Foot Drop

Foot drop is weakness of ankle dorsiflexion (and often toe extension and foot eversion) that causes the forefoot to drag or slap on the ground during walking. It is a sign rather than a diagnosis, and it can arise anywhere from the cerebral cortex to the tibialis anterior muscle.

• Lower motor neurone causes: common peroneal neuropathy at the fibular head (the commonest), L5 radiculopathy, sciatic neuropathy, lumbosacral plexopathy, anterior horn cell disease (motor neurone disease, poliomyelitis), polyneuropathy (diabetic, alcoholic, Charcot-Marie-Tooth, leprosy, Guillain-Barre syndrome) and mononeuritis multiplex from vasculitis.
• Muscle causes: distal myopathies, facioscapulohumeral and myotonic dystrophy, inclusion body myositis, anterior compartment syndrome.
• Upper motor neurone causes: stroke, multiple sclerosis, parasagittal meningioma or other mid-line lesion, spinal cord lesion, cerebral palsy, in which spasticity and a plantar flexed, inverted foot occur with brisk reflexes.
• Compression is the usual reversible mechanism: leg crossing, prolonged squatting, tight casts or bandages, lithotomy position and weight loss.
• Cauda equina compression and acute stroke are the time critical causes.

• Steppage gait: the hip and knee are lifted high to clear the toes; foot slap at heel strike; tripping and falls; inability to walk on the heels.
• Pattern of weakness gives the level:
  • Common peroneal nerve: weak dorsiflexion and eversion, preserved inversion and hip abduction, sensory loss over the lateral lower leg and dorsum of the foot, normal ankle jerk.
  • L5 root: weak dorsiflexion, inversion, hip abduction and great toe extension, back pain radiating to the lateral leg, sensory loss in the L5 dermatome, normal reflexes.
  • Sciatic nerve: weakness of the peroneal and tibial divisions, loss of the ankle jerk, hamstring weakness.
  • Upper motor neurone lesion: spasticity, hyperreflexia, extensor plantar response, circumduction gait.
  • Distal polyneuropathy: bilateral weakness, glove and stocking sensory loss, absent ankle jerks, and in leprosy thickened nerves and anaesthetic skin patches.
• Examine the back and hips, and perform a straight leg raise, power of hip abduction, ankle reflexes, plantar responses, peripheral pulses and the skin.
• Red flags: bilateral symptoms with saddle numbness, urinary retention or faecal incontinence (cauda equina); sudden onset with facial droop or speech disturbance (stroke); rapidly progressive weakness (Guillain-Barre syndrome, motor neurone disease); fasciculations; severe leg pain with tense swollen compartments.

• Clinical localisation from the pattern of weakness and sensory change, then targeted tests.
• Nerve conduction studies and EMG from 3 weeks after onset to separate nerve, root, plexus and anterior horn cell lesions.
• MRI of the lumbar spine for suspected L5 radiculopathy (emergency if cauda equina features); MRI or ultrasound of the knee and fibular neck for a mass, ganglion or injury; MRI brain and spine for central causes.
• Blood tests: glucose and HbA1c, FBC, ESR, CRP, vitamin B12, TSH, renal and liver function, creatine kinase, autoantibodies and ANCA when vasculitis is suspected, HIV and syphilis serology when indicated.
• Skin slit smear or nerve biopsy for suspected leprosy.
• Differentials: ankle sprain or Achilles problems, peroneal tendon injury, pain related weakness, functional weakness, hip abductor weakness with Trendelenburg gait.

Urgent

• Suspected cauda equina syndrome or spinal cord compression: emergency admission and same day MRI.
• Stroke features: emergency stroke care.
• Compartment syndrome: urgent surgical review.

Treat the cause

• Compressive peroneal neuropathy: remove the pressure (stop leg crossing, loosen casts and bandages, pad the fibular head); most recover within 3 to 6 months.
• L5 radiculopathy: conservative care for 6 to 12 weeks if the deficit is mild (activity, physiotherapy, ibuprofen 400 mg three times daily with food for up to 2 weeks, gabapentin 300 mg at night increasing to 300 to 600 mg three times daily if neuropathic pain); microdiscectomy for severe or progressive weakness.
• Diabetes: optimise glycaemic control. Alcohol: abstinence with thiamine 100 mg orally daily. Vitamin B12 deficiency: hydroxocobalamin 1 mg intramuscularly alternate days for 2 weeks then every 3 months. Leprosy: multidrug therapy with specialist input. Vasculitis: immunosuppression by a specialist.

Support function and prevent complications

• Ankle foot orthosis (lightweight plastic or spring leaf) to hold the ankle in neutral and stop toe drag; fit shoes with a firm heel counter.
• Physiotherapy: twice daily passive ankle dorsiflexion and Achilles stretching to prevent equinus contracture, strengthening of dorsiflexors and evertors, gait training, balance work; functional electrical stimulation of the peroneal nerve for upper motor neurone and persistent lesions.
• Falls prevention: clear walkways, appropriate footwear, walking aid, home assessment.
• Examine the feet and skin if sensation is reduced.

Surgery

• Nerve decompression, repair, graft or transfer for compression or injury without recovery by 3 to 6 months.
• Tibialis posterior tendon transfer to the dorsum of the foot when no recovery is expected by 12 to 18 months; ankle arthrodesis in selected cases.

Follow up

• Review at 4 to 6 weeks and 3 months with repeat power grading; refer to neurology or a peripheral nerve surgeon when recovery stalls or the cause remains unclear.