Drop foot is the inability or significant difficulty in lifting the front part of the foot, a movement known as dorsiflexion. This complication is a recognized, though relatively infrequent, risk following lumbar spine surgery. The estimated incidence rate is about 3.33% after spinal procedures, though this figure can rise significantly in more complex operations, such as those for high-grade spinal deformities. The causes range from direct mechanical contact with the nerve to indirect compression from post-operative swelling.
Understanding the Anatomy of Foot Movement
The ability to lift the foot and toes is controlled by a neurological pathway starting in the lower back. Dorsiflexion relies primarily on the tibialis anterior muscle, which runs along the front of the shin and attaches to the foot. This muscle receives its motor signal from nerves originating in the spinal column.
The most frequent site of injury leading to post-operative drop foot is the L5 nerve root, which exits the spinal column at the L4-L5 level. The L5 nerve root contributes significantly to the formation of the sciatic nerve. Damage at this spinal level causes weakness in the muscles it supplies, resulting in the characteristic foot dragging.
Another common injury site is the common peroneal nerve, a major division of the sciatic nerve, further down the leg. This nerve wraps around the head of the fibula near the knee and controls the muscles responsible for lifting the foot. Damage to either the L5 nerve root or the common peroneal nerve interrupts the signal to the tibialis anterior, manifesting as drop foot.
Direct Mechanisms of Nerve Damage During Surgery
Post-operative drop foot is often caused by the surgical manipulation of neural elements within the spinal canal. One mechanism is retraction injury, where instruments used to hold soft tissue away from the operative site apply prolonged or excessive pressure. This pressure can compress the L5 nerve root, disrupting its blood supply and causing temporary or sustained damage. Mechanical compression can lead to ischemia, making the nerve vulnerable to injury.
Direct mechanical trauma occurs when the nerve root is accidentally nicked, stretched, or manipulated during the procedure. During decompression procedures, such as microdiscectomy or laminectomy, the surgeon works closely around the nerve root. Even subtle manipulation of an already compressed nerve can exacerbate pre-existing damage, leading to a new motor deficit.
In procedures involving bone work, such as spinal fusion, heat generated by drills or electrocautery can cause thermal injury to nearby nerve tissue. This heat damages the cellular structures of the nerve root, affecting signal transmission. Additionally, a misplaced pedicle screw used to stabilize the spine can breach the spinal canal and directly injure the L5 nerve root.
Acute post-operative complications also involve direct compression from a hematoma or edema forming near the surgical site. A collection of blood or significant swelling can accumulate in the epidural space, placing extrinsic pressure on the nerve root. This compression can occur hours to days after the operation and requires immediate investigation to prevent permanent nerve damage.
Indirect and Pre-existing Contributing Factors
The patient’s positioning during the procedure can increase the risk of developing drop foot. For long surgical cases, especially those involving spinal fusion, the patient remains in a fixed position for extended periods. Improper padding can compress the common peroneal nerve as it passes around the fibular head near the knee. This injury is separate from the spinal procedure but results in foot weakness.
The duration of the surgery is also correlated with increased risk. Prolonged operative times intensify the effects of positioning and retraction. Extended time under anesthesia increases the total duration of potential nerve compression, raising the likelihood of nerve ischemia. Longer procedures also increase the risk of excessive intraoperative blood loss.
A patient’s pre-existing condition significantly influences the nerve’s vulnerability to injury. If the L5 nerve root was already severely compressed due to spinal stenosis or a large disc herniation, it is considered compromised. This pre-existing damage means the nerve requires less additional trauma to fail, making it hypersensitive to minimal manipulation. Patients with uncontrolled diabetes also face a higher risk because their peripheral nerves are already in a fragile state (peripheral neuropathy).
Expected Recovery and Management
The prognosis for post-operative drop foot depends primarily on the severity of the initial nerve injury. If the nerve damage is mild (neurapraxia), the condition may resolve fully over several weeks or months. More severe injuries, which involve damage to the nerve’s internal fibers (axonotmesis or neurotmesis), have a longer and less predictable recovery timeline, sometimes taking a year or more.
Management focuses on protecting the foot and supporting mobility. An Ankle-Foot Orthosis (AFO) is prescribed to hold the foot in a neutral position, preventing toe dragging and reducing the risk of tripping. This device assists with gait while nerve regeneration occurs.
Physical therapy is a core component of recovery, focusing on strengthening weakened muscles and maintaining the range of motion in the ankle joint. A key predictor of a good outcome is the strength of the tibialis anterior muscle before surgery and the duration of foot weakness prior to treatment. Early diagnosis and intervention maximize the potential for nerve function to return.

