Foot drop most often results from disruption of the neural pathways that control ankle dorsiflexion, particularly those innervating the tibialis anterior and associated dorsiflexor muscles. The underlying neurological causes can be broadly grouped into central (brain and spinal cord), intraspinal root, and peripheral nerve or neuromuscular disorders, each producing weakness or paralysis of these muscles through different pathophysiological mechanisms.
Overview of neural control
Normal dorsiflexion depends on an intact chain from the motor cortex through descending tracts, spinal motor neurons, peripheral nerves, neuromuscular junction, and muscle fibers. Lesions at any level of this chain can impair voluntary activation of the dorsiflexors, but the resulting clinical picture differs depending on whether upper or lower motor neurons are primarily affected.
The motor cortex for the leg is located in the medial aspect of the precentral gyrus, and its axons descend via the corona radiata, internal capsule, cerebral peduncle, and corticospinal tracts of the brainstem and spinal cord to synapse on anterior horn cells in the lumbosacral spinal cord. From there, lower motor neurons exit as L4–S2 roots, contribute to the lumbosacral plexus and sciatic nerve, and ultimately form the common and deep peroneal nerves that innervate the tibialis anterior, extensor hallucis longus, and extensor digitorum longus.
Central (brain and spinal cord) causes
Central causes of foot drop arise from upper motor neuron lesions affecting the leg area of the motor cortex or corticospinal tract. These include ischemic or hemorrhagic stroke in the anterior cerebral artery territory, parasagittal tumors, traumatic brain injury, and demyelinating diseases such as multiple sclerosis.
In these conditions, the primary pathophysiology is interruption of descending excitatory drive from the cortex to spinal motor neurons, leading to weakness with characteristic upper motor neuron signs such as spasticity, hyperreflexia, and Babinski sign. Cortical or subcortical lesions may produce “pseudoperipheral” foot drop, where weakness is disproportionately prominent in ankle dorsiflexion despite a central lesion, because of the dense somatotopic representation and fiber condensation for the foot and leg in the interhemispheric cortex and internal capsule.
Spinal cord pathology can also produce central foot drop when corticospinal fibers for the legs are compressed or damaged, as seen in cervical or thoracic myelopathy, spinal cord infarction, or inflammatory myelitis. In these cases, foot drop often coexists with other signs such as sensory level, sphincter dysfunction, and bilateral spastic paraparesis, reflecting more widespread cord involvement.
Radiculopathy and intraspinal nerve root lesions
Below the spinal cord, one of the most frequent neurological causes of foot drop is lumbosacral radiculopathy, especially involving the L5 root. L5 radiculopathy typically results from intervertebral disc herniation, foraminal stenosis due to spondylosis, or extraforaminal compression by osteophytes or ligaments.
The key pathophysiology is mechanical compression and ischemia of the nerve root, which impair axoplasmic transport and conduction in motor and sensory fibers supplying the dorsiflexors. Patients often report low back pain radiating down the lateral leg with sensory changes in the L5 dermatome, and examination may show weakness of ankle dorsiflexion and toe extension, often accompanied by weakness of hip abduction and inversion because these share L5 root innervation.
Chronic compression can cause demyelination and secondary axonal loss, leading to more persistent weakness and muscle atrophy. In contrast, acute massive disc herniation may produce rapid-onset foot drop with severe radicular pain, representing abrupt disruption of root function, and may require urgent decompression to optimize neurological recovery.
Peripheral nerve and plexus lesions
Peripheral neuropathies of the sciatic, common peroneal, or deep peroneal nerves are among the most common neurological causes of foot drop. The common peroneal nerve is particularly vulnerable where it winds around the fibular neck, making it susceptible to compression from leg crossing, tight casts or braces, trauma, and space-occupying lesions near the fibular head.
Focal compression produces segmental demyelination with conduction block at the compression site, leading to weakness of dorsiflexion and eversion, as well as sensory loss over the dorsum of the foot and lateral shin. More severe or prolonged compression causes Wallerian degeneration distal to the lesion, with axonal loss that prolongs recovery and may leave permanent deficits.
Sciatic neuropathy, often due to hip surgery, pelvic trauma, or deep gluteal injection injury, can also cause foot drop when fibers destined for the peroneal division are preferentially affected. In sciatic lesions, weakness typically involves hamstrings and all muscles below the knee, with sensory loss extending over most of the leg and foot, reflecting the broader distribution of the nerve.
Lumbosacral plexopathy, due to diabetes, retroperitoneal hematoma, pelvic tumors, or radiation, can likewise result in foot drop by damaging multiple roots or fascicles contributing to the peroneal nerve. The underlying mechanism often combines ischemic microvasculitis and inflammatory injury, especially in diabetic lumbosacral radiculoplexus neuropathy, which produces painful asymmetric weakness including the dorsiflexors.
Generalized neuropathies and motor neuron disease
Generalized peripheral neuropathies frequently involve the peroneal-innervated muscles early, producing bilateral or asymmetric foot drop. Length-dependent axonal polyneuropathies, such as those caused by diabetes, chronic alcohol use, or certain toxins, preferentially affect distal sensory and motor fibers, so dorsiflexor weakness and distal sensory loss in the feet are prominent features.
Hereditary neuropathies like Charcot–Marie–Tooth disease cause slowly progressive demyelination or axonal degeneration of peripheral nerves, resulting in distal weakness, pes cavus, and often bilateral foot drop in adolescence or early adulthood. In these conditions, the neurological cause is intrinsic genetic dysfunction of myelin or axonal proteins, leading to chronic conduction failure and loss of motor units supplying the dorsiflexors.
Motor neuron diseases such as amyotrophic lateral sclerosis or spinal muscular atrophy damage anterior horn cells and corticospinal tracts, combining upper and lower motor neuron features. Foot drop can be an early manifestation when lower motor neuron loss is prominent in the lumbosacral segments, and progressive denervation reduces the number of functioning motor units in the tibialis anterior and related muscles.
Pathophysiology at the neuromuscular junction and muscle
Although many cases of foot drop are neuropathic, disorders of the neuromuscular junction and muscle can contribute to or mimic neurological foot drop. Myopathies such as muscular dystrophy, inflammatory myositis, or metabolic myopathies can weaken the dorsiflexors directly, but in practice these conditions usually present with more generalized proximal weakness rather than isolated foot drop.
In these diseases, the primary pathology is degeneration or inflammation of muscle fibers, leading to reduced force generation even when neural input is preserved. From a functional perspective, the gait abnormality is similar: the forefoot cannot be adequately lifted during swing, so patients develop a high-stepping or slapping gait to compensate.
Clinical implications of neurological mechanisms
Understanding the precise neurological cause of foot drop has important diagnostic and therapeutic implications, because prognosis and management differ substantially between central and peripheral lesions. Central causes may respond to stroke rehabilitation, antithrombotic therapy, or disease-modifying treatments for multiple sclerosis, whereas compressive radiculopathy or peroneal neuropathy may require surgical decompression, bracing, and targeted physiotherapy.
Electrodiagnostic studies, including nerve conduction studies and electromyography, are crucial for localizing the lesion along the neuroaxis by demonstrating patterns of denervation, conduction block, or chronic reinnervation in specific muscles. Imaging of the brain, spine, and peripheral nerves further delineates compressive, vascular, or inflammatory lesions, allowing treatment to focus on relieving neural injury and preventing further axonal loss that would worsen or prolong the foot drop.