Neurologic Causes of Foot Pain: Part II

Neurologic Causes of Foot Pain: Part II

Ernest Megdanis

Simran K. Chhabra

Andrew Gunter

Ginette Illuzzi

Amanda Johnson

Anita Krish

Raymond Morales

Mary Ann Picone


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.

Clinical Course

Patient was prescribed a short course of physical therapy for his knees when these symptoms were first noticed. Magnetic resonance imaging (MRI) showed multilevel degenerative changes with moderate central canal stenosis most notable at L4-5 secondary to a grade I retrolisthesis of L4 on L5 and buckling of the ligamentum flavum. As symptoms were largely positional, sleeping modifications that would allow patient to not lie flat while sleeping were discussed. Patient also started physical therapy focusing on improving core strength and his hips, postural alignment, and lower extremity strengthening. Gabapentin was discussed as a treatment for his pain, but the patient was not interested at the time. If pain in the legs or claudication symptoms were to develop, epidural steroid injection would be considered.


Spinal stenosis can be caused by congenital or acquired factors. Only 9% of the cases are congenital. The most common congenital causes are achondroplasia, shortened pedicles, osteopetrosis, apical vertebrae, spinal dysraphism, early vertebral arch ossification, kyphosis, morquio syndrome, and bony exostosis. Acquired pathology occurs from trauma, degenerative changes, and systemic disease. Trauma usually affects the vertebral canal acutely with a mechanical force. Degenerative changes occur when there is a narrowing of the central canal and lateral recess from posterior disk herniation, ligamentum flavum hypertrophy,
and spondylolisthesis. Additionally, stenosis is a sequela of laminectomy, fusion, and diskectomy procedures.2

Patients may report numbness and tingling in the extremities bilaterally, although not all patients will have both burning pain and numbness and tingling. Once the pressure reaches a critical level, weakness can occur in one or both legs. Some patients will present with foot drop. Patients report that leaning forward can actually increase the space available for the nerves, and they may note relief when leaning, especially with sitting. Pain is usually made worse by standing up straight and walking.3

Nonsurgical Treatment

Nonsurgical treatment options focus on restoring function and relieving pain. Although nonsurgical methods do not improve the narrowing of the spinal canal, some patients report that these treatments do help relieve symptoms.

  • Physical therapy: Stretching exercises, massage, and lumbar and abdominal strengthening often help manage symptoms.

  • Lumbar traction: Although it may be helpful in some patients, traction has very limited results. There is no scientific evidence of its effectiveness.

  • Anti-inflammatories: Because stenosis pain is caused by pressure on a spinal nerve, reducing inflammation (swelling) around the nerve may relieve pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) initially provide pain relief. When used over the course of 5 to 10 days, they can also have an anti-inflammatory effect.

  • Steroid injections: Cortisone injections around the nerves or in the “epidural space” can decrease swelling, as well as pain. They also reduce numbness, but not weakness, in the legs.

  • Acupuncture: Acupuncture can be helpful in treating some of the pain for less severe cases of lumbar stenosis. Although safe, long-term success with this treatment has not been proven.4

Surgical Treatment

Surgery for lumbar spinal stenosis is generally reserved for patients with poor quality of life and limitations in function. There are 2 main surgical options to treat lumbar spinal stenosis: laminectomy and spinal fusion.

  • Laminectomy/decompression: This procedure involves removing the bone and mass
    effects compressing the nerves. Laminectomy can be performed open or minimally invasive.

  • Spinal fusion: If arthritis has progressed to spinal instability, a combination of decompression and stabilization or spinal fusion may be jointly employed.4


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

Case Presentation

A 37-year-old woman with no significant past medical history presents with severe back and right leg pain without inciting event or trauma. She has had back pain off and on for years. Pain is localized in the lower back and radiates to the plantar aspect of the right foot. The leg feels numb and patient describes tingling. She has difficulty with bending, standing, walking, and sitting. She denies bladder/bowel incontinence. On physical examination, she was noted to have diminished sensation in the right lateral foot, and weakness with right great toe extension (4+/5) and plantar flexion (4+/5).

Clinical Course

Patient was started on a Medrol dose pack and gabapentin. Spinal x-rays were largely unremarkable with slight narrowing noted at L5-S1. She was sent for a transforaminal epidural injection of the L5-S1 nerve roots and started on a course of physical therapy.


L2, L3, and L4 lumbar radiculopathy manifest similar presentations and are grouped together on examination. This group innervates the anterior thigh. Acute pathology of L2, L3, and L4 will most commonly present with radiating pain to anterior thigh and knee, and possibly radiate to the medial aspect of the lower leg and foot. The patient may have weakness in knee extension, hip adduction, or flexion. There is often a loss of sensation over the anterior thigh as well, in addition to a reduced patellar reflex (L4). Other aggravating factors include coughing, leg straightening, or sneezing.5

In L5 radiculopathy, patients complain of lateral leg and foot pain that radiates. There may be a reduction in muscle strength to the extensor hallucis longus, and in foot eversion, inversion, toe extension, and foot dorsiflexion. Chronic L5 radiculopathy can cause atrophy of the extensor digitorum brevis as well as the tibialis anterior. In severe cases, L5 radiculopathy can cause weakness in leg abduction and weakness of the gluteal muscles. In S1 radiculopathy, sacral or buttock pain will radiate into the posterior aspect of the patient’s leg, into the foot, and weakness in plantar flexion can be seen. The ankle reflex (S1) can also be diminished.5

Patients may complain of inability to get up from a chair, knee buckling, and toe drag, suggestive of iliopsoas or quadriceps weakness, quadriceps, and tibialis anterior involvement. Straight leg raising can be painful in lumbosacral radiculopathy. Pain or reproduction of paresthesias is considered a positive test
(Lasegue sign). The straight leg raising test is most helpful in the diagnosis of L4 and S1 radiculopathies. An internal hamstring reflex for L5 radiculopathy has also been shown to be useful. When there is an asymmetry of the reflex between legs, this can be significant for radiculopathy. In nonradicular back pain, the pain localizes to the spinal or paraspinal areas.6


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


PLP is usually reported within the first week after amputation and will generally decrease in severity and frequency for most patients. Symptoms include sensations such as tingling, burning, cramping, heat and cold sensitivities, and throbbing in addition to normal postoperative pain. The patient may report continued sensation in the limb as well as residual limb pain or “stump pain” at the actual site of the amputation.10 The onset of symptoms can be elicited by physical, emotional, and environmental changes.


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

Case Presentation

A 64-year-old female patient presented with past history of L4 laminectomy that was complicated by weakness of left ankle dorsiflexion and plantar flexion, PVD, and hypertension. She reported difficulty with balance, foot clearance, and secondary back pain due to her alterations in gait. Physical examination revealed weakness of left ankle dorsiflexion (1/5) and plantar flexion (4/5). Sensation was diminished throughout the foot. Gait was wide based with exaggerated hip flexion to allow for clearance of the left foot, with foot slap gait.

Clinical Course

The patient was fitted for a leaf spring ankle-foot orthosis (AFO), which allowed for a more normal gait. She developed secondary pressure ulcerations due to her history of PVD and required a modification of the AFO. Secondary back pain due to abnormal gait was treated with caudal epidural steroid injections.


The diagnosis of foot drop is reliant on a meticulous physical examination in order to ascertain the site of the lesion injury. Musculoskeletal testing (Medical Research Council [MRC]) including single-limb heel rise and muscle strength testing are standard. MRC scale rating 0 to 5 for the major muscle groups to the lower extremities, including ankle plantar flexion, ankle dorsiflexion, ankle inversion, ankle eversion, knee extension, knee flexion, and hip flexion, should be performed. Neurosensory examination including sharp-dull and Semmes-Weinstein testing should be done for peripheral nerves as well as lumbar dermatomes. A gait examination is also an essential component in isolating a skeletal-muscular deficit.

Compensation for weak anterior compartment muscles can be seen during the swing phase of gait. Normally, the extensors would assist in clearing the ground before initiating early contact phase. The consequence results in step page or slap gait patterns where the patient clears the ground by increasing flexion at the knee raising the foot higher than normal. Another manifestation is the subsequent contracture of the digits due to an increase in flexor tone to help stabilize the foot. Patients will often relate the need for assistive devices in order to aid in mobility.

Any damage affecting the neuraxis from the roots to the peripheral nerve can lead to weakness of the muscles supplied by that nerve. A lesion of the L5 root can potentially lead to foot drop due to the weakness of the anterior compartment musculature. There may or may not be associated pain. Radiculopathy affecting the fifth lumbar nerve root typically results in neuropathic pain radiating down the posterior thigh, anterolateral leg to the hallux, and first webspace.17

Sciatic neuropathy classically presents with sensory loss of the whole foot and weakness of the triceps surae as well as ankle inversion and can result in a flail foot. It is not uncommon for an incomplete sciatic neuropathy to present as a common peroneal neuropathy, as many times the peroneal fascicles in the sciatic nerve are more susceptible to injury.18

In common peroneal neuropathy, the patient presents with sensory and motor deficits. History may include prolonged kneeling, immobility, or trauma. Suspected neuropraxia and/or neurotmesis of the common peroneal nerve can lead to sensory loss or paresthesia of the lateral leg below the knee and the anterolateral foot. Muscle weakness affects ankle dorsiflexion, toe extension, and ankle evertors.13

If only the deep peroneal portion is affected, only minimal sensory deficits and isolated weakness of toe and ankle extensors are seen. Ankle eversion and inversion are normal. Isolated superficial peroneal neuropathy is rare and presents as the sensory deficit of the foot except for the first webspace.18


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.

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Sep 8, 2022 | Posted by in ORTHOPEDIC | Comments Off on Neurologic Causes of Foot Pain: Part II

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