Neuropathy refers to peripheral nerve damage or disease leading to dysfunction, which can manifest clinically as hypesthesia, paresthesia, neuropathic pain, or weakness. The fibular, tibial, sural, and saphenous nerves are all in close proximity to the knee and are susceptible to injury. When evaluating knee-region neuropathic symptoms, it is also important to consider lumbar radiculopathy and proximal neuropathies (e.g., femoral, obturator, sciatic).
- Mass lesion such as tumor (schwannoma, neuroma, neurofibroma) or intraneural ganglion cyst
- Hereditary neuropathy with tendency to pressure palsies
- Mononeuritis multiplex
- Other: inflammatory, infectious, metabolic, neoplastic, paraneoplastic, toxic (drugs, metals), inherited, degenerative
- Transection or traction/stretch (trauma, iatrogenic surgery/biopsy/injection complication)
- Compression from surrounding structures (tumors, compartment syndrome, cysts/ganglia, muscle hypertrophy/hernia, venous or arterial aneurysms, hematoma, weight loss) or external sources (bracing, tight clothing, leg crossing, bed rest)
Epidemiology including risk factors and primary prevention
Fibular (peroneal) nerve
- Most common lower limb mononeuropathy1
- Diabetes mellitus increases risk2
- Common fibular nerve (CFN) more often affected than superficial fibular nerve (SFN) or deep fibular nerve (DFN) branches
- Injury usually occurs at fibular neck or as nerve pierces fibularis longus muscle. Causes include:
- Extrinsic compression such as leg crossing, bed rest, casting/bracing, lithotomy position, prolonged squatting or kneeling, knee high footwear
- Weight loss
- Knee dislocation
- Proximal fibular fracture or proximal tibiofibular joint laxity3
- Proximal tibiofibular joint ganglion cyst (extraneural or intraneural)4
- Lateral meniscal cyst5
- Repetitive ankle inversion and pronation in runners, cyclists, or machine drivers1
- Postoperative complication e.g. following total knee arthroplasty6
- 0.3-1.3% of those who had TKA may develop a peroneal neuropathy
- Compression at popliteal fossa (e.g. Baker cyst7, popliteal pseudoaneurysm8) is less common
- Anterior compartment syndrome of lower leg
- Autoimmune conditions causing nerve infarcts (polyarteritis nodosa, microscopic polyangitis) Tibial nerve
- Less common than fibular neuropathy
- Deep course in leg with abundant surrounding fat and muscle
- Ganglion cysts are rare1
- Most causes are related to compression at the popliteal fossa
- Space-occupying lesions such as Baker cyst, or less commonly popliteal aneurysm or tumor7,9
- Popliteal entrapment syndrome
- Popliteus injury
- Gastrocnemius or popliteus hypertrophy10 or anomalous muscle slip1
- Compression beneath tendinous arch at origin of soleus muscle or an accessory soleus muscle (rare)
- Knee dislocation, posterior capsule injuries, or a tibial shaft fracture may lead to tibial neuropathy
- Posterior compartment syndrome
- Rarely injured in popliteal fossa and more commonly entrapped in leg or foot secondary to trauma1
- Compilation of sural neuropathy case reports revealed following etiologies11
- Trauma (67%) – compression, missile injury, foot fracture (more common in 5th metatarsal fractures), ankle inversion injuries
- Venous disorders (15%)
- Ganglion (10%)
- Idiopathic lesions (5%)
- Baker cyst (3%)
- Iatrogenic (sural nerve biopsy or vein stripping, foot and ankle surgeries – 1% incidence with ankle arthroscopy)
- Most common neurovascular complication after medial knee surgery12
- 7-22% of meniscal repairs13 and 30-59% of ACL reconstructions14
- Can develop spontaneous compression of infrapatellar branch as it passes beneath or through the sartorius tendon over the medial femoral condyle.15
- Also reported following patellar dislocations, varicose vein stripping, saphenous vein harvesting, femoral artery catheterization or thrombectomy, dashboard injuries, excessive genu valgus or internal tibial torsion, surfers gripping board between their knees1 bodybuilders due to muscle hypertrophy, pes anserine bursopathy, prolonged kneeling, and knee injection.3
- Origin L4-S2 nerve roots, posterior division of sacral plexus, sciatic nerve (common fibular division)
- CFN branches laterally proximal to popliteal fossa
- Wraps around the fibular head/neck in peroneal tunnel and then branches to form DFN and SFN
- CFN innervates short head of biceps femoris
- SFN innervates lateral leg compartment muscles (fibularis longus/brevis) and sensation to lateral leg and dorsum of the foot
- DFN innervates anterior leg compartment muscles (tibialis anterior, extensor hallucis longus, extensor digitorum longus, fibularis tertius)
- Passes underneath the anterior tarsal tunnel to innervate extensor hallucis brevis/extensor digitorum brevis and cutaneous branch supplies first web space sensation
- Origin L4-S3 nerve roots, anterior division of sacral plexus, sciatic nerve (tibial division)
- Tibial nerve branches proximal to popliteal fossa
- Travels in deep posterior compartment of leg, then travels in close proximity to the tibia and posterior tibial artery
- Enters tarsal tunnel at medial ankle, dividing into medial calcaneal, medial plantar, and lateral plantar nerves
- Tibial nerve supplies muscles of superficial posterior compartment (gastrocnemius, soleus and plantaris) and deep posterior compartment of leg (popliteus, tibialis posterior, flexor digitorum longus, flexor hallucis longus)
- Medial calcaneal branch provides cutaneous sensation to the plantar heel
- Medial plantar branch supplies abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, first lumbrical and cutaneous sensation to medial three-fourths of plantar forefoot and arch
- Lateral plantar branch supplies quadratus plantae, adductor hallucis, interossei, lumbricals 2-4, flexor digitorum minimi brevis, abductor digiti minimi and cutaneous sensation to lateral one-fourth of plantar forefoot and arch
- Origin S1 nerve root; arises from union of medial and lateral sural cutaneous nerves (branches of tibial and CFN, respectively) between gastrocnemius heads at the distal third of the gastrocnemius
- Purely sensory to the posterolateral aspect of the distal third of lower leg and lateral aspect of foot
- Origin L3-L4 nerve roots; terminal branch of femoral nerve
- Purely sensory to medial knee, leg, and foot
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
- Pain at compression site
- Neuropathic pain or paresthesia/anesthesia along lateral lower leg and dorsal foot
- Dorsiflexion and toe extension weakness, which can result in stubbing toe, tripping, foot slap or steppage gait
- If proximal SFN involved, may report recurrent ankle sprains/instability due to weak ankle evertors
- Chronic: anterior or lateral leg compartment atrophy
- Neuropathic pain or paresthesia/anesthesia in posterior calf (medial/lateral sural cutaneous nerve), lateral foot (sural nerve) and plantar foot (medial calcaneal, medial/lateral plantar nerves)
- Weakness in ankle plantar flexors (soleus, gastrocnemius), invertors (tibialis posterior), toe flexors (flexor digitorum longus, flexor hallucis longus), or intrinsic foot muscles
- Chronic: posterior leg compartment atrophy, intrinsic foot muscle atrophy/claw toes
- Neuropathic pain or paresthesia/anesthesia in posterior leg or lateral ankle/foot
- Symptoms may be worse at night and exacerbated with exercise (e.g. plantarflexion and foot inversion)
- Neuropathic pain or paresthesia/anesthesia in medial leg or pain in anterior/medial knee
- Symptoms may be provoked with knee flexion3 and may be mistaken for medial knee compartment pathology if infrapatellar branch involved
Specific secondary or associated conditions and complications
- Complex regional pain syndrome
- Gait instability/falls due to weakness or sensory abnormalities
- Skin breakdown due to sensory loss
- Ankle contractures due to weakness
Essentials of Assessment
- Onset, symptom quality and severity, location, duration and timing, palliative and provocative factors
- Medical and social history (diabetes mellitus, hypothyroidism, autoimmune diseases, viral infectious diseases (HIV), kidney or liver disease, weight loss, cancer, alcohol use, metal exposures)
- Medications (chemotherapy, amiodarone, Isoniazid, supplements)
- Activities (leg crossing, squatting, compressive clothing/bracing or tight shoes)
- Personal/family history of neurologic conditions (pressure palsies or plexitis)3
- Surgical History (Total knee arthroplasty)
- Skin assessment for anhidrosis or warmth (vasomotor paralysis) during first 48 hours, hair loss, ulcers, temperature changes, trauma, sensation changes
- Muscle bulk or atrophy, swelling/hematomas
- Abnormal limb positioning
- Range of motion/contracture
- Palpation: Tinel sign over fibular head
- Strength: Weak dorsiflexion and great toe extension (DFN), foot eversion (SFN). When testing eversion strength, have the patient plantarflex while everting to isolate the fibularis longus/brevis (SFN). In dorsiflexion, the extensor digitorum longus (DFN) acts as an evertor; thus, the examiner may miss eversion weakness secondary to injury to the SFN.
- Sensory: Hypesthesia anterolateral leg and foot (SFN), first web space (DFN)
- Palpation: Popliteal fossa for Baker cyst or other mass
- Strength: Weak plantarflexion and foot inversion (proximal injury) and/or toe flexors (mid-leg injury).
- Sensation: Hypesthesia in posterolateral leg, sole of the foot, and lateral border of the foot in the sural distribution, though this may be variable as the sural nerve also receives fibular nerve contribution
- Reflexes: Diminished or absent Achilles tendon reflex
- Sensation: Hypesthesia in the posterolateral leg and lateral foot
- Palpation: Tinel sign over medial tibial fossa16
- Sensation: Hypesthesia in medial leg; may be provoked with passive thigh hyperextension or deep palpation proximal to medial femoral condyle
Screen electrolyte imbalances, diabetes, thyroid dysfunction, infection, amyloidosis, sarcoidosis, systemic vascular or connective tissue diseases, renal dysfunction, heavy metal intoxication (lead, copper, arsenic), alcohol, nutritional/vitamin deficits (B1, B6, B9, B12, Folate) or supplement misuse3
- Radiographs assess for fracture or bony lesion if history of trauma, cancer, or implant impinging on nerve
- Direct signs1
- Nerve compression
- Compressive lesion (e.g. Baker cyst, ganglion cyst)
- Swelling/hyperemia of nerve
- Comparison of cross-sectional area (CSA) of nerve at site of compression to area at site proximal or distal to site of compression17
- Comparison of CSA of nerve to asymptomatic side
- Neuroma formation
- Nerve discontinuity
- Dynamic assessment (snapping, gliding, compression)
- Nerve compression
- Indirect signs
- Muscle atrophy
- Fatty infiltration—muscle will appear hyperechoic in comparison to normal muscle
- Visualize course of nerve and anatomic variation to optimize surgical planning and injection targeting; minimize iatrogenic complications18,19,20
- Direct signs1
- Direct signs
- Displaced nerve, focal swelling, signal intensity changes1
- Compressive lesion
- Indirect signs
- Denervation edema or fat infiltration to muscle1
- May show nerves and surrounding anatomic structures with better broadscale view
- Direct signs
Supplemental assessment tools
- MRI or CT arthrography can evaluate communication between a joint and ganglion cyst
- Compartment pressure measurements in suspected cases of acute or chronic compartment syndrome
- Electrodiagnostic testing (nerve conduction studies and electromyography)
- Evaluate for conduction block or slowing, demyelination, axonal loss, and muscle denervation
- Localize lesion (and rule out proximal injuries including radiculopathy or plexopathy)
- Assess severity, chronicity, and prognosis
- Abnormal EMG/NCS findings may take up to 3-4 weeks to fully develop20
- Nerve conduction study amplitudes and insertional/spontaneous EMG activity are normal in the acute phase
- Recruitment changes on EMG should be apparent immediately
- Nerve conduction studies across an injured nerve segment will be abnormal immediately21
- Diagnostic injections with local anesthetic may distinguish nerve pain from other potentially painful structures about the knee
Early predictions of outcomes
Prognosis improves if neurophysiologic studies find a focal conduction block and the source of compression can be resolved.3 In general, early assessment and intervention is recommended.
Rehabilitation Management and Treatments
Available or current treatment guidelines
- Physical therapy
- range of motion to prevent contracture (heel cords)
- gradual strengthening
- gait and proprioceptive retraining
- neural gliding
- TENS, desensitization11
- Low frequency electrical stimulation22
- Acupuncture, CBT for diabetic neuropathy
- AFO for foot drop or calf weakness to stabilize ankle during push-off phase of gait
- bracing to protect the nerve or prevent joint injury
- Oral pain medications
- tricyclic antidepressants (Amitriptyline)
- membrane-stabilizing agents (gabapentin or pregabalin)
- SNRI’s (Duloxetine)
- Topical compounds
- nerve block (anesthetic/corticosteroid)
- hydrodissection of entrapment site
- Involves the injection of solution to separate the nerve from surrounding structures commonly the tissue and fascia which may cause decompression of the surrounding nervi nervosum or vasa nervorum
- Injections may include saline, steroids, PRP, dextrose, various anesthetics
- Peripheral nerve Stimulators/Radiofrequency Ablations
- Genicular, saphenous nerve are common
- Usually target 3 of the 6 branches including the superior medial branch, the superior lateral branch, and the inferior medial genicular nerves
- Typically trial stimulator for 60 days and if significant relief can proceed to permanent options
- resection of mass/tumor/displaced bone fragment or dense scar tissue
- fasciotomy for acute/chronic compartment syndrome
- immediate nerve repair for transection
- surgical exploration and release if intrinsic compression
- tendon transfers to restore function in chronic injury
Algorithm suggested for peripheral nerve injuries
- If laceration: immediate surgical exploration and repair
- If entrapment or traction injury:
- Relieve external compression and conservative treatment
- Relative rest, environmental modifications (avoid leg crossing, modification to cast or orthoses, repositioning in bed)
- If deteriorating and no signs of improvement within 3 months, surgical referral
- Surgical consultation if anatomic source compression
- Relieve external compression and conservative treatment
- If metabolic/toxic: initiate lab workup for deficiencies/toxicity, EMG
- Infectious/inflammatory/neoplastic: labs, imaging, EMG
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
- Injury to nerves may occur due to intrinsic factors or extrinsic factors following knee surgery, leg fractures, and in the setting of vascular disease or inflammatory conditions.
- Early evaluation and treatment of nerve injuries can avoid long-term impairments and irreversible nerve damage.
- Injections may be useful for both diagnostic and potentially therapeutic purposes. Imaging with radiographs, ultrasound, and MRI can evaluate for structural signs of nerve pathology.
- Peripheral nerve stimulators and Hydrodissection of entrapment sites
- EMG can help localize nerve lesion and determine severity/prognosis.
- EMG with Diagnostic Ultrasound for peripheral nerve evaluation showing morphological changes
- Acute trauma may reveal hypoechogenicity, thickening of nerves, perineural fat stranding while chronic trauma may reveal thinning of nerves, thickened perineurium and surrounding fatty replacement
- Treatment may include both conservative measures and surgical intervention, depending on nature of injury.
Cutting Edge/ Emerging and Unique Concepts and Practice
Peripheral nerve injuries and surgical repair techniques may result in incomplete recovery due to:
- Neuroma formation
- Lipid peroxidative damage
- Other poorly understood factors
Peripheral nerve stimulators may be emerging as an option for certain neuropathies and chronic pain associated with neuropathies.
Surgical repair techniques have been suggested, including:
- Direct end-to-end nerve suturing for short discontinuities (0.5mm)
- Fibrin glue adhesive may be comparable or superior to microsurgery24
- Nerve grafts for repair of peripheral nerve discontinuities
- Nerve conduits can be used to serve as a pathway for axonal reconnection25,26
- Materials for conduits include muscle tissue, vessels, and synthetic materials (silicone, porous stainless steel, bioabsorbable tubes)
- Growth Factors and supportive cells have been hypothesized to facilitate regeneration (Neurotrophic factor, Insulin-like growth factor, Basic fibroblast growth factor, Hepatocyte Growth Factor, Platelet-rich plasma,Schwann cells) 25,26,27
- Stem cells(Human Umbilical Cord Stem cells, Mesenchymal stem cells, Olfactory ensheathing cells26,32
- Pharmaceutical adjuvant therapies which have been shown to promote nerve recovery in animal models include Immunosuppressants (Tacrolimus, Sirolimus, Dexamethasone, Glatimer Acetate), Calcium-Dependent Drugs (Nimodipine, Lithium, Gabapentin, Valproic acid), and other drugs including Erythropoietin and Riluzole25, 26
- Alpha Lipoic Acid for diabetic neuropathy
Gaps in the Evidence-Based Knowledge
- Continue research exploring pathophysiology of nerve injury and repair.
- Increasing role of ultrasound in diagnosis of neuropathy — establish additional normative data regarding nerve diameter and cross-sectional area.
- Randomized controlled trials for interventions, including pharmacologic, growth factor and cell-based therapies.
- Optimal timing, repeating, and type of injection solution for hydrodissections
- Optimal timing and technique for surgical repair of nerve lesions.
- Understand why permanent functional deficits occur despite current nerve injury repair strategies.
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Original Version of the Topic
Jacob L. Sellon, MD, Matthew Pingree, MD, Marisa J. Terry, MD. Knee neuropathies. 9/20/2014
Previous Revision(s) of the Topic
William A. Anderson, MD. Knee neuropathies. 7/3/2018
Tyler Williamson, MBBCh, BS
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Luke Guminik, DO
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