Foot drop and wrist drop

Foot drop is weakness of ankle dorsiflexion, and wrist drop is weakness of wrist and finger extension. Both are signs of weakness whose localisation (nerve, root, plexus, cord, brain or muscle) determines treatment. The commonest causes are common peroneal neuropathy at the fibular head and L5 radiculopathy for foot drop, and radial nerve injury for wrist drop.

Clinical relevance. Acute foot drop can be the first sign of cauda equina syndrome, a disc prolapse with a surgical window, stroke, or compartment syndrome. Acute wrist drop after trauma may accompany a humeral fracture or vascular injury.

Anatomy.

• Dorsiflexion of the ankle is by tibialis anterior (deep peroneal nerve, L4 to L5); eversion by peroneus longus and brevis (superficial peroneal nerve, L5 to S1); inversion by tibialis posterior (tibial nerve, L5). Toe extension is by extensor hallucis longus (L5).
• Wrist extension is by extensor carpi radialis longus, brevis and ulnaris, and finger extension by extensor digitorum (radial nerve and its posterior interosseous branch, C6 to C8). Triceps (C7) and brachioradialis are supplied by the radial nerve proximal to the elbow.

Localisation of foot drop:

• Common peroneal neuropathy: weak dorsiflexion and eversion with preserved inversion, sensory loss on the lateral lower leg and dorsum of the foot, normal ankle reflex.
• L5 radiculopathy: weak dorsiflexion, eversion and inversion, hip abduction and big toe extension, back pain with sciatica, sensory loss on the dorsum of the foot and big toe.
• Sciatic nerve or lumbosacral plexus: involvement of hamstrings and plantar flexion, absent ankle jerk.
• Upper motor neuron: spasticity, brisk reflexes, extensor plantar response, and circumduction gait.

Localisation of wrist drop:

• Radial nerve in the spiral groove: weak wrist and finger extension and brachioradialis, preserved triceps, sensory loss over the first dorsal web.
• Posterior interosseous nerve: finger drop with wrist extension still possible (radial deviation), no sensory loss.
• Axillary (high) radial lesion: triceps also weak.
• C7 radiculopathy: weak triceps, wrist flexion and finger extension with reduced triceps reflex.
• Posterior cord of the brachial plexus: deltoid, triceps and extensors involved.
• Central: stroke with spasticity and a flexed wrist.

Temporal patterns. Sudden (compression palsy, trauma, stroke, ischaemia, disc), days to weeks (disc, vasculitis, inflammatory), subacute to chronic (tumour, hereditary neuropathy, motor neuron disease, myopathy).

History. Onset and speed, back or neck pain, sciatica, sensory symptoms, bilateral symptoms, other nerve involvement, bladder or bowel dysfunction, and systemic features.

Preceding event: prolonged sleep in an awkward posture, intoxication, leg crossing, kneeling or squatting, weight loss, casts or tight bandages, surgery and positioning, injections, fracture, knee dislocation, humeral injury, sustained arm hang over a chair or crutch use.

Background and drugs. Diabetes, alcohol, vasculitis or connective tissue disease, HIV, hepatitis B and C, leprosy exposure, lead exposure (battery recycling, paint, smelting, glazes, traditional remedies), cancer, family history of neuropathy or foot deformity (pes cavus), anticoagulation, vincristine, dapsone, nitrofurantoin and isoniazid.

Examination

• Grade power (0 to 5) for ankle dorsiflexion, eversion, inversion, big toe extension, plantar flexion, hip abduction and extension, and knee flexion; for the arm, shoulder abduction, elbow extension and flexion, brachioradialis, wrist extension, finger extension, thumb extension, grip and the first dorsal interosseous.
• Tone, bulk (wasting of tibialis anterior or forearm extensors), fasciculation, reflexes (knee, ankle, triceps, brachioradialis), plantar response, and sensory map.
• Tinel sign at the fibular head and spiral groove, straight leg raise, spine and neck examination, and signs of an upper motor neuron lesion.
• Gait: steppage, inability to heel walk, slapping foot.
• Skin, nerve thickening (leprosy), pulses and compartment tension, fracture or deformity, bruising, and signs of vasculitis. Mees lines, gum lines and abdominal pain in lead toxicity.

Red flags

• Bilateral foot drop, saddle anaesthesia, bladder or bowel dysfunction, or sensory level
• Rapidly progressive weakness, or multifocal involvement (vasculitis, mononeuritis multiplex)
• Trauma with fracture, knee dislocation, tense swollen leg, severe pain on passive toe stretch, or absent pulses
• Wrist drop after humeral fracture manipulation or surgery, or with open injury
• Weakness with speech disturbance, facial droop or hemisensory loss
• Lead exposure with abdominal pain, anaemia or encephalopathy
• Severe pain, fever, weight loss, cancer history or injecting drug use
• Post-operative or post-injection palsy

Special groups. Pregnancy and labour: lumbosacral trunk compression by the foetal head causing foot drop, peroneal compression from stirrups. Children: Charcot Marie Tooth disease, trauma, sciatic nerve injury after gluteal injection, and cerebral palsy. Older adults: lumbar stenosis and diabetes. Region specific: leprosy (common peroneal, ulnar and radial nerves), post-injection palsy, poliomyelitis, and lead toxicity from informal recycling.

Foot drop

• Common peroneal neuropathy: compression at the fibular head (leg crossing, casts, positioning, weight loss, squatting, fibular fracture), traction injury (knee dislocation, ankle inversion injury), ganglion cyst, nerve tumour
• L5 radiculopathy: disc herniation, lateral recess or foraminal stenosis, tumour
• Lumbosacral plexopathy and sciatic neuropathy: pelvic mass, hip surgery, injection injury, diabetic amyotrophy, malignant infiltration, radiation, labour
• Cauda equina syndrome
• Mononeuritis multiplex and polyneuropathy: diabetes, vasculitis, leprosy, HIV, Charcot Marie Tooth disease, hereditary neuropathy with pressure palsies, chronic inflammatory demyelinating polyneuropathy, lead
• Motor neuron disease and spinal muscular atrophy
• Distal and scapuloperoneal myopathy, facioscapulohumeral dystrophy
• Upper motor neuron causes: stroke, multiple sclerosis, parasagittal tumour, spinal cord lesion
• Anterior compartment syndrome
• Mimics: foot pain, ankle arthritis, Achilles contracture, functional weakness

Wrist drop

• Radial nerve palsy: compression in the spiral groove (Saturday night palsy), humeral shaft fracture, crutch use, tourniquet, injection, lipoma
• Posterior interosseous neuropathy: ganglion, tumour, entrapment at the arcade of Frohse
• C7 radiculopathy, brachial plexopathy (posterior cord), neuralgic amyotrophy
• Lead neuropathy, mononeuritis multiplex (vasculitis, diabetes, leprosy), multifocal motor neuropathy
• Stroke or brain lesion, motor neuron disease
• Mimics: tendon rupture (rheumatoid arthritis), extensor tendon injury, wrist arthritis, functional weakness

Reasoning. Establish the muscle group pattern, find which muscles are spared (inversion in peroneal neuropathy, triceps in a spiral groove lesion), then image the likely level. Exclude cauda equina syndrome, compartment syndrome and vascular injury on the day.

Immediate checks. Bladder scan and anal tone when a spinal cause is possible, limb pulses and capillary refill, compartment tension, X-ray of fracture sites (knee, fibula, humerus), glucose.

Imaging.

• Emergency MRI lumbar spine for foot drop with back pain, bilateral signs, saddle loss or sphincter dysfunction.
• MRI lumbar spine within days for any acute or progressive foot drop with sciatica (L5 radiculopathy).
• MRI or high resolution ultrasound of the nerve for suspected compressive lesion, cyst or tumour at the fibular head or spiral groove.
• MRI of the pelvis or plexus for suspected plexopathy.
• CT angiography for knee dislocation or suspected popliteal injury.
• MRI brain for upper motor neuron signs.

Neurophysiology. Nerve conduction studies and electromyography localise the lesion, grade axon loss and predict recovery. Look for conduction block or slowing across the fibular head or spiral groove. Involvement of tibialis posterior and short head of biceps femoris separates L5 or sciatic lesions from peroneal neuropathy at the fibular head. Findings are most informative 10 to 14 days after acute injury, and repeat testing at 3 to 4 weeks shows the full extent.

Blood tests. Full blood count and film, glucose and HbA1c, urea, creatinine, electrolytes, calcium, liver function, creatine kinase, ESR and C reactive protein, antinuclear antibody, ANCA, rheumatoid factor, complement, cryoglobulins, HIV, hepatitis B and C and syphilis serology, vitamin B12, thyroid stimulating hormone, serum protein electrophoresis.

In suspected lead toxicity: venous blood lead level, with film for basophilic stippling and microcytic anaemia, and urinary coproporphyrin.

Other tests. Nerve and muscle biopsy for suspected vasculitis, slit skin smear and skin or nerve biopsy for leprosy, genetic testing for hereditary neuropathy after counselling, and compartment pressure measurement when clinical compartment syndrome is uncertain (a difference between diastolic pressure and compartment pressure of under 30 mmHg supports fasciotomy).

Limitations. Early electrophysiology can be normal. MRI of the lumbar spine shows disc bulges in asymptomatic adults, so clinical correlation is needed. Weak ankle dorsiflexion with preserved inversion does not exclude a peroneal division sciatic lesion.

Emergencies

• Cauda equina syndrome: emergency MRI and surgical decompression, ideally within 24 hours of onset of retention or bladder dysfunction.
• Anterior compartment syndrome: remove constrictive dressings and casts, keep the limb at heart level, and arrange urgent fasciotomy.
• Knee dislocation or suspected vascular injury: vascular assessment, CT angiography, and urgent vascular surgical review.
• Open injury, nerve laceration or humeral fracture with new radial palsy after manipulation: urgent orthopaedic or plastic surgical referral for exploration.
• Stroke: alteplase 0.9 mg/kg IV (maximum 90 mg) or tenecteplase 0.25 mg/kg IV (maximum 25 mg) within 4.5 hours when haemorrhage is excluded, with aspirin 300 mg orally daily when thrombolysis is not given.

Compression neuropathy (common peroneal, radial)

• Remove the cause: stop leg crossing, kneeling and squatting, remove or loosen casts, avoid pressure from crutches, change positioning.
• Foot drop: ankle foot orthosis or a dorsiflexion assist splint, physiotherapy for range of motion and strengthening of unaffected muscles, gait training and footwear review. Falls prevention.
• Wrist drop: wrist and finger extension splint (cock up splint) to keep the wrist extended and allow grip, with passive range of motion exercises to prevent contracture.
• Most compression palsies are neurapraxic and recover over weeks to 4 months. Repeat electrophysiology at 3 to 4 weeks, and refer for exploration or decompression when there is no recovery by 3 months, or earlier with a mass or progression.
• Persistent palsy after 6 to 12 months: reconstructive options by a nerve surgeon: tendon transfer (tibialis posterior transfer for foot drop; pronator teres and flexor carpi radialis transfers for wrist drop), nerve grafting or transfer, and ankle arthrodesis.

Lumbar radiculopathy with foot drop.

• Paracetamol 1 g orally every 6 hours (maximum 4 g daily; 2 g daily in weight under 50 kg, chronic alcohol use or liver disease).
• Ibuprofen 400 mg orally three times daily with food for short courses (maximum 2.4 g daily; avoid in renal impairment, heart failure, peptic ulcer).
• Neuropathic pain drugs as needed.
• Urgent spinal surgical referral for a motor deficit that is severe (power of 3 or less), progressive or persistent, because decompression within days to a few weeks gives the best recovery.

Diabetic and vasculitic neuropathy. Optimise glycaemic control. Vasculitis: prednisolone 1 mg/kg orally daily (maximum 60 to 80 mg) with cyclophosphamide or rituximab, by specialists.

Lead toxicity. Remove the source of exposure. Chelation under a poisons service for symptomatic patients or high blood lead levels, with monitoring of renal function and blood count. Iron and calcium repletion, and screening of household members.

Leprosy. Adults with multibacillary disease take rifampicin 600 mg once monthly (supervised), clofazimine 300 mg once monthly (supervised) and 50 mg daily, and dapsone 100 mg daily for 12 months. Paucibacillary disease uses the same three drugs for 6 months. Nerve function impairment and reactions: prednisolone 40 mg orally daily reduced gradually over several months. Specialist care.

Motor neuron disease, myopathy and hereditary neuropathy. Specialist neurology care, orthoses, physiotherapy and genetic counselling.

Pain control.

• Amitriptyline 10 mg at night increased by 10 mg weekly to 25 to 75 mg.
• Gabapentin 300 mg at night increased every 3 to 7 days to 1.8 to 3.6 g daily in 3 doses (adjust to creatinine clearance).
• Pregabalin 75 mg twice daily increased to a maximum of 300 mg twice daily.

Monitoring. Power grading and sensory map at each visit, repeat nerve conduction at 3 to 4 weeks and 3 months, foot and skin inspection in insensate limbs, orthosis fit and skin checks, and mood.

Referral and escalation. Immediate: cauda equina syndrome, compartment syndrome, vascular injury, open nerve injury, stroke. Urgent spinal surgery for radicular foot drop with severe or progressive deficit. Neurology for polyneuropathy, mononeuritis multiplex, motor neuron disease and myopathy. Nerve surgery or orthopaedics for failed recovery, tumour or cyst. Rehabilitation and orthotics for all persistent palsies.

Admission criteria. Cauda equina syndrome, compartment syndrome, vascular injury, acute stroke, rapidly progressive or multifocal weakness, suspected vasculitis, or severe pain with inability to cope.

Discharge and safety netting. Review in 1 to 2 weeks, then at 3 months. Return for new weakness, numbness in the saddle area, bladder or bowel change, a swollen tense limb, severe pain, a cold or discoloured limb, or spreading weakness.