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Disorders of the Neck and Back

  • James WingerEmail author
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Abstract

Low back pain (LBP) is a heterogeneous condition with high prevalence, high morbidity, and large economic burden. According to the 2010 Global Burden of Disease Study, low back pain ranked highest among 291 studied disorders in terms of years lived with disability (YLDs), with a global point prevalence estimated to be 9.4% (95% CI 9.0–9.8). In 2005, direct expenditures for spine problems in the United States were estimated at $85.9 billion, which represented 9% of the total national healthcare expenditures, similar to costs associated with arthritis, cancer, and diabetes, and only exceeded significantly by those for heart disease and stroke. In the United States between 2004 and 2008, it is estimated that over two million episodes of back pain resulting in presentation for emergency care occurred, yielding an incidence rate of 1.39/1000 person-years. In workers 40–65 years of age, back pain costs employers an estimated $7.4 billion/year in lost productive time. Commonly, disorders of the neck and back are self-limiting conditions, which require only judicial use of imaging and rarely more invasive treatments. Many national and international groups have produced high-quality, evidence-based recommendations to aid in the diagnosis and treatment of low back pain.

Keywords

Back pain Nerve root Cervical spondylotic myelopathy Roland Morris Disability Questionnaire Cervical radiculopathy 

Disorders of the Back

Low Back Pain (LBP)

General Principles

Definition/Background
Low back pain (LBP) is a heterogeneous condition with high prevalence, high morbidity, and large economic burden. According to the 2010 Global Burden of Disease Study, low back pain ranked highest among 291 studied disorders in terms of years lived with disability (YLDs), with a global point prevalence estimated to be 9.4% (95% CI 9.0–9.8) [1]. In 2005, direct expenditures for spine problems in the United States were estimated at $85.9 billion, which represented 9% of the total national healthcare expenditures, similar to costs associated with arthritis, cancer, and diabetes, and only exceeded significantly by those for heart disease and stroke [2]. In the United States between 2004 and 2008, it is estimated that over two million episodes of back pain resulting in presentation for emergency care occurred, yielding an incidence rate of 1.39/1,000 person-years [3]. In workers 40–65 years of age, back pain costs employers an estimated $7.4 billion/year in lost productive time [4]. Commonly, disorders of the neck and back are self-limiting conditions, which require only judicial use of imaging and rarely more invasive treatments. Many national and international groups have produced high-quality, evidence-based recommendations to aid in the diagnosis and treatment of low back pain (Table 1) [5].
Table 1

2007 recommendations on the diagnosis and treatment of low back pain from the American College of Physicians and the American Pain Society

1. Patients should be classified at initial presentation into the following groups: Nonspecific low back pain, back pain potentially associated with radiculopathy or spinal stenosis, or back pain potentially associated with another specific spinal cause. The history should include assessment of psychosocial risk factors that predict the risk for chronic disabling back pain

2. Clinicians should not routinely order imaging or other diagnostic testing in patients with nonspecific back pain

3. Diagnostic imaging and testing should be pursued when severe or progressive neurological deficits are present or when severe underlying conditions are suspected

4. Patients suspected to have either radiculopathy or spinal stenosis should be evaluated with MRI or CT only if potential candidates for surgery or epidural steroid injection

5. Clinicians should provide patients’ educational materials regarding the course and prognosis of back pain, advice to remain active, and self-care options

6. For most patients, the first-line medication options are acetaminophen or nonsteroidal anti-inflammatory drugs

7. Clinicians should consider the addition of nonpharmacologic therapy with proven benefits in those not initially improving. For acute low back pain, spinal manipulation; for chronic or subacute low back pain, intensive interdisciplinary rehabilitation, exercise therapy, yoga, acupuncture, massage therapy, spinal manipulation, cognitive-behavioral therapy, or progressive relaxation

Epidemiology

A 2002 survey in the United States indicated that low back pain, defined as posterior trunk pain between the costal margins and inferior gluteal folds, was present for at least 1 day in the last 3 months in 26.4% of respondents, with men and women exhibiting similar responses. Prevalence rates were reported highest among Native Americans and lowest among Asian Americans. Increasing income and higher education levels had moderating effects on reported back pain [6]. Throughout the adult life cycle, prevalence rates increase until the 60–65 year age group and then again decline, with the peak incidence of LBP in the third decade of life [7]. Commonly reported factors associated with LBP include anxiety, depression, job dissatisfaction, low levels of social support, low educational status, poor coping skills, ongoing litigation, smoking, and obesity [8]. While the incidence of LBP is increasing, as are its associated medical costs, no commensurate improvements are seen in health status [2].

Progression to chronic LBP that lasts more than 6 weeks is a costly complication, both in terms of medical expenditures and work absences. In those experiencing activity-limiting pain, most will experience recurrent episodes [7], and up to 40% of those with initial back pain episodes will experience pain chronically [9]. Psychosocial factors (depression, anxiety, coping mechanisms, attitudes, stress, and job satisfaction) better predict the transition from acute to chronic back pain than do patient-specific anatomic factors [8].

The majority of the societal morbidity associated with LBP is accounted for by disability. Disability 1 year after initial lumbosacral injury has been shown to be predicted by injury severity, specialty of the first healthcare provider seen after injury, worker-reported physical disability, number of pain sites, “very hectic” job, no offer of accommodation, and previous injury involving a month or more off of work. These factors produce a model predicting disability with a 0.88 (95% CI 0.86–0.90) area under the receiver operating characteristic (ROC) curve [10].

Natural History

LBP is frequently described as a self-limiting condition in that initial episodes resolve in 90% of individuals within 3 months of onset [9]. Pooled data analysis indicates that the greatest improvement occurs in the first 6 weeks following initial injury with slower improvement through 52 weeks. However, LBP has a high propensity for recurrence and persistence, and levels of pain, disability, and work absence remain mostly constant after 90 days. A 2008 study indicated that in a cohort of nearly 1,000 patients, more than half of those initially absent from work had returned by 14 days and 83% by 3 months; nearly 30% had persistent pain at 12 months’ time [9]. Many patients experience at least one recurrence in the first 12 months following a low back pain episode with a prior episode of LBP being the only strong predictor of future recurrence [11].

Anatomic sites of acute lumbosacral pain vary and may include paraspinal musculature, collagenous structures (tendon and ligament), intervertebral disk, annulus fibrosus, facet joints, central canal stenosis, spinal nerve roots, and the vasculature.

Clinical Presentation

The experience of many individuals with LBP is that of pain and dysfunction that gradually resolve over several days and allow return to the usual activities of daily living [9]. Most individuals with an episode of LBP will not present to medical attention.

History

Focused history in a patient presenting with LBP will include onset of symptoms, location of pain, timing of pain, interventions that provide palliation or provocation, and any associated symptoms. Assessment for signs suggesting neurological involvement, such as radiation of pain, weakness, numbness, sensory changes, or bowel and bladder dysfunction, is likewise important. Description of any previous episodes of back pain should be elicited during the interview, as well as any current or pertinent past medical history. Interview of a patient presenting with low back pain should pay particular attention to established risk factors for back pain such as known trauma, previous low back pain, missed work, occupational mechanism, and preexisting mood disorder [12].

In addition to standard interviewing approaches, certain additional queries in individuals with low back pain are aimed at identifying neurosurgical emergency, vertebral fracture, or malignancy. A retrospective study of 206 patients with spinal cord or cauda equina compression noted that the presence of bowel and bladder dysfunction as well as saddle sensory disturbance yielded a specificity of 0.92 and a likelihood ratio of 3.46 of such compression [13]. Interestingly, this same study noted that these symptoms showed stronger association with MRI diagnosis than did physical examination of the lower extremities, even while only marginally raising the clinical suspicion of neurological compression. A 2013 study evaluating the benefit of screening questions addressing the presence of malignancy indicated that only a prior history of malignancy is informative [14]. The same study also found that prolonged corticosteroid use, older age, and trauma increased the pretest probability of spinal fracture by 15–43% when present individually and greater when present in combination. Thus, there is relatively little evidence favoring reliance on the so-called “red flag” symptoms to trigger changes in management.

Physical Exam

Examination of the patient with back pain is attentive to the presence and extent of signs indicating neurological involvement. Observation of the patient’s gait, stance, and posture (absence or alteration of normal lordosis or kyphosis) may provide diagnostic clues. Inspection while attending to patient modesty should include the entire back and posterior pelvis but also the upper and lower extremities. The sequelae of trauma may present as disfigurement, edema, or ecchymosis. Asymmetry and muscle wasting may indicate chronic motor neuropathy. Palpation of bony and other landmarks may assist in the localization of a primary pain source. The spinal range of motion in coronal, sagittal, and axial planes may be useful as an indicator of which movement types trigger a patient’s pain; however, this specific assessment is noted to be highly examiner dependent.

A neurologic exam is performed on all patients and should include both upper and lower extremities (Table 2). Manual muscle testing should focus on nerve root myotome testing rather than on specific individual muscles, and strength should be scored with the standard 0–5 scale. Testing of nerve root strength may be assessed as follows: single-leg rising from a chair without the use of hands (quadriceps/L4), heel walking (tibialis anterior/L5), and toe walking (gastrocnemius/S1). The examiner must be aware that deficits in balance or preexisting weakness may affect motor strength testing results. Assessment of pinprick and light touch sensation should be compared to the unaffected contralateral side. Numbness should be specified by dermatomal distribution and may include examination of the perineum and sacral distributions. Evaluation of vibration and position sense may be useful if central processes are included in the differential diagnosis. Signs of upper motor neuron (UMN) dysfunction, such as Hoffmann’s reflex, a positive Babinski’s sign, or hyperreflexia, may suggest etiology for lower motor neuron dysfunction. Pertinent reflexes include the knee jerk (L4), hamstring reflex (L5, S1), and ankle jerk (S1), as graded on the standard 0–4 scale. Depending on the extent of neurological manifestations, assessment of perineal sensation and anal sphincter tone may be appropriate.
Table 2

Strength, sensation, and deep tendon reflexes associated with the commonly impinged nerve roots

Nerve root

Strength testing

Sensory innervation

Deep tendon reflexes

C5

Shoulder abduction

Lateral arm

Biceps (C5, C6)

C6

Elbow flexion, wrist extension

Lateral forearm

Brachioradialis

C7

Elbow extension, wrist flexion

Middle of the hand dorsum

Triceps

C8

Finger flexion

Medial forearm

T1

Finger abduction

Medial arm

L3

Hip flexion

Distal upper leg

L4

Knee extension

Anterior knee

Knee jerk (patellar)

L5

Ankle dorsiflexion (heel walking)

Dorsum of the foot

Hamstring reflex (L5, S1)

S1

Ankle plantar flexion (toe walking)

Lateral foot

Ankle jerk (Achilles)

Nerve tension tests such as the straight-leg raise (SLR) and seated slump test (SST) may suggest neural impingement but are positive in most symptomatic individuals with and thus have a poor positive predictive value when applied to all patients with low back pain. In the SST, the patient is seated on the edge of the examination table. With the hands clasped behind the back and neck flexed with the upper body “slumped” forward, the examiner passively extends the knee. A positive finding is reproduction and radiation of the patient’s pain beyond the knee. Having the patient extend his or her neck, thus relieving neural tension and lessening or relieving the pain, may provide confirmation of this finding. The SLR is performed with the patient supine and the ipsilateral hip flexed to 90° while the examiner passively extends the ipsilateral knee. A positive test is reproduction and radiation of the patient’s pain prior to 60° of knee extension and further relief of such pain with knee flexion. This maneuver may be modified by Lasègue’s sign: dorsiflexion of the ipsilateral ankle increasing neural tension and thus worsening the pain response. The femoral stretch test (FST) for upper (L2, L3, L4) lumbar nerve root impingement is performed with the patient prone as the examiner passively and slowly flexes the ipsilateral knee. Reproduction of the patient’s typical lower extremity pain constitutes a positive test. The crossed SLR (cSLR) and crossed FST (cFST) are performed on the lower extremity contralateral to a patient’s typical radiating pain.

The cSLR and cFST are poorly sensitive but highly (>90%) specific [15]. Thus, neural tension tests may be better applied only to those with presenting symptoms already suggestive of radiculopathy.

In 2011, Suri et al. evaluated the accuracy of physical exam maneuvers for the diagnosis of midlumbar (L2, L3, L4) and low lumbar (L5, S1) nerve root impingement. The study compared standardized, expert-level examinations to MRI findings in patients presenting to a physiatry spine practice with acute or subacute symptoms suggestive of nerve root impingement. Exam maneuvers testing positive that either increased the likelihood ratio >4.0 or exhibited 100% specificity for midlumbar nerve root impingement were FST, cFST, sit-to-stand test, medial ankle sensation, and patellar reflex assessment. Achilles reflex testing was the only exam maneuver in which a positive test either increased the likelihood ratio >5.0 (+LR 7.1) [15].

Further examination should include the hips and sacroiliac joints. Range of motion of the femoroacetabular joints should be assessed along with the response to the loading of the acetabular labra. The acronymically named FABER test, also known as Patrick’s test, stresses the SI joint by flexing, abducting, and externally rotating the contralateral hip while applying posterior pressure to the ipsilateral anterior pelvis and contralateral knee. A positive response is reproduced pain in the contralateral SI joint.

Given the contribution of psychosocial issues to acute and chronic low back pain, assessment of biopsychosocial stressors should be performed. Minimally, screening for common mood disorders such as anxiety and depression should be done. The presence of nonorganic signs or nonanatomic pain distributions does not exclude orthopedic pain generators but may indicate a need for further psychiatric workup.

It is estimated that a brief physical examination and neurological examination of the L4, L5, and S1 dermatomes, myotomes, and deep tendon reflexes should be sufficient to identify 99% of potentially serious spinal pathology [16].

Radiographic and Laboratory Diagnosis

There has been much studied and written about the utilization of imaging strategies as applied to back pain. Published recommendations discourage imaging in the first 4 weeks after presentation [17, 18]. In a 2007 clinical guideline paper, the American College of Physicians and the American Pain Society wrote: “Clinicians should not routinely obtain imaging or other diagnostic tests in patients with nonspecific low back pain [5].” Supporting these recommendations, a 2009 random effects meta-analysis of 1,806 patients evaluated the effect of immediate lumbar imaging on clinical outcomes at 3 and 6 months’ time when compared to usual care without imaging; no differences were found with regard to pain or function levels at the specified time points [18]. Risks of unnecessary imaging include radiation exposure (CT, roentgenography), identification of abnormal tissues with unknown relation to a patient’s pain source, diminished self-perceived health, and unnecessary healthcare utilization [17].

Plain-film radiography is best used as an initial evaluation only when vertebral compression fracture is of utmost concern, such as those with osteoporosis or with chronic steroid use. When appropriate, plain-film radiography of the spine should include standing anteroposterior and lateral view of the lumbar spine. In adolescent athletes in whom spondylolisthesis is considered, oblique views of the lumbosacral spine should be obtained. European guidelines actively discourage the use of plain-film radiography and MRI for nonspecific back pain unless in the context of referral for a second opinion [19].

Advanced imaging may play an important role in the evaluation of a patient when severe (urinary retention, saddle anesthesia) or progressive neurologic deficits are present (Fig. 1) or when high-morbidity conditions such as metastatic cancer, vertebral infection, or the cauda equina syndrome are suspected [5]. Magnetic resonance imaging is generally preferred over CT due to the lack of ionizing radiation and better visualization of soft tissues and the spinal canal. In patients with signs and symptoms suggestive of nerve root compression or spinal stenosis, evaluation with MRI or CT should only be done in individuals who are potential candidates for surgery or image-guided epidural steroid injection [5].
Fig. 1

Imaging of the pathologic spine. (a) T2-weighted sagittal MRI image of the lumbar spine of a 64-year-old man reveals multilevel spondylosis with disk pathology including protrusion and extrusion with migration at levels L3–L4, L4–L5, and L5–S1. (b) Plain-film x-ray image of lateral cervical spine in an 84-year-old woman shows extensive and widespread spondylosis and osteoarthritis with anterior bridging osteophytes and ossification of the anterior longitudinal ligament and moderate to severe disk degeneration. (c) T2-weighted axial MRI image of the lumbar spine of a 22-year-old man at the L5–S1 level demonstrates right foraminal disk protrusion and disk bulge, causing mild central canal stenosis, severe right-sided neuroforaminal narrowing, and moderate left-sided neuroforaminal narrowing with mild bilateral facet hypertrophy

Radiographic abnormalities are common in the spine and show poor correlation with patients’ presenting pains [20]. A 2000 study of 408 patients demonstrated no significant associations between segmental distribution of symptoms and the presence of anatomic impairment, while only severe nerve compression and disk extrusion were shown to be strongly predictive (OR 2.72 and 3.34) of pain present below the knee [21].

Differential Diagnosis

Nonspecific Low Back Pain

It is theorized that the majority of acute low back pain has paraspinal anatomic structures as a pain generator. Paraspinal musculature, spinal ligaments, and annulus fibrosis of the intervertebral disk are all poorly imaged and may be sites of injury that account for the most common types of low back pain [17].

Osteoarthritis

Degenerative osteoarthritis of the axial spine is estimated to be present in 40–85% of individuals [21], and arthritis in general is a leading cause of disability and decreased quality of life. Spondylosis (lumbar spine degeneration) has been defined as intervertebral disk degeneration and same vertebral-level osteophytosis. As in other joints, spinal arthritis is characterized by changes to the articular cartilage and subchondral bone, inflammatory response of the synovium, and inappropriate bone and cartilage overgrowth. Radiographic features of spondylosis include vertebral osteophytosis, disk space narrowing, and facet joint osteoarthritis. Recent longitudinal studies with a large number of patients have highlighted the discordance between radiographic findings and patient symptoms [21].

Intervertebral Disk Herniation

Progressive failure of the successive layers of the annulus fibrosus is responsible for the ultimate failure of the structure of the intervertebral disk. Gradual desiccation of nuclear material results in a centrifugal disorganization of collagenous layers in the inner and outer annuli. This disorganized tissue cracks and fissures, eventually resulting in channels that permit herniation of the nuclear material through the annulus.

Disk herniation occurs typically in a posterior (paramedian) or posterolateral direction, these being the weakest areas of the disk. Depending on the anatomic location of the disk disfigurement, resultant symptoms may border on radiculopathy (posterolateral) to frank myelopathy or neurogenic claudication (paramedian). Disk disfigurement may range from disk bulge to herniation, protrusion, and extrusion [22].

The hallmark of disk herniation presentation is radiating pain. While the outer layer of the annulus fibrosus is poorly innervated, like other chronically degenerative collagenous tissues, the pathologic outer annuli exhibit neoinnervation that show positive staining for substance P, which has been associated with pain generation [22]. Paresthesias and numbness may be present and with prolonged symptoms weakness may occur in the distal musculature from lower motor neuron compromise.

Diagnosis is commonly clinical, based on a combination of reported radicular pain in a dermatomal distribution, neuropathic signs, and positive nerve-tension testing findings. As up to 30% of asymptomatic individuals have radiographic evidence of lumbar disk pathology, radiographic study is not commonly indicated without severe or rapidly progressive neuropathic symptoms [23].

Spinal Stenosis

Degenerative lumbar spinal stenosis describes the effects of degenerative changes in the spinal canal on the vascular and neural elements of the lumbar spine [24]. Symptoms vary and may include gluteal or lower extremity pain that may occur with or without back pain, especially when seen in older patients. Walking and upright exercise typically worsen symptoms, and patients may relieve symptoms with forward flexion or recumbent posture. As in other syndromes mediated by degeneration, symptoms are slowly progressive. While not supported by extant literature, certain exam findings may be associated with the diagnosis of spinal stenosis: the Romberg test, thigh pain exacerbated by extension, sensorimotor deficits, leg cramps, and abnormal Achilles tendon reflexes all may be present. Prognosis may only be favorable in up to one half of patients, with few treatments significantly altering the course of the disease. If needed for diagnostic or interventional purposes, MRI or CT myelogram are the preferred imaging modalities.

Osteoporosis

Osteoporosis is estimated to affect up to 30% of all women over the age of 65. Associated fractures occur in up to 50% of all affected individuals, leading to profound morbidity and healthcare resource utilization. The United States Preventive Services Task Force currently recommends screening via dual-energy x-ray absorptiometry (DEXA) in women with increased fracture risk aged 60–64 and all women aged greater than 65 [25]. In addition to age and sex, risk factors include low BMI, personal history of fracture, Caucasian or Asian race, > two alcoholic drinks daily, caffeine and tobacco use, history of falls, low level of physical activity, low calcium and vitamin D intake, and use of certain predisposing medications. Initial treatment includes fall prevention education, intake of calcium >1,200 mg/day, intake of vitamin D >800 IU/day, and treatment with bisphosphonate osteoclast inhibitor medication. Compression fractures of the vertebra are the most common type of osteoporotic fracture and may be painful; symptoms usually resolve over the course of 3–4 months. Up to 4% of patients presenting to primary care offices with back pain will have a vertebral compression fracture [14]. Patients with vertebral compression fractures usually do not present with pain radiation, as there typically is no neural compromise. Plain-film radiography may indicate a loss of vertebral height associated with compression fracture, and diagnosis of low-impact fractures in susceptible individuals should prompt further investigation. Currently, there are no serum biochemical markers used to aid in diagnosis [25].

Neoplasia

Fewer than 1% of individuals presenting to primary care offices with back pain will be diagnosed with a malignancy [14], and the spine is a more common site of metastasis than primary tumor. Risk factors for spinal malignancy include age >50 years, history of malignancy, and recent unintended weight loss. Symptoms include unrelenting pain that is not improved with rest and may be worse at night. Initial evaluation may include plain-film radiography enhanced by the erythrocyte sedimentation rate.

Symptomatic secondary metastases are estimated to occur in approximately 10% of all cancer patients, and cadaveric studies find 30–90% prevalence of spinal metastases [26]. Spinal metastases are most likely to originate from the breast, lung, prostate, or hematopoietic system and may arise via hematogenous spread, local extension via lymphatics, or perineurium or extension through the intervertebral foramina.

Primary spinal tumors are rare, affecting 2.5–8.5/100,000 patients yearly [27]. Multiple myeloma is a malignant clonal proliferation of plasma cells characterized by the presence of these cells in the bone marrow and monoclonal immunoglobulins in the serum and/or urine. Rarely, a solitary plasmacytoma may be the only manifestation of disease and may be present in the vertebral column. These tumors commonly present with spinal cord compression; thus, serum and urine protein electrophoresis should be performed in all patients with pathological vertebral fractures in which primary malignancy is not evident. Lymphomas may arise in the bones or compress the spinal cord via invasion of the epidural space.

Facet Syndrome

The lumbar zygapophyseal joint is a commonly cited source of spinal pain; dysfunction may be associated with unilateral or bilateral pain radiating to one or both buttocks, groin, and thighs but not proceeding below the knee. Pathological degeneration of the synovial joint may be noted on CT evaluation, and thus intra-articular anesthetic injection has long been a treatment for this condition. However, as with many other areas of degeneration within the axial skeleton, there is incomplete correlation between radiographic findings and patients’ reports of pain [28]. Thus, today diagnostic anesthetic block of the small nerve fibers innervating the facet joints (medial branch block or MBB) is considered a gold standard for lumbar facet joint syndrome diagnosis. Due to the fleeting response to MBB seen in treated patients, a longer-lived treatment is now utilized: lumbar medial branch neurotomy (LMBN). Thermal coagulation at temperatures in excess of 80 °C denature intracellular proteins and produce results that last on average, longer than those achieved with MBB [28]. A 10-year clinical audit noted that among 174 patients treated with LMBN, 68% exhibited good or excellent results.

Ankylosing Spondylitis

Characteristic of the spondyloarthropathies is ankylosing spondylitis (AS). It is an inflammatory arthritis that commonly affects the axial spine with possible extension to peripheral joints, eyes, and bowel. AS exhibits symptoms onset in the late teens, but the delay between the symptom presentation of lumbosacral pain and stiffness and eventual diagnosis averages 8 years [29], primarily due to the difference in distinguishing the symptoms of AS from nonspecific mechanical low back pain in the young active population. While there is limited diagnostic utility in plain-film radiology, MRI has permitted the identification of the inflammatory sequelae of this disease, aided by serum markers of inflammation such as ESR and CRP.

Visceral Diseases

Uncommonly, back pain may be the only presenting concern in a patient with organ system-based disease. Typically, visceral pain referred from intra-abdominal and retroperitoneal organs differs in quality from musculoskeletal pain; however, this difference may be subtle and overlooked.

Dissecting thoracic or abdominal aortic aneurysm is described as “tearing” pain that is acute and severe. This condition is found in up to 4% of those patients over 50 with increased prevalence in smokers and those with diagnosed hypertension and hyperlipidemia. Some patients will have a pulsatile abdominal mass, and presentation may include diaphoresis and signs of impending circulatory failure such as hypotension and tachycardia [30].

Myocardial infarction may present as mid-thoracic pain that radiates to the left arm or axilla. It is most common in those older than 45, with risk factors including family history, hyperlipidemia, hypertension, obesity, and others. Presenting symptom constellation may include diaphoresis, dyspnea, anterior chest heaviness or pain, nausea, vomiting, and a sense of impending doom.

Acute low back pain associated with abdominal pain in a woman of childbearing age may indicate ectopic pregnancy. Back pain is described as part of a classic symptom triad including amenorrhea and vaginal bleeding. Hypovolemic shock may be present in up to 20% of cases, and associated back pain may be located in the L1 and L2 dermatomes of the pelvic organs.

Acute pancreatitis commonly presents with “boring” thoracolumbar pain when the pancreatic duct is obstructed. Patients with acute pancreatitis may have a history of gallstones or binge drinking, and diagnosis is usually achieved with assessment of serum lipase and amylase as well as CT demonstration of glandular inflammation.

Vague back pain that occurs with increasing gastric acidity levels may represent a duodenal ulcer. Inflammation, injury, and ulceration of the mucosal lining of the digestive tract are associated with H. pylori infection, smoking, and alcohol ingestion.

Urological conditions such as nephrolithiasis and urinary tract infection commonly present with varying back pain. Ascending urinary tract infections may exhibit low lumbar pain or perinephric pain from ribs 9–11 on either side of the low thoracic spine if pyelonephritis has developed. Unilateral thoracolumbar pain radiating to the ipsilateral flank and toward the groin may indicate a ureteral stone [30].

Management

Stratified Primary Care Management

Multiple international management recommendations for low back pain recommend stratification of patients into groups based on risk for morbid pathology and risk of progression to chronic back pain. A 2011 study known as STarT Back evaluated this model on the basis of economic and patient-centered metrics when compared to usual care in English general practices [31]. This study included greater than 850 adult patients and evaluated changes in the Roland Morris Disability Questionnaire (RMDQ) at 12 months’ time as well as quality-adjusted life years (QALY) and healthcare costs between stratified and nonstratified groups. Individuals were stratified into one of three groups: “low-risk” patients had one visit and were educated as to the good prognosis and that further treatment was not necessary nor beneficial; the medium-risk group was referred for further physiotherapy; and the high-risk group was referred for “psychologically informed physiotherapy” [31]. The stratified (interventional) group had significantly improved RMDQ scores at 4 and 12 months and 0.039 additional QALYs and cost savings compared to the nonstratified control group. The low-risk group intervention was found to be noninferior to usual care, indicating that the minimum intervention did not lead to worse outcomes than the current best practices. Differences were present between matched risk groups at 4 and 12 months but lost statistical superiority at the latter time point [31].

Another study of stratification in family medicine practice demonstrated similar results. In 2014, Foster published results showing modest improvements in patient overall outcomes, improved use of healthcare resources, and reduced sick certification without increased healthcare costs. Direct patient benefits of stratification intervention included improvements to physical function, fear avoidance beliefs, satisfaction, and work absenteeism. Changes to physician behaviors included decreased NSAID prescription, increased appropriate referral to physical therapy, and fewer sickness certifications [32].

A subsequent 2018 study of 1,700 patients was unable to reproduce these positive findings and demonstrated no improvement in patient function or healthcare utilization with stratified care [33].

Thus, stratified care for low back pain may demonstrate clinical and economic benefits and can be implemented successfully into a family medicine practice. Further research may reveal if certain populations show improved outcomes from stratified care.

Activity

For most patients, especially those with nonspecific low back pain, rapid return to normal activities, including work, are recommended. However, these patients should initially avoid heavy lifting, twisting, and bodily vibration [5].

Bed Rest

The harmful physiological adaptations to organismal inaction are dramatic and well established. The complications of bed rest are myriad. Muscle mass loss may approach 2% daily in the first 3 weeks of enforced rest; this is primarily due to catabolism of muscle proteins by enzymes activated by inactivity. Joint stiffness and loss of capsular compliance begin soon after immobilization. The risk of thromboembolic event, pulmonary atelectasis, and pressure ulcers rise along with inactivity.

When bed rest is prescribed for acute lumbosacral injury, the aforementioned complications are risked. Bed rest in acute low back pain is not associated with either quicker resolution of pain or return to regular activity. Regular activity as tolerated maximizes the return to function and decreases patient pain score report.

Pharmacological
Nonopiate Analgesics

For most patients with low back pain, acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line pharmacological treatment. Acetaminophen is recommended by the American Pain Society and American College of Physicians as the initial pharmacological treatment of nonspecific back pain due to its record of safety in other settings of musculoskeletal pain. Acetaminophen carries a low risk of harm; it is not associated with the risk of either gastrointestinal bleeding or myocardial infarction and is relatively well tolerated [34]. Hepatotoxicity may be seen at doses approaching the recommended maximum daily allowance (3 g/day), and so caution must be taken in those patients with preexisting liver conditions or heavy alcohol use.

NSAIDs exert their anti-inflammatory, analgesic, and antipyretic effects via the inhibition of the cyclooxygenase (COX)-2 enzyme. Nonselective NSAIDs (celecoxib) also inhibit COX-1, which is responsible for gastric mucosal protection via prostaglandin production. A review of different NSAID formulations indicates similar efficacy when compared to placebo in acute and chronic back pain and similar intrafamily efficacy. Thus, treatment decisions may rely on side effect profile, prior response to NSAIDs, cost, and dosing schedule. Each member of the class is associated with gastrointestinal and renal adverse effects, including gastrointestinal ulcers, hemorrhage, and perforation, as well as decreased glomerular filtration. A 2006 meta-analysis of 138 individual studies revealed an approximate twofold class-wide risk elevation in myocardial infarction when compared to placebo, except naproxen, which showed no such increased risk. Cardiovascular, gastrointestinal, and renal risks should be taken into account prior to prescribing or recommending NSAIDs for nonspecific low back pain. The long-term use of NSAIDs may be combined with misoprostol, a prostaglandin that decreases the risk of gastrointestinal ulceration, or a proton pump inhibitor [34].

Opiate Receptor Agonists

There exists significant controversy regarding the use of opiate receptor agonist medication in low back pain. Opiate receptors are widely distributed throughout the brain, spinal cord, and intestinal tract and are activated by morphine and its derivatives and homologues. While considered the strongest class of pain relievers, they carry significant potential for dependence and abuse due to their effects on the dopaminergic reward system of the brain. In 2009, the American Pain Society and the American Academy of Pain Medicine published joint guidelines on the use of opioids for chronic noncancer pain to aid practitioners in decisions regarding this class of medication [35]. Primary among these recommendations include time-limited rather than symptom-limited course of medication. Common adverse effects include constipation, nausea, somnolence, and pruritus.

Tramadol is a synthetic agent with weak affinity for the α-opiate receptor. Clinically, it has greater efficacy than NSAIDs and is relatively comparable to weak opiates [35]. Tramadol has similar adverse effect tolerability to acetaminophen-opioid combinations; however, it has been linked to the serotonin syndrome when used in combination with serotonin receptor antagonists.

Skeletal Muscle Relaxants

Medicines known as “skeletal muscle relaxants” are related neither pharmacologically nor structurally. Those commonly used for the relief of musculoskeletal spasticity are baclofen, carisoprodol, cyclobenzaprine, metaxalone, methocarbamol, tizanidine, and orphenadrine. It is unclear if these medications work to relax muscles or if their effects stem mostly from sedation [34]. Medications in this grouping have been shown to demonstrate short-term pain relief for acute low back pain, but no agent has been shown to be more effective than others [36]. These medications carry a high rate of adverse side effects, and sedation commonly limits their use. Several studies have indicated the equivalence of benzodiazepines when compared to skeletal muscle relaxants for acute low back pain, suggesting similar benefit. All medications here referenced may be more effective when combined with an NSAID or acetaminophen [36].

Antidepressants

Certain antidepressants with noradrenergic antagonist activity may have pain-modulating properties independent from their effects on mood disorders. Tricyclic antidepressants (TCAs) such as amitriptyline have long been used in chronic pain conditions, and, in recent years, serotonin and norepinephrine reuptake inhibitors (SNRIs) such as duloxetine, venlafaxine, desvenlafaxine, and others carry similar indications. TCAs show small benefit over placebo for chronic nonspecific pain in some meta-analyses, while SNRIs have shown benefits for certain types of chronic pain. High rates of adverse effects limit the use of these medications and prevent their use as a first-line treatment [36].

Systemic Corticosteroids

While it has been suggested that the inflammatory response associated with extruded intervertebral disk nuclear material may be stemmed with oral corticosteroids, several studies in the setting of lumbar radicular pain have demonstrated no improvement versus placebo. Similarly, despite the euphoric effect achieved by some patients, these medications are also without effect in nonspecific acute low back pain [34].

Disease-Modifying Antirheumatic Drugs (DMARDs)

There is no role for antitumor necrosis factor (TNF)-α biologic therapy in the treatment of nonspecific low back pain [34].

Exercise

Whether done in the home setting or under the guidance of a physical therapist, stretching, and strengthening activities are commonly prescribed for acute nonspecific back pain. A meta-analysis of 11 studies utilizing the McKenzie (directional preference) method indicated significant improvement in pain and disability after 1 week of therapy [37], resulting in a recommendation for usage [strength of recommendation taxonomy (SORT) B]. Evidence suggests that there is a mild benefit for exercise protocols in chronic nonspecific back pain and little to no improvement when compared to other treatments in acute back pain [38].

Back School

Education is commonly utilized in the treatment of low back pain; it is apparent, however, that there is little to no standardization on what constitutes back school curriculum, and thus, these approaches vary widely. A 2016 review analyzed 273 trials that studied the effects of back schools on nonspecific low back pain; four were deemed to be rigorous enough to meet inclusion criteria. Given the paucity of high-quality evidence available, the authors were unable to comment on the efficacy of back schools for acute and subacute nonspecific LBP [39].

Psychological Intervention

Cognitive-behavioral therapy (CBT) is a method of psychotherapy that attempts changing cognitive processes to affect changes in behavior, thought, and emotional responses. CBT has been applied to chronic pain settings with varying results. In the setting of chronic pain, CBT has improved pain experience, positive coping, and social role function when compared to placebo or other treatments [40].

Spinal Manipulation

A 2004 Cochrane meta-analysis concluded that spinal manipulation was superior only to sham treatments and inert interventions. It demonstrated no advantage over “usual care,” analgesic medication, physical therapy, exercise, or back school. Chronic pain applications were found to yield similar results. These results were unaffected by the presence of pain radiation, study quality, manipulator, nor therapy combinations [41].

Acupuncture

A Cochrane review of studies investigating the use of acupuncture in the treatment of low back pain found acupuncture to be effective for pain relief and equivalent to other complementary or conventional treatments. For short-term relief of chronic pain, acupuncture was more effective than sham procedure and placebo. Data regarding the effects on short-term low back pain were inconclusive [42].

Epidural Steroid Injection

The use of epidural steroid injections in the treatment of pain for lumbar radiculopathies as well as spinal stenosis is increasing. A meta-analysis of 38 placebo-controlled trials evaluating the effect of epidural steroid injection in lumbar radiculopathy and spinal stenosis showed brief and nonsustained effects of injection in lumbar radiculopathy that were below predefined set points for clinical significance. There were no effects in spinal stenosis. Neither patient characteristics nor technical factors had an effect on these results [43].

Surgery

Evidence is very clear that there are limited roles for surgery of the spine outside the conditions of sciatica, pseudoclaudication, or spondylolisthesis [44]. Prolonged or worsening neurological symptoms in the setting of diagnosed disk disease unresponsive to or inappropriate for ESI should stimulate referral for surgical evaluation.

Lumbar diskectomy is the most common operation in the United States for reasons related to disk herniation, but there remains poor evidence supporting its use when compared to conservative treatments. Newer treatments in minimally invasive spine surgery (MISS) offer lower perioperative morbidity to patients.

The largest and longest-term comparison between nonsurgical and surgical approaches was published as the 10-year follow-up to the Maine lumbar spine study (n = 400) [44]. Ten years after initial presentation, postsurgical patients were more likely to be satisfied with their current condition when compared to the medically managed patients (71% vs. 56%, P = 0.002), whereas there was insignificant difference between the two groups with regard to improvement in the initial presenting symptom and work and disability status [44].

Chronic Low Back Pain

Low back pain of greater than 6 months duration develops in a small percentage of patients. These conditions carry a very low likelihood of a specific diagnosis, and symptomatic cure is unlikely. Treatment should be supportive, with efforts aimed at improving pain and function. While the mechanisms of initial injury and chronic pain propagation are unclear, it is proposed that these disorders are primarily mechanically induced, and then maladaptive physical and cognitive compensations produce a mechanism for an ongoing pain.

A recent systematic review demonstrated predictors favoring persistent disabling back pain: maladaptive coping behaviors, nonorganic signs, functional impairment, significant comorbidities, and psychiatric comorbidities. Factors such as low level of fear avoidance and functional impairment predict recovery at 1-year time [45].

The transition from acute to subacute to chronic pain appears to be one strongly mediated by psychosocial factors rather than anatomic or disease-based factors. Therefore, interventions attempting to prevent chronicity transformation have utilized psychological approaches.

Disorders of the Neck

Cervical Radiculopathy

General Principles

A common cause of neck pain is impingement of the cervical nerve roots exiting the spine. This is frequently caused by disk pathology, facet joint osteophytes, or degenerative disk disease, further affected by intraneural edema or inflammatory mediators such as substance P. The annual incidence of cervical radiculopathy has been found to be 83 in 100,000 persons [22].

The nomenclature of the cervical nerve roots differs from that elsewhere in the spine. The presence of an eighth cervical nerve root determines that most cervical nerve roots exit the spinal canal superior to their correspondingly named vertebra; the C7 nerve root exits at the level of the C6–C7 intervertebral disk. The exception to this rule is the eighth cervical nerve root, which exits between the C7 and T1 vertebral levels. The most commonly affected nerve root is the C7 root, which is impinged at the level of the C6–C7 intervertebral disk.

Presentation

When compared to chronic spondylosis of the cervical spine, pain associated with radiculopathy is more commonly unilateral [46]. The most common mechanism of acute cervical radiculopathy is that of annular failure of the intervertebral disk resulting in disk deformation or frank extrusion of nuclear material. Chronic radicular symptoms, which may persist in up to two thirds of patients, are more commonly associated with chronic spondylosis, usually characterized by facet joint osteophytosis or disk degeneration [22].

As with lumbar radiculopathy, the clinical presentation is highly dependent on the exact impinged nerve root or roots; however, clinical and symptom overlap does occur. Pain in proximal nerve root distribution is accompanied by distal distribution neuropathy (paresthesias or other sensory dysfunction). Commonly, referred pain from unilateral cervical radiculopathy is vaguely localized to the ipsilateral neck, shoulder, or medial scapular border [46], whereas radicular pain may follow a dermatomal distribution.

On physical examination, pain is usually exacerbated by neck extension as well as neck rotation toward a patient’s symptomatic side, which narrows the neural foramen (Spurling’s sign). Conversely, a patient may find mild relief with neck flexion, shoulder abduction, and scapular retraction. Altered deep tendon reflexes corresponding to the affected nerve root may be present. Upper motor neuron findings such as hyperreflexia, clonus, and Hoffman’s sign should be absent: their presence should stimulate search for myelopathic conditions.

Diagnosis

The differential diagnosis of cervical radiculopathy encompasses pathologies of the neck, shoulder, viscera, and extremities. Thus, trauma, myelopathy, degenerative spondylosis, rotator cuff pathology, myocardial ischemia, zoster, and other conditions should be considered at differential diagnosis [46]. As noted with lumbar radiculopathy, plain-film x-ray is of limited use, given the poor correlation between findings and the patient’s report of symptoms. Similarly, in the absence of certain findings suggesting cancer, myelopathy, or acute pathologies, it is recommended that practitioners delay advanced imaging until after a suitable period of conservative treatment has failed [47]. MRI or CT are best utilized as a confirmatory test of nerve root compromise, in anticipation of referral to spine subspecialist and possible interventional treatment, with limited evidence available to recommend for or against the use of electromyography (EMG) [47].

Management

The prognosis of cervical radiculopathy is optimistic and well described [26, 46]. The majority of patients will improve over time, with 75–90% having no or minimal further sequelae. Management decisions must be made with reference to this high rate of recovery.

The following interventions have insufficient evidence to recommend or discourage their use: medication, physical therapy, traction, cervical manipulation, and cervical collar. Several of these have demonstrated improvement in patients’ symptoms in uncontrolled trials. Cervical manipulation has been rarely associated with emergent vascular and nonvascular complications then requiring definitive surgical treatment [47]. Similar consideration should be used when applying pharmacological treatments to cervical radiculopathy as were discussed with regard to lumbar radiculopathy.

Injection of an anti-inflammatory steroid and anesthetic mixture into the epidural space may provide symptom relief for up to 60% of patients and delay or negate the need for surgery in an additional 25% [47]. Rare but potential complications such as spinal cord damage and death may be considered when developing an interventional treatment plan for those patients with cervical radiculopathy.

Surgical referral is appropriate in individuals who have documented cervical radicular symptoms that are intolerable and resistant to a prolonged (6 weeks) course of conservative treatment.

Acute Cervical Strain

General Principles

The acute cervical strain caused by acceleration-deceleration and subsequent energy transfer to the neck is known as whiplash. It commonly occurs during motor vehicle accidents, but also during sporting activities. It may result in a variety of bony and soft tissue injuries, manifest by myriad symptoms. This constellation is known as whiplash-associated disorders (WAD) [48]. These conditions generally have a positive prognosis, with 87% and 97% cited as having recovered from their injuries at 6 and 12 months; however, this optimism is debated [48].

Presentation

Common symptoms after motor vehicle accident (MVA) are neck pain (88–100%) and headache (54–66%), but also commonly seen are neck stiffness, shoulder pain, arm pain or numbness, and others [48]. As in other injuries of the axial spine, issues surrounding the compensation for injury and work delay clinical improvement. In 2001, Côté reviewed a Canadian study investigating the association between insurance systems and claim-closure and compensation times after WAD. In the no-fault province of Quebec, the median claim-closure time was 30 days and 4.1% of claimants were still compensated at 1 year. In Saskatchewan under the tort system, the median claim-closure time was 433 days and 57% were still compensated at 1 year, implying extra-physiological influences to recovery [49].

Diagnosis

An acute cervical injury in the setting of an appropriate mechanism of injury is suitable for the diagnosis of whiplash-associated disorders. Care must be taken not to overlook other conditions that can be present with cervical and cranial trauma, such as fracture, intracranial hemorrhage, mild traumatic brain injury (mTBI), and others. Typically, diagnostic testing and imaging are only utilized to exclude these other conditions.

Management

Management of whiplash should be multimodal and include an assessment of psychological wellness in accordance with the biopsychosocial model. Patients’ beliefs, coping strategies, locus of control, and disability should also be measured [48]. It has been suggested that active interventions may be more effective in those with WAD. These have been shown to be beneficially long term on pain, global perceived effort, or participation in daily activities [48]. Patients should be educated and reassured regarding the positive prognosis. Active therapy for comorbid mood disorders should be addressed immediately. Return-to-clinic and emergency room visit criteria should be discussed. If applicable, continuing care of mTBI should be provided.

Prognosis

The prognosis of acute whiplash is favorable for most individuals. Age, gender, baseline neck pain, baseline headache, and radicular complaints all have independent influence on recovery. It is well recognized that nonmedical factors may also strongly affect recovery. The above Canadian study further noted that when Saskatchewan changed its insurance systems from tort to no-fault, it achieved a 54% reduction in median time to claim closure [49]. The influence of jurisdiction on recovery is further highlighted by chronic whiplash, which is low in historically no-fault provinces (Québec), less litigious countries (Greece), and where whiplash is not compensated (Lithuania) [49].

Cervical Myelopathy

General Principles

Chronic atraumatic compression of the cervical spinal cord due to spondylosis is the most common cause of spinal cord compression in the world [50]. It is understood that 40–60% of untreated cervical spondylotic myelopathy (CSM) cases will progress with worsening neuropathy, neuroinflammation, and apoptosis. Radiographic evidence of cervical stenosis is insufficient to produce the syndrome, as some patients with significant stenosis never develop myelopathy for reasons that are unclear.

Presentation

The clinical presentation in CSM varies greatly, depending on the site and type of lesion and whether it produces motor or sensory and upper motor neuron or lower motor neuron signs in the upper or lower limbs [50]. Onset is typically between ages 50 and 70, of insidious onset and progressive and unremitting. These characteristics may help distinguish it from other neuropathic syndromes, such as peripheral compression or multiple sclerosis.

Symptoms may include neck and/or upper limb pain, weakness, numbness or loss of sensation in the upper or lower extremities, and bladder symptoms such as incontinence or urinary frequency.

Physical exam may reveal signs consistent with upper motor neuron dysfunction: hyperreflexia and/or clonus, Hoffman’s sign, Babinski’s reflex, multilevel nerve root weakness, sensory loss, or signs of spasticity in the lower limbs [50].

Diagnosis

Plain-film x-ray is commonly obtained in individuals with CSM. With the advent of cross-sectional imaging, however, MRI and intrathecal enhanced CT (CT myelography) have become the studies of choice to evaluate this condition [50], as they are able to aid in the calculation of intracanalar dimensions. The role of EMG is to evaluate for the presence of other conditions that may mimic the findings of CSM, such as peripheral compressive lesions. Cerebrospinal fluid and blood analysis may be used to similarly exclude other neurological conditions [50].

Management

Myelopathy is a progressive disorder and little evidence exists that nonoperative treatment halts or reverses its progress. Thus, nonoperative treatment (intermittent bed rest, the use of collar, anti-inflammatory medication, and discouragement of high-risk activities) is reserved only for asymptomatic patients or those with mild symptoms [50]. Referral or comanagement with a neurologist or neurosurgeon is recommended. For individuals with moderate to severe or rapidly progressive myelopathic symptoms, immediate surgical referral is warranted.

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Copyright information

© Springer International Publisher Switzerland 2020

Authors and Affiliations

  1. 1.Department of Family MedicineLoyola University Chicago Stritch School of MedicineMaywoodUSA

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