Keywords
bariatric surgery - cycling - exercise - peroneal neuropathies - weight loss
Introduction
Common fibular nerve (CFN) palsy is one of the most common mononeuropathies in the
body, the most common in the lower limbs, and several etiologies have been described.[1] When considered a non-traumatic lesion, compressions remain the most common cause.
There are several risk factors for fibular compression: tumors, position of the legs,
muscular edema and small hematoma on asthenic athletes, fibrous bands, changes in
the bones, iatrogenic conditions, and others.[2]
[3] The association of rapid weight loss with prolonged physical exercise as a cause
of CFN palsy has not been well reported.[4] We herein described a case of an amateur cyclist who experienced foot drop after
a bariatric surgery.
Case Report
The present case report was approved by the institutional ethics committee, and the
patient signed the free and informed consent form.
A 39-year-old man weighing 123.80 Kg and 1.80 m tall (body mass index: 38.2Kg/m2; body surface area: 2.404m2), classified grade-II obese,[5] had been submitted to a bariatric surgery through the Santoro method (vertical gastroplasty).[6] He had only one kidney that had been transplanted four years before the bariatric
surgery.
Two weeks after the bariatric surgery, the patient lost 14.3 Kg (11.6% of his initial
weight). After 1 month, his weight was of 103.6 Kg (a loss of 16.6% of his initial
weight). Eight months and a half after the surgery, he weighed 84 Kg (loss of 39.4
Kg and of 32.1% of his initial weight). During this period, the patient started to
practice amateur long-distance cycling. Eleven months after the bariatric surgery,
after a strenuous 70-Km ride in a straight route, he experienced paresthesia in anterior
region of the distal leg and in the dorsal part of the foot. The next day, he rode
another 45 Km downhill, and the day after that, he woke up feeling his left foot drop
and loss in extension force ([Fig. 1A]).
Fig. 1 (A) The maximum extension of the left foot shows the disability twenty days after the
onset of symptoms. (B) Planning and (C,D) surgical decompression of the CFN. (E,F) Clinical evidence of complete recovery of the extension and full range of motion
of the left feet 24 months after the surgery.
He sought care two weeks after symptom onset. The physical examination did not show
muscular atrophy, but showed an M2 in the anterior tibialis and paresthesia in the
region of the CFN. An electroneuromyographic study was performed 20 days after the
initial clinical symptoms, and it showed subacute sensory mononeuropathy and motor
demyelinating neuropathy that was initially moderate to severe (with presence of conduction
block and secondary degenerative axonal sign) at the level of the head of the fibula;
thus, the diagnosis was confirmed. A metabolic study was performed, but the hemogram
and the levels of B-complex vitamins were completely normal. Decompression was indicated
and performed 15 months after bariatric surgery, 4 months after the onset of the neurological
symptoms.
The surgery was performed with the patient under general anesthesia, using pneumatic
tourniquets on the thigh with 340 mmHg. A 6-cm incision was made over the fibular
neck ([Fig. 1B]) and, after a careful dissection, the compression of the CFN was revealed in the
osteofibrous band of the origin of the long peroneal muscle. The nerve featured an
hourglass with aspects of chronic compressive neuropathy. The fibrous band was released
throughout the course of the nerve course, and a careful external neurolysis was performed
with a 3.2 magnifying glass ([Fig. 1C] and [1D]).
The anterior sensitivity in the distal leg and dorsal region of the left foot was
partially recovered immediately after surgery. During the follow-up, there was a gradual
improvement in the strength of the anterior muscles on physical examination. Seven
days after the surgery, the patient experienced subsidence of the pain. After 10 weeks,
the clinical examination revealed total recovery of strength and sensitivity, which
is illustrated in photos taken 24 months postoperatively ([Fig. 1E] and [1F]).
Discussion
The CFN is the minor and lateral division of the sciatic nerve, and it originates
in the lumbar sacral division (L4 to S2, posterior division). In the popliteal fossa,
sciatic nerve divides into the CFN and the tibial nerve. The CFN crosses the lateral
head of the gastrocnemius muscle and, as it courses to the head of the fibula, it
emerges more subcutaneously and divides into superficial and deeper peroneal nerves.
The former innervate the lateral muscle of the leg and provide sensitivity to the
dorsal side of the feet, except to the first interdigital space. The latter innervate
the muscles of the anterior compartment of the leg and provide sensitivity to the
first space of the interdigital web.[1] On its course to the peroneal neck, the CFN takes the path of the peroneal tunnel,
an osteofibrous band located at the origin of the long peroneal muscle that it is
a common site of entrapment.[4]
Several risk factors for compression of the CFN have been described in the literature:
behavior of prolonged crossing and squatting of the legs, intra- and extraneural compressive
masses, recent anesthesia, surgery and prolonged hospitalization, diabetes, and metabolic
alterations such as malnutrition and vitamin complex deficiency,[4] a usual finding in obese patients, for 20% to 30% of them have nutritional disorders
that may worsen after surgery.[5]
Weight loss has been reported as a habitual cause of CFN neuropathy. The frequency
of neurological complications among bariatric patients has been reported to range
from 1.3% to 4.6% of the cases.[6] Some pathological causes have been described: loss of the protection of the subcutaneous
tissue, which causes compression of the nerve against the hard structure of the bone,
an immune mechanism of inflammatory infiltration into the microstructure of the nerve,
such as cachexia, and the nutritional deficiencies.[7]
Conversely, in athletic patients, the CFN is the nerve most affected by traumatic
lesions, and blunt trauma is the most common mechanism. On the other hand, traction
injuries, although less common, could be more severe.[8] Few sports have been associated with non-traumatic CFN palsy, such as chronic exertional
compartment syndrome. In a study involving patients who were runners, Peck et al.[9] reported that a repetitive movement combining plantar flexion and inversion while
running downhill or on uneven surfaces could cause a distension in the fibular head
of the CFN.[9] The case herein reported is that of an amateur cyclist with a CFN lesion that may
have worsened after extreme weight loss and a strenuous leg exercise, which was an
unusual presentation of CFN palsy. Strenuous exercise can cause microtrauma in the
muscle belly, which results in local edema and small hematomas, which may be another
cause of compression due to physical exercise.[8]
The treatment is based on the cause and severity of the nerve palsy. When the symptoms
are intermittent and it is possible to make changes regarding lifestyle, a conservative
treatment should be administered. Changing behavior in terms of position of the legs,
sleep, exercises, posture, protecting the prominent fibular head and rehabilitation
to stretch the contralateral muscle groups, and progressive strengthening of the dorsiflexors
are some practices that must be performed. When any traumatic lesion or full motor
or sensory function is lost, or there are no signs of improvement within 6 weeks to
3 months of the conservative treatment, a surgical approach and microneurolysis of
the CFN are indicated. Good outcomes have been reported after neurolysis surgery,
with 3% of cases of some motor or sensitive deficit.[2]
[9]
[10]
Palsy of the CFN has countless causes, both traumatic and non-traumatic. However,
weight loss followed by bariatric surgery and strenuous sports may be a possible etiology
of CFN palsy.
