damage as a result of torsional injuries to the ankle is
uncommon. It does appear however, that subclinical injury to the
common peroneal nerve following ankle injuries is more prevalent
than previously thought. This case report highlights the
importance of neurological assessment in all patients who
present with ankle sprains no matter how benign the mechanism of
injury may be. An excellent end result was obtained in this
patient with conservative treatment alone.
forty year old gentleman presented to the emergency department
having twisted his right ankle on rough ground one day earlier.
His main complaint at the time of presentation was that of
lateral ankle pain and swelling and inability to weight bear. In
addition he was noted to have a complete foot drop which had
progressed overnight following his injury. He also described
altered sensation over the lateral aspect of the leg and dorsum
of the foot.
past history included low back pain with left sided sciatica
which had responded to physiotherapy. He had also sustained two
previous inversion type injuries to his right ankle from which
he had made a complete recovery.
examination he held his foot in plantar flexion and was found to
have significant swelling and tenderness over the lateral
ligament complex. There was also tenderness over the posterior
aspect of the lateral malleolus. Ankle passive range of motion
was uncomfortable and restricted. Distal pulses were palpable.
Knee and hip examination revealed no focal swelling or
tenderness with normal pain free range of motion. Neurological
assessment showed altered sensation to pin prick in the
distribution of the common peroneal nerve and MRC grade 1 power
in the ankle dorsiflexors. Left lower limb neurology was normal.
anteroposterior and lateral radiographs of the right ankle
showed no fracture. Urgent MRI scan of the lumbar spine showed a
small L4/L5 disc bulge on the left side which was not in keeping with the clinical findings.
EMG studies, performed within two weeks of the injury, showed
evidence of a severe demyelinating lesion of the right common
peroneal nerve around the fibula neck.
conduction velocity was in the demyelinating range in the right
common peroneal nerve around the fibula neck (velocity of 23 m/s
on the right compared to 48 m/s on the left). Sensory nerve
action potential was of significantly reduced amplitude in the
right superficial peroneal nerve when compared to the left
(amplitude of 7uV on the right compared to 21uV on the left).
needle EMG sampling showed evidence of marked chronic
denervation with reinnervation in the right tibialis anterior
and right peroneous brevis. The right tibialis anterior showed
scanty fibrillation potential and positive sharp waves but on
voluntary effort there were long duration low amplitude
re-innervation motor units firing at abnormally rapid rates. The
right peroneus brevis also showed evidence of re-innervation.
The presence of re-innervation activity indicated continuity of
the nerve. This study confirmed that the patientsí lesion was
peripheral in the common peroneal nerve and was not due to
patient was managed non-operatively with a foot drop splint and
an intensive physiotherapy programme. He was reviewed regularly
in the fracture clinic and by six weeks there was clinical
evidence of nerve function recovery. He progressed well and at
final follow up five months following his injury he was found to
have a stable ankle with normal pain free range of motion.
Sensation was improving with MRC grade 5 power in the ankle
, an estimated 302,000 ankle sprains are seen each year in
Accident and Emergency Departments. This common injury is most
frequently sustained during sporting activity usually as a
result of forced ankle plantar flexion and inversion. Lateral
ankle sprains account for 85% of all ankle sprains (1).
lateral ankle ligament complex consists of anterior talofibular
ligament (ATFL), the calcaneofibular ligament (CFL), and the
posterior talofibular ligament (PTFL). ATFL is the weakest and
most frequently injured element of the lateral ankle ligament
complex. Lateral ankle ligament injuries are graded from I to
III, based on increasing ligament damage and morbidity. In a
grade I sprain, the ATFL is stretched with some of the ligament
fibres torn, but no frank ligamentous disruption is present. A
grade II sprain frequently involves complete tear of the ATFL
and an additional partial tear of the CFL. A grade III injury
implies complete disruption of both ATFL and CFL, possibly with
a capsular tear. An accompanying tear of the PTFL can be present
complication of common peroneal nerve palsy following an ankle
sprain has been rarely reported in the English language medical
literature (2,3,4,5,6). Isolated superficial peroneal nerve
palsy has also been reported (7).
nerve injury is thought to be rare, a study by Nitz AJ et al (8)
found that in their study group 86% of patients with grade 3
ankle sprains had EMG evidence of injury to the peroneal nerve
at two week follow up although clinical neurological examination
remained normal. In addition 83% of patients with grade 3
sprains had EMG evidence of injury to the posterior tibial
nerve. This would suggest that subclinical injury to peripheral
nerves may be more common following severe ankle sprains than
aetiology of peroneal nerve paralysis following ankle sprain is
not clearly understood. It is postulated that several mechanisms
act alone or in combination to result in the clinical picture.
Oppenheim (9) suggested nerve traction as a possible cause, as
the nerve rounds the fibular neck.
(10) postulated that the peroneal nerve is compressed against
the fibular neck when the investing fibrous origin of the
peroneus longus is drawn tight as the muscle resists ankle
inversion. The effects of the nerve damage would be immediate in
these situations. In Hyslopís three cases of peroneal-nerve
palsy following inversion sprains of the ankle, paralysis
occurred immediately followed the injury in only one. In another
the palsy did not develop until the day after the inversion and
planter flexion sprain; and in the third, not until one week
after the sprain. In cases of delayed onset of paralysis,
traction-compression mechanism does not fully explain the mode
of injury. In these cases, it is more likely to be the result of
a gradually expanding hematoma within the nerve sheath
consequent to rupture of a nutrient vessel.
two cases of common peroneal nerve injury following spiral
fractures of the distal fibula, reported by Nobel (4), the
dramatic disappearance of pain and paralysis after early
evacuation of the hematoma strongly suggest that the hematoma in
the nerve sheath was the sole cause of the paralysis.
our patient neurological symptoms developed overnight resulting
in footdrop. Leg pain was not significant at the time of
presentation. The late onset of the paralysis in this case
favours the diagnosis of paralysis by a hematoma which developed
gradually and was subsequently resorbed without permanent
sequelae. Function of the peroneal nerve should be evaluated in
all patients with the history of inversion ankle sprain. Manual
muscle testing and neurological exams should be performed. This
examination helps in making a differential diagnosis between
overstretched nerve fibres and hematoma.
is usually immediate after overstretching, but if the paralysis
has a gradual onset and causalgia-like pain develops, a hematoma
within the sheath is more likely. Early evaluation with EMG
studies is invaluable and provided the EMG studies show
continuity of the nerve with evidence of re-innervation we feel
that this unusual case can be managed safely by non-operative
measures. There does not appear to be convincing evidence to
suggest that early surgical exploration of the nerve is
appropriate in all cases.
case acts as a reminder of the importance of neurological
assessment in patients who present with ankle sprains even if
the mechanism of injury appears benign. An excellent recovery
occurred in our patient with conservative treatment measures
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