Chapter 11. Neurodynamic Mobility and Mobilizations

At the completion of this chapter, the reader will be able to:

1. Summarize the various types of neurodynamic examination and mobilization techniques.

2. Describe the proposed mechanisms behind the neurodynamic examination and mobilization techniques.

3. Apply knowledge of the various neurodynamic mobilization techniques in the planning of a comprehensive rehabilitation program.

4. Recognize the manifestations of abnormal nervous tissue tension and develop strategies using neurodynamic mobilization techniques to treat these abnormalities.

5. Evaluate the effectiveness of a neurodynamic mobilization technique when used as a direct intervention.

Neurodynamics is the study of the mechanics and physiology of the nervous system. The nervous system is an electrical, chemical, and mechanical structure with continuity between its two subdivisions: the central and peripheral nervous systems (see Chapter 3). In addition to permitting inter- and intra-neural communication throughout the entire network, the nervous system is capable of withstanding mechanical stress as a result of its unique mechanical characteristics. Nervous tissue, a form of connective tissue, is viscoelastic. This viscoelasticity allows for the transfer of mechanical stress throughout the nervous system during trunk or limb movements. This adaptation results from changes in the length of the spinal cord1 and the capacity of the peripheral nerves to adapt to different positions. The peripheral nerves adapt through a process of passive movement relative to the surrounding tissue via a gliding apparatus around the nerve trunk.2,3 Three mechanisms appear to play an important role in this adaptability3:

• Elongation of the nerve against elastic forces. In normal daily movement, nerves may slide up to 2 cm in relation to surrounding tissues and contend with a strain of 10%.4
• Longitudinal movement of the nerve trunk in the longitudinal direction.
• An increase and decrease of tissue relaxation at the level of the nerve trunk.

According to Millesi,3 the efficiency of this mechanism partially depends on the capacity of the loose connective tissue around the nerve (adventitia, conjunctiva nervorum, perineurium) to allow any traction forces to be distributed over the whole length of the nerve.3 If this distribution of forces is compromised, an unfavorable rise in traction forces can occur at certain segments, depending on the anatomic site (see next section).3

The role that tension on the neural tissue plays in pain and dysfunction has been studied for over a century. During this time, a number of specific tests have been designed to examine the neurological structures for the presence of adaptive shortening and inflammation.5–7 The more common of these neurodynamic mobility tests are described in this chapter.

The spinal dura (see Chapter 3) forms a loose sheath around the spinal cord from the foramen magnum to the level of the second sacral tubercle. From there it continues as the filum terminale to the end at the coccyx. Laterally, the dura surrounds the exiting spinal nerve roots at the level of the intervertebral foramen. There are three areas called tension sites, in which the dura is tethered to the bony canal, providing stability to the spinal cord. These tension sites are found at the segmental levels of C6, T6, and L4; the elbow; the shoulder; and the knee have similar sites.5,8 As a result of these sites of tension, the neurologic tissues move in different directions, depending on where the stress is applied and in which order it is applied.7

During movement, neural tissue takes its lead from the movement of joints and muscles, with the physical loading of the nerve dependent on the location of the nerve in relation to the joint axis.4 Various studies have demonstrated excursion of the nerve complex during movements of the extremity.1,8–12 Under normal circumstances, the tension sites are not adversely affected by motion of the extremities. However, if the dura becomes adherent, excessive stress may be produced in the areas of adhesion, increasing the length of the dura beyond its normal limit of tension (Table 11-1).13 Theoretically, increased dural tension may be felt throughout the neuromeningeal system and, potentially, it may affect the range of motion available to the trunk and to an extremity. Pathomechanically, a decrease in the mobility of a nerve along its entire length makes the nerve more vulnerable to additional injuries during repetitive movements.13,14

The nerves and their microcirculation are vulnerable to tension, friction, and compressive forces at multiple sites along their routes.14 A number of mechanisms (excluding diseases such as diabetes mellitus, hypothyroidism, immune deficiency syndromes, rheumatoid arthritis, and alcoholism) are hypothesized to contribute to an injury of the peripheral nerve trunk. These include the following18:

• Posture. Sustained postures that produce changes in the natural curves of the spine can result in a shortening of the distance traveled by the peripheral nerve trunk and eventual adaptive shortening of these structures. Correction of this posture, after sufficient time has elapsed for it to have taken place, may produce a stretching of the neural tissues.
• Direct trauma. Orthopaedic injuries account for some of the injuries to peripheral nerves. For example, the radial nerve is injured through orthopaedic trauma more than any other major nerve.19 Nerve injuries can occur as the result of a direct blow to the nerve or secondary to damage of an adjacent structure such as a fracture,20,21 joint dislocation,22 or tendon rupture.23 Other causes of direct nerve trauma have included injections,24 joint manipulation,25 and surgical procedures.26 Neurological injury is one of the more serious complications of fracture and dislocation, both in the short and long term. For example, the prevalence of injury to the sciatic nerve after acetabular fracture or fracture-dislocation of the hip has been reported to be between 10–25%.27
• Extremes of motion. Given the course of many of the peripheral nerve trunks, it is not difficult to envision movements of the extremities that could place a traction force on these trunks. Indeed, those very same movements are exploited in some of the neurodynamic mobility tests.
• Electrical injury. In a 17-year review of burn unit admissions, permanent nerve injuries were found in 22% of electrocuted patients.28 The upper limb was most commonly involved with the median and ulnar nerves most commonly injured.28 Postneurologic symptoms in such cases can vary from neuropathy to complex regional pain syndrome (CRPS).
• Compression. Compression to a nerve can occur during muscle contraction and as a result of tight fascia, osteochondroma, ganglia, lipomas and other benign neoplasms, and bony protuberances.

Double-Crush Injuries

The double-crush syndrome (DCS) is a general term referring to the coexistence of dual neuropathies along the course of a peripheral nerve. The concept was proposed by Upton and McComas in 197329 who suggested that proximal compression of a nerve may decrease the ability of the nerve to withstand a more distal compression.

From the pathophysiological viewpoint, impairment of neural excursion, loss of elasticity, underlying abnormality of the connective tissue as well as direct pressure on the nerve may lead to disruption of axons, impairment of axonal transport, endoneural edema, or ischemic changes in nerves.29 For example, according to this theory, a cervical radiculopathy, manifesting as little more than neck pain and stiffness, could precipitate a distal focal entrapment neuropathy.29 The term double-crush syndrome is used to describe this mechanism of nerve injury: serial compromise of axonal transport along the same nerve fiber causing a subclinical lesion at the distal site to become symptomatic.

At least eight other etiologic mechanisms have been proposed to explain the relationship between the proximal and distal nerve fiber lesions29–33:

1. A proximal nerve lesion renders the distal nerve segment more vulnerable to compression because of serial constraints of axoplasmic flow.

2. The peripheral nerves possess an underlying susceptibility to pressure.

3. Interruption of lymphatic and venous drainage at the proximal nerve lesion site renders the distal nerve segment more vulnerable.

4. Endoneurial edema at one lesion site compromises neural circulation, rendering nerve fibers at the other site more vulnerable.

5. A connective tissue abnormality common to both sites along the nerve fibers.

6. Tethering of the nerve at one site causes injurious shear forces at the other site.

7. Entrapment of the nerve at one site causes decreased use of the muscle pump, which creates a slight, generalized edema of the limb. This increases tissue pressure in certain anatomic passages, which causes an additional entrapment nerve lesion.

8. The initial nerve lesion releases a metabolite that passes through the free intraneural circulation and increases the vulnerability of other segments of the nerve.

Since its introduction, the double-crush hypothesis has been invoked to explain a great number of coexisting proximal and distal nerve impairments. In fact, it has been expanded in various ways (i.e., to triple-crush, quadruple-crush, and multiple-crush syndromes, as well as the reversed DCS).31,34,35 Despite its acceptance, there are situations where the double-crush hypothesis has anatomic and pathophysiologic restrictions that render it inapplicable in some clinical situations.36 For the DCS to occur, there must be anatomic continuity of nerve fibers between the two (or more) lesions sites. If this is lacking, then sequential impairment of axoplasmic flow obviously cannot occur. Consequently, two focal nerve disorders along the same neural pathway (e.g., cervical root lesions and carpal tunnel syndrome) do not automatically fulfil this anatomic criterion of DCS unless the same axons are compromised at both sites.36

Although, experimental studies of the double-crush hypothesis have shown that successive lesions along a peripheral nerve can summate,32,37,38 studies that have attempted to demonstrate the existence of DCS have proved inconclusive.39–41

Neurophysiological examination is critical in distinguishing between a single or a double lesion as well as determining the comparative severity of the two lesions.

Both Elvey42 and Butler13 have been credited with the development of the examination techniques for neurodynamic mobility. Elvey42 developed what he named the brachioplexus tension test, which was later called the upper limb tension test (ULTT). Similar tests, such as the straight leg raise (SLR) and prone knee flexion tests, have been designed for the lower extremity. The slump test is considered to be a general test of neurodynamic mobility. The tension tests are designed to apply controlled mechanical and compressive stresses to the dura and other neurologic tissues, both centrally and peripherally.43 These neurodynamic tests are designed to assess the contribution of the spinal nerve roots and peripheral nerves to extremity pain by employing a sequential and progressive stretch to the dura. The tests place tensile stresses on the dura of spinal nerve roots and peripheral nerves using a longitudinal traction force of the nerve until the patient's symptoms are reproduced.6

The examination of neural adhesions is by no means an exact science, but the principles are based on sound anatomic theory. Knowledge of the course of each of the peripheral nerves is thus essential in order to put a sequential and adequate tension through each of them (see Chapter 3).

Breig's tissue-borrowing phenomenon offers a plausible explanation for the neurodynamic tests.44 Breig observed that tension produced in a lumbosacral nerve root results in displacement of the neighboring dura, nerve roots, and lumbosacral plexus toward the site of tension.13,44–46 In effect, a borrowing of the resting slack in neighboring meningeal tissues occurs as neural structures are pulled toward the site of increased tension. This results in a decrease in the available slack and potential mobility of the neural tissues throughout the region.7,44–48 This stretching and displacement of the nerve roots plexi reduces the available mobility of the peripheral nerves.7,44–48

Positive symptoms for the presence of neuropathic dysfunction include pain, paresthesia, and spasm.18 Unfortunately, these signs and symptoms are also associated with a host of musculoskeletal injuries. Asbury and Fields49 hypothesized that the type of pain that results from an injury to a peripheral nerve is characteristic and has two varieties:

1. Dysesthetic pain. This type of pain is felt in the peripheral sensory distribution of a sensory or mixed nerve and results from nociceptive afferent fibers.

2. Nerve trunk pain. This type of pain results from the nociceptors within the nerve sheaths and exhibits a pain distribution following the course of the nerve trunk.18

However, relying on the reproduction of a type of pain (a subjective issue at the best of times) is not sufficient to make the diagnosis of neural tissue dysfunction.

Because the subject of neural provocation tests and the intervention of neurodynamic mobilization remain controversial, the clinician should ensure that the results of these tests are always used in conjunction with findings from a complete neuromusculoskeletal examination, including the following:18,43,50,51

• Observation. An injury to a peripheral nerve trunk may result in visible atrophy within its motor distribution.
• Palpation. The clinician should carefully palpate along each of the nerve trunks in the region where they are superficial. Physical deformation of an irritated nerve should reproduce pain with palpation.
• Range of motion. In areas of decreased neural mobility, both active and passive range of motion may be diminished in the same direction. However, a lesion to the musculotendinous unit would also reproduce pain with the same maneuver, particularly in muscles that cross two joints.
• Resistive testing. Resistive tests can be used to examine for the presence of weakness in the distribution of a peripheral nerve and to help differentiate between pain reproduced with active or passive range of motion that indicates damage to the musculotendinous unit and pain that results from neural tension. For example, pain reproduced in the posterior thigh with the SLR may indicate a lesion of the hamstring muscle belly or a lesion to the sciatic nerve. If resisted knee flexion does not reproduce pain, the musculotendinous unit is unlikely to be at fault, leaving the sciatic nerve as the likely cause.

The purpose of the physical examination is to determine which tissue is at fault. This is accomplished by isolating (where possible) each tissue that has the potential to produce those symptoms and selectively stressing that tissue. Part of the problem with this approach lies in the fact that a positive finding for many of the techniques designed to assess the integrity of a neural structure may just be the result of a sensitive movement, rather than a stretch of the dura.52 For example, when wrist extension is performed with the elbow in extension and the shoulder abducted, in addition to placing stress through the elbow and wrist joints, wrist flexors, and elbow flexors, the loading of the nervous system is continued proximally, at least up to the level of the axilla.53

Some of the so-called dural symptoms could also result from the imparted stretch on the dura during the various maneuvers, producing changes in the axoplasmic flow inside the nerves, provoking the firing of abnormal impulses, and decreasing the vascular supply to the nerve.54–56

A neural tension test performed in a sitting position is necessary to simulate the extremes of spinal motion associated with symptom-provoking activities such as slouched sitting or entering and exiting a car.57–59

The slump test, popularized by Maitland,59 is a combination of other neuromeningeal tests, namely, the seated SLR, neck flexion, and lumbar slumping. In the slump test, the patient is seated in full flexion of the thoracic and lumbar regions of the spine.60 Sensitizing maneuvers are then systematically applied and released to the cervical spine and lower extremities while the tester maintains the patient's trunk position. The slump test assesses the excursion of neural tissues within the vertebral canal and intervertebral foramen58 and detects impairments to neural tissue mobility from a number of sources as identified by Macnab61 and Fahrni.62 Maitland asserted that the slump test enables the tester to detect adverse nerve root tension caused by spinal stenosis, extraforaminal lateral disk herniation, disk sequestration, nerve root adhesions, and vertebral impingement.57,58

Several studies44,48,63,64 have demonstrated the effects of trunk and head position on neural structures within the vertebral canal and intervertebral foramen during slump testing. These studies reported that full spinal flexion or flexion of the cervical, thoracic, and lumbar regions of the spine produces lengthening of the vertebral canal. This elongation of the vertebral canal stretches the spinal dura and transmits tension to the spinal cord, lumbosacral nerve root sleeves, and nerve roots.44,48,63–65 During full spinal flexion, the cauda equina becomes taut and the lumbosacral nerve roots and root sleeves are pulled into contact with the pedicle of the superior vertebra.44,63,64,66

When extension of the cervical spine is introduced, the dura and the nerve roots slacken as the vertebral canal begins to shorten.44,63–66,68 Extending the thoracic and lumbar spines increases the slack in the neural tissues as the vertebral canal continues to shorten.44,63–66,68

Because the slump test is a combination of other tests, a choice as to its use needs to be made. Either the classic SLR test or its variations should be performed; or the slump test should be used.69 The only advantage of the slump test over the SLR test is that it increases the compression forces through the intervertebral disks and will highlight the presence of dural adhesions.69 Depending on which text is read, there is a wide variety of progressive steps to the slump test; particularly when the lumbar kyphosis stage is introduced. Although the specific order of implementation remains controversial, it is important that the clinician consistently use the same sequence with each patient.

As soon as symptoms are reproduced during these tests, the test should be terminated. It is worth remembering that during a dural tension test, the dura itself does not move. It is merely stressed; hence, the name for the tests. One such method of sequencing is described next.

The patient is positioned sitting with the hands behind the back, the popliteal creases just off the edge of the bed and a slight arch in the back (Fig. 11-1), and the head flexed and then placed in neutral. This initial position is then followed by a slump of the lumbar and thoracic spine with a posterior pelvic tilt as the clinician maintains the patient's neck in neutral (Fig. 11-2). This maneuver has the effect of tightening the entire dura including the thorax dura. If the test is still negative, the patient is asked to flex the neck by first applying a chin tuck and placing the chin on the chest and then to straighten the knee as much as possible. Overpressure is then gently applied to the upper thoracic and the lower cervical spine and maintained throughout the examination (Fig. 11-3). The subject's ankle is then passively dorsiflexed to the point of slight resistance, while the knee is slowly passively extended to full extension or to the point when the subject reports an onset of neural mediated symptoms (Fig. 11-4). If the patient is unable to straighten the knee because of a reproduction of symptoms, he or she is asked to actively extend the neck. Following extension of the neck, if the patient cannot straighten the knee further, the test can be considered positive.

The test can also be performed in reverse because a positive response may occur in one direction but not the other.

It is important to note that no diagnostic accuracy studies have been performed to determine the sensitivity and specificity of the slump test. A recent study by Davis and colleagues70 found the slump test had a high false positive rate in asymptomatic individuals and recommended that the current criteria for determining a positive test should be examined using new range of motion cutoff scores. The study also recommended that the test should be considered positive only when peripheral symptoms are reproduced before 22 degrees of knee extension.70

Sciatica is defined as pain along the course of the sciatic nerve or its branches and is most commonly caused by a herniated disk or by spinal stenosis.71 Characteristically, patients with sciatica report gluteal pain radiating down the posterior thigh and leg, paresthesia in the calf or foot, and varying degrees of motor weakness. Extraspinal entrapment of the sciatic nerve (i.e., along its course within the pelvis or the lower extremity), although infrequent, is difficult to diagnose because its symptoms are similar to those of the more frequent causes of sciatica.72–74

Straight Leg Raise

The SLR test is recognized as the first neural tissue tension test to appear in the literature. It was first described by Lasègue well over 100 years ago.75

The patient is positioned supine with no pillow under the head. The patient's trunk and hip should remain neutral, avoiding internal or external rotation, and excessive adduction or abduction. Each leg is raised individually (uninvolved side first). To ensure that there is no undue stress on the dura, the tested leg is placed in slight internal rotation and adduction of the hip and extension of the knee. The clinician holds the patient's heel, maintaining the extension and neutral dorsiflexion at the ankle, and raises the straight leg (Fig. 11-5) until complaints of pain or tightness in the posterior thigh are elicited.13 At this point, the range of motion is noted and the clinician then lowers the straight leg slightly until the patient reports a decrease in symptoms.

The evaluation of the findings from the SLR test requires that the range of motion measured and the symptoms produced are compared with the contralateral side and with expected norms.7,77–80 Because sitting knee extension and the SLR culminate in essentially identical positions, symptomatic responses to the two types of maneuvers should be similar, although the angle at which pain is elicited may vary.81

It is generally agreed that the first 30 degrees of the SLR serves to take up the slack or crimp in the sciatic nerve and its continuations. Using symptom reproduction below 40 degrees as a criterion for a positive SLR test result has been found to increase the sensitivity to 72%.83

Pain in the 0- to 30-degree range may indicate the presence of

• acute spondylolisthesis
• tumor of the buttock
• gluteal abscess
• very large disk protrusion or extrusion84
• acute inflammation of the dura
• malingering patient
• the sign of the buttock

Between 30 and 70 degrees, the spinal nerves, their dural sleeves, and the roots of the L4, L5, S1, and S2 segments are stretched with an excursion of 2–6 mm.85 After 70 degrees, although these structures undergo further tension, other structures also become involved. These additional structures include the hamstrings, gluteus maximus, hip, lumbar, and sacroiliac joints. An SLR test is positive if

• the range is limited by spasm to less than 70 degrees, suggesting compression or irritation of the nerve roots. A positive test reproduces the symptoms of sciatica, with pain that radiates below the knee, not merely back or hamstring pain.76 When the SLR is severely limited, it is considered diagnostic for a disk herniation.86
• the pain reproduced is neurologic in nature. This pain should be accompanied by other signs and symptoms such as pain with coughing, tying of shoe laces and so on but not necessarily by muscle weakness.

The following caveats are important for accurate assessment of the SLR:

• The patient must have the necessary available range of hip flexion (30–70 degrees).
• The SLR produces a posterior shear and some degree of rotation in the lumbar spine (a region not well suited to shearing or rotational forces). Thus, back pain alone with the SLR is not a positive test.81

Sensitizers

Passive dorsiflexion of the ankle (Braggard's test) (Fig. 11-6) and/or passive cervical flexion (Soto-Hall test) may be used as sensitizers for the SLR test. The cervical flexion can also be performed actively (Fig. 11-7). In addition, further internal rotation or extreme adduction of the hip may also be added to the SLR. These additional maneuvers increase the tension exerted on the spinal cord, spinal dura, and lumbosacral nerve roots.7,13,44–46,48,89 Research studies44–47,63,89 have demonstrated that cervical flexion lengthens the spinal cord and dura. This action may provoke radicular symptoms without stressing nonneural tissues in the lower extremity.13,58,90

Thus, the dura can be pulled from below, using dorsiflexion, or from above, using cervical flexion. Further modifications can be incorporated to place stress through different branches of the sciatic and common fibular (peroneal) nerves by adjusting the ankle and foot position. Coppieters and colleagues91 evaluated the clinical hypothesis that strain in the nerves around the ankle and foot caused by ankle dorsiflexion can be further increased with hip flexion. Linear displacement transducers were inserted into the sciatic, tibial, and plantar nerves and plantar fascia of eight embalmed cadavers to measure strain during the modified SLR. Nerve excursion was measured with a digital caliper. Ankle dorsiflexion resulted in a significant strain and distal excursion of the tibial nerve. With the ankle in dorsiflexion, the proximal excursion and tension increases in the sciatic nerve associated with hip flexion were transmitted distally along the nerve from the hip to beyond the ankle. As hip flexion has an impact on the nerves around the ankle and foot but not on the plantar fascia, the modified SLR may be a useful test to differentially diagnose plantar heel pain. Although the modified SLR caused the greatest increase in nerve strain nearest to the moving joint, mechanical forces acting on peripheral nerves are transmitted well beyond the moving joint. Based on these findings, the following ankle and foot adjustments can be made:

• Dorsiflexion, foot eversion, and toe extension stress the tibial branch.
• Dorsiflexion and inversion stress the sural nerve.
• Plantar flexion and inversion stress the common fibular (peroneal) nerve (deep and superficial).

If symptoms are not reproduced with the SLR but the slump test is positive, numerous reasons have been proposed, and the following are few among them69:

• The presence of a soft disk protrusion, particularly a central soft protrusion. Soft central protrusions need loading through weight bearing and are often negative in a non–weight-bearing position.
• Acute spondylolisthesis.
• Posterior instability.
• Malingering patient/nonorganic symptoms.

Crossed Straight Leg Raise Sign

The crossed SLR sign, or Well leg raising test of Fajersztajn,80 is associated with the SLR test. There are three recognized types:

1. SLR that produces pain in the contralateral leg but not when the contralateral leg is raised.

2. SLR that produces pain in both legs.

3. SLR of either leg that produces pain in the contralateral limb. For example, SLR of the right leg produces pain in the left leg and SLR of the left leg produces pain in the right leg.

There are many theories as to the cause and significance of the crossover sign. One theory suggests that the neuromeninges are pulled caudally, resulting in compression of the dural sleeve against a large or medially displaced disk herniation. The crossed SLR is considered relatively insensitive but highly specific and is thought to be more significant than the SLR test in terms of its diagnostic powers to indicate the presence of a large disk protrusion.92 For example, Kosteljanetz and colleagues 93 found the test to have 24% sensitivity and 100% specificity, and Kerr and colleagues94 found the test to have a sensitivity of 25% and a specificity of 95%. One study goes so far as to recommend using the combined results from the SLR and crossed SLR for a more accurate diagnosis.88

The following findings are strongly predictive of disk herniation84,92,95:

• Severely limited SLR.
• Positive crossover SLR.
• Severely restricted and painful trunk movements.

Bilateral Straight Leg Raise

Once the unilateral SLR test is completed, the clinician should test both legs simultaneously (Fig. 11-8). A limitation of the unilateral SLR is that it may not highlight the presence of a central disk protrusion, particularly a soft disk protrusion.78 By performing a bilateral SLR and incorporating both neck flexion and dorsiflexion, central protrusions may be detected.69

Because a central protrusion may mimic a lateral recess stenosis, a differentiation test is needed. The bicycle test of van Gelderen96 is advocated. The patient is appropriately positioned on a bicycle and asked to pedal against resistance.

• A patient with lateral spinal stenosis tolerates this position well.
• A patient with intermittent claudication of the lower extremities typically experiences an increase in symptoms with continued exercise, regardless of the position of the spine.
• A patient with intermittent cauda equina compression typically has an increase of symptoms with an increase in lumbar lordosis.
• A patient with a disk herniation usually fairs well if the lumbar spine remains extended.

Bowstring Tests

The bowstring tests are named after the technique applied to the nerve under examination. Both the tibial and the common fibular (peroneal) nerves can be tested and although the tests impart an insufficient stretch of the dura to detect chronic adhesions, they can be used to make a prognosis about acute disk herniations. A positive bowstring test is a strong indicator for surgery but it need only be performed if the SLR is positive with the addition of dorsiflexion.69

Sciatic Tension Test

The sciatic tension test, also referred to as the Deyerle and May test, reproduces the mechanics of the Bowstring test in a seated position. The tibial nerve travels down the middle of the posterior thigh between the femoral condyles and down the back and middle of the calf entering the foot under the medial malleolus of the ankle (see Chapter 3). The involved extremity is extended at the knee to the point of pain and then lowered slightly to decrease pain. The clinician supports the patient's leg on his or her shoulder and then applies finger pressure to the popliteal fossa in an attempt to tension the sciatic nerve (Fig. 11-9). If the symptoms return with this maneuver, the test is considered positive.

Common Fibular (Peroneal) Test

Typically, the common fibular (peroneal) nerve travels with the tibial branch to the posterior distal thigh region (see Chapter 3). It then wraps itself around the fibular head and has strong attachments to the tendon of the biceps femoris. The procedure for this test is similar to that of the tibial version of the test except that after the knee is slightly flexed, the clinician pulls the biceps femoris tendon at the fibular head medially and laterally (Fig. 11-10). If this maneuver reproduces the symptoms, it is considered a positive test.

Prone Knee Bending Test

The prone knee bending (PKB) test stretches the femoral nerve using hip extension and knee flexion to stretch the nerve termination in the quadriceps muscle.69 This test has been used to indicate the presence of upper lumbar disk herniations,97 particularly when hip extension is added.98 The femoral nerve travels anteriorly to both the hip and the knee (as does the rectus femoris). Therefore, the nerve roots and the rectus femoris are stretched with a combination of knee flexion and hip extension. The lateral cutaneous nerve of the thigh and the hip flexors travel anterior to the thigh and may be stressed with the hip extension component of this maneuver.

Some clinicians recommend performing a PKB test before executing a sacroiliac “upslip” correction because there is a small potential to avulse the L2–L3 nerve roots with this maneuver.

The PKB test is performed as follows: the patient is positioned prone, and the clinician stabilizes the ischium to prevent an anterior rotation of the pelvis. The clinician then gently moves the lower extremity into knee flexion, bending the knee until the onset of symptoms (Fig. 11-11). This maneuver is likely to produce a stretching sensation on the anterior aspect of the patient's thigh. The zone at which the dura is stretched is 80–100 degrees of knee flexion. Knee flexion greater than 100% introduces both a rectus femoris stretch and lumbar spine motion into the findings. A number of sensitizing maneuvers can be used including hip extension, plantar flexion, dorsiflexion, or head movements.

The test is positive if there is a reproduction of unilateral pain in the lumbar area, buttock, posterior thigh, or a combination in the 80–100 degree range of knee flexion which could indicate an L2, L3, or L4 nerve root impairment although an acute L4–S1 disk protrusion may also produce positive findings.99

The reliability and validity of the PKB is not known.87 Porchet and colleagues100 found the test to have a sensitivity of 84% but the positive findings were associated with severe lateral disk herniations.

Crossed Prone Knee Bending Test

This is a variation of the PKB test except that the uninvolved lower extremity is moved into knee flexion. A positive test is the reproduction of the patient's symptoms in the untested (opposite) leg. No diagnostic accuracy studies have been performed to determine the sensitivity and specificity of this test.

See reference 13

The role of adverse neuromechanics in the upper limb and trunk has received much attention over the past three decades,42,101,102 and has been linked to chronic neck and arm pain and upper limb disorders.16,29,103,104

Upton and McComas29 demonstrated that the peripheral nerve and its cervical roots may manifest irritation at simultaneous sites. A further study, which investigated adverse tension in the neural system in 20 subjects suffering from unilateral symptoms of tennis elbow, appeared to suggest that the adverse tension could be a factor.103

The relative mobility between the nerve root and its investing sheath, which occurs in the lumbar spine,8 also has been demonstrated in the cervical spine.42 This mobility is produced with certain movements of the arm and occurs maximally at C5 and C6, to a lesser degree at C7, and to an even lesser degree at C8 and T1.16

The ULTTs, or brachial plexus tension tests, involve an ordered sequence of movement of the shoulder girdle, arm, elbow, forearm, wrist, and hand. Because there are a number of tissues in the cervicobrachial region that could be stressed by these maneuvers, cervical side bending or cervical flexion, which are thought to be more selective to the nervous system, are added.105,106

The principles behind the ULTT are the same as those described for the lower extremity tension tests. Therefore, only the procedures themselves are described here. During these procedures, care must be taken to maintain the cervical spine in neutral flexion–extension, side bending, and rotation.

ULTT 1 (Median Nerve Dominant)

The patient is positioned supine. The clinician depresses the shoulder girdle, abducts the humerus to approximately 110 degrees, supinates the forearm, and extends the elbow, wrist, and fingers (Fig. 11-12). The sensitizers for this test are cervical spine side flexions either toward or away from the involved side. The test is repeated on the contralateral extremity and the results are compared.

Several studies have shown that the longitudinal motion of the median nerve is affected by motion of the fingers and wrist, with digital flexion resulting in a proximal slide into the forearm, and wrist and finger extension both producing a distal slide of the nerve toward the hand.10,12 Hyperextension of the wrist has been shown to cause the median nerve to slide 10–15 mm distally relative to a fixed bony landmark in the carpal tunnel whereas flexion of the wrist and fingers moves the nerve 4 mm proximally.10

ULTT 2 (Radial Nerve Dominant)

The patient is positioned supine. The clinician depresses, abducts, and internally rotates the shoulder, pronates the forearm, extends the elbow, and flexes the wrist and thumb (Fig. 11-13). The sensitizers for this test are cervical spine side flexions either toward or away from the involved side. The test is repeated on the contralateral extremity and the results are compared.

ULTT 3 (Ulnar Nerve Dominant)

The patient is positioned supine. The clinician extends the wrist, supinates the forearm, fully flexes the elbow, and depresses and abducts the shoulder. The sensitizers for this test are side flexion of the head and neck, both toward and away from the test side. The test is repeated on the contralateral extremity and the results are compared.

Evans107 described a modification of the basic ULTT 3. The patient actively abducts the humerus with the elbow straight, stopping just short of the onset of symptoms. The patient then externally rotates the shoulder just short of symptoms and the clinician holds this position. Finally, the patient flexes the elbows so that the hand is placed behind the head. Reproduction of the symptoms with elbow flexion is considered a positive test.

Musculocutaneous Nerve

The patient is positioned supine with the head unsupported by a pillow. The clinician, facing the patient's feet, supports the patient's arm in about 80 degrees of elbow flexion. The shoulder is placed in full external rotation and approximately 10 degrees of abduction. Shoulder depression is then applied followed by glenohumeral extension (the “sensitizer”), elbow extension, and wrist ulnar deviation.

Axillary Nerve

The patient is positioned supine with the head unsupported by a pillow. The clinician places one hand on top of the patient's shoulder and depresses the shoulder. The glenohumeral joint is then externally rotated and the patient side flexes the head away from the tested side. The shoulder is then abducted to approximately 40 degrees.

Suprascapular Nerve

The patient is positioned supine with the head unsupported by a pillow. The clinician places a hand on top of the patient's shoulder. The patient's arm is placed in internal rotation and shoulder girdle protraction. The arm is then moved into horizontal adduction followed by the patient side bending the head away from the test side. The clinician now depresses the shoulder.

Adverse neural tension is an abnormal response to mechanical stimuli of neural tissue. The genesis of this abnormal tissue response can be from a variety of factors to include injuries (compression, vibration, and postsurgical), intraneural, extraneural, and anatomic.108 A factor that receives a significant amount of attention involves that of repetitive strain injuries specifically with the upper extremities.

The detrimental effects of immobilization on musculoskeletal structures are well documented as are the benefits of early mobilization protocols.109–118 The rationale behind the use of neural mobilization techniques is to attempt to restore the dynamic balance between the relative movement of neural tissues and surrounding mechanical interfaces, thereby allowing reduced intrinsic pressures on the neural tissue and improving nerve conduction velocity.13,43 By applying early mobilization to the neural system, it seems possible that similar benefits should occur. The hypothesized benefits from such techniques include facilitation of nerve gliding, reduction of nerve adherence, dispersion of noxious fluids, increased neural vascularity, and improvement of axoplasmic flow.43,119,120 However, an important distinction needs to be made between techniques that lengthen or stretch the dura and techniques that stretch the anatomic structures that surround the involved neural tissue.

Elvey18 recommends an initial intervention of passive, gentle, and controlled oscillatory movements to the anatomic structures that surround the neural tissue before progressing to the techniques that stretch both the surrounding tissues and the neural tissues together. Using this approach, the treatment barrier is represented by the onset of muscle activity.102 For example, in the cervical spine, the sequence of neurodynamic mobilizations is initiated with shoulder depression with the neck in neutral and the arm by the side followed by shoulder depression with fixation of the cervical spine, then shoulder depression, cervical fixation, and arm traction with the arm by the side. Once this progression has been performed without any adverse effects, the more specific movements used to isolate the nerve are employed.

Evidence for the efficacy of this gradual approach has been demonstrated in subjects with low back pain and radiculopathy,58,59,121 lateral epicondylalgia,122 and chronic cervicobrachial pain.18,123 Cleland and colleagues124 performed a pilot clinical trial to determine if slump stretching resulted in improvements in pain, centralization of symptoms, and disability in 30 patients with nonradicular low back pain with suspected mild to moderate neural mechanosensitivity. Patients were randomized to receive lumbar spine mobilization and exercise (n = 14) or lumbar spine mobilization, exercise, and slump stretching (n = 16). All patients were treated in physical therapy twice weekly for 3 weeks for a total of six visits. Upon discharge, outcome measures were reassessed. Independent t-tests were used to assess differences between groups at baseline and discharge. No baseline differences existed between the groups (P > 0.05). At discharge, patients who received slump stretching demonstrated significantly greater improvements in disability (9.7 points on the Oswestry Disability Index, P > 0.01), pain (0.93 points on the numeric pain rating scale, P > 0.001), and centralization of symptoms (P > 0.01) than patients who did not. The authors suggested that slump stretching is beneficial for improving short-term disability, pain, and centralization of symptoms and also recommended that future studies should examine whether these benefits are maintained at a long-term follow-up.124

A recent systematic review of randomized controlled trials with an analysis of therapeutic efficacy of neural mobilizations found only limited evidence to support its use.120 However, choosing the right technique for the right patient based on causal mechanism is fraught with difficulty when it comes to heterogenous groups.125

Stretching Program for the Sciatic Nerve

The home stretching exercise to improve tissue mobility and neural extensibility is performed in three phases or positions as follows:117

1. The patient is positioned supine with the hips and knees are flexed at a comfortable range. Using the uninvolved leg, the patient lifts the heel of the involved side up until he or she experiences a stretch (Fig. 11-14). This position is maintained for approximately 1 minute (can be performed up a wall to provide additional support).

2. From the position in step 1, the patient slides the heel further up. If this maneuver provokes any paresthesias, the patient allows the heel back down. Progress is measured by timing the period during which the patient is able to keep the knee straight.

3. The patient performs the same maneuver as in step 2 but with a pillow under the head. This stretch is performed 3–5 times a day for 3–5 minutes at a time.

Stretches for the Upper Extremity Nerves

The recommended home stretching exercise to improve tissue mobility and neural extensibility of the peripheral nerves throughout the upper extremity is performed in four phases or positions as follows:117

1. The patient is seated with the cervical spine in neutral sidebending and the arm abducted to 90 degrees. The patient is asked to extend the fingers and to begin flexing the elbow while sidebending toward the elevated arm (Fig. 11-15A).

2. Keeping the upper extremity in the same position, the patient is asked to side bend the head away from the elevated arm (Fig. 11-15B). When a gentle stretch is felt, the position is held for 10–15 seconds.

3. When the patient is able to maintain the previous stretch for 30–60 seconds, trunk rotation away from the involved side is added.

4. Once full trunk rotation is achieved, various positions of cervical side bending and elbow flexion/extension can be attempted (Fig. 11-15C). For example, elbow extension combined with contralateral cervical side bending. To increase tension, forearm supination or pronation can be superimposed on the elbow motions.

Each position is held for 7 seconds and is repeated five times per session.

A series of home stretching exercise to improve tissue mobility and neural extensibility of the median nerve in cases of carpal tunnel syndrome have been advocated. Theoretically, stretching exercises of the median nerve affect symptom resolution in a carpal tunnel syndrome by126

• stretching the adhesions
• broadening the longitudinal area of contact between the median nerve and the transverse carpal ligament
• reducing tenosynovial edema by a milking action
• improving venous return from the nerve bundles
• reducing pressure inside the carpal tunnel

Six positions are used for mobilization of the median nerve at the wrist:

1. The wrist in neutral, with the fingers and thumb in flexion

2. The wrist in neutral, with the fingers and thumb extended

3. The wrist and fingers extended, with the thumb in neutral

4. The wrist, fingers, and thumb extended

5. The wrist, fingers, and thumb extended, with the forearm supinated

6. The wrist, fingers, and thumb extended, with the forearm supinated and the other hand gently stretching the thumb

Each position is held for 7 seconds and is repeated five times per session.126 All of the exercises performed in the clinic should be performed by the patient at home whenever possible.

• 1. List the number of mechanisms that are hypothesized to contribute to an injury of the peripheral nerve trunk.

• 2. Which term is used to describe a serial compromise of axonal transport along the same nerve fiber, causing a subclinical lesion at the distal site to become symptomatic?

• 3. In addition to complaints of pain, what other signs and symptoms are likely to be present with a diagnosis of neurodynamic tension?

• 4. The SLR test exerts a caudal traction on which of the lumbosacral nerve roots?

• 5. Within which range of the SLR are positive findings more significant for a decrease in neurodynamic mobility?

Answers