Stephanie G Wheeler, MD
Joyce E Wipf, MD
Thomas O Staiger, MD
Richard A Deyo, MD, MPH
Jeffrey G Jarvik, MD, MPH
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — It is estimated that up to 84 percent of adults have low back pain at some time in their lives [1,2]. For many individuals, episodes of back pain are self-limited. Patients who continue to have back pain beyond the acute period (four weeks) have subacute back pain (lasting between 4 and 12 weeks) and may go on to develop chronic back pain (persists for ≥12 weeks) . Rarely, back pain is a harbinger of serious medical illness.
This discussion will focus on an approach to the initial evaluation, including diagnostic tests, of a patient presenting with low back pain in the primary care setting. The treatment of acute, subacute, and chronic low back pain are discussed separately. (See "Treatment of acute low back pain" and "Subacute and chronic low back pain: Pharmacologic and noninterventional treatment" and "Subacute and chronic low back pain: Nonsurgical interventional treatment" and "Subacute and chronic low back pain: Surgical treatment".)
TERMINOLOGY — Several terms are used to describe conditions related to the back, based upon radiologic findings (eg, spondylosis), physical findings (radiculopathy), and symptoms (sciatica). These terms are defined in the table (table 1).
EPIDEMIOLOGY — In 2010, back symptoms were the principal reason for 1.3 percent of office visits in the United States . Spinal disorders accounted for 3.1 percent of diagnoses in outpatient clinics.
Prevalence — The prevalence of back pain has been estimated with surveys [1,5]. A 2012 systematic review estimated that the global point prevalence of activity-limiting low back pain lasting for more than one day was 12 percent and the one-month prevalence was 23 percent .
Other survey estimates of the prevalence of low back pain have ranged from 22 to 48 percent, depending on the population and definition [2,7-9]. For example, the 2002 National Health Interview Survey found that 26 percent of respondents reported low back pain lasting at least one day in the last three months .
Risk factors — Risk factors associated with back pain complaints include smoking, obesity, age, female gender, physically strenuous work, sedentary work, psychologically strenuous work, low educational attainment, Workers' Compensation insurance, job dissatisfaction, and psychologic factors such as somatization disorder, anxiety, and depression [2,8,10-15].
ETIOLOGIES — Although there are many etiologies of low back pain (table 2), the majority of patients seen in primary care will have nonspecific low back pain.
Nonspecific back pain — The vast majority of patients seen in primary care (>85 percent) will have nonspecific low back pain, meaning that the patient has back pain in the absence of a specific underlying condition that can be reliably identified [16-18]. Many of these patients may have musculoskeletal pain . Most patients with nonspecific back pain improve within a few weeks. (See "Treatment of acute low back pain".)
Serious systemic etiologies — Among patients who present with back pain to primary care settings, less than 1 percent will have a serious systemic etiology (cauda equina syndrome, metastatic cancer, and spinal infection) [5,19]. Almost all patients with these conditions will have risk factors or other symptoms .
●Spinal cord or cauda equina compression – There are many causes of cauda equina syndrome, the most common being herniation of the intervertebral disc. One systematic review found that cauda equina syndrome was caused by herniation of the intervertebral disc in 22.7 percent of cases, ankylosing spondylitis in 15.9 percent, lumbar puncture in 15.9 percent, trauma in 7.6 percent, malignant tumor in 7.2 percent, benign tumor in 5.7 percent, and infection in 5.3 percent . While the incidence of cord compression in patients known to have cancer varies depending on the cancer, among patients who are diagnosed with cord compression, it is the initial manifestation of malignancy in 20 percent . Metastatic disease from any primary cancer can cause cord compression. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression, including cauda equina syndrome", section on 'Epidemiology' and "Clinical features and diagnosis of neoplastic epidural spinal cord compression, including cauda equina syndrome", section on 'Pathophysiology'.)
Pain is usually the first symptom of cord compression, but motor (usually weakness) and sensory findings are present in the majority of patients at diagnosis. Bowel and/or bladder dysfunction are generally late findings. Early diagnosis and treatment improves outcomes. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression, including cauda equina syndrome", section on 'Clinical features' and "Treatment and prognosis of neoplastic epidural spinal cord compression, including cauda equina syndrome", section on 'Impact of treatment delay on posttreatment ambulation'.)
●Metastatic cancer – The bone is one of the most common sites of metastasis. A history of cancer (excluding nonmelanoma skin cancers) is the strongest risk factor for back pain from bone metastasis . Among solid cancers, metastatic disease from breast, prostate, lung, thyroid, and kidney cancers account for 80 percent of skeletal metastases. Approximately 60 percent of patients with multiple myeloma have skeletal lytic lesions present at diagnosis. (See "Overview of the epidemiology, clinical presentation, diagnosis, and management of adult patients with bone metastasis", section on 'Epidemiology' and "Clinical features, laboratory manifestations, and diagnosis of multiple myeloma", section on 'Skeletal surveys'.)
Pain is the most common symptom. In patients with a history of cancer, sudden, severe pain raises concern for pathologic fracture. Patients may also have neurologic symptoms from either spinal cord compression or spinal instability. (See "Overview of the epidemiology, clinical presentation, diagnosis, and management of adult patients with bone metastasis", section on 'Clinical presentation'.)
●Spinal epidural abscess – Spinal epidural abscess is a rare but serious cause of back pain. Initial symptoms (eg, fever and malaise) are often nonspecific; over time, localized back pain may be followed by radicular pain and, left untreated, neurologic deficits. Risk factors include recent spinal injection or epidural catheter placement, injection drug use, and other infections (eg, contiguous bony or soft tissue infection or bacteremia). Immunocompromised patients may also be at higher risk. Urgent antibiotic treatment and surgical therapy for those with neurologic symptoms is required for patients with spinal epidural abscess. (See "Spinal epidural abscess".)
●Vertebral osteomyelitis – The incidence of vertebral osteomyelitis generally increases with age. Men are more commonly affected than women. Many cases are thought to be health care-related or postprocedural from hematogenous spread of bacteremia. Less specific risk factors include an immunocompromised state and injection drug use. (See "Vertebral osteomyelitis and discitis in adults", section on 'Epidemiology' and "Vertebral osteomyelitis and discitis in adults", section on 'Pathogenesis'.)
Acute osteomyelitis typically presents with gradual onset of symptoms over several days. Most patients with vertebral osteomyelitis will present with back pain but may not have fevers or other systemic symptoms. Prompt antibiotic treatment improves outcomes. (See "Overview of osteomyelitis in adults", section on 'Clinical manifestations' and "Vertebral osteomyelitis and discitis in adults", section on 'Clinical features' and "Vertebral osteomyelitis and discitis in adults", section on 'Treatment'.)
Less serious, specific etiologies — Less than 10 percent of patients who present in primary care settings with low back pain will have less serious but specific etiologies for their pain [19,23].
●Vertebral compression fracture – Approximately 4 percent of patients presenting in the primary care setting with low back pain will have a vertebral compression fracture [19,23]. While some produce no symptoms, other patients present with acute onset of localized back pain which may be incapacitating. There may be no history of preceding trauma. Risk factors for osteoporotic fracture include advanced age and chronic glucocorticoid use (table 3). A history of an osteoporotic fracture is a risk factor for subsequent fractures, which can be mitigated by pharmacologic therapy. (See "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment", section on 'Clinical manifestations' and "Osteoporotic fracture risk assessment" and "Overview of the management of osteoporosis in postmenopausal women", section on 'Postfracture'.)
Approximately 3 to 4 percent of patients who present in primary care settings with have a symptomatic disc herniation or spinal stenosis [19,23].
●Radiculopathy – Radiculopathy refers to symptoms or impairments related to a spinal nerve root. Damage to a spinal nerve root may result from degenerative changes in the vertebrae, disc protrusion, and other causes. The clinical presentations of lumbosacral radiculopathy vary according the level of nerve root or roots involved. Over 90 percent are L5 and S1 radiculopathies . Patients present with pain, sensory loss, weakness, and/or reflex changes consistent with the nerve root involved; these are summarized in the table and discussed in more detail separately (table 4). Testing for lumbar nerve root compression is shown in a figure (figure 1). Many patients with symptoms of acute lumbosacral radiculopathy improve gradually with supportive care. (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Pathophysiology and etiology' and "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Clinical presentations' and "Acute lumbosacral radiculopathy: Treatment and prognosis", section on 'Prognosis'.)
Sciatica is a nonspecific term used to describe a variety of leg or back symptoms. Usually, sciatica refers to a sharp or burning pain radiating down from the buttock along the course of the sciatic nerve (the posterior or lateral aspect of the leg, usually to the foot or ankle) . Most sciatica is attributable to radiculopathy at the L5 or S1 level from a disc disorder.
●Spinal stenosis – Lumbar spinal stenosis is most often multifactorial. Spondylosis (degenerative arthritis affecting the spine) spondylolistheses, and thickening of the ligamentum flavum are the most common causes, typically affecting patients >60 years (figure 2). (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Etiologies'.)
Ambulation-induced pain localized to the calf and distal lower extremity resolving with sitting or leaning forward ("pseudoclaudication" or "neurogenic claudication") is a hallmark of lumbar spinal stenosis. Other symptoms of lumbar spinal stenosis can include back pain and sensory loss and weakness in the legs, though many patients may present with a normal neurologic exam. Symptoms of neurogenic claudication can usually be distinguished from vascular claudication (table 5). Rare patients develop a cauda equina syndrome. Patients often have symptoms only when active. Most patients with spinal stenosis related to osteoarthritis will have stable symptoms over time. A trial of conservative, nonsurgical treatment is the initial therapy for most patients . (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Clinical presentation' and "Lumbar spinal stenosis: Treatment and prognosis", section on 'Prognosis' and "Lumbar spinal stenosis: Treatment and prognosis", section on 'Nonsurgical treatment'.)
●Ankylosing spondylitis – Among patients who present in primary care settings for back pain, it is estimated that approximately 0.5 percent will have ankylosing spondylitis [19,23]. It is most commonly diagnosed in men under the age of 40 years. (See "Clinical manifestations of ankylosing spondylitis in adults", section on 'Epidemiology'.)
Almost all patients report back pain, which often has characteristics suggesting an inflammatory etiology (morning stiffness, improvement with exercise, pain at night) . Patients may also have extraskeletal disease manifestations (eg, uveitis). (See "Clinical manifestations of ankylosing spondylitis in adults", section on 'Musculoskeletal symptoms and findings' and "Clinical manifestations of ankylosing spondylitis in adults", section on 'Extraarticular comorbidities'.)
●Osteoarthritis – Low back pain may be a symptom of osteoarthritis of the facet joints spine. Patients may also complain of hip pain, either from osteoarthritis of the hip or referred pain from the spine. Osteoarthritis most commonly presents in patients over the age of 40. Pain is typically exacerbated by activity and relieved by rest (table 6). Osteoarthritis can lead to spinal stenosis. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Facet joint'.)
●Scoliosis and hyperkyphosis – Back pain can be associated with scoliosis and hyperkyphosis. (See "Adolescent idiopathic scoliosis: Management and prognosis", section on 'Outcome' and "Overview of hyperkyphosis in older persons", section on 'Other health-related consequences'.)
●Psychologic distress – Psychologic distress (eg, depression or somatization) may contribute to the severity symptoms of low back pain or may be a cause of nonorganic back pain . (See "Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis", section on 'Clinical presentation'.)
●Etiologies outside the spine – Low back pain may be a symptom of problems outside the back. Examples of other etiologies include pancreatitis, nephrolithiasis, pyelonephritis, abdominal aortic aneurysm, or herpes zoster [3,17]. Patients generally have other accompanying symptoms. (See "Clinical manifestations and diagnosis of acute pancreatitis", section on 'Clinical features' and "Diagnosis and acute management of suspected nephrolithiasis in adults", section on 'Clinical manifestations' and "Acute complicated cystitis and pyelonephritis", section on 'Clinical manifestations' and "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Clinical presentations' and "Clinical manifestations of varicella-zoster virus infection: Herpes zoster", section on 'Clinical manifestations'.)
There are also clinical entities that are possibly associated with low back pain symptoms:
●Piriformis syndrome – The piriformis syndrome is thought by some to be a condition in which the piriformis muscle, a narrow muscle located in the buttocks, compresses or irritates the sciatic nerve [25,27,28].
●Sacroiliac joint dysfunction – "Sacroiliac joint dysfunction," a term to describe pain in the region of the sacroiliac joint believed to be due to malalignment or abnormal joint movement, is a controversial topic. Tests of pelvic symmetry or sacroiliac joint movement have been shown to have low intertester reliability [29-35], and provocative maneuvers such as fluoroscopically guided injections of the sacroiliac joint have been unreliable in diagnosis and treatment [34,36]. The sacroiliac joint may be a referred site of pain, including from a degenerative disc at L5-S1, spinal stenosis, or osteoarthritis of the hip.
●Bertolotti's syndrome – Back pain in the setting of a transitional vertebra is known as "Bertolotti's syndrome." A transitional vertebra is a common finding on radiologic studies. It is a congenital anomaly with a naturally occurring articulation or bony fusion between the transverse processes of L5 and the sacrum. Estimates of prevalence of transitional vertebra range from 4 to 36 percent . It remains unclear whether these individuals have a higher risk of back pain than those without such an anomaly. Generally, patients with Bertolotti's syndrome should initially be treated similarly as patients with nonspecific back pain. Whether and when surgical intervention is appropriate remains unclear.
INITIAL EVALUATION — The clinical evaluation of low back pain includes a history and physical to evaluate for signs or symptoms that indicate need for immediate imaging and further evaluation. For most patients with acute back pain (<4 weeks), laboratory tests and imaging are not necessary in the initial evaluation.
History — While it may not be possible to define a precise cause of low back symptoms for most patients, it is important to evaluate for evidence of specific etiologies of back pain. The history should include location, duration, and severity of the pain, details of any prior back pain, and how current symptoms compare with any previous back pain.
We also ask about constitutional symptoms (eg, unintentional weight loss or night sweats), history of malignancy, precipitants or precipitating events, therapies attempted, neurologic symptoms (eg, weakness, falls or gait instability, numbness or other sensory changes, or bowel/bladder symptoms), stability or progression of symptoms, history of recent bacterial infections (particularly bacteremia), recent history or current use of injection drugs, history or current use of corticosteroid medications, and recent history of procedures in the back.
Patients should also be evaluated for social or psychologic distress that may be contributing . Potentially useful items are a history of failed previous treatments, substance abuse, and disability compensation. Screening for depression may be helpful. (See "Screening for depression in adults".)
Features that may suggest underlying systemic disease include history of cancer, age >50 years, unexplained weight loss, duration of pain >1 month, nighttime pain, and unresponsiveness to previous therapies . Injection drug use, recent bacterial infection (particularly bacteremia), or fever increase the suspicion of spinal infection. (See "Spinal epidural abscess" and "Vertebral osteomyelitis and discitis in adults".)
Physical examination — In general, the purpose of the physical examination is to identify features that suggest that further evaluation is indicated, rather than to make a primary diagnosis. The physical examination should include the following components:
●Inspection of back and posture – Inspection of the patient on physical examination can reveal anatomic abnormalities such as scoliosis or hyperkyphosis (table 1). (See "Overview of hyperkyphosis in older persons".)
●Palpation/percussion of the spine – Palpation and/or percussion of the back is usually performed to assess vertebral or soft tissue tenderness. Vertebral tenderness is a sensitive, but not specific, finding for spinal infection, and may also be seen in patients with vertebral metastases and osteoporotic compression fracture . (See "Vertebral osteomyelitis and discitis in adults", section on 'Symptoms and signs'.)
●Neurologic exam – Patients should have a neurologic exam including evaluation of the reflexes, strength, sensation, and gait. (See "The detailed neurologic examination in adults".)
For patients suspected of having a radiculopathy, neurologic testing should focus on the L5 and S1 nerve roots (table 4), since most clinically significant radiculopathies occur at these levels. (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Physical examination'.)
●Straight leg raising – The straight leg raise and other maneuvers can be helpful in identifying whether symptoms are radicular in nature. These are described separately. (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Maneuvers'.)
●Nonorganic signs (Waddell's signs) – Patients with psychologic distress that is contributing to back pain symptoms may have associated inappropriate physical signs, also known as "Waddell's signs" (table 7). These include superficial tenderness, straight leg raise that improves when the patient is distracted, patient overreaction during the physical examination, nondermatomal distribution of sensory loss, sudden giving way or jerky movements with motor examination, inconsistency in observed spontaneous activity (dressing, getting off table) and formal motor testing, and pain elicited by axial loading (pressing down on top of head, or rotating the body at hips or shoulders) . The presence of multiple Waddell's signs suggests a psychologic component to a patient's pain .
●Other – For patients with new or worsening urinary incontinence, we measure bladder post void residual (eg, by ultrasound) to differentiate overflow incontinence from urge and/or stress incontinence. If a patient's history strongly suggests malignancy, we evaluate as appropriate (eg, lymph node exam, breast exam, prostate evaluation). Other physical examination components (eg, hip examination or examination for peripheral vascular disease) should be performed based on the history. (See "Evaluation of the adult with hip pain", section on 'Examination' and "Clinical features and diagnosis of lower extremity peripheral artery disease", section on 'Physical examination'.)
Laboratory studies — Most patients with acute low back pain do not require any laboratory testing. In some patients with suspected infection or malignancy, we use the erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP) in addition to plain radiographs to determine the need for advanced imaging [22,40-42]. Because of its higher sensitivity, CRP may have similar or greater value than the ESR; however, CRP has not been similarly evaluated in the evaluation of low back pain. (See 'Risk assessment for acute back pain' below.)
The ESR and CRP are also used in the diagnosis of ankylosing spondylitis. (See "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial spondyloarthritis) in adults", section on 'Laboratory testing'.)
Limited utility of imaging — Earlier use of imaging for low back pain without associated symptoms is not associated with improved outcomes but increases the use of invasive procedures. A 2009 systematic review and meta-analysis of six trials that compared immediate imaging (magnetic resonance imaging [MRI], computed tomography [CT], or radiography) with usual care for patients with acute and subacute low back pain, without signs or symptoms of infection or malignancy, found no significant differences in short-term (up to three months) or long-term (6 to 12 months) outcomes for measures of patient pain or function . A subsequent prospective observational study in patients ≥65 years with back pain but without radiculopathy found no differences in disability at one year for patients who received early imaging (within six weeks of the index visit) compared with those who did not .
Additionally, imaging exams often show abnormal findings in adults without low back pain, which can make it difficult to correlate symptoms with imaging findings. Disc herniations on MRI are seen in 22 to 67 percent of asymptomatic adults and spinal stenosis in 21 percent of asymptomatic adults over age 60 [45-47]. Evidence of osteoarthritis is often seen on imaging but correlates poorly with symptoms . In a community-based study of 188 individuals 40 to 80 years old, 60 percent of males and 67 percent of females had facet joint osteoarthritic changes on lumbar CT scans; radiologic facet joint osteoarthritis increased with age and there was no correlation with low back pain . (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Neuroimaging' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Neuroimaging'.)
Even when the radiographic findings are consistent with clinical presentation, the magnitude of radiographic findings does not necessarily correlate with clinical severity and outcome, and clinical improvement may not correlate with resolution of the radiographic defect [50,51]. As an example, in one follow-up of a trial of 283 patients with lumbar disk herniation and sciatica who had undergone surgery, MRI at one-year follow-up showed disk herniation in 35 and 33 percent of patients with favorable and unfavorable outcomes, respectively .
Some findings on MRI are clinically insignificant or of uncertain significance. These include:
●Annular fissures (tears) – Annular fissures, colloquially termed tears, are separations between the annular fibers of the intervertebral disc or separations of annular fibers from their attachments to the vertebral bone. Several small studies found no correlation between the presence of annular fissure and back pain [52-54]. As an example, a prospective study of asymptomatic patients found that 38 percent had evidence of annular fissures at baseline . Follow-up after three years showed that annular fissures were not associated with new back pain .
●Schmorl's nodes – Schmorl's nodes, representing herniation of the nucleus pulposus into the adjacent end plate, can be seen in approximately 20 percent of MRI studies in patients without back pain (image 1) . Although Schmorl's nodes are associated with degenerative changes in the lower back, they are not an independent risk factor for back pain .
●Modic changes – Modic changes are of unclear clinical significance. They refer to specific signal changes in the vertebral endplate and adjacent bone marrow on a spine MRI . These changes occur in 6 to 10 percent of asymptomatic adults and are common in patients with back pain, with any type of Modic change typically reported in about 20 to 40 percent of patients [59,60]. The prevalence of Modic changes increases with age and appears to be associated with degenerative disc changes. A systematic review found only a small number of treatment studies involving patients with Modic changes and concluded that it is unclear whether the presence of these changes is helpful in guiding the selection of treatment options . Additionally, the type of Modic change in a single patient may progress or regress over time .
Modalities — The main imaging modalities to evaluate back pain are MRI, CT, and plain radiographs. Imaging is not indicated in many patients with low back pain. (See 'Indications for imaging' below.)
●Advanced imaging – MRI without contrast is generally considered the best initial exam for most patients with low back pain who require advanced imaging [63,64]. It provides axial as well as sagittal views which can demonstrate normal and pathologic discs, ligaments, nerve roots, epidural fat, as well as the shape and size of the spinal canal. MRI is more sensitive and specific than plain radiographs for the detection of spinal infection and malignancy . MRI enhancement with gadolinium allows the distinction of scar from disc in patients with prior back surgery.
In patients who require advanced imaging but cannot undergo MRI, we generally proceed with CT. Radionuclide scans are an alternative to MRI for evaluation of possible osteomyelitis. Myelography is rarely performed in the primary care setting and generally used when a patient is not able to undergo CT or MRI. (See "Principles of magnetic resonance imaging", section on 'Precautions' and 'Infection' below.)
●Plain radiographs – When plain radiographs are indicated, anteroposterior and lateral views of the lumbar spine are usually adequate. Oblique and spot views substantially increase the risks of radiation exposure, particularly for women, and add little new diagnostic information . Flexion-extension views may be helpful in patients who have had surgical fusion procedures or for whom instability is a concern. Plain radiographs are a reasonable option for imaging in patients when concerned for infection or malignancy, but clinical suspicion is not high . They are often combined with the erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) for evaluation. (See 'Infection' below and 'Cancer' below and 'Cancer risk' below.)
Indications for imaging — The majority of patients with low back pain of less than four weeks duration do not require imaging . Most patients who present to primary care settings will have nonspecific pain without associated symptoms and will improve rapidly. (See 'Etiologies' above and "Treatment of acute low back pain".)
Approximately one-quarter of patients 18 to 50 years of age with acute low back pain who underwent imaging exams had no identifiable indication for imaging . Inappropriate lumbar imaging can lead to irrelevant findings and trigger additional costly studies, unneeded treatments, and unwarranted surgical interventions [67-69].
Joint guidelines from the American College of Physicians (ACP) and the American Pain Society explicitly recommend that "clinicians should not routinely obtain imaging or other diagnostic tests in patients with nonspecific low back pain" and reserve imaging for patients with severe or progressive neurologic deficits or when serious underlying conditions are suspected on the basis of history and physical examination [17,18]. Guidelines from the National Institute for Health and Care Excellence (NICE) in the United Kingdom advise clinicians to “not routinely offer imaging in a non-specialist setting for people with low back pain with or without sciatica” . The ACP provides practical advice about when imaging studies should be considered in patients with acute low back pain (table 8), and our recommendations below are consistent, with the exception of imaging for suspected vertebral compression fracture. Avoiding imaging in acute low back pain has been identified as a recommendation in the American Board of Internal Medicine's "Choosing Wisely" campaign.
Red flags — Some guidelines suggest "red flag" symptoms, which may identify patients at risk for a more dangerous cause of back pain and represent an indication for earlier imaging exams [5,17,18,71]. There are limited data to support the use of most of the red flags as an indication for early imaging . Systematic reviews of studies that used one or more of these indications for imaging found that only a history of cancer has been shown to increase the probability of finding spinal malignancy [73,74]. Systematic reviews have found that the red flags associated with the highest post-test probability of a vertebral fracture were older age, prolonged use of corticosteroids, severe trauma, and presence of contusion or abrasion [73,75].
Risk assessment for acute back pain — Among patients seen in primary care, less than 1 percent will have a serious systemic etiology that requires evaluation with immediate advanced imaging (algorithm 1). (See 'Serious systemic etiologies' above and 'Modalities' above and 'Less serious, specific etiologies' above.)
Neurologic deficits — Any patient with symptoms of spinal cord or cauda equina compression or progressive and/or severe neurologic deficits should have immediate MRI for further evaluation and urgent specialist referral (algorithm 1). Such symptoms and signs include new urinary retention, urinary incontinence from bladder overflow, new fecal incontinence, saddle anesthesia, and significant motor deficits not localized to a single unilateral nerve root. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression, including cauda equina syndrome", section on 'Radiologic confirmation' and "Spinal epidural abscess", section on 'Diagnosis'.)
Patients with symptoms of radiculopathy at one level or spinal stenosis with stable symptoms do not need immediate imaging unless there is a history of cancer or significant clinical suspicions of infection. If there is no improvement in symptoms, we image after four to six weeks of conservative therapy. (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis", section on 'Evaluation and diagnosis' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Diagnosis' and 'Radiculopathy or lumbar spinal stenosis' below.)
Infection — Patients for whom there is a high clinical suspicion for spinal infection should have immediate imaging (algorithm 1). Patients with neurologic symptoms should have MRI as noted above. In patients without neurologic symptoms, the choice of modality depends on the level of clinical suspicion. (See 'Neurologic deficits' above.)
●High clinical suspicion – Patients with a high clinical suspicion for either vertebral osteomyelitis or epidural abscess should have MRI (algorithm 1). Features which may raise suspicion for infection include recent spinal procedure or current intravenous drug use with high fever and localized back pain and tenderness.
MRI is the most sensitive imaging modality for detecting spinal infection with sensitivity of 0.96 and specificity of 0.92 . For patients who are unable to obtain an MRI, a CT scan is a useful alternative to evaluate for epidural abscess, while radionuclide scans are an option to evaluate for osteomyelitis. The evaluation and diagnosis of these conditions are discussed in detail separately. (See "Spinal epidural abscess", section on 'Diagnosis' and "Spinal epidural abscess" and "Vertebral osteomyelitis and discitis in adults", section on 'Suggested clinical approach' and "Vertebral osteomyelitis and discitis in adults", section on 'Radiographic imaging'.)
●Concern for infection present but not high – When a concern for infection is present but not high, it is reasonable to evaluate patients with plain radiographs and ESR (or CRP) (algorithm 1). Patients with a positive plain radiograph should undergo appropriate further evaluation for infection. The choice of subsequent evaluation will depend on a variety of factors (eg, whether the concern is for epidural abscess or vertebral osteomyelitis, if blood culture data is available). Patients with a positive ESR (or CRP) but a negative plain radiograph should be evaluated with MRI. (See "Spinal epidural abscess", section on 'Diagnosis' and "Vertebral osteomyelitis and discitis in adults", section on 'Suggested clinical approach'.)
Plain radiographs are less sensitive than MRI for spinal infection, particularly early in the disease course. The sensitivity of plain radiograph for spinal infection is 0.82 and specificity 0.57 . Because of the lower sensitivity and specificity of plain radiographs, we combine the evaluation with ESR (or CRP). In patients with osteomyelitis or other spinal infection, the sensitivity of an elevated ESR is 0.76 to 0.95 and CRP is 0.82 to 0.98 percent [3-5]. Infection is very unlikely in patients with an ESR <20 and no more than one risk factor for a systemic illness [22,40]. While a leukocytosis is suggestive of infection, the sensitivity of elevated white blood cell (WBC) count for spinal infection is only between 0.35 to 0.61. (See "Vertebral osteomyelitis and discitis in adults", section on 'Laboratory findings' and "Spinal epidural abscess", section on 'Diagnosis'.)
Cancer — Patients with cancer or risk factors for cancer and neurologic deficits should have immediate imaging as noted above. In patients without neurologic deficits, the decision to image is based on risk. (See 'Neurologic deficits' above.)
●Current or recent cancer – Imaging for these patients will vary depending on a variety of factors (eg, what the primary cancer is, when the patient's most recent imaging studies were, whether or not the patient has known bone metastasis). For such patients, we consult with their oncologist to discuss the most appropriate imaging exam (algorithm 1). The diagnosis of bone metastasis is discussed separately. (See "Overview of the epidemiology, clinical presentation, diagnosis, and management of adult patients with bone metastasis", section on 'Overview of the diagnostic approach'.)
●Moderate to high risk for cancer – In patients at moderate to high risk for cancer, we start the evaluation with plain radiographs and ESR (or CRP) (algorithm 1) . Patients with a positive radiograph should have appropriate further evaluation for malignancy (eg, evaluation for primary site, other metastatic disease). Patients with a positive ESR (or CRP) but negative plain radiograph should be further evaluated with MRI. (See "Overview of the classification and management of cancers of unknown primary site".)
What constitutes a moderate to high risk for cancer (aside from a history of cancer) is not well-defined and the approach likely differs among clinicians. Factors to consider include the patient's age, smoking history, family history, physical examination findings, and any associated concerning symptoms (eg, recent weight loss). Vertebral metastases are often associated with localized pain and focal tenderness on examination. It is likely that patients having more than one such finding or feature are at higher risk than those with a single risk factor.
The sensitivity of plain radiographs for malignancy is 0.60 and specificity 0.95 . The yield of plain radiographs is increased when combined with the ESR . Cancer is very unlikely in a patients with an ESR <20 and no more than one risk factor (table 9) [22,40].
●Low risk for cancer – We do not obtain immediate imaging in patients with acute back pain who are at low risk for cancer (eg, one risk factor). If the pain is persistent, we image after four to six weeks. (See 'Cancer risk' below.)
Compression fracture — Patients with suspected vertebral compression fracture should have plain radiographs for evaluation (algorithm 1). Features in the history that indicate an increased risk for vertebral fractures include prolonged glucocorticoid use, advanced age, significant trauma or presence of contusion or abrasion, or recent mild trauma in a patient with a known diagnosis of or risk factors for osteoporosis (table 3) [65,73,75,76]. Patients can have osteoporotic vertebral compression fractures in the absence of trauma.
Symptomatic patients with osteoporotic fractures typically describe a sudden onset of pain and have localized pain and tenderness on examination. While the American College of Physicians (ACP) guidelines suggest that imaging should be deferred in patients with suspected vertebral compression fracture, when clinical suspicion is high it is reasonable to obtain plain radiographs on initial evaluation in order to institute appropriate symptomatic and preventive therapies. The diagnosis and management of osteoporotic vertebral compression fractures is discussed in detail separately. (See "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment", section on 'Diagnosis'.)
Minor trauma — Indications for imaging in patients with trauma are discussed in detail elsewhere. (See "Evaluation of thoracic and lumbar spinal column injury", section on 'Decision rules for imaging thoracic or lumbar spine injury'.)
Risk assessment subacute back pain — Patients who have not improved after four to six weeks of conservative therapy and who did not receive imaging on initial evaluation are reevaluated. Patients who have developed neurologic deficits or symptoms of infection in the interim should have imaging as noted above. (See 'Neurologic deficits' above and 'Infection' above.)
Patients who present initially with low back pain of more than four to six weeks duration should undergo the initial risk assessment as presented above. (See 'Indications for imaging' above.)
In patients who had indications for immediate imaging and had negative findings, we do not repeat imaging in patients if symptoms are unchanged . Repeat imaging is indicated in patients with new or worsening symptoms or new concerns that develop in the interim. The modality will depend on the suspected diagnosis and the modality of the initial imaging exam.
Radiculopathy or lumbar spinal stenosis — Patients with persistent symptoms due to a lumbosacral radiculopathy or spinal stenosis who have not responded to conservative treatment and who are candidates for and interested in invasive therapies (eg, surgery or epidural injection for radiculopathy) should have an MRI for further evaluation and be referred for consideration for these therapies . (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Neuroimaging' and "Acute lumbosacral radiculopathy: Treatment and prognosis", section on 'Epidural glucocorticoids' and "Acute lumbosacral radiculopathy: Treatment and prognosis", section on 'Surgery' and "Lumbar spinal stenosis: Treatment and prognosis", section on 'Surgical treatment'.)
Cancer risk — In patients with low back pain who did not meet criteria for immediate imaging but who have risk factors for cancer and do not improve with conservative therapy after four to six weeks, we evaluate with plain radiographs and ESR (or CRP) . Patients with a positive radiograph should have appropriate further evaluation for malignancy (eg, evaluation for primary site, other metastatic disease). Patients with a positive ESR (or CRP) but negative plain radiograph should be further evaluated with MRI. (See 'Cancer' above.)
●Concern for ankylosing spondylitis – Patients with persistent back pain despite four to six weeks of conservative therapy who also have signs or symptoms concerning for ankylosing spondylitis should have a plain radiograph to evaluate the sacroiliac joints . These can often be well-evaluated on a lumbosacral plain radiograph. (See "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial spondyloarthritis) in adults", section on 'Diagnostic approach'.)
●Concern for osteoarthritis – Lumbosacral, pelvic, and/or hip radiographs may be considered for older patients with persistent back pain in whom there is concern for osteoarthritis of the hip referred to the back or for whom the mechanical adaptions to hip osteoarthritis are causing back pain. If a patient's low back symptoms do not lateralize, a standing pelvis radiograph will evaluate both hips for the presence of osteoarthritis; if symptoms lateralize, a two-view hip (standing frontal and frog-leg views) is appropriate. The diagnosis and management of osteoarthritis is discussed in detail separately. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Imaging' and "Overview of the management of osteoarthritis".)
●Patients without specific concerns – In other patients where there are no concerns for a particular etiology, we generally treat with conservative therapy for another eight weeks.
Risk assessment chronic back pain — Patients who present initially with low back pain >12 weeks duration should undergo the risk assessment for acute and subacute back pain. (See 'Risk assessment for acute back pain' above and 'Risk assessment subacute back pain' above.)
In patients without specific concerns who have not received any imaging for indications noted above, if there is no improvement after 12 weeks, we generally image with a plain radiograph and consider the need for referrals for further evaluation and treatment.
Counseling patients who request imaging — Patients often expect that imaging will be ordered during their initial visit for back pain. Although it is not possible to provide a definitive physiologic diagnosis for low back pain in the majority of patients, clinicians can reassure patients without concerning history or physical exam findings that they appear to have "mechanical" or nonspecific low back pain, and that it is very unlikely that they have a serious underlying problem. Patients should be assured that improvement is to be expected and should be advised that:
●They are unlikely to have a serious underlying condition. (See 'Etiologies' above.)
●Incidental imaging findings, unrelated to their pain, are common, and may lead to unnecessary further tests or interventions. (See 'Limited utility of imaging' above.)
In addition, a careful physical exam with ongoing commentary ("I am checking strength for any sign of nerve injury") may be reassuring for patients and help make it clear that the clinician is not inappropriately bypassing a further diagnostic evaluation or dismissing the symptoms.
Patients who perceive that they have received an adequate explanation for the cause of their problem are less likely to want additional diagnostic tests and more likely to be satisfied with the visit than those who do not think they have been given an adequate explanation . In one randomized trial, low-risk patients who received an educational intervention rather than a plain radiograph were equally satisfied with their care and had equally good clinical outcomes .
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Low back pain in adults (The Basics)" and "Patient education: Spinal stenosis (The Basics)" and "Patient education: Herniated disc (The Basics)" and "Patient education: Muscle strain (The Basics)" and "Patient education: Do I need an X-ray (or other test) for low back pain? (The Basics)")
●Beyond the Basics topics (see "Patient education: Low back pain in adults (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Most patients who present with back pain to primary care settings will have nonspecific back pain. Such patients will typically improve over a few to several weeks with conservative or self-care. (See 'Etiologies' above.)
Less than 1 percent will have serious systemic etiologies (eg, malignancy or infection). Less than 10 percent will have less serious, specific etiologies (eg, vertebral compression fracture, radiculopathy, or spinal stenosis). (See 'Etiologies' above.)
●A focused history and physical examination are sufficient to evaluate most patients with back pain of less than four weeks duration. The history and physical examination should identify features that suggest that imaging and/or other evaluations are indicated. (See 'History' above and 'Physical examination' above.)
●The majority of patients with low back pain of less than four weeks duration do not require imaging. Among patients seen in primary care, less than 1 percent will require immediate advanced imaging (eg, magnetic resonance imaging [MRI] or computed tomography [CT]) (algorithm 1). (See 'Indications for imaging' above.)
•Any patient with symptoms of spinal cord or cauda equina compression or progressive and/or severe neurologic deficits should have immediate MRI for further evaluation and urgent specialist referral. Such symptoms and signs include new urinary retention, incontinence from bladder overflow, new fecal incontinence, saddle anesthesia, and significant motor deficits not localized to a single unilateral nerve root. (See 'Neurologic deficits' above.)
•Other patients who may require imaging on initial evaluation include those with a high suspicion for spinal infection, a current or recent history of cancer, major risk factors for cancer, and those with suspected vertebral compression fracture. (See 'Risk assessment for acute back pain' above.)
●Patients who have not improved after four to six weeks of conservative therapy and who did not receive imaging on initial evaluation are reevaluated:
•Patients with persistent symptoms due to a lumbosacral radiculopathy or spinal stenosis who are candidates for and are interested in invasive therapies (eg, surgery or epidural injection for radiculopathy) should have an MRI for further evaluation. (See 'Radiculopathy or lumbar spinal stenosis' above.)
•In patients with low back pain who have risk factors for cancer, we evaluate with erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) and plain radiographs. (See 'Cancer risk' above.)
•Other patients that may need imaging include those with concerns for ankylosing spondylitis and osteoarthritis. (See 'Other patients' above.)
•In other patients where there are no concerns for a particular etiology, we generally treat with conservative therapy for another eight weeks.
●For patients without concerns for a particular etiology who have not improved after 12 weeks total, we generally image with a plain radiograph and consider referrals for further evaluation and treatment. (See 'Risk assessment chronic back pain' above.)
- Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low-back pain and its related medical care in the United States. Spine (Phila Pa 1976) 1987; 12:264.
- Cassidy JD, Carroll LJ, Côté P. The Saskatchewan health and back pain survey. The prevalence of low back pain and related disability in Saskatchewan adults. Spine (Phila Pa 1976) 1998; 23:1860.
- Chou R. In the clinic. Low back pain. Ann Intern Med 2014; 160:ITC6.
- Centers for Disease Control and Prevention. National Ambulatory Medical Care Survey: 2010 Summary Tables. http://www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf (Accessed on September 30, 2014).
- Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992; 268:760.
- Hoy D, Bain C, Williams G, et al. A systematic review of the global prevalence of low back pain. Arthritis Rheum 2012; 64:2028.
- Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: estimates from U.S. national surveys, 2002. Spine (Phila Pa 1976) 2006; 31:2724.
- Skovron ML, Szpalski M, Nordin M, et al. Sociocultural factors and back pain. A population-based study in Belgian adults. Spine (Phila Pa 1976) 1994; 19:129.
- Papageorgiou AC, Croft PR, Ferry S, et al. Estimating the prevalence of low back pain in the general population. Evidence from the South Manchester Back Pain Survey. Spine (Phila Pa 1976) 1995; 20:1889.
- Katz JN. Lumbar disc disorders and low-back pain: socioeconomic factors and consequences. J Bone Joint Surg Am 2006; 88 Suppl 2:21.
- Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990; 112:598.
- Croft PR, Papageorgiou AC, Ferry S, et al. Psychologic distress and low back pain. Evidence from a prospective study in the general population. Spine (Phila Pa 1976) 1995; 20:2731.
- Croft PR, Papageorgiou AC, Thomas E, et al. Short-term physical risk factors for new episodes of low back pain. Prospective evidence from the South Manchester Back Pain Study. Spine (Phila Pa 1976) 1999; 24:1556.
- Macfarlane GJ, Thomas E, Papageorgiou AC, et al. Employment and physical work activities as predictors of future low back pain. Spine (Phila Pa 1976) 1997; 22:1143.
- Steffens D, Ferreira ML, Latimer J, et al. What triggers an episode of acute low back pain? A case-crossover study. Arthritis Care Res (Hoboken) 2015; 67:403.
- Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001; 344:363.
- Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med 2007; 147:478.
- Chou R, Qaseem A, Owens DK, et al. Diagnostic imaging for low back pain: advice for high-value health care from the American College of Physicians. Ann Intern Med 2011; 154:181.
- Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002; 137:586.
- Sun JC, Xu T, Chen KF, et al. Assessment of cauda equina syndrome progression pattern to improve diagnosis. Spine (Phila Pa 1976) 2014; 39:596.
- Schiff D, O'Neill BP, Suman VJ. Spinal epidural metastasis as the initial manifestation of malignancy: clinical features and diagnostic approach. Neurology 1997; 49:452.
- Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med 1988; 3:230.
- Underwood MR, Dawes P. Inflammatory back pain in primary care. Br J Rheumatol 1995; 34:1074.
- Acute low back problems in adults: assessment and treatment. Agency for Health Care Policy and Research. Clin Pract Guidel Quick Ref Guide Clin 1994; :iii.
- Ropper AH, Zafonte RD. Sciatica. N Engl J Med 2015; 372:1240.
- Delitto A, Piva SR, Moore CG, et al. Surgery versus nonsurgical treatment of lumbar spinal stenosis: a randomized trial. Ann Intern Med 2015; 162:465.
- Papadopoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. Orthop Clin North Am 2004; 35:65.
- Hopayian K, Song F, Riera R, Sambandan S. The clinical features of the piriformis syndrome: a systematic review. Eur Spine J 2010; 19:2095.
- Potter NA, Rothstein JM. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985; 65:1671.
- Russel AS, Maksymowych W, LeClercq S. Clinical examination of the sacroiliac joints: a prospective study. Arthritis Rheum 1981; 24:1575.
- Freburger JK, Riddle DL. Measurement of sacroiliac joint dysfunction: a multicenter intertester reliability study. Phys Ther 1999; 79:1134.
- Levangie PK. Four clinical tests of sacroiliac joint dysfunction: the association of test results with innominate torsion among patients with and without low back pain. Phys Ther 1999; 79:1043.
- McCombe PF, Fairbank JC, Cockersole BC, Pynsent PB. 1989 Volvo Award in clinical sciences. Reproducibility of physical signs in low-back pain. Spine (Phila Pa 1976) 1989; 14:908.
- Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79:288.
- Riddle DL, Freburger JK. Evaluation of the presence of sacroiliac joint region dysfunction using a combination of tests: a multicenter intertester reliability study. Phys Ther 2002; 82:772.
- Irwin RW, Watson T, Minick RP, Ambrosius WT. Age, body mass index, and gender differences in sacroiliac joint pathology. Am J Phys Med Rehabil 2007; 86:37.
- Jancuska JM, Spivak JM, Bendo JA. A Review of Symptomatic Lumbosacral Transitional Vertebrae: Bertolotti's Syndrome. Int J Spine Surg 2015; 9:42.
- Chandrasekar PH. Low-back pain and intravenous drug abusers. Arch Intern Med 1990; 150:1125, 1128.
- Waddell G, McCulloch JA, Kummel E, Venner RM. Nonorganic physical signs in low-back pain. Spine (Phila Pa 1976) 1980; 5:117.
- Chelsom J, Solberg CO. Vertebral osteomyelitis at a Norwegian university hospital 1987-97: clinical features, laboratory findings and outcome. Scand J Infect Dis 1998; 30:147.
- Beronius M, Bergman B, Andersson R. Vertebral osteomyelitis in Göteborg, Sweden: a retrospective study of patients during 1990-95. Scand J Infect Dis 2001; 33:527.
- Kapeller P, Fazekas F, Krametter D, et al. Pyogenic infectious spondylitis: clinical, laboratory and MRI features. Eur Neurol 1997; 38:94.
- Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet 2009; 373:463.
- Jarvik JG, Gold LS, Comstock BA, et al. Association of early imaging for back pain with clinical outcomes in older adults. JAMA 2015; 313:1143.
- Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69.
- Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990; 72:403.
- Weishaupt D, Zanetti M, Hodler J, Boos N. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 1998; 209:661.
- Eno JJ, Boone CR, Bellino MJ, Bishop JA. The prevalence of sacroiliac joint degeneration in asymptomatic adults. J Bone Joint Surg Am 2015; 97:932.
- Kalichman L, Li L, Kim DH, et al. Facet joint osteoarthritis and low back pain in the community-based population. Spine (Phila Pa 1976) 2008; 33:2560.
- Oland G, Hoff TG. Intraspinal cross-section areas measured on myelography--computed tomography. The relation to outcome in nonoperated lumbar disc herniation. Spine (Phila Pa 1976) 1996; 21:1985.
- el Barzouhi A, Vleggeert-Lankamp CL, Lycklama à Nijeholt GJ, et al. Magnetic resonance imaging in follow-up assessment of sciatica. N Engl J Med 2013; 368:999.
- Jarvik JG, Hollingworth W, Heagerty PJ, et al. Three-year incidence of low back pain in an initially asymptomatic cohort: clinical and imaging risk factors. Spine (Phila Pa 1976) 2005; 30:1541.
- Munter FM, Wasserman BA, Wu HM, Yousem DM. Serial MR Imaging of Annular Tears in Lumbar Intervertebral Disks. AJNR Am J Neuroradiol 2002; 23:1105.
- Slipman CW, Patel RK, Zhang L, et al. Side of symptomatic annular tear and site of low back pain: is there a correlation? Spine (Phila Pa 1976) 2001; 26:E165.
- Jarvik JJ, Hollingworth W, Heagerty P, et al. The Longitudinal Assessment of Imaging and Disability of the Back (LAIDBack) Study: baseline data. Spine (Phila Pa 1976) 2001; 26:1158.
- Williams FM, Manek NJ, Sambrook PN, et al. Schmorl's nodes: common, highly heritable, and related to lumbar disc disease. Arthritis Rheum 2007; 57:855.
- Yin R, Lord EL, Cohen JR, et al. Distribution of Schmorl nodes in the lumbar spine and their relationship with lumbar disk degeneration and range of motion. Spine (Phila Pa 1976) 2015; 40:E49.
- Nguyen C, Poiraudeau S, Rannou F. From Modic 1 vertebral-endplate subchondral bone signal changes detected by MRI to the concept of 'active discopathy'. Ann Rheum Dis 2015; 74:1488.
- Zhang YH, Zhao CQ, Jiang LS, et al. Modic changes: a systematic review of the literature. Eur Spine J 2008; 17:1289.
- Jensen TS, Karppinen J, Sorensen JS, et al. Vertebral endplate signal changes (Modic change): a systematic literature review of prevalence and association with non-specific low back pain. Eur Spine J 2008; 17:1407.
- Jensen RK, Leboeuf-Yde C. Is the presence of modic changes associated with the outcomes of different treatments? A systematic critical review. BMC Musculoskelet Disord 2011; 12:183.
- Hutton MJ, Bayer JH, Powell JM. Modic vertebral body changes: the natural history as assessed by consecutive magnetic resonance imaging. Spine (Phila Pa 1976) 2011; 36:2304.
- Bradley WG Jr, Seidenwurm DJ, Brunberg JA, et al. Low back pain. American College of Radiology (ACR), 2005. Available at: www.guideline.gov/summary/summary.aspx?doc_id=8599#s24 (Accessed on October 11, 2011).
- Miller GM, Forbes GS, Onofrio BM. Magnetic resonance imaging of the spine. Mayo Clin Proc 1989; 64:986.
- Bigos SJ, Bowyer OR, Braen GR, et al. Acute low back pain problems in adults. Clinical practice guideline No 14. Agency for Health Care Policy and Research, Public Health Service; US Department of Health and Human Services, Rockville, MD, 1994.
- National Committee for Quality Assurance. The state of health care quality 2006. Available at: www.ncqa.org (Accessed on October 11, 2011).
- Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain: a randomized controlled trial. JAMA 2003; 289:2810.
- Srinivas SV, Deyo RA, Berger ZD. Application of “less is more” to low back pain. Arch Intern Med 2012; 172:1016.
- Deyo RA, Jarvik JG, Chou R. Low back pain in primary care. BMJ 2014; 349:g4266.
- Bernstein IA, Malik Q, Carville S, Ward S. Low back pain and sciatica: summary of NICE guidance. BMJ 2017; 356:i6748.
- American College of Radiology. ACR Appropriateness Criteria. Low back pain. Available at: http://www.acr.org/SecondaryMainMenuCategories/quality_safety/app_criteria/pdf/ExpertPanelonNeurologicImaging/LowBackPainDoc7.aspx (Accessed on April 05, 2012).
- Hooten WM, Cohen SP. Evaluation and Treatment of Low Back Pain: A Clinically Focused Review for Primary Care Specialists. Mayo Clin Proc 2015; 90:1699.
- Downie A, Williams CM, Henschke N, et al. Red flags to screen for malignancy and fracture in patients with low back pain: systematic review. BMJ 2013; 347:f7095.
- Henschke N, Maher CG, Ostelo RW, et al. Red flags to screen for malignancy in patients with low-back pain. Cochrane Database Syst Rev 2013; :CD008686.
- Williams CM, Henschke N, Maher CG, et al. Red flags to screen for vertebral fracture in patients presenting with low-back pain. Cochrane Database Syst Rev 2013; :CD008643.
- Black DM, Cummings SR, Karpf DB, et al. Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Fracture Intervention Trial Research Group. Lancet 1996; 348:1535.
- Deyo RA, Diehl AK. Patient satisfaction with medical care for low-back pain. Spine (Phila Pa 1976) 1986; 11:28.
- Deyo RA, Diehl AK, Rosenthal M. Reducing roentgenography use. Can patient expectations be altered? Arch Intern Med 1987; 147:141.