Foot drop is also known and "drop foot." This is where the patient cannot lift their forefoot secondary to weakness of the dorsiflexor muscles. Foot drop can be caused by muscular, skeletal, or nervous system disorders.
|Compartment||Muscles||Action||Nerve Supply||Blood Supply|
|Anterior||Sartorius and quadriceps muscles (rectus femoris, vastus lateralis, vastus intermedius, vastus medialis)||Hip flexion||Femoral nerve||Superficial femoral artery|
|Medial||Pectineus, obturator externus, gracilis, and adductor muscles (longus, brevis, magnus, minimus)||Hip adduction||Obturator nerve|
|Posterior||Biceps femoris, semimembranous, and semitendinous muscles||Hip extension||Sciatic nerve||Deep femoral artery|
|Compartment||Muscles||Action||Nerve Supply||Blood Supply|
|Anterior||Tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius||Dorsiflexion and inversion/eversion of the ankle and extension of the toes||Anterior tibial artery||Deep peroneal nerve|
|Lateral||Peroneus longus and peroneus brevis||Eversion of the foot and ankle, and weak plantarflexion of the foot||Peroneal artery||Superficial peroneal nerve|
|Superficial posterior||gastrocnemius, the soleus, +/- plantaris||Plantarflexion and inversion of the foot at the ankle, and toe flexion||Posterior tibial and peroneal arteries||Tibial nerve|
|Deep posterior||Tibialis posterior, flexor hallucis longus, flexor digitorum longus, and popliteus muscles.||Plantarflexion and inversion of the foot at the ankle, and toe flexion||Posterior tibial and peroneal arteries||Tibial nerve|
|Nerve||Segment||Motor Supply||Action||Sensory Supply|
|Iliohypogastric nerve||T12/L1||Transversus abdominis and internal oblique muscles||N/A||Lower abdomen|
|Ilioinguinal nerve||L1||Inferior abdominal muscles||N/A||Inguinal region, small area of media thigh, and upper scrotum/labia|
|Genitofemoral nerve||L1, L2||Cremasteric muscle in men||N/A||Skin of femoral triangle. Lower scrotum/labia|
|Lateral femoral cutaneous nerve||L2,L3||N/A||N/A||Lateral thigh|
|Obturator nerve||L2, L3, L4 anterior rami||Adductor magnus (anterior half), adductor longus, adductor brevis, gracilis, obturator externus||Hip adduction||Medial thigh|
|Femoral nerve||L2, L3, L4 anterior rami, posterior divisions||Quadriceps femoris, sartorius, pectineus, iliacus||Knee extension||Medial lower leg (through saphenous nerve|
|Lumbosacral trunk / furcal nerve||L4-5, mainly L5||Ankle dorsiflexion, eversion, inversion||L5 sensory loss|
|Nerve||Segment||Motor Supply||Action||Sensory Supply|
|Superior gluteal||L4-S1||Gluteus medius, gluteus minimus, tensor fasciae latae||hip abduction||buttock pain|
|Inferior gluteal||L5-S2||Gluteus maximus||hip external rotation and power extension||N/A|
|Sciatic trunk/nerve||L5–S3||Tibial portion: Posterior compartment of the thigh and leg
Common peroneal division: short head of biceps femoris, and anterior, and lateral compartments of the leg, and extensor digitorum brevis. and leg through common peroneal and tibial nerves
|Tibial portion: Sole of the foot (medial and lateral plantar nerves)|
Common peroneal division: Anterolateral surface of the leg (sural nerve), first webspace of foot (deep peroneal nerve), and dorsal aspect of the foot (superficial peroneal nerve)
|Posterior femoral cutaneous nerve||-||-||Posterior surface of the thigh, leg, and perineum (perineal branches and inferior cluneal nerves)|
|Pudendal nerve||S2-4||Muscles of the perineum||Penis, clitoris, most of the perineum|
|Nerve to piriformis|
|Nerve to obturator internus and superior gemellus|
Compression of the peroneal nerve can occur anywhere along its course. It is more common in patients with a history of significant weight loss, in those who frequently cross their legs, or who do squatting exercises.
- The most common site is at the fibular head. This area is vulnerable due to the bony prominence of the fibular head, the superficial position of the nerve, and tethering of the nerve by the peroneus longus tendon in the peroneal tunnel.
- Compression at the level of the hip
- Compression at the popliteal fossa. This is immediately after the division of the sciatic nerve into the tibial and common peroneal nerve. Baker's cysts are the most common compressive lesion. Mononeuropathy multiplex is another cause in this area with resultant nerve infarction.
- The deep peroneal nerve can be compressed at the level of the ankle from a tight-fitting rim or strap from a shoe.
- There can be an anatomical variation of the biceps femoris muscle resulting in the formation of the muscular tunnel between the gastrocnemius muscle and distal biceps femoris, resulting in peroneal nerve entrapment.
- It can also be trapped when there is a high division of the sciatic nerve. In this situation the peroneal component pierces the piriformis muscle and especially in cases of piriformis scarring or hypertrophy it may become entrapped.
- The presence of a fabella, an accessory sesamoid bone, can cause compression at the lateral gastrocnemius attachment.
- Intraneural or extraneural lesions can cause compression.
Lumbar spine disease can also cause foot drop such as with lumbar disc herniation and lumbar spinal stenosis. The L5 nerve root at the L4-5 segment is the most commonly affected nerve root, often in association with S1 or L4 (double nerve root compression), or all of L4-S1 (triple nerve root compression).
Trauma is the second most common cause of peroneal nerve injury. This can occur following knee and posterior hip dislocations, ACL injury, severe ankle inversions (stretches the peroneal nerve), fractures (e.g. tibial plateau - 1%, acetabular, femur), blunt trauma, nerve tract, or direct nerve laceration. The nerve is most susceptible at the level of the knee, but it there can also be problems secondary to injury involving the sciatic nerve or at the ankle.
Compartment syndrome can lead to peroneal nerve ischaemia. This can be due to trauma or related to ischaemia-reperfusion injury.
Injury can occur with surgical procedures (hip, knee, or ankle), prolonged positioning during anaesthesia (especially lithotomy), prolonged bed rest, splinting, and pneumatic compression devices.
There are primary and secondary neurologic disorders that can cause foot drop.
Charcot-Marie-Tooth is a primary peripheral nerve disorder, and is the most commonly inherited peripheral nerve disorder with an incidence of 1 in 2500 people. It affects both sensory and motor peripheral nerve fibres. Patients generally start having symptoms during childhood or early adulthood, but in some cases it may present later in life. Foot drop is one of the initial symptoms, but there is variation in disease progression.
Amyotrophic lateral sclerosis and multiple sclerosis are other primary neurological causes of foot drop.
Diabetes is a secondary cause of foot drop in those who have peripheral neuropathy.
Foot drop may be partial or complete. It can develop acutely or worsen over days to weeks. Patients may report that they are dragging their toes. They may have problems walking or climbing stairs, and may have frequent falls. There may be other symptoms depending on the aetiology of the foot drop.
- Common peroneal nerve entrapment: foot drop with decreased sensation, paraesthesias, or burning of the lower lateral leg to the dorsum of the foot and/or first toe webspace. Sensory manifestations are common at 79%, but pain is only present in 17% of cases.
- Deep peroneal nerve entrapment: There is usually pain with minimal weakness, and sensory deficit only involves the webspaces between the 1st and 2nd toes.
- Mononeuritis multiplex: pain is usually a significant feature with vasculitic conditions.
- L5 radiculopathy: foot drop with radicular pain, and concurrent low back pain.
- Sciatic nerve compression: foot drop with radicular pain, and weakness of knee flexion and hip extension.
- Lumbosacral plexopathy: foot drop with weakness of knee flexion, internal hip rotation, and hip abduction.
- Neurological disorders: Additional symptoms depending on the condition
Peripheral nerve lesions cause weakness in two or more muscles from a single peripheral nerve (which may belong to different spinal segments) and spare muscles from other nerves (see complete myotome chart). Over 85% of patients with foot drop secondary to peroneal nerve injury have weak ankle dorsiflexion (L4-L5) and eversion (L5-S1) but have preservation of inversion. The tibial nerve innervates tibialis posterior (L4-L5) but is spared in a peroneal nerve injury. So with L4-L5 working for inversion, but not working for ankle dorsiflexion and eversion, suggests that the lesion is not in the spine, but in the peroneal nerve.
Another important thing to remember is that the sciatic trunk divides into the peroneal and tibial nerves just above the knee. Therefore a lesion of the sciatic trunk (sciatic neuropathy) can affect any of the muscles of the sciatic trunk, peroneal nerve, and tibial nerve .
The peroneal nerve does not contribute to the Achilles reflex. So in patients with foot drop, an absent or asymmetrically diminished ankle jerk reduces the probability that they have a peroneal nerve palsy, and increases the chance that they have a more proximal lesion such as a sciatic neuropathy or radiculopathy.
Assess for Tinel's sign over the peroneal nerve at the head of the fibula.
Assess for signs of trauma, previous surgery, peripheral vascular disease, ulcers, and oedema. Observe the gait without any braces, looking for steppage.
Electromyography and nerve conduction studies can be used to help localise the lesion. Motor nerve conduction studies are done on the peroneal and tibial nerve, and sensory nerve conduction studies are done on the sural and superficial peroneal nerves. EMG generally examines a selection of leg muscles to evaluate the function of the different branches, with further examination of more proximal muscles if abnormal. The availability of neurophysiology studies is generally poor in New Zealand.
Plan x-ray or CT can be used to assess for fractures, masses, arthritis, or tumours. MRI of the lumbar spine, knee, or ankle can evaluate soft tissue lesions causing nerve compression.
In cases where there hasn't been traumatic or iatrogenic nerve transection then the initial management is often conservative due to the possibility of partial or complete recovery. The goals of conservative treatment are to improve the gait, prevent foot slap, and prevent contracture of the denervated muscles. Conservative management options include physiotherapy, splinting, and analgesia. Electromyography can be useful to evaluate for possible improvement.
- Physiotherapy - Strengthening and electrical stimulation of the affected dorsiflexors and evertors, and their antagonists, stretching of the contralateral muscle groups. At the point of autonomous muscle contraction, then there is a transition to strengthening of the muscles.
- Splinting - Different types of splints are used depending on the problem. In isolated superficial peroneal nerve palsy with weakness of the evertors then a lateral wedge shoe insert can be used to prevent supination. If there is dorsiflexion weakness then an ankle foot orthosis is needed. Splinting is also important to prevent contractures.
For traumatic or iatrogenic nerve transection, the patient should have surgical nerve reconstruction within 72 hours. After 72 hours there is irreversible degradation making repair impossible. Direct primary repair is used in cases of a minimal gap, otherwise an autologous nerve graft is used (usually the sural nerve) or a nerve conduit.
In other cases surgical management may be considered at three to six months after the onset of symptoms if there are no signs of improvement or if there is further deterioration. Nerve decompression is performed at the site of the problem such as at the fibular head, fibular tunnel, or other area. If there is an extraneural compressive mass then this may need to be resected. Intraneural lesions may be dissected out using microsurgical techniques with intraoperative nerve monitoring.
In those with irreversible nerve impairment or in those who are unresponsive to decompression then nerve transfers, tendon transfers, and combined procedures may be able to be performed. Nerve transfer can restore ankle dorsiflexion, and patients with limited improvement after nerve transfer can subsequently undergo tendon transfer. Alternatively combined nerve and tendon transfer may be done. Nerve transfer involves transferring a functional but less important nerve to a distal but more important denervated nerve. In deep peroneal nerve denervation, the superficial peroneal or tibial nerve are used as a donor. Tendon transfer involves transferring one of the flexor or invertor muscles to the dorsum of the foot to enable dorsiflexion function, usually by transferring the posterior tibial tendon to the anterior tibialis tendon, or a double tendon transfer with additionally transferring the flexor digitorum longus to the extensor digitorum longus and extensor hallucis longus tendons.
If the patient has an equinus contracture then they should have surgical treatment for this at the same time.
In those who the above is not appropriate or if they have failed, then ankle fusion may improve pain and function as a last resort. The ankle is fused to 90 degrees with either a tibiotalar fusion or pantalar fusion. Complications include malunion, hardware related problems, and adjacent joint osteoarthritic changes.
Common Peroneal Nerve Entrapment
In a study of 523 patients with knee-level common peroneal nerve lesions, 318 were operated on. 
- Stretch/contusion without fracture/dislocation
- The time between the injury and operation varied between 4 and 8 months.
- In those where nerve action potentials were recorded and had external neurolysis, 88% had functional outcomes of motor grade 3 or better. In those who did not have nerve action potentials or complete nerve disruption, interfascicular nerve graft was done, and 42% had good outcomes.
- For graft repair patients, proximal peroneal muscle contraction could be seen at 9-12 months. Dorsiflexion of the anterior tibialis muscle when it occurred in graft repairs, appeared at 18-24 months. Whereas extensor hallucis longus muscle function improvement, if it occurred, was variable and usually greatly delayed. Prognosis was poor for recovery of the remaining toe muscle extensors.
- Direct repair achieved achieved grade 3 or better functional outcomes in 84% of patients, but this was only feasible in 19 patients.
- Sharp lacerations in which transection is suspected should was aimed to be repaired immediately, or within 2 or 3 days, whereas the time frame for blunt laceration was 2 to 4 weeks after injury to allow delineation of proximal and distal stump damage.
- Recovery of foot eversion because of reinnervation of the peronei muscles occurred earlier and to a greater extent than did dorsiflexion of the foot.
In another study of 30 patients who had neuroplasty of the common peroneal nerve, average symptom duration to surgery was 122.9 weeks, and clinical improvement was seen in 24 of the 26 patients.
In a study of the post operative course of 135 patients with foot drop due to lumbar degenerative disease, the muscle strength of tibialis anterior (TA) improved in 83.7%. The strength recovered to grade 4 or 5 in 15.6%, with only one third of those recovered achieving grade 5 power. The most important influences on prognosis were duration of palsy, preoperative muscle strength of TA, and age. The recovered group had a median symptom duration of 86.3 days, while the unrecovered group had a median symptom duration of 204.9 days. The preoperative muscle strength was 2.55 and 1.83 in the recovered and unrecovered groups respectively. All patients with grade 0 power recovered to grade 1 but no higher. Overall, postoperative strength seems to have been at its maximum at three months.
|Duration of palsy (days)||>180||150-180||120-150||90-120||60-90||30-60||<30|
|Preop muscle strength of TA||0||1||2||3|
Early Stage: 10-13, Good recovery
Middle Stage: 5-9, Incomplete recovery
Late Stage: 0-4, Poor recovery
- Elkwood et al. Foot drop: Etiology, diagnosis, and treatment. Uptodate. May 2021.
- ↑ 1.0 1.1 1.2 Liu et al.. Foot drop caused by lumbar degenerative disease: clinical features, prognostic factors of surgical outcome and clinical stage. PloS one 2013. 8:e80375. PMID: 24224052. DOI. Full Text.
- ↑ Katirji & Wilbourn. Common peroneal mononeuropathy: a clinical and electrophysiologic study of 116 lesions. Neurology 1988. 38:1723-8. PMID: 2847078. DOI.
- ↑ Kim et al.. Management and outcomes in 318 operative common peroneal nerve lesions at the Louisiana State University Health Sciences Center. Neurosurgery 2004. 54:1421-8; discussion 1428-9. PMID: 15157299. DOI.
- ↑ Souter et al.. Surgical Results of Common Peroneal Nerve Neuroplasty at Lateral Fibular Neck. World neurosurgery 2018. 112:e465-e472. PMID: 29355794. DOI.
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