Radicular Back Pain

Radicular Back Pain

Article Author:
Alexander Dydyk
Article Editor:
Joe M Das
10/24/2020 5:53:59 PM
For CME on this topic:
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Radicular Back Pain


The definition of acute lumbosacral radiculopathy is a diffuse disease process that affects more than one underlying nerve root, causing pain, loss of sensation, and motor function depending on severity. Muscle strength is often preserved in the case of radiculopathy because muscles often receive innervation from multiple roots. There is built-in redundancy to human anatomy, despite a potentially significant injury to a single nerve root. Thus, muscle strength is often only effected in severe cases of radiculopathy.[1] Lumbosacral radiculopathy is very common.[1] Most cases of lumbosacral radiculopathy are self-limited. The most common symptom in radiculopathy is paresthesia.[2] Sensory loss or paraesthesia into the lower extremity, back pain radiating into the foot, with a positive straight leg raising test are a common presentation of lumbar radiculopathy.[3][4][5][6]

The most common cause of lumbar radiculopathy is a herniated disc. A herniated disc can cause nerve root compression. This process can be acute or can develop chronically over time.  Imaging is not always a helpful modality in diagnosis. Almost 27% of patients without back pain have been found to have disc herniation on magnetic resonance imaging (MRI). Complicating the diagnosis of radicular pain is how an abnormality such as disc herniation found on an MRI does not appear to be predictive of future development of back pain.[7][8] To diagnose a herniated disc as a source of a patient's pain, it is important to review the complete history and physical, making sure the symptoms fit the imaging results. 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.  Referral from the primary team to a specialist for alternative therapies such as an epidural glucocorticoid injection should be considered as well at that time, depending on the severity of symptoms.[9]


The most common origin of lumbar radiculopathy is nerve root compression. Nerve root compression is most commonly results from either disc herniation or spondylosis. Spondylosis occurs when there is a narrowing of the canal, neural foramen, or the lateral recess, with the most cause of the canal narrowing being degenerative arthritis of the lumbar spine. Other etiologies of lumbosacral radiculopathy include inflammation, infection, trauma, vascular disease, and neoplasm. Acute or chronic compression of the spinal nerve root can lead to underlying ischemia, inflammation, or edema.

The nerve root and the surrounding tissues generate the pain experienced by patients with radicular symptoms. The surrounding tissues include the ligaments, vasculature, and dural matter. The pain fibers of these tissues are activated when there is disc herniation.[10] The erosion of the intervertebral disc, uncovertebral joints, and zygapophyseal joints damages the spinal nerve roots. Osteophytes or herniation along the damaged areas can cause direct impingement of the spinal cord and underlying spinal nerve roots. If degeneration becomes severe enough, it can cause a misalignment of the spine. This degenerative misalignment is called spondylolisthesis. 

The areas which are most susceptible to injuries are L4-L5 and L5-S1. These levels are the areas that are responsible for the majority of the movement of the spine. Roughly 90% of compressive lumbosacral radiculopathies occur at these levels.[11]


Lumbosacral radiculopathy is very common. On average, 3 to 5% of adults will experience symptoms in their lifetime.[12] L5 radiculopathy is a single most common lumbar radiculopathy.  

Between 63 and 72% of patients with lumbar radiculopathy will experience paresthesia, 35% will experience radiation of pain in the lower limb, and 27% of patients will endorse numbness.[2] Muscle weakness presents in up to 37%, absent ankle reflexes in up to 40%, and absent knee reflexes in 18% of patients.[13][14][15]

About 27% of patients without back pain have been found to have disc herniation on MRI.[7]

Disc disease is the underlying etiology of less than 5% of patients with acute low back pain.[16]

If a patient has a positive Romberg test with a wide-based gait, this can be specified over 90% of the time for possible lower spine syndrome.[17]

Electromyography (EMG) has a sensitivity between 50 and 85% for radiculopathy.[18][19]


When discussing radicular pain, it is crucial to review human neuro-anatomy; where nerve roots exit the spinal cord. A pathological fracture of a vertebra can cause injury to a nerve root at a lower vertebral level. Injuries to the spine often affect the areas where nerve roots exit the spinal canal, not the degree in which the damage occurs.[20]

The compressive radicular disease often occurs in the area proximal to where the dorsal root ganglia attach to its respective vertebral body.[21] When there is an injury to the dorsal rami of the spinal cord, it can be challenging to evaluate thoroughly. There are overlapping innervations that can cause pain, which can make it challenging to assess pathology within paraspinal muscles fully. Muscle strength is often preserved in the case of radiculopathies because multiple roots often innervate muscles. However, when motor fibers are injured, deep tendon reflexes can be lost or diminished. 

The ventral rami are responsible for motor and sensory function. Typically this is assessed on physical exam with various myotomes and dermatomes.[22] The areas of the body which we can contribute to a single nerve root are called autonomous zones. These independent areas of lumbosacral radiculopathy include the anterior thigh (L2 and L3), the medial calf (L4), and the dorsum of the foot (L5), and the sole (S1).  

An L5 nerve root compression occurs from central disc protrusion of L2-L3 or L3-L4, a lateral disc protrusion at L4-L5, or from a far-lateral protrusion at the foramen at L5-S1.  

The cauda equina contains multiple nerve roots. When compression occurs at one level, there is an increased likelihood of compression at multiple, possibly bilateral, nerve roots simultaneously. The pain will often occur alongside neurological deficits. Nerve roots injury can occur at any disc level.[10]

History and Physical

L2, L3, L4 lumbar radiculopathy are considered a group. This group has a marked overlap of the innervation of the anterior thigh muscles.[1] An acute injury in the distribution of L2, L3, L4 will most commonly present with the patient experiencing radiating back pain to the anterior aspect of the thigh, which may progress into their knee, and possibly radiate to the medial aspect of the lower leg, into the foot. On examination, patients can have weakness in knee extension, hip adduction, and or hip flexion. There is often a loss of sensation over the anterior thigh along the area of pain. The patient may show a reduced patellar reflex (L4).[1] Activities that can make symptoms worse include coughing, leg straightening, or sneezing.

In L5 radiculopathy, patients will often complain of acute back pain, which radiates down the lateral leg, into the foot. On examination, there may be a reduction in muscle strength with big toe extension (extensor hallucis longus), foot eversion, inversion, toe extension, and foot dorsiflexion. Chronic L5 radiculopathy can cause atrophy of the extensor digitorum brevis (the marker of L5 radiculopathy in EMG) as well as the tibialis anterior of the anterior leg. If severe enough, L5 radiculopathy can cause weakness in leg abduction when the gluteus minimus and medius are affected.[1]

For S1 radiculopathy, sacral or buttock pain will radiate into the posterior aspect of the patient's leg, into the foot or the perineum. On examination, there can be a weakness in plantar flexion. There can also be a sensation loss along the posterior leg and lateral aspect of the foot. The ankle reflex (S1) can also be lost or diminished.[1]

The marked motor deficit patterns characterized by an L5 or S1 radiculopathy, help aid in their diagnosis compared to other radiculopathies: L4, and S1 nerve roots have their distinct innervations for sensation and muscle strength testing.

Examination findings helpful in the diagnosis of radiculopathy would include a patient's inability to get up from a chair, history of a knee-buckling, and toe drag on ambulation. These exam findings are suggestive of iliopsoas or quadriceps weakness, quadriceps, and tibialis anterior weakness, respectively. Diminished deep tendon reflexes for L4, L5 are also useful to support a diagnosis of lumbar radiculopathy.[11]

A straight leg raising can be painful in lumbosacral radiculopathy. The mechanism of pain during a straight leg raise is increased dural tension placed upon the lumbosacral spine during the test. Patients are supine during the test. The physician will flex the patient's quadriceps with the leg in extension as well as dorsiflex the patient's foot on the symptomatic side. Pain or reproduction of paresthesias is considered a positive test (Lasegue sign). Separately, a Bowstring sign is a relief of this underlying radicular pain with flexion of the patient's knee on the affected side. The straight leg raising test is most helpful in the diagnosis of L4 and S1 radiculopathies.[11][3]

An internal hamstring reflex for L5 radiculopathy has also been shown to be a useful test. Tapping either the semimembranosus or the semitendinosus tendons proximal to the popliteal fossa elicits the reflex. When there is an asymmetry of the reflex between legs, this can be significant for radiculopathy.[23]

A contralateral straight leg raising test is the passive flexion of the quadriceps with the leg in extension and foot in dorsiflexion of the unaffected leg by the physician. This test is positive when the unaffected leg reproduces radicular symptoms in the patient's affected limb. However, the straight leg raising test is more sensitive but less specific than the contralateral straight leg raising test.[4][24][3]

In non-radicular back pain, the pain localizes to the spinal or paraspinal regions.


Urgent utilization of neuroimaging is for cases of severe acute radiculopathy. Severe symptoms include progressive worsening of neurological deficits, a suspected underlying neoplasm, epidural abscess, or cauda equina syndrome.[12] A problem that arises with imaging is that there is a very high prevalence of abnormal findings seen on neuroimaging in even asymptomatic patients.

MRI of the lumbosacral spine is the most useful imaging to identify underlying pathology and the need for surgical intervention. Sensitivities for computed tomograms (CT) and MRI are similar for lumbosacral radiculopathy. Plain radiographs of the patient's lumbar spine offer limited value in the evaluation of underlying radiculopathy. An MRI can be useful to distinguish between inflammatory, malignant, or vascular disorders when compared to CT scan. The recommendation is for an MRI with contrast unless otherwise contraindicated when evaluating lumbar radiculopathy. When imaging is either equivocal or negative, with high suspicion for radiculopathy, nerve conduction studies are warranted. A CT is a poor test for the visualization of nerve roots, making it challenging to diagnose radicular disease. Standard CT scans are useful to assess bony structures. With better efficacy than an MRI.[25][26] 

Use of CT myelography is when the patient has either a contraindication to having an MRI such as having a pacemaker device or defibrillator or be used when a standard CT or MRI is negative or equivocal. Myelography is a CT scan or an MRI with intrathecal administration of contrast. CT myelography visualizes a patient's spinal nerve roots in their passage through the neuroforamina. CT myelography can be used to assess the underlying root sleeve. A unique population to recommend a CT myelogram is for patients with surgical spinal hardware. A CT is a poor test for the visualization of nerve roots, making it challenging to diagnose radicular disease.[25][26] 

More advanced tests, such as nerve conduction studies or electromyography (EMG), are complete after three weeks of symptoms, not before. Diagnostic tests such as EMG or nerve conduction studies are accurate only after three weeks of persistent symptoms. The primary reason why ordering an EMG or nerve conduction study is delayed three weeks following the development of pain is because fibrillation potentials after an acute injury lead to an axonal motor loss. These do not develop until two to three weeks following injury.[18][19]

When the origin of the patient's pain is thought to be from the dorsal rami, such as the case of pain originating from the paraspinal muscles, EMG cans be beneficial in helping to make the diagnosis.[1]. An EMG helps establish the relationship between the nerve root and muscle, innervation. An EMG is usually not ordered until neuroimaging findings have been negative and there are no signs of severe radiculopathies, such as muscular weakness on exam.[27][26]

The usefulness of EMG is in helping distinguish pain, which is related to neurogenic weakness; the pain is similar to the decreased muscular effort. A nerve conduction study or an EMG helps localize specific nerve roots that are damaged. These diagnostic tests can also help distinguish between new and old nerve damage and support demyelination at a nerve level leading to a conduction block.[1] EMG can provide physiological information that can aid in diagnosis alongside the anatomical information given by an MRI. EMG also provides evidence of direct denervation when there are uncertain motor deficits or when there are no motor deficits. EMG is beneficial in helping to determine if denervation is either chronic or currently ongoing. An example of this would be patients who have undergone previous spinal surgery but continue to have significant radicular back pain following surgery.[18][19]

Separately, cerebrospinal fluid analysis is a useful test if there is a suspected neoplasm or infectious cause or radiculopathy symptoms. The recommendation for a lumbar puncture is in the case of a patient with negative or nondiagnostic neuroimaging, without known primary cancer, who has progressive neurological symptoms and has failed to improve promptly.[28]

A systematic review found insufficient evidence to support the use of somatosensory evoked potentials in helping make the diagnosis of radiculopathy. Discography is a diagnostic modality with the injection of contrast into the nucleus of the disc under fluoroscopy. It also has not demonstrated usefulness in the diagnosis of lumbosacral radiculopathy.[29]

Treatment / Management

 There are three categories of radicular symptoms and signs. Mild radiculopathy is considered a sensory loss and pain without motor deficits, moderate radiculopathy is the sensory loss or pain with mild motor deficits, and severe radiculopathy is considered sensory loss and pain with marked motor deficits. Management of patients underlying symptoms will depend on the severity of the radiculopathy. 

Most cases of lumbosacral radiculopathy are self-limited. Counseling is essential for patients with radicular symptoms since most cases are mild and will resolve within six weeks after the onset of symptoms. It is vital to discuss weight loss reduction considering the majority of patients with lumbar radicular pain will have an elevated body mass index. Spontaneous improvement following a disc herniation or lumbar spinal stenosis is very high.[30]

The primary treatment for lumbar radiculopathy will include conservative managements such as acetaminophen, nonsteroidal anti-inflammatories (NSAIDs), and activity modification. Opiate analgesia is only for patients with radiculopathy and severe pain who have failed non-opiate analgesics. Studies have shown that acetaminophen was more effective than placebo but less effective than morphine for reducing pain in patients with lumbar-sacral radiculopathy.[31][32][33]

Muscle relaxants and benzodiazepines are not efficacious in patients with suspected compression of the nerve root. 

A randomized trial showed no significant difference in outcome for treatment with bed rest versus watching and waiting. There is similar evidence for bed rest versus physical therapy. Separately, a systematic review showed no benefit of bed rest as well. There is no convincing evidence for physical therapy to prescribed in the case of lumbosacral radiculopathy.  It is recommended to delay the prescription of physical therapy until symptoms have persisted for over three weeks in duration.[34][35][36]

There have been some experts who previously recommended systemic glucocorticoids to provide pain relief in patients with acute radiculopathy. The evidence has not shown systemic glucocorticoids to offer any benefit for pain.[37] Disability scores were marginally better in the group receiving oral steroids versus placebo [38]. Furthermore, if patients are prescribed NSAIDs alongside oral steroids, they may require further protection against gastrointestinal bleeding with a daily proton pump inhibitor.

Epidural steroid injections are beneficial for up to three months in duration in patients with acute lumbar radiculopathy. This benefit is modest yet clinically significant in the short-term.[39][40][41] If a patient has not improved after six weeks of conservative management, they would be eligible for an epidural glucocorticoid injection. When assessing a patient undergoing surgical intervention versus conservative management; patients who undergo surgery such as discectomy have a more favorable outcome after a short 12-week follow-up. However, at one to two years follow up, there are equal outcomes between the surgical and nonsurgical groups. The patient should not consider surgical options until at least six weeks of symptoms have passed.

Controlled studies have been done to evaluate epidural etanercept injection. These results have been conflicting. One study showed similar results between patients receiving saline and etanercept.[42] Separate studies show that when compared to a placebo, there was significant pain relief with etanercept compared to saline at a six-month follow-up. Furthermore, additional studies have also demonstrated the benefits of etanercept are similar to an epidural glucocorticoid injection.[43][44]

Differential Diagnosis

The differential diagnosis of lumbosacral radiculopathy includes herniated disc, lumbosacral plexopathy, lumbar spinal stenosis, mononeuropathies, diabetic amyotrophy, cauda equina syndrome, and non-radicular back pain.

A microvascular complication of the spine most commonly seen with diabetes can occur in diabetic amyotrophy. Weakness, dysesthesias, and pain in the proximal leg along the L2, L3, and L4 nerve roots can occur over the course of days to weeks, in patients suffering from diabetic amyotrophy.[45]

Vertebral body fracture is highly suspected in a patient with osteoporosis, experiencing acute back pain.

A patient with acute back pain in the setting of fever raises concerns for discitis or epidural abscess.  

Pain which wakes the patient at night or an inability to become comfortable in various positions is concerning for malignancy, alongside symptoms such as weight loss, fatigue, fever, and chills.

A spinal stenosis is a form of degenerative spondylosis. Patients with symptomatic spinal stenosis will experience symptoms of neurogenic claudication. Patients with neurogenic claudication often have bilateral and asymmetrical radicular pain, weakness, and or sensory loss of the lower extremities. These symptoms are made worse by walking or standing for prolonged periods.

 A disc herniation can be either an acute injury or secondary to chronic degeneration of the spine.

New-onset urinary incontinence is a concern for cauda equina syndrome.[11] Cauda equina syndrome is an infrequent complication of lumbar spinal stenosis. Patients can present with progressive weakness, saddle anesthesia, changes to their gait, and or bowel and bladder dysfunction. Injury to the S2, S3, S4 nerves can affect sexual dysfunction as well. Cases of cauda equina syndrome warrant immediate surgical decompression within 24 hours. Decompression is recommended to be done within 12 hours if possible, to minimize damage from the nerve root compression.


Most cases of lumbosacral radiculopathy are self-limited. Counseling is crucial for patients with radicular symptoms since most cases are mild and will resolve within six weeks. It is vital to discuss weight loss reduction as well considering the vast majority of these patients will have an elevated body mass index. Spontaneous improvement following a disc herniation or lumbar spinal stenosis is very high.[30] Concerns arise when a patient's symptoms worsen or are severe. Severe symptoms warrant further imaging and/or emergent surgical intervention.


Lumbar radiculopathy is often self-limited but can be extremely painful while patients recover. An immediate complication that can arise from acute radicular pain is the loss of function and decreased quality of life.

Concern for patients who do not improve within the six to twelve weeks following the onset of pain is the development of chronic pain.

Slowly progressing radicular symptoms can eventually lead to muscle atrophy as the nerves innervating the lower extremity musculature are affected. Deconditioning can occur over time.

Emergent complications include cauda equina syndrome and severe lumbar radiculopathy. Both of these complications often require emergent surgical decompression. 

Deterrence and Patient Education

Lumbar radiculopathy is a self-limited injury to the nerve roots of the lumbar spine. It can be excruciating, including burning, stinging pain, radiation of pain down the leg, decreased sensation of the legs, numbness, and tingling, and in more severe cases, muscle weakness. 

The recommendation is for patients to see their healthcare provider for further evaluation if they present with radicular pain symptoms.

Most symptoms resolve within six weeks with moderate activity and over the counter pain management. 

Patients with symptoms persisting for over six weeks can benefit from an epidural corticosteroid injection.

If lumbar radicular pain symptoms continue to worsen and the patient develops numbness and tingling between their legs, bowel or bladder incontinence, difficulty walking, and or sexual dysfunction this warrants an immediate emergent evaluation and surgical consultation. 

Enhancing Healthcare Team Outcomes

Lumbar radiculopathy pain is a significant but often a self-limited injury to the nerve roots of the lumbar spine. The condition affects millions of people and has enormous morbidity because of the pain. Thus the condition is best managed by an interprofessional team.

Rarely, the condition correlates with a few severe complications, including severe spondylolisthesis and cauda equina syndrome. These complications often require surgical intervention and advanced imaging modalities. Severe symptoms must receive treatment immediately, as permanent damage may occur, leading to an increase in healthcare costs. Thus, it is imperative to identify the risk factors and perform a thorough assessment of the patient with radicular pain as well as monitor for progression of symptoms. A team approach is an ideal way to limit the complications of such an injury. 

  • Evaluation of a patient with lumbar radicular pain by the primary care provider to rule out severe radiculopathy or alarm symptoms is the recommended first step.
  • Conservative management should commence when symptoms are mild or moderate; including moderate activity, stretches, and pharmacological management. A pharmacist should evaluate dosing and perform medication reconciliation to preclude any drug-drug interactions, and alert the healthcare team regarding any concerns.
  • The patient should follow up with primary care physicians one to two weeks following initial injury to monitor for progression of the nerve damage.
  • If symptoms worsen on follow up or there is a concern for the development of a severe radiculopathy referral to neurosurgery or hospitalization for possible spinal decompression. 
  • If radicular symptoms persist three weeks after injury, physical therapy referral can be a consideration. 
  • When symptoms persist for greater than six-week duration, imaging such as MRI or CT can are options for better visualization of the nerve roots.
  • The patient should consult with a dietitian and eat a healthy diet and maintain a healthy weight.
  • The pharmacist should encourage the patient to quit smoking, as this may help with the healing process. Further, the pharmacist should educate the patient on pain management and available options.
  • Persistent pain at six weeks follows up may warrant a referral to interventional pain management or neurosurgery for an epidural steroid injection.
  • If mild to moderate symptoms continue at three months following the onset of symptoms, referral for possible surgical intervention merits consideration as well. 

The interprofessional team should openly discuss the management of each patient so that the patient receives optimal care delivery. This area is where nursing can play a crucial role, by verifying patient compliance, monitoring for progress (or lack of) with the present treatment plan, and monitoring for adverse medication effects; communicating any areas of concern to the treating physician. Only through open, interprofessional communication can optimal management of radicular low back pain occur. [Level 5]

While surgery does work, it is usually not the first choice treatment, unless the patient has cauda equina syndrome. Further, there is no guarantee that surgery will bring the desired results.


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