Evaluation and Management of Neck and Back Pain

John W. Martel, MD, PhD, FACEP; Samuel B. Potter, MD


Semin Neurol. 2019;39(1):41-52. 

In This Article

Acute Back Pain

Emergent Differential Diagnosis

• Spinal cord or nerve root compression

   - Cauda equina syndrome

   - Disk herniation with neurologic compromise

   - Malignancy

• Vascular catastrophe

   - Aortic dissection

   - Ruptured abdominal aortic aneurysm (rAAA)

• Infection

   - Epidural abscess

   - Vertebral osteomyelitis

• Malignancy

   - Primary spinal neoplasm

   - Metastatic disease

Spinal cord or nerve root compression: Intervertebral disks experience mechanical degradation over time. In addition to trauma, age-related tears in the ligamentous annulus fibrosis increase the risk of paracentral disk herniation, thereby placing local nerve roots or the spinal cord itself at risk for acute compression (Figure 1). Spinal cord injury can also be caused by a wide variety of other mechanical and infectious etiologies, including spinal epidural abscess (SEA), osteomyelitis, primary neoplasm or metastatic disease, postoperative hematoma, or trauma.[11]

Figure 1.

L4/L5 paracentral disc herniation. T2-weighted MRI image. MRI, magnetic resonance imaging.

The adult spinal cord generally terminates at the level of L1. Spinal roots known collectively as cauda equina are located distal to this terminus. The primary role of this cord region is sensorimotor innervation to multiple structures, including the urinary bladder, perineum, and lower extremities (Figure 2). Cauda equina syndrome is an acute surgical emergency that has traditionally been described by several key "red flag" symptoms, including urinary retention, decreased rectal tone, loss of perineal sensation referred to as "saddle anesthesia," as well as fecal and/or urinary overflow incontinence. It is often attributed to large central disc herniations and has the potential to be a permanent function-limiting process requiring emergent surgical decompression. However, it can also occur with several of the other pathologies described above.[7]

Figure 2.

Cauda equina syndrome. Schematic of (a) cauda equina syndrome associated with paracentral disc herniation and (b) lateral disc herniation causing unilateral radicular symptoms due to nerve root compression.

Vascular catastrophe: Aortic dissection and rAAA both can both present with acute back pain, and are associated with high morbidity and mortality. Although abdominal pain is more commonly reported in rAAA, back pain has been reported to occur in nearly 20% of cases.[12] Patients experiencing aortic dissection typically report severe acute back pain, often described as a sudden-onset, sharp, ripping/tearing sensation. Mortality in acute aortic dissection increases by as much as 1% per hour. In untreated patients, mortality approaches 50% in the first 48 hours and increases to 90% within 3 months. Similarly, rAAA is associated with 90% mortality when untreated.[13–16]

Infection: SEA and vertebral osteomyelitis (Figure 3) represent serious infectious etiologies in a subset of patients complaining of back pain.[7] SEA is a relatively uncommon but potentially function-/life-threatening infection of the central nervous system (CNS) that generally involves three to five contiguous vertebral levels and most commonly manifests in the thoracolumbar region. It has been reported that the larger epidural spaces and fat-containing tissues in this region contain a more extensive extradural venous plexus and are subsequently at risk for acute infection via hematogenous spread.[17–19] However, they can occur at any point along the spine and may feature noncontiguous lesion distributions as well.[17] This process may also arise as a result of local muscle or disc infection (discitis), or from direct inoculation of the spinal canal during invasive procedures. SEA is associated with a wide array of morbidities, including acute spinal cord compression, compromise of local blood supply, thrombophlebitis, and sepsis. Risk factors include compromised immunity (diabetes mellitus, alcohol abuse, end stage renal disease, malignancy, and acquired immune deficiency syndrome [AIDS]), recent instrumentation (spinal surgery or epidural catheter), and local or hematogenous spread of bacteria (intravenous [IV] drug users [IVDU] and recent infection—particularly skin and soft tissue).[20–22] These infectious etiologies can often initially present without systemic symptoms, and are frequently diagnosed only after multiple clinic visits, as only 33% of patients present with the "classic triad" of fever, back pain, and neurological deficit.[18] Providers should therefore be vigilant when evaluating patients with new onset low back pain with any of the above comorbidities, as well as patients for whom it is not their first visit for back pain.

Figure 3.

Epidural abscess. T2-weighted MRI image depicting an abscess extending from the T12/L1 level to the sacrum, with associated spinal canal stenosis and cauda equina nerve root compression. MRI, magnetic resonance imaging.

Malignancy: Metastatic involvement of bone is commonly seen in a variety of neoplastic processes, including primary breast, lung, prostate, kidney, and thyroid carcinomas (Figure 4). An estimated 80% of cancer patients who present with acute back pain may have associated underlying metastatic disease. In contrast, primary neoplastic processes of the spine are much less common and comprise only 0.7% of total patients presenting with this complaint.[7]

Figure 4.

Spinal neoplasm. T2-weighted MRI image of schwannoma that fills the spinal canal in a patient with classic symptoms of cauda equine syndrome. MRI, magnetic resonance imaging.


A targeted history focused on risk factors and comorbidities is vital in assessing the pretest probability of a patient presenting with an emergent underlying etiology of acute back or neck pain. The past medical history may point to a particular organ system as the root cause of the complaint, including known previous AAA, peripheral vascular disease, IVDU, prior/current indwelling vascular access, previous back surgery, recent instrumentation, or malignancy. Any significant trauma associated with the onset of pain should prompt consideration of acute fracture.

Surveillance for emergent pathology may be facilitated via screening for so-called red flag signs and symptoms that are widely used to help identify potentially life-threatening etiologies of acute back pain (see Table 1). It is important to note that screening in this manner is often complicated by a high false-positive rate. One recent study showed that only 0.9% of patients presenting with acute low back pain ultimately are determined to have an emergency diagnosis, yet 80% of the patients reported at least one positive red flag sign or symptom.[23] Therefore, it is crucial that clinicians gather key historical information and consider the entire clinical context before moving forward with aggressive diagnostics.

Physical Examination

A complete physical examination in the setting of back pain includes evaluation of the musculoskeletal, neurologic, and vascular systems, with several maneuvers tailored to the specific complaint. Failure to do so may lead to unnecessary imaging that does not improve patient outcome, places patients at additional risk, and inappropriately increases health care expenditures.[24–27]

Abnormal vital signs are an important facet of the physical exam as well, and may reveal fever, tachycardia, or hypotension. All of these abnormalities would be unexpected in the setting of low-acuity acute mechanical back pain and are concerning for potentially serious underlying pathologies.

The musculoskeletal examination itself comprises systematic palpation of paravertebral musculature and midline vertebral evaluation of the entire spine, including the sacroiliac joints and hips. These maneuvers may elucidate focal muscle or vertebral tenderness. Midline tenderness is generally more concerning than focal paravertebral muscle soft tissue tenderness, though this is not specific to any particular pathology, and inter-rater reliability has been reported to be poor.[7,27]

In addition, it is important to perform a thorough neurologic examination to surveil for focal deficits; key elements include evaluation of motor power, sensation, and reflexes (Figure 5, Table 2). The majority of symptomatic disc herniations occur at the L4, L5, and/or S1 levels, and often present with predictable patterns of sensorimotor deficit.[7,28] The straight leg raise, crossed straight leg raise, and slump test elicit radicular symptoms with varying degrees of sensitivity and specificity. The former is performed while the patient is supine by elevating the affected lower extremity after extending the knee. A positive test occurs when pain radiates distal to the knee in a dermatomal distribution when the leg is at an angle less than 90 degrees. In contrast, the slump test is performed in the seated position. While both hips and knees flexed to 90 degrees, the patient "slumps" forward while the examiner applies pressure over the thoracic spine to flex the patient's neck. The knee and foot of the affected extremity are then extended and dorsiflexed, respectively. In this case, a positive test elicits radicular lower extremity symptoms in a dermatomal distribution. Sensitivities of these tests are variable. There is a reported sensitivity range of 28 to 92%, with specificities between 28 and 90%.[5,7,26,29] Of note, a positive test does not mandate further emergent evaluation if no additional sensorimotor deficits are identified. Examination results simply help narrow the differential for the cause of discomfort and may aid in establishing appropriate outpatient follow-up. Gait testing also provides invaluable information with regard to overall mechanical and neurologic functioning, and should be assessed in patients that are able to comply. Note that some patients presenting with low-acuity mechanical lower back pain and muscle spasm without red flag symptoms, other focal neurological deficits, or vital sign abnormalities may initially have difficulty ambulating due to discomfort. Refractory discomfort and an inability to ambulate despite aggressive analgesia should raise concern for potentially serious underlying pathology.

Figure 5.

Dermatomal symptoms associated with L4-S1 nerve root compromise. (Adapted from Bigos et al. 19956.)

Saddle anesthesia, diminished rectal tone, urinary retention, and fecal or urinary overflow incontinence are all part of an alarming suite of symptoms concerning for cauda equina syndrome as described above.[30,31] Urinary retention has a reported diagnostic sensitivity of 90%, and the absence of a significant postvoid residual (PVR) has a negative predictive value of 99.9%.[27] Although PVR greater than 100 cc may be abnormal in the appropriate clinical context, PVR greater than 300 cc is considered pathologic and warrants extensive diagnostic evaluation. Nearly 75% of patients with acute spinal cord compression have objective impairment of perineal sensation (saddle anesthesia) as well as lower extremity sensorimotor deficits. Up to 50% of patients present with an associated foot drop and an absent ankle reflex.[3] Diminished rectal tone is also very concerning within this clinical context, and should be assessed per digital rectal exam.[32,33]

In addition to a thorough neurological examination, evaluation of peripheral pulses helps screen for serious vascular pathology such as aortic dissection or rAAA, and a thorough abdominal examination may yield pulsatile masses indicative of rAAA. A combination of severe pain often refractory to analgesia, a palpable abdominal pulsatile mass, and hypotension is seen in ~50% of rAAA.[12,34] When combined with widened mediastinum (chest X-ray [CXR]), peripheral pulse deficits and/or hypotension are associated with 96% of dissections.[35] Bedside ultrasonography (US) is a vital tool to rapidly evaluate for the presence of AAA.

Given the sheer volume of annual ED visits in the US for back pain, it is also important to evaluate for potential psychosocial and nonorganic causes. This is crucial for efficient use of clinical resources as well as minimizing the risk of adverse effects associated with unnecessary radiation and contrast exposure. The Waddell signs (Table 3) were developed to evaluate nonorganic components of acute back pain complaints; the overall test is considered positive when a patient scores positively in three or more categories, thereby suggesting a potentially nonorganic basis of the complaint in association with coexisting psychiatric pathology.[36]

Emergency Department Work-up

In the event that there is significant concern for an underlying function- or life-threatening etiology per physical examination, neuroimaging is warranted in several specific cases.


The vast majority of patients presenting to the ED with acute back pain do not require emergent imaging, and routine X-rays are not indicated given the low utility and adverse effect of radiation exposure.[6] If the pain has been present for less than 4 weeks and there are no red flag signs or symptoms present, further diagnostic evaluation is usually unnecessary. However, in the setting of concerning historical or physical exam elements, advanced imaging may be warranted.

Spinal Cord Compression. Magnetic resonance imaging (MRI) is the diagnostic imaging test of choice in the evaluation of compressive etiologies due to SEA (Figure 3) and disc herniation, as well as in vertebral osteomyelitis, discitis, and vertebral bony metastatic lesions.[36] Gadolinium-enhanced MRI is generally used for SEA and vertebral osteomyelitis/discitis evaluation, and is considered both highly sensitive and specific for each entity.[37,38] Evaluation of neoplastic spinal mass and metastatic disease is usually performed both with and without contrast. However, IV contrast is not typically used when evaluating exclusively for acute disc herniation.

When evaluating for cord compression due to suspected unstable fracture or spondylolisthesis, an initial X-ray may be performed for expedient evaluation followed by MRI. In children especially, computed tomography (CT) is often inadequate as an initial test and comes at the cost of significant radiation.[38]

Vascular Emergencies. Bedside, US may aid in rapid diagnosis of AAA, as both sensitivity and specificity approach 100% for non-ruptured AAA with an aortic diameter greater than 3.0 cm.[39] CT angiogram (CTA) is considered to be better than US for evaluating suprarenal aneurysms, distinguishing ruptured versus nonruptured aneurysms, and screening for potential endovascular leak in patients that have undergone prior repair.[37,38] CTA is the study of choice when evaluating for aortic dissection.[40,41]

Treatment of Muscular and Radicular Pain

Given the frequency with which patients present with muscular and radicular low back pain in the context of a national opioid misuse epidemic, providers should be aware of the evidence and guidelines surrounding available treatment options, and the guidelines for the treatment of both acute and chronic low back pain are constantly evolving. There is growing interest and research that supports the use of nonpharmacologic strategies, such as superficial heat, massage, acupuncture, spinal manipulation, or noncontrolled substance pharmacologic treatments such as nonsteroidal anti-inflammatory drug (NSAID) medications or muscle relaxants as first-line therapies.[42–47] This is echoed in the 2017 American College of Physicians (ACP) guidelines.[48] These guidelines differ from the 2007 guidelines in that acetaminophen is no longer recommended as a first-line therapy for acute muscular and radicular pain.

For chronic low back pain, the 2017 ACP guidelines also recommend initial treatment with nonpharmacologic treatment such as exercise, rehab, acupuncture, mindfulness-based stress reduction, tai chi, yoga, motor control exercise, progressive relaxation, electromyography biofeedback, low-level laser therapy, operant therapy, cognitive behavioral therapy, or spinal manipulation. For those who do not respond to these nonpharmacological first-line treatments, they recommend initiating pharmacological therapy with NSAIDs, tramadol or duloxetine.

Of particular note, there is a growing body of research which concludes that the use of opioid medications for back pain should only be considered as an option in patients that have failed the treatment options mentioned above.[47,48] There are well-known risks and potential harm associated with opioid therapy, and these types of medications should only be considered if potential benefits outweigh these risks for individual patients. Shared decision making regarding known risks and realistic benefits should be undertaken whenever considering opioid therapy, particularly in patients with chronic low back pain. Lastly, the 2017 ACP guidelines no longer recommend the use of tricyclic antidepressants for chronic back pain.[48]