History and Physical Examination
Direct injury to dorsiflexors
With dorsiflexor injury due to laceration or contusion, both cause and effect are readily apparent on clinical examination. (See the video below.) A young healthy patient or an active healthy elderly patient usually benefits from surgical repair of the injury.
If the patient develops a degenerative rupture of the tibialis anterior, foot drop may be observed, but the cause may not be immediately apparent. Such a patient is often an elderly man who suffers a minor trauma with the foot in plantarflexion. The patient stands with the foot everted and has some loss of dorsiflexion when attempting to heel-walk. The degree of foot drop varies, depending on the time elapsed since the rupture.
Active function in the other muscles innervated by the deep and superficial branches of the peroneal nerve essentially rules out the possibility of a peripheral neuropathy. Functional recovery is achieved over time and is aided by bracing of the affected ankle. Surgery may not be required in this situation.
Compartment syndromes
Increased pain with passive stretch of the involved muscles is a consistent diagnostic indicator of a compartment syndrome. The usual initial presenting symptom is pain that is out of proportion to the injury. Paresthesias follow, but at this point, irreversible myoneural injury is likely to have occurred. Foot drop also may be noted; the time of presentation varies with the compartment involved.
Anterior compartment syndrome
Clinical presentation of an acute anterior compartment syndrome includes pain with passive toe flexion, some weakness of toe extension, and diminished sensation in the first web space because of deep peroneal nerve compression. The extensor hallucis longus (EHL) usually is the first muscle to show weakness. Anterior compartment syndrome may follow trauma to the extremity but also can be observed in march gangrene (ie, ischemic myositis of leg muscles following exercise [9] ). In march gangrene, local erythema, heat, and brawny edema over the anterior compartment are present.
Regardless of the cause, wide fasciotomy of the anterior compartment must be performed to salvage the ischemic muscles.
Deep posterior compartment syndrome
An acute deep posterior compartment syndrome presents as pain and some weakness of toe flexion and ankle inversion. Pain on passive toe extension is referred to the calf. Diminished sensation over the sole of the foot, especially on the medial side, is noted, resulting from posterior tibial nerve compression. Foot drop develops because of ischemic contracture of the posterior compartment and is seen if the acute syndrome is not treated.
Once again, wide fasciotomy of the involved compartment is mandatory at the time of acute presentation.
Chronic compartment syndrome
Chronic compartment syndrome occurs in athletes in their third or fourth decade who have exercise-induced pain in the lower leg or foot within 20-30 minutes after beginning to exercise. Often, this occurs after a recent increase in intensity or duration of training or after a change in the training routine. The symptoms resolve after 15-30 minutes of rest; however, as the syndrome progresses, pain occurs earlier and takes longer to resolve. The anterior compartment is the one that is most commonly involved.
Unless the patient has been exercising just before being examined, the physical examination may yield nonspecific or normal results. Patients with a chronic anterior compartment syndrome may have diminished sensation in the first dorsal web space.
Recording of intracompartmental pressures before, during, and after exercise can provide useful diagnostic information as to which compartments may be involved. The following, individually or in combination, are believed to be indicative of the syndrome:
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Resting pressure of 15 mm Hg or higher
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Pressure of 30 mm Hg or higher 1 minute after exercise
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Pressure of 20 mm Hg or higher 5 minutes after exercise
A slit catheter may be used to measure these pressures, with the understanding that the accuracy of the readings is influenced by the depth of needle insertion; the positioning of the leg, ankle, and foot; and the force of muscle contraction.
Some preliminary investigation has been completed into the use of magnetic resonance imaging (MRI) as a potential test for chronic compartment syndrome.
Nonsurgical treatment of a chronic compartment syndrome can succeed only if the patient is willing to discontinue the inciting activity. The surgical treatment of choice is fasciotomy of the involved compartment.
Neurologic defects
Several neurologic defects can cause foot drop. Equinovarus deformity associated with toe contracture is the most common lower-extremity manifestation of stroke. This can be differentiated from a peripheral neuropathy on examination by eliciting hyperactive deep tendon reflexes and a positive Babinski sign. The patient’s gait pattern can also suggest the etiology. For example, patients with a paretic foot drop bear weight on the heel during initial foot strike, whereas those with a spastic deformity strike with the forefoot.
Another central-nerve insult that can be associated with foot drop is L5 compression. In addition to weakness in the peroneal nerve distribution, weakness of the tibialis posterior is noted. Back pain, sciatica, and limitation of straight leg raising also are seen. Motor conduction velocity may remain normal.
Peroneal neuropathy also may be spontaneous, traumatic, or, less frequently, progressive. It is characterized by weakness in dorsiflexion without back pain, sciatica, or other symptoms. Leprosy neuritis, for example, affects nerves where they are close to the skin and pass through a narrow fibrous or osseous canal. In addition to peroneal nerve palsy, patients with leprosy may have involvement of the posterior tibial nerve at the tarsal tunnel that leads to anesthesia of the sole of the foot.
Foot drop from neuropathy may develop in patients who have undergone bariatric surgery, especially those who experience rapid postoperative weight loss. [10] Deficiencies of micronutrients (eg, vitamin B12) may be a factor in these cases. [11]
Combination of neurologic, muscular, and anatomic dysfunction
Patients with a combination of neurologic, muscular, and anatomic dysfunction typically are diabetic and develop loss of protective sensation and proprioception that leads to unperceived trauma. This is coupled with an autonomic neuropathy that results in loss of sympathetic vasoconstriction and enhanced pedal blood flow, causing demineralization and subsequent bone weakness.
Unperceived trauma, demineralization, and bone weakness culminate in destruction of the tarsal bones. This, in turn, leads to formation of a bony block at the ankle joint and foot drop. Progressive motor neuropathy is also present, in which the muscles weaken in a distal-to-proximal manner, resulting in loss of strength in the anterior compartment. The anterior muscles are overpowered by the Achilles tendon, and this leads to abnormal pronator stress at the midtarsal joint, which further encourages osseous breakdown and foot drop.
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Diagram of ground reaction vector during heel strike.
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Common and superficial peroneal nerves, branches, and cutaneous innervation.
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Deep peroneal nerve, branches, and cutaneous innervation.
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Incisions for Bridle procedure.
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Posterior leg with retrieved posterior tibial tendon above ankle. Window in interosseous membrane is labeled with X.
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Posterior tibial tendon (C) is pulled through slit in anterior tibial tendon (A) and inserted into second cuneiform. Posterior tibial tendon is anastomosed to anterior tibial tendon and distal stump of peroneus longus (B) that has been rerouted anterior to lateral malleolus.
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Gait of patient with foot drop.
