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Radicular Back Pain
Introduction
Acute lumbosacral radiculopathy is a diffuse disease process that affects more than 1 underlying nerve root, causing pain, loss of sensation, and motor function depending on the severity of nerve compression. Lumbosacral radiculopathy is very common.[1] Most cases of lumbosacral radiculopathy are self-limited. The most common symptom in radiculopathy is paresthesia.[2] Another common presentation is back pain radiating into the foot, with a positive straight leg raising test.[3][4][5][6] Muscle strength is often preserved in the case of radiculopathy because muscles often receive innervation from multiple roots. Thus, muscle strength is often only affected by severe cases of radiculopathy.[1] The most common causes of lumbar radiculopathy are either a herniated disc with resultant nerve root compression or spondylosis. This process can be acute or can develop chronically over time. Imaging is not always a helpful diagnostic modality, as almost 27% of patients without back pain have been found to have disc herniation on magnetic resonance imaging (MRI). Furthermore, this incidental finding does not predict future back pain development.[7][8]
To diagnose a herniated disc as a source of a patient's pain, reviewing the complete history and physical and ensuring that the symptoms match the imaging results is important. Patients with lumbar radicular pain often respond to conservative management. Patients who do not respond to conservative therapies likely need an MRI for further evaluation and characterization of nerve root involvement. Referral from the primary team to a specialist for interventional therapies, such as an epidural steroid injection or surgical decompression, should be considered, depending on the severity of symptoms.[9]
Etiology
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Etiology
The most common origin of lumbar radiculopathy is nerve root compression. It commonly results from either disc herniation or spondylosis. A disc herniation can be either due to an acute injury or secondary to chronic degeneration of the spine. Disc herniation activates the pain fibers of surrounding tissues such as ligaments, vessels, and dura mater.[10] Separately, spondylosis narrows the spinal canal, neural foramen, or the lateral recess. The most common cause of canal narrowing is degenerative arthritis of the lumbar spine. Other etiologies 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 erosion of the intervertebral disc, intervertebral 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 spine misalignment. This degenerative misalignment is called spondylolisthesis. The areas 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 lumbar spine. Roughly 90% of compressive lumbosacral radiculopathies occur at either of these levels.[11]
Epidemiology
Lumbosacral radiculopathy is very common. On average, 3 to 5% of adults experience symptoms in their lifetime.[12] L5 radiculopathy is the single most common lumbar radiculopathy. Between 63 and 72% of patients with lumbar radiculopathy experience paresthesia, 35% experience radiation of pain in the lower limb, and 27% of patients endorse numbness.[2] Muscle weakness is present in up to 37%, absent ankle reflexes in up to 40%, and absent knee reflexes in 18% of patients.[13][14][15] Disc herniation is the underlying etiology of less than 5% of patients with acute low back pain.[16] In patients presenting with a positive Romberg test with a wide-based gait, there is over a 90% chance of possible lower spine syndrome.[17] Electromyography (EMG) has a sensitivity between 50 and 85% for radiculopathy.[18][19]
Pathophysiology
Reviewing human neuroanatomy, where nerve roots exit the spinal cord, is crucial when discussing radicular pain. A pathological vertebra fracture can cause injury to a nerve root at a lower vertebral level. Injuries to the spine often affect the nerve roots where they exit the spinal canal.[20] Compressive radicular disease often occurs in the area proximal to the dorsal root ganglia relative to the neuroforamen and vertebral body.[21] When there is an injury to the dorsal rami of the spinal cord, it can be challenging to perform and evaluate a thorough neurological examination. There are overlapping innervations that can cause pain, making 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, deep tendon reflexes can be lost or diminished when motor fibers are injured. The ventral rami are responsible for motor and sensory function. Typically, this is assessed on a physical exam with various myotomes and dermatomes.[22] The areas of the body which can be attributed 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), the dorsum of the foot (L5), and the sole (S1). An L5 nerve root compression occurs from a central disc protrusion of L2-L3 or L3-L4, a lateral disc protrusion at L4-L5, or a far-lateral protrusion at the foramen at L5-S1. The cauda equina contains multiple nerve roots. When compression occurs at 1 level, there is an increased likelihood of compression simultaneously at multiple, possibly bilateral, nerve roots. The pain often occurs alongside neurological deficits. Nerve root injury can occur at any disc level.[10]
History and Physical
L2, L3, and L4 lumbar radiculopathies 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, and L4 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 during knee extension, hip adduction, and 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 the symptoms worse include coughing, leg straightening, or sneezing.
In L5 radiculopathy, patients often complain of acute back pain, which radiates down the lateral leg into the foot. On examination, muscle strength may be reduced 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) and the tibialis anterior of the anterior leg. Severe L5 radiculopathy can affect the gluteus minimus and medius, causing weakness in leg abduction.[1]
S1 radiculopathy causes radiation of sacral or buttock pain into the posterior aspect of the patient's leg, into the foot, or the perineum. On examination, there can be weakness in plantar flexion. There can also be a loss of sensation 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 their diagnosis compared to other radiculopathies. L4 and S1 nerve roots have distinct innervations for sensation and muscle strength testing.
Examination findings helpful in diagnosing radiculopathy include a patient's inability to get up from a chair, a history of knee buckling, and toe drag on ambulation. These exam findings suggest iliopsoas or quadriceps, quadriceps, and tibialis anterior weakness, respectively. Diminished deep tendon reflexes for L4 and L5 are also useful to support a diagnosis of lumbar radiculopathy.[11] A straight leg raising can be helpful in lumbosacral radiculopathy. During a straight leg raise, the pain mechanism is increased dural tension placed upon the lumbosacral spine during the test. Patients lay supine during the test. The physician flexes the patient's quadriceps with the leg in extension and dorsiflex the patient's foot on the symptomatic side. Pain or reproduction of paresthesias is considered a positive test (Lasegue sign). A Bowstring sign relieves this underlying radicular pain with flexion of the patient's knee on the affected side. The straight leg raising test is most helpful in diagnosing L4 and S1 radiculopathies.[11][3]
A contralateral straight leg raising test is the passive flexion of the quadriceps with the leg in extension and the 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][23][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 the legs, radiculopathy is suspected.[24] In non-radicular back pain, the pain localizes to the spinal or paraspinal regions.
Evaluation
Urgent utilization of neuroimaging is recommended for cases of severe acute radiculopathy. Severe symptoms include progressive worsening of neurological deficits, suspected underlying neoplasm, epidural abscess, or cauda equina syndrome.[12] A problem with imaging is a very high prevalence of abnormal neuroimaging findings in even asymptomatic patients.
MRI of the lumbosacral spine is the most useful imaging tool for identifying underlying pathology and the need for surgical intervention. An MRI can be more useful to distinguish between inflammatory, malignant, or vascular disorders when compared to a CT scan. The recommendation is 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 nerve root visualization, making it challenging to diagnose radicular disease. Standard CT scans are better than MRI to assess bony structures.[25][26] Plain radiographs of the patient's lumbar spine offer limited value in evaluating underlying radiculopathy.
CT myelography is used when the patient has a contraindication for an MRI, such as having a pacemaker device or defibrillator, or 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. It can also be used to assess the underlying root sleeve. A unique population for whom to recommend a CT myelogram is patients with surgical spinal hardware.
More advanced tests, such as EMG or nerve conduction studies, are accurate only after 3 weeks of persistent symptoms. This is because they depend on fibrillation potentials after an acute injury, which does not develop until 2 to 3 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 can help diagnose.[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 the exam.[27][26] EMG is useful because it helps distinguish neurogenic weakness from decreased muscular effort or muscle inhibition due to pain.
A nerve conduction study or an EMG helps localize specific damaged nerve roots. These diagnostic tests can also help distinguish between new and old nerve damage and support the presence of 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 or 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]
Cerebrospinal fluid analysis is another useful test for a suspected neoplasm or infectious cause or radiculopathy symptoms. The recommendation for a lumbar puncture is progressive neurological symptoms, negative or non-diagnostic neuroimaging without known primary cancer, and failure of prompt improvement.[28] A systematic review found insufficient evidence to support using somatosensory evoked potentials in diagnosing radiculopathy. Discography, a diagnostic modality with the injection of contrast into the disc's nucleus under fluoroscopy, has also not demonstrated usefulness in diagnosing lumbosacral radiculopathy.[29]
Treatment / Management
There are 3 categories of radicular symptoms and signs. Mild radiculopathy is considered sensory loss and pain without motor deficits, moderate radiculopathy is sensory loss or pain with mild motor deficits, and severe radiculopathy is sensory loss and pain with marked motor deficits. The severity of the radiculopathy determines the management of the patient's underlying symptoms. Most cases of lumbosacral radiculopathy are self-limited. Counseling is essential for patients with radicular symptoms since most cases are mild and resolve within 6 weeks after the onset of symptoms. It is vital to discuss weight loss reduction, considering that most patients with lumbar radicular pain have an elevated body mass index. Spontaneous improvement following a disc herniation or lumbar spinal stenosis is very high.[30](A1)
The primary treatment for lumbar radiculopathy includes conservative management, 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. (A1)
A randomized trial showed no significant difference in outcome for treatment with bed rest versus watching and waiting. Also, there is no significant difference between bed rest and physical therapy. A systematic review showed no benefit from bed rest. Similarly, there is no convincing evidence in favor of physical therapy in the case of lumbosacral radiculopathy. It is recommended to delay physical therapy initiation until symptoms have persisted for over 3 weeks duration.[34][35][36] Some experts have previously recommended systemic glucocorticoids to provide pain relief in patients with acute radiculopathy. There is no evidence that systemic glucocorticoids provide any benefit for radicular 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.(A1)
Epidural steroid injections are beneficial for up to 3 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 6 weeks of conservative management, they would be eligible for an epidural glucocorticoid injection. However, the outcomes are less favorable in a chronic setting. On comparing surgical intervention versus conservative management, researchers found that patients who underwent surgery such as discectomy had a more favorable outcome after a 12-week follow-up. However, 1 to 2 years of follow-up showed similar outcomes between the surgical and nonsurgical groups. The patient should not consider surgical options until at least 6 weeks of symptoms have passed. Controlled studies evaluating the efficacy of epidural etanercept injection have conflicting results. One study showed similar results between patients receiving saline and etanercept.[42] Other studies show that compared to a placebo, there was significant pain relief with etanercept compared to saline at a 6-month follow-up. Furthermore, additional studies have also demonstrated that the benefits of etanercept are similar to those of an epidural glucocorticoid injection.[43][44](A1)
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. Diabetic patients are prone to diabetic amyotrophy, which is a microvascular complication of the spinal blood vessels. It presents as weakness, dysesthesias, and pain in the proximal leg along the L2, L3, and L4 nerve roots, progressing over days to weeks.[45] New-onset acute back pain in a patient with osteoporosis should raise the suspicion of vertebral body fracture. A patient with acute back pain in the setting of fever raises concerns for discitis or epidural abscess. Pain that 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.
Spinal stenosis is a form of degenerative spondylosis. Patients with symptomatic spinal stenosis experience symptoms of neurogenic claudication. These symptoms include bilateral and asymmetrical radicular pain, weakness, and sensory loss of the lower extremities. These symptoms are made worse by walking or standing for prolonged periods. New-onset urinary incontinence, in the presence of progressive weakness, saddle anesthesia, changes to the gait, and bowel dysfunction are concerning for cauda equina syndrome.[11] It is an infrequent complication of lumbar spinal stenosis. Injury to the S2, S3, and 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.
Prognosis
Most cases of lumbosacral radiculopathy are self-limited. Counseling is crucial for patients with radicular symptoms since most cases are mild and resolve within 6 weeks. It is vital to discuss weight loss reduction, as most of these patients have an elevated body mass index. Chances of spontaneous improvement following a disc herniation or lumbar spinal stenosis are very high.[30] Concerns arise when a patient's symptoms worsen or are severe. Severe symptoms warrant further imaging and/or emergent surgical intervention.
Complications
The complications that can manifest with radicular back pain are as follows:
- Lumbar radiculopathy is often self-limited but can be extremely painful. An immediate complication that can arise from acute radicular pain is the loss of function and decreased quality of life.
- Emergent complications include cauda equina syndrome and severe lumbar radiculopathy. Both of these complications often require emergent surgical decompression.
- Patients who do not improve within the 6 to 12 weeks following the onset of pain can develop 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.
Deterrence and Patient Education
Lumbar radiculopathy is a self-limited injury to the nerve roots of the lumbar spine. It can present as excruciating, burning, or stinging pain radiating down the leg, decreased sensation of the legs, numbness and tingling, and, in more severe cases, muscle weakness. If patients present with radicular pain symptoms, they should see their healthcare provider for further evaluation. Most symptoms resolve within 6 weeks with moderate activity and over-the-counter pain management. Patients with symptoms persisting for over 6 weeks can benefit from an epidural corticosteroid injection. Suppose 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. In that case, this warrants an immediate emergent evaluation and surgical consultation.
Enhancing Healthcare Team Outcomes
Lumbar radiculopathy pain is a significant but often 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 inter-professional 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 be treated immediately, as permanent damage may occur, leading to decreased quality of life and increased healthcare costs. Thus, it is imperative to identify the risk factors, perform a thorough assessment of the patient with radicular pain, and monitor for the progression of symptoms. A team approach is an ideal way to limit the complications of such an injury.
The recommended first step is for the primary care provider to evaluate a patient with lumbar radicular pain to rule out severe radiculopathy or alarm symptoms. 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 drug-drug interactions and potential dependence on certain pain medications and alert the healthcare team regarding any concerns.
- The patient should follow up with primary care physicians 1 to 2 weeks following the initial injury to monitor for the progression of the nerve damage.
- If symptoms worsen on follow-up or there is a concern for the development of severe radiculopathy, referral to neurosurgery or hospitalization for possible spinal decompression.
- If radicular symptoms persist 3 weeks after injury, a physical therapy referral can be a consideration.
- When symptoms persist for over 6 weeks, imaging such as an MRI or CT scan is an option for better visualization of the nerve roots.
- The patient should consult a dietitian to eat 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 6 weeks' follow-up may warrant a referral to interventional pain management or neurosurgery for an epidural steroid injection.
- If mild to moderate symptoms continue 3 months following the onset, referral for possible surgical intervention also merits consideration.
The interprofessional healthcare 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 thereof) with the present treatment plan, monitoring for adverse medication effects, and communicating any areas of concern to the treating physician. Only through open, interprofessional communication can optimal management of radicular low back pain occur. 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 can bring the desired results.
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