The last 2 chapters focused on neurologic disorders such as multiple sclerosis and stroke and the neurologic causes of foot pain associated with these conditions. Common causes of neuropathic pain involving the foot and ankle were also covered. This chapter will focus on radicular pain, spinal stenosis, traumatic causes of foot and ankle nerve injury and phantom limb pain.

A common cause of low back and lower extremity pain is lumbar spinal stenosis. The normal wear and tear effects of aging can lead to narrowing of the spinal canal. Degenerative changes of the spine are seen in up to 95% of the general population by the age of 50 years. Spinal stenosis most often occurs in adults older than 60 years. Pressure on the nerve roots is equally common in men and women. The phrase spinal stenosis directly refers to a narrowing in the vertebra, in any of the anatomical regions of the central canal, lateral recess, or the neural foramen. When both or either the lateral recess and neural foramen are narrowed, the symptomatology of lumbar radiculopathy may also present concomitantly. In spite of the fact that it is widely prevalent, currently there is no universally accepted definition of presentation for lumbar spinal stenosis, and there is also much variability in radiographic interpretation to make a diagnosis. Lumbar spinal stenosis is a significant cause of disability in the elderly, and it is the most significant cause of spinal surgery in this particular patient population. Therefore clinicians need to recognize and treat lumbar spinal stenosis effectively, and the podiatric physician must also recognize this particular pathology as our patient population continues to age and develop lower extremity symptomatology secondary to this condition.

A smaller portion of patients present prior to the sixth decade and usually have some underlying structural deformity, causing congenital spinal stenosis. It occurs most often in men. Patients with this presentation usually first notice symptoms between the ages of 30 and 50 years.¹

Spinal stenosis occurs when the space around the spinal cord narrows, which puts pressure on the spinal cord and the spinal nerve roots, causing pain, numbness, or weakness in the legs. Degenerative spondylosis is the most common etiology of lumbar spinal stenosis. With senescence, wear and tear degenerative changes, and posttraumatic degeneration, among other factors, the intervertebral disks can degenerate, and clinically the disks will protrude posteriorly,
which will lead to increased uneven wear and loading of the posterior aspects of each particular vertebral segment. These changes can lead to posterior vertebral osteophytosis, also known as uncinate spurs, facet hypertrophy, synovial facet cysts, and ligamentum flavum hypertrophy, which all in turn will create a space-occupying lesion that will ultimately cause the symptomatology of spinal stenosis.

Additionally, degenerative spondylolisthesis is another cause of lumbar spinal stenosis. When degenerative changes of the spine occur, the structures of the concomitant pars interarticularis can be fractured, and it is this destabilization that will result in the symptoms. Sufficient anterior slippage of one vertebra on top of the next vertebral segment, which is most commonly seen L4-on-L5, can narrow the spinal canal, leading to stenosis.

There are several other acquired conditions, although significantly rarer than the conditions mentioned above, which can and should also be considered by the clinician in the workup. These include other space-occupying lesions such as malignancy, postsurgical fibrosis that can be deduced from the surgical history, and rheumatologic conditions as well as other skeletal diseases like ankylosing spondylitis or diffuse idiopathic skeletal hyperostosis. Rarely, lumbar spinal stenosis may be secondary to congenital factors such as achondroplasia.

Arthritis is the most common cause of spinal stenosis. In the spine, arthritis can result as the disk degenerates and loses water content. In children and young adults, disks have high water content, causing settling, or collapse, of the disk spaces and loss of disk space height. As the spine settles, weight is transferred to the facet joints. Progressively, the tunnels that the nerves exit through become smaller. As the facet joints experience increased pressure, they also begin to degenerate.

Eventually, the cartilage that covers and protects the joints wears away, resulting in pressure on spinal nerves and in pain in the areas that the nerves supply. The pain may be described as an aching or a burning sensation, starting in the area of the buttocks and radiating down the leg. As it progresses, it can result in pain in the foot.²

Case description: A 71-year-old male patient with past history of obesity and knee osteoarthritis, s/p right total knee arthroplasty performed in February 2020 complicated by deep vein thrombosis (DVT) and cellulitis, right shoulder osteoarthritis, and hypertension, presented with complaint of numbness and cramping in the feet when lying down flat. He denied pain, just an intolerable sensation of the legs falling asleep, which impeded his ability to sleep. He had no symptoms when walking. He denied weakness or foot drop. He had no history of bowel/bladder incontinence.

Acute lumbosacral radiculopathy is a diffuse disease process that often affects multiple nerve roots. It manifests as pain, loss of sensation, and motor function depending on severity and levels involved. Muscle strength is often preserved in the case of radiculopathy because muscles typically receive innervation from multiple roots, and so muscle strength is often only affected in severe cases of radiculopathy. Most cases of lumbosacral radiculopathy are self-limiting. The most common symptom in radiculopathy is paresthesia. Sensory loss or paresthesia into the lower extremity and back pain radiating into the foot, with a positive straight leg raising test, are common presentations of lumbar radiculopathy.

The most common cause of lumbar radiculopathy is disk herniation, causing nerve root compression. This process can be acute or chronic. Imaging is not always diagnostic. Almost a quarter of patients without back pain have been found to have disk herniation on MRI. To diagnose a herniated disk as a source of pain, it is important to clinically correlate examination to imaging. Patients with lumbar radicular pain often respond to conservative management. Patients who do not respond to conservative therapies will likely undergo an MRI for further evaluation.⁵

Limb salvage is a major component of podiatry in order to preserve the function and length of the lower extremity in the setting of managing comorbidities and other pathologies. However, in the United States alone, 30,000 to 40,000 amputations are performed each year due to vascular disease, trauma, infection, and cancer.⁷ Painful postamputation sensation, also known as phantom limb pain (PLP), is a common sequela of amputations that was first recorded in the 16th century but is still poorly understood. Approximately 60% to 80% of amputees will experience phantom limb sensations.⁸ PLP is often mild in nature but can progress to such a chronic and debilitating point that it leads to poor quality of life, compromised social settings, and increased restrictions of activity. Although the extremity is gone, the nerve endings at the site of the amputation continue to send pain signals to the brain. Anecdotally, for the podiatric physician, PLP is a presenting sequela of forefoot or digital amputation and should be discussed with patients in the perioperative setting. Researchers have found dorsal root ganglion cells become altered and adapt
after a nerve is transected. The ganglion cells become more active and sensitive to chemical and mechanical changes with potential for plasticity development.⁹

Foot drop is the condition in which a disturbance in the motor nerve pathway results in the inability to actively lift the foot from weakness of the dorsiflexor muscles of the foot. This condition can cause limping or antalgic gait pattern that will affect both phases of gait and leads to compensatory hyperflexion in the hip and knee joints. As the result of the muscular imbalance, which causes permanent strain of the plantar flexors and shortening of the Achilles tendon, equinus position of the foot may develop.¹⁶ The clinical condition may also lead to frequent falls and injury.

Diagnosis and localization of the injury is necessary for successful treatment and outcome. Injury to the motor pathways of muscles can occur from either central, peripheral, or both locations.¹⁶ The most common cause of foot drop is associated with common peroneal nerve neuropathy at the level of the fibular neck. The common peroneal nerve is responsible for innervation of the ankle and foot extensor muscles in the anterior compartment of the lower extremity. Other etiologies may include muscular, neurologic, spinal, autoimmune, and musculoskeletal disorders
such as L5 radiculopathy, lumbosacral plexopathy, and sciatic neuropathy. Depending on the etiologic cause, the treatment options will vary.¹⁶

Treatment is contingent upon the etiology of foot drop and the nature of the compressive lesion. Based on the evaluation and diagnostic findings, many options exist. Naturally, the goal is to reach a normal physiologic gait pattern as a sum of both coordination and musculotendon balancing.

Surgical management can include neurolysis of the nerve, end-to-end repair, autogenous nerve grafts, nerve transfers, and tendon transfers. In trauma cases, for nerve transection, nerve reconstruction should take place within 72 hours. Primary nerve repair techniques and autologous nerve grafts are commonly used in acute clinical scenarios. For complete nerve compression, neurolysis and nerve decompression should be performed. In cases of significant nerve dysfunction, nerve or tendon transfer may be required and is pathology specific.¹⁹ A tibialis posterior tendon transfer can be ideal for both recurrent congenital deformities and/or acquired weaknesses to compensate for the lack of dorsiflexion at the ankle. This out-of-phase tendon transfer is accomplished by rerouting the posterior tibia tendon proximally through the interosseous membrane with fixation at the lateral cuneiform. For the other etiologies, treatment is initially conservative because there may be a chance of partial or complete resolution of symptoms spontaneously over time.