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Recognizing Nerve Injuries In Patients With Acute Ankle Sprains
Noting that early recognition can facilitate a quicker rehabilitation, these authors provide salient pearls for diagnosing nerve injuries in patients with acute ankle sprains.
Up to 85 percent of ankle sprains are due to an inversion mechanism causing damage to the three main lateral ankle ligaments.1,2 While ankle sprains most often result from trauma causing injury to either the ligaments or bones about the ankle, there are other structures at risk that clinicians should keep in mind.
Coining “sprained ankle syndrome,” Fallat and colleagues demonstrated and reiterated the point that more than just the lateral ligaments are harmed in an inversion ankle sprain.3 The varied and concomitant structures injured in an ankle sprain may include the bones, joints and their capsules, muscles and tendons and, as we discuss in more depth, nerves. One should evaluate all of these structures in order to perform an optimal exam and direct appropriate treatment.
What happens when a patient comes in complaining of additional nerve-related symptoms (i.e., numbness, paresthesias, burning, radiating/shooting pain, cramping, weakness or motor function deficits) after an inversion or eversion ankle sprain?
During an ankle sprain, the mechanism of injury can lead to damage to the common peroneal nerve and/or its branches, the superficial peroneal or deep peroneal nerves as well as the sural, saphenous or tibial nerves.4–10 Oppenheim and coworkers reported the first documented case of peroneal nerve palsy after an ankle sprain over 100 years ago.11 Researchers often cite the common peroneal nerve as the most frequently injured nerve in the lower extremity, producing a range of symptoms from sensory deficits to motor function loss (e.g., foot drop).11,12
Anselmi stated that 15 percent of all grade 2 and 3 ankle sprains have some level of peroneal nerve damage.12 In a large prospective review of 639 acute ankle sprain patients, Fallat and coworkers found 80 patients (12.5 percent) with associated neuritis.3 Most patients in the study demonstrated injury to the superficial peroneal nerve’s terminal branches, resulting in tingling/burning along the nerve’s course or decreased pedal sensation in the nerve’s area of distribution.
A neuropathy to these structures can occur in either an acute or delayed manner.13 Acutely, traction on the nerve can result in either axon disruption (i.e., neuropraxia or axonotmesis, terms coined by Seddon, Sunderland and their respective colleagues) or entrapment along its course (see the table “A Guide To Nerve Injury Classifications” above”).9,14–16 Entrapments can be external (i.e., direct trauma, compression) or internal (i.e., compression, increased compartment pressure secondary to hematoma, traction or strain secondary to violent motion or ligament instability).17
We can divide the entrapment pathology into three stages with correlated histological nerve changes (see the table “What You Should Know About The Stages Of Nerve Entrapment” above). Nerve histological and functional changes occur between 6 and 50 percent strain while intraneural microcirculation may be impaired and can cease with as little as 8 and 15 percent elongation to the nerve respectively.9,14
Using electromyographic (EMG) measurements, Nitz and coworkers demonstrated that grade II ankle sprains resulted in peroneal and tibial nerve injury in 17 and 10 percent of patients studied respectively.9 These injury rates increased to 86 percent for the peroneal nerve and 83 percent for the tibial nerve in grade III sprains. Examples of delayed injury include intraneural ganglion cyst formation, neuroma formation or neuromuscular alterations resulting in various pathologies, most commonly chronic ankle instability.13
Ensuring An Accurate Diagnosis
Diagnosis is often difficult with symptoms being diffuse and poorly defined. In addition, the patient may be unable to fully express the issue. Furthermore, sites of nerve injury may cause referred pain to other anatomic locations (e.g., common peroneal nerve compression at the fibular head causing dorsal foot sensory deficits).
Although nerves can be injured at any point along their course, common and cited sites of injury include the common peroneal nerve, deep peroneal nerves, the superficial peroneal nerve, the sural nerve and the tibial nerve.
Common peroneal nerve. At the proximal fibula or peroneal ring, nerve injury occurs as the common peroneal nerve travels around the fibular neck and passes deep to the peroneal longus insertion. Pathology may be due to multiple variations of anatomy at this location, a direct blow against the fibula, tight overlying fascia, traction or the acute change in the nerve’s anatomic course.12,18,19
Deep peroneal nerves. At the anterior tarsal tunnel, the deep peroneal nerve passes through a fibro-osseous tunnel located between the inferior extensor retinaculum and the talus/navicular.4,17 There are actually three main regions of entrapment for the deep peroneal nerve as it courses under the various bands of the superficial and inferior extensor retinaculum with muscular and/or tendinous (deeper) compression against these more superficial structures.17 An entrapment injury can be secondary to trauma, either a direct blow or sprain of the ankle or midfoot.4
Superficial peroneal nerve. At a fibro-osseous tunnel located 8 to 12.5 cm proximal to the fibular tip, the nerve exits the deep fascia of the lateral compartment of the leg and enters into the anterior compartment where it becomes superficial.4 Superficial peroneal nerve entrapment is uncommon but can be the result of acute or chronic ankle sprains. One should consider this for any sensory symptoms (i.e., numbness, tingling) extending from the distal lateral leg and ankle into the dorsum of the foot, especially on palpation at the tunnel.4,7,20
Sural nerve. Injuries can occur at multiple locations along the sural nerve’s anatomic course in the lateral leg. The nerve runs posterior to the lateral mallelous and superficial to the extensor retinaculum, between 20 and 25 mm posterior to and 10 to 15 mm distal (inferior) to the fibular tip, terminating in the distal lateral aspect of the foot.21
A Pertinent Overview Of Testing For Nerve Injuries
Every patient who comes in for a lower extremity exam for any ankle sprain or acute/chronic ankle instability should have a thorough physical exam with a focused neurological exam using techniques to assess the culpable nerves.6,23
Common peroneal nerve at the fibular neck. Testing maneuvers include the palpation test.11,12,24
• Palpation test: Press/percuss the nerve as it wraps around the fibular neck.
• Note: Induced symptoms upon exam include sensory symptoms along the anterior and lateral leg and dorsum of the foot while motor symptoms may include weakness in dorsiflexion and eversion at the ankle or, more severely, full-on dropfoot. There may also be tenderness at the fibular neck.
Superficial peroneal nerve at the anterior lateral leg. Testing maneuvers include the provocative test, the percussion test and the passive/palpsation test.4,7,11,1,20
• Provocative test: Apply direct pressure over the entrapment site (8 to 12 cm proximal to the distal tip of the fibula) while the patient actively dorsiflexes and everts the foot against resistance.
• Percussion test: Percuss the nerve at its entrapment site while the foot is passively plantarflexed and inverted.
• Passive/palpation test: Press the nerve at the point where it transitions from deep to superficial fascia.
• Note: positive superficial peroneal nerve injury reported when pain and paresthesia elicited over the superficial peroneal nerve distribution in 2/3 tests.
• Note: Presenting or exam-induced symptoms include sensory symptoms (i.e. numbness, tingling) extending from the distal lateral leg and ankle into the dorsum of the foot. Motor and reflex function should be preserved with a pure superficial peroneal nerve injury.
Deep peroneal nerve at the anterior tarsal tunnel. Testing maneuvers include the palpation test.4,5,17
• Palpation test: Applying direct pressure at the entrapment site may cause altered sensation or pain in the distal first intermetatarsal space while percussion of the extensor hallucis brevis may cause a Tinel’s sign.
• Note: Presenting or exam-induced symptoms include dorsal midfoot aching pain or nerve symptoms (i.e., decreased sensory) in the first web space. Symptoms are often increased with activity or sleep and decreased with rest (plantarflexion of the foot places traction on the nerve through the tarsal tunnel).
Tibial nerve medially at the tarsal tunnel. Testing maneuvers include the palpation test and the provocative test.22
• Palpation test: Attempt to demonstrate the classic Tinel's sign at the tarsal tunnel with pressing the nerve against its deep osseous border.
• Provocative test: Position the foot in eversion while dorsiflexing the foot upon the ankle and toes upon the metatarsal heads. Holding this position for 10 seconds may increase symptoms.
• Note: Presenting or exam-induced symptoms include local or radiating sensory changes to the medial ankle or plantar foot (i.e. burning, paresthesias, temperature perception changes) while motor (i.e. intrinsic muscle weakness, toe contractures) symptoms are secondary to chronic or repetitive injury.
Sural nerve at the posterior lateral leg. Testing maneuvers include the palpation test and the provocative test.4,17
• Palpation test: Apply direct pressure along the sural nerve’s anatomic path.
• Provocative test: Applying passive stretch to the nerve through foot plantarflexion and inversion may reproduce symptoms.
• Note: Injury to the sural nerve should result in purely sensory deficits. Reflex and motor function along its course should be normal.
During the patient interview, consider the mechanism of injury (inversion versus eversion versus rotation) to determine what structures are at risk. Nerves on the tension side of the injury would be placed on traction (i.e. common peroneal nerve and superficial peroneal nerve for inversion, tibial nerve for eversion). For example, the superficial peroneal nerve is tethered proximally and distally so forced inversion and plantarflexion pulls the nerve taut against its fascial opening, and can cause subsequent injury.7
Ask patients what they remember from the sprain regarding direction of the foot and ankle. To complicate matters, multidirectional ankle sprain patterns may occur with the same injury. Although a presumed lateral sprain would put nerves like the common peroneal or superficial peroneal nerve on traction, the senior author had one patient who, in correcting her inversion sprain from falling, "wobbled" and everted the ankle. Her main subjective complaint on presentation was medial-related tibial nerve symptoms, creating a self/sprain-induced tarsal tunnel syndrome.
Regardless of the mechanism of injury, one should evaluate the obvious and sometimes self-reported injured nerve, but do not exclude an examination of the other aforementioned nerves. Additionally, perform neurological testing at the initial evaluation as well as at all follow-up exams in order to track changes with hopes of improvement rather than potential worsening or new symptoms.
Key Insights On Conservative Treatments
There are multiple conservative treatments one can attempt for nerve injuries.4,5,7,24 Elevation and ice will help decrease the localized swelling and external environmental pressure on the nerve. Immobilization, daily and nightly, allows removal of the aggravating maneuver of plantarflexion and inversion that often puts many of these nerves on traction, especially at night.5
Mitsiokapa and colleagues have mentioned the use of topical non-steroidal anti-inflammatory drugs (NSAIDs) or topical medications such as lidocaine, capsaicin, and topical diclofenac 1-2% to help treat nerve injuries.24 Oral medications including gabapentin, pregabalin (Lyrica, Pfizer), amitriptyline and clonazepam (Klonopin, Genentech) may assist in symptom reduction through their various mechanisms of action.6
One can also implement local corticosteroid injection at the point of entrapment, which acts both diagnostically and therapeutically in treatment.20 Musculoskeletal ultrasound can prove to be a valuable tool in targeting sites of entrapment or neuromas along the nerve in real time with the added benefit of more exact needle placement during injection therapy. Electromyography may also be useful in determining sensory and motor impairment to establish prognosis and treatment protocols.24
If a physical exam or advanced study demonstrates positive neural injury, one may implement physical therapy treatments earlier than normal, regardless of patient readiness for activity based on the concomitant injuries (i.e., high grade sprain, osseous injury where delayed motion or weightbearing may be enacted). Electrical stimulation modalities decrease pain through modulation of the gate mechanism of pain while cryotherapy slows nerve conduction velocities in addition to the gate theory effect for pain relief.1,23 Even without obvious nerve symptoms after a sprain, therapy directed to the nerves can be of benefit in the recovery process. This can include ankle isometric and TheraBand exercises, gait training, and desensitization modalities.25
Recently, Plaza-Manzano and colleagues demonstrated that by adding manual therapy techniques (“mobilizations to influence joint and nerve structures”) to the ankle and surrounding nerves in addition to basic strengthening and propioceptive exercises, patients had lower pain levels, reduced subjective instability, increased ankle strength, and increased active range of motion in the dual treatment group.10 This technique of neuromobilization, movement patterns to move and challenge the nervous system, has been well described in the literature and can be an important additional focus during physical therapy for ankle sprains.26
What Are The Surgical Options For Nerve Injuries?
When all else fails, surgical intervention may be warranted.7 Authors have recommended waiting at least three to seven months post-injury if symptoms do not resolve.24 The presentation of more severe neural injuries such as a dropfoot can shorten the threshold time to surgery to four to five weeks if little improvement has occurred.11
Dependent upon exam findings and the course of a patient’s symptoms, surgical procedures include exploration with neurolosyis, nerve excision or decompression at the known entrapment points.7,24 Multiple articles and case reports exist for techniques on specific sites of entrapment.5,22,27 Intra-operative ultrasound can be a valuable tool to identify and target anatomic regions or nerve deformity like a neuroma during surgery.4 Using surgical decompression, two of the dropfoot cases by Brief and coworkers showed improved motor and sensory function respectively (while having continued sensory and motor deficit respectively).11
The literature is filled with case examples of nerve-related pathology status for post-acute ankle sprains. Neuropraxia, the least severe form of neural injury, can take three to six weeks for recovery while axonotmesis may require months.15,17,28 In the aforementioned series by Fallat and colleagues, most nerve symptoms (e.g., tingling, burning, numbness) resolved within a week. However, reported symptoms for some patients lasted several months.3 Interestingly, several of the authors’ cases listed neuritis as the last symptom to resolve prior to full ankle sprain recovery.
Consequences of an ankle sprain can also be more severe. These consequences may include drop foot and complex regional pain syndrome (CRPS). Brief and colleagues discussed four examples of ankle sprains causing dropfoot via common peroneal nerve injury (the authors found another 16 cases in their literature review) with two patients having complete return of common peroneal nerve function while the other two patients showed partial sensory and motor function return respectively.11 With the superficial peroneal nerve being one of the most commonly involved nerves in CRPS in the foot and ankle, researchers have documented examples of post-acute sprain CRPS.25
In Conclusion
Nerve injury and associated pain/symptoms that manifest at the time of injury or even weeks later can cause a delayed recovery from the normal progression of healing an ankle sprain, requiring prolonged rehabilitation and therapy.9,24 Moreover, nerve injury should always be a differential diagnosis for a patient with either recurrent sprains or longstanding pain after a sprain. Approximately 70 percent of patients with acute ankle sprain will experience further sprains, recurrent joint instability, residual symptoms and decreases in functional capacity for up to two years after injury while approximately 30 percent will develop a chronic ankle instability.29,30 Long-term complications can result in more permanent nerve damage including: decreases in range of motion, proprioception and motor strength; muscle atrophy; and even CRPS.9,31 Anselmi discussed that residual peroneal weakness of neurogenic origin (sprain) is often misdiagnosed as an incomplete rehabilitation or recurrent instability.12
These are important points to remember in managing and treating these patients. By identifying a potential nerve injury early in the treatment of your patients, you can set better expectations as you coach patients through the rehabilitation process back to health.
Dr. Hood is a fellowship-trained foot and ankle surgeon practicing in Nashville. Follow him on Twitter at @crhoodjrdpm or check out his website www.footankleresource.com, which contains information on student/resident/new practitioner transitioning as well as links to academic and educations resources found throughout the Internet.
Dr. Morrison is a second-year resident with the Bryn Mawr Hospital/Main Line Health System PMSR/RRA residency in Bryn Mawr, Pa.
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