ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 1 مورد

Evaluation of low back pain in adults

Evaluation of low back pain in adults
Authors:
Stephanie G Wheeler, MD
Jeffrey G Jarvik, MD, MPH
Roger Chou, MD
Section Editor:
Steven J Atlas, MD, MPH
Deputy Editor:
Karen Law, MD, FACP
Literature review current through: Apr 2025. | This topic last updated: May 06, 2025.

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) [3]. Rarely, back pain is an indicator of serious medical illness.

This discussion will focus on an approach to the initial evaluation of a patient seeking evaluation of low back pain with a health care professional, including diagnostic testing. Most patients in this group will have acute low back pain; however, the initial evaluation described in this topic is recommended at the presenting visit and with any acute changes in back pain, regardless of the overall duration of symptoms.

The treatment of acute, subacute, and chronic low back pain is discussed separately:

(See "Treatment of acute low back pain".)

(See "Subacute and chronic low back pain: Management".)

(See "Subacute and chronic low back pain: Nonsurgical interventional treatment".)

(See "Subacute and chronic low back pain: Surgical treatment".)

The evaluation of low back pain in patients with a recent history of significant trauma is also discussed separately. (See "Acute traumatic spinal cord injury" and "Thoracic and lumbar spinal column injury in adults: Evaluation".)

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 — 

Back symptoms are the principal reason for 1.3 percent of office visits in the United States [4]. A systematic review of 165 studies from 54 countries 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 [5]. Other survey estimates of the prevalence of low back pain have ranged from 22 to 48 percent, depending on the population and definition [2,6-8]. For example, in one United States National Health Interview Survey, 26 percent of respondents reported low back pain lasting at least one day in the preceding three months [6].

Risk factors associated with back pain complaints include smoking; obesity; age; female sex; physically strenuous work; sedentary work; psychologically strenuous work; workers' compensation insurance; job dissatisfaction; and psychologic factors such as somatization disorder, anxiety, and depression [2,7,9-14].

ETIOLOGIES — 

Although there are many etiologies of low back pain, the majority of patients seen in primary care will have nonspecific low back pain. Almost all patients with a serious etiology will have risk factors or other suggestive symptoms to prompt additional evaluation [15]. The approach to evaluating for serious etiologies of back pain is outlined in the algorithm (algorithm 1) and associated content. (See 'Initial evaluation' below.)

Nonspecific back pain is most common — The majority of patients seen for initial consultation will have nonspecific low back pain (>85 percent), meaning that the patient has back pain in the absence of a specific underlying condition that can be reliably identified [15-17]. Nonspecific low back pain is sometimes referred to as "mechanical back pain," but this designation also does not identify a specific etiology. Because there is no confirmatory diagnostic test for nonspecific low back pain, it is presumptively diagnosed in the absence of features suggestive of other etiologies of back pain. The presence of degenerative changes on spinal imaging does not exclude the diagnosis of nonspecific back pain because such findings do not reliably correlate with symptoms.

Urgent and acute conditions — Among patients who present with back pain to primary care settings, less than 1 percent will have a serious etiology (eg, cauda equina syndrome, metastatic cancer, spinal infection, etc) [18,19]. Key features and suggestive symptoms to prompt additional evaluation for a serious etiology are described below:

Spinal cord compression and cauda equina syndrome – Pain in the affected area is usually the first symptom of cord compression. Weakness and other motor or sensory findings are present in most patients at diagnosis. Among patients who are diagnosed with cord compression, it is the initial manifestation of malignancy in 20 percent [20].

Cauda equina syndrome is due to spinal canal narrowing or compressive lesions below the level of the conus medullaris. It is defined as compression of more than two lumbosacral nerve roots, typically causing bowel or bladder dysfunction and/or saddle anesthesia. There are many causes of cauda equina syndrome, the most common being herniation of the intervertebral disc [21]. Other causes include lumbar puncture, ankylosing spondylitis, trauma, malignancy, and infection.

Additional details regarding the clinical manifestations of spinal cord compression and cauda equina syndrome are discussed separately. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression" and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Cauda equina syndrome'.)

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 to the level of nerve root or roots involved. Over 90 percent are L5 and S1 radiculopathies [22].

Patients present with pain, sensory loss, weakness, and/or reflex changes consistent with the nerve root involved; these are summarized in the table (table 2) and discussed in more detail separately. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

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) [23]. Most sciatica is due to a disc disorder causing radiculopathy at the L5 or S1 level.

Metastatic cancer – In patients with a history of cancer, sudden, severe back pain raises concern for pathologic vertebral fracture. Patients may also have neurologic symptoms from either spinal cord compression or spinal instability. Among solid cancers, metastatic disease from breast, prostate, lung, thyroid, and kidney cancers accounts for 80 percent of skeletal metastases [24]. Approximately 60 percent of patients with multiple myeloma have skeletal lytic lesions present at diagnosis. The diagnosis and management of bone metastasis are reviewed in detail separately. (See "Epidemiology, clinical presentation, and diagnosis of bone metastasis in adults".)

Spinal infection – Vertebral osteomyelitis and spinal epidural abscess may present separately or concomitantly. Shared risk factors include recent spinal injection or epidural catheter placement, injection drug use, chronic indwelling catheter, and other recent infection (eg, contiguous bony or soft tissue infection, endocarditis, or bacteremia). Immunocompromised patients and patients receiving hemodialysis may also be at higher risk. Fever is suggestive but is an inconsistent finding.

Vertebral osteomyelitis – Patients with vertebral osteomyelitis present with gradually increasing back pain over weeks to months, along with features of positional discomfort, pain on palpation, and varying degrees of neurologic signs and symptoms [25]. The intervertebral disc may also become infected (discitis). When left untreated, the infection may extend into the epidural space and present with features of epidural abscess.

The incidence of vertebral osteomyelitis generally increases with age, and males are more commonly affected than females. The diagnosis and management of vertebral osteomyelitis are discussed in detail separately. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

Spinal epidural abscess – Spinal epidural abscess is a rare but serious cause of back pain. Initial symptoms (eg, fever and malaise) are often nonspecific. If left untreated, localized back pain is followed by radicular pain and neurologic deficits as the infection progresses to include the epidural space. The diagnosis and management of spinal epidural abscess are reviewed in detail separately. (See "Spinal epidural abscess".)

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]. Patients may be asymptomatic or may present with acute, localized back pain ranging from mild to incapacitating.

Risk factors for compression fracture related to osteoporosis include advanced age and chronic glucocorticoid use (table 3). A history of an osteoporotic or traumatic fracture is a risk factor for subsequent fractures. Additional details are discussed separately [22,23,26]. (See "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment".)

Subacute and chronic conditions — Less than 10 percent of patients who present in primary care settings will have low back pain from a specific subacute or chronic etiology [19,27]; approximately 3 to 4 percent have symptomatic disc herniation or spinal stenosis. Key features and suggestive symptoms to prompt additional evaluation for a serious subacute or chronic etiology are described below:

Spinal stenosis – Lumbar spinal stenosis is most often multifactorial. Spondylosis (degenerative arthritis affecting the spine), spondylolisthesis, and thickening of the ligamentum flavum are the most common causes, typically affecting patients >60 years of age (figure 1).

Ambulation-induced pain localized to the calf and distal lower extremity and resolving with sitting or leaning forward ("pseudoclaudication" or "neurogenic claudication") is a hallmark of lumbar spinal stenosis. Symptoms of neurogenic claudication can usually be distinguished from vascular claudication (table 4). Other symptoms of lumbar spinal stenosis can include sensory loss and weakness in the legs, though many patients may present with a normal neurologic examination. Most patients with spinal stenosis related to osteoarthritis will have stable symptoms over time. Rarely, patients may develop a cauda equina syndrome [28]. (See 'Urgent and acute conditions' above.)

Further details regarding the diagnosis and treatment of lumbar spinal stenosis are discussed separately. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis" and "Lumbar spinal stenosis: Treatment and prognosis".)

Osteoarthritis – Low back pain may be a symptom of osteoarthritis of the facet joints in the spine. Osteoarthritis most commonly presents in patients over the age of 40. Pain caused by osteoarthritis is typically exacerbated by activity and relieved by rest (table 5). The presence of osteoarthritic changes on imaging does not reliably correlate with symptoms; determining whether osteoarthritis is the cause of low back pain is a challenge due to the lack of a reliable diagnostic "gold standard."

Osteoarthritis can also lead to spinal stenosis. Additional features of lumbar facet joint osteoarthritis are discussed separately. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Facet joint'.)

Axial spondyloarthritis (including ankylosing spondylitis and nonradiographic axial spondyloarthritis) – Almost all patients with axial spondyloarthritis report back pain due to sacroiliitis. The back pain often has characteristics suggesting an inflammatory etiology (morning stiffness, improvement with exercise) [3]. Patients may also have extraskeletal disease manifestations (eg, uveitis, psoriasis).

Among patients with chronic low back pain, approximately 0.7 to 5 percent have axial spondyloarthritis, depending on the population studied [19,27,29]. Ankylosing spondylitis is more common among males, while the prevalence of nonradiographic axial spondyloarthritis is similar in males and females [30]. Ankylosing spondylitis is most commonly diagnosed in males under the age of 40 years.

Additional details regarding the diagnosis and treatment of axial spondyloarthritis are discussed separately. (See "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)

Scoliosis and hyperkyphosis – Back pain can be associated with scoliosis and hyperkyphosis. Patients have a history of congenital vertebral anomaly, osteoporosis with compression fractures, or degenerative disc disease. Excess spinal curvature and asymmetry may be notable on examination. Additional details regarding the management of scoliosis are discussed separately. (See "Adolescent idiopathic scoliosis: Management and prognosis" and "Hyperkyphosis in older persons".)

Nonspinal etiologies and referred pain conditions — Numerous nonspinal conditions may refer pain to the lower back. These conditions are reviewed below:

Nonspinal musculoskeletal conditions – Patients with musculoskeletal conditions of the hip and pelvis may present initially with back pain or may describe back pain as a component of their symptoms.

Primary pathology of the hip – Primary hip pathology may refer pain to the lower back. Pain is typically exacerbated by internal or external rotation of the hip; hip range of motion may also be reduced. (See "Approach to the adult with unspecified hip pain".)

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 [23,31,32]. Patients report gradual-onset pain in the buttock that increases with sitting. Piriformis symptoms may resemble sciatica. The neurologic examination is usually normal. (See "Approach to hip and groin pain in the athlete and active adult", section on 'Piriformis syndrome'.)

Sacroiliac joint dysfunction – The sacroiliac joint may be a referred site of pain, including from a lumbosacral degenerative disc, spinal stenosis, or osteoarthritis of the hip. "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. Diagnosing this condition is difficult due to the absence of an agreed-upon "gold standard" and low interrater reliability of specific sacroiliac examination maneuvers [33-40]. Moreover, provocative maneuvers such as fluoroscopically guided injections of the sacroiliac joint have been unreliable in diagnosis and treatment [39,41,42]. Additional detail regarding the examination of the sacroiliac joint is discussed separately. (See "Musculoskeletal examination of the hip and groin", section on 'Tests of sacroiliac region'.)

Psychologic conditions – Psychologic conditions (eg, depression or somatization) may contribute to the severity of symptoms of low back pain or may be a cause of nonorganic back pain [3]. (See "Somatic symptom disorder: Epidemiology, clinical features, and course of illness", section on 'Clinical features'.)

Herpes zoster – Herpes zoster, or shingles, results from reactivation of latent varicella-zoster virus infection. Patients typically exhibit a painful, unilateral vesicular eruption in a dermatomal distribution that can occur in the back region. In some cases, the pain may precede the onset of rash. Long-term pain is the most common complication of shingles. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Clinical manifestations'.)

Peripheral artery disease – Lower extremity peripheral artery disease presents with pain of one or more lower extremity muscle groups related to activity; back pain, if present, is referred and much less severe than the associated pain in the extremities. If arterial narrowing is severe, patients may have pain at rest and associated nonhealing wounds, skin discoloration, or ulceration. Risk factors include older age, history of smoking, hypertension, and other risk factors for cardiovascular disease. (See "Lower extremity peripheral artery disease: Clinical features and diagnosis", section on 'Clinical features' and "Overview of established risk factors for cardiovascular disease".)

Intra-abdominal pathologies – Intra-abdominal pathologies may refer pain to the lower back [3,17]. Patients generally have other accompanying symptoms that indicate a nonspinal etiology of low back pain:

Pancreatitis – Patients may have epigastric pain and abdominal distension; in severe cases, signs of obstructive jaundice and critical illness (eg, fever, hypoxemia, hypotension) may be present. (See "Clinical manifestations, diagnosis, and natural history of acute pancreatitis".)

Pyelonephritis – Patients typically present with acute flank pain and costovertebral angle tenderness. Nausea and vomiting are common features. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults".)

Nephrolithiasis – Pain with nephrolithiasis can vary from a mild ache to intense discomfort localized to the flank or lower back. It is usually "colicky" or waxing and waning in nature. Gross or microscopic hematuria may also be present. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis".)

Abdominal aortic aneurysm – Pain with abdominal aortic aneurysm may vary widely from the abdomen to the back, flank, or pelvis depending on the location of the aneurysm. With nonruptured aneurysms, the pain is indolent and nonspecific; pain associated with aneurysmal rupture is acute and severe. (See "Clinical features and diagnosis of abdominal aortic aneurysm".)

INITIAL EVALUATION — 

The clinical evaluation of low back pain includes a focused history and physical to evaluate for signs or symptoms that suggest a serious etiology of back pain or indicate the need for immediate imaging and further evaluation (algorithm 1). This evaluation should be completed at the initial evaluation of back pain by a health care professional, regardless of back pain duration, and with any acute worsening or change in back pain symptoms. For most patients with acute back pain (<4 weeks), laboratory tests and imaging are not necessary in the initial evaluation.

History — 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. While nonspecific low back pain is the most common etiology, it is a presumptive diagnosis in the absence of features suggestive of other etiologies. Therefore, history-taking should focus on identifying symptoms or risk factors that predict a serious etiology of back pain, as below and in the table (table 6):

Timing – Acute, rapidly progressive pain may suggest an urgent or acute etiology, including spinal cord compression, cauda equina, metastatic cancer, or infection. Gradual onset of pain and intermittent pain episodes may suggest osteoarthritis, spinal stenosis, or inflammatory arthritis. The timing of nonspecific back pain varies from acute to chronic.

Character and location

Burning pain in a nerve root distribution suggests lumbar radiculopathy.

Local tenderness to spinal percussion suggests vertebral osteomyelitis, discitis, or metastatic disease.

Pain induced by ambulation and alleviated with rest suggests osteoarthritis. Pseudoclaudication from spinal stenosis may present similarly, but with more pronounced pain in the calf and distal lower extremity, in addition to back pain.

Pain and associated stiffness that is worse in the morning and with rest and improved with exercise, suggests axial spondyloarthritis or other inflammatory arthritis.

Primary pain in the hip, pelvis, or buttocks suggests a referred pain condition such as piriformis syndrome, primary hip osteoarthritis, or other nonspinal etiology.

Associated symptoms

Acute fecal or urinary incontinence or urinary retention, progressive weakness or falls, saddle anesthesia, or other sensory changes suggest spinal cord compression.

Fever, chills, and malaise suggest an infectious etiology, though these are inconsistent findings depending on the extent of the infection; fever at presentation has been reported in 30 to 52 percent of patients with spinal infection [43-45].

Constitutional symptoms, including unintentional weight loss and night sweats, may suggest underlying malignancy.

Patients with axial spondyloarthritis may have associated extra-articular features, including uveitis, inflammatory bowel disease, and psoriasis. (See "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)

Psychosocial symptoms, including pre-existing psychologic conditions, somatization, chronic pain, job dissatisfaction, or stress, should also be assessed as these may indicate psychosocial contributors to pain and are risk factors for progression to chronic, disabling low back pain [3]. (See 'Nonspinal etiologies and referred pain conditions' above and "Subacute and chronic low back pain: Management", section on 'Risk assessment for chronic, disabling pain'.)

Past medical history – Information relevant to the evaluation of low back pain includes the following:

A history of injection drug use, recent bacteremia, or recent epidural or spinal procedure suggests epidural abscess or vertebral osteomyelitis. Current immunosuppression or hemodialysis are additional risk factors.

A history of smoking or personal or family history of cancer, specifically multiple myeloma or cancer of the breast, lung, prostate, thyroid, or kidney, is suggestive of skeletal metastatic disease.

A history of osteoporosis, prolonged glucocorticoid use, and recent trauma is associated with vertebral compression fractures [46-49]. Additional clinical risk factors for vertebral compression fractures are reviewed in the table (table 3).

Physical examination — The physical examination is performed to identify features that suggest a specific etiology of low back pain. The physical examination should include the following components:

Evaluation for most patients

Inspection of back and posture – Inspection may reveal anatomic abnormalities such as scoliosis or hyperkyphosis (table 1). (See 'Subacute and chronic conditions' above and "Hyperkyphosis in older persons".)

Palpation/percussion of the spine – Palpation and/or percussion of the back is 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 fractures [50]. A palpable mass suggests possible abscess or metastatic disease. (See 'Urgent and acute conditions' above and "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

Neurologic examination – Neurologic examination should include evaluation of the reflexes, strength, sensation, and gait. (See "The detailed neurologic examination in adults".)

In patients with radiculopathy, the neurologic examination should focus on identifying affected lumbosacral nerve roots (table 2), though this is not always possible. Testing for lumbar nerve root compression is as shown in the figure (figure 2) and discussed in further detail separately. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

Straight leg raising – The straight leg raise test and other maneuvers can be helpful in identifying whether symptoms are radicular in nature. These maneuvers are described separately. (See 'Urgent and acute conditions' above and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Physical examination'.)

Additional evaluation in select patients – Patients with key elements elicited from the history, including urinary retention, constitutional symptoms suggestive of malignancy, or pain suggestive of a nonspinal or referred pain etiology, should prompt additional evaluation:

Urinary retention – For patients with new or worsening urinary retention or incontinence, the physical examination should include palpation for a distended bladder. When feasible, we measure bladder postvoid residual by urethral catheterization or ultrasound to differentiate overflow incontinence from urge and/or stress incontinence (see "Acute urinary retention", section on 'Prompt diagnosis of retention'). Confirmed urinary retention or incontinence from bladder overflow warrants prompt evaluation with advanced imaging for cauda equina syndrome. (See 'Determining if imaging is indicated' below.)

Malignancy – If a patient's history includes features suggestive of malignancy, including constitutional symptoms, unexplained weight loss, and/or a personal or family history of cancer, we evaluate as appropriate (eg, lymph node examination, breast examination, prostate evaluation, imaging).

Nonspinal etiologies and referred pain – Other physical examination components to evaluate for nonspinal etiologies and referred pain should be performed based on the history. Details regarding these evaluations are discussed separately. As examples:

-(See "Approach to the adult with unspecified hip pain".)

-(See "Approach to hip and groin pain in the athlete and active adult".)

-(See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Physical examination'.)

-(See "Lower extremity peripheral artery disease: Clinical features and diagnosis", section on 'Physical examination'.)

Psychogenic back pain – Psychologic conditions may underlie or magnify back pain symptoms in some patients. Such patients may exhibit maladaptive coping behaviors and/or associated physical signs, also known as "Waddell's signs" (table 7). These include patient overreaction during physical examination, superficial tenderness, straight leg raise that improves when the patient is distracted, nonanatomic neurologic deficits (eg, nondermatomal distribution of sensory loss, sudden giving way or jerky movements with motor examination, inconsistency in observed spontaneous activity [dressing, getting off table]), and pain elicited by axial loading (pressing down on top of head or rotating the body at hips or shoulders) [51].

The data supporting Waddell's signs are mixed. Some studies suggest Waddell's signs are associated with a psychologic component to a patient's pain [3,52,53]. In one systematic review, while Waddell's signs did not correlate well with psychologic distress or accurately diagnose psychogenic back pain, they were associated with poorer treatment outcomes and greater pain levels [54].

The management of low back pain associated with psychologic conditions and maladaptive coping behaviors is discussed separately. (See "Subacute and chronic low back pain: Management", section on 'Risk assessment for chronic, disabling pain'.)

Laboratory studies — Most patients with acute low back pain do not require any laboratory testing. Additional testing with inflammatory markers and/or blood and urine cultures is indicated based on clinical suspicion of a specific etiology (algorithm 1):

Nonspecific, acute low back pain – Patients with nonspecific, acute low back pain without features suggestive of a specific etiology do not require initial laboratory testing.

Suspected malignancy – In patients with suspected malignancy (eg, current cancer history, constitutional symptoms, vertebral tenderness, palpable mass), we order an erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP) [24]. Because of its higher sensitivity, CRP may have a similar or greater value than the ESR; however, CRP has not been similarly evaluated in the evaluation of low back pain. The results are interpreted with plain radiography (algorithm 1) to determine the need for advanced imaging. (See 'Determining if imaging is indicated' below.)

Suspected infection – In patients with suspected spinal infection (eg, fever, current immunosuppression, recent invasive spinal procedure, or history of injection drug use), blood and urine cultures should be sent as they are positive in up to 50 percent of patients with vertebral osteomyelitis and guide antimicrobial therapy selection [25,55].

In patients with risk factors for infection but with a low index of suspicion (absence of suggestive physical examination findings), the ESR and/or CRP can inform the need for advanced imaging (algorithm 1) [56-58]. Patients with a high index of suspicion for infection warrant additional imaging regardless of ESR/CRP results. (See 'Determining if imaging is indicated' below.)

Suspected axial spondyloarthritis – The ESR and CRP are also used in the diagnosis of axial spondyloarthritis, along with imaging for sacroiliitis and other testing. (See "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Laboratory testing'.)

DIAGNOSTIC IMAGING

Nonspecific low back pain: Limited role of imaging — Patients with low back pain of less than four weeks' duration, without associated symptoms or risk factors suggestive of specific etiologies, do not require imaging [17]. Most patients who present to primary care settings will have nonspecific back pain and will improve rapidly with conservative measures (algorithm 1). The treatment of nonspecific, acute low back pain is discussed separately. (See "Treatment of acute low back pain".)

Our recommendations are consistent with guidelines from the American College of Physicians (ACP) (table 8), the United Kingdom's National Institute for Health and Care Excellence, the American Board of Internal Medicine's "Choosing Wisely" campaign, and the American College of Radiology's "Appropriateness Criteria" for low back pain [15,17,59,60], with the exception of imaging for suspected vertebral compression fracture, as discussed below. (See 'Determining if imaging is indicated' below.)

Studies indicate that early imaging for patients with nonspecific low back pain is associated with:

Minimal impact on symptoms – Studies report no improvement in pain, disability, or other patient-important outcomes when early imaging is pursued in patients with nonspecific back pain [61-64].

Findings of uncertain significance – Imaging may show abnormal findings that are clinically insignificant or of uncertain significance. (See 'Findings of uncertain significance' below.)

Unnecessary treatment – Early imaging in patients with nonspecific back pain is associated with increased treatment with opioids, unnecessary additional studies and overtreatment (including invasive and costly procedures), and increased health care costs [61-63,65].

If a patient with nonspecific back pain does not improve after four to six weeks of conservative management, we re-evaluate with additional history and a repeat examination and pursue diagnostic imaging, as below. (See 'Determining if imaging is indicated' below.)

Determining if imaging is indicated — Among patients seen in primary care, less than 1 percent will have a serious etiology that requires evaluation with advanced imaging (algorithm 1) (see 'Nonspecific low back pain: Limited role of imaging' above). While some guidelines suggest "red flag" symptoms to identify patients at risk for a more dangerous cause of back pain, there are limited data to support their utility in determining if early imaging is warranted [15,17,18,60,66]. Red flags associated with the highest posttest probability of a vertebral fracture on systemic reviews include older age, prolonged use of corticosteroids, severe trauma, and presence of contusion or abrasion over the spine [47,48].

We pursue diagnostic imaging when the initial evaluation raises suspicion for a serious underlying etiology of low back pain. If a serious etiology of low back pain is suspected, we use the following approach to select the appropriate imaging modality.

Address neurologic deficits, if present — We assess the nature of neurologic symptoms along with the clinical suspicion for cancer and/or infection to determine the imaging study and study urgency (algorithm 1).

Significant neurologic deficits, including cauda equina – Any patient with progressive weakness and/or severe other neurologic deficits or symptoms of spinal cord compression should have immediate magnetic resonance imaging (MRI) for further evaluation and urgent specialist referral. Such symptoms and signs include new urinary retention, urinary incontinence from bladder overflow, new fecal incontinence, saddle anesthesia, and severe or progressive motor deficits. Lumbar spine MRI without contrast is usually appropriate; if there is concern for cancer or infection or history of prior surgery at the involved site, we recommend MRI with and without contrast. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression", section on 'Magnetic resonance imaging of the spine' and "Spinal epidural abscess", section on 'Evaluation and Diagnosis'.)

Mild or moderate neurologic symptoms and risk of cancer or infection – Patients with significant neurologic deficits, regardless of the risk of cancer or infection, should prompt referral for MRI as per above.

Patients with mild or moderate radicular pain, motor weakness, or sensory changes and either current malignancy or moderate to high risk of cancer or infection should have imaging with plain radiography or MRI in consultation with treating specialists (oncology, infectious diseases), as discussed below and in the algorithm (algorithm 1).

Stable radiculopathy, low risk of cancer or infection – Patients with radiculopathy reliably localized to a single nerve root level or with stable symptoms due to spinal stenosis do not need immediate imaging. For all patients with radiculopathy attributable to a single nerve root level, we image with MRI without contrast if symptoms do not improve after four to six weeks of conservative therapy.

There is no indication to reimage patients with spinal stenosis symptoms if a previous MRI was performed and symptoms are stable. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Evaluation and diagnosis' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Diagnosis'.)

Determining risk for malignancy or infection is not well defined and is guided largely by individual clinical assessment, as below.

Assess the risk of infection — If vertebral osteomyelitis, spinal epidural abscess, or other spinal infection is suspected in the absence of neurologic deficits, we pursue imaging as below and in the algorithm (algorithm 1). However, the risk for infection (aside from a recent history of infection) is not well defined and is informed primarily by clinical suspicion:

Moderate to high clinical suspicion for infection – While fever is highly suggestive of infection, it is an inconsistent finding in patients with spinal infection [43,44]. Additional risk factors and examination findings that are suggestive of infection are reviewed above. (See 'Initial evaluation' above.)

For patients with low back pain in whom there is moderate to high clinical suspicion for spinal infection, including recent bacteremia or invasive spinal procedure, immediate MRI without and with contrast is indicated (algorithm 1) [60]. MRI is the most sensitive imaging modality for detecting spinal infection, with a sensitivity of 0.96 and specificity of 0.92 [19]. For patients who are unable to obtain an MRI, a computed tomography (CT) with contrast is an acceptable alternative to evaluate for epidural abscess. 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 'Evaluation and Diagnosis' and "Spinal epidural abscess" and "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis" and "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Imaging studies'.)

Lower concern for infection – As above, determining the risk for infection is not well defined and is informed by clinical suspicion. Though immunosuppression, hemodialysis, or a history of injection drug use are risk factors, given the prevalence of nonspecific low back pain, only a small percentage of patients with a history of one or more of these conditions will develop a spinal infection. Additional risk factors and examination findings suggestive of infection are reviewed above. (See 'Initial evaluation' above.)

In the absence of fever or other suggestive physical examination findings, it is reasonable to classify the patient as having a lower concern for an infectious cause of back pain. In such patients, inflammatory markers (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]) can assist with determining the need for MRI (algorithm 1). If inflammatory markers are not elevated, conservative management may be pursued without immediate additional imaging. If inflammatory markers are elevated, an MRI with and without contrast should be obtained. (See "Spinal epidural abscess", section on 'Evaluation and Diagnosis' and "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

In patients with osteomyelitis or other spinal infection, the sensitivity of an elevated ESR is 0.76 to 0.95, and the sensitivity of an elevated CRP is 0.82 to 0.98 [3,4,18]. Infection is very unlikely in patients with an ESR <20 without additional findings suggestive of a systemic illness (fever, leukocytosis, or persistent pain and tenderness over the spine) [24,56]. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Laboratory findings' and "Spinal epidural abscess", section on 'Evaluation and Diagnosis'.)

Assess the risk of malignancy — Patients with neurologic deficits and cancer or risk factors for cancer should have immediate imaging as discussed above. In patients without neurologic deficits, the decision to image is based on the assessment of cancer risk:

Current or recent cancer – Imaging for these patients will vary depending on a variety of factors (eg, primary cancer type and propensity to metastasize to the spine, the timing of the most recent imaging studies, and whether the patient has known metastases) and should be considered in consultation with the patient's oncology team. Diagnostic imaging in the evaluation of osseous metastases in a patient with cancer and back pain is reviewed in detail separately (algorithm 2). (See "Epidemiology, clinical presentation, and diagnosis of bone metastasis in adults", section on 'Overview of the diagnostic approach'.)

Moderate to high risk for cancer – Determining 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 symptoms (eg, recent weight loss). Vertebral metastases are often associated with localized pain and focal tenderness on examination. Patients with more than one such finding are at higher risk than those with a single risk factor.

In patients with moderate to high risk for cancer, we start the evaluation with plain radiographs and inflammatory markers (ESR, CRP) (algorithm 1) [15]. Patients with a positive radiograph should have further evaluation for malignancy (eg, evaluation for primary site or other metastatic disease). We pursue MRI with and without contrast for patients with normal radiographs and elevated inflammatory markers, multiple risk factors for cancer, and/or high clinical suspicion for cancer. (See "Overview of the classification and management of cancers of unknown primary site".)

The sensitivity and specificity of plain radiographs for malignancy are 0.60 and 0.95, respectively [19]. The yield of plain radiographs is increased when combined with the ESR [24]. Cancer is very unlikely in patients with an ESR <20 and no more than one risk factor (table 9) [24,56].

Low risk for cancer – As above, determining risk for cancer is not well defined. We classify patients with acute back pain, no personal history of cancer, and no more than one risk factor for cancer as "low risk" for cancer. "Risk factors" for cancer in this setting include older age, smoking, heavy alcohol use, failure to improve after one month, and anemia [67]. In these patients, we do not obtain immediate imaging. If the pain persists beyond six weeks with conservative therapy, we consider imaging and specialty referral. (See 'Nonspecific low back pain: Limited role of imaging' above.)

Imaging for less urgent conditions

Suspected compression fracture – Features in the history that indicate an increased risk for vertebral fractures are reviewed in further detail in the table (table 3) and above (see 'Initial evaluation' above). While the ACP guidelines suggest that imaging should be deferred in patients with suspected vertebral compression fractures, we recommend plain radiographs on initial evaluation when clinical suspicion for fracture is high (algorithm 1). Early diagnosis in these cases facilitates prompt initiation of appropriate symptomatic and preventive therapies.

The diagnosis and management of osteoporotic vertebral compression fractures are discussed in detail separately. (See "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment", section on 'Diagnosis'.)

Spondyloarthritis symptoms – Back pain with inflammatory features, including morning stiffness, improvement with exercise, and pain at night, is suggestive of axial spondyloarthritis. Patients may also have a history of additional disease manifestations, including eye inflammation, psoriasis, and peripheral arthritis.

If axial spondyloarthritis is suspected, the sacroiliac joints should be evaluated with a lumbosacral plain radiograph. Patients whose symptoms or examination also suggests hip involvement should also have radiographs of the affected hip. The diagnosis of these conditions is discussed separately. (See "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)

Imaging for persistent symptoms

Persistent symptoms – Patients with nonspecific back pain are managed with conservative therapy for four to six weeks (see "Treatment of acute low back pain" and "Subacute and chronic low back pain: Management"). If back pain persists despite conservative management, we re-evaluate as follows:

Patients who experience some improvement with conservative therapy should continue this regimen for a total of 12 weeks; in these patients, if pain persists beyond 12 weeks, we image with a plain radiograph.

For patients who have minimal or no improvement with conservative therapy, it is reasonable to pursue earlier imaging (eg, at six weeks).

The management of patients with subacute or chronic low back pain, including additional treatment and imaging, is discussed separately. (See "Subacute and chronic low back pain: Management" and "Subacute and chronic low back pain: Nonsurgical interventional treatment".)

Acute change or worsening of symptoms – In a patient with back pain of greater than four weeks' duration, worsening of symptoms may represent an acute flare of low back pain or a new cause of low back pain. These patients should be evaluated for new symptoms suggestive of a specific etiology of back pain (see 'Initial evaluation' above). Imaging is pursued according to the presence of new concerning signs or symptoms. (See 'Determining if imaging is indicated' above.)

An acute flare of chronic low back pain is a presumptive diagnosis once the patient has been evaluated and no features suggestive of serious etiologies are found (see 'Etiologies' above and 'Initial evaluation' above). In such patients, we revisit specific strategies that were effective during the initial episode of back pain. As above, additional imaging is warranted for persistent symptoms beyond 12 weeks.

The management of acute flares of chronic low back pain is discussed separately. (See "Subacute and chronic low back pain: Management", section on 'Management of acute flares' and "Subacute and chronic low back pain: Management".)

Imaging modalities

Plain radiographs – When plain radiographs are indicated, anteroposterior and lateral views of the lumbar spine are usually adequate. Flexion-extension views may be helpful in patients for whom instability is a concern (eg, spondylolisthesis that worsens with flexion). Oblique and spot views substantially increase the radiation dose and add little new diagnostic information [46].

We use plain radiographs for the detection of compression fractures in patients with osteoporosis [60]. We also use plain radiographs for initial imaging in patients with risk factors for malignancy (algorithm 1), though, for patients with high clinical suspicion for cancer, MRI is also a reasonable initial test (algorithm 2) [19,68].

Advanced imaging

Lumbar MRI – For most patients with low back pain who require advanced imaging, lumbar spine MRI is the appropriate initial examination [69,70]. MRI provides both axial and sagittal views and demonstrates discs, ligaments, nerve roots, and epidural fat, as well as the shape and size of the spinal canal. MRI is also more sensitive and specific than plain radiographs for the detection of spinal infection and malignancy [19]. When cancer or infection is suspected, MRI without and with intravenous contrast offers the ability to distinguish infection or mass from other structures. Enhancement with gadolinium also allows the distinction of scar from disc in patients with prior back surgery.

Lumbar CT – In patients who require advanced imaging but cannot undergo MRI, we pursue lumbar spine CT with contrast [70]. While MRI is the preferred method for detecting spinal cord pathology and imaging soft tissues, CT also offers a reasonable degree of detail to diagnose similar conditions. If iodinated contrast is contraindicated, CT without contrast is acceptable.

Other imaging modalities – We do not routinely perform radionuclide scans or myelography in the initial evaluation of patients with low back pain.

Findings of uncertain significance — Imaging examinations often show abnormal findings in adults without low back pain, making it difficult to determine which imaging findings are clinically significant. For example, degenerative changes (osteoarthritis of the spine and degenerative disc disease) are often seen on imaging but correlate poorly with symptoms [71]. Numerous studies have shown that the prevalence of radiologic facet joint arthritis increases with age but does not correlate with low back pain [72,73]. In addition, disc herniations on MRI have been reported in 22 to 67 percent of asymptomatic adults; spinal stenosis has been detected by MRI in 21 percent of asymptomatic adults over age 60 [74-76].

Furthermore, even when radiographic findings are consistent with the clinical presentation, studies suggest the magnitude of radiographic findings does not correlate with clinical severity and outcome, and clinical improvement may not correlate with the resolution of the radiographic defect [77,78]. In one study 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 [78].

Specific findings on MRI that are clinically insignificant or of uncertain significance 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 fissures and back pain [79-81]. As an example, a prospective study of asymptomatic patients found that 38 percent had evidence of annular fissures at baseline [82]. Follow-up after three years showed that annular fissures were not associated with new back pain [79].

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) [83]. Although Schmorl's nodes are associated with degenerative changes in the lower back, they are not an independent risk factor for back pain [84].

Modic changes – Modic changes (also known as degenerative end plate changes) are of unclear clinical significance. They refer to specific signal changes in the vertebral end plate and adjacent bone marrow on a spine MRI [85]. 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 approximately 20 to 40 percent of patients [86,87]. 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 [88]. Additionally, the type of Modic change in a single patient may progress or regress over time [89].

While the significance of Modic changes remains uncertain, their presence on imaging has been used to determine candidacy for interventional treatment for subacute and chronic low back pain. This is discussed in further detail separately. (See "Subacute and chronic low back pain: Nonsurgical interventional treatment", section on 'MRI'.)

Transitional vertebrae – A transitional vertebra is a common finding in radiologic studies. It is a congenital anomaly involving a naturally occurring articulation or bony fusion between the transverse processes of L5 and the sacrum. Back pain in the setting of a transitional vertebra is known as "Bertolotti's syndrome." Estimates of the prevalence of transitional vertebrae range from 4 to 36 percent [90]. It remains unclear whether these individuals have a higher risk of back pain than those without such an anomaly. Patients with transitional vertebra and associated Bertolotti's syndrome should undergo the same initial management as patients with nonspecific back pain.

Patient counseling when imaging is not indicated — Patients often expect that imaging will be ordered during their initial visit for back pain. When counseling patients presenting with nonspecific low back pain, we underscore the following:

They are unlikely to have a serious underlying condition. (See 'Nonspecific back pain is most common' above.)

The prognosis for acute, nonspecific low back pain is excellent. (See "Treatment of acute low back pain", section on 'Prognosis'.)

When imaging has been performed for nonspecific low back pain, it has not led to faster resolution of symptoms. Furthermore, incidental imaging findings unrelated to their pain are common and may lead to unnecessary further tests or interventions. (See 'Nonspecific low back pain: Limited role of imaging' above.)

Imaging is appropriate if they do not improve as expected or if symptoms worsen or change. (See 'Determining if imaging is indicated' above.)

We find that designating the nonspecific back pain as "mechanical" assists patients with understanding the condition, even when a definitive physiologic diagnosis cannot be provided. In addition, a careful physical examination with ongoing commentary ("I am checking strength for any sign of nerve injury") can reassure patients that the clinician is not dismissing the symptoms or inappropriately bypassing a further diagnostic evaluation.

Compared with patients who are unsatisfied with the counseling they receive, 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 [91]. 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 [92].

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Lower spine disorders".)

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 email 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: Lumbar 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 topic (see "Patient education: Low back pain in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Epidemiology and etiology of low back pain – Most patients who present with back pain to primary care settings will have nonspecific, self-limited back pain that improves over several weeks with conservative or self-care. Less than 1 percent will have serious etiologies (eg, malignancy or infection). Other, less urgent etiologies (eg, vertebral compression fracture, radiculopathy, or spinal stenosis) are identified in less than 10 percent of patients. (See 'Etiologies' above.)

Initial evaluation – A focused history and physical examination identifies signs and symptoms suggestive of serious etiologies of back pain requiring further evaluation (table 6). Most patients do not require any laboratory testing. Inflammatory markers and/or blood and urine cultures are indicated based on clinical suspicion of malignancy, infection, or other serious etiology. (See 'Initial evaluation' above.)

Diagnostic imaging

Limited role of imaging for most patients – The majority of patients with low back pain of less than four weeks' duration do not require imaging (algorithm 1). Among patients seen in primary care, less than 1 percent will require advanced imaging (eg, MRI or CT). (See 'Nonspecific low back pain: Limited role of imaging' above.)

Patients with neurologic deficits – Urgent imaging is indicated for patients with symptoms of spinal cord compression or neurologic deficits. Any patient with symptoms of spinal cord compression, including progressive and/or severe neurologic deficits, should have immediate MRI for further evaluation and urgent specialist referral. Lumbar spine MRI without contrast is usually appropriate; if there is concern for cancer or infection or history of prior surgery at the involved site, we order an MRI with and without contrast.

Patients with suspected cancer or infection – Imaging is also indicated if the initial evaluation raises suspicion for infection or metastatic cancer. In such patients, we obtain plain radiography, CT, or MRI for further evaluation based on the clinical scenario (algorithm 1).

Other indications – Other patients who may require imaging on initial evaluation include those with suspected vertebral compression fractures (algorithm 1) or spondyloarthropathy and patients with nonspecific back pain who have completed four to six weeks of conservative therapy without improvement. (See 'Determining if imaging is indicated' above.)

Patient counseling – Patients often expect that imaging will be ordered during their initial visit for back pain. When counseling patients presenting with nonspecific low back pain, we underscore the following:

They are unlikely to have a serious underlying condition. (See 'Nonspecific back pain is most common' above.)

The prognosis for acute, nonspecific low back pain is excellent. (See "Treatment of acute low back pain", section on 'Prognosis'.)

When imaging is performed for nonspecific low back pain, incidental imaging findings unrelated to their pain are common and may lead to unnecessary further tests or interventions. (See 'Nonspecific low back pain: Limited role of imaging' above.)

Imaging is appropriate if they do not improve as expected. (See 'Determining if imaging is indicated' above.)

ACKNOWLEDGMENTS — 

The UpToDate editorial staff acknowledges Joyce E Wipf, MD, Thomas O Staiger, MD, and Richard A Deyo, MD, MPH, who contributed to earlier versions of this topic review.

  1. 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.
  2. 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.
  3. Chou R. In the clinic. Low back pain. Ann Intern Med 2014; 160:ITC6.
  4. National Ambulatory Medical Care Survey: 2010 summary tables. Centers for Disease Control and Prevention. https://archive.cdc.gov/#/details?url=https://www.cdc.gov/nchs/data/ahcd/namcs_summary/2010_namcs_web_tables.pdf (Accessed on September 30, 2014).
  5. Hoy D, Bain C, Williams G, et al. A systematic review of the global prevalence of low back pain. Arthritis Rheum 2012; 64:2028.
  6. 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.
  7. 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.
  8. 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.
  9. Katz JN. Lumbar disc disorders and low-back pain: socioeconomic factors and consequences. J Bone Joint Surg Am 2006; 88 Suppl 2:21.
  10. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990; 112:598.
  11. 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.
  12. 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.
  13. 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.
  14. 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.
  15. 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.
  16. Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001; 344:363.
  17. 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.
  18. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992; 268:760.
  19. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002; 137:586.
  20. 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.
  21. 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.
  22. 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.
  23. Ropper AH, Zafonte RD. Sciatica. N Engl J Med 2015; 372:1240.
  24. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med 1988; 3:230.
  25. Nolla JM, Ariza J, Gómez-Vaquero C, et al. Spontaneous pyogenic vertebral osteomyelitis in nondrug users. Semin Arthritis Rheum 2002; 31:271.
  26. Crandall CJ, Larson JC, LaCroix AZ, et al. Risk of Subsequent Fractures in Postmenopausal Women After Nontraumatic vs Traumatic Fractures. JAMA Intern Med 2021; 181:1055.
  27. Underwood MR, Dawes P. Inflammatory back pain in primary care. Br J Rheumatol 1995; 34:1074.
  28. 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.
  29. Riis A, Olesen JL, Thomsen JL. Early differential diagnosis of ankylosing spondylitis among patients with low back pain in primary care. BMC Fam Pract 2020; 21:90.
  30. de Winter JJ, van Mens LJ, van der Heijde D, et al. Prevalence of peripheral and extra-articular disease in ankylosing spondylitis versus non-radiographic axial spondyloarthritis: a meta-analysis. Arthritis Res Ther 2016; 18:196.
  31. 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.
  32. Hopayian K, Song F, Riera R, Sambandan S. The clinical features of the piriformis syndrome: a systematic review. Eur Spine J 2010; 19:2095.
  33. Szadek KM, van der Wurff P, van Tulder MW, et al. Diagnostic validity of criteria for sacroiliac joint pain: a systematic review. J Pain 2009; 10:354.
  34. Potter NA, Rothstein JM. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985; 65:1671.
  35. Russel AS, Maksymowych W, LeClercq S. Clinical examination of the sacroiliac joints: a prospective study. Arthritis Rheum 1981; 24:1575.
  36. Freburger JK, Riddle DL. Measurement of sacroiliac joint dysfunction: a multicenter intertester reliability study. Phys Ther 1999; 79:1134.
  37. 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.
  38. 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.
  39. 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.
  40. 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.
  41. 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.
  42. Juch JNS, Maas ET, Ostelo RWJG, et al. Effect of Radiofrequency Denervation on Pain Intensity Among Patients With Chronic Low Back Pain: The Mint Randomized Clinical Trials. JAMA 2017; 318:68.
  43. Torda AJ, Gottlieb T, Bradbury R. Pyogenic vertebral osteomyelitis: analysis of 20 cases and review. Clin Infect Dis 1995; 20:320.
  44. Sapico FL, Montgomerie JZ. Pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. Rev Infect Dis 1979; 1:754.
  45. Chen WC, Wang JL, Wang JT, et al. Spinal epidural abscess due to Staphylococcus aureus: clinical manifestations and outcomes. J Microbiol Immunol Infect 2008; 41:215.
  46. Bigos SJ, Bowyer OR, Braen GR, et al. Acute low back problems in adults. Clinical practice guideline no. 14, Agency for Health Care Policy and Research; US Department of Health and Human Services, Rockville, MD 1994.
  47. 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.
  48. 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.
  49. 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.
  50. Chandrasekar PH. Low-back pain and intravenous drug abusers. Arch Intern Med 1990; 150:1125, 1128.
  51. Waddell G, McCulloch JA, Kummel E, Venner RM. Nonorganic physical signs in low-back pain. Spine (Phila Pa 1976) 1980; 5:117.
  52. Fritz JM, Wainner RS, Hicks GE. The use of nonorganic signs and symptoms as a screening tool for return-to-work in patients with acute low back pain. Spine (Phila Pa 1976) 2000; 25:1925.
  53. Polatin PB, Cox B, Gatchel RJ, Mayer TG. A prospective study of Waddell signs in patients with chronic low back pain. When they may not be predictive. Spine (Phila Pa 1976) 1997; 22:1618.
  54. Fishbain DA, Cole B, Cutler RB, et al. A structured evidence-based review on the meaning of nonorganic physical signs: Waddell signs. Pain Med 2003; 4:141.
  55. Patzakis MJ, Rao S, Wilkins J, et al. Analysis of 61 cases of vertebral osteomyelitis. Clin Orthop Relat Res 1991; :178.
  56. 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.
  57. 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.
  58. Kapeller P, Fazekas F, Krametter D, et al. Pyogenic infectious spondylitis: clinical, laboratory and MRI features. Eur Neurol 1997; 38:94.
  59. Bernstein IA, Malik Q, Carville S, Ward S. Low back pain and sciatica: summary of NICE guidance. BMJ 2017; 356:i6748.
  60. ACR Appropriateness Criteria: Low back pain. American College of Radiology. https://acsearch.acr.org/docs/69483/Narrative/ (Accessed on May 13, 2019).
  61. Jacobs JC, Jarvik JG, Chou R, et al. Observational Study of the Downstream Consequences of Inappropriate MRI of the Lumbar Spine. J Gen Intern Med 2020; 35:3605.
  62. 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.
  63. Srinivas SV, Deyo RA, Berger ZD. Application of “less is more” to low back pain. Arch Intern Med 2012; 172:1016.
  64. Deyo RA, Jarvik JG, Chou R. Low back pain in primary care. BMJ 2014; 349:g4266.
  65. Powell AC, Rogstad TL, Elliott SW, et al. Health Care Utilization and Pain Outcomes Following Early Imaging for Low Back Pain in Older Adults. J Am Board Fam Med 2019; 32:773.
  66. 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.
  67. 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.
  68. Spinal metastases and metastatic spinal cord compression: Evidence reviews for investigations – diagnosis. National Institute for Health and Care Excellence, 2023. https://www.nice.org.uk/guidance/ng234/evidence/f-investigations-diagnosis-pdf-13134698178 (Accessed on April 07, 2025).
  69. Miller GM, Forbes GS, Onofrio BM. Magnetic resonance imaging of the spine. Mayo Clin Proc 1989; 64:986.
  70. Patel ND, Broderick DF, Burns J, et al. ACR Appropriateness Criteria Low Back Pain. J Am Coll Radiol 2016; 13:1069.
  71. 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.
  72. 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.
  73. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol 2015; 36:811.
  74. 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.
  75. 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.
  76. 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.
  77. 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.
  78. 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.
  79. 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.
  80. 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.
  81. 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.
  82. 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.
  83. 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.
  84. 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.
  85. 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.
  86. Zhang YH, Zhao CQ, Jiang LS, et al. Modic changes: a systematic review of the literature. Eur Spine J 2008; 17:1289.
  87. 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.
  88. 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.
  89. 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.
  90. Jancuska JM, Spivak JM, Bendo JA. A Review of Symptomatic Lumbosacral Transitional Vertebrae: Bertolotti's Syndrome. Int J Spine Surg 2015; 9:42.
  91. Deyo RA, Diehl AK. Patient satisfaction with medical care for low-back pain. Spine (Phila Pa 1976) 1986; 11:28.
  92. Deyo RA, Diehl AK, Rosenthal M. Reducing roentgenography use. Can patient expectations be altered? Arch Intern Med 1987; 147:141.
Topic 7782 Version 91.0

References