SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 17

The differential diagnosis of 
neurogenic and referred leg pain

JA Louw MBChB(Pret), MMed(Orth), PhD, MD
Full-time private practice, Pretoria, South Africa

Correspondence:
Dr JA Louw
PO Box 24

Moreleta Plaza
0167

Introduction
Leg pain is a common presenting symptom of lumbar disc
herniation due to neurological compression. If conser-
vative management fails, a large number of these patients
might undergo lumbar spine surgery. Magnetic resonance
imaging (MRI) is considered to be the cornerstone special
investigation to confirm the diagnosis of a lumbar disc
herniation. However, between 38% and 52% of asympto-
matic individuals demonstrated significant lumbar disc
bulging on MRI.1,2 Given the high prevalence of these
findings and of back pain, the discovery by MRI of disc
bulges may frequently be coincidental and the leg pain
caused by an unrelated condition. It is therefore essential
to consider all possible aetiological factors when evalu-
ating leg pain.

Literature reviews combined with the author’s personal
experience in the examination of more than 15 000 patients
with back pain were used to propose an aetiological classi-
fication of conditions to consider when evaluating leg
pain.

Conditions to consider when evaluating leg pain

1. Systemic conditions
Metabolic neuropathy
Diabetes mellitus is the most common metabolic
neuropathy. Its most common presentation is the distal
symmetrical polyneuropathy with bilateral symmetrical
pain in the lower extremities starting distally and moving
proximally.3,4 Other subtypes include proximal diabetes,
truncal, cranial, median and ulnar neuropathies. Diabetic
autonomic neuropathy affects each tissue, organ and
system in the whole body and is strongly involved in the
development of foot ulceration.5

A less common diabetes presentation is diabetic
amyotrophy6 which has most probably a vasculitis
aetiology with ischaemia followed by axonal degeneration
and demyelination. The main features are unilateral
weakness, wasting and pain most commonly in the
quadriceps. It spreads later to the contralateral side in an
asymmetrical manner.

Abstract
Background:
Neurogenic and referred leg pain are some of the most challenging clinical problems in spinal surgery due to the
diversity of conditions that can act as aetiological factors.
Methods:
The literature was reviewed and combined with case studies to demonstrate different aetiological factors.
Results:
At least 300 conditions were identified that might cause neurogenic and referred leg pain. An aetiological classi-
fication of neurogenic and referred leg pain is presented. The classification includes systemic conditions, condi-
tions from the brain, spinal cord, cervical and thoracic spinal canal, lumbar spinal canal, lumbar nerve root canal,
lumbar extraforaminal area, the pelvis and the lower extremity. Each one of these conditions can mimic a lumbar
disc herniation accurately.
Conclusion:
The aetiological classification can be used as a checklist when evaluating neurogenic and referred leg pain. Each
condition deserves careful consideration and when overlooked might result in a missed diagnosis.
Key words: neurogenic, leg pain, nerve root

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 17



Page 18 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

Other metabolic neuropathies to consider are alcoholic
and uraemic neuropathies.7,8

Vasculitic neuropathy
The primary pathology of vasculitic neuropathies is a
vasculitis of the small and medium-sized vessels in the
peripheral nervous system9 with an area of infarction in
the nerve.10,11 The presenting symptoms are severe pain
localised to the region of the infarction, motor deficit,
numbness and paraesthesias. Vasculitic neuropathies are
classified into primary and secondary vasculitides.10
Primary vasculitic neuropathy includes Churg-Strauss
syndrome, microscopic polyangiitis, classic polyarteritis
nodosa and Wegener granulomatosis. Secondary
vasculitis occurs as a complication of connective tissue
disease (systemic lupus erythematosus, rheumatoid
arthritis and Sjögren syndrome), infection (hepatitis B and
C, human immunodeficiency virus, Lyme disease,
cytomegalovirus, Herpes zoster virus and various bacterial
infections), medication (sulphonamides, other antibiotics
and anti-viral agents) and malignancies representing a
paraneoplastic vasculitis.11-15

Paraneoplastic peripheral neuropathy
In addition to the paraneoplastic vasculitis and the local
effect of the tumour, malignancies can also cause a parane-
oplastic sensorimotor neuropathy which might even be
more debilitating than the cancer itself.16 The detection of
anti-neuronal antibodies and EMG changes help to
identify the neuropathy as paraneoplastic. A paraneo-
plastic myopathy might also develop which can cause leg
pain.16,17

Case 1
This 53-year-old female patient presented with severe
acute onset unilateral pain in the L5 nerve root distri-
bution. The MRI of the lumbar spine failed to demonstrate
any neurological compression. The coronal images of the
MRI thoracic spine demonstrated a lesion in the lung
which was biopsied and turned out to be a bronchus
carcinoma (Figure 1). The antineuronal antibodies and
EMG confirmed a paraneoplastic neuropathy.

Case 2
This 64-year-old male patient presented with severe
unilateral pain in the L5 and S1 nerve root distribution
25 months after an uncomplicated L4 to S1 decom-
pression and fusion procedure. The plain radiographs
demonstrated an uncomplicated fusion and the MRI a
wide decompression without neurological compression.
The anti-neuronal antibodies demonstrated a positive
anti-PNMA(Ma/Ta) which is associated with small cell
bronchus carcinoma. This prompted a chest CT scan
which demonstrated a small lesion in the apex of the
right lung. A lung biopsy demonstrated a bronchus
carcinoma.

Vascular occlusion
Vascular occlusion can mimic neurogenic claudication.
The peripheral pulses should therefore be palpated in
every back pain examination.

2. Brain
Brain-related causes of leg pain include multiple
sclerosis,18,19 Parkinson’s disease,20 motor neurone disease,21
post-stroke pain in lenticulo-capsular haemorrhages22 and
space-occupying lesions.

Case 3
This 57-year-old male patient presented with spontaneous
onset pain in the right lower extremity 12 years after an L4
to S1 fusion, neurological decompression and instrumen-
tation. The plain radiographs failed to demonstrate any
complications and no neurological compression could be
demonstrated on the MRI lumbar spine. The history of the
systemic diseases revealed resection of a melanoma
behind the right scapula three years before. A CT scan of
the brain demonstrated multiple melanoma metastases
(Figure 2).

3. Spinal cord
Spinal cord conditions which should be excluded in the
evaluation of leg pain are multiple sclerosis,18,19 motor
neurone disease,21 transverse myelitis,22,23 syringomyelia,24,25
and any posterior (compression of substantia gelatinosa at
the tip of the posterior column) or anterolateral
(compression of lateral spino-thalamic tract)26 situated
space-occupying lesion, for example intervertebral disc
herniation,27,28 tumour, haematoma or abscess. An atypical
Brown-Sequard lesion can also be produced, with loss of
pain and thermal sensation on the contralateral side and
leg pain on the ipsilateral side.27,29

Figure 1. The coronal MRI demonstrated a lesion in the
lung apex (bronchus carcinoma)

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 18



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 19

Case 4
This 73-year-old female patient presented with excruci-
ating pain in the L5 distribution of the right lower
extremity and was booked for an emergency laminectomy.

When the patient presented for a second opinion, the MRI
of the lumbar spine demonstrated a small disc bulging on
the asymptomatic side. An MRI thoracic spine was
requested which demonstrated a posterior situated
meningioma at T7 (Figure 3) which was removed and the
L5 nerve root symptoms resolved completely.

4. Cervical and thoracic spinal canal
Any posterior or anterolateral situated space-occupying
lesion in the cervical and thoracic spinal canal may cause
compression on the lateral spino-thalamic tract and
substantia gelatinosa at the tip of the posterior column of
the spinal cord with resulting leg pain, for example
haematoma, abscess, soft tissue or bone tumours, etc.26-29

5. Conus medullaris
At the conus medullaris the nerve roots are positioned
lateral to the spinal cord (Figure 4). A parasagittal disc
herniation or any other space-occupying lesion (for
example intradural or extradural tumours, haematoma,
abscess, primary bone tumours, metastases, etc.) can
therefore cause compression of the nerve roots with leg
pain without much compression on the spinal cord. 

An MRI thoracic spine demonstrated a posterior 
situated meningioma at T7

Figure 2. Brain CT scan with multiple melanoma 
metastases in a patient who presented with leg pain
only

Figure 4. The conus medullaris. The nerve roots (between
the arrows) are positioned lateral to the spinal cord.

Figure 3 (a) Figure 3 (b)

Figure 3. A patient with leg pain only. Figure 3 (a)
demonstrates a small disc bulging on the asymptomatic
side on the lumbar spine MRI. Figure 3 (b) demonstrates
a T7 meningioma responsible for the leg pain.

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 19



Page 20 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

Case 5
This 58-year-old male patient presented with severe pain
in the right lower extremity in the L4 nerve distribution
seven years after a T12 to S1 fusion and pedicle instru-
mentation. The CT myelogram demonstrated interver-
tebral disc and gas sequestration in the right parasagittal
position with severe compression on the nerve roots but
only slight displacement of the conus medullaris (Figure 5).
Removal of the gas and disc sequestration alleviated the
L4 symptoms completely.

6. Lumbar spinal canal
As far back as 1933, Baastrup30 reported on the interspinous
bursa (kissing spines, Baastrup’s disease) as a cause of leg
pain31,32 (Figure 6). The bursa can communicate with an
epidural cyst with severe neurological compression.33

In facet joint syndrome, osteoarthrosis of the facet joint
with a normal spinal canal and nerve root canal can give
buttock and leg pain34,35 (Figure 7). Hypertrophy of the facet
joints gives spinal stenosis and leg pain (Figure 8). 

A facet joint cyst can compress the nerve root with leg
pain. With both superior or inferior rotational instability,
the facet joints may rotate into the spinal canal with neuro-
logical compression and leg pain (Figure 9).

In degenerative spondylolisthesis, the vertebral body and
inferior facet joints displace anteriorly. The inferior facet
joints move forwards and compress the dural sac and
nerve roots against the posterior aspect of the cranial
vertebral body. If the flexion radiographs demonstrate
superimposed instability with further anterior translation
of the inferior facet joints in the flexed position, the
compression on the dural sac is aggravated significantly.
This dynamic compression on the dural sac is not demon-
strated on the MRI and can only be appreciated on the
stress radiographs (Figures 10 and 11).

Any space-occupying lesion in the lumbar spinal canal can
give leg pain, for example intervertebral disc herniation or
sequestration, soft tissue or bone tumours, haematoma, etc. 

7. Lumbar nerve root canal
Inside the nerve root canal the facet joint might give leg
pain with a combination of loss of disc height and posterior
subluxation when the superior articular process moves
upwards and forwards and might impinge the nerve root
against the pedicle or the posterior aspect of the vertebral
body, especially the inferior endplate (Figure 12).

In spondylosis osteophytes from the superior facet joint or
posterior inferior vertebral endplate (Figure 13) may
compress the nerve root.
Anterior subluxation of the vertebra in degenerative

spondylolisthesis might be associated with hypertrophy of
the superior facet joint with extension of the superior facet
joint into the nerve root canal with compression of the
nerve root and resulting leg pain.

Any nerve root lesion, for example a nerve root cyst or
nerve root tumour, should be considered. The most
common benign nerve root tumours are the schwannomas,
neurofibromas36 and less common haemangioblastomas37,38
and non-Hodgkin lymphomas.39 Nerve sheath tumours can
originate from the intradural or extradural position.40

Figure 6. The interspinous bursas are demonstrated
between the red arrows.

Figure 5 (a) Figure 5 (b)

Figure 5. A patient with L4 leg pain. In Figure 5 (a) gas
(blue arrows) and disc (red arrows) sequestrations are
demonstrated. In Figure 5 (b) the gas sequestration (blue
arrow) is positioned over the nerve roots lateral to the
spinal cord with only slight displacement of the spinal
cord. 

Figure 7 Figure 8

Facet joint disease. Facet joint osteoarthrosis in 
Figure 7 and facet joint hypertrophy with spinal
stenosis in Figure 8.

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 20



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 21

Malignant peripheral nerve sheath tumours (MPNSTs) are
grouped together by the World Health Organisation as
MPNST and include previous terminology such as
malignant neurilemmomas, neurogenic sarcoma and
neurofibrosarcoma.41

In isthmic spondylolisthesis the nerve root canal is
narrowed by the combination of disc bulging and pars
interarticularis hypertrophy.

The pedicle moves down and might compress the nerve
root in complete loss of disc height in combination with
spondylolisthesis (Figure 14) and degenerative scoliosis.
Intervertebral disc herniation into the nerve root canal is

the most common cause of nerve root canal narrowing and
neurological compression.

A nerve root anomaly might easily be mistaken for a disc
fragment with grave consequences. The most common
anomaly is the conjoint nerve root with two nerve roots
derived from a common dural sheath followed by two
nerve roots in one foramina.42-44

8. Lumbar extraforaminal area
A far lateral disc herniation may compress the nerve root
after it has left the nerve root canal (Figure 15).

The corporotransverse ligament extends from the
vertebral body to the transverse process of the same
vertebra.45 It may entrap the nerve root in rotatory
subluxation in combination with complete disc space
narrowing.
Psoas pathology, for example abscess, haematoma,

tumour or any other space-occupying lesion, may
compress the nerve root in its course through the psoas.46

In spondylolisthesis with severe disc space narrowing,
the L5 nerve root may be impinged between the L5
transverse process and the ala of the sacrum (Figure 14).
This may also occur in degenerative scoliosis with tilting
of L5 and depression of the concave L5 transverse
process (Figure 16).

Figure 9 (a) Figure 9 (b) Figure 9 (c)

Figure 9. Rotational instability. Both the superior in Figure 9 (b) and inferior facet joint
in Figure 9 (c) can rotate into the spinal canal with neurological compression.

Figure 10 (a) Figure 10 (b)

Figure 10. Degenerative spondylolisthesis. The space
available for the dural sac between the posterior aspect
of the vertebral body and the anterior aspect of the
inferior facet joints (between the red arrows) measured
15 mm with the back in extension with 4 mm anterior
displacement [Figure 10 (a)] and decreases to only 4 mm
in flexion when the anterior displacement increases to 16
mm with severe dural sac compression [Figure10 (b)].

Figure 11 (a) Figure 11 (b)
Figure 11. The MRI was done with 4 mm anterior
displacement of L4 on L5 in Figure 11 (a) and (b). At 16 mm
anterior displacement, as demonstrated on the stress
radiographs in Figure 10, the inferior facet joints and
lamina at the position of the white arrows in Figure 11 (b)
will move forwards to the position of the red arrows with
severe aggravation of the existing compression. The MRI
fails to demonstrate the effect of this additional dynamic
compression of instability which is well demonstrated on
plain stress radiographs (Figure 10).

A facet joint cyst can compress the 
nerve root with leg pain

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 21



Page 22 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

9. Pelvis
At the entrance to the pelvis, a large osteophyte from the
L5 transitional vertebra pseudoarthrosis might compress the
L5 nerve root (Figure 17).

The lumbosacral ligament47 extends from the L5 vertebra to
the ala of the sacrum and forms the roof of the lumbosacral
tunnel through which the L5 nerve root passes.
Ossification of the lumbosacral ligament in combination
with osteophytes from the inferior L5 vertebral body
endplate may impinge the L5 nerve root.47

A stress fracture of the sacrum can give back, buttock, groin
and thigh pain.48 It may also give direct compression or a
neuropathy of the nerve root.49 The most common
associated stress fracture is that of the ipsilateral,
contralateral or both pubic rami.50 It may remain
undetected on plain radiographs for months but readily
demonstrated on the STIR and T2 weighted MRI images
(Figure 18).51 MRI alone identifies 99, 2% of stress fractures
compared to 69% with the CT scan alone.51 The MRI
remains the investigation of choice in these cases.

Figure 15. The position of a far lateral disc herniation is
demonstrated on the cadaver dissection (black arrow) on
the left side and the MRI (red arrow) on the right.

Figure 12. The superior
facet joint moves
upwards and forwards
(red arrow) in loss of
disc height with possible
nerve root compression. 

Figure 13. An osteophyte
from the inferior
vertebral endplate
extends into the nerve
root canal with nerve
root compression.

Figure 14. The pedicle moves down with nerve root
compression.

Figure 16. Tilting of L5 with dipping down of the left L5
transverse process (red arrows) and L5 nerve root
compression

Figure 17. An osteophyte from the L5 transitional
vertebra pseudoarthrosis extends medially with L5 nerve
root compression.

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 22



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 23

Degenerative sacroiliitis can give buttock, groin and thigh
pain.52 An osteophyte from the sacroiliac joint extending
anteriorly can compress a nerve root. Any type of infec-
tious sacroiliitis (tuberculosis, brucellosis and piogenic)53
and tumours of bone and the soft tissue in and around the
sacroiliac joint can give pain in a similar distribution.54 The
sero-negative spondyloarthropathies (ankylosing
spondylitis, psoriatic arthritis, reactive arthritis and
Behcet’s disease) should also be considered.55

A lumbosacral radiculoplexus neuropathy presents with
asymmetrical lower limb pain, weakness, atrophy and
paraesthesia.56 It can be caused by diabetic lumbosacral
radiculoplexus neuropathy, non-diabetic lumbosacral
radiculoplexus neuropathy, chronic inflammatory
demyelinating polyneuropathy, connective tissue disease,
Lyme disease, sarcoidosis, HIV and cytomegalovirus-
related polyradiculopathy.56,57 The typical MRI neurog-
raphy findings (Figure 19) are increased signal intensity
and enlargement of the nerve and blurring of the perifas-
cicular fat on the T2 weighted neurography sequences58,59
(long echo times, radiofrequency saturation pulses to

suppress signals from adjacent vessels and frequency-
selective fat suppression).60,61 EMG, fasting blood glucose
levels, sedimentation rate, rheumatoid factor, antinuclear
antibodies, antineutrophil cytoplasmic antibodies,
extractable nuclear antigen, HIV,56 serum antibodies
associated with neurological disorders (antineuronal,
antiganglioside and anti-astrocyte antibodies)62 and CSF
evaluation are some of the special investigations of
diagnostic value.

In the piriformis muscle syndrome hypertrophy, spasm,
contracture or inflammation of the piriformis muscle may
compress the ischiadic nerve with pain in any part of the
ischiadic nerve distribution (Figure 20). 

The diagnostic accuracy of a wide variety of clinical tests
(tenderness on deep palpation over the piriformis,63 Pace’s
sign,64 Freiberg’s sign,65 FAIR test [flexion- adduction-
internal rotation],66 persistent piriformis position in
external rotation) remain controversial.67 The imaging
diagnosis with an MRI of the pelvis is based on
enlargement of the piriformis and MRI neurography.59
Enlargement of the piriformis alone has a specificity of
66% and a sensitivity of 64%. If in addition the MRI
neurography demonstrates an increased signal intensity
and enlargement of the ischiadic nerve (Figure 21), the
specificity increases to 93% and the sensitivity to 64%.68

Figure 18 (a) Figure 18 (b)

Figure 18. The stress fracture of the sacrum is not visible
on the plain radiographs in Figure 18 (a) but well demon-
strated (red arrow) on the STIR sequences of the MRI in
Figure 18 (b). 

Figure 21 (a) Figure 21 (b)

Figure 21. The piriformis syndrome. Figure 21 (a) demon-
strates enlargement of the right piriformis muscle
(between red arrows) and the normal size on the left side
(yellow arrows). Figure 21 (b) demonstrates a
neuropathy of the underlying ischiadic nerve with
enlargement and increased signal intensity (between red
arrows).

Figure 19. The MRI neurography demonstrates a
neuropathy of the left ischiadic nerve (between black
arrows) with enlargement, increased signal intensity,
blurring of the perifascicular fat and loss of the normal
fascicular appearance. A normal nerve is demonstrated
between the red arrows.

Figure 20. Posterior
view of the right
gluteal area. The
ischiadic nerve

emerges from under-
neath the piriformis
and courses over the
obturator internus.
(Ipf: Infrapiriformis

foramina; ssl:
sacrospinalis

ligament; sg: superior
gemellis muscle; ig:
inferior gemellis

muscle; qf: quadratus
femoris muscle; pfcn:
posterior femoral
cutaneous nerve)

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 23



Page 24 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

The ischiadic nerve passes underneath the piriformis and
then over the obturator internus (Figure 20). Swelling and
inflammation of the obturator internus might displace and
irritate the ischiadic nerve with resultant leg pain (Figure
22).69
Superior gluteal nerve entrapment syndrome is caused by

any condition which narrows the suprapiriformis foramen
(Figure 20), for example enlargement or spasm of the
piriformis muscle,70 superior gluteal nerve perforating the
piriformis,71 aneurysm or pseudoaneurysm of the superior
gluteal artery,72 direct injury to the superior gluteal nerve
during hip surgery,73 percutaneous placement of iliosacral
screws,74 abscess and pelvic fracture. The clinical diagnosis
is based on the triad of buttock pain, weakness of hip
abduction and marked tenderness on deep palpation in
the region just lateral to the greater schiadic notch.75

Case 6
This 55-year-old male patient presented with the clinical
triad of superior gluteal nerve entrapment. The MRI pelvis
demonstrated sacroiliitis on the right side with an effusion
and a neuropathy of the superior gluteal nerve with
enlargement and an increased signal intensity (Figure 23).

The inferior gluteal nerve entrapment syndrome is caused by
any condition which narrows the infrapiriformis foramen,
for example an aneurysm of the inferior gluteal artery,63
pelvis fracture and abscess.76

In the pudendal nerve entrapment syndrome the pudendal
nerve is compressed in the pudendal or Alcock’s canal
between the sacrospinous and sacrotuberous ligaments.
The nerve might become ensheathed by ligamentous
expansions that form a perineural compartment, by the
falciform process of the sacrotuberous ligament or by
duplication of the obturator fascia.77-79 It causes chronic
perineal pain typically presenting as pain in the penis,
scrotum, labia, perineum, anorectal area and medial
proximal thighs.77

There are special considerations in female patients regarding
leg pain which deserve mentioning. Sciatica in pregnancy
can be caused by direct compression of the gravid uterus
on the lumbosacral plexus and blood vessels.80,81
Incorrectly positioned leg stirrups on the obstetrical table
can cause common peroneal nerve pain and weakness.80,82
Obstetric neuropathy of the sciatic nerve during vaginal
labour can be caused by continuous pressure of the foetus
on the lumbosacral plexus as it crosses the pelvic brim
during prolonged labour.83 Piriformis syndrome can be
caused during labour following a piriformis haematoma
after prolonged labour, and a piriformis abscess after
epidural anaesthesia and forceps delivery.84 Sciatica
secondary to pathological conditions80 include
leiomyomas with lumbosacral plexus compression,85
endometriosis with infiltration or compression of the
sciatic nerve86 and a large retroverted uterus with
compression on the lumbosacral plexus.80 Sciatica
secondary to iatrogenic trauma includes vaginal proce-
dures which might be complicated by ischiadic
neuropathy,87 superior gluteal artery aneurysm with
superior gluteal nerve compression and the superior
gluteal nerve neuropathy due to stretching of the superior
gluteal nerve.

Case 7
This 29-year-old female patient presented after two years
of diligent conservative treatment for a small L5/S1 disc
bulging with progressive deterioration of buttock and leg
pain. The MRI pelvis demonstrated a large ovarian cyst
which displaced a large uterus lateral and posterior with
an underlying large piriformis muscle, and an increased
signal intensity and enlargement of the ischiadic nerve
(Figure 24).

Figure 22. The ischiadic nerve (black arrows) is displaced
posteriorly by the obturator internus muscle (between
red arrows) with an area of increased signal intensity in
the muscle.

Figure 23. The MRI pelvis demonstrates a sacroiliitis on
the right side (black arrow) with an effusion and area of
high signal intensity around the joint. A neuropathy of
the right superior gluteal nerve is demonstrated (red
arrow) with enlargement and an increased signal
intensity.

Piriformis syndrome can be caused during 
prolonged labour, and a piriformis abscess 

after epidural anaesthesia and forceps delivery

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 24



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 25

10. Lower extremity
Greater trochanter bursitis and gluteus medius tendinitis
remain some of the most common causes of leg pain in
patients above 60 years of age.

A stress fracture of the femur neck, intertrochanteric area
and the proximal femur presents with pain in the groin
and anterior aspect of the proximal thigh. Plain
radiographs may remain normal for a considerable time.
An MRI and bone scan are useful in the early stages to
confirm the diagnosis.
Iliopsoas88 and iliopectineal89 bursitis and synovitis present

with pain in the groin and anterior aspect of the proximal
thigh. They might also give femoral nerve palsy and pain.
Non-traumatic focal mononeuropathies may present with

symptoms indistinguishable from a lumbar disc herni-
ation and include the following conditions:
1. Compression neuropathies: Acute, chronic and hered-

itary.90
2. Infectious neuropathies: Herpes zoster, Lyme disease,

acquired immunodeficiency syndrome (AIDS), leprosy
mononeuropathy, hepatitis B and C, cytomegalovirus,
Epstein-Barr virus, various bacterial infections.11-15

3. Inflammatory/vasculitic neuropathies: Churg-Strauss
syndrome, microscopic polyangiitis, classic
polyarteritis nodosa, Wegener granulomatosis,
systemic lupus erythematosus, rheumatoid arthritis,
Sjögren syndrome.11-15

4. Drug-related neuropathies: Sulphonamides, other
antibiotics, anti-viral agents.11-15

5. Metabolic neuropathies: Diabetic amyotrophy,
alcoholic and uraemic.6-8

6. Paraneoplastic neuropathies: Paraneoplastic vasculitis,
paraneoplastic sensorimotor neuropathy.16,17

7. Radiation neuropathy.90
8. Nerve and nerve sheath tumours.90
9. Hereditary: Familial amyloid polyneuropathy,91 hered-

itary compression neuropathy.90
The nerve entrapment syndromes of the lower extremity
include the following conditions:

The iliohypogastric (T12, L1), ilioinguinal (T12, L1) and
genitofemoral (L1, 2) entrapment syndromes usually occur
after lower abdominal surgery.92

Entrapment of the lateral femoral cutaneous nerve (L2-4) is
also known as meralgia paraesthetica. Symptoms include
anterior and lateral thigh burning, tingling and numbness.92

The femoral nerve (L2-4) is usually entrapped below the
inguinal ligament where it lies in close proximity to the
femoral head, the tendon insertion of the vastus inter-
medius, the psoas tendon, and the hip joint and hip joint
capsule, all of which can cause entrapment.92 Other causes
of entrapment include methylmethacrylate heat during
total hip arthroplasty, pelvic procedures requiring acutely
flexed, abducted and externally rotated positioning,
compression by a foetus in difficult childbirth, pelvic
fractures and radiation.92

The saphenous nerve (L3,4) is the terminal and longest
branch of the femoral nerve. It can become entrapped as it
pierces the roof of the adductor canal, by femoral vessels,
pes anserine bursitis, varicose vein operations and medial
knee surgery.92,93
Common peroneal neuropathy is the most common

mononeuropathy of the lower extremity. It is most
commonly entrapped as it courses along the lateral aspect of
the fibula neck through a fibro-osseous tunnel by tight
plaster casts, knee surgery, osteophytes, synovial cysts or
ganglions and sitting in a prolonged crossed leg position.93-96
Repetitive exercises involving inversion and pronation
(for example runners and cyclists) stretch the common
peroneal nerve against the fibula neck and fibrous arch of
the peroneal tunnel.93 Many cases are idiopathic in origin.97

The deep peroneal nerve travels in the anterior
compartment of the leg between the extensor digitorum
longus and the extensor hallucis longus tendon until it
reaches the ankle where it courses under the extensor
retinaculum to enter the anterior tarsal tunnel where most
of the entrapment occurs, referred to as the anterior tarsal
tunnel syndrome with symptoms referring to the dorsum
of the foot.98,99 The entrapment is usually sport related.93

The superficial peroneal nerve courses through the antero-
lateral compartment of the leg until it pierces the deep
fascia of the lateral compartment approximately 
10 to 15 cm above the ankle where it may become
entrapped. This is commonly seen in dancers in whom the
nerve may become stretched during inversion or plantar
flexion injuries.99,100
Proximal tibial entrapment neuropathy is uncommon,

owing to the deep location of the nerve and abundant
surrounding muscle tissue. Entrapment is usually related
to space-occupying lesions in the popliteal fossa such as
tumours, popliteal cyst, popliteal artery aneurysm and
ganglia.99

Figure 24 (a) Figure 24 (b) Figure 24 (c)

Figure 24. The MRI pelvis demonstrates a large ovarian cyst, displacing a large uterus (a) against a large piriformis (b)
with an underlying large ischiadic nerve with an increased signal intensity on MRI neurography (c).

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 25



Page 26 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

Distal tibial entrapment usually occurs in the tarsal tunnel
causing tarsal tunnel syndrome. Entrapment follows
trauma (fracture, surgery and scarring), space-occupying
lesion (tumour, ganglia, varicosities and an anomalous
muscle) and foot deformities.99,101

The sural nerve runs distally between the two heads of the
gastrocnemius beneath the crural fascia until it pierces the
fascia between the middle and distal thirds of the calf.
Compression of the nerve by mass lesion, scar tissue,
ganglion, surgical trauma and thrombophlebitis has been
reported. Extrinsic compression can occur from tight ski
boots or casts. The crural fascia may act as a compression
or fixation point in athletes with stretching of the
nerve.92,102-104

At the distal branches of the tibial nerve, medial plantar
nerve neuropathy (Jogger’s foot) can develop owing to
repetitive trauma to the nerve while running with
increased heel valgus and foot pronation.99,105

Entrapment of the inferior calcaneal nerve, the first branch
of the lateral plantar nerve, often manifests as heel pain
(Baxter neuropathy).99
Interdigital neuropathy (Morton neuroma) is caused by a

fibrotic nodule of the interdigital nerve most commonly at
the second and third intermetatarsal spaces. The patients
present with web space pain, tingling, numbness and
paraesthesias.99,106
Medial plantar proper digital neuropathy (Joplin’s neuroma)

is an entrapment neuropathy of the plantar proper digital
nerve which is particularly susceptible to repetitive
trauma.99,107,108

The diagnosis of an entrapment neuropathy is based on
a good clinical examination, typical EMG findings, MRI of
the nerves and muscle, and blood investigations as
mentioned under lumbosacral radiculoplexus
neuropathy. The MRI includes signs of nerve entrapment,
increased signal intensity, enlargement of the nerve, loss
of the normal fascicular appearance or blurring of perifas-
cicular fat.57 The indirect signs of nerve injury are seen in
the muscles supplied by the nerve with an increased signal
intensity followed by atrophy and fat placement of the
muscle.59,99

Leg pain may also be caused by myositis or myopathy.
Palpation of the muscle may reveal local tenderness which
is more pronounced than what would be expected of
neurological compression, swelling and oedema, atrophy
or hypertrophy and overlying skin changes. 

One of four basic patterns of abnormality may be present
on the MRI, namely muscle oedema with an increased
signal intensity, muscle atrophy with an increased fat
content, mass within a muscle or an accessory muscle.109
The aetiology of muscle oedema is inflammatory
myopathy (dermatomyositis, polymyositis and inclusion
body myositis), polymyositis, myositis in collagen
vascular disease (rheumatoid arthritis, systemic lupus
erythematosus, mixed connective tissue disease and
Sjögren syndrome), radiation myositis, Graves’ disease,
drug-induced myositis (lipid-lowering statins, antiretro-
viral medication), HIV myositis, myositis due to infection
(high risk patients include diabetes, immuno-compro-
mised patients, penetrating wounds), polymyositis, necro-
tising fasciitis and sarcoidosis. The denervation phases
include a normal MRI in the acute phase, mixed oedema
and paradoxical hypertrophy in the early subacute phase,
mixed oedema and atrophy in the late subacute phase and
atrophy in the chronic phase.109
Sport-related leg pain110 includes tibial and fibular stress

fractures,111 medial tibial stress syndrome,112 chronic
exertional compartment syndrome,113 tendinopathies,114,115
nerve entrapment syndromes,116 vascular syndromes117,118
and myopathies.119

Finally, leg pain may be associated with three poorly
understood neurological conditions, namely complex
regional pain syndrome,120,121 restless leg syndrome122 and
painful legs and moving toes syndrome.123

Discussion
At least 300 conditions were identified that might cause
neurogenic and referred leg pain. Table I is presented as an
aetiological classification for neurogenic and referred leg
pain and can serve as a checklist to ascertain that all
appropriate conditions are evaluated. Each one of these
conditions deserves careful consideration and if
overlooked might result in a missed diagnosis or even the
disaster of the creation of yet another failed back. Our
treatment can only be as good as our diagnosis. If the
diagnosis is missed, the treatment will obviously fail.

Each one of these conditions deserves careful consideration 
and if overlooked might result in a missed diagnosis

Continued on next page

1. Systemic diseases

Table I: Aetiological  classification of neurogenic and referred leg pain

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 26



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 27

2. Brain 8. Lumbar extraforaminal area

9. Pelvis

3. Spinal cord

4. Cervical and thoracic spinal canal

5. Conus medullaris

6. Lumbar spinal canal

7. Lumbar nerve root canal

10. Lower extremity

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 27



Page 28 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

The content of this article is the sole work of the authors, and no
benefit of any form has been received or will be received from any
commercial party.

References
1. Quiros-Moreno R, Lezama-Suárez G, Gómes-Jimenez C.

Disc alterarions of the lumbar spine on magnetic resonance
images in asymptomatic workers. Rev Med Inst Mex Sequro
Soc. 2008;46:185-90.

2. Jensen MC, Brant-Zawadski MN, Obuchowski N, et al.
Magnetic resonance imaging of the lumbar spine in people
without back pain. N Engl J Med. 1994;331:69-73.

3. Pasnoor M, Dimachkie MM, Kluding P, et al. Diabetic
neuropathy part 1: overview and symmetric phenotypes.
Neurol Clin. 2013;31(2):425-45.

4. Pasnoor M, Dimachkie MM, Barohn RJ. Diabetic
neuropathy part 2: proximal and asymmetric phenotypes.
Neurol Clin. 2013:31(2):447-62.

5. Kamenov ZA, Traykov LD. Diabetic autonomic
neuropathy. Adv Exp Med Biol. 2012;771:176-93.

6. Indiculla J, Shirazi N, Opacka-Juffry J, et al. Natl Med J India.
2004;17:200-202.

7. Arnold R, Kwai NC, Krishnan AV. Mechanisms of axonal
dysfunction in diabetic and uraemic neuropathies. Clin
Neurophysiol. 2013 May 14; In print.

8. Lozeron P, Adams D. Metabolic neuropathies. Rev Prat.
2008;58:1903-909.

9. Collins MP, Periquet-Collins I. Nonsystemic vasculitic
neuropathy: update on diagnosis, classification, patho-
genesis, and treatment. Front Neurol Neurosci. 2009;26:26-66.

10. Gorson KC. Vasculitic neuropathies. An update. Neurol.
2007;13:12-9.

11. Collins MP, Periquet MI. Nonsystemic vasculitic
neuropathy. Curr Opin Neurol. 2004;17:587-98.

12. Said G, Lacroix C. Primary and secondary vasculitic
neuropathy. J Neurol. 2005;252:633-41.

13. Somer T, Finegold SM. Vasculitides associated with infec-
tions, immunization, and antimicrobial drugs. Clin Infection
Dis. 2004;36:392-93.

14. Ferrari S, Lanzafame M, Faggian F, et al. Painfull
neuropathy vasculitis in 2 patients with longstanding
human immunodeficiency virus-1 infection. Scand J Infection
Dis. 2004;36:392-93.

15. Oh SJ. Paraneoplastic vasculitis of the peripheral nervous
system. Neurol Clin. 1997;15:849-63.

16. Dalmau J. Carcinoma associated paraneoplastic peripheral
neuropathy. J Neurol Neurosurg Psychiatry. 1999;67:4.

17. Campbell MJ, Paty DW. Carcinomatous neuromyopathy:
Electrophysiological studies. J Neurol Neurosurg Psychiatry.
1974;37:131-41.

18. Tsang BK, Macdnell R. Multiple sclerosis- diagnosis,
management and prognosis. Aust Fam Physician.
2011;40:948-55.

19. Piwko C, Desjardins OB, Bereza BG, et al. Pain due to
multiple sclerosis: analysis of the prevalence and economic
burden in Canada. Pain Res Manag. 2007;12:259-65.

20. Sage JI. Pain in Parkison’s disease. Curr Treatm Opti Neurol.
2004;6:191-200.

21. Brettschneider J, Kurent J, Ludolph A. Drug therapy for
pain in amyotrophic lateral sclerosis. Cochrane Database of
Systematic Reveiws. 2013; Issue 6.

22. Kim JS. Central post-stroke pain or parasthesias in lenticulo-
capsular hemorrhages. Neurol. 2003;61:679-82.

23. Berman M, Feldman S, Alter M, et al. Acute transverse
myelitis: incidence and etiological considerations. Neurol.
1981;31:966.

24. Campos WK, Almeida de Oliviera YS, Campi de Andrade
D, et al. Spinal cord stimulation for the treatment of neuro-
pathic pain related to syringomyelia. Pain Med. 2013;14:767-
68.

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 28



SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2 Page 29

25. Waseem M, Raja A, Jeun E, et al. Paroxysmal neuropathic
pain in an adolescent female with syringomyelia: a review
of the literature. Pediatr Emerg Care. 2012;28:472-74.

26. Last, RJ. Anatomy: Regional and Applied, 5th ed. Churchill
Livingstone, Edinburgh and London 1973.

27. Yeung JT, J----ohnson JI, Karim AS. Cervical disc herniation
with neck pain and contralateral symptoms: a case report. J
Med Case Reports. 2012;6:166.

28. Sasaoka R, Nakamura H, Yamano Y. Idiopathic spinal cord
herniation in the thoracic spine as a cause of intractable leg
pain: Case report and review of the literature. J Spinal Disord
Techn. 2003;16:288-94.

29. Langfitt TW, Elliot FA. Pain in the back and legs caused by
cervical spinal cord compression. JAMA. 1967;200:112-15.

30. Baastrup C. On the spinous processes of the lumbar
vertebrae and the soft tissue between them, and on patho-
logical changes in that region. Acta Radiol. 1933;14:52-54.

32. Sartoris DJ, Resnick D, Haghighi P. Age-related alterations
in the vertebral spinous processes and intervening soft
tissue: radiologic-pathologic correlation. Am J Roentgenol.
1985;145:1025-30.

33. Chen CKH, Yeh L, Resnick D, et al. Interspinous posterior
epidural cyst associated with Baastrup’s disease: Report of
10 patients. Am J Roentgenol. 2004;182:191-94.

34. Lilius G, Laasonen EM, Myllynen P, et al. Lumbar facet joint
syndrome. A randomised clinical trial. J Bone Joint Surg Br.
1989;71B:681-84.

35. McCall IW, Park WM, O’Brein JP. Induced pain referral
from posterior lumbar elements in normal subjects. Spine.
1979;4:441-46.

36. Coulon A, Milin S, Laban E, et al. Pathological characteristics
of the most frequent peripheral nerve tumours. Neurosurg.
2009;55:454-58.

37. Lonser RR, Wait SD, Butman JA, et al. Surgical management
of lumbosacral nerve root haemangiomablastomas in von
Hippel-Lindau syndrome. J Neurosurg. 2003;99:64-69.

38. Gläsker S, Bertis A, Pagenstecher A, et al. Characterization
of heamangioblastomas of the spinal nerves. Neurosurg.
2005;56:503-509.

39. Tsai MC. Non-Hodgkin’s B-cell lymphoma of a lumbar
nerve root: A rare cause of lumbar radiculopathy. J Clin
Neurosci. 2013;20:1029-31.

40. Jinnai T, Koyama T. Clinical characteristics of nerve sheath
tumours: analysis of 149 cases. Neurosurg. 2005;56:510-15.

41. Gupta G, Mammis A, Maniker A. Malignant peripheral
nerve sheath tumours. Neurosurg Clin N Am. 2008;19:533-43.

42. Neidre A, Macnab I. Anomalies of the lumbosacral nerve roots:
review of 16 cases and classification. Spine. 1983;8:294-99.

43. Kadish LJ, Simmons EH. Anomalies of the lumbosacral
nerve roots: An anatomical investigation and myelographic
study. J Bone Surg Br. 1984;66-B:411-16.

44. Taghipour M, Razmkon A, Hosseini K. Conjoined
lumbosacral nerve roots. Analysis of cases diagnosed intra-
operatively. J Spinal Disord Tech. 2009;22:413-16.

45. Transfeldt EE, Robertson D, Bradford DS. Ligaments of the
lumbosacral spine and their role in possible extraforaminal
spinal nerve entrapment and tethering. J Spinal Disord.
1993;6:507-12.

46. Demetriou GA, Nair MS, Navaratnam R. Right-sided
colonic tuberculosis: a rare cause of ilio-psoas abscess. BMJ.
2013; in press.

47. Nathan H, Weizenbluth M, Halperin N. The lumbosacral
ligament (LSL), with special emphasis on the lumbosacral
tunnel and entrapment of the 5th lumbar nerve. Intern
Orthop. 1982;6;197-202.

48. Tsirides E, Upadhyay N, Giannoudes PV. Sacral insuffi-
ciency fractures : current concepts of management.
Osteoporos Int. 2006;17:1716-25.

49. Jones JW. Insufficiency fracture of the sacrum with
displacement and neurological damage: a case report and
review of the literature. J Am Geriatr Soc. 1991;39:280-3.

50. Aretxabala I, Fraiz E, Perez-Ruiz F, et al. Sacral insufficiency
fractures. High association with pubic rami fractures. Clin
Rheumatol. 2000;19:399-401.

51. Cabarrus MC, Ambekar A, Lu Y, et al. MRI and CT of insuf-
ficiency fractures of the pelvis and the proximal femur. Am
J Roentgenol. 2008;191:995-1001.

52. Strak JG, Fuentes J, Fuentes TI, et al. The history of sacroiliac
joint arthrodesis: a critical review and introduction of a new
technique. Cur Orthop Pract. 2011;22:545-57.

53. Hermet M, Minichiello E, Flipo RM, et al. Infectious
sacroiliitis: a retrospective, multicentre study of 39 adults.
BMC Infect Dis. 2012;12:305.

54. Wang J, Tang Q, Xie X, et al. Iliosacral resection of pelvic
malignant tumors and with reconstruction non-vascular
bilateral fibular autografts. Ann Surg Oncol. 2012;19:4043-51.

55. Deesomchok U, Tumrasvin T. Clinical comparison of
patients with ankylosing spondylitis, Reiter’s syndrome and
psoriatic arthritis. J Med Assoc Thai. 1993;76:61-70.

56. Dyck PJB, Norell JE, Dyck PJ. Non-diabetic lumbosacral
radiculoplexus neuropathy. Natural history, outcome and
comparison with the diabetic variety. Brain. 2001;124:1197-207. 

57. Chanin N, Temesgen Z, Kurtin PJ, et al. HIV lumbosacral
radiculoplexus neuropathy mimicking lymphoma: Diffuse
infiltrative lymphocytosis syndrome (DILS) restricted to
nerve? Muscle Nerve. 2010;41:276-82.

58. Filosto M, Pari E, Cotelli M, et al. MR neurography in
diagnosing nondiabetic lumbosacral radiculoplexus
neuropathy. J Neuroimaging. 2013; June 10: In press.

59. Petchprapa C, Rosenburg ZS, Sconfienza LM, et al. MR
Imaging of entrapment neuropathies of the lower extremity
Part 1. The pelvis and hip. Radiographics. 2010;30:983-1000.

60. Grant GA, Goodkin R, Maravilla KR, et al. MR
Neurography: diagnostic utility in the surgical treatment of
peripheral nerve disorders. Neuroimaging Clin N Am.
2004;14:115-33.

61. Maravilla KR, Brown BC. Imaging of the peripheral nervous
system: evaluation of peripheral neuropathy and
plexopathy. Am J Neuroradiol. 1998;19:1011-23.

62. Vincent A. Antiganglioside antibodies in the peripheral
neuropathies. J Clin Pathol. 1998;51:641-42.

63. Papadopoulos SM, McGillicuddy JE, Albers JW. Unusual
case of piriformis muscle syndrome. Arch Neurol.
1990;47:1144-46.

64. Pace JB, Nagle D. Piriformis syndrome. West J Med.
1976;124:435-39.

65. Freiberg AH. Sciatic pain and its relief by operations on the
muscle and fascia. Arch Surg. 1937;34:337-50.

66. Kean Chen C, Nizar AJ. Prevalence of piriformis syndrome
in chronic low back pain patients. A clinical diagnosis with
modified FAIR test. Pain Pract. 2013;13:276-78.

67. Miller TA, White KP, Ross DC. The diagnosis and
management of piriformis syndrome: myths and facts. Can J
Neurol Sci. 2012;39:577-83.

68. Filler AG, Haynes J, Jordan SE, et al. Sciatica of non-disc
origin and piriformis syndrome: diagnosis by magnetic
resonance neurography and interventional magnetic
resonance imaging with outcome study of resulting
treatment. J Neurosurg Spine. 2005;2:99-115.

69. Meknas K, Christensen A, Johansen O. The internal
obturator muscle my cause sciatic pain. Pain. 2003;104:275-
80.

70. Diop M, Parratte B, Tatu L, et al. Anatomical basis of
superior gluteal nerve entrapment syndrome in the
suprapiriformis foramen. Surg Radiol Anat. 2002;24:155-59.

71.  Yadav Y, Mehta V, Roy S et al. Superior gluteal nerve
entrapment between two bellies of piriformis muscle. Int J
Anat Variations. 2010;3:203-204.

72. Lowenthal RM, Taylor BV, Jones R et al. Severe persistent
sciatic pain and weakness due to gluteal artery pseudoa-
neurysm as a complication of bone marrow biopsy. J Clin
Neurosci. 2006;13:384-85.

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 29



Page 30 SA Orthopaedic Journal  Winter 2014 | Vol 13 • No 2

73. Ramesh M, O’Byrne JM, McCarthy N, et al. Damage to the
superior gluteal nerve after the Hardinge approach to the hip.
J Bone Joint Surg Br. 1996;78:903-906.

74. Collinge C, Coons D, Aschenbrenner J. Risks to the superior
gluteal neurovascular bundle during percutaneous iliosacral
screw insertion: an anatomical cadaver study. J Orthop Trauma.
2005;19:96-101.

75. Rask MR. Superior gluteal nerve entrapment syndrome.
Muscle Nerve. 1980;3:304-307.

76. Fielder J, Miriti K, Bird P. Mycotic aneurysm of the inferior
gluteal artery caused by non-typhi salmonella in a man
infected with HIV. A case report. J Med Case Rep. 2010;18:273

77. Hough DM, Wittenberg KH, Pawlina W, et al. Chronic
perineal pain caused by pudendal nerve entrapment: anatomy
and CT-guided perineum injection technique. Am J Roentgen.
2003;181:561-67.

78. Robert R, Prat-Pradal D, Labat JJ, et al. Anatomical basis of
chronic perineal pain: role of the pudendal nerve. Surg Radiol
anat. 1998;20:93-98.

79. Shafik A, el-Sherif M, Youssef A, et al. Surgical anatomy of the
pudendal nerve and its clinical implications. Clin Anat.
1995;8:110-15.

80. Al-Khodairy A-WT, Bovay P, Gobelet C. Sciatica in the female
patient: anatomical considerations, aetiology and review of
the literature. Eur Spine J. 2007;16:721-31. 

81. Ashkan K, Casey ATH, Powel M, et al. Back pain during
pregnancy and after childbirth: an unusual case not to miss. JR
Soc Med. 1998;19:88-90.

82. Tubridy N, Redmond JM. Neurological symptoms attributed
to epidural analgesia in labour: an observational study of
seven cases. Br J Obstet Gynecol. 1996;103:832-33.

83. Gonik B, Stringer CA, Cotton, DB. Intrapartum maternal
lumbosacral plexopathy. Obstet Gynecol. 1984;63:45S-6S.

84. Ku A, Kern H, Lachman E, et al. Sciatic nerve impingement
from piriformis haematoma due to prolonged labour. Muscle
Nerve. 1995;18:789-90.

85. Heffernan LPM, Fraser RC, Purdy RA. L-5 Radiculopathy
secondary to uterine leiomyoma in a primigravid patient. Am
J Obstet Gynecol. 1980;138:460-61.

86. Vilos GA, Vilos AW, Haebe JJ. Laparoscopic findings,
management, histopathology, and outcome of 25 woman with
cyclic leg pain. J Am Assoc Gynecol Laparosc. 2002;9:145-51.

87. Ras S. Complications of vaginal surgery. In: Raz S, editor.
Atlas of transvaginal surgery. Philadelphia: Saunders;1992, pp
37-47.

88. Tokita A, Ikari K. Tsukahara S, et al. Iliopsoas bursitis-
associated femoral nerve neuropathy exacerbated after
internal fixation of an intertrochanteric hip fracture in
rheumatoid arthritis: a case report. Mod Rheumatol.
2008;18:394-8.

89. Tatsumura M, Mishima H, Shiina I, et al. Femoral nerve palsy
caused by a huge iliopectineal synovitis extending to the iliac
fossa in a rheumatoid arthritis case. Mod Rheumatol.
2008;18:81-85.

90. Bodur H. Nontraumatic focal neuropathies. Turk J Phys Med
Rehab. 2012;58:114-20.

91. Adams D. Recent advances in the treatment of familial
amyloid polyneuropathy. Ther Adv Neurol Disord. 2013;6:129-
39.

92. Hollis MH, Lemay DE. Nerve entrapment syndromes of the
lower extremity. Medscape Reference. 2010;Nov 10.

93. McCoy P, Bell S, Bradshaw C. Nerve entrapments of the lower
leg, ankle and foot in sport. Sports Med. 2002;32:371-91.

94. Flu HC, Breslau PJ, Hamming JF, et al. A prospective study of
saphenous nerve injury after total great saphenous vein
stripping. Dermtol Surg. 2008;34:1333-39.

95. Kaminsky F. Peroneus palsy by crossing the legs. JAMA.
1947;134:206.

96. Anselmi SJ. Common peroneal nerve compression. J Am
Podiatr Med Assoc. 2006;96:413-17.

97. Kopell HP, Thompson W. Peripheral nerve entrapments of the
lower extremity. New Engl J Med. 1962;266:16-19.

98. DiDomenico LA, Masternick EB. Anterior tarsal syndrome.
Electromyography. 1968;8:123-34.

99. Donovan A, Rosenburg ZS, Cavalcanti CF. MR Imaging of
entrapment neuropathies of the lower extremity.
Radiographics. 2012;30:1001-19.

100. Kennedy JG, Baxter DE. Nerve disorders in dancers. Clin
Sports Med. 2008;27:329-34.

101. Sammarco GF, Conti SF. Tarsal tunnel syndrome caused by an
anomalous muscle. J Bone Joint Surg Am. 1994;76:1308-14.

102. Coert J, Dellon A. Clinical implications of the surgical
anatomy of the sural nerve. Plast Reconstr Surg. 1994;94:850-55.

103. Pringle R, Protheroe K, Mukherjee S. Entrapment neuropathy
of the sural nerve. J Bone Joint Surg Br. 1974;56:465-68.

104. Schon L. Nerve entrapment, neuropathy and nerve
dysfunction in athletes. Orth Clin North Am. 1994;25:47-59.

105. Schon L. Chronic pain. In: Meyerson’s foot and ankle disorder.
Vol 2. Philadelphia. Saunders, 2000;851-81.

106. Morscher E, Ulrich J, Dick W. Morton’s intermetatarsal
neuroma: morphology and histological substrate. Foot Ankle
Int. 2000;21:558-62.

107. Merritt GN, Subotnick SI. Medial plantar digital proper nerve
syndrome (Joplin’s neuroma): typical presentation. J Foot Surg.
1982;21:166-69.

108. Still GP, Fowler MB. Joplin’s neuroma or compression
neuropathy of the plantar proper digital nerve to the hallux:
clinicopathologic study of three cases. J Foot Ankle
Surg.1998;37:524-30.

109. Pathria M, Bradshaw J. Muscle MR imaging- Part 2. Non-
traumatic changes. In: The Radiology Assistant; Jan 2010.

110. Reinking MF. Exercises related leg pain (ERLP): A review of
the literature. North Am J Sports Phys Ther. 2007;2:170-80.

111. Verma RB, Sherman O. Athletic stress fracture: Part1. History,
epidemiology, physiology, risk factors, radiology, diagnosis,
and treatment. Am J Orthop. 2001;30:798-806.

112. Mubarak SJ, Gould RN, Lee YF, et al. The medial tibial stress
syndrome. A cause of shin splints. Am J Sports Med.
1982;10:201-205.

113. Mavor GE. The anterior tibial syndrome. J Bone Joint Surg Br.
1956;38B:513-7.

114. Khan KM, Cook JL, Taunton JE, et al. Overuse tendinosis, not
tendinitis. Phys Sportsmed. 2000;28:38-47.

115. Kaufman KR, Brodine SK, Shaffer RA, et al. The effect of foot
structure and range of motion on musculoskeletal overuse
injuries. Am J Sports Med. 1999;27:585-93.

116. Hirose CB, McGarvey WC. Peripheral nerve entrapments. Foot
Ankle Clin. 2004;9:255-69.

117. Korkola M, Amendola A. Exercise-induced pain. Phys
Sportsmed. 2001;29:35-38.

118. Bradshaw C. Exercise-related lower leg pain: Vascular. Med
Sci Sports Exerc. 2000;32(3 Suppl):S34-6.

119. McCrory P. Exercise related leg pain: Neurological
perspective. Med Sci Sports Exerc. 2000;32(3 Suppl):S11-4.

120. Grande LA, Loeser JD, Ozuna J, et al. Complex regional pain
syndrome as a stress response. Pain. 2004;110:495-98.

121. Wasner G, Schattschneider J, Binder A, et al. Complex regional
pain syndrome- diagnostic, mechanisms, CNS involvement
and therapy. Spinal Cord. 2003;41:61-75.

122. Bogan RK, Cheray JA. Restless legs syndrome: A review of
diagnosis and management in primary care. Postgrad Med.
2003;125: 99-111.

123. Reich SG. Painfull legs and moving toes. Handb Clin Neurol.
2011;100:375-83.

This article is also available online on the SAOA website
(www.saoa.org.za) and the SciELO website (www.scielo.org.za).
Follow the directions on the Contents page of this journal to access it.

• SAOJ

SAOJ Winter 2014 BU_Orthopaedics Vol3 No4  2014/05/05  9:51 PM  Page 30