Steppage gait is the inability to lift the foot while walking due to the weakness of muscles that cause dorsiflexion of the ankle joint. Foot drop is not a commonly seen condition. The typical presentation is one of a patient who presents with a sudden onset of weakness of the muscles that extend the foot during walking. The history usually consists of unusual activity, a surgical procedure, prolonged bed rest, accident leading to fracture, or a tight cast applied to the lower extremity. The other possibilities include a history of collagen vascular diseases leading to nerve ischemia. Peripheral neuropathies, the most common cause being diabetes, can lead to unilateral or bilateral foot drop. Upper motor neuron lesions can also present as foot drop. However, the presentation also includes hemiplegia and aphasia.

Any damage or compression of the neuraxis anywhere along this pathway can potentially lead to foot drop, and steppage gait.  Frequent reasons include traumatic injuries, pelvic fractures, tibia or fibular head fractures, tight casts, prolonged positioning in lithotomy during surgical procedures, compression by a space-occupying lesion, vascular impairments as in conditions as lupus, or Waldenstrom macroglobulinemia which can lead to vasculitis causing nerve ischemia. Neuropathies affecting the nerves of the peripheral nervous system are referred to as peripheral neuropathies. These can be primarily demyelinating, primarily axonal, or mixed. Primary demyelinating neuropathies can be acquired or congenital. Examples of acquired neuropathies include acquired inflammatory demyelinating polyneuropathy (AIDP) and chronic inflammatory demyelinating polyneuropathy (CIDP). Hereditary neuropathies include Charcot-Marie Tooth (CMT), and hereditary preponderance to pressure palsies (HNPP).

Predominantly axonal neuropathies are seen with exposure to toxins, viral or bacterial infections, chemotherapeutic agents as vincristine or vinblastin.

Diabetes, alcohol intoxication and renal disease can lead to mixed peripheral polyneuropathies. 

The primary causes of foot drop include cerebral vascular accident (CVA) and amyotrophic lateral sclerosis. CVA presents as hemiparesis or hemiplegia, associated with dysphagia, dysarthria, or aphasia.[1][2]

Foot drop with high steppage gait is of the upper motor neuron type.

Peroneal neuropathy is more common in males (male-to-female ratio, 2.8 to 1). Approximately 90% of peroneal lesions are unilateral, with no preference to the side.

• The frequency of occurrence is - 0.3 to 4% after total knee arthroplasty (TKA).
• 3 to 13% of cases may end up with foot drop after proximal tibial osteotomy.

• To understand the pathophysiology and prognosis, a knowledge of nerve injury classification is necessary. In 1943 Seddon and 1953 Sunderland have proposed a classification that is still in use. Accordingly, there are three degrees 1) neurapraxia, 2) axonotmesis, and 3) neurotmesis.
• In neurapraxia, the nerve remains intact, but due to a temporary injury to myelin, the propagation of the signal is affected. The endoneurium, perineurium, and the epineurium remain intact. Conduction is unaffected in the distal segment and proximal segment, but no conduction occurs across the area of injury; the term for this is conduction block. Conduction studies reveal signs of demyelination as prolonged latency and slow nerve conduction velocity across the compressed segment. The prognosis for recovery is the best of the three classifications.
• In axonotmesis, the axon becomes damaged, but the surrounding connecting tissue, i.e., the epineurium and perineurium, remain intact. Wallerian degeneration takes place distal to the site of injury. Nerve conduction studies show sensory and motor deficits distal to the site of the lesion. Some conduction which may initially be present disappears after 3 to 4 days following the injury. In 3 to 4 weeks after the injury, signs of axonal damage, i.e., fibrillation potentials (FP), and positive sharp waves appear. Eventually, axonal regeneration occurs, and recovery is possible, although it may not always be complete.
• The last degree is neurotmesis, in which both the axon and connective tissue suffer damage. Wallerian degeneration occurs distally to the injury site. Sensory-motor problems and autonomic function defects accompany this. Nerve conduction distal to the injury site is not possible. Since electromyography (EMG) and nerve conduction velocity (NCV) findings are similar to those of the second degree, the distinction is difficult. Surgical intervention is sometimes necessary.[3][4]
• There are five lumbar vertebrae. From each of the five lumbar vertebrae nerves, roots emerge. They extend from L1 to S4. These nerve roots emerge from the lateral spinal recess formed by the superior facet of the distal vertebra and inferior facet of the proximal. They join to form the lumbosacral plexus. The lumbosacral plexus has only two main components: the portion made of nerve fibers from the L2 through L5 roots is called lumbar plexus, and the other from S1 through S4 roots is called sacral plexus.
• Anteriorly, the largest branch that emerges from the LS plexus is the femoral nerve. Posteriorly, another large branch emerges through the sciatic notch and is called the sciatic nerve. At or around the popliteal fossa, this nerve divides into two branches — the tibial and fibular or peroneal nerve. The tibial nerve travels down to the posterior thigh supplying the hamstring group, then continues to supply the calf muscles, the gastric soleus tibialis posterior, flexor hallucis, and flexor digitorum and all the intrinsic muscles of the foot.
• The sural nerve is a large sensory nerve that gets contributions from both tibial and peroneal nerves; this is the primary sensory nerve that supplies the posterior leg and heel.
• The common peroneal nerve continues down the lateral side of the leg at the fibular head. It divides into the superficial peroneal nerve, which supplies the peroneus longus and brevis, the main eversion muscles of the foot.  
• The superficial branch supplies sensation to the dorsum of the foot and lateral calf.  The deep branch supplies a small area at the first webspace.[5] The deep peroneal nerve innervates the dorsiflexors, i.e., tibialis anterior, extensor digitorum longus and brevis, and extensor hallucis longus muscles. These are responsible for ankle dorsiflexion.
• Because of its superficial location, the peroneal nerve is vulnerable to compression during surgical procedures, tight cast placements, and other traumatic conditions sustained during sports. Patients with diabetes seem to be affected more often. Any compression of the common peroneal nerve leads to foot drop.
• The normal gait cycle consists of stance phase 60% and the swing phase, 40%. When the one foot is in the swing phase, the other is in the stance phase. The gait cycle starts with a heel strike and ends with a heel strike on the same side. During the stance phase, the foot remains flat on the ground. In the heel strike, the foot is in dorsiflexion, preparing for gradual lowering before the stance phase. Any damage affecting the neuraxis from the roots to the peripheral nerve can lead to weakness of the muscles supplied by that nerve. Therefore a lesion of the L5  root, lumbar plexus, sciatic nerve, common peroneal, or the deep peroneal nerve can potentially lead to foot drop due to the weakness of the anterior compartment musculature. The presenting symptom is the inability to ambulate as before. More specifically, there is a weakness of the muscles in the foot that assist in dorsiflexion. There may or may not be a pain. The person will be unable to dorsiflex during the heel strike, and the foot remains flat on the ground. Sometimes this can also cause toe drag and inability to clear the foot, potentially leading to falls.