Sports Medicine: Just the Facts

CHAPTER 67 • NERVE ENTRAPMENTS OF THE LOWER EXTREMITY 399

(Baxter, 1993). A history of prior ankle injuries with

instability is common.

SYMPTOMS ANDSIGNS

• Neuropathic medial heel pain radiating along the
  medial arch toward the plantar aspect of the first and
  second toes.


• Tenderness at the superior aspect of the AHM at the
  navicular tuberosity, with distally radiating pain or tin-
  gling. Provocative testing includes forceful passive
  heel eversion, standing on the balls of the feet, or per-
  cussion over the nerve. Sensory loss, weakness, or
  atrophy is rarely reported. The athlete should be exam-
  ined for ankle instabilities, malalignments, hallux
  rigidus, AHM hypertrophy, and a valgus running style.

DIFFERENTIALDIAGNOSIS ANDEVALUATION

• Differential diagnosis parallels that of TTS, with the
  exception of additional local pathological processes.


• Resisted great toe plantarflexion or passive toe dorsi-
  flexion will induce pain with flexor tendonitis, but not
  typically with nerve entrapment (McCluskey and
  Webb, 1999). Hindfoot and midfoot synovitis, arthri-
  tis, and stress fractures should be considered.


• Evaluation is similar to that for TTS.

TREATMENT

• Treatment principles are parallel to those for TTS.
  Rigid orthoses should be modified, replaced, or
  removed to avoid MPN compression. Functional
  hyperpronation may be addressed.


• Therapeutic injection should avoid direct nerve con-
  tact. Surgical release has been successful in refractory
  cases and is generally a distal extension of the surgery
  performed for TTS.

COMMON PERONEAL NERVE (CPN)

DEFINITION

• Common peroneal nerve(CPN) entrapment typically
  occurs at the fibular head, proximal to the bifurcation
  into the SPN and DPN, and produces dorsiflexion
  weakness and possibly neuropathic pain extending
  over the anterolateral leg and foot dorsum (Smith and
  Dahm, 2001).

ANATOMY, PATHOPHYSIOLOGY, ANDRISKFACTORS

• The CPN consists of sensory and motor fibers from
  the L4-S2 segments and is the smaller terminal
  branch of the sciatic nerve. The CPN separates from
  the sciatic nerve just above the knee, where it sup-
  plies innervation to the short head of the biceps
  femoris (the only thigh muscle innervated by the

peroneal nerve) and divides into the SPN, DPN, and

lateral sural cutaneaous nerve(LSCN) at the level of

the fibular head. The SPN innervates leg lateral com-

partment muscles, and then emerges from the lateral

compartment by penetrating the crural fascia 10.5 to

12.5 cm proximal to the tip of the lateral malleolus. It

supplies sensation to the anterolateral leg, and then

divides into its terminal medial and intermediate

cutaneous branches about 6 cm above the lateral

malleolus. These branches enter the foot dorsum

superficial to the inferior extensor retinaculum and

supply sensation to the foot dorsum, including the

medial aspect of the first toe, and the adjacent sides

of the third and fourth, and fourth and fifth toes. The

DPN traverses the leg anterior compartment, inner-

vating all the muscles including the peroneus tertius,

divides into medial and lateral branches 1 to 2 cm

proximal to the ankle, and enters the foot deep to the

inferior extensor retinaculum. Its medial branch sup-

plies sensation to the first web space, and its lateral

branch innervates the EDB as well as local joints. Up

to 20% of individuals may have accessory innerva-

tion of the EDB from the SPN (McCluskey and

Webb, 1999).

• The CPN is vulnerable to compression at the fibular
  head. Reported etiologies of SPN injury include exter-
  nal compression (knee crossing, bed rest, casts,
  orthoses), aneurysms, tumors, (e.g., neurofibroma),
  tibiofibular joint ganglion, fibular head dislocation,
  Baker’s cyst, generalized ligamentous laxity, genu
  varum, genu recurvatum, and compartment syndrome
  (Moller and Kadin, 1987; Di Risio, Lazaro, and Popp,
  1994; Nagel et al, 1994). Repetitive combined plan-
  tarflexion and inversion while running downhill or on
  uneven surfaces may also produce stretching of the
  CPN at the fibular head.

SYMPTOMS ANDSIGNS

• The DPN is often more severely affected than the
  SPN. The athlete may report neuropathic symptoms
  extending into the dorsal foot and toe web spaces. The
  most common complaint is dorsiflexion weakness.


• The athlete may complain of foot drop, steppage gait,
  recurrent ankle sprains, and/or an otherwise funny
  sound when running.

DIFFERENTIALDIAGNOSIS ANDEVALUATION

• Differential diagnosis includes compartment syn-
  drome, sciatic neuropathy, lumbosacral plexopathy
  and L5 radiculopathy.


• EDX studies may be extremely helpful for localiza-
  tion, prognostication, and differential diagnosis; how-
  ever, EDX abnormalities may only occur postexercise
  (Leach, Purnell, and Saito, 1987).