SHORT REPORT
We
SURAL NEUROPATHY: ETIOLOGIES AND
PREDISPOSING FACTORS
D. E. STICKLER, MD,1 K. N. MORLEY,2 and E. W. MASSEY, MD2
1
Division of Neurology, Medical University of South Carolina, 96 Jonathan Lucas Street,
Clinical Sciences Building, Suite 307, P.O. Box 25060, Charleston, South Carolina 29464, USA
2
Division of Neurology, Duke University Medical Center, Durham, North Carolina, USA
Accepted 4 April 2006
The sural nerve is a sensory nerve that originates in
the lower leg and provides sensory innervation to the
lateral surface of the foot and ankle. It is derived
primarily from the S1 nerve root and originates in
the popliteal fossa. This medial sural branch of the
tibial nerve receives a communicating branch of the
common peroneal nerve in the lower leg. The ana-
tomical course of the nerve in the distal leg and
ankle makes it susceptible to local trauma.6,8,13 Sim-
ilarly, this location also increases the risk of trauma
during surgical interventions at the ankle.9
Sural neuropathy is suspected in patients with
numbness, pain, or paresthesias in the distribution
of the sural nerve and can be confirmed by electro-
diagnostic testing. We retrospectively examined the
electrodiagnostic reports of 36 patients with isolated
sural neuropathy to classify etiologies and predispos-
ing factors for developing this mononeuropathy.
MATERIALS AND METHODS
The Duke University Medical Center institutional re-
view board approved this study. A search of electrodi-
agnostic studies performed in the Duke Electromyo-
graphy (EMG) Laboratory since 1986 was undertaken
Abbreviation: EMG, electromyography
Key words: electrodiagnosis of sural neuropathy; neuropathy; sural nerve;
trauma
Correspondence to: D. Stickler; e-mail: stickle@musc.edu
© 2006 Wiley Periodicals, Inc.
Published online 11 May 2006 in Wiley InterScience (www.interscience.wiley.
com). DOI 10.1002/mus.20580
482 Short Reports
ABSTRACT: Isolated sural neuropathy is an uncommon diagnosis.
identified 36 patients with isolated sural neuropathy. Sixteen had various
forms of ankle trauma, in three of whom the associated sural neuropathies
developed following medical intervention. Three patients developed sural
neuropathy associated with vasculitis, and there were single patients with
schwannoma and ganglionic cyst. In patients without a history of trauma,
structural causes, such as schwannoma or ganglionic cysts and vasculitis,
should be considered and managed as appropriate.
Muscle Nerve 34: 482– 484, 2006
and identified 36 patients meeting inclusion criteria.
Sural sensory responses were obtained using standard-
ized techniques with a distance of 14 cm between the
stimulating and active recording electrodes.12 Limb
temperature was maintained at 34°C or above, and
patients in whom foot and ankle edema may have
limited the study were excluded. Patients with absent
or abnormal sural responses but normal contralateral
sural studies were included. Based on our laboratory
normal values, an abnormal response was defined as a
response that had either an abnormal peak latency
exceeding 4.2 ms or an amplitude of less than 5 ␮V. We
then compared these abnormal values to the contralat-
eral sural response and included only studies that fell
outside of the 95% confidence interval for published
data for normal sural symmetry.3 For the ratios of
abnormal-to-normal sural studies, amplitude ratios less
than 0.39 and latency ratios greater than 1.24 were
considered abnormal.3 Patients without contralateral
studies for comparison, patients with evidence of ab-
normal ipsilateral peroneal or tibial motor conduction
studies, and patients with polyneuropathy were ex-
cluded. We included a single patient with normal sural
conduction studies using standardized techniques who
demonstrated evidence of a more proximal conduction
block at a distance greater than the standard 14 cm.
RESULTS
The distribution of electrodiagnostic abnormalities
with etiologies is presented in Table 1. Trauma to
the sural nerve in the distal leg or ankle was the
identified etiology in 16 patients, whereas compres-
sion from a mass occurred in 2 patients. Vasculitis
was the suspected etiology in 3 patients with isolated
MUSCLE & NERVE October 2006
 Table 1. Patient characteristics and etiologies.
with vasculitis. Confirmatory sural nerve biopsies
were not performed these 2 patients. An additional
Sural Response
patient presented with lateral foot numbness and a
Abnormal Contralateral
history of a steroid-responsive mixed connective tis-
Latency Amplitude Latency Amplitude
Etiology (ms) (␮V) (ms) (␮V)
sue disease with levido reticularis, myalgias, and ex-
tremity edema.
Trauma (16)
Ankle fracture 4.3 10 3.4 7
Although 27 patients demonstrated sensory abnor-
Ankle fracture NR 3.3 10 malities in the sural distribution, only 6 patients were
Ankle fracture NR 3.6 9 referred for specific evaluation of the sural nerve. Pe-
Ankle fracture NR 3.4 14
Ankle fracture NR 3.6 19 ripheral neuropathy was the referring assessment in 15
Ankle sprain NR 3.9 6 patients, lumbosacral radiculopathy in 11 patients, and
Ankle sprain NR 4.2 6 tarsal tunnel syndrome in 4 patients.
Lipoma excision NR 4.0 21
Vein stripping NR 3.8 19
Knee surgery 4.0 5 4.0 16 DISCUSSION
Long-distance runner 4.0 5 3.9 14
Shrapnel injury NR 3.7 6 Sural neuropathy is an uncommon electrophysiologi-
Ankle laceration NR 3.9 12
Ankle laceration NR 3.9 10
cal diagnosis. A search of our database containing over
Gunshot NR 3.9 16 50,000 electrodiagnostic studies resulted in the 36
External compression 4.6 4.0 3.7 16 cases of sural neuropathy described herein, which rep-
Vasculitis (3)
Wegener’s granulomatosis NR 3.8 14 resents the largest reported sample of sural mononeu-
Polyarteritis nodosa NR 3.4 10 ropathies, at least to our knowledge. Trauma is the
Nonsystemic vasculitis NR 4.0 15 most frequently cited cause of sural neuropathy in the
Connective tissue disease (1)
Mixed connective tissue literature and neuropathies secondary to ankle frac-
disease NR 3.5 25 ture,10,16,24 trauma,4,7,18,20,21,24 and external compres-
Other (3) sion at the ankle have been reported.2,5,11,19,22,24 Struc-
Ganglion cyst NR 3.1 11
Schwannoma NR 3.8 11 tural lesions secondary to Baker’s cyst15 and intraneural
Prior nerve harvesting NR 3.0 20 ganglions1,17 have also been reported. Sural neuropa-
Unknown (13)
thy is also an uncommon complication of ankle sur-
Neurofibromatosis 5.3 3.0 4.1 10
Diabetes NR 3.9 12 gery, and cases similar to our vein-stripping neuropa-
Diabetes NR 3.7 7 thy14,24,26 and neuropathy following sural harvesting for
Diabetes NR 4.0 10
nerve graft25 have been reported.
NR 3.6 7
NR 3.6 21 Although sural nerve involvement in sensory
5.2 12 4.0 12 polyneuropathy associated with vasculitis is com-
NR 3.7 17
NR 3.7 6
mon, with a high frequency of diagnostic sural nerve
NR 3.6 18 biopsies,23 isolated sural nerve impairment as the
NR 3.9 5 initial manifestation of peripheral nervous system
3.7 24* 3.8 27
NR 3.8 11
impairment in both systemic and nonsystemic vascu-
litis has only been suspected in a single case to our
NR, no response recorded. knowledge and has not previously been confirmed
*Patient with abnormal response recorded at a distance greater than 14
cm. by biopsy.24 In our patients with polyarteritis nodosa
and Wegener’s granulomatosis, the suspected link
between the mononeuropathy and systemic vasculitis
sural neuropathy. Nonsystemic vasculitis was diag- was not confirmed by sural biopsy. All 3 patients with
nosed in a patient presenting with pain and numb- presumed vasculitis-associated neuropathy were
ness on the lateral surface of the left leg and foot. women under the age of 45 years. A similar case of
The sural nerve biopsy demonstrated vasculitic sural neuropathy linked to connective tissue disease
changes with no history or subsequent discovery of a has been reported, also without biopsy confirma-
systemic vasculitic condition. Sural mononeuropathy tion.24 A single patient with a normal study using our
was also found in a patient with Wegener’s granulo- routine sural nerve conduction methods had abnor-
matosis diagnosed by biopsy of the nasal septum. malities with more proximal stimulation, demon-
Serial studies demonstrated the sural neuropathy strating the importance of inching studies for sus-
was the initial manifestation of mononeuritis multi- pected proximal sural nerve lesions in the calf.
plex. Another patient with polyarteritis nodosa con- In 13 patients the etiology could not be deter-
stituted the third case of sural neuropathy associated mined. Three of these patients were diabetic without

Short Reports MUSCLE & NERVE October 2006 483

evidence of polyneuropathy. One had a history of neu-
rofibromatosis but a sural neurofibroma could not be
identified. None of these 13 patients underwent sural
nerve biopsy. Anatomical studies have demonstrated
the presence of potential sites for entrapment of the
sural nerve as it travels through deep fascia, particularly
with knee extension,6 which may be clinically relevant,
especially in patients with a history of diabetes.
When encountering patients with symptoms sug-
gestive of isolated sural neuropathy, the history is
likely to reveal evidence of prior ankle trauma or
history of compression. In the absence of this infor-
mation, appropriate imaging should be obtained to
evaluate for a structural lesion involving the sural
nerve. If these evaluations are nondiagnostic, then
screening for systemic vasculitis and consideration of
sural nerve biopsy is recommended.
This study was presented in part at the annual meeting of the
American Association of Neuromuscular and Electrodiagnostic
Medicine, Monterey, California, September 2005.
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