Clinician’s Corner
Case 1: Foot drop and
numbness in a 16-year-old girl
A
16-year-old girl presented with a two-week history of right
foot drop and numbness along the dorsum of her right foot
and anterolateral aspect of the lower limb. She also described a
pinching pain behind the medial aspect of the right knee. There
were no complaints of bowel or bladder incontinence, radiating
back pain or saddle paresthesia. Review of systems revealed a
three-month history of constipation, believed to be related to a
two-year self-imposed dietary restriction. Her medical history
included appendectomy as a child and a right patellar subluxation
one year previously. The patient reported no recent trauma or
previous neurological problems.
Pertinent neurological findings included: weakness in right
dorsiflexion (2 of 5), ankle eversion (4+ of 5) and toe extension
(4+ of 5); decreased pin-prick sensation in the right anterolateral
calf, dorsolateral aspect of the foot and webspace between the first
and second toes; and dragging of the right foot during gait analysis,
with impaired dorsiflexion on heel strike. All other neurological
findings were normal. Her head circumference was 54 cm, height
was 165 cm and weight was 47.5 kg. The patient’s body mass index
was 17.4 kg/m2 (eighth percentile for age). Before food restriction,
the patient had weighed 59 kg (body mass index 21.7 kg/m2, 70th
percentile). At the time of presentation, she was awaiting hospital
admission for treatment of a newly diagnosed eating disorder. Her
general physical examination revealed no other pertinent
findings.
Further investigations confirmed the diagnosis and underlying
cause.
Correspondence (Case 1): Dr Evan Cole Lewis, Department of Pediatrics – Children’s Hospital of Eastern Ontario, Division of Neurology, 401 Smyth
Road, Ottawa, Ontario K1H 8L1. Telephone 613-737-7600 ext 2159, e-mail [email protected]
Correspondence (Case 2): Dr Julian AJ Raiman, Division of Clinical & Metabolic Genetics, Hospital for Sick Children, Department of Paediatrics,
University of Toronto, 555 University Avenue, Toronto, Ontario M5G 1X8. Telephone 416-813-5753 (clinical) or 416-813-5753 ext 5340 (academic),
fax 416-813-4940, e-mail [email protected]
Case 1 accepted for publication May 15, 2013. Case 2 accepted May 21, 2013
Paediatr Child Health Vol 18 No 10 December 2013
©2013 Pulsus Group Inc. All rights reserved
515
Clinician’s Corner
case 1 Diagnosis: Compressive Peroneal
Neuropathy Secondary to Weight Loss
The clinical examination led to a preliminary diagnosis of peroneal
mononeuropathy. Pointed questioning revealed that the patient was
prone to habitual leg crossing. Family history for hereditary neuropathies was negative. The patient denied alcohol or drug abuse and
recent prolonged bedrest. Laboratory testing revealed a normal
erythrocyte sedimentation rate and normal antinuclear antibody,
thyroid-stimulating hormone, T4, vitamin B12 and folate levels.
Nerve conduction studies and electromyography confirmed the
diagnosis of a common peroneal neuropathy. Nerve conduction
studies revealed a conduction block across the fibular head and
below-normal compound motor action potential amplitudes.
Conduction slowing was not observed. Remaining sensory and
motor nerve responses in both legs were normal. Electromyography
of the right tibialis anterior muscle revealed active and chronic
denervation changes. The right peroneus longus, biceps femoris
and gastrocnemius muscles were normal.
The peroneal nerve wraps around the neck of the fibula (between
the fibula and the peroneus longus muscle) in what is referred to as
the fibular tunnel (1). At this point, the common peroneal nerve
divides and compression of the peroneal nerve can occur. The deep
peroneal nerve innervates the tibialis anterior muscle (dorsiflexion
of the foot) and the toe extensors (the digitorum longus, digitorum
brevis and hallucis muscles) (1). The superficial nerve innervates
the peroneus longus and brevis muscles (assisting in ankle eversion
and plantar-flexion) (1). In terms of sensory function, the superficial
peroneal nerve innervates the skin on the lower two-thirds of the
anterolateral aspect of the lower leg, while the deep peroneal nerve
innervates the webspace between the first and second toes (1).
For common peroneal neuropathy presentations, history typically
reveals a description of weakness in muscles supplied by the superficial
and deep peroneal nerves with or without associated sensory complaints (1). Physical examination should exclude other possible
neuroanatomical localizations such as a lumbosacral radiculopathy,
lumbosacral plexopathy, sciatic neuropathy or polyneuropathy.
Compressive peroneal neuropathy can result from habitual leg
crossing or other prolonged posturing, unadjusted foot/ankle
orthoses, compression from a lower limb cast, prolonged illness
resulting in being bedridden, surgery or trauma (1-3). Tumours and
cysts can compress the peroneal nerve, and magnetic resonance
imaging should be considered in this context (1,2,4). Hereditary
neuropathy with liability to pressure palsies, an autosomal dominant disorder, may be a consideration, particularly with a positive
family history. Diabetes, thyroid dysfunction, vitamin B12 deficiency, alcohol abuse and systemic lupus erythematosus should be
considered as causes of noncompressive peroneal neuropathy.
Several studies have reported that patients can develop peroneal nerve compression following significant weight loss (5,6). The
decrease in fat tissue surrounding the nerve exposes it to mechanical
damage from adjacent skeletal structures. Important determinants
include amount of weight lost and time period of weight reduction. A
reduction in body fat >10% is clinically significant (7) and weight loss
in a short period of time is associated with a higher risk of developing
peroneal neuropathy (7). An underlying cause for the weight loss
should always be elicited because weight loss may be secondary to
a variety of medical or psychiatric conditions, such as malignancy,
pituitary hypofunction, syringomyelia, anorexia nervosa or depression
(8,9), or due to nonpathological conditions such as recent bariatric
surgery or dietary modification independent of psychiatric illness
(7,10).
Our patient had lost 19% of her body weight over the course of
two years and was on the waitlist for the in-patient treatment program
for anorexia nervosa. The present case is an example of compressive
516
peroneal neuropathy secondary to excessive weight loss due to anorexia nervosa. Peroneal neuropathy in the context of anorexia nervosa
was first documented in 1979 (11), and multiple case reports regarding
patients with anorexia nervosa presenting with foot drop have subsequently been published (4,12-15). While the relationship was initially
unclear, peroneal neuropathy is most likely due to mechanical compression neuropathy associated with the weight loss, as opposed to a
specific vitamin deficiency (14). Particular postures, such as leg crossing, appear to be important precipitating factors (11), whereas the
role of inactivity as an exacerbating or protective factor remains
unclear (11,15).
CLINICAL PEARLS
• Ankle inversion is weak in L5 radiculopathy but spared in a
common peroneal neuropathy.
• Patients with anorexia nervosa are at risk for compressive
neuropathy.
• Consider screening for causes of a noncompressive peroneal
neuropathy including diabetes, thyroid dysfunction, vitamin B12
deficiency, alcohol abuse and systemic lupus erythematosus.
Jeanette W Evans BSc
University of Ottawa
Erick Sell MD
Evan Cole Lewis MD
Department of Pediatrics, Division of Neurology
Children’s Hospital of Eastern Ontario
Ottawa, Ontario
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Paediatr Child Health Vol 18 No 10 December 2013