Acute low back pain spontaneously resolves within 2–4 weeks in the majority of cases. Therefore, in the absence of trauma, fever, known malignancy, or focal neurologic signs or symptoms (such as incontinence or leg weakness), acute low back pain does not require imaging or intervention other than conservative symptomatic management.
Patients with new low back pain following trauma require emergent imaging of the lumbar spine, usually with computed tomography (CT), to identify conus medullaris or lumbosacral nerve root injury secondary to fracture, ligamentous injury, or compression from hematoma. Left untreated, such injuries may result in permanent neurologic disability. Other specific clinical features may suggest a cause for pain for which imaging is indicated. The most frequent presenting symptoms of epidural abscess are back pain (~ 50%) and fever or chills (~ 33%). Delayed diagnosis is common and a high index of suspicion is necessary. Recent systemic infection or spinal procedure, including lumbar puncture, epidural anesthesia, or spine surgery, should raise concern for this diagnosis. Spinal cord infarction and Guillain-Barré syndrome, while rare, often feature prominent low back pain. In neither condition, however, is pain the only symptom; associated leg weakness and reflex abnormalities, along with the temporal course of symptoms, suggests these diagnoses.
Nontraumatic low back pain involving new bowel or bladder incontinence, regardless of the presence of other symptoms, requires emergent imaging of the lumbar spine. Magnetic resonance imaging (MRI) provides better visualization of the conus medullaris, nerve roots, and intervertebral disc pathology compared to CT and is therefore preferred if available. Asymmetric weakness, pain radiating into the legs (radicular pain), or absent knee reflexes suggests cauda equina pathology. In contrast, symmetric leg weakness with absent Achilles and preserved patellar reflexes suggests a conus medullaris lesion.
The presence of radicular pain suggests lumbosacral radiculopathy. Nonradicular low back pain associated with unilateral leg weakness should also prompt consideration of lumbosacral radiculopathy. A forward flexed stance when standing or walking to reduce low back pain suggests the lumbosacral radiculopathy is due to spinal canal stenosis. This posture provides symptomatic relief by widening the spinal canal.
The absence of leg weakness or radicular low back pain is most suggestive of a musculoskeletal source of pain. In the acute phase, these patients may benefit from nonsteroidal antiinflammatory drugs (NSAIDs). With more chronic pain, an interdisciplinary approach including physical therapy, massage, yoga, and cognitive-behavioral therapy may be helpful. Patients should be instructed to resume normal activities and limit themselves to 1–2 hours of rest daily when the pain is most severe.
Radicular pain without leg weakness suggests a mild or sensory-predominant lumbosacral radiculopathy, though a musculoskeletal source of pain cannot be excluded. Acute symptomatic treatment may include NSAIDS and physical therapy. Additionally, treatment for neuropathic pain with gabapentin may be beneficial. Time-limited trials of opioids or benzodiazepines can be considered for severe, disabling pain but, given their potential for abuse and addiction, should not be used as first-line treatment. Although frequently used, systemic steroids or epidural steroid injections have not clearly demonstrated a long-term benefit. Failure to respond to conservative treatment should prompt reevaluation for progressive neurologic deficits. For chronic low back pain, additional approaches such as tricyclic antidepressants and radiofrequency ablation are frequently used in addition to the treatments above.
Isolated unilateral weakness of hip flexion suggests an L2 radiculopathy, which is quite uncommon. Weakness of unilateral hip flexion, hip adduction, and knee extension with a reduced or absent patellar reflex suggests an L3 radiculopathy. These findings can also be seen with a lumbar plexopathy (see Chapter 95 ).
The evaluation of unilateral knee extension weakness is discussed in Chapter 29 .
Unilateral foot drop is commonly caused by L5 radiculopathy and peroneal neuropathies. The evaluation of foot drop from ankle dorsiflexion weakness is discussed in Chapter 30 .
Unilateral ankle plantarflexion weakness and a reduced or absent Achilles reflex suggests an S1 radiculopathy or tibial neuropathy.
The presence of leg weakness in a presumed lumbosacral radiculopathy indicates the loss of motor axons with the potential for further axonal loss if the underlying cause is not addressed. MRI of the lumbar spine (with contrast if there is clinical suspicion for infection or malignancy) should be performed to evaluate for the need for surgical decompression. Be aware that degenerative lumbar spine changes, such as disc herniation or osteophytes, are very common in older patients and may represent an incidental finding unrelated to symptoms. If there is clinical uncertainty regarding whether the degenerative changes seen on MRI are causing the patient’s symptoms, nerve conduction studies/electromyography (NCS/EMG) should be performed. NCS/EMG can confirm the localization of the lesion in the peripheral nervous system, assess the severity of motor axon loss, and provide information on the acuity of the injury. Symptomatic treatment of these patients consists of the conservative treatment approach discussed in section E.
If lumbar spine MRI is normal in patients with leg weakness or bowel or bladder incontinence, consider imaging of the thoracic and cervical spine to evaluate for myelopathy.