SHORT REPORT ABSTRACT: Accessory deep peroneal nerve (ADPN), a common ana-

tomic variant, is traditionally suspected when common peroneal nerve stimu-

lation evokes a greater amplitude extensor digitorum brevis compound
muscle action potential than deep peroneal nerve (DPN) stimulation. Pos-
terolateral ankle stimulation over the ADPN is confirmatory. We report a rare
patient with ADPN neuropathy in whom the collision technique was neces-
sary to confirm the presence of an ADPN and to distinguish between neu-
ropathy of the ADPN and the DPN. © 1998 John Wiley & Sons, Inc. Muscle
Nerve, 21: 121–123, 1998.
Key words: electromyography; collision technique; peroneal nerve

ACCESSORY DEEP PERONEAL

NEUROPATHY: COLLISION
TECHNIQUE DIAGNOSIS
HOWARD W. SANDER, MD,1,2* CHRISTINE QUINTO, MD,1,2 and
SUDHANSU CHOKROVERTY, MD1,2,3

1
Department of Neurology, Saint Vincents Hospital and Medical Center of New
York, 153 West 11th Street, New York, NY 10011, USA
2
Division of Clinical Neurophysiology, Saint Vincents Hospital and Medical Center
of New York, New York, NY, USA
3
Robert Wood Johnson Medical School, Piscataway, NJ, USA

Accepted 15 June 1997

Accessory deep peroneal nerve (ADPN) is a com-
mon anatomic variant with a prevalence of 17–
28%7,10–13,15,16 and probable autosomal dominant
transmission.3 It originates from the superficial pe-
roneal nerve, runs within peroneus brevis, winds pos-
terior to the lateral malleolus, and innervates the
lateral aspect of the extensor digitorum brevis
muscle (EDB).2,7,16 It provides sensory innervation
to tarsal and metatarsal articulations.2,7,16 The pres-
ence of an ADPN is suspected when common pero-
neal nerve stimulation at the fibular head (FHS)
evokes a greater amplitude EDB compound muscle
action potential (CMAP) than deep peroneal nerve
(DPN) stimulation at the anterior ankle (AAS). Pos-
terolateral ankle stimulation (PLAS) over the ADPN
will evoke a primarily negative CMAP and verify its
presence.1,3–7,10–13,15 We now report a patient with
pathology of the ADPN which required the collision
technique for diagnosis.
PATIENT
A 39-year-old woman was evaluated for carpal tunnel
syndrome and mild, transitory, ill-defined leg pain.
*Correspondence to: Dr. Howard W. Sander
CCC 0148-639X/98/010121-03
© 1998 John Wiley & Sons, Inc.
She had sustained bilateral distal leg trauma during
childhood. Upper extremity examination revealed a
median distribution sensory loss without weakness.
Lower extremity motor examination revealed left
EDB atrophy and weakness. Other muscles had nor-
mal bulk and strength. Reflexes, lower extremity sen-
sation, and gait were normal.
METHODS AND RESULTS
Upper extremity electrodiagnostic studies were con-
sistent with a median neuropathy at the wrist bilat-
erally. Bilateral tibial CMAPs, F waves, H reflexes,
and sural and superficial peroneal sensory nerve ac-
tion potentials were normal. The right peroneal mo-
tor nerve conduction study is discussed below.
Needle electromyography of right EDB revealed pro-
longed duration motor units and a decreased inter-
ference pattern. The left peroneal CMAP was absent
upon AAS, PLAS, and FHS.
Left EDB electromyography was not performed
at the patient’s request. Electromyography of bilat-
eral tibialis anterior, peroneus longus, gastrocnemi-
us, vastus lateralis, biceps femoris (short head), and
paraspinous muscles was normal. These studies indi-
cate the presence of a left deep peroneal neuropa-
thy. Localization is likely distal to the extensor hal-
lucis longus branch, which is clinically spared.

Short Reports MUSCLE & NERVE January 1998 121

 Details of the right peroneal motor nerve con-
duction study (skin temperature 32°C) with surface
recording over EDB follow (Fig. 1). Measurements
were obtained at a gain of 200 µV/division. Duration
was calculated from the initial negative deflection
until the first baseline crossing.
AAS over the DPN (Fig. 1A) produced a CMAP
with a normal latency (5.9 ms), a decreased ampli-
tude (1.3 mV), and a duration of 4.9 ms. PLAS over
the ADPN (Fig. 1B) evoked a CMAP with a similar
latency (5.4 ms) and amplitude (1.2 mV), and a du-
ration of 6.4 ms. FHS over the common peroneal
nerve (Fig. 1C) evoked a bifid waveform with an am-
plitude (1.2 mV) approximately equivalent to the
AAS and PLAS evoked waves but with an increased
duration of 9.6 ms. Peroneal nerve conduction ve-
locity was 52 m/s.
The recordable CMAP following PLAS indicates
an ADPN is present. The bifid morphology of the
FHS evoked wave in conjunction with a normal maxi-
mum conduction velocity suggests that the second of
the two contributing components is delayed. This
delayed component, and the abnormal right EDB
electromyogram raised, the possibility of neuropathy
FIGURE 1. Peroneal motor nerve conduction studies recording
over right extensor digitorum brevis. (A) Anterior ankle stimula-
tion (AAS) of the deep peroneal nerve (DPN). (B) Posterolateral
ankle stimulation (PLAS) of the accessory deep peroneal nerve
(ADPN). (C) Fibular head stimulation (FHS) of the common pe-
roneal nerve. (D) AAS followed by FHS. Arrow and bracket indi-
cate the ADPN derived component (which is delayed) remaining
after the DPN component has been abolished by collision. (E)
PLAS followed by FHS. Arrowhead and bracket indicate the DPN
derived component remaining after the ADPN component has
been abolished by collision.
122 Short Reports
of either the DPN or the ADPN. Upon visual inspec-
tion of the FHS evoked bifid wave (Fig. 1C), the
second (delayed) component appears similar in
morphology to the AAS evoked wave (Fig. 1A), and
the first (normal) component appears similar to the
PLAS evoked wave (Fig. 1B), possibly suggesting a
deep peroneal neuropathy. Visual inspection, how-
ever, cannot be relied upon to correctly attribute
CMAP components to a particular nerve, as mor-
phology may have been altered by phase cancella-
tion. Collision studies were therefore performed to
separate the components and determine which
nerve was pathologic.
Collision Studies. Collision technique8 with AAS
followed by FHS in 7 ms (Fig. 1D) clearly resolves the
two components of the bifid waveform. The DPN
contribution has been eliminated by collision. The
ADPN derived remaining component (bracket) is
clearly coincident (arrow) with the second (delayed)
component of the FHS evoked wave (Fig. 1C), and it
morphologically is most similar to the PLAS evoked
wave (Fig. 1B). The ADPN conduction velocity is 29
m/s.
Similarly, collision technique8 with PLAS fol-
lowed by FHS in 7 ms (Fig. 1E) also resolves the two
components. In this instance, following elimination
of the ADPN contribution by collision, the DPN de-
rived remaining component (bracket) clearly coin-
cides (arrowhead) with the first (normal) compo-
nent of the FHS evoked wave (Fig. 1C), and it
morphologically resembles the AAS evoked wave
(Fig. 1A).
DISCUSSION
On the basis of the above studies our patient has a
right accessory deep peroneal neuropathy between
the ankle and the fibular head. The etiology is likely
local trauma sustained as a child. The remarkable
change in morphology and duration with proximal
stimulation of the peroneal nerve suggested both the
presence of an ADPN as well as the presence of pa-
thology in either the DPN or the ADPN. Collision
studies were necessary to identify the ADPN as the
pathologically affected nerve.
One previous case of accessory deep peroneal
neuropathy has been reported by Dessi et al.4 Fol-
lowing a distal lower extremity stab wound their pa-
tient developed EDB weakness and atrophy. AAS did
not evoke a CMAP. PLAS evoked a 1.35-mV wave,
while knee stimulation evoked a 0.27-mV wave, indi-
cating an ADPN conduction block. Three cases of
deep peroneal neuropathy in the presence of an
ADPN have been reported.4,6 These four cases differ
MUSCLE & NERVE January 1998
from our subject in that they had an absent or very
low amplitude CMAP upon AAS, and FHS accord-
ingly produced a monophasic CMAP. Correct iden-
tification of the pathologic nerve was therefore easily
accomplished with routine studies. In our case the
CMAP amplitudes evoked by AAS and PLAS were
comparable. Furthermore, ADPN conduction slow-
ing (relative to DPN) allowed for phase cancellation
following FHS and resulted in a bifid CMAP. This
‘‘double hump’’ sign is analogous to some cases of
carpal tunnel syndrome with a concomitant median–
ulnar anastomosis.9,13,14 Collision studies were essen-
tial in determining that the ADPN was responsible
for the delayed peak and was therefore the patho-
logic nerve. Visual inspection alone might have led
to an erroneous diagnosis of deep peroneal neurop-
athy.
In summary we have described a rare case of ac-
cessory deep peroneal neuropathy. Additionally we
describe a new application of the collision technique
in distinguishing between DPN or ADPN pathology.
The authors thank Lisa Feldman for assistance in preparation of
the figure.
REFERENCES
1. Azouvi P, Bouche P, Cathala HP: Nerf peronier accessoire.
Etude electrophysiologique. Rev Electroencephalogr Neurophysiol
Clin 1986;16:87–91.
2. Bryce TH: Long muscular branch of the musculocutaneous
nerve of the leg. Proceedings of the Anatomical Society of
Great Britain and Ireland. J Anat 1896;31:5–7.
Short Reports
3. Crutchfield CA, Gutmann L: Hereditary aspects of accessory
deep peroneal nerve. J Neurol Neurosurg Psychiatry 1973;36:
989–990.
4. Dessi F, Durand G, Hoffmann JJ: The accessory peroneal
nerve: a pitfall for the electromyographer. J Neurol Neurosurg
Psychiatry 1992;55:214–215.
5. Gutmann L: AAEM Minimonograph [2: Important anoma-
lous innervations of the extremities. Muscle Nerve 1993;16:
339–347.
6. Gutmann L: Atypical deep peroneal neuropathy in presence
of accessory deep peroneal nerve. J Neurol Neurosurg Psychiatry
1970;33:453–456.
7. Infante E, Kennedy WR: Anomalous branch of the peroneal
nerve detected by electromyography. Arch Neurol 1970;22:
162–165.
8. Kimura J: Collision technique. Neurology 1976;26:680–682.
9. Lambert EH: Diagnostic value of electrical stimulation of mo-
tor nerves. Electroencephalogr Clin Neurophysiol 1962;22:9–16.
10. Lambert EH: The accessory deep peroneal nerve: a common
variation in innervation of extensor digitorum brevis. Neurol-
ogy 1969;19:1169–1176.
11. Mapelli G, Pavoni M, DiBari M, Baroncini W, Manente A,
Bellelli T: The accessory deep peroneal nerve. Acta Neurol
1978;33:349–354.
12. Neundorfer B, Seiberth R: The accessory deep peroneal
nerve. J Neurol 1975;209:125–129.
13. Oh SJ: Clinical Electromyography: Nerve Conduction Studies, 2nd
ed. Baltimore, Williams and Wilkins, 1993, pp 321–330.
14. Sander HW, Quinto C, Chokroverty S: Median-ulnar anasto-
mosis to thenar, hypothenar, and first dorsal Interosseous
muscles: collision technique confirmation. Muscle Nerve (in
press).
15. Stamboulis E: Accessory deep peroneal nerve. Electroencepha-
logr Clin Neurophysiol 1987;27:289–292.
16. Winckler G: Le nerf peronier accessoire profond: etude
d’anatomie comparee. Arch Anat Histol Embryol 1934;18:
181–219.
MUSCLE & NERVE January 1998 123