbits by 0, 6 or 12 percent of its length and held the strain for one hour (Wall 1992). At 6 percent the amplitude of the action potential fell by 70 percent, then returned to normal during a one-hour recovery period. At 12 percent conduction blocked completely and showed minimal recovery.
Those are small numbers. Six percent is inside the range a limb crosses in ordinary reaching, which is why a position held for hours matters more than a position reached for a moment. Strain that stopped short of injury reversed within the hour.
Why an irritated nerve hurts when it is lengthened
Inflammation changes what a stretch means. Dilley and colleagues wrapped rat peroneal and sciatic nerves in material saturated with complete Freund adjuvant to produce a local neuritis (Dilley 2005). Fibers then appeared that fired to small stretches and to local pressure. No such fibers were found in control preparations.
The most responsive fibers answered a 3 percent stretch, which the authors put inside the range seen during normal limb movement. A nerve chemically irritated along its trunk, with no visible lesion, becomes mechanosensitive. It generates pain from movement it once tolerated without complaint.
Adaptive shortening and the loss of reserve
When a limb stops moving well, the nerve loses reserve along with the muscle and the joint capsule. Reduced movement from a frozen shoulder, a sustained posture or prolonged guarding leads to adaptive shortening, so the nerve can no longer elongate on demand. Attempt to lengthen it again and the result is adverse neural tension. Our model reads that shortening as constraint the nervous system itself produced and still maintains, which is why it is reversible.
Reduced glide is measurable in patients. Greening and colleagues used high-frequency ultrasound to record longitudinal median nerve movement in the forearm during maximal inspiration (Greening 2005). Movement was reduced by 71 percent in nine post-whiplash patients and by 68 percent in eight patients with non-specific arm pain. Transverse movement through 30 degrees of wrist extension to 30 degrees of flexion ran radially in the whiplash group and the other way in controls.
Tension also reduces blood flow inside the nerve, which produces tingling and numbness, and it slows axoplasmic flow, the transport of materials along the axon. The Nerve Root carries the occlusion pressures for the root itself. This is a mechanical story with a reversible mechanism, not a sign of catastrophe.
04Reading the arm
The guarded arm posture is the body protecting a sensitized nerve
The first clue often arrives before any test, in posture. A person with upper limb neural tension tends to elevate the shoulder girdle, internally rotate the arm and flex the elbow and wrist. That position puts slack into the brachial plexus. Increased tone in the upper trapezius on the same side is a common companion.
These are not random habits. They are neuroprotective, the body avoiding the movements that lengthen an irritated nerve. The upper limb neurodynamic test runs those provocation movements in reverse, adding tension through a sequence of joints and looking for two things. One is reproduction of the patient symptoms. The other is a restriction of movement compared with the other side.
Which version of the test carries weight
The cadaver work narrowed the field. Kleinrensink and colleagues concluded that only the median nerve test and its version with contralateral cervical rotation proved sensitive and specific (Kleinrensink 2000). The radial and ulnar variants did not. The same study found that these tests cannot selectively stress an individual cervical nerve root, because the tension distributes across the plexus.
A review of validity reached a matching verdict from the clinical side. Limited evidence supports the median nerve test for deciding whether a patient has cervical radiculopathy, and the radial nerve test does not help with that question (Nee 2012). The median nerve test does not help diagnose carpal tunnel syndrome. The same review defined a positive result: the test reproduces at least part of the patient symptoms, and moving a distant joint changes those symptoms. Defined that way it is reliable in clinical use. Double Crush and the Arm carries the diagnostic accuracy of the upper limb test and the carpal tunnel picture in full.
A positive tension test is not a verdict. It is a hypothesis that neural tissue is part of the story, and it earns its weight only when the side to side difference and the symptom pattern agree.
05Slump against straight leg raise
The slump test adds the cord to what the straight leg raise loads
In the lower limb the same reasoning splits across two tests that load different lengths of one structure. The straight leg raise tensions the sciatic nerve and the lumbosacral roots from below. The slump test adds the neuraxis above by flexing the trunk and tucking the chin, then extends the knee and dorsiflexes the ankle to pull from below at the same time.
The cord measurements explain why that combination reaches further. In five volunteers, neck flexion elongated the cervical cord by 10 percent along its posterior surface and 6 percent along its anterior surface (Yuan 1998). Average displacement ran 1 to 3 millimeters. The upper cord moved caudad and the lower cord moved cephalad, so the whole structure was drawn toward the middle of the flexed canal.
The qualifying movements that make the test mean something
Breig and Troup studied the sacral plexus in six cadavers and showed that medial hip rotation raises tension in it (Breig 1979). They then applied a standard protocol to 442 patients, using three qualifying movements: ankle dorsiflexion, medial hip rotation and cervical flexion. Positive signs on medial hip rotation were frequently associated with increased tension and neurologic dysfunction of the lumbosacral roots.
Their conclusion is the practical one. Uncontrolled hip rotation reduces the value of the raise, and a standardized protocol improves both its diagnostic value and its repeatability. Extending the neck to relieve leg symptoms works the same way, removing tension from above to separate true neural tension from simple hamstring tightness.
The two tests work best together, and each answers a different question. When It Looks Like the Nerve carries the measured sensitivity and specificity of the straight leg raise and the slump test for lumbar disc herniation. The mechanics are this page, and the accuracy figures are that one.
06The membrane that anchors it
The dural anchors decide where neural tension lands during movement
Neural tension is a property of a membrane system with fixed ends. The cord does not float freely in the canal, and neither does the membrane around it. The dura anchors at the foramen magnum, dorsally to the posterior arches of the atlas and axis, and at the sacrum. Along its whole length it is fixed to the vertebral column by the meningovertebral ligaments. Those ligaments are thickest behind the cord at the atlas and the axis, and again at the fifth lumbar and first sacral segments.
Ventrally the dural sac is adherent to the posterior longitudinal ligament from the sixth cervical to the second thoracic segment. Beyond the Single Joint carries the lumbosacral dissection work on those ligaments, and Coccydynia and Its Mimics works out what the sacral anchor means at the bottom end.
What happens when an anchor fails
Shinomiya and colleagues found abundant posterior epidural ligaments running between the posterior dura mater and the ligamentum flavum in 11 embalmed cervical spines (Shinomiya 1995). No one had reported them in the cervical spine before. In five young men with isolated wasting of the hand muscles, the posterior dural wall displaced forward during neck flexion and compressed the cord from C7 to C8. The authors attributed that displacement to a lack or an insufficiency of those ligaments.
The membrane is doing the mechanical work in that finding. A dura that is anchored behaves one way in flexion, and the same dura unanchored crushes the cord in front of it.
Alf Breig established the spinal cord as a tensioned structure whose shape is maintained by the dentate ligaments anchoring it inside the canal. Those ligaments run from the pia mater to the dura and suspend the cord within its sleeve like a hammock. The Slow Cord Compression carries the modeling work showing that dentate-mediated tensile stress explains cervical cord dysfunction better than compression alone.
07Gentle restoration
Neural mobilization moved back and neck-arm pain, and did not move carpal tunnel
Movement is the treatment that matches the mechanism, and the trial evidence separates cleanly by condition. Basson and colleagues pooled 40 randomized trials of neural mobilization, 17 of them at low risk of bias (Basson 2017). In chronic low back pain, disability improved by 9.26 points on the 50-point Oswestry questionnaire, with a confidence interval from 4.01 to 14.50. Pain improved by 1.78 of 10.
Chronic neck-arm pain improved by 1.89 points of 10. For most clinical outcomes in carpal tunnel syndrome, neural mobilization was not effective, with p values above 0.11, while it still produced measurable neurophysiological effects including reduced intraneural edema. The intervention reached the tissue and did not move the symptom in that condition.
Choosing the dose
The technique chosen decides how much the nerve actually travels. A sliding technique produced 10.2 millimeters of median nerve excursion and a tensioning technique produced 1.8 (Coppieters 2009). Those are different mechanical inputs, and a sensitized nerve meets them differently. Loading a nerve that already fires to a 3 percent stretch is a different act from sliding it through its bed.
The guardrails matter as much as the technique. Progressive weakness, reflex loss and objective sensory loss point away from mobilization and toward further workup, because those signal conduction failure rather than mechanosensitivity. When Conservative Care Stops sets those thresholds. Conservative care here is not timid care. It is the safe and rational starting point, and it earns the confidence that comes from having first ruled out the dangerous.
08Claims removed from this page
Neural tension claims from the earlier version that were corrected or removed
The earlier version credited Lasegue with proposing a mechanical test for sciatica in 1864. He did not. His 1864 paper analyzed the theories of sciatica then current and described his own clinical observations. In it he held that flexion or extension of the lower limb did not exacerbate the pain (Sugar 1985). The straight leg raise was described and illustrated in 1881, in the Paris thesis of his pupil Forst, who ascribed it to his teacher.
Three figures came off. The claim that the straight leg raise stretches the L5 and S1 roots by 2 to 6 millimeters could not be matched to a published measurement. Neither could the figure putting a stretch response in 80 to 90 percent of healthy people during the upper limb test. The same applies to the 68 percent of patients with neck and arm pain said to show asymmetrical elbow motion.
The stretching protocols came off for the same reason. The earlier text gave 10 seconds of tension with 10 seconds of rest across 10 cycles, and 30 seconds across 5 cycles for the slump, with no source for either. Nothing in the neural tension literature fixes a dose that precisely, and the pooled trial results above replace those numbers.
09The model on neural tension
What the Unified Model of Tone claims about adverse neural tension
Everything above is established science, including the excursion study that found no difference between the groups and the carpal tunnel result that did not move. What follows is this model’s reading, stated as ours rather than drawn from the papers cited.
The dura is innervated by autonomic branches and its tension is dynamic. Like a string, tighter dura carries higher frequencies and looser dura lower ones, and that tension decides which signals propagate cleanly through the cord. Our model treats the meninges as a sensing and transducing part of spinal control, which makes dural tension a regulated quantity rather than a passive consequence of where the bones sit.
The claim that runs both ways
The usual account runs one way. An outside force displaces a bone, the displaced bone irritates the nerve, and the nerve reports it. Our model holds that the vertebra is not pushed out of place from outside. It is twisted into position by the combined torque of asymmetric membrane tension and asymmetric muscular tone, and held there by tissue whose tone the nervous system itself produced.
Both directions are real: the bone can pull the cord, and the cord can pull the bone. Shinomiya and colleagues documented the first direction, where a dural wall free of its posterior anchors moved forward in flexion and compressed the cord (Shinomiya 1995). The second direction is ours to state, and it is measurable. Record paired left and right neurodynamic range at one segment, paired paraspinal surface electromyographic tone, and the axial rotation of that vertebra. Our model predicts the three vary together, and that reducing the tension asymmetry changes the rotation.
Why the excursion study came back flat
Longitudinal sciatic excursion did not differ between 16 asymptomatic participants and 60 with spinally referred leg pain (Ridehalgh 2015). Only the direction of transverse motion varied between groups. Our model expects that result, because millimeters of travel describe the input and not the state receiving it. Fibers in an inflamed nerve fired to 3 percent stretch while control fibers ignored the same stretch (Dilley 2005).
The same reading explains the validity problem in the diagnostic literature. Neurodynamic tests are scored against electrophysiological reference standards, and a patient whose nerve is mechanosensitive without conduction loss is classified by that standard as not having neuropathic pain (Nee 2012). The test and the standard read two different variables. An input interacting with a tone creates the outcome, and neither instrument records the tone.
The prediction
From that follows a claim the neurodynamics literature does not make. Our model predicts that four measures recorded together in the same people share one underlying factor. The first two are longitudinal nerve excursion in millimeters on ultrasound and the side to side difference in joint range at symptom onset on the same neurodynamic test. The others are pressure pain threshold over the nerve trunk and time to return to baseline after a sustained neurodynamic load.
Our model further predicts the direction of change under an input that restores regulation. People who begin with a wide neurodynamic range and people who begin with a narrow one both move toward the middle, and the spread narrows. A stretching account predicts something different, that everyone gains range in the same direction.
This is a claim about how neural tension is organized rather than a claim about what treatment does. If nerve excursion, side to side difference in neurodynamic range, pressure pain threshold over the nerve trunk and recovery time after a neurodynamic load are shown to move together, the unification claim is confirmed.
10The tone reading
How adverse neural tension expresses tone
Every topic in this library expresses all of tone. In adverse neural tension three aspects carry the signature, because the same stretch is unremarkable in one nerve and painful in the next.
Load
A nerve carries strain from wherever the movement happens. Six percent of strain held for one hour cut action potential amplitude by 70 percent in rabbit tibial nerve.
Gain
An inflamed nerve fires to stretches it once ignored. In rat neuritis the most responsive fibers answered 3 percent stretch, inside the range of ordinary limb movement.
Constraint
Guarding shortens what the nerve can be asked to do. Median nerve longitudinal movement fell about 70 percent in patients with whiplash and non-specific arm pain.
The remaining foundations run through neural tension as well. Input quality: a nerve bed that no longer slides reports limb position through a degraded stream, and the brain estimates the limb from what it gets. Coupling: the neck, the trunk and the leg share one membrane, which is why extending the neck changes a symptom felt in the calf. Set point: the resting tension a nerve sits at decides how much added lengthening it takes to provoke a symptom. Prediction: an arm that expects the next reach to hurt guards before the reach begins, and the guarding is what removes the slack. Time course: strain at 6 percent reversed within an hour and strain at 12 percent did not, so duration and magnitude decide the outcome together. Oscillation: symptoms that arrive with a held posture and fade when it breaks are reporting the regulator rather than the tissue. These are readings of one organization rather than separate systems, which is the core claim of the Unified Model of Tone.
11Across the library
How this page relates to the rest of the library
The mechanics on this page are what several neighboring lessons are quietly assuming.
The root inside its dural sleeve, with the pressures at which its blood supply is occluded.
The diagnostic accuracy of the upper limb neurodynamic test, and one nerve compromised at two levels.
The measured sensitivity and specificity of the straight leg raise and the slump test.
Why dentate-mediated tensile stress explains cervical cord dysfunction better than compression alone.
The suboccipital tissue whose held tension is also held dural tension.
The structure of the nerve trunk that makes gliding and stretching possible in the first place.
Leg pain read as a regulatory state, with the instruments used to measure it.
12Frequently asked
Questions patients ask about neural tension
What is a neural tension test?
It is a movement that loads a nerve along its length to see whether the nerve is the source of a symptom. The straight leg raise and the upper limb neurodynamic test are the common ones. A clinician then moves a joint far from the painful area and watches whether the symptom changes, which is what separates a nerve from a muscle. Cadaver work with force transducers confirmed that tension applied at the wrist is transmitted upward into the cords of the brachial plexus.
What does it mean if a nerve feels tight?
Nerves are meant to glide as a limb moves, and a sensitized nerve reports ordinary lengthening as tightness or pain. Inflammation is one route. In rats with a local neuritis, fibers appeared that fired to a 3 percent stretch, which is inside the range of normal limb movement, while control nerves ignored the same stretch. Tightness in that setting reflects a lowered threshold in the nerve rather than a shortened muscle behind it. It also explains why pushing harder into the stretch usually makes the sensation worse.
How much does a nerve actually move?
Enough to measure with ultrasound. In 15 healthy volunteers a sliding technique produced 10.2 millimeters of longitudinal median nerve excursion in the upper arm, while a tensioning version produced 1.8 millimeters. The spinal cord moves too. Between neutral posture and full neck flexion the cervical cord elongated 10 percent along its posterior surface, displacing 1 to 3 millimeters, with the upper cord travelling down and the lower cord travelling up. Nerves are therefore loaded by movements that no one would call a stretch.
Can stretching a nerve damage it?
Sustained strain changes conduction well before anything tears. In rabbit tibial nerve held for one hour, 6 percent strain dropped action potential amplitude by 70 percent and then recovered fully, while 12 percent strain blocked conduction completely with minimal recovery. That is why neural work is applied briefly and at the edge of a symptom rather than pushed into it. Progressive weakness, reflex loss or objective sensory loss point toward further workup rather than toward more movement, because those findings indicate conduction failure.
Does neural mobilization work?
The pooled trials separate cleanly by condition. Across 40 randomized trials, neural mobilization improved chronic low back disability by 9.26 points of 50 on the Oswestry questionnaire and pain by 1.78 of 10. Chronic neck-arm pain improved by 1.89 of 10. For most clinical outcomes in carpal tunnel syndrome it was not effective, although it still reduced intraneural edema, so the input reached the tissue without moving the symptom. Seventeen of the 40 trials carried a low risk of bias.
Why do neurodynamic tests give false positives?
Because the test and the reference standard measure different things. Neurodynamic tests are scored against electrophysiological studies, which detect conduction loss. A nerve can be mechanosensitive with conduction intact, and that patient is then classified as not having neuropathic pain. Cadaver work adds a second reason. These tests distribute tension across the plexus and cannot selectively stress one cervical root, so a positive result localizes poorly on its own. A side to side difference and a matching symptom pattern are what give the result weight.
What does the Unified Model of Tone say about neural tension?
That dural and neural tension is a regulated quantity rather than a fixed length, and that it runs in both directions. The bone can pull the cord, and the cord can pull the bone, because asymmetric membrane tension and asymmetric muscle tone converge on a vertebra as a rotational moment. From that the model predicts that nerve excursion, side to side neurodynamic range, pressure pain threshold over the nerve trunk and recovery time after a load share one underlying factor, with compensation deciding how far each one moves.
13The sources
References
12 primary sources, each linked to its record. Figures quoted on this page were checked against the published abstract.
Related evidence