Ski Season is here! This article discusses the most common ski nerve injuries…
Lower-limb neuropathies in skiers most commonly arise from a convergence of biomechanical and environmental factors, particularly external compression from ski boots, sustained postures, and cold exposure. High-energy trauma and exertional compartment syndromes are less frequent but important differentials.
Risk is amplified by tight or poorly contoured boots, tall rigid cuffs creating focal edge pressure, overly tightened buckles or tongues compressing the dorsum of the foot, ill-fitting footbeds, and prolonged static loading while queuing or sitting on chairlifts.
Cold-induced slowing of nerve conduction, boot-related oedema within a noncompliant shell, and pre-existing metabolic or polyneuropathic risk further increase susceptibility.
The skiing stance itself predisposes to nerve compression, with the ankle held in dorsiflexion and the shank inclined forward into a rigid cuff, transmitting pressure to the anterior tibia and laterally toward the fibular head.
Compression beneath the boot tongue and dorsal buckles can affect the region of the inferior extensor retinaculum, where the deep peroneal nerve is particularly vulnerable, while misplaced medial buckles or narrow medial shells may load the tarsal tunnel.
Malaligned cuffs biasing the tibia into varus or valgus can further concentrate pressure at the fibular neck or medial malleolus. Race boots and over-tightened micro-adjust buckles increase contact stress, and behaviours such as prolonged squatting in lift lines or leg-crossing on chairlifts are well-recognised contributors to fibular neck compression.
Clinical assessment should focus on early differentiation of peripheral mononeuropathies from L5/S1 radiculopathy and exertional compartment syndromes.
Neurapraxias typically present acutely with paraesthesia or numbness and may resolve rapidly once compression is relieved, whereas axonotmesis can evolve over days with progressive weakness and delayed denervation changes.
Electrodiagnostic testing, nerve conduction studies early to identify conduction block, followed by needle EMG after 2–3 weeks to assess axonal loss, remains central to localisation.
High-resolution ultrasound can demonstrate focal entrapment or neuroma, while targeted MRI or radiographs are indicated where trauma or space-occupying pathology is suspected.
In cases of suspected exertional syndromes, dynamic compartment pressure testing remains the reference standard.
LATERAL NERVES
Common Peroneal Nerve
- Function: Motor and sensory
- Muscles Innervated: Innervates the muscles of the anterior and lateral compartments of the leg (e.g., tibialis anterior, extensor digitorum longus, fibularis longus, and fibularis brevis).
- Clinical Significance: Injury can result in foot drop (inability to dorsiflex the foot), loss of eversion, and sensory loss over the anterolateral aspect of the leg and dorsum of the foot.
Common peroneal nerve palsy at the fibular neck is the archetypal ski-boot neuropathy. The nerve wraps superficially around the fibular neck before dividing into deep and superficial branches, leaving it vulnerable to tall cuff edge pressure, prolonged squatting, and chairlift leg-crossing.
Varus knee stress, fibular head avulsion, or fibular neck fractures after falls can coexist. Patients report numbness over the anterolateral leg and dorsum of the foot and may develop foot drop with tripping, often after a long day in tight boots or time spent waiting in lift lines.
Examination reveals weakness of dorsiflexion (tibialis anterior), toe extension (extensor hallucis and digitorum longus), and eversion (peronei) if the lesion is proximal to the bifurcation, with preservation of plantarflexion and inversion (tibial nerve).
Sensory loss involves the anterolateral leg and dorsum of the foot; a Tinel sign is often present at the fibular neck. Steppage gait may be observed. L5 radiculopathy is the key differential; inversion strength (tibialis posterior, tibial nerve) and hip abduction (gluteus medius) help distinguish proximal causes, as do back symptoms and reflex changes.
Management begins with immediate pressure relief by loosening or modifying the cuff and adding padding over the fibular neck, followed by an ankle – foot orthosis when foot drop compromises safety, physiotherapy with nerve gliding and strengthening, and neuropathic pain control.
Ultrasound can identify focal compression or swelling of the common peroneal nerve at the fibular head.
NCS and EMG localize and grade injury; knee imaging is warranted after trauma. Refractory compression or structural lesions may require surgical decompression.
Prevention hinges on avoiding leg-crossing and prolonged squatting, ensuring cuff alignment and adequate flare and padding at the fibular neck, selecting appropriate shell height and last, avoiding overtightening, and maintaining warmth, particularly in patients with metabolic risk.
Superficial Peroneal Nerve
- Function: Motor and sensory
- Muscles Innervated: Fibularis longus and fibularis brevis.
- Clinical Significance: Injury can lead to weakness in eversion of the foot and sensory loss over the lower leg (anterolateral aspect) and the dorsum of the foot.
Superficial peroneal nerve entrapment typically occurs where the nerve exits the lateral compartment fascia in the distal leg to become subcutaneous.
Boot shell or liner seams, lateral cuff edges, or oedema can compress the fascial exit point; chronic inversion sprains with scarring predispose to entrapment.
Patients report burning or dysesthesia over the anterolateral leg and dorsum of the foot, often aggravated by tight cuffs or prolonged edging; eversion weakness may occur if the motor branch is involved. Sensory loss spares the first web space.
Percussion tenderness and a Tinel sign at the fascial exit, pain with nerve glide testing, and preserved dorsiflexion strength relative to common peroneal palsy help localize the lesion. Dynamic ultrasound can confirm focal entrapment.
This ultrasound diagram shows the superficial peroneal nerve moving from a deep to superficial position exiting the crural fascia, where it is most likely to become entrapped.
Consider testing for chronic exertional compartment syndrome when symptoms are exertion-dependent. Management includes lateral cuff and liner modification, padding and smoothing of seams, orthoses to reduce lateral shear, physiotherapy, and, for refractory cases, perineural hydro dissection or surgical release.
ANTERIOR NERVES
Deep Peroneal Nerve
- Function: Motor and sensory
- Muscles Innervated: Innervates the extensor muscles in the anterior compartment of the leg (e.g., tibialis anterior, extensor hallucis longus, extensor digitorum longus, and fibularis tertius).
- Clinical Significance: Injury can cause foot drop, reduced dorsiflexion, and numbness in the web space between the first and second toes.
Deep peroneal nerve entrapment at the inferior extensor retinaculum – the so-called anterior tarsal tunnel or the more classic “ski-boot syndrome” – results from pressure by the tongue or dorsal buckles over the dorsum of the foot.
The deep peroneal nerve traverses beneath the retinaculum with the extensor tendons and supplies sensation to the first web space and motor innervation to extensor digitorum and hallucis brevis. Patients develop dorsal foot pain and paraesthesia maximal in the first web space that worsen with tight lacing or buckling, commonly in racers who aggressively cinch the tongue. There may be weakness or atrophy of the short toe extensors.
A Tinel sign at the dorsum near the retinaculum and symptom reproduction with plantarflexion–inversion or with simulated lacing support the diagnosis. Nerve conduction studies may show reduced sensory amplitude to the first web space; ultrasound can demonstrate retinacular thickening.
Management is mechanical: loosening or reconfiguring dorsal buckles, adding padding with cut-outs to redistribute pressure, heat-moulding tongues, and allowing sufficient toe box height. Persistent deficits can be treated with decompression.
MEDIAL NERVES
Tibial Nerve
- Function: Motor and sensory
- Muscles Innervated: Innervates muscles in the posterior compartment of the leg (e.g., gastrocnemius, soleus, tibialis posterior) and some plantar muscles in the foot.
- Clinical Significance: Injury can result in weakness of plantarflexion, difficulty walking on toes, and sensory loss in the plantar aspect of the foot.
Tarsal tunnel syndrome in skiers arises from compression of the tibial nerve beneath the flexor retinaculum posterior to the medial malleolus.
Medial shell or buckle pressure, pronation within the boot, oedema, and unmasked space-occupying lesions can contribute. Patients describe burning and tingling of the plantar foot and toes, often with nocturnal worsening and exacerbation by tight medial buckles or long runs; intrinsic foot cramping may be reported.
Examination reveals a Tinel sign over the tarsal tunnel, plantar sensory loss, and, in later stages, intrinsic muscle weakness and atrophy; the dorsiflexion–eversion with toe extension manoeuvre reproduces symptoms.
Nerve conduction may show prolonged distal latencies; ultrasound or MRI can detect masses; foot mechanics should be assessed. Management includes relocating or loosening medial buckles, padding or cut-outs over the medial malleolus, custom footbeds to control pronation, and analgesic strategies, with surgical decompression reserved for refractory cases.
Sural Nerve
- Function: Sensory
- Muscles Innervated: No motor function; provides sensory innervation.
- Clinical Significance: Injury typically leads to sensory loss along the lateral aspect of the foot and the heel.
Sural nerve neuropathy presents with burning or numbness over the lateral heel and foot due to pressure along the posterolateral cuff, at the Achilles strap, or behind the lateral malleolus; race straps and lateral ankle sprains are additional culprits. Examination demonstrates a Tinel sign along the retro-malleolar course and purely sensory deficits. Management is typically mechanical, with posterior cuff and strap adjustments, padding, and avoidance of focal pressure; neuroma formation may require targeted interventions.
Saphenous Nerve
- Function: Sensory
- Muscles Innervated: No motor function; provides sensory innervation.
- Clinical Significance: Injury can cause numbness along the medial aspect of the leg and foot; often affected by trauma or surgery in the region.
Saphenous nerve irritation results from medial cuff or liner seam pressure or from kneeling during boot adjustments that compress the medial tibial border.
Patients experience medial leg or ankle paraesthesia and allodynia under the medial shell without motor deficit. Redistribution of pressure, padding, and liner modification generally lead to resolution once the inciting pressure is eliminated.
Lateral Plantar Nerve
- Function: Motor and sensory
- Muscles Innervated: Innervates intrinsic muscles of the foot (e.g., abductor digiti minimi, quadratus plantae, and the third and fourth lumbricals).
- Clinical Significance: Injury can lead to weakness of the intrinsic foot muscles, resulting in issues with foot function and sensory loss on the lateral side of the foot.
Entrapment of the first branch of the lateral plantar nerve (Baxter’s nerve) manifests as medial plantar heel pain and sometimes abductor digiti quinti weakness. Rigid footbeds, aggressive varus posting, and prolonged forefoot loading in stiff boots can exacerbate compression deep to the abductor hallucis.
Examination reveals tenderness anteromedial to the calcaneus; distinguishing features from plantar fasciitis include less prominent “first-step” pain. Footbed modifications with a softer heel cup and neutral posting, intrinsic strengthening, and, rarely, surgical decompression are effective.
Exertional compartment syndromes
Exertional compartment syndromes of the anterior or lateral leg raise intracompartmental pressures during runs, compromising perfusion and the deep or superficial peroneal nerves. Patients describe aching tightness and paraesthesia over the relevant territories that resolve with rest; transient foot drop may occur.
Post-exertional firmness and tenderness of the compartments, symptom reproduction on provocation, and diagnostic intracompartmental pressure measurements confirm the diagnosis. Management involves training modification, attention to boot fit to reduce anterior compression, technique changes, and fasciotomy when criteria are met.
Proximal injuries
Proximal injuries of the sciatic nerve, particularly the peroneal division, and femoral neuropathies are uncommon and usually follow high-energy trauma such as hip dislocation or pelvic fractures, or prolonged compression during immobilisation.
Sciatic involvement produces foot drop accompanied by hamstring weakness, while femoral neuropathy causes quadriceps weakness, loss of the patellar reflex, and anterior thigh sensory changes. These are not primarily boot-related and should be managed within trauma protocols with appropriate imaging and neurodiagnostics.
Cold-related neurapraxia
Cold-related neurapraxia deserves emphasis in skiers. Cold exposure reduces conduction velocity and local perfusion, increasing vulnerability to compression; frostbite causes axonal injury with prolonged dysesthesia after rewarming. History of inadequate insulation, wet socks, and prolonged exposure, along with skin changes, guide management toward aggressive rewarming, insulation optimization, moisture control, and avoidance of tight boots that further compromise perfusion.
Clinical assessment
A structured examination begins with red flags for fractures, dislocations, and acute compartment syndrome – pain out of proportion, pain with passive stretch, and tense compartments – and careful documentation of progressive motor deficits.
Territory-based sensory and motor testing then localizes lesions: first web space sensation and extensor digitorum/hallucis brevis function for the deep peroneal nerve; eversion strength and dorsum foot sensation excluding the first web space for the superficial peroneal nerve; dorsiflexion and eversion together for common peroneal lesions at the fibular neck; plantar sensation and intrinsic strength with a Tinel sign at the tarsal tunnel for tibial nerve involvement; lateral and medial foot/leg territories for sural and saphenous nerves.
Provocative and percussion tests at the fibular neck, inferior extensor retinaculum, and tarsal tunnel assist in localization. Testing inversion (tibialis posterior) and hip abduction helps separate L5 radiculopathy from peroneal neuropathies.
Investigations are timed to the pathophysiology. Early nerve conduction studies identify conduction block in neurapraxia; needle EMG at two to three weeks reveals denervation in axonal injuries and aids prognosis. Ultrasound maps focal entrapments, neuromas, and dynamic compression at fascial exits. Radiographs or MRI identify fractures, osteophytes, or masses in chronic cases. Intracompartmental pressure testing confirms exertional or acute compartment syndromes. In recurrent or bilateral presentations, metabolic screening with glucose, B12, and TSH is prudent.
Management and prevention
Management principles are straightforward: remove or redistribute external pressure immediately by loosening buckles, modifying shells and liners, and adding targeted padding or cut-outs over known nerve hotspots; warm the extremity, elevate to reduce oedema, and consider a short course of anti-inflammatories when appropriate. Rehabilitation focuses on restoring dorsiflexor and evertor strength, intrinsic foot conditioning, proprioception, and nerve mobility, with gait retraining as needed. An ankle–foot orthosis protects patients with foot drop.
Neuropathic pain is addressed with standard agents. Image-guided perineural injections or hydro-dissection and surgical decompression are reserved for focal refractory entrapments or structural causes. Prognosis depends on injury grade: neurapraxia typically resolves over weeks to a few months; axonotmesis may require three to twelve months for meaningful recovery; progressive or persistent deficits warrant re-evaluation.
Preventive strategies emphasise meticulous boot fitting and behaviour modification. Proper shell length, last, and cuff height, with cuff alignment to the tibial axis, reduce focal contact. Heat-moulded liners, pressure-relief channels over the fibular neck, inferior extensor retinaculum, and medial malleolus, and smoothing of liner seams protect vulnerable nerves. Tongue padding with localised cut-outs reduces dorsal compression, and sufficient toe box height prevents dorsal crowding. Footbeds should maintain neutral alignment and avoid aggressive posting that concentrates heel or forefoot stresses; a cushioned heel cup can reduce Baxter’s nerve irritation. Buckles must secure the foot without constriction; micro-adjustment and periodic loosening on lifts help maintain perfusion.
Technique and behaviour matter: avoid prolonged squatting and leg-crossing, take pressure breaks each run, and keep feet warm and dry with moisture-wicking socks or heated liners.
Conditioning programs that strengthen dorsiflexors, evertors, intrinsic foot musculature, and hip abductors, combined with balance training, reduce varus stress and improve control.
Skiers with diabetes, prior neuropathy, or hypothyroidism merit extra caution and may benefit from less aggressive race-style setups. Regularly reassessing liners for packing-out and replacing them when new edges develop, as well as ensuring binding and stance settings do not force excessive dorsiflexion or pronation, completes equipment-based prevention.
Return to skiing depends on deficits and control of provoking factors. Patients with mild neurapraxia without weakness can return once symptoms are minimal and boot modifications are in place. Those with motor deficits require protection with an ankle–foot orthosis and should not return until antigravity strength is restored and gait is safe, with a progressive on-snow loading plan.
After surgical decompression or fasciotomy for chronic exertional compartment syndrome, staged return follows surgical protocols with objective strength and symptom thresholds.
In summary, most ski-related lower-limb palsies are preventable through careful boot fit, targeted pressure management at predictable nerve hotspots, attention to stance and behaviour, and early recognition of evolving neuropathy. A neuroanatomically organized examination and appropriately timed diagnostics separate mononeuropathies from radiculopathy and compartment syndromes. Prompt decompression of external pressure, structured rehabilitation, and judicious escalation to interventions optimize outcomes and facilitate safe return to sport.
