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Strain and Excursion of the Sciatic, Tibial, and

Plantar Nerves during a Modified Straight Leg Raising Test


Michel W. Coppieters,1,2 Ali M. Alshami,1 Awais S. Babri,3 Tina Souvlis,1 Vaughan Kippers,3 Paul W. Hodges1
1

Division of Physiotherapy, School of Health and Rehabilitation Sciences, The University of Queensland,
QLD 4072 St. Lucia, Australia
2

Neuro Orthopaedic Institute, 19 North Street, Adelaide, SA 5000, Australia

3
Department of Anatomy and Developmental Biology, School of Biomedical Sciences,
The University of Queensland, QLD 4072 St. Lucia, Australia

Received 7 December 2005; accepted 2 March 2006


Published online 12 July 2006 in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jor.20210
ABSTRACT: A modified straight leg raising (SLR) in which ankle dorsiflexion is performed before
hip flexion has been suggested to diagnose distal neuropathies such as tarsal tunnel syndrome. This
study evaluates 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 calliper.
Ankle dorsiflexion resulted in a significant strain and distal excursion of the tibial nerve. With the
ankle in dorsiflexion, the proximal excursion and tension increase in the sciatic nerve associated with
hip flexion were transmitted distally along the nerve from the hip to beyond the ankle. As hip flexion
had 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 the moving joint, mechanical forces acting on peripheral
nerves are transmitted well beyond the moving joint. 2006 Orthopaedic Research Society.
Published by Wiley Periodicals, Inc. J Orthop Res 24:18831889, 2006

Keywords:
fasciitis

nerve biomechanics; straight leg raise; diagnosis; neurodynamics; plantar

INTRODUCTION
Passive straight leg raising (SLR) is performed in
patients with low back or leg pain to test for
lumbosacral nerve root irritation.1,2 It is considered a diagnostic standard and is used widely.1
However, the range of SLR does not uniquely
reflect nerve involvement in lumbar spine conditions as the test is also frequently used to measure
the length of the hamstring muscles.3,4 Structural
differentiation is made by the addition of sensitizing maneuvers or qualifying signs, such as ankle
dorsiflexion,5 to increase strain in the lumbosacral
plexus without affecting the hamstring muscles.
The addition of ankle dorsiflexion at the angle of
hip flexion at which pain is produced has become
an integral part of the SLR.1

Correspondence to: Michel W. Coppieters (Telephone: 61


(0)7 3365 4590; Fax: 61 (0)7 3365 2775;
E-mail: m.coppieters@uq.edu.au)
2006 Orthopaedic Research Society. Published by Wiley Periodicals,
Inc.

While maintaining the knee in extension, Smith


et al.2 demonstrated that hip flexion induced a 0.5
5 mm longitudinal excursion of the L4, L5, and S1
spinal nerves, a transverse movement toward the
pedicle, and a 2%4% increase in strain. The
amount of longitudinal movement was in agreement with earlier findings.6 Despite the widespread use of ankle dorsiflexion as a sensitizing
maneuver, the supposition that this additional
movement increases strain in the lumbosacral
plexus remains unexamined.
To diagnose more distally located neuropathies,
such as tarsal tunnel syndrome, and medial
and lateral plantar neuropathies, a modified SLR
with a tibial nerve bias (SLRTIBIAL) has been
suggested.79 Compared to the traditional SLR,
the main modification comprises reversal of the
movement sequence. In the modified SLR, ankle
dorsiflexion is performed before hip flexion. Hip
flexion can therefore be regarded as a sensitizing
maneuver, as the strain increase in the sciatic
nerve associated with hip flexion is thought to be
transmitted distally to place greater mechanical
JOURNAL OF ORTHOPAEDIC RESEARCH SEPTEMBER 2006

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COPPIETERS ET AL.

forces on the nerves around the ankle and foot


without challenging local structures, such as the
plantar fascia. A second modification consists of a
more precise positioning of the ankle and foot. Ankle
dorsiflexion is combined with eversion to further
challenge the tibial nerve. In a case report, Meyer
et al.10 were able to reproduce a patients neurogenic
plantar heel pain utilizing the SLRTIBIAL.
Symptoms could not be reproduced when SLR was
performed without ankle dorsiflexion.
The first reference to using the SLR in patients
with tarsal tunnel syndrome was published in
1974,11 and various textbooks describe the modified
SLR as a diagnostic test to differentially diagnose
foot and ankle conditions.8,9,12 However, there is
limited clinical and no anatomical evidence for the
assumption that increased tension in the sciatic
nerve as a result of hip flexion is transmitted
distally as far as the tibial and plantar nerves.
Since the modified SLR aims to investigate
increased mechanosensitivity of a peripheral
nerve around the ankle or foot, an increase in
strain with hip flexion in the tibial nerve and its
branches is essential in order to be able to
differentially diagnose nerve involvement from
other conditions.
The primary aim of the present study was to
measure strain in the sciatic, tibial, and
plantar nerves during the different components of
SLRTIBIAL. We hypothesize that in addition to
ankle dorsiflexion, hip flexion will significantly
increase strain in the tibial nerve around the ankle
and its branches. The secondary aim was to
measure strain in the plantar fascia during
SLRTIBIAL. Confirmation of the primary hypothesis
in combination with no change in strain in the
plantar fascia will provide support to use SLRTIBIAL
to differentiate between plantar heel pain caused
by a neuropathy or by plantar fasciitis.

METHODS
Cadavers
Eight male embalmed cadavers (age range at time of
death: 7690 years) which displayed no evidence of
trauma or deformity to the spine or lower extremity
were used in this study. Kleinrensink et al.13,14 investigated the effect of embalmment and concluded that it
is justified to obtain data from embalmed cadavers to
analyze the effect of limb movement on strain in
peripheral nerves. It should be noted however that an
in depth analysis of the effects of embalmment on
mechanical properties of nerves, such as elasticity and
maximal tensile strength, is not available. Ethical
approval for the study was obtained from the Institutional Ethics Committee.
JOURNAL OF ORTHOPAEDIC RESEARCH SEPTEMBER 2006

Electrogoniometer
Inclinometer

Figure 1. The modified straight leg raising test


(SLRTIBIAL). To bias the test towards the tibial
nerve, the ankle is dorsiflexed (1) before hip flexion is
performed (2).

Straight Leg Raising Test


SLRTIBIAL was performed with the cadavers in supine
(Fig. 1). In the first stage, the ankle was moved from
plantar flexion into dorsiflexion. The mobility of the
ankle did not allow the addition of eversion. In the
second stage, the hip was flexed while the ankle was
maintained in dorsiflexion and the knee in extension.
Depending on the available range of motion, the ankle
was moved into 1520 degrees dorsiflexion and the hip
was flexed 7080 degrees.
An electronic inclinometer (Accustar, Schaevitz Sensors, Hampton, Virginia) was placed proximal to the
lateral femoral condyle to measure the range of hip
flexion during SLRTIBIAL. A twin axis electrogoniometer
(SG65, Biometrics, Blackwood, UK) was attached to the
lateral side of the ankle to measure the position of the
ankle. A second electrogoniometer (SG110) was attached
to the lateral side of the knee to verify that the knee was
maintained in extension throughout the experiment.
During the test, the angle of the hip, knee, and ankle were
displayed on a monitor, which also displayed the target
angles. Real-time feedback assisted the investigator to
exactly reach the target positions for each test.
Strain Measurements
Two linear displacement transducers with a stroke
length of 6 mm and a resolution of 1.5 mm were used to
measure strain in the sciatic, tibial, and plantar nerves,
and in the plantar fascia [differential variable reluctance transducers (DVRT), Microstrain, Burlington,
VT]. Although previous studies have demonstrated the
usefulness of these transducers to measure strain in
nerve trunks,1517 we used three consecutive repetitions
of SRLTIBIAL in five cadavers to calculate the intraclass
correlation coefficient [ICC(2,1)] and standard error of
measurement (SEM) as measures of reliability for
the strain in the tibial nerve around the ankle. The
analysis revealed that the strain measurements were
reliable in the different position of SLRTIBIAL [mean
ICC(2,1) 0.75; mean SEM 0.34%].
The strain gauges were fixed by insertion of two
barbed pins into, but not through, the structure under
DOI 10.1002/jor

NERVE STRAIN DURING STRAIGHT LEG RAISING

investigation. For the smaller nerves and plantar fascia,


the barbed pins provided by the manufacturer were
shortened to accommodate for the thinness of the
structures. Calibration equations provided by the manufacturer were used to convert voltage measurements
into length measurements. An arbitrary reference position was chosen in relation to which changes in strain
were expressed. In the reference position, the angle
between the lower leg and the fifth metatarsal was
90 degrees, the knee was in extension and there was no
hip flexion. Changes in strain (percentage strain)
were calculated based on the change in nerve length
compared to the length in the arbitrary reference
position. Throughout the experiment, the investigator
was blinded to the output of the strain gauges.
Excursion Measurements
A digital Vernier calliper was used to measure the
excursion of the nerve in relation to its surrounding
structures. A fixed marker was screwed into the cortical
bone and consisted of a metal L-shaped pin which
was placed perpendicularly over the nerve bedding. As a
mobile marker, a suture was placed around the nerve in
the vicinity of the fixed marker.15 The locations for the
fixed markers were (1) the medial side of the tibia,
proximal to the malleolus, to measure tibial nerve
excursion at the ankle; (2) the dorsal side of the femur,
proximal and lateral to the medial condyle for tibial
nerve excursion at the knee; and (3) the dorsal side of the
femur, distal to the greater trochanter for sciatic nerve
excursion.
Dissection
Although all dissections were carefully planned to
minimize disruption of surrounding soft tissues and
local biomechanics, some structures had to be excised.
To insert the DVRT in the tibial nerve at the ankle, a
window of approximately 7  4 cm was made into the
skin and underlying subcutaneous tissues. An 8-cm
section of the Achilles tendon was excised close to the
insertion into the calcaneus to obtain a physiological
range of ankle dorsiflexion. The deep fascia was incised
to expose the neurovascular bundle, and the posterior
tibial vessels were excised as these vessels cover the
tibial nerve. The flexor retinaculum remained intact.
The DVRT was positioned 2.53.0 cm proximal to the tip
of the medial malleolus. If the muscle belly of the flexor
hallucis longus hindered the sliding of the DVRT, the
belly was trimmed, leaving the tendon intact. An
incision of a similar size was made in the skin of the
sole of the foot for the strain measurements in
the plantar fascia. Subcutaneous fat was cleared and
the DVRT was inserted in the proximal third of the
plantar fascia, in line with the second digit.
At the knee, the skin and popliteal fascia were incised
to expose the tibial nerve. The DVRT was inserted
approximately 2 cm proximal to the level of the knee joint.
If fibers of the semimembranosus muscle hindered the
DOI 10.1002/jor

1885

sliding of the DVRT, the belly was trimmed. The popliteal


vessels were kept intact. A larger incision had to be
made for the sciatic nerve (10  15 cm). Given its deep
location, the lower part of the gluteus maximus, and
proximal parts of the long head of biceps femoris
and semimembranosus were excised. The DVRT was
inserted in the medial (tibial) component of the sciatic
nerve, approximately 2 cm distal to the ischial tuberosity.
The DVRTs for the medial and lateral planter nerve
were inserted through the same window that was made
to expose the plantar fascia. The plantar fascia was
released from the calcaneus and excised to the level of the
heads of the metatarsals. The flexor digitorum brevis
which overlies the plantar nerves was removed. The
second muscle layer was left intact, although in some
cadavers the muscle belly of the abductor hallucis was
trimmed if its fibers hindered the sliding of the DVRT in
the medial plantar nerve, which was inserted approximately 8 cm distal to the calcaneal tuberosity. The DVRT
for the lateral plantar nerve was inserted approximately
5 cm distal to the calcaneal tuberosity, before the nerve
divides into its terminal branches.
Data Collection and Analysis
Strain and excursion measurements were first collected
for the tibial nerve at the ankle and the plantar fascia;
subsequently for the tibial nerve at the popliteal fossa
and the sciatic nerve, and finally for the medial and
lateral plantar nerves. The dissection was also performed in three stages to minimize the time that
structures were exposed before the measurements were
obtained. For all sites, strain and excursion measurements were obtained during three consecutive repetitions of SLRTIBIAL.
The output from the strain gauges, electrogoniometers, and inclinometer was connected to a data
acquisition system (Micro 1401, Cambridge Electronic
Design, Cambridge, UK), which sampled at 50 Hz using
Spike 2 software. From the continuous data sets, the
strain in the different positions was determined. Results
were analyzed using a two-way repeated-measures
analysis of variance (ANOVA) with two repeated-measures factors (STRUCTURE with six levels, and POSITION with three levels). Duncans multiple comparison
tests were used for post-hoc comparison. In addition,
Friedman ANOVAs and Wilcoxon matched pairs tests
were calculated if an increase in strain was observed in at
least two-thirds of the cadavers, with a mean increase of
at least 1%, when the parametric tests failed to reach
significance due to a relatively small sample size and
large variability. For all tests, the level of significance
was set at p < 0.05.

RESULTS
Test Characteristics
In the first stage of SLRTIBIAL, the ankle was
moved 55.3  8.5 degrees, from 39.4  7.1 degrees
plantar flexion to 15.9  1.8 degrees dorsiflexion.
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COPPIETERS ET AL.

During this maneuver, the angle at the knee and


hip remained practically unchanged (0.8  0.7
degrees extension at the knee and 0.6  0.5
degrees extension at the hip). In the second stage,
the hip was flexed 74.6  2.9 degrees, while the
position of the other joints remained virtually
unchanged (0.3  0.2 degrees extension at the
knee and 0.3  0.1 degrees dorsiflexion at the
ankle).
Strain

Sciatic nerve (medial portion)


Tibial nerve (knee)

+6%

Tibial nerve (ankle)


Medial plantar nerve

+5%
+4%

Lateral plantar nerve


Plantar fascia

+3%
+2%
+1%
Strain in
reference
position
-1%
-2%
-3%

Location
Sciatic nerve
Tibial nerve (knee)
Tibial nerve (ankle)
Medial plantar nerve

Figure 2 illustrates the strain in the different


structures for the three different positions of
SLRTIBIAL. The change in strain as a result of
ankle dorsiflexion and hip flexion with the ankle in
dorsiflexion is summarized in Table 1.
The analysis of variance revealed a significant interaction (STRUCTURE  POSITION,
p < 0.0001), indicating that the pattern of changes
in strain during SLRTIBIAL differed between structures. Post-hoc analysis indicated that during
ankle dorsiflexion, strain increased significantly
in the tibial nerve around the ankle ( p 0.0002)
and in the medial ( p 0.009) and lateral plantar

+7%

Table 1. Mean Change (SD) in Strain as a Result of


the Movements Ankle Dorsiflexion (DF) and Hip Flexion
During SLRTIBIALa

ANKLE in PF

ANKLE in DF

HIP in FLEXION

NO HIP FLEXION

NO HIP FLEXION

ANKLE in DF

Figure 2. Differences in strain relative to the reference position for the different nerves and plantar fascia
in the three different positions of the SLRTIBIAL. In the
reference position, there was a 90 degree angle between
the fifth metatarsal and the lower leg, the knee was in
extension, and there was no hip flexion. ANKLE in PF:
ankle positioned in plantar flexion with the knee in
extension and no hip flexion; ANKLE in DF: ankle in
dorsiflexion with the knee in extension and no hip flexion;
HIP in FLEXION: hip in flexion with the ankle in
dorsiflexion and the knee extended.
JOURNAL OF ORTHOPAEDIC RESEARCH SEPTEMBER 2006

Lateral plantar nerve


Plantar fascia

Ankle DF

Hip Flexion

0.02 (0.02)NS
[1/8]
0.48 (0.36)NS
[8/8]
3.28 (1.64)S
[8/8]
2.24 (2.19)S
[7/8]
1.67 (2.06)S
[8/8]
2.74 (4.90)S*
[7/8]

6.61 (1.52)S
[8/8]
5.49 (1.43)S
[8/8]
2.30 (0.82)S
[7/8]
1.22 (0.88)S*
[8/8]
1.06 (1.88)NS
[7/8]
0.17 (0.13)NS
[7/8]

S, significant change; NS, nonsignificant change; S*, significant change but only with nonparametric tests.
a
For both test components, the number of cadavers demonstrating an increase in strain is indicated between square
brackets.

nerve ( p 0.038). There was no significant


increase in strain in the sciatic ( p 0.959) or tibial
nerve at the knee ( p 0.239). Despite the relatively
large increase in strain in the plantar fascia, and
the fact that an increase was observed in all but one
of the cadavers, the increase did not reach the level
of significance ( p 0.072). As this was partly due to
a relatively large variability in strain between
subjects, the nonparametric test showed a significant difference ( p 0.025).
While keeping the ankle in dorsiflexion, hip
flexion resulted in an increase in strain in the
sciatic nerve ( p < 0.0001), and in the tibial nerve at
the knee ( p 0.0002) and ankle ( p 0.0007). There
was no increase in strain in the plantar fascia
( p 0.906). The relatively large increase in strain
was not significant for the medial ( p 0.123) or
lateral plantar nerve ( p 0.167), despite the fact
that all (medial plantar nerve) or 7/8 (lateral
plantar nerve) cadavers showed an increase.
However, when analyzed with nonparametric
tests, the increase was significant for the medial
plantar nerve ( p 0.017), but did not reach the
level of significance for the lateral plantar nerve
( p 0.068).
Excursion
The greatest movement of the nerve occurred
nearest the moving joint, but the excursion was
not limited to this area (Fig. 3). The direction of the
excursion was always towards the moving joint.
Ankle dorsiflexion resulted in a distal excursion of
DOI 10.1002/jor

NERVE STRAIN DURING STRAIGHT LEG RAISING

9.5

Tibial nerve (ankle)

6.4
Tibial nerve (knee)

3.1

*
**

12.2
Sciatic nerve (medial portion)

NS

28.0
35

30

25

20

Ankle dorsiflexion
Hip flexi
flexion

15

**
**

10

**
5

10
Distal

15

Nerve excursion (mm)


Proximal

Figure 3. Excursion of the sciatic and tibial nerve


following ankle dorsiflexion and hip flexion during
SLRTIBIAL. Nerve excursion was the largest nearest the
moving joint, but extended to neighboring joints with
ankle dorsiflexion and even to nonadjacent joints with
hip flexion. The asterisks indicate the level of significance
for the excursion (*: p < 0.01; **: p  0.001). Black bars
indicate distal excursion, whereas white bars indicate
proximal excursion. Note that the nerve always moved
toward the moving joint.

the tibial nerve at the ankle ( p 0.0001) and knee


( p 0.004), but caused no significant excursion of
the sciatic nerve ( p 0.192). While maintaining
the ankle in dorsiflexion, hip flexion resulted in a
proximal excursion of the sciatic ( p < 0.0001) and
tibial nerve at the knee ( p < 0.0001) and ankle
( p 0.0001).

DISCUSSION
Strain and excursion in the sciatic, tibial, and
plantar nerves were measured to evaluate the
clinical assumption which underpins the use of a
modified SLR (SLRTIBIAL) in the diagnosis of distal
neuropathies, such as tarsal tunnel syndrome. It is
assumed that following ankle dorsiflexion, the
component of hip flexion in SLRTIBIAL further
increases the mechanical forces acting on the tibial
nerve in the tarsal tunnel. The findings of this
study support this hypothesis.
The results demonstrate that joint movements
which elongate the nerve bedding result in a
significant increase in strain in nearby nerves
and excursion of the nerve towards the moving
joint. This is consistent with human upper limb16,17
and animal studies.18 In agreement with earlier
work by Daniels et al.,19 ankle dorsiflexion
increased strain in the tibial nerve around the
ankle (3.3%) and resulted in a considerable distal
excursion (9.5 mm). With dorsiflexion, the tibial
DOI 10.1002/jor

1887

nerve is further challenged by a considerable


increase in pressure in the tarsal tunnel, from
47 mm Hg in a neutral position to 1520 mm
Hg.20 However, more interestingly is that although
the greatest strain and excursion occurred nearest
the moving joint, the strain was transmitted
along the nerve well beyond the neighboring joint.
The component of hip flexion in SLRTIBIAL resulted
in a significant excursion (6.5 mm) and increase in
strain (2.3%) in the tibial nerve at the ankle. It is
remarkable that the effect of hip flexion on the
increase in strain and excursion of the tibial nerve
around the ankle was as large as approximately
two-thirds of the strain induced by ankle dorsiflexion. This is especially interesting when considering
that the tibial nerve was already pre-stretched by
ankle dorsiflexion. Furthermore, the increase in
tension as a result of hip flexion was transmitted
into the medial (1.2%) and lateral (1.1%) plantar
nerves in the foot. Due to the variability, however,
this increase did not reach the level of statistical
significance for the LPN.
The findings of this study reflect the ability of the
nervous system to stretch and glide to accommodate for an increase in length of the nerve bedding.
Distribution of tension over a longer section of a
nerve may avoid localized peak elongation of a
magnitude that would impair nerve function, such
as microcirculation,2123 axonal transport,24 and
nerve conduction.25 Animal models have demonstrated that 5%10% elongation results in
impaired blood flow,21,22 with a complete arrest of
intraneural circulation at an elongation of approximately 15%.23 At 11% strain, axonal transport is
inhibited24 and the amplitude of the action potential is reduced by 70% following a 1 h sustained
elongation of 6%.25
Under normal conditions, nerve fibers are able to
comply with low to moderate strain or compression
associated with physiological joint movements.
However, in peripheral neuropathies, mechanosensitivity increases and ectopic activity may
occur.26,27 Following local neural inflammation,
nerve fibers become sensitive to stretch as little as
3% and to low intensity pressure.28 Increased
mechanosensitivity of the tibial nerve or its
branches to tension and pressure is the most likely
mechanism behind the reproduction of pain with
SLRTIBIAL in patients with tarsal tunnel syndrome,
as demonstrated in a case report by Meyer et al.10
Furthermore, an animal model showed that 7 days
after nerve injury, nerve strain induced with SLR
and ankle dorsiflexion was increased, demonstrating that nerve injury changes the mechanical
properties of the nerve.18
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COPPIETERS ET AL.

The findings of this study lend support for the


use of SLRTIBIAL in the differential diagnosis of
plantar heel pain. Plantar heel pain is common29,30
and several conditions, such as plantar fasciitis,
tarsal tunnel syndrome, entrapment of the plantar
nerves, calcaneus fracture, rupture of the plantar
fascia, and atrophy of the heel pad may lead to
plantar heel pain.30 Although plantar fasciitis
is the most prevalent cause of plantar heel pain,
tarsal tunnel syndrome is common31 and is considered one of the most commonly overlooked
causes of chronic heel pain.32 When the symptom triad of pain, paresthesia, and numbness
is present, the diagnosis of tarsal tunnel syndrome is straightforward. However, clinical
findings may vary and symptoms are commonly vague and diffuse, which makes diagnosis
difficult.33,34
Several clinical tests have been suggested to
differentiate tarsal tunnel syndrome from other
sources of plantar heel pain. Analogous to clinical
tests for carpal tunnel syndrome, Tinels test, the
plantar flexion-inversion test and a nerve compression test have been suggested.35,36 However, sound
validity studies which demonstrate the diagnostic
accuracy of these tests are lacking. Kinoshita
et al.37 described a test for tarsal tunnel syndrome
in which the ankle is everted and dorsiflexed and
the metatarsophalangeal joints dorsiflexed.
Although the authors state that the pain induced
with this test is different from pain associated with
plantar fasciitis, the test resembles the Windlass
test. In the Windlass test, which was designed to
asses the plantar fascia, the first metatarsophalangeal joint is dorsiflexed with the ankle in
90 degrees.38,39 A recent anatomical study demonstrated that both the Windlass and the dorsiflexioneversion test increase strain in both the tibial nerve
and plantar fascia, complicating the differential
diagnosis of plantar heel pain.40 As the component
of hip flexion in SLRTIBIAL stretches the tibial nerve
in the tarsal tunnel, but has no effect on the plantar
fascia, the SLRTIBIAL may be a useful clinical test
to structurally differentiate the tissue origin of
plantar heel pain. The cumulative effect of ankle
dorsiflexion and hip flexion on strain in the tibial
nerve in the tarsal tunnel demonstrates that
elongation of a larger segment of the nerve bedding
places larger mechanical forces on the tibial
nerve in the tarsal tunnel than ankle dorsiflexion
alone. This increased mechanical provocation
may be useful in patients with vague and diffuse
symptoms in which it is often harder to reproduce
symptoms and more difficult to make the diagnosis
of tarsal tunnel syndrome.33,34
JOURNAL OF ORTHOPAEDIC RESEARCH SEPTEMBER 2006

A limitation of the present study was that the


Achilles tendon had to be transected to obtain a
physiological range of ankle dorsiflexion. A continuous fascial network has been described to run
between the hip and ankle.41 Although there is no
data to confirm that mechanical forces can be
transmitted along this myofascial system from the
hip to the ankle and into the foot, we cannot
rule out that this system may alter strain in the
plantar fascia during the hip flexion component of
SLRTIBIAL. It should also be noted that ankle
eversion was not included during SLRTIBIAL in this
study. Given the limited range of eversion when
combined with ankle dorsiflexion, we do not believe
that the addition of ankle eversion would have
altered our conclusions. In the clinical setting,
however, we do recommend including eversion to
further challenge the tibial nerve and its branches
at the foot and ankle.
In conclusion, when the diagnosis of tarsal
tunnel syndrome is based on history and
clinical findings, the diagnosis will gain strength
if symptoms can be reproduced or increased with
SLRTIBIAL, as the findings of this study demonstrate that hip flexion increases the strain in the
tibial nerve at the tarsal tunnel, without affecting
other musculoskeletal structures at the painful
site, such as the plantar fascia.

REFERENCES
1. Rebain R, Baxter GD, McDonough S. 2002. A systematic
review of the passive straight leg raising test as a
diagnostic aid for low back pain (1989 to 2000). Spine 27:
E388E395.
2. Smith SA, Massie JB, Chesnut R, et al. 1993. Straight leg
raising. Anatomical effects on the spinal nerve root
without and with fusion. Spine 18:992999.
3. Feland JB, Marin HN. 2004. Effect of submaximal
contraction intensity in contract-relax proprioceptive
neuromuscular facilitation stretching. Br J Sports Med
38:E18.
4. Halbertsma JP, Goeken LN, Hof AL, et al. 2001. Extensibility and stiffness of the hamstrings in patients with
nonspecific low back pain. Arch Phys Med Rehabil 82:232
238.
5. Troup JD. 1981. Straight-leg-raising (SLR) and the
qualifying tests for increased root tension: their predictive value after back and sciatic pain. Spine 6:526
527.
6. Goddard MD, Reid JD. 1965. Movements induced by
straight leg raising in the lumbo-sacral roots, nerves and
plexus, and in the intrapelvic section of the sciatic nerve.
J Neurol Neurosurg Psychiatry 28:1218.
7. Butler DS. 1991. Mobilisation of the nervous system.
Melbourne: Churchill Livingstone.
8. Butler DS. 2000. The sensitive nervous system. Unley,
Australia: Noigroup Publications.
DOI 10.1002/jor

NERVE STRAIN DURING STRAIGHT LEG RAISING

9. Magee D. 1997. Orthopedic physical assessment. Philadelphia: Saunders.


10. Meyer J, Kulig K, Landel R. 2002. Differential diagnosis
and treatment of subcalcaneal heel pain: a case report.
J Orthop Sports Phys Ther 32:114122.
11. Mann RA. 1974. Tarsal tunnel syndrome. Orthop Clin
North Am 5:109115.
12. Grieve GP, Boyling JD, Palastanga N. 1994. Grieves
modern manual therapy: the vertebral column. Edinburgh:
Churchill Livingstone.
13. Kleinrensink GJ, Stoeckart R, Mulder PG, et al. 2000.
Upper limb tension tests as tools in the diagnosis of nerve
and plexus lesions. Anatomical and biomechanical aspects.
Clin Biomech 15:914.
14. Kleinrensink GJ, Stoeckart R, Vleeming A, et al. 1995.
Peripheral nerve tension due to joint motion. A comparison
between embalmed and unembalmed human bodies. Clin
Biomech 10:235239.
15. Byl C, Puttlitz C, Byl N, et al. Strain in the median and
ulnar nerves during upper-extremity positioning. J Hand
Surg [Am] 27:10321040.
16. Wright TW, Glowczewskie F Jr, Cowin D, et al. 2001.
Ulnar nerve excursion and strain at the elbow and wrist
associated with upper extremity motion. J Hand Surg [Am]
26:655662.
17. Wright TW, Glowczewskie F, Wheeler D, et al. 1996.
Excursion and strain of the median nerve. J Bone Joint
Surg [Am] 78:18971903.
18. Boyd BS, Puttlitz C, Gan J, et al. 2005. Strain and
excursion in the rat sciatic nerve during a modified
straight leg raise are altered after traumatic nerve injury.
J Orthop Res 23:764770.
19. Daniels TR, Lau JT, Hearn TC. 1998. The effects of foot
position and load on tibial nerve tension. Foot Ankle Int
1998; 19:7378.
20. Kumar K, Deshpande S, Jain M, et al. 1988. Evaluation of
various fibro-osseous tunnel pressures (carpal, cubital and
tarsal) in normal human subjects. Indian J Physiol
Pharmacol 32:139145.
21. Driscoll PJ, Glasby MA, Lawson GM. 2002. An in vivo
study of peripheral nerves in continuity: biomechanical
and physiological responses to elongation. J Orthop Res
20:370375.
22. Lundborg G, Rydevik B. 1973. Effects of stretching the
tibial nerve of the rabbit. J Bone Joint Surg [Br] 55:390
401.
23. Ogata K, Naito M. 1986. Blood flow of peripheral nerve
effects of dissection, stretching and compression. J Hand
Surg [Br] 11:1014.
24. Dahlin LB, McLean WG. 1986. Effects of graded experimental compression on slow and fast axonal transport in
rabbit vagus nerve. J Neurol Sci 72:1930.

DOI 10.1002/jor

1889

25. Wall EJ, Massie JB, Kwan MK, et al. 1992. Experimental
stretch neuropathy. Changes in nerve conduction under
tension. J Bone Joint Surg [Br] 74:126129.
26. Devor M, Seltzer Z. 1999. Pathophysiology of damaged
nerves in relation to chronic pain. In: Wall PD, Melzack R,
editors. Textbook of pain, 4th ed. Edinburgh: Churchill
Livingstone.
27. Eliav E, Benoliel R, Tal M. 2001. Inflammation with no
axonal damage of the rat saphenous nerve trunk induces
ectopic discharge and mechanosensitivity in myelinated
axons. Neurosci Lett 311:4952.
28. Dilley A, Lynn B, Pang SJ. 2005. Pressure and stretch
mechanosensitivity of peripheral nerve fibres following
local inflammation of the nerve trunk. Pain 117:462
472.
29. Schepsis AA, Leach RE, Gorzyca J. 1991. Plantar fasciitis.
Etiology, treatment, surgical results, and review of the
literature. Clin Orthop Relat Res 266:185196.
30. Schon LC, Glennon TP, Baxter DE. 1993. Heel pain
syndrome: electrodiagnostic support for nerve entrapment.
Foot Ankle 14:129135.
31. Barrett SJ, OMalley R. 1999. Plantar fasciitis and other
causes of heel pain. Am Fam Physician 59:22002206.
32. Pfeffer GB. 1995. Plantar heel pain. In: Baxter DE, editor.
The foot and ankle in sport. St. Louis: Mosby; p 195
206.
33. Finkel JE. 1994. Tarsal tunnel syndrome. Magn Reson
Imaging Clin N Am 1994; 2:6778.
34. Kuper BC. 1998. Tarsal tunnel syndrome. Orthop Nurs 17:
915.
35. Bailie DS, Kelikian AS. 1998. Tarsal tunnel syndrome:
diagnosis, surgical technique, and functional outcome.
Foot Ankle Int 19:6572.
36. Jolly GP, Zgonis T, Hendrix CL. 2005. Neurogenic heel
pain. Clin Podiatr Med Surg 22:101113.
37. Kinoshita M, Okuda R, Morikawa J, et al. 2001. The
dorsiflexion-eversion test for diagnosis of tarsal tunnel
syndrome. J Bone Joint Surg [Am] 83:18351839.
38. Brown C. 1996. A review of subcalcaneal heel pain
and plantar fasciitis. Aust Fam Physician 1996; 25:875
881.
39. De Garceau D, Dean D, Requejo SM, et al. 2003. The
association between diagnosis of plantar fasciitis and
Windlass test results. Foot Ankle Int 24:251255.
40. Alshami AM, Babri AS, Souvlis T, et al. 2007. Biomechanical evaluation of two clinical tests for planter heel pain:
the dorsiflexion-eversion test for tarsal tunnel syndrome
and the windlass test for plantar fasciitis. Foot Ankle Int
28: in press.
41. Gerlach UJ, Lierse W. 1990. Functional construction of the
superficial and deep fascia system of the lower limb in man.
Acta Anat (Basel) 139:1125.

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