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.

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:

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  Standing relaxed: defined at 100%.

  
  
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  Lying prone: 20%.

  
  
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  Sitting unsupported: 92%.

  
  
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  Standing and flexing forward: 220%.

  
  
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  Sitting and flexing forward: 166%.

  
  
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  Lifting a 45-lb weight with rounded flexed back: 460%.

  
  
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  Lifting a 45-lb weight with flexed knee: 340%.

  
  
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  Lifting a 45-lb weight with flexed knee and weight close to body: 220%.

  
  
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  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.

MYOFASCIAL PAIN

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.

SPINAL STENOSIS

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 ARTHROPATHY

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.

SACROILIAC JOINT PAIN

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.

PIRIFORMIS SYNDROME

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.

SCOLIOSIS

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.