Low back pain (LBP) is the leading cause of disability in adults under 45 years of age, the second most common cause of missed work days after upper respiratory conditions, and the fifth most common reason for all visits to a physician. It is the number-one most common pain condition, the second being headaches. Jobs that are thought to increase the risk of low back pain include nursing, construction, factory work, farm work, law enforcement, firefighting, sanitation, sedentary office work, nursery school teaching, and occupational driving. Low back pain is the leading cause of expenditures for workers’ compensation. The economic burden for low back pain to American society is up to $200 billion annually, with one-third of this total occurring as direct medical costs and the remainder from lost productivity. Approximately 5% of low back pain patients account for 75% of these costs. Chronic pain of all types, including low back pain, costs American society up to $635 billion annually in both medical costs and lost productivity.
About 70% to 80% of all people will experience low back pain in their lives. Of these, approximately 70% will resolve in 6 to 12 weeks. Approximately 85% will have recurrences of low back pain. Approximately 7% will go on to have significant chronic pain.
The prevalence of back pain is highest in the age groups of 45 to 64 years old, yet people under 45 experience the most activity limitations. The majority of younger patients are men, while the majority of patients over 60 years old are women. Return-to-work rates for back pain are dismal for pain lasting 6 months or longer. For those out of work for 6 months, the return-to-work rate is 50%, and for those out of work for 1 year, the return-to-work rate is 25%. After 2 years of unemployment due to back pain, the return-to-work rate is nearly zero.
The literature demonstrates a higher prevalence of chronic back pain in those with depression, anxiety, substance abuse, somatization, and personality disorders. Major depression was found in 30% to 65% of chronic low back pain patients compared to the rate of depression in the general population of 5% to 17%. The relationship between obesity and the prevalence of back pain continues to be controversial. One study found that a BMI higher than 30 (obese) increased the risk for chronic low back pain by 20% but that this risk is reduced with exercise. A systematic review involving 56 studies found, at best, a very weak correlation between obesity and low back pain. On the other hand, exercise has been shown to reduce the risk of low back pain regardless of weight, while lack of exercise increases the risk for low back pain. Smoking has been independently linked in some studies to an increased risk of chronic low back pain.
Table 38-1 shows ranks the etiological sources of back pain.
Final Diagnosis in 2374 Chronic Low Back Pain Patients Participating in the National Low Back Pain Study
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Final Diagnosis in 2374 Chronic Low Back Pain Patients Participating in the National Low Back Pain Study
Osteoarthritis root compression
Pain with psychiatric component
HERNIATED NUCLEUS PULPOSUS
In herniated nucleus pulposus (HNP), patients present with low back pain that is typically worsened with increasing pressure on the disc, such as when the patient coughs or sneezes, or strains on the toilet (Valsalva maneuvers). MRIs often show protruded or extruded discs. In more than 95% of cases, HNP occurs at either the L4–5 or L5–S1 levels. Approximately 50% of HNP found on MRIs is asymptomatic. MRIs may show multiple herniations, not all of which have clinical relevance. It is not uncommon to have a poor correlation between patient complaints and MRI findings. In this case, an experienced clinician can formulate diagnoses and treatment planning on the comprehensive collection of data, possibly including electromyography, which may offer additional information.
A recent study measuring in vivo intradiscal pressures allows for comparison of intradiscal pressure with different positions and conditions:
Standing relaxed: defined at 100%.
Lying prone: 20%.
Sitting unsupported: 92%.
Standing and flexing forward: 220%.
Sitting and flexing forward: 166%.
Lifting a 45-lb weight with rounded flexed back: 460%.
Lifting a 45-lb weight with flexed knee: 340%.
Lifting a 45-lb weight with flexed knee and weight close to body: 220%.
Nighttime lying down: 96%.
The preceding list demonstrates that lifting objects the “correct” way reduces intradiscal pressures. Despite this, most disc herniations do not occur from lifting heavy objects. One study found that 62% of all herniated discs have no particular inciting event, with an additional 25% due to activities such as tying shoes or releasing a handbrake on a car. Only 6.5% of herniated discs are due to heavy lifting, 2% are due to light lifting, and 1.3% are due to trauma. Thus, disc herniations occur during routine activities that are generally unavoidable, such as sitting, bending to unplug an appliance, or putting on a winter coat. The most likely reason discs herniate is simply from degenerating discs, as studies have found an inverse relationship between the force required to herniate a nucleus pulposus and the degree of degeneration. The term age-appropriate degeneration can be applied to most patients, and this phenomenon seen on MRI should not warrant excessive concern or invasive procedures. Instead, patients’ complaints and concerns should be met with appropriate treatment, education, and reassurance.
Interestingly, evidence has shown that lifting crates while keeping the crate's center of gravity close to the body but allowing the actual work to be done by the back muscles, rather than the leg muscles, in a therapeutic regimen under supervision can, in fact, benefit back pain sufferers of most etiologies in terms of pain and function. Inclusion of this particular exercise in a therapeutic regimen along with use of a Roman Chair and back extension weight machines do not seem to increase the incidence of HNP.
Whereas the outer annulus of the disc is recognized as “self” by the body's immunological system, the herniated portion of the disc is not recognized, resulting in an immune-mediated inflammatory response to this “foreign body.” This inflammatory process recruits cells, proteins, and fluid that serve to increase the mass effect. A large immunogenic reaction to even a small herniation can cause well-defined radiculopathy, but because this inflammation is not well visualized on MRI, the actual disc pathology may be visually underappreciated. This is often referred to as a “chemical radiculopathy.” Over 4 to 6 weeks, but often up to 6 months, this inflammation subsides, and most patients with an acute herniated disc will improve spontaneously without medical intervention. Improvement involves immunogenic removal of the herniated disc material, potentially leading to resolution of symptoms. Therefore, observation is often appropriate care for acute disc herniations. Patients should be encouraged to stay active during this process.
Some patients experience intense pain that affects their ability to work and enjoy a high quality of life. In these individuals, conservative medical treatments are recommended. They range from nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen to intravenous or oral Prednisone. The latter should be of a moderately high dose and tapered quickly to temper the inflammatory response thought to be responsible for acute pain. Although there are no studies that define effective and appropriate steroid dosing, in our clinic, we typically prescribe Prednisone 60 mg for 2 days followed by 40 mg for 2 days, and finally 20 mg for 2 days. At least anecdotally, this has been shown to be effective and safe for back pain and, particularly, radiculopathy. This seems especially true for a chemical radiculopathy when the MRI is unimpressive. Other clinics have used Medrol dosepaks with reported efficacy for their patients, although the Prednisone taper used by our clinic seems to be more effective. Patients should be warned of the potential side effects from oral steroids, including increased hunger, sleep disturbance if taken near bed time, agitation, psychosis, and increased blood glucose in diabetics. Serious side effects include avascular necrosis, especially of the hip, and glaucoma exacerbation. These can occur with prolonged duration of oral steroids. Our office limits the use of oral Prednisone to a maximum of two 6-day tapering courses. Typically, the efficacy of oral steroids is the greatest within the first 6 weeks of low back pain when inflammation is thought to be maximal.
Great care should be taken in prescribing opioids for long-term use as this may lead to progressive opioid-induced hyperalgesia, escalating opioid dosages due to tolerance, and aberrant behaviors. Studies have also shown that patients prescribed high-dose opioids as initial treatment can lead to increased work days lost, increased physician visits, and increased surgical and interventional procedures without satisfactory relief of pain. Although opioids clearly provide some benefit for acute back pain episodes compared to placebo, there is scant evidence to support their use for chronic back pain. For many patients, a weak opioid agonist with dual functions such as Tramadol or Tapentadol can provide a safe and effective alternative.
Interventional procedures such as epidural steroid injections can be employed to place steroids in the area where the inflammation is believed to be occurring. It has been shown that while both particulate and nonparticulate steroids provide statistical benefit compared to controls, particulate steroids result in better and longer-lasting pain relief. It is often advised to choose a level below the area of herniation where the epidural space is larger as this is thought to minimize complications during the procedure, but there is no evidence to support this. However, the Artery of Adamkiewicz lies above L2, and epidural injection above the L2–3 level increases the risks for spinal cord injury. A small number of patients have this artery at a level lower, so care must be taken to avoid complications, especially with particulate steroids.
Exercise has long been shown to be an important way to treat chronic back pain. However, for acute disc herniation, there is little evidence for its efficacy. Exercise does not accelerate the healing process for an acute herniated disc. It can be expensive for both patients with copays and for insurance companies that, in turn, pass these expenses on to the general public. Along with medications (nonopiates) and ice, observation is an appropriate course of action for an acute herniated disc. Exercise can become beneficial if back pain persists longer than the acute phase, typically 6 weeks or more, with increasing symptoms but with a benign MRI. Systematic reviews almost universally support the efficacy of exercise for chronic low back pain.
Surgery for herniated discs is indicated in a minority of cases. The conditions widely acknowledged to be indications for emergent surgery include bowel or bladder incontinence with accidents that occur generally without the patient being aware during the episode, only to discover its occurrence after the accident. This is in distinction to overflow or stress incontinence when a patient senses leakage while it happens. Other emergent indications include new onset of urinary retention, new sexual dysfunction, cauda equina, or saddle anesthesia. An indication for urgent surgery includes physical exam findings of progressive weakness occurring over the course of weeks. Manual muscle testing and atrophy can be measured at the initial visit and remeasured at a follow-up visit 2 to 3 weeks later. Historical evidence such as progressive difficulty climbing stairs or foot drop can also be helpful in making a decision for surgical referral. Surgery for intractable pain, failure of conservative treatments, and poor quality of life due to pain is elective and dependent on patient choices, keeping in mind that discogenic pain can resolve spontaneously without any intervention. In clinical trials comparing surgical decompression to conservative management for neuropathic low back pain, where all studies demonstrate a benefit for surgery at 6 months, most show no statistically significant benefit after 2 years.
Finally, a note about bed rest as a course of treatment. Studies have shown that bed rest has, at best, a neutral effect, and, at worse, it is detrimental. Patients should, therefore, be encouraged to stay active regardless of treatment course. Extreme physical activity, on the other hand, should be avoided during the first 4 to 6 weeks of herniation.
Table 38-2 lists favorable and unfavorable prognosticators for HNP with nonoperative care.
Prognostic Factors of Positive and Negative Outcomes with Nonoperative Care for Lumbar Disc Herniation
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Prognostic Factors of Positive and Negative Outcomes with Nonoperative Care for Lumbar Disc Herniation
Absence of crossed straight-leg raising (SLR)
Positive crossed SLR
Absence of leg pain during spinal extension
Reproduction of leg pain during spinal extension
Large extrusion or sequestration
Subligamentous contained lumbar disc herniation
>50% reduction in leg pain within first 6 weeks of onset
<50% reduction in leg pain within 6 weeks of onset
Positive response to corticosteroids
Poor response to corticosteroids
Limited psychosocial issues
Overbearing psychosocial issues
Receiving workers’ compensation
Educational level >12 years
Educational level <12 years
Good fitness level
Poor fitness level
Absence of spinal stenosis
Presence of spinal stenosis
Progressive return of neurologic deficits within first 12 weeks
Progressive neurologic deficits and cauda equina syndrome
Myofascial pain is a common cause of LBP, with one study conducted by spine surgeons finding its prevalence to be almost 20%, second only to herniated discs. In addition, some studies have found LBP to be associated with elevated levels of paraspinal muscle tension. Myofascial LBP often presents as a deep, achy pain that is aggravated by activity and position changes. It may be localized to the low back or radiate into the buttock, sacrum, thigh, abdominal wall, or even calf, depending on the affected muscle(s). Pain-induced weakness or paresthesias, or both, may be present but are nonmyotomal and nondermatomal in distribution. On physical examination, a tender, taut band of muscle may be noted (trigger point) that, when palpated, results in a characteristic referral pattern, but, often, a discrete trigger point cannot be appreciated in the deeper muscle layers. When a trigger point is appreciated, deep, traverse “snapping” palpation or needle insertion often elicits the characteristic local twitch response. In severe cases, decreased lumbar lordosis, or if the muscle spasm is unilateral, functional scoliosis—or “listing”—may be noted. Patients may present with significant concern because their posture has changed suddenly, listing to one side or the other. Patients should be reassured that this condition will likely resolve spontaneously as their back pain resolves.
The treatment of myofascial LBP is mainly conservative. Some of the therapies used for myofascial pain include ischemic compression massage, the so-called spray-and-stretch technique, iontophoresis, and physical therapy. Ice applied to the low back slows the metabolism required for muscle contraction and subsequently reduces painful spasms. Ice also decreases the conduction velocity of pain fibers, thereby decreasing pain and, debatably, also floods the central neurologic gateway with temperature signals that override pain signal transmission. Ice should be applied 20 minutes at a time with 1 hour in between applications. Ice should not be in direct contact with the skin, and a towel barrier is recommended.
A large, randomized controlled trial compared osteopathic manipulation with conventional noninvasive therapy in patients with axial LBP of less than 6 months’ duration. The osteopathic treatment group required less pain medication than the conventional treatment group but had similar outcomes. When trigger points are identified, trigger-point injections using local anesthetic can be helpful. A recent, randomized, double-blind study in patients with chronic LBP found injections with botulinum toxin A to be an effective treatment. When myofascial pain is associated with other pathology of the lumbar spine, as is often the case, these problems need to be treated as well.
This is a common occurrence as people age. Spinal stenosis can refer to central canal narrowing, foraminal narrowing, or lateral recess stenosis. Axial and/or radiating pain is often provoked with hyperextension, walking, and descending stairways or hills. It is often relieved by leaning over a shopping cart, counter, or walker. Disc protrusions, hypertrophied ligamentum flava, enlarged facet joints, facet cysts, osteophytosis, and spondylolisthesis can all contribute to central canal stenosis. Patients may present with unilateral or bilateral neuropathic symptoms of pain, numbness, tingling, or weakness that often extends to multiple dermatomes. In addition, they may also have signs such as lower extremity hyperreflexia compared to the upper extremities, clonus, and a positive Babinski, especially if significant stenosis occurs in the high lumbar or thoracic regions. MRI findings of myelomalacia are concerning, but, often, surgery is not required. Aggressive physical therapy may improve pain scores and quality of life, especially if pain is movement induced (so-called dynamic pain, see the later section on chronic back pain), or if the patient has kinesiophobia, fear-avoidance beliefs, pain behaviors or is deconditioned. However, these patients should be closely monitored for symptomatic progression, and if this is observed over time, a surgical referral is warranted. Surgical referral is also warranted if conservative treatments fail to improve pain or quality of life. While facet blocks or radiofrequency denervation may relieve axial pain, it is thought by some that facet blocks, in particular, may cause inflamed and hypertrophic facet joints to reduce in size, thereby relieving the stenosis and radicular pain. This has anecdotally been observed frequently in our office, although the exact mechanism remains unknown.
Decreased disc height from desiccation or herniation, as well as bony changes and osteophyte complexes, may cause foraminal stenosis or lateral recess stenosis, and these changes are usually detected on an MRI. These usually affect a single nerve root or multiple nerve roots at different levels, causing pain, radiculopathy, dermatomal numbness and tingling, and myotomal weakness as the lower motor neurons are affected. Deep tendon reflexes can be hyporeflexic. Epidural steroid injections that allow for steroid and local anesthetic dispersion through multiple levels may provide relief to those who are symptomatic at these levels, though the duration of effect tends to be shorter than that achieved for a herniated disc. A transforaminal approach may benefit those with unilateral pain in a well-delineated dermatomal distribution.
As with lumbar disc herniations, treatments to avoid if possible are bed rest and opioids. Bed rest tends to cause deconditioning and reinforce fear-avoidance beliefs, while opioids increase the risk of falling, especially in seniors, and increase the risk of continued use and long-term hyperalgesia. Neuropathic medications such as gabapentin have been shown to increase walking distances and reduce pain.
For spinal stenosis unrelated to spondylolisthesis, treatment outcomes, whether surgical or nonsurgical, are poorer for those patients with duration of symptoms longer than 12 months. This is not true for degenerative spondylolisthesis. Therefore, an MRI should be ordered early, and nonoperative treatments should be exhausted promptly to remain within the window of surgical efficacy. In a randomized, multicenter study comparing surgery to conservative care for spinal stenosis without spondylolisthesis, the surgical group did better through 2-year follow-up in the “as treated” analysis.
DEGENERATIVE DISC DISEASE AND DISCOGENIC PAIN
The intervertebral disc over time loses proteoglycans and chondroitin, which are molecules that attract and retain water. Losing these molecules means that the disc loses its water content. Loss of water translates to loss of compressive strength of the disc. This water is then replaced with collagen, which makes the disc less compliant under pressure and more susceptible to tears. With significant loss of water, the disc is less likely to herniate, but disc space is reduced, possibly narrowing the foramina through which nerve roots exit.
The annulus fibrosus is innervated anteriorly by the ventral rami and gray rami communicans. The posterior part of the annulus is innervated by the sinuvertebral nerves. Therefore, tears within the lamellae of the disc without herniation can produce back pain without radiation. An MRI may show a zone of high intensity. With decreased lamellae, the integrity of the disc is reduced and the stress increases, especially with activities that are associated with increased pressure such as prolonged sitting. Over time, chemical sensitization may occur that can lead to axial pain with even normal activities, which did not produce pain previously. Desensitization may occur chemically at the level of the disc. Alternatively, regional or generalized nonchemical desensitization usually occurs over time in most people, resulting in a recalibrated and electrically stable neurophysiological pain system. When these desensitization processes or systems fail, pain continues and becomes chronic.
Patients with low back pain often have degenerative disc disease (DDD). According to many studies, DDD is the most common cause of nonradicular chronic low back pain. Similar to HNP, a majority of patients, 85% in one study, with DDD on MRI are asymptomatic, and this percentage increases with age.
Discogenic pain can present with back pain radiating into the buttock, hip, groin, or even the lower limb. It is typically worsened by prolonged sitting. Often, this pain mimics HNP, and it is sometimes difficult to discriminate between HNP and discogenic pain. However, there should be an absence of focal neurologic findings, and the radiation pattern tends to be nondermatomal.
Treatment for acute discogenic pain involves NSAIDs, acetaminophen, Tramadol, and the passage of time. For the aforementioned reasons, prescribing opioids should be done with great care. Discograms are usually not indicated and can produce false positives, especially in those with abnormal psychometric testing, multiple somatic complaints, and previous back surgery. The results of the few studies conducted yield mixed evidence as to whether they improve fusion outcomes. The use of Intradiscal Electrothermal Annuloplasty (IDET) has been shown in uncontrolled studies to provide moderate pain relief. However, for chronic discogenic pain, IDET has been shown to be of benefit only in the short term. Only one of four randomized studies demonstrated significant improvement of fusion compared to conservative care, and the benefit experienced with fusion tends to be modest. Fusing the spine may also be associated with juxtafusional degenerative changes such as accelerated disc and facet joint degeneration, spondylolisthesis and scoliosis. Disc replacement may be considered for patients with no significant radicular or facetogenic component to their pain and may be as effective as fusion for one- or two-segment disease. The advantages of disc replacement include more rapid recovery and better preservation of spinal motion. As mentioned in the chronic back pain section, desensitization through aggressive physical therapy or cognitive interventions are viable options should the patient choose to exhaust nonsurgical options before deciding on surgery.
DDD is thought to facilitate facet arthropathy from redistribution of load forces from the disc to the facet joints (loads are normally shared when both discs and facets are healthy).
Facet joints (also called zygapophysial joints or Z-joints) are estimated to be involved in up to 40% of all back pain sufferers. Facet joints are paired, true synovial joints that connect adjacent vertebrae posterolaterally. The function of facet joints in the lumbar spine (as opposed to the function in the cervical spine) is to limit rotation and assist the intervertebral discs in resisting compressive forces during lordotic postures, such that maximal stress on the facet joints occurs during lumbar extension and rotation.
The mechanism of how facet arthropathy develops is unclear. Kirkaldy-Willis described the three-joint complex at a given level and how the deterioration of this complex occurs in three phases. In the dysfunctional phase, circumferential and radial tears occur in the disc, and synovitis and hypomobility occur in the facet joints. This results in disc herniations and dysfunction of the three-joint complex. In the instability phase, disc herniations and resorption of the disc material, combined with facet capsular laxity and subluxation, cause instability and lateral nerve entrapment. In the stabilization phase, osteophytes form and facet enlargement occurs, causing stenosis at that particular level. The three phases collectively describe the process of spondylosis. Multilevel spondylosis results in multilevel stenosis.
The degenerative changes observed in facet arthropathy include microtrauma, capsular tears, synovial inflammation (seen on MRI as fluid in the joints), chondromalacia, microhemorrhage, and meniscoid entrapment. Facet joint degeneration can also involve outpouching of the synovium, forming a synovial cyst. Rupture of synovial cysts by fluoroscopic-guided, contrast-enhanced cystic distention has been shown to have potential for safe, long-term pain relief of back pain.
Similar to other forms of arthritis, the prevalence of facet joint pain increases with age. Facet pain is often described as back pain that does not radiate. It is often worse with hyperextension and with rotation, such as when swinging a golf club. Facet pain may also radiate down the buttocks and thighs unilaterally or bilaterally, but weakness and paresthesias are usually not present. This pain rarely radiates distal to the knees, except when facet hypertrophy results in clinically significant foraminal stenosis. Facet joints share similar anatomical features to nonaxial joints such as knuckles, knees, and hips. They are encapsulated with joint fluid, their articular surfaces are lined with cartilage, and the periosteum is innervated. As people age, these joints degenerate, resulting in loss of cartilage, irregularity of articulating surfaces, and joint pain. Joints at each level are innervated by medial branches of the dorsal rami at that level and the one above. For example, at the L4–5 articulation, the superior aspect of the facet is innervated by the L3 medial branch, while the inferior aspect of the facet is innervated by the L4 medial branch.
Facet pain can also be treated with aggressive quota-based, non-pain-contingent therapy if pain is movement induced. Alternatively, facet blocks can quiet inflammation within the joint. Fluid in the joint may be present on an MRI, but this is not always the case. Studies suggest that there is little difference whether the steroid/local anesthetic is actually deposited within the joint capsule or merely in the vicinity of the joint. That is, good efficacy can be achieved in either instances, although this remains controversial. Medial branch blocks that reduce pain by 80% are diagnostic, and medial branch radiofrequency ablation (often called “rhizotomy”) may then be beneficial. On the other hand, it is believed by some that if facet blocks do not relieve pain, medial branch blocks may not be warranted. It is also believed by some that medial branch blocks should be performed instead of facet blocks, but this is also controversial.
The sacroiliac (SI) joint is a large joint connecting the sacrum to the iliac bones. The joint is heterogeneous in that while the anterior surface of the articulation between the sacrum and ilium is a true diarthrodial joint, the dorsal surface is mostly comprised of an intricate network of ligamentous and muscular connections. It functions to dissipate shock forces from the upper trunk to the lower extremities. SI pain can present as unilateral buttock pain, but it is also known to cause pain radiation down to the feet bilaterally. It can also present as groin pain or as clicking or popping in the posterior pelvis. There should be no associated weakness or paresthesias in SI joint pain.
SI joint pain as a cause of low back pain is controversial for many reasons. Many believe that its relative lack of movement; the complex force distribution among the SI joint, hips, pubic symphysis, and spine; and overlapping symptoms of other more common and identifiable pathologies make it difficult to define the SI joint as a definite pain generator in a patient's complaints of back pain. Furthermore, while there are many physical exam maneuvers to evaluate for SI joint pathology, no single test has been shown to be very sensitive or specific, including tenderness to palpation over the joint itself. Similar to facet joint pain, the only way to diagnose a painful SI joint is by diagnostic blocks. Imaging such as CT and MRIs is usually not helpful in evaluating SI joint pain but could be ordered to rule out other concerning pathologies.
Several conditions may be associated with a higher risk of SI joint pain that include ankylosing spondylitis, pregnancy (which involves hormonal-induced ligamentous laxity and exaggerated hyperlordosis), true or apparent leg length discrepancies, and, rarely, infection or tumors. Among patients with axial low back pain predominantly below L5, the estimated prevalence is between 20% and 35%.
Other sources of pain should be investigated before concluding that a patient has pure SI joint pain. Treatments for SI joint pain ranges from ice and NSAIDs in the acute phase (1–3 days) and physical therapy for muscle balancing in the recovery phase (3 days–8 weeks). Maladaptations of movement due to pain should be addressed during this time. Functional leg length discrepancies (measured from the umbilicus to the medial malleoli) in the absence of actual leg length discrepancies (measured from the Anterior Superior Iliac Spine (ASIS) to the medial malleoli) should be addressed with muscle balancing and not with shoe lifts. One study showed that 32% of Army recruits had actual leg length discrepancies of up to three-fifths of an inch (15 mm) without symptoms. The subsequent recommendations are to address leg length discrepancies only for values exceeding this.
In any event, while many may attribute pain to mechanical abnormalities such as leg length discrepancy or pelvic malrotation, it should be pointed out that these abnormalities likely persisted long before the patient's development of back pain and that the patients’ neurophysiologic pain system had, up to the point of an exacerbating event, suppressed pain signal transmission. The exacerbating event then pushed the stimulus beyond the pain threshold of transmission, resulting in a new onset of pain perception. Retraining of the pain system to increase the pain threshold (through aggressive physical therapy) is a reasonable first-line treatment option associated with less adverse side effects than fixing the anatomic abnormality. Muscular stretching, strengthening, and balancing can also be performed as part of the therapy.
In terms of interventional procedures, both intraarticular and periarticular injections have been shown to provide benefit. In those who respond with only short-term relief to injections, the use of radiofrequency ablation of the L4 and L5 dorsal rami and lateral branches of S1 to S3 may provide pain relief lasting up to 1 year.
The piriformis is a flat, pyramidal muscle extending from the anterior sacrum, greater sciatic foramen, and sacrotuberous ligament to the greater trochanter of the femur. The major function of the piriformis is to abduct and externally rotate the femur. The possibility that sciatic symptoms may stem from the piriformis muscle dates back to 1928, when Yeoman examined the relationship of the sacroiliac joint, sciatic nerve, and piriformis muscle. Although six anatomic variations between the sciatic nerve and piriformis muscle have been described, in the large majority of cases, the sciatic nerve passes anterior to the muscle. Any process that causes the piriformis to hypertrophy, spasm, or contract inappropriately can cause sciatic nerve impingement, leading to piriformis syndrome.
The typical presentation of piriformis syndrome is buttock pain, sciatica, or both, exacerbated by activities that necessitate hip adduction and internal rotation, such as cross-country skiing or prolonged sitting. Pain that accompanies bowel movements may be present and, for women, dyspareunia. Physical examination may reveal tenderness in the buttock extending from the lateral border of the sciatic foramen to the greater trochanter. Both pelvic and rectal examinations may reproduce the pain pattern. Pain is also elicited during resistance to hip flexion, adduction, and internal rotation (FADIR test), otherwise known as the Freiberg's sign. The neurologic examination is usually nonfocal, with most patients having a negative straight-leg raising test. Although CT, MRI, and electrodiagnostic studies may be helpful, by themselves, these tests are insufficient to make the diagnosis. Imaging should be used with caution as they may lead to misdiagnoses. For example, an L5-S1 herniation seen on imaging, a very common finding that is commonly non-painful, may be assumed to be the cause for leg pain, when the actual cause may be from the piriformis muscle. This may result in a series of invasive treatments for the wrong target.
For most patients with piriformis syndrome, conservative treatment is sufficient. This includes physical therapy and correction of leg-length discrepancies, pelvic obliquity, abnormalities in gait or posture mechanics, and associated back or leg problems. Medications such as NSAIDs and muscle relaxants can sometimes be helpful. Other treatments that have been advocated include transrectal massage, vapocoolant spray coupled with soft-tissue stretching maneuvers, and Transcutaneous Electrical Nerve Stimulation (TENS) therapy. When conservative treatment fails, injection of the piriformis with local anesthetic and corticosteroids can relieve muscle spasm and pain. This treatment should be done using either a nerve stimulator to locate the sciatic nerve or fluoroscopy with contrast. In instances in which relief is short term, piriformis injections can be repeated with botulinum toxin. In rare instances, surgical sectioning of the piriformis muscle may be necessary.
One disorder that is easily mistaken for piriformis syndrome is ischiogluteal bursitis. Patients with ischiogluteal bursitis usually complain of severe pain in the center of the buttock, which is worse with sitting or walking. This pain may radiate into the thigh, but rarely extends below the knee. Tests involving motion at the hip joint, such as the straight-leg raise and Patrick's tests, are often positive. Pressure applied on the lateral rectal wall during a digital rectal examination can elicit excruciating pain. Conservative treatment includes NSAIDs and soft pillows or so-called doughnuts for sitting. For patients with severe pain, bursa injections performed with corticosteroids and local anesthetic are indicated.
It has been shown that patients with progression of congenital scoliosis or idiopathic juvenile scoliosis have a higher incidence of herniated discs and back pain. On the other hand, those with degenerative scoliosis are not more likely to have back pain compared with the general population. One study showed the presence of scoliosis in 68% of elderly patients (mean age 70.5) without significant correlation to pain. Another study following patients (ages 50–84) over a 12-year period showed de novo development of scoliosis in more than 36% of patients. Patients should not attribute their pain primarily to scoliosis, though it is thought by some that the asymmetric loading present in scoliosis may predispose patients to other abnormalities such as facet and disc degeneration. Potential sources of back pain in the setting of scoliosis include facet pain, discogenic pain, disc herniations and degeneration, and stenosis. These conditions should be treated the same way as they would in the absence of scoliosis.
CHRONIC BACK PAIN AND EXERCISE TREATMENT
Chronic pain is usually defined as pain that has persisted beyond the expected duration of an acute pain event. In discogenic back pain for example, this is usually 4 to 6 weeks. However, as noted earlier, pain from disc herniations may take as long as 6 months to resolve. Chronic back pain occurs when the neurophysiologic pain response from acute changes in the spinal column continues to transmit pain signals to the brain. In theory, most neurophysiologic systems continue to adjust and adapt to these changes, increasing the threshold to which stimulus input produces pain. This may explain why older people are not in excruciating pain despite having significantly degenerated spines seen on an MRI. This may also explain why patients “get better” despite showing a persistent disc herniation on a follow-up MRI. Another example is when a microdiscectomy is performed. While 23% of patients reherniate the same disc postoperatively, only 56% of these patients are symptomatic.
When this threshold is increased sufficiently, the neurophysiologic system is said to have adjusted to the anatomic change (e.g., disc herniation) that previously occurred. The patient does not feel pain despite the fact that the spinal column is permanently changed. These changes occur throughout our adult lives, and our neurophysiologic system continuously adjusts and adapts; hence, back pain often appears in episodes that resolve spontaneously in most cases. It is overwhelmingly common to have significant anatomic changes in the spine without significant pain. On the other hand, some patients have relatively mild changes in their spines seen on MRI, yet have significant pain. Practitioners should be cautious in correlating pain to anatomic changes because, often, these correlations are poor.
When threshold fails to adjust, pathologic pain ensues. Pathologic pain serves no functional purpose. This is in contrast to physiologic or “Darwinistic” pain, which serves to protect the body and prevent injury. Patients should be educated that while they may have significant degenerative changes, resuming all the activities that they enjoy doing without fear of injury may improve long-term outcomes because their chronic pain is pathologic and not physiologic.
When the pain threshold is kept low, pain is recreated intermittently or constantly. Pain provoked with movement is called dynamic pain and is the most common type of pain associated with mechanical, nociceptive pain (e.g., facet arthropathy, SI joint pain, discogenic pain). Dynamic pain is produced when the pain threshold is low to the point where a small stimulus produced by benign movement activates pain fibers. In patients with normal or adequately adjusted pain thresholds, pain fibers do not activate with normal movements.
It is important to distinguish to patients the difference between “pain threshold” and “pain tolerance.” Threshold is the amount of stimulus necessary to activate pain fibers. If the stimulus fails to activate pain fibers, the event goes unnoticed by the patient. On the other hand, tolerance describes what the patient chooses to do after the pain threshold is exceeded, that is, what the patient does when he or she feels pain. Thus, a low-threshold, high-tolerant patient may feel pain with the slightest of movements but choose to go to work despite the pain because of the fear of lost income. The low-threshold, low-tolerant patient may choose to minimize movements by staying in bed or purchasing a wheelchair.
A decrease in pain threshold is thought to be facilitated by chronic use of narcotic medication, hypervigilence to avoid activities that are thought to provoke the pain (known as fear-avoidance beliefs or kinesiophobia), depression and anxiety, personality disorders, and other psychosocial phenomena such as compensation. Compensation can be in the form of financial or other compensation, such as having family members perform the daily chores that the patient would normally have done but is now excused from doing because of perceived disability. This may explain opioid-induced hyperalgesia, higher prevalence of back pain with psychiatric or personality disorders, and the failure to improve when compensated financially, for example. Studies have shown that return-to-work rates are significantly lower when patients are financially compensated compared with those who are not compensated. Additionally, attorney involvement further decreases return-to-work rates. When threshold- or tolerance- lowering factors are present, chronic pain is likely to continue despite aggressive physical therapy, interventional procedures, and even surgery.
Even in those with a fully adjusted neurophysiologic system, high thresholds can be overcome with a large stimulus. This may explain why a pain-free patient with a large osteophyte complex from an old disc herniation may be painfully symptomatic after a fall—because the subsequent inflammatory reaction stimulated pain fibers that exceeded the threshold. These patients improve over time with resolution of said inflammation with or often without treatment.
Dynamic chronic pain from a lowered pain threshold is often amenable to aggressive physical therapy combined with a cognitive behavioral component. Many studies have shown profound effectiveness with this approach. Fear-avoidance beliefs are dispelled and kinesiophobia is remedied. Constant exposure to the familiar pain by repetition of pain-provoking movements increases the threshold to which these movements induce pain. This is written on a physical therapy order as “quota-based, non-pain-contingent” exercises. The prescription should also contain “no passive modalities” because most have no proven long-term benefit and therapy time is better allocated to active physical exercises. Therapy should be twice weekly for 6 weeks because one study has shown that thrice-weekly physical therapy has no added benefit. While MRIs should not be routinely ordered for chronic back pain unless concerning signs or symptoms are reported, or if a procedure is planned, patients often present to the pain specialist with a recent MRI. In this case, and if the results are benign, health care providers should provide reassurance that there is nothing concerning about their back anatomy other than age-appropriate degeneration. Again, it should be explained to patients that age-appropriate degeneration is common in all people of that particular age group but typically produces no pain. Finally, patients need to be instructed to continue their exercises in their own gym twice a week because complete resolution of pain takes longer than 6 weeks, often up to 6 months. They should be told that the main reason for aggressive physical therapy is for desensitization (increasing the pain threshold), and that the secondary benefits are a stronger core, increased cardiovascular fitness and health, confidence in returning to activities that they enjoy, reduction in pain behaviors and fear avoidance, cessation of catastrophic thinking patterns, and a better sense of well-being.
Static pain—that is, pain with sitting or lying in bed, but improved with standing or moving around—is often more challenging to manage. It is important to note that static pain may fail to respond to aggressive physical therapy and other methods of treatment should be prescribed, usually interventional procedures.
Pain in the setting of depression may be improved with simple aerobic exercise. Babyak showed that aerobic exercise three times per week for 10 months treated depression better than antidepressants and better than antidepressants plus exercises. For those patients unable to or who decline exercise as a treatment plan, antidepressants have been FDA approved for chronic back pain. The antidepressant Duloxetine is FDA approved for musculoskeletal pain, including low back pain, and systematic reviews have generally found that tricyclic antidepressants may provide a slightly greater beneficial effect (compared with newer antidepressants) in some individuals with LBP regardless of the etiology. The fact that serotonin- and norepinephrine-specific reuptake inhibitors are weakly effective analgesic agents suggests that both neurotransmitters are involved in the pain modulatory effects. When antidepressants are used to treat pain, the dosing regimen, total dosage, and onset are all lower or shorter than when they are used to treat depression. For nortripytline, a dose range of 25 to 75 mg at night is often therapeutic.
In addition to exercise treatment for chronic low back pain, chiropractic manipulation, acupuncture, interventional procedures, and surgery have been shown to benefit many patients. Ergonomic evaluation of the workplace or home can be of benefit. Many patients will ask a physician for a recommendation for a particular bed or mattress that will alleviate back pain. One study showed reduced back pain with a “medium-firm” mattress versus “soft” or “firm” mattresses, but these terms are ill-defined. In the absence of compelling evidence, practitioners should be wary of making a recommendation because mattresses, especially those that are advertised to be therapeutic, tend to be expensive.
FAILED BACK SURGERY SYNDROME
The definition of failed back surgery syndrome (FBSS) is the persistence or development of low back or leg pain following surgery on the lumbosacral spine. Two statistics highlight the magnitude of FBSS as a pain problem in the United States. First, approximately 300,000 lumbosacral spine procedures are performed each year in the United States as a treatment for chronic LBP. Second, depending on the definition of failure, the incidence of FBSS can be as high as 60%.
The reasons patients continue to have pain following spine surgery can be broadly categorized as follows: (1) poor patient selection (e.g., patients with threshold lowering factors); (2) surgery was performed on a structure that was incorrectly thought to be the primary pain generator (e.g., a patient thought to have an L4–5 discogenic radiculopathy because it was seen on an MRI, but actually had a piriformis syndrome as the primary cause of pain); (3) clear indication for surgery, but the procedure did not correct the original problem; (4) complication from surgery (e.g., discitis, pseudomeningocele, or a pars defect, especially from far lateral discectomies); (5) recurrent disc herniation; (6) secondary instability or degenerative changes occurring as a consequence of surgery (e.g., adjacent level discogenic pain, facetogenic pain, sacroiliac joint pain developing after a spinal fusion, spondylolisthesis following laminectomy, or pain that develops over the site of a donor graft); (7) persistent or established neural injury (e.g., arachnoiditis or epidural scarring); and (8) an intercurrent diagnosis, such as cancer.
The workup of patients with FBSS begins with a detailed history and physical examination. Of particular importance is determining whether the patient's pain is of the same character and quality as before the surgery or if it represents a new symptom that has arisen. For instance, a new pain complaint might indicate a surgical complication. Equally crucial is determining whether or not, and for how long, the patient experienced a pain-free interval. The three most common scenarios are as follows:
No relief or the worsening of pain shortly after surgery. This category includes a retained disc fragment, failure to remove the offending disc, and certain iatrogenic infections. No relief following surgery might also indicate an incorrect diagnosis or poor patient selection.
Initial relief followed shortly thereafter by pain, numbness, or weakness. Examples of this group of disorders are arachnoiditis, epidural fibrosis, and battered-root syndrome with perineural scarring. Note that this pattern can also occur as the patient is weaned off of their post-op pain medications.
Excellent relief after the surgery followed by development of pain months or years later. This group includes a recurrent disc at the same or different level, pseudoarthrosis, juxtafusional degeneration, and lumbar instability.
Overall, the most frequent causes of pain in patients with FBSS syndrome are recurrent disc herniation, spinal stenosis, epidural scarring, and arachnoiditis. Table 38-3 lists the most frequent diagnoses conferred at one pain management center in patients with failed back surgery syndrome.
Pain Center Diagnosis in 78 Patients with Failed Back Surgery Syndrome
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Pain Center Diagnosis in 78 Patients with Failed Back Surgery Syndrome
Number of Cases
Minor spondylitic/expected postoperative changes
Musculoskeletal abnormality only
Lateral foraminal stenosis
Tarsal tunnel syndrome
After obtaining a detailed history, the physician should arrive at a reasonable differential diagnosis. At this point, diagnostic studies are usually necessary. If a recurrent herniated disc or spinal stenosis is suspected, an MRI scan is indicated. Because scar tissue is relatively vascular, a gadolinium-enhanced MRI or contrast CT scan is usually necessary to detect epidural fibrosis. This diagnosis can be confirmed with epidural mapping by the injection of contrast media through the caudal canal. In patients with epidural fibrosis, a filling defect is present. When arachnoiditis is suspected, myelography is the diagnostic imaging study of choice. Additional accuracy can be obtained when a myelogram is followed by a CT scan. For osteomyelitis, a bone scan is the preferred test.
The treatment of FBSS is aimed at the underlying cause. Depending on the diagnosis, nerve blocks—including epidural corticosteroid injections, sacroiliac joint blocks, and facet blocks—can sometimes be of benefit. In patients with radicular symptoms, neuropathic pain medications may provide relief. Some clinicians report good results with epidural lysis of adhesions (i.e., Racz procedure) in FBSS patients with epidural fibrosis, although, in our experience, the analgesia conferred by this procedure tends to be short-lived. Causes of FBSS that may be amenable to surgery include a recurrent disc herniation, postlaminectomy instability, recurrent spinal stenosis, nonunion, and a host of surgical complications. However, in a study by North and colleagues that followed 102 patients who underwent repeat back surgery, only 34% had a successful outcome. In patients who do not respond to nerve blocks, repeat surgery, or other medications, opioids are indicated. Finally, spinal cord stimulation may be of benefit for patients with FBSS who have intractable pain, especially those for whom leg pain is the predominant complaint.
In addition to the usual causes of LBP, the astute clinician must also consider the unusual. Because of their effects on the musculoskeletal system, a host of different metabolic and endocrine disorders can result in LBP, including hyperthyroidism, hyperparathyroidism, and Cushing's disease. For similar reasons, virtually any rheumatologic disorder can present as LBP. Visceral pain emanating from internal organs can be referred to the back secondary to convergence in the spinal cord. These sources of visceral pain include genitourinary organs, the kidneys, gallbladder, bowel, liver, and pancreas. Vascular disease can manifest as LBP, which, if not detected, can be catastrophic. Not only is the spine a common site of metastatic tumors, but primary tumors may originate there as well. In some patients, hematologic disorders such as mastocytosis and hemoglobinopathies can lead to low back pain, as can diseases such as sarcoidosis, Paget's disease, and infectious endocarditis. Finally, psychiatric and functional disorders can manifest as chronic back pain, which can be extremely difficult to treat.
Back pain that is constant or worse at night, night sweats or fever, unintentional weight loss, or a history of cancer warrants an MRI or CT scan if an MRI is contraindicated.
Infection of the Lumbosacral Spine
Infectious causes of LBP include vertebral osteomyelitis, epidural abscess, and discitis. Vertebral osteomyelitis accounts for between 2% and 4% of all cases of osteomyelitis, with males being affected more than females and the elderly more than young people. In descending order, the most common sources of infection are the genitourinary system, skin, respiratory tract, and spine surgery. Risk factors include intravenous drug abuse, immune suppression, and rectosigmoid disease. Although vertebral osteomyelitis may sometimes begin abruptly, more often, the presentation is insidious. Back pain typically is described as sharp, persistent, and exacerbated with movement. Fever may be minimal or absent. On physical examination, there is usually marked tenderness over the affected vertebra, guarding, and paraspinal muscle spasm. Treatment involves antibiotics and immobilization.
Because of its poor blood supply, most cases of discitis either are iatrogenic or occur secondary to direct spread from an infected vertebra. Classically, patients report the onset of intense, spasmodic pain appearing 1 to 2 weeks after spine instrumentation. Fever is usually absent. In patients without previous surgery, the diagnosis may take months or even years to make. Pain from discitis may be referred into the groin, flanks, hips, abdomen, or lower extremities. It usually is exacerbated by movement and relieved by rest. In one study, 3 of 13 patients with discitis had neurologic deficits at diagnosis. Physical examination of the spine reveals localized tenderness and restricted range of motion. Treatment is supportive, with antibiotics and pain medication being the mainstays of therapy. Although the treatment course is usually prolonged, surgical debridement is rarely necessary. Some studies have shown discitis to be associated with an increased incidence of chronic LBP.
Epidural abscesses account for approximately 1 in 10,000 hospital admissions. Predisposing factors include intravenous drug abuse, cirrhosis, and alcoholism, with men being affected at a greater rate than women. Although severe back pain that follows a spinal procedure should arouse suspicion, spinal instrumentation is usually not the cause of an epidural abscess. In a review of 39 cases of spinal epidural abscess over 27 years at Massachusetts General Hospital, only one was secondary to epidural placement.
The four cardinal signs of an epidural abscess are back pain, tenderness, leukocytosis, and fever. Interestingly, although it is the most common symptom of epidural abscess, back pain itself is not universal. If left untreated, symptoms progress over a period of hours to weeks. Generally, the order of progression proceeds from localized back pain to radicular pain, weakness, incontinence, and paralysis. An epidural abscess is a surgical emergency. In one study, in which patients diagnosed within 36 hours of the onset of symptoms had minimal residual weakness, no recovery was observed in patients paralyzed longer than 48 hours. Other infections that can result in back pain include herpes zoster, Lyme disease, and infectious sacroiliitis.
Vertebral Fractures and Spondylolysis
As the life expectancy of the U.S. population has continued to increase, so, too, has the incidence of spinal fractures. There are two main reasons for this: increasing disability with age and a higher incidence of osteoporosis. In clinical practice, only 30% of vertebral fractures come to the attention of physicians, primarily because lack of severe back pain in many patients does not trigger obtaining radiologic studies. However, the prevalence of radiographically demonstrated vertebral deformities rises from 5% of individuals between the ages of 50 and 54, to 50% in women over 80 years. The most common locations for vertebral fractures are at the thoracolumbar junction, the mid-thoracic spine (T7–8), and the lumbar vertebral column. The prevalence of spinal fractures is highest in Caucasian and Asian women, owing to their increased incidence of osteoporosis. Aside from the increased propensity for vertebral fractures, some experts believe osteoporosis in and of itself can cause spinal pain.
The patient with a vertebral fracture typically presents with acute pain overlying the fracture site. For sacral fractures, pain may radiate into the buttocks or leg. The precise incidence of neurologic deficit depends on the extent, type, and location of injury but is usually cited as being greater than 30%. One fact that distinguishes spinal fractures from those with other types of fractures or other acute pain conditions is the fact that more than half of all patients with severe vertebral fractures go on to develop chronic pain. Physical examination of the patient with a vertebral fracture(s) usually reveals marked tenderness on palpation. In patients with lumbar fractures who develop radiculopathy, straight-leg-raising tests may be positive.
Exercise programs for elderly patients suffering from spinal fractures have been shown to increase bone density, decrease the use of analgesics, and improve quality of life. Because patients with vertebral fractures are at increased risk to develop hip and other fractures, walking programs, fall-prevention courses, and even Tai Chi may be beneficial. One study showed that Tai Chi may reduce the risk falls by up to 55% in the elderly. Tai Chi also helps protect stroke survivors from falls and improve balance and motor control in those with Parkinson's disease.
In most patients with isolated spinal fractures, NSAIDs and/or short-acting opioids are sufficient for pain relief. In those with constant pain, sustained release opioids may be necessary. For patients whose main symptoms are consistent with radiculopathy, an epidural steroid injection(s) or trial with neuropathic pain medications may be a worthwhile endeavor. Two treatments that have been shown to both reduce subsequent fractures and provide analgesia for fracture patients are bisphosphonates and salmon calcitonin. In patients with focal pain and limited acute spinal fractures who do not respond to conservative measures, vertebroplasty or kyphoplasty can be considered. Finally, surgical intervention may be necessary in patients with unrelenting pain, spinal instability, or worsening neurologic deficit. In many patients, analgesics and activity modifications are sufficient treatment.
One particular type of vertebral fracture is spondylolysis, also known as pars interarticularis. For the Caucasian adult population, the incidence of spondylolysis has been reported to range between 3% and 6%. There is general agreement that most pars defects occur during childhood, with the large majority of cases being asymptomatic. Risk factors for pars fractures include spondylolisthesis, involvement in sports, and genetics. In active adolescents, spondylolysis can be a significant cause of LBP.
Patients with pars interarticularis usually present with focal LBP, although radiation into the buttock or thigh can occur. This pain may be increased during activities that require extension or rotation of the spine. On physical examination, many patients are noted to have a hyperlordotic posture with tight hamstrings. Diagnosis can be confirmed with plain radiographs, CT, or MRI.
The treatment of patients with symptomatic spondylolysis includes analgesics, bracing, cessation of sports activities, hamstring stretching, and strengthening of the abdominal muscles. In patients who require further pain management, pars injections may be helpful. In some cases, surgery may be necessary.
Bone is the third most common location of tumor metastases after the lungs and liver. In patients with metastatic cancer, tumor invades bone in 60% to 84% of cases, with the vertebral column and pelvis being the most frequently affected sites. In one study, 39% of all skeletal metastases were to the spine. The pain associated with spinal metastases develops slowly over weeks or months, gradually becoming more intense. Frequently, it can be localized to the involved vertebral bodies. Patients typically characterize it as a dull, but constant, pain. Aggravating factors may include weight bearing, activity, and nighttime, when the patient is trying to sleep. Besides back pain, other signs of spinal metastases include fever, chills, weight loss, and generalized fatigue. Pain treatment includes NSAIDs, neuropathic pain medications, opioids, orthotics, and activity modification. In patients with neurologic deficits, surgical decompression may be necessary. As an adjunct to conventional modalities, chemotherapy, hormone treatment, corticosteroids, bisphosphonates, salmon calcitonin, radioisotopes, and radiotherapy can be helpful.
Kidney stones, which can be identified by imaging, may be the source of low back pain, and, in these cases, medical referral is the best course of action. Pyelonephritis should also be considered with costovertebral angle tenderness and fever.
Table 38-4 shows the typical associated pattern of pain, numbness, weakness, and atrophy by lumbar disc level.
Level of Disc Herniation as Differentiated by History and Physical Examination
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Level of Disc Herniation as Differentiated by History and Physical Examination
L2–3 Disc (L3 nerve root)
Pain: low back, upper buttock to anterior thigh, anterior knee, medial lower leg
Numbness: anterior thigh, knee (may be absent)
Weakness: hip flexion, hip adduction, knee extension
Atrophy: iliopsoas, quadriceps femoris, sartorius, hip adductors
Associated reflex: patellar
L3–4 Disc (L4 nerve root)
Pain: low back, hip, thigh, anterior leg, inner leg to medial portion of foot
Numbness: anteromedial thigh, medial aspect of lower leg (may be absent)
Weakness: knee extension, sometimes dorsiflexion of foot
Atrophy: quadriceps femoris, tibialis anterior, gluteus medius, gluteus minimus, tensor fasciae latae
Associated reflex: patellar, gluteal
L4–5 Disc (L5 nerve root)
Pain: low back, buttock, hip, posterolateral thigh, lateral aspect of lower leg, dorsum of foot, first two toes
Numbness: lateral leg, dorsum of foot, first two toes
Weakness: dorsiflexion of foot and great toe, difficulty walking on heels, possible foot drop
Atrophy: hamstrings, tibialis posterior, extensor hallucis longus, extensor digitorum brevis, sometimes gluteals
Associated reflex: tibialis posterior, gluteal
L5–S1 Disc (S1 nerve root)
Pain: sacroiliac joint, hip, buttock, posterolateral thigh and leg, lateral edge of foot, heel, sole
Numbness: calf, lateral border of foot, heel, sole, sometimes fourth and fifth toes
Weakness: gastrocnemius, soleus, gluteus maximus, hamstrings, peroneus
Associated reflex: ankle jerk, hamstring
The initial visit to a spine or pain specialist should be comprehensive. The magnitude of pain (0–10 on a 10-point scale or other descriptors as “mild,” “moderate,” or “severe”), location (“in the middle,” “off to the right/left side,” “in the buttock”), radiation pattern (medial, lateral, anterior, or posterior thigh; medial, lateral, or posterior lower leg; lateral, dorsal, or plantar foot; and medial or lateral toes), whether the patient is experiencing more back pain than leg pain or vice versa, and aggravating and remitting factors should be noted. Worsening pain with Valsalva maneuvers that increase intradiscal pressure (coughing, sneezing, bearing down when defecating) or prolonged sitting suggests disc pathology with or without radiculopathy. Pain with standing or walking with pain relief while leaning forward (on a shopping cart, counter, or walker) or sitting may indicate stenosis or facet arthropathy. Sacroiliac joint pain is typically worsened when arising from sitting. Other information to note are changes pain with lying down and changes in relation to the time of day or with particular activities such as swinging a golf club or driving. Pain with swinging a golf club (“the golf sign” should be reproducible on a physical exam) could indicate facet joint pain. Pain that is aggravated more with driving than just sitting can imply increased tension through the sciatic nerve because the knee is held in extension for an extended period of time.
Leg pain experienced going up stairs is often due to vascular claudication because plantar flexors are oxygen depleted due to significant vascular disease. Pain typically decreases when a patient stands still either upright or seated. In contrast, leg pain that occurs while descending stairs or walking down a hill may indicate neurogenic claudication because patients are usually leaning backward slightly as they descend (in order to shift their center of gravity posteriorly to minimize falling forward), which narrows the neuroforamina. Standing upright at the bottom of the stairway or hill does not relieve pain, but it is relieved by leaning forward or sitting. The “shopping cart sign” describes the behavior of leaning over a shopping cart in the grocery store to relieve pain. Alternatively, patients say that they lean on the bathroom sink while performing activities of daily living (ADLs) that relieves the pain. Note that while this behavior may classically be associated with spinal stenosis, it may also relieve discogenic pain by providing traction, so the “cart sign” should be used in the proper context. Note the presence of numbness, tingling, or subjective weakness, with examples for the latter often described as difficulty climbing stairs or subjective knee buckling. It is important to try to distinguish between pain-induced weakness and true neurological weakness, which may be associated with muscle atrophy or hyporeflexia. Difficulty putting on socks or shoes may indicate hip pathology.
A review of back-related symptoms should include questions regarding bowel or bladder incontinence, recent fevers, unintentional weight loss, or falling. Red flags to keep in mind include gait ataxia/upper motor neuron complaints that could indicate myelopathy. Bowel, bladder, or sexual dysfunction could indicate cauda equina syndrome. Night pain, fevers, chills, or unintentional weight loss could indicate infection or cancer. In order to better identify these conditions, a detailed history should include questions directed toward previous drug abuse (for infection) and family history (for cancer). Frequent falling is a dangerous condition particularly in seniors or in patients on anticoagulation. These red flags may require urgent or emergent medical care. A general review of systems should always be performed when evaluating a new patient with back pain (discussed later).
The evaluator should note the date and the activity or event that the patient associates with the onset of pain and whether there has been an increase or decrease in symptoms since the event. Sacroiliac joint pain is more likely to be associated with a specific inciting event than facet joint or discogenic pain, as is radicular pain from a herniated disc more likely to have a distinct onset than spinal stenosis. The course of pain may have been altered by therapeutic interventions prescribed by prior health care providers, including opioid medications, oral Prednisone, “muscle relaxers,” antiepileptics, antidepressants, aspirin or other anti-inflammatories, acetaminophen, or other medications, including herbal remedies. Prior interventional procedures should be listed, such as epidural steroid injections, facet blocks, nerve blocks, medial branch blocks, radiofrequency ablations, SI joint injections, and the like and whether they were performed under fluoroscopy. The percentage of relief from these procedures, as well as duration of effect, should be noted because this information can guide future treatments. Previous physical therapy courses should include details such as the number of sessions, whether modalities were used, stretching and methods of strengthening that were employed, and whether the patient is continuing a home exercise program after the completion of the therapy prescription. Other forms of therapy such as acupuncture, chiropractic manipulation, and cognitive behavioral therapy should be documented.
Dose and duration of opioid use should be noted, as well as changes in use over time (increasing, decreasing, or relatively constant) and conversion to stronger opioids, such as going from oral Oxycodone to Fentanyl patches. Recent studies have shown that chronic opioid use is associated with chronic opioid-induced hyperalgesia and effectively lowers pain threshold such that susceptibility to pain is increased. Evidence suggests that patients on high doses of opioids are more likely to fail procedural interventions, such as radiofrequency denervation and surgery. One study showed that patient treated for acute low back pain with a morphine equivalent amount (MEA) of 450 mg or more over the first 15 days are out of work 69 days longer, are three times more likely to have surgery, and are six times more likely to continue on opioids than those who were not treated with opioids. Finally, another study showed that patients with compensable back injuries on long-term opioids tend to increase opioid dosages without significant improvement of pain. It also concluded that the dosages used to treat acute low back pain predict long-term usage.
A careful medical, surgical, family, and social history should be done. Studies have shown that smoking increases susceptibility to chronic pain. Return to work was approximately 70% more likely in married workers than unmarried workers. A poor social support system has been linked to a higher risk of low back pain. Family history offers clues and may be a useful prognosticator. In patients with painful herniated disc, 35% of them had a first-degree relative with a history of a painful herniated disc compared with 12% for controls. Five percent of herniated disc patients had a family member who had back surgery for a herniated disc compared with 1% for controls.
The patient's relationship to work should be assessed. Patients who “hardly ever enjoyed their job” were 2.5 times more likely to report back pain than those who “almost always enjoyed their job.” Many studies have shown a decreased return-to-work rate with higher compensation in the form of workers’ compensation, disability insurance, and other forms of financial compensation. Financially compensated low back pain lasted, on average, 12 months in one study compared with 1 week on average for uncompensated low back pain. Low back injuries that occurred at work were associated with up to four times longer “out-of-work” duration than injuries that did not occur at work. Assessment should include whether an attorney is involved in the patient's case of back pain and whether it is in the setting of workers’ compensation, a motor vehicle accident, or other settings that may involve litigation. One study showed that when an attorney is involved in a workers’ compensation case, the return-to-work rate decreased by approximately 50% compared with cases without attorney involvement. Other studies show similar trends. Recommendations to employers to reduce work injury claims should not only include safety and ergonomic optimization, but also improve employee satisfaction, fitness for specific job tasks, and relationships among fellow employees and supervisors.
The patient's attitude toward exercise and details of their routine exercise regimen should be assessed. Patients who exercise regularly tend to have fewer episodes of back pain and recover more quickly. Monitoring of progressive return to their normal exercise routine is a positive prognosticator. If physical therapy is prescribed, knowledge of their normal exercise routine could allow for better integration of their therapeutic regimen.
A general medical evaluation should be performed, which includes listing the patient's medications and allergies and a general review of systems. Each of the patient's medical conditions should be surveyed to determine if they are controlled medically, in quiescence, or otherwise being followed by the patient's primary care physician or a particular specialist. If not, recommendations can be made to the patient and his or her primary care physician to get the issue(s) addressed.
The physical exam is a key component of the complete evaluation of the spinal pain patient. However, it is important to understand that a definitive diagnosis can rarely be conferred based on physical examination alone. Each part of the comprehensive patient visit represents one piece of a complex puzzle that includes history, psychosocial and family history, physical exam, imaging, and ancillary tests as deemed necessary (e.g., electromyography/nerve conduction studies). In some respects, the main value of the physical examination is to identify those patients who may benefit from advanced diagnostic testing (e.g., MRI) and/or for referral to an interventional pain specialist for injections or to a spine surgeon for surgical evaluation.
Look for open wounds, rashes, skin lesions, signs of infection, edema, or other issues that should be addressed. Port wine or other birth marks or doughy lipomata may indicate spina bifida. An unusual patch of hair on the spine can signify underlying bony abnormalities. Patients may present in the examination room unable to sit, pacing back and forth, leaning over the exam table, lying down as means to minimize back pain, or otherwise express and demonstrate the physical and emotional content of their pain experience, which may include these and other behaviors.
Abnormal gait can indicate pain-associated movement, muscle weakness that may indicate level of pathology (e.g., foot slap for L4 pathology), or fear-avoidance beliefs (FABs). Scissoring gait, where the legs cross when walking, can be observed after cerebrovascular events, spinal cord injury or syringomyelia, or cervical myelopathy. Steppage gait often accompanies foot drop and can occur with a herniated disc, with peroneal neuropathy or polyneuropathy, and after spinal cord injury. Waddling gait often ensues with muscular dystrophies, gluteus medius weakness, spinal muscle atrophy, and hip problems.
FABs are maladaptations from misinformation regarding the potential for physical injury of the low back stemming from generalized or specific activities. They involve avoidance of repeating the emotional content of the pain experience. FABs can stem not only from the patient, but also from misinformation, misinterpretation of information, and transference of these fears from health care providers or the Internet. It has been shown that excessive FABs result in hypervigilence in monitoring a patient's own pain and represent a significant obstacle for recovery from low back pain. It has also been shown that those who confront their pain and are able to increase physical and social activities over time have improved recovery rates, while those who respond to their pain with avoidance are more likely to develop chronic pain, increased impairment, and eventual disability.
Pain behavior, on the other hand, refers to the cognitive and emotional expression of pain such as limping, grimacing, moaning, crying, and asking for more pain medications. It has been suggested that these behaviors, through perceived validation, are reinforced with positive rewards by family, friends, and even health care providers; they also reinforce patient identity as being disabled. Further reinforcement comes in the form of financial rewards and excuses from returning to work and doing household chores. Ultimately, pain behaviors, through multiple studies, have been shown to be a significant barrier to recovery, and they enhance the perception of pain. When positive reinforcement ceases, the behavior is vulnerable to extinction, and the barrier to recovery is removed.
Lumbosacral Range of Motion, Including Flexion, Extension, Side Bending, and Rotation
It is not practical to try to isolate lumbar motion, and it has been shown that lumbosacral motion is an equivalent measure of function of the lumbar spine. If any motion causes pain, it should be documented. These quantitative measures can be monitored in subsequent follow-up visits to track progress. Pain with movement may indicate a potentially greater benefit from aggressive physical therapy as opposed to pain while sitting, lying down, or otherwise not moving. Normal ranges for lumbosacral spinal flexion are commonly between 70° and 100°; for extension, between 20° and 35°; for lateral bending, between 15° and 25°; and for axial rotation, between 20° and 30°.
The sit-to-stand test is 50% to 54% sensitive and 77% to 81% specific for L3/L4 nerve root impingement, respectively, and possibly the best test for this. The patient stands from a seated position on one leg while the examiner maintains patient's balance if needed.
Great Toe Extensor Strength
The great toe extensor strength test is 61% sensitive and 86% specific for an L5 nerve root impingement. Results are best if performed in isolation with foot flat on step stool with the great toe extending beyond edge of step stool and with examiner applying resistance.
The hip abductor strength test is 29% sensitive and 97% specific for an L5 nerve root impingement. Results are best if performed with the patient lying on his or her side with the hip slightly flexed. The test is performed when the patient abducts the hip against examiner's resistance. The test may differentiate between Tensor Fascia Lata (TFL) and gluteal weakness if first performed with the hip in slight flexion and then in extension, keeping the knee fully extended at all times. If there is a difference, a nerve root impingement is unlikely.
Plantar flexor strength is 4% sensitive and 86% specific for an L2, L3, and/or L4 impingement but does not differentiate among these levels. Likewise, this test is 14% sensitive and 96% specific for an L5 and/or S1 nerve root impingement. The patient is asked to stand on one foot and plantar flex his or her weight maximally 10 times. The test is then repeated on the contralateral foot.
The heel walking test is 20% sensitive and 86% specific for an L2, L3, and/or L4 impingement but does not differentiate among these levels. Likewise, this test is 14% sensitive and 80% specific for an L5 and/or S1 nerve root impingement.
The dorsiflexor strength test is for L4–L5, but it may not be specific for a particular root. Results are best when performed with the patient's ankles in firm contact on a step stool and dorsiflexed against examiner's resistance.
The hip flexors and adductors should also be tested.
In comparing different modes of sensory testing, it can be generally agreed that vibration is the first to be affected by radiculopathy and, therefore, would be the most sensitive but least specific test for radiculopathy at a given level. On the other hand, it is also known that light touch, pin prick, and temperature dermatomes do not overlap precisely. The quantitative findings in detecting levels in radiculopathy were performed using pinprick and so they are presented here. Anterior thigh pinprick is 50% sensitive and 96% specific for an L2 nerve root impingement.
This test is 61% sensitive and 86% specific for an L4 nerve root impingement.
This test is 17% sensitive and 96% specific for an L2, L3, and/or L4 impingement but does not differentiate among these levels. Likewise, this test is 4% sensitive and 83% specific for an L5 and/or S1 nerve root impingement.
Dorsal Great Toe Pinprick
This test is 13% sensitive and 82% specific for an L2, L3, and/or L4 impingement but does not differentiate among these levels. Likewise, this test is 18% sensitive and 87% specific for an L5 and/or S1 nerve root impingement.
This test is 8% sensitive and 79% specific for an L2, L3, and/or L4 impingement but does not differentiate among these levels. Likewise, this test is 21% sensitive and 92% specific for an L5 and/or S1 nerve root impingement. This test is best performed at the most distal areas of the lateral foot.
Patellar Reflex Abnormality
Patellar reflex abnormality test is 39% sensitive and 95% specific for an L4 nerve root impingement. Together with an abnormal medial ankle pinprick, it is 62% sensitive and 95% specific for an L4 nerve root impingement.
Achilles Reflex Abnormality
Achilles reflex abnormality test is 33% sensitive and 91% specific for an L5 nerve root impingement. Together with a weak hip abduction, it is 61% sensitive and 89% specific for an L5 nerve root impingement.
Ipsilateral Straight Leg Raise
The ipsilateral straight-lef raise test is 67% sensitive and 67% specific for an L5 nerve root impingement. It is 73% sensitive and 63% specific for an S1 nerve root impingement. It is 69% sensitive and 84% specific for either an L5 or S1 nerve root impingement. Reproduction of the patient's radiating pain pattern when hip is passively flexed between 30° and 70° is a positive result.
Contralateral Straight Leg Raise
The contralateral straight-leg raise test is 7% sensitive and 96% specific for either an L5 or S1 nerve root impingement. Reproduction of the patient's radiating pain pattern when contralateral hip is passively flexed between 30° and 70° is a positive result.
Ipsilateral Femoral Stretch Test
The ipsilateral femoral stretch test is 70% sensitive and 88% specific for an L3 nerve root impingement. It is 50% sensitive and 100% specific for an L2, L3, and/or L4 impingement, but does not differentiate among these levels. Reproduction of the patient's radiating pain pattern is a positive result.
Contralateral Femoral Stretch Test
The contralateral femoral stretch test is 9% sensitive and 100% specific for an L4 nerve root impingement. Reproduction of the patient's radiating pain pattern is a positive result.
Babinksi and Clonus tests evaluate for upper motor neuron involvement.
FABER/FADIR/Hip Grind/Hip External/Internal Rotation
These tests are used to evaluate hip pain and limited ROM due to degenerative joint disease in the hip or labral tear. The majority of pain should be in the groin, but patients may complain of lateral hip pain from these maneuvers. Applying pressure to the SI joint while in FABRE may indicate SI joint pain, but this is nonspecific. Applying pressure to the piriformis while in the FADIR position with reproduction of radiating symptoms may indicate piriformis syndrome, especially if the patient's hip rests in external rotation compared to the contralateral hip or if the patient has difficulty in active hip internal rotation. In practice, however, this is also nonspecific.
Applying Pressure to Spinous Processes at Midline
When testing in this manner, tenderness may indicate a fracture, interspinous ligamentous sprain, or underlying disc pathology.
Applying Pressure Paraspinally
When applying pressure of this kind, tenderness may indicate primary muscular spasm or strain (i.e. trigger point) or may occur secondarily in response to other pathology, such as with facetogenic or sacroiliac joint pain. Identifying the primary source of pain by palpation is controversial. Because the facet joint lies as much as 7 cm below the skin, it is not likely that a particular painful facet joint can be palpated with specificity. Multiple studies have demonstrated increased levels of myoelectric activity during electromyography (EMG) testing.
Arguably antiquated, Wadell's Signs were originally described more than 30 years ago. The presence of signs from the following five categories has been the subject of widespread misinterpretation and misuse over the ensuing decades. A review by Fishbain and colleagues found either negative or conflicting evidence for an association between Waddell's signs and psychological stress or secondary gain and their ability to reliably distinguish organic from nonorganic pathology. However, the authors concluded that the presence of signs in three of the five categories was positively associated with greater baseline pain and disability and poorer treatment outcomes. During the physical exam, there should be ample opportunities to observe these physical signs in five categories that may caution the examiner when considering invasive procedures, and may prompt a more detailed psychological evaluation:
Overreaction: Excessive pain behaviors and verbal expressions while doing maneuvers that require patient to move either actively or passively.
Tenderness: Pain behaviors with light touching or pinching of skin in a nonanatomic pattern.
Nonanatomic findings: Patients with signs and symptoms that do not correlate well with known anatomy. Examples include discord between myotomal findings and dermatomal findings or findings that include parts of dermatomes but exclude other parts of the same dermatomes. An example of this would be entire right foot pain without pain above the right ankle or numbness of the entire leg but not the foot.
Distraction: Tests that are abnormal but become normal when patient is distracted or that stay abnormal without following through with the test. An example is a patient who shows marked weakness in the plantar flexors or quads in isolation but is later climbing stairs without difficulty alongside the examiner who is carrying on a conversation about a distracting topic. Another example is when a patient is hyperreflexic at the patellae and also hyperreflexic when the examiner stops the hammer before striking the patellar tendon.
Simulation: Low back pain exacerbation by pushing down on the top of the patient's head or shoulders.
Other physical exam maneuvers are performed as deemed necessary. Patients with complaints of balance problems or exam findings of clonus should receive a full neurological exam, including cranial nerve evaluation, tightrope walking, Rhomberg test, heel-to-toe walking, and so forth. Patients with hip, knee, or foot pain should receive appropriate examinations to rule in or rule out nonspinal causes of pain. Often, these are the reasons for referral to a pain or spine physician to help determine whether the pain is coming from the hip, knee, or foot or from the spine. For example, it would be a mistake for surgeons to perform hip surgery for groin pain that is referred from the spine.
See the Chapter Addendum for other exam maneuvers that may be useful in a physical exam.
With the advent of new procedures, neuroimaging has taken on a greater role in recent years for the diagnosis of LBP. Conventional radiographs are frequently used during an initial evaluation of LBP, especially in patients with known musculoskeletal disease, or when a fracture is suspected. Disorders likely to be picked up on plain x-rays include spondylolisthesis, pars interarticularis defects, scoliosis, ankylosing spondylitis, Scheuermann's disease, spinal stenosis, and osteoporosis. However, because of the low yield with radiographs, their utility in patients with LBP is controversial.
Magnetic resonance imaging is the diagnostic test of choice for evaluating patients with radiculopathy. Other disorders in which MRI is the preferred imaging tool include myelomalacia, syringomyelia, intramedullary tumors of the spinal cord, spinal cord infarction, traumatic injury, and multiple sclerosis. In a study by Jensen et al. published in the New England Journal of Medicine, 64% of individuals without LBP were found to have abnormal intervertebral disks on MRI scans of their lumbar spine. The results of this study have been confirmed by numerous other investigators, with the prevalence of abnormalities increasing with age. Currently, the American College of Physicians recommends an MRI only for serious or progressive neurological deficits or when referring patients for surgical evaluation or epidural steroid injections.
The strength of computed tomography in evaluating patients with LBP lies not in its resolution but in its ability to define spatial relationships between anatomic structures. As such, CT is helpful in patients with spinal stenosis, spinal infections, primary metastatic tumors of the spine, and spinal cord injuries. Because CT provides better images of bone than does MRI, it is preferred for patients with suspected bony abnormalities. Frequently, CT is used in conjunction with myelograms for the evaluation of radiculopathy and following discography to better delineate disk disease.
Radionuclide bone scanning is the procedure of choice for detecting a variety of bone disorders. Bone scanning is the primary modality used to diagnose and follow skeletal metastases. Whereas osteomyelitis may not be detectable radiographically for more than a week after onset, a bone scan usually shows areas of enhancement within hours of onset. Other indications for bone scanning include occult vertebral fractures, bone disease associated with metabolic disorders, and spondyloarthropathies.
The complexity of low back pain and radiation can be daunting to the unfamiliar practitioner. In any given patient, the number of pain generators can range from a single source (such as a herniated disc) to multiple sources (such as multilevel disc herniations, facet arthropathy, and stenosis) plus pain generated from remote sources (such as the hip, sacroiliac joint, or piriformis muscle). In addition, psychosocial factors are likely to affect the diagnosis, treatment, or prognosis of any given patient. Finally, there is often no single piece of historical information, no particular physical exam finding, nor a particular MRI result that can reliably result in a definitive diagnosis or prognosis. It often takes a well-informed and experienced practitioner, as well as a motivated patient, to arrive at a meaningful diagnosis, prescribe viable treatment options, and improve patient outcomes. A patient visit of at least 30 minutes is often required to gather all pertinent information from the patient, formulate treatment options, and provide meaningful education and reassurance to the patient.
It is also important to closely monitor patient progress in the form of follow-up visits. Often during these visits, a patient may report increased pain from a particular treatment course, and the experienced practitioner should understand the side effects of these treatments and also the natural course of the particular etiology being treated. Increased pain is expected in the early course of any effective physical therapy and it is rarely is a cause to cease therapy. Injections can also cause transient increases in pain. Finally, some etiologies, such as disc herniations, most often have a natural course of waxing and subsequently waning regardless of whether treatment has been prescribed or not. The experienced practitioner should be able to rule out very rare but concerning processes, such as a new vertebral fracture or more commonly a painful reherniation. Most often, however, increased pain is benign. The practitioner should be comfortable with complaints of increased pain and also with reassuring the patient that his or her increased pain is part of the neurologic or muscular pathology and does not indicate harmful anatomic events.
ADDENDUM: SPECIAL TESTS BY CATEGORY FOR LOW BACK PAIN WITH OR WITHOUT RADICULOPATHY
Bow String Sign. The patient is seated with the body bent forward and knee flexed to 70°, a position that lengthens the course of the sciatic nerve. The examiner then applies pressure on the sciatic nerve by pressing the fingers into the popliteal fossa. An increase in leg pain signifies a radiculopathy.
Brudzinski's Test. With the patient supine, the head is passively flexed to the chest. Reproduction of the patient's leg pain signifies nerve root irritation.
Kernig's Test. The patient lies supine with the hip flexed 90°. The patient is then asked to extend the knee. Back pain may be a sign of nerve root irritation.
Lasegue's Test. The patient lies supine with the hip flexed 90°. The patient is then asked to slowly extend the knee. A positive test occurs with the elicitation of sciatic pain.
Milgram's Test. The patient, lying supine, is asked to elevate both extended legs approximately 2 inches off the examining table. If the patient can hold this position for 30 seconds without pain, it aids the examiner in eliminating intrathecal pathology as a cause of pain. If the patient experiences pain during this maneuver or cannot hold the position, intrathecal pathology, such as a herniated disk, must not be ruled out.
Stoop Test. The patient is asked to walk briskly for several minutes. When back, posterior thigh, and leg pain appear, the patient sits and flexes forward. Disappearance of the pain suggests neurogenic claudication. During this time, reflexes may be diminished.
Valsalva's Test. The patient is asked to bear down, as during a bowel movement or coughing, thus increasing intrathecal pressure. A positive test suggests intrathecal pathology.
TESTS FOR SACROILIAC JOINT DYSFUNCTION
Cranial Shear Test. With the patient prone and the pelvis immobilized through the hip, pressure is applied to the coccygeal end of the sacrum. This test may be positive in patients with sacroiliac joint pain.
Extension Test. The patient is placed in the prone position, with one hand of the examiner on the thigh of the affected side and other hand over the opposite iliac crest. Downward pressure is exerted on the iliac crest, while pulling slightly on the anterior thigh, to elicit sacroiliac joint pain.
Flamingo Test. The patient is asked to stand on the involved leg and hop. Pain in the sacroiliac region may be indicative of sacroiliac joint dysfunction.
Gaenslen's Test. The patient lies supine on the examining table with both knees drawn to the chest. The patient is then asked to shift over to the edge of the table, so that the leg being tested hovers over the edge. The examiner presses down on the affected side, hyperextending the hip. A positive Gaenslen's test is generally considered a sign of sacroiliac joint pain but may indicate hip pathology as well.
Gillet's Test. While the patient stands with the feet approximately 12 inches apart, the examiner sits behind the patient and palpates the S2 spinous process with one thumb and the posterior superior iliac spine with the other. As if taking a large marching step, the patient then flexes the knee and hip of the side being tested. If the posterior superior iliac spine fails to move posteroinferiorly with respect to S2, the test is positive. This may be indicative of sacroiliac joint dysfunction.
Patrick's Test. The patient is positioned supine with the foot of the involved side against the opposite knee. The sacroiliac joint is then stressed by pressing simultaneously against the flexed knee and contralateral anterior superior iliac supine. The Patrick's test is used to assess both sacroiliac joint dysfunction as well as hip pathology when, in the latter, pain is elicited in the inguinal or hip area. Because this test involves flexion, abduction, and external rotation of the hip, it is also called the FABER test.
Pelvic Compression Test. This test compresses the pelvis by the application of lateral pressure to the uppermost iliac crest, directed toward the opposite iliac crest. It is believed to stretch the posterior sacroiliac ligaments and compress the anterior part of the joint.
Pelvic Distraction Test. For this test, the examiner applies pressure to both anterior superior iliac spines, directed posteriorly and laterally. This test is alleged to stretch the anterior sacroiliac ligaments.
Pelvic Rock Test. The patient lies supine, and the examiner cups both hands around the iliac crests with the thumbs on the anterior superior iliac spine and the palms on the iliac tubercles. The examiner then forcibly compresses the patient's pelvis toward the midline of the body. Complaints of pain may indicate pathology in the sacroiliac joint.
Sacroiliac Shear Test. With the patient lying prone, the examiner crosses both hands over the sacrum. The overlying hand delivers a postero-anterior thrust, while the underlying hand is used to detect motion in the joint.
Shift Test. Patient stands with feet 12 inches apart and is asked to shift his or her weight from foot to foot, back and forth. Transient pain is felt on the offloading side with each shift. Again as with all SI joint testing, this test is nonspecific for SI joint pathology.
Thigh Thrust Test. This test applies a posterior shearing stress to the sacroiliac joint through the femur.
TESTS FOR PIRIFORMIS SYNDROME
Beatty's Maneuver. From the lateral decubitus position with the nonpainful side dependent, the patient is asked to abduct the thigh by moving the nonpainful leg off the table. Contraction of the piriformis muscle elicits pain in patients with piriformis syndrome.
Freiberg's Sign. Recreation of buttock or leg pain, or both, occurs during internal rotation of the hip. This test may be positive in patients with piriformis syndrome.
Pace Sign. An indicator of piriformis syndrome, this test is positive when the patient experiences weakness during resisted abduction and external rotation of the leg.
TESTS FOR MUSCLE PATHOLOGY
Beevor's Sign. While the examiner observes the patient's umbilicus, the patient is asked to do a quarter sit-up with the arms crossed over the chest. Normally, the umbilicus should not move. If the umbilicus is drawn up, down, or over to one side (the stronger side), weakness, atrophy, or asymmetry of the anterior abdominal or paraspinal muscles may be present. This sign is frequently positive in patients with meningomyelocele or poliomyelitis.
Sit-up Test. Patient's with severe discogenic pain or paraspinal muscle spasm have difficulty sitting up unassisted when flexed at their lumbar spine. They have a tendency to push up with their arms for support.
Tripod Sign. As the patient sits with legs dangling and hips flexed 90°, the knees are passively extended. Patients with hamstring muscle tightness will extend the trunk to relieve the pressure.
TESTS FOR NONORGANIC COMPONENTS TO DYSFUNCTION
Hoover's Test. This test should be performed in conjunction with the straight-leg raise test. A patient who is making a genuine effort to raise the affected leg will automatically put pressure on the calcaneus of his opposite leg in order to gain leverage. By placing one hand under the patient's heel, the examiner can determine whether or not the patient is making a concerted effort.
Ratcheting versus Smooth Strength Testing. When attempting a sustained muscle contraction such as dorsiflexion at the ankle, patients with nonorganic components to dysfunction exhibit ratcheting and jerking movements and, eventually, breakaway weakness. In contrast, patients with isolated myotomal weakness are overcome in a smooth fashion.
TESTS FOR UPPER MOTOR LESIONS
Babinski's Reflex. Stimulation is applied to the plantar surface of the foot with a dull object. When the lateral four toes flex and fan and the large toe extends, an upper motor lesion is suspected.
Chaddock Reflex. This test is similar to the Babinski's reflex test, except that the lateral aspect of the foot beneath the lateral malleolus is stimulated.
Oppenheim's Test. A dull object is run down the anterior portion of the tibia. A positive response is similar to Babinski's reflex.
Schober's Test. This test measures the flexibility of the lumbar spine. The patient's back is marked twice, once at the level of the sacroiliac dimples and again 10 cm above this point. As the patient flexes forward, the distance between the two points should increase by at least 4 cm. An abnormal test may indicate spondyloarthropathy.
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