The Use of Imaging in Management of Patients with Low Back Pain.

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I NTRODUCTION

Lower back pain (LBP) affects up to 80%–85% of the population during their lifetime.[ 1 ] More than 85% of patients will have nonspecific LBP, which usually improves within a few weeks. LBP is associated with substantial direct health care costs as well as indirect costs related to disability and loss of productivity.[ 2 ] A 2014 study by Schwartz et al., estimated that annual medicare spending on imaging for uncomplicated low back pain ranged from $82 million to $226 million, which does not include costs associated with follow-up testing and care due to the results.[ 3 ] Due to the fact that the plain radiographs are insensitive for spinal pathology, magnetic resonance imaging (MRI) and computerized tomography (CT) are increasingly being utilized for low back pain, however, much of the utilization occurs outside of appropriateness guidelines.[ 4 ]

Imaging findings, such as disk degeneration, facet arthropathy, and disk herniations, have been attributed as causative factors for LBP; however, these structural abnormalities are present in a large proportion of asymptomatic individuals and the incidence of these findings increases with age.[ 5 6 7 8 ]

MRI is highly sensitive in detecting degenerative changes in the spine, however, several studies have shown degenerative changes to have no association with low back pain.[ 9 10 11 ] Perhaps, more importantly, the prognostication of surgical outcomes based on imaging findings has not been established.[ 12 13 ] One study found that patients undergoing early MRI in the workup of LBP were more likely to have prolonged disability, higher medical costs, and greater utilization of surgery.[ 14 ]

Concerns about the use of improper advanced imaging have led to the issuance of practice guidelines regarding the use of imaging in the diagnosis and treatment of LBP.[ 15 ] In 2012, the Board of Internal Medicine's Choosing Wisely campaign supported selective use MRI and CT imaging in patients with LBP.[ 16 ] The American Academy of Family Physicians recommends withholding imaging for low back pain within the first 6 weeks of symptom onset unless clinical “red flags” are present [ Table 1 ]. The American Association of Neurological Surgeons and Congress of Neurological Surgeons recommend withholding all imaging of the spine in patients with nonspecific acute low back pain and without “red flags.” However, advanced imaging of the spine with MRI and/or CT is appropriate in several circumstances [ Table 2 ], which will be reviewed.

R ADICULOPATHY

Uncomplicated LBP with or without radiculopathy is often a self-limiting benign condition in that does not warrant imaging studies in the first 4–6 weeks after symptom onset.[ 10 17 18 ] The majority of disk herniations resorb, and patients usually become asymptomatic within 8 weeks after symptom onset.[ 19 ] Over 90% of patients with radiculopathy have symptoms in an L5 or S1 distribution.[ 20 ] MRI should be considered in patients with radiculopathy symptoms who do not responded to conservative management consisting of pain control, medical management and physical therapy after 4–6 weeks of symptom onset [ Figure 1 ]. Alternatively, if motor weakness or muscle atrophy accompanies radiculopathy symptoms, emergent neurosurgical evaluation, and MRI should be obtained.

R ADICULOPATHY AFTER M ICRODISKECTOMY

Within the first 6 months after microdiskectomy for the treatment of radiculopathy symptoms, postoperative granulation tissue can manifest clinically with recurrent or residual symptoms. Recurrent or residual disk herniations can also occur.[ 19 ] The clinical symptoms of residual or recurrent disk herniation and postoperative scarring may be identical. MRI of the lumbar spine with and without gadolinium can be useful in differentiating postoperative granulation tissue from recurrent or residual disk herniations.[ 21 22 23 ] Granulation tissue tends to enhance homogenously, [ Figure 2a ] whereas herniated nucleus pulposis demonstrate peripheral enhancement [ Figure 2b ]. In addition, nerve roots may become damaged during surgery and enhance after gadolinium administration [ Figure 2b ].[ 24 ] While useful in the postoperative period, no consensus criteria have been published regarding the length of time after surgery in which administration of gadolinium is necessary. In our institution, gadolinium is used for patients who have had microdiskectomy within the past 2 years. Physicians should consult their local radiologists for recommendations on usage of gadolinium for patients who need postoperative imaging.

L UMBAR S PINAL S TENOSIS

Lumbar spinal stenosis is an anatomic condition that commonly affects patients over the age of 60 years. Degenerative lumbar spinal stenosis is caused by decreased space for neural and vascular elements in the lumbar canal secondary to degenerative arthritic lumbar changes.[ 25 ] Spinal stenosis can occur as a congenital-developmental problem with diminutive caliber of the spinal canal but is usually an acquired condition due to disk bulges, herniations, facet hypertrophy, and ligamentum flavum redundancy [ Figure 3 ]. Patients with lumbar canal stenosis can present with buttock or lower extremity pain, radiculopathy, or neurogenic claudication. Neurogenic claudication is defined as radiculopathy or pain and weakness in one or both lower extremities that worsen with walking and may be relieved with sitting or bending forward.[ 26 27 ] MRI without gadolinium is considered the best imaging modality for diagnosing spinal stenosis.[ 27 28 29 ] Specific measurements of spinal canal size on radiological imaging have not been shown to correlate with clinical symptoms of spinal canal stenosis. However, a cross-sectional area of the dural sac of <110 mm 2 on MRI with can be useful in decision making for patients with clinically suspected lumbar stenosis.[ 25 ]

C AUDA E QUINA S YNDROME

Cauda equine syndrome (CES) results from dysfunction of the sacral and lumbar nerve roots resulting in motor impairment of the bladder, bowel, sexual function, and perineal numbness. The patients can present with low back pain with or without radiculopathy, lower extremity weakness or sensory changes, or absent reflexes. The most common symptom of CES is low back pain.[ 30 ] A prospective cohort study by Bell et al., recommends urgent unenhanced lumbar MRI in all patients with new-onset urinary symptoms with low back pain or sciatica.[ 31 ] The most common cause of CES is lumbar disc herniation at the L4-5 or L5-S1 levels, but can also occur secondary to trauma, metastatic disease or spinal hemorrhage [ Figure 4 ]. In patients who are unable to undergo MRI, myelography can be used as an alternative.[ 18 ]

I NFECTION

Spinal infection is usually secondary to a primary source elsewhere in the body. Infection can spread to the spine hematogenously through direct adjacent infection as a complication of recent surgery or spinal procedure, intravenous drug use, or penetrating trauma. Symptoms of spinal infection are nonspecific. Patients often complain of low back pain that is not relieved with analgesics. Fever is not consistently present. Constitutional symptoms such as chills, night sweats, and weight loss may not be consistently present, but raise suspicion for infection when present.[ 32 ] White blood cell count may be normal, while erythrocyte sedimentation rate and C-reactive protein are usually, but not always, elevated.[ 32 33 ] The lumbar spine is most commonly affected, followed by the thoracic spine and the cervical spine.[ 34 ] Pyogenic discitis osteomyelitis most commonly involves one lumbar segment, beginning in the anterior portion of the endplates of adjacent vertebral bodies and the intervertebral disk. MRI with and without gadolinium is the preferred imaging study to diagnose and localize spinal infection because of its high sensitivity and specificity.[ 34 35 36 37 38 ] T1-weighted images display low signal intensity along the endplate with loss of definition of the cortex with corresponding high signal intensity of T2 and short tau inversion recovery (STIR) images [ Figure 5a ]. The disk space usually demonstrates fluid like signal intensity on all pulse sequences.[ 36 ] Epidural and paraspinal abscess develops later in disease course and are characterized by peripheral enhancing fluid collections on MRI [ Figure 5b ].

Modic Type 1 degenerative changes can mimic early discitis osteomyelitis. Type 1 degenerative change is defined edema such as signal on fluid-sensitive sequences with enhancement of the vertebral body endplates and disk [ Figure 6 ]. However, these imaging features can occur both in Type 1 changes and discitis osteomyelitis. Aggressive imaging features such as endplate destruction can also occur in both scenarios. If the fluid signal in the disk or soft tissue or epidural abscess are present, infectious etiology rather than Type 1 degenerative changes should be favored.[ 39 ] Correlation with the patient history for risk factors, spinal infection, and us of inflammatory markers is essential in differentiating imaging findings in infection from Modic 1 changes. Serial follow-up MRI examinations may be useful in distinguishing the infection from degenerative changes and monitoring therapeutic responses.

Atypical infections, such as tuberculosis and fungal infections, have a different appearance on imaging than most typical bacterial infections. Mycobacterial and fungal pathogens frequently involve the vertebral bodies, but initially spare the intervertebral disks. This type of infection spreads beneath the anterior and posterior longitudinal ligaments leaving intervertebral disks unaffected until late in the disease course [ Figure 7 ].[ 40 ]

M ALIGNANCY

Although a history of malignancy is the strongest risk factor for pain from bone metastasis, <1% of patients in a primary care center have malignancy as the etiology for low back pain.[ 41 ] Other risk factors such as insidious onset, age >50, and failure to improve with conservative management have high false positive rates. Among solid cancers, metastatic disease to the spine is most commonly from breast, prostate, lung, thyroid, and renal cancers. Around 60% of patients with multiple myeloma present with skeletal lytic lesions.

The osseous spinal metastatic disease most often occurs with pain, and a specific complaint of sudden severe pain should raise concern for pathologic fracture. The spine is the third most common site for metastatic disease to manifest and is the most common site for the osseous metastatic disease.[ 42 43 ] Osseous metastasis most frequently involves the thoracic spine. Metastatic lesions can occur within the bone, the epidural space, the intradural extramedullary space (i.e., leptomeningeal carcinomatosis), or intramedullary (within the parenchyma of the spinal cord).

Spinal X-ray is relatively insensitive for the detection of bone metastases to the spine, with false negative results approaching 40%.[ 44 ]

Nuclear medicine bone scans are the standard for initial screening for skeletal metastasis, but the results should be correlated with CT or MRI scans because of a lack of specificity.[ 45 ] FDG-PET scans detect increased glucose metabolism, when combined with CT have a reported sensitivity of 74% and 98% respectively.[ 46 ]

CT provides excellent spatial resolution and can demonstrate sclerotic or lytic changes in the marrow space or cortex, however MRI with and without gadolinium is significantly superior to CT for detection of osseous metastases with higher sensitivity and similar specificity.[ 46 ] MRI is also superior for tumor characterization, allowing evaluation of both bone and soft tissue components that may involve the spinal cord and nerve roots [ Figure 8 ]. The combination of T1 hypointensity and STIR hyperintensity has been shown to be the most useful in the detection of metastatic lesions and in discrimination of malignant from benign bone changes. The MRI appearance of metastatic lesions depends on the nature of the bone replacement or destruction. Lytic lesions are typically hypointense on T1-weighted images and exhibit diffuse enhancement. Blastic metastatic lesions are typically hypointense on T1 and T2-weighted pulse sequences. Mixed lytic and sclerotic lesions will have features of both.[ 46 ]

S PINAL H EMORRHAGE

Spinal hematomas should be considered in patients with signs of acute or progressive paraparesis, paresthesia or bowel, and bladder incontinence.[ 47 ] Intraspinal hematomas can occur in the setting of trauma or recent procedure, secondary to anticoagulation, or can occur spontaneously. MRI without gadolinium is considered the study of choice for diagnosis for diagnosis.[ 48 49 ] Intraspinal hematomas can occur in the epidural space (epidural hematomas [EDH]) [ Figure 9 ], subdural space (subdural hematomas [SDH]), subarachnoid space or within the spinal cord. The location of intraspinal hematoma can be determined by the location of signal changes and the effect of the hematoma on adjacent structures. SDH are classified if blood products do not displace epidural fatty tissue. EDH can be suspected if epidural fat is displaced, and if there is displacement of the dura toward the spinal canal. A subarachnoid hemorrhage will be in an extramedullary intradural location.[ 50 ]

O STEOPOROSIS

Vertebral fractures secondary to osteoporosis are common, affecting 30 million American women and 14 million American men.[ 51 ] Vertebral fractures are associated with lower quality of life. Risk factors for osteoporotic fractures include increasing age, female gender, and steroid use. In a large study in Europe, the prevalence of osteoporotic fractures ranged from 10% to 24%.[ 52 ] Many vertebral fractures are asymptomatic; however, even asymptomatic fractures can have significant consequences because of the increased risk of future fractures.[ 53 54 55 ] Vertebral fractures may present with spinal pain that is worse with walking or standing and relieved by lying flat but are difficult to diagnose due to the nonspecific nature of such symptoms. Only one in four vertebral fractures is clinically recognized.[ 56 ] When there is concern for osteoporotic fracture, noncontrast CT is recommended [ Figure 10 ].[ 18 ]

A NKYLOSING S PONDYLITIS

Ankylosing spondylitis (AS) most commonly occurs in men under the age of 40 who present with back pain and morning stiffness that improves with exercise. Systemic disease manifestations such as uveitis and iritis may also be present. No comprehensive studies have been conducted regarding the use of MRI in the management of inflammatory spondyloarthropathies.[ 57 ] Plain radiography is used routinely for the initial evaluation of patients with AS, while MRI is used for subsequent evaluations.[ 57 58 59 ] MRI can show signal changes at the corners of the vertebral bodies, known as Romanus lesions or “shiny corners.” [ Figure 11 ]. Sacroiliitis can also be seen on MRI and CT and can be an isolated cause of LBP. MRI has a sensitivity of 25%–85% with a specificity of 90%–100% for the evaluation of AS.[ 48 49 51 ] MRI has also been used to assess treatment response with anti-TNF factor therapy in patients with AS.[ 57 ]

S UMMARY

Routine acute LBP is usually a benign, self-limiting condition that does not warrant evaluation with any imaging modality. Advanced imaging modalities such as CT and MRI can provide useful clinical information if used correctly in patients with radiculopathy that unresponsive to conservative management, myelopathy, neurogenic claudication, or patients with “red flag” symptoms. A thorough history and physical exam is essential to identifying patients who would most benefit from advanced imaging. Plain films are insensitive to many pathologies. Noncontrast CT is the initial study of choice if a fracture of the spine is suspected. MRI is the gold standard diagnostic imaging modality for many disease states associated with LBP, with use of intravenous gadolinium contrast reserved for patients in whom infection, malignancy, or postoperative sequelae are suspected. In patients who cannot safely undergo MRI, CT with or without myelography can be considered as a less sensitive alternative diagnostic imaging tool.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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