Key points

Introduction

FBSS is persistent or recurring low back pain with or without lumbosacral radiculopathy after 1 or more spine surgeries. The incidence of FBSS is reported as between 10% and 40% but ranges between 5% and 50% have been quoted for microlaminectomy alone. The incidence is known to increase with more complex surgeries and has not improved with the development of less-invasive advanced surgical techniques. The failure rate for lumbar fusion is reported between 30% and 46% based on previous reviews whereas the failure rate for microdiskectomy is thought to range between 19% and 25%. The financial costs are considerable.

Introduction

FBSS is persistent or recurring low back pain with or without lumbosacral radiculopathy after 1 or more spine surgeries. The incidence of FBSS is reported as between 10% and 40% but ranges between 5% and 50% have been quoted for microlaminectomy alone. The incidence is known to increase with more complex surgeries and has not improved with the development of less-invasive advanced surgical techniques. The failure rate for lumbar fusion is reported between 30% and 46% based on previous reviews whereas the failure rate for microdiskectomy is thought to range between 19% and 25%. The financial costs are considerable.

Risk factors for failed back surgery syndrome

Chan and Peng provide an excellent review of the risk factors for the development of FBSS. Specific psychosocial risk factors that have been found to result in poor outcome for spinal surgery are significant levels of depression, anxiety, poor coping, somatization, and hypochondriasis. The presence of a worker’s compensation claim is consistently cited in the literature as a risk factor associated with poor surgical outcomes and is often dismissed as due to secondary gain. It is important to differentiate true secondary gain from symptom magnification imposed by inability to obtain timely diagnosis and treatment. In addition, FBSS patients often pursue disability claims after job loss to retain insurance coverage for ongoing treatment. FBSS is, therefore, a biopsychosocial problem where indirect and intangible costs play a significant role in defining morbidity.

A major difficulty in preventing FBSS is that the ideal time to operate is not well defined in the literature. Surgical decision making is clear when there is progressive motor loss or cauda equina syndrome. But the timing and indications for surgery when pain is the primary complaint are not well defined. A general dictum is that 6 to 12 weeks of conservative care is reasonable prior to surgery.

It has been stated that the 2-year outcome for patients treated with either laminectomy or microlaminectomy is the same as for those treated with conservative care. The time to pain improvement is faster, however, with the surgical groups. If considerations for lost productivity and lifestyle compromise are openly discussed, surgery may be a reasonable option for refractory pain as an earlier option.

Earlier surgical intervention for low back pain may make sense in selected cases on a physiologic basis. Since the 1970’s it has been accepted that untreated pain promotes persistent pain patterns in the central nervous system in as little as 3 months. This is often attributed to “wind-up phenomena” or central sensitization at the levels of the spinal cord and central nervous system. Once chronic pain patterns develop treatment because more complicated and the likelihood of a successful outcome diminishes.

Deciding on the ideal time to operate is further complicated by disuse atrophy and chronic inflammation promoting physical deconditioning, making restoration of function and pain control more difficult after surgery. Prolonged pain and distress also may exacerbate preexisting psychosocial stressors, which is especially problematic with hypervigilant patients who have poor pain tolerance because they may simply refuse to normalize their activities, thereby creating a vicious cycle of pain and deconditioning. Thus, although an ounce of prevention may be worth a ton of cure, nihilism with respect to surgical decision making is not reasonable.

Preoperative risks

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  Prior surgery

  
  
  
  
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    Spinal instability has been noted to occur in 12% of cases after a first surgery and increases to greater than 50% after 4 or more revisions.

  
  
  
  
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  Surgery based on imagining abnormalities without good clinical correlation

  
  
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  Nonsurgical causes of radiculopathy and neuropathy, including toxic-metabolic neuropathies (eg, diabetes), viral and inflammatory radiculitis, vascular disease, and plexopathies due to a pelvic mass or trauma

Intraoperative risks

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  Difficult radiographic localization intraoperatively during microsurgical cases or when there are segmentation defects causing operation at the wrong level, thus leaving the true pain generator without intervention

  
  
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  Inadequate decompression may leave a pain generator intact.

  
  
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  Aggressive decompression may lead to spinal instability and pain.

  
  
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  Loss of disk height after diskectomy may lead to vertical stenosis, compression, and pain.

  
  
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  Unrecognized pathology, such as disk fragments in the neural foramen, kinking of the nerve root by the adjacent pedicle, root compression by the articular process, spinal stenosis, extraforaminal disk herniation, and conjoined nerve roots may frustrate a successful outcome.

  
  
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  Excessive retraction, bleeding, or use of cottonoid patties may lead to battered root syndrome. Battered root syndrome is thought to occur in as many as 13% of cases with diskectomy and should be suspected if there is incomplete resolution of sciatic symptoms with or without progressive neurologic deficit that progresses over 3 to 6 months. It may be more common if there are conjoined nerve roots.

  
  
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  Pars interarticularis fracture may occur during decompression.

  
  
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  Use of methyl methacrylate as a primary means of stabilization or as a salvage technique for stripped screws may damage neural elements through compression or heat.

  
  
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  Roots may be damaged by graft extrusion after posterior lumbar interbody fusion (PLIF) or from excessive retraction.

  
  
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  Finally, the aim of surgery may be difficult to achieve. Proper decompression for foraminal stenosis due to ligamentous hypertrophy or far lateral disk herniation may cause destabilization of the segment and postoperative pain.

Postoperative factors

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  Postsurgical complications

  
  
  
  
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    Hematoma or infection

    
    
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    Symptomatic pseudoarthrosis after fusion surgery

    
    
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    Epidural fibrosis may tether spinal nerve roots and interfere with cerebrospinal fluid–mediated nutrition of the nerve roots or interfere with the vascular supply of the nerve roots.

    
    
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    Pseudomeningocele, which can result from inadequate closure or inadvertent meningeal tear. This is a pseudocyst with no true meningeal lining that is secondary to postoperative dehiscence and can affect up to 2% of postlaminectomy patients. Patients with pseudomenigocele complain of wound swelling, headache, and focal neurologic symptoms, including radicular pain and cauda equina symptoms.

    
    
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    Persistent irritation of the nerve roots may also result from postsurgical arachnoiditis and can result in both axial and lower limb pain. MRI T2-weighted fast spin-echo sequences provide the best evaluation for arachnoiditis. There are 3 patterns of presentation on MRI:

    
    
    
    
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      Type 1 is a conglomerate of nerve roots seen as nerve root clumping, and this pattern is associated with the mildest involvement.

      
      
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      Type 2 is due to peripheral adhesions of the nerve roots to the thecal sac producing the so-called empty sac appearance and is associated with moderate involvement.

      
      
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      Type 3 refers to an intermediate attenuation mass obliterating the subarachnoid space below the conus medullaris and is thought to produce the most severe presentation.

    
    

  
  
  
  
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  Anatomic or biomechanical alterations

  
  
  
  
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    Spinal instability has been noted to occur in 12% of cases after a first surgery and increases to greater that 50% after 4 or more revisions.

    
    
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    Loss of disk height after diskectomy may lead to vertical stenosis, compression, and pain.

    
    
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    Transition syndrome, or adjacent level disease, is due to altered biomechanics that imposes increased load across adjacent spinal segments after diskectomy, thereby accelerating preexisting disk degeneration. Similar mechanisms are thought to predispose to sacroiliac (SI) dysfunction, especially after fusion, and this is thought to occur in up to 36% of patients after lumbar fusion.

    
    
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    Recurrent disk herniations are known to occur in approximately 15% of patients at the site of operation or in adjacent segments because of altered load distributions. Altered load distributions may exacerbate adjacent level spondylolisthesis or further stenosis as part of a transition syndrome.

    
    
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    Myofascial pain

  
  

Myofascial pain may result from dissection or prolonged retraction of the paraspinals during surgery, causing denervation and atrophy. Altered postural changes postoperatively may also create permanent chronic strain. There are no large studies to demonstrate that development of minimally invasive fusion surgeries, such as PLIF, axial lumbar interbody fusion, and transforaminal lumbar interbody fusion, have an impact on the incidence of FBSS or this component of FBSS, despite that these surgeries do not disrupt the dorsal musculature extensively. The author’s anecdotal experience over 10 years in a university-affiliated spine center is that there is little if any difference.

Fusion disease is a form of myofascial pain that has been attributed to compensatory hyperextension of the lumbar spine exacerbating poor posture. It has been attributed to paraspinal and hamstring muscle spasm or atrophy. In the author’s experience, however, flexed posture and difficulty arising from sitting is even more common after low lumbar fusion. Short-term relief can be afforded with manipulation and focused physical therapy but recurrent and persistent pain, spasm, and limited of range of motion is common. In the author’s view, the recurrence of these symptoms is most likely due to a combination of permanently altered postural biomechanics from fusion hardware constructs and self-perpetuating muscle imbalances with the hip flexors overpowering the multifidi, short lumbar rotators, paraspinals, and transversus abdominis.

The difficulty demonstrated by long-term treatment of this problem emphasizes that myofascial pain is a complex problem demanding an individualized approach that targets specific deficits. Complicating factors include

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  Differentiating referred versus true radicular pain

  
  
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  Differentiating the role of osteoligamentous structures versus the role of neuromuscular coordination (motor control) for pain-free motion

  
  
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  Understanding how predominantly tonic muscles and phasic muscles respond to injury

Myofascial referred pain can be easily confused with radicular pain. The description of chronic ligamentous strain or musculotendinous pain as deep burning ache is similar to dysesthesia and the patterns of pain can also confound diagnosis. Travell and Simons provide several examples of pain patterns responsive to trigger point therapy that seem indistinguishable from dermatomal radicular pain, for example, trigger points in the gluteus minimus and gluteus medius that mimic L5 radiculopathy.

The clinical presentation of myofascial pain is important for 2 reasons: (1) it is not responsive to many of the treatments commonly offered to chronic FBSS patients, such as opioids and interventional spine techniques; and (2) if left untreated, it becomes worse, making it more difficult to resolve. This is important because it feeds patient perceptions of incapacity and hopelessness and contributes to the vicious cycle of pain and deconditioning commonly seen with FBSS patients. There are 2 dominant theories of myofascial pain propagation. One focuses on peripheral mechanisms where damaged motor endplates locally propagate more trigger points, and the other posits that central sensitization in the dorsal horn causes expanded receptive fields in the spinal cord and amplifies perception. The issues of posture and balance most likely also play a significant role.

Another major consideration, relative to lumbar myofascial pain, is the issue of motor control if overloading of muscles, tendons, ligaments, disks, and joints are to be minimized. Motor control is the regulation of coordinated muscular activity allowing efficient transfer of loads to joint services. Motor control requires (1) accurate instantaneous feedback from mechanoreceptors at the joint/soft tissue interface, (2) appropriate interpretation of this input, and most importantly, (3) modulation and timing of the responses to accomplish specific tasks. The loss or perturbation of these neuromuscular adaptations can result in refractory pain, inefficient movement, and inappropriate force closure of joints during motion. These, in turn, can lead to articular microtrauma and inflammation, ligamentous laxity, and disuse atrophy, which can mimic neurogenic weakness.

The role of the inner ring muscles, consisting of the multifidus, thoracolumbar fascia, and transverses abdominis, and, their interaction with the diaphragm and pelvic floor muscles to create a cylindrical supporting system for the lumbar spine through the regulation of intra-abdominal pressure is especially important. This is not an issue of strength but rather of timing and coordination, which are fundamentally important because the posterior portion of this ring, the multifidus, receives its innervation from the posterior rami and medial branches of the lumbar roots. Consequently, if there is injury to the lumbar roots, coordination of the multifidus can be compromised. Richardson and colleagues presented persuasive data that these timing issues play an important role and are common denominators in many cases of chronic low back pain. Motor control is generally regulated by reflex mechanisms at the level of the spinal cord but it can be affected by supraspinal influences, such as mood and arousal, and this too is consistent with chronic pain variability.

The propagation of myofascial pain is also affected by how tonic and phasic muscles respond to injury. Physicians learn that muscle fibers can be categorized histologically and by their speed of contraction:

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  Type I, or slow oxidative muscle fiber, has high mitochondrial content.

  
  
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  Type IIa, or fast glycolytic muscle fiber, has low mitochondrial content.

  
  
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  Type IIb, or fast oxidative muscle fiber, has a high mitochondrial content like type I fiber, but, it has a lower glycogen content than type IIa fiber and an intermediate range of fatigue between type I and type IIa fiber.

Most human skeletal muscle is not truly represented by any of these types, however. A more functional classification characterizes muscles as either predominantly tonic or phasic. Tonic muscles are postural and not susceptible to early fatigue. Phasic muscles provide ballistic function (movement) and are less suited to endurance activities. Some muscles serve both functions depending on situational context, such as the vastus medialis, which stabilizes the knee during loading and standing (tonic function) but also extends the leg ballistically during activities, such as drop kicking a football (phasic activity). The point of this classification is how these muscle types respond to overloading and injury. Tonic muscles tend to shorten with injury and overloading. Phasic muscles tend to weaken with injury and overloading. Examples of tonic muscles include the erector muscles of the lumbar spine, piriformis, and hip flexors. Examples of phasic muscles include the abdominal muscles, knee extensors, and gluteus muscles. The important point is that shortened tonic muscles can inhibit phasic antagonists and synergists, thereby preventing maximal activation and optimal trainability. Consequently, a vicious cycle is created and compounded by faulty substitution patterns that develop after injury and surgery. This situation is especially problematic after denervation or if fusion constructs prevent range of motion, because normal muscle balance may not be recoverable. Consequently, any successful rehabilitation strategy has to account not only for strength and flexibility but also for posture and motor control issues. Treatment of myofascial pain is also thought dependent on improving a patient’s aerobic capacity.

Evaluation of the postoperative spine: history and physical

History and physical examination are the most important parts of evaluating FBSS. There is considerable overlap, however, of the types of pain associated with this syndrome. The potential anatomic and pathologic processes responsible for postoperative pain complaints are difficult to differentiate. The types of pain include myofascial pain, arthropathic joint pain, and radicular pain that follows true dermatomal patterns associated with dysesthesia, loss of sensation, or loss of power. Chronic neural pain of any kind, whether visceral, sympathetically mediated, or phantom pain, is diffuse, poorly localized, and not well described anatomically. It is sometimes described with combinations of cramping, aching, and tight or burning sensations and is, therefore, similar to myofascal pain; it is ill described. It may also be associated with hyperalgesia or allodynia, which is important because, like myofascial pain, chronic neural pain is less responsive to opioids and better treated with adjuvant medications and therapies.

Physical examination typically focuses on neurologic findings, such as deep tendon reflexes and motor and sensory examination. Musculoskeletal examination, however, should include flexibility and tests of hip mobility, seated and standing trunk rotation, lumbar flexion and extension, lumbar side-bending, and palpation of the SI joints and trochanters. The entire spine should be examined and concomitant disease causing myelopathy with increased tone, clonus, and Babinski and Hoffmann signs should be ruled out. Spondylosis is a generalized condition and does not affect the lumbar spine in isolation.

Side-to-side asymmetry of motion is more important than measured range of motion. Straight leg raise and femoral nerve stretch test are also important with respect to the postoperative spine. True radicular pain with numbness or dysesthesia in dermatomal patterns is important to differentiate from decreased flexibility and discomfort due to lost range of motion from chronic injury or postsurgical guarding. A good representative neurologic examination is available from the American Spinal Injury Association, and the American College of Rheumatology has excellent materials on trigger/tender point examination. Patients should be assessed for leg length discrepancies and focal weakness, especially footdrop, because orthotics and bracing may be necessary to minimize repetitive strain over the kinetic chain. Finally, screening tests for motor control and stabilization are also recommended. Two easy tests include

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  Assessing balance from the hands and knee position with opposite arm and leg extension (the pointer dog test)

  
  
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  Maintaining a stable prone plank position from a modified push-up position where the patient starts prone and elevates to the elbows and balls of the feet

The entire physical examination should not take more than 8 to 10 minutes of office time. Evaluation of functional potential is more important than immediate relief of pain. The initial cause of surgery, prior symptoms and neurologic deficits, type of surgery, current symptoms, and time since surgery are critical to know to evaluate the advantages and limitations of particular imaging studies, further work-up, and treatment modalities. It is also imperative to assess compliance with previous treatments and rehabilitation efforts to appreciate any psychosocial overlay that has an impact on care.

Evaluation of the postoperative spine: work-up

Radiographic evaluation is an important tool because it may reveal anatomic aberrations, allowing for definitive treatment and better prognostication, such as residual lateral recess stenosis. Diagnostic studies may also provide reassurance that serious pathology is not present and that neurologic deterioration is not likely to occur with increased activity.

Radiologic findings specific to FBSS should not be confused with postoperative normal variants. Small seromas and edema of the subcutaneous tissue after surgery should be expected and herniation of the thecal sac through a new laminectomy defect may produce a mass effect that is normal if it is seen to decrease on serial films over the first 30 to 60 days.

MRI demonstrating epidural fibrosis has to be interpreted with caution because most patients with epidural fibrosis are asymptomatic. Nerve root enhancement is often seen in asymptomatic patients for 6 months after surgery, but if nerve root thickening and displacement are seen, the positive predictive value of imaging improves. The main differential in this setting is recurrent disk herniation, and recurrent disk herniation needs to be ruled out in symptomatic patients.

Similarly, postoperative inflammation and fibrosis due to disruption of the annulus fibrosis and epidural edema may simulate recurrent disk herniation with noncontrast MRI studies. Vertebral endplates can demonstrate edema and enhancement in 19% of patients between 6 and 18 months after surgery and nerve root enhancement may linger for 6 weeks or longer in 20% to 62% of patients after surgery. Consequently, careful correlation with progressive clinical signs and symptoms is mandatory during any investigation for postoperative or persistent pain.

MRI is generally the modality of choice in the postoperative setting because it allows for evaluation of soft tissues, bone marrow, and intraspinal content. Metallic hardware may lead to magnetic artifact but this can be minimized with fast spin-echo sequences, short echo time, and longer repetition time. Titanium and vitallium hardware produce less artifact than stainless steel on MRI. T2-weighted sequences should also afford better visualization with less artifact and short time inversion recovery sequences and should be used for fat suppression to improve homogeneity of the image.

Contrast administration with T1 imaging is useful to distinguish inflammatory tissue from recurrent disk herniation. Contrast is also useful when infection is suspected because bacterial diskitis is associated with particularly intense contrast enhancement compared with normal inflammatory change that can be seen postoperatively. A heightened index of suspicion for infection should arise if fluid collections are seen in paraspinal areas or the anterior epidural space; if they are located adjacent to the disk involved; or if there is psoas enhancement. Contrast-enhanced MRI with fat saturation is the modality of choice when infection is suspected because it allows for evaluation of bone edema and diskitis earlier than other modalities. Contrast-enhanced CT allows for assessment of associated bone involvement, phlegmons, and abscesses and both CT and ultrasound are useful for guiding biopsies.

CT is the modality of choice for bone and abnormal calcification assessment. Intravenous iodine contrast is required to investigate suspected infection. Metal artifact can be reduced with attenuation techniques, and software manipulation and orthopedic hardware with lower attenuation coefficients are known to produce less distortion. Titanium produces less distortion than stainless steel, which, in turn, produces less distortion than cobalt-chrome.

CT is particularly useful for investigating suspected misplaced or loosened hardware. Root irritation can be seen with misplaced pedicle screws encroaching on the lateral recess or foramen. In general, root irritation is associated with low or medial screw placement. Loosening of hardware can be seen with infection or stress fatigue and is associated with a halo or hypoattenuation greater than 2 mm around the hardware.

Conventional radiographs are particularly useful when there is hardware because there is no metallic artifact. Anteroposterior, lateral, oblique views and flexion/extension views are all useful when planning diagnostic or therapeutic interventional procedures and to diagnose structural problems, such as postoperative loss of disk height or spondylolisthesis with instability.

Electrodiagnostic evaluation of the postoperative spine can be useful for both localization and prognosis, especially if there is a preoperative study to compare with. A change in compound motor action potential and increase in peripheral membrane irritability may reflect worsening postoperative axonopathy. Similarly, membrane irritability may localize to the involved nerve root when there is multilevel disease. The presence of membrane irritability that correlates with at least one grade of motor loss on physical examination may assist treatment considerations if differentiating motor loss from involuntary guarding is difficult. For example, assistive devices and lifestyle management may be more appropriate in the presence of extensive neurogenic atrophy whereas aggressive strengthening exacerbates joint pain and instability.

Interpreting electrodiagnostic evaluations requires some caution. Sampling size always has an impact on recognition of membrane irritability and both positive and negative findings have to be measured against the clinical picture and radiology. As a rule, MRI is more sensitive than electromyogram (EMG) for diagnosing the cause of radiculopathy but EMG is more specific for the presence of radiculopathy. If both sensory and motor nerve conduction abnormalities are seen, a peripheral nerve problem is more likely than a preganglionic root problem. It is, however, possible for vertical stenosis or a large lateral disk herniation to affect the dorsal root ganglion and cause sensory nerve conduction abnormalities too, most commonly at L5.

Paraspinal denervation does not always equal lumbar disease. It can be seen in diabetics and, if associated with extensive denervation in more than the expected peripheral myotomes, the differentials for myopathic, neuropathic, or motor neuron diseases should come to mind. Finally, irritability in the paraspinals may persist because of incisional muscle damage and therefore, muscle sampling should be further than 2 cm from an incision line and interpretation must still be made with caution.

Treatment

The goals of treatment are to maximize neuromuscular and musculoskeletal efficiency with activity, control pain, and interrupt and reverse the progression of debility. Medical therapy should be advanced with the goal of increasing physical activity and community involvement. Pharmacologic management includes

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  Nonsteroidal antiinflammatory drugs or acetaminophen

  
  
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  Muscle relaxants, such as cyclobenzaprine, methacarbamol, and metaxalone

  
  
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  True antispastic medications, such as baclofen or tizanidine

  
  
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  Antidepressants, such as tricyclics, selective serotonin reuptake inhibitors, and combined serotonin and norepinepherine reuptake inhibitors

  
  
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  Gabapentinoids

  
  
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  Tramadol

  
  
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  Opioids

Medication prescription should take into account mechanisms of action, presumed modification of specific symptom complexes, and side-effect profiles. In actuality, off-label indications, trial and error, and empiric decision making are common in community medicine settings; for example, low-dose amitriptyline or tizanidine may prescribed at hour of sleep to promote better sleep hygiene and improve myofascial pain.

The American Pain Society has published clinical practice guidelines for chronic low back pain but not specifically for FBSS. Cochrane reviews are also available for symptomatic relief of low back pain but again these do not specifically address FBSS. There is at least 1 case report of decreased pain and improved function with gabapentin as monotherapy for FBSS, but there are no formal studies of gabapentinoids and the effect on FBSS. Side effects and drug interactions often limit these therapies, and polypharmacy increases the risk of serious complications, such as serotonin syndrome. Consequently, opioids are commonly prescribed.

All of these medications have been well reviewed in Braddom’s textbook, Physical Medicine and Rehabilitation, 4th ed, with respect to mechanisms of action and dosage ranges. Another focused review is available from the American Pain Society/American College of Physicians Clinical Practice Guideline.

Nonopioid medications are considered adjunctive pain medications and are usually insufficient in the setting of FBSS. Opioids are generally considered safe and effective for moderate to severe pain but the use of opioids for chronic noncancer pain is becoming more controversial. This is especially true in the setting of FBSS, especially in the setting of instrumented lumbar fusion. Chan and Peng comment on a recent publication investigating mortality after lumbar fusion:

In this study, the leading cause of mortality (accounting for 31% of all deaths) was analgesic related. The overwhelming majority of deaths were related to opioids (20/22 patients with analgesic related death). While the majority were accidental, three deaths were the result of suicide. Of those patients who suffered from analgesic related mortality, all had undergone either instrumented fusion or intervertebral cage procedure. No patient with receiving lumbar fusion from autograft or allograft suffered from analgesic related death. While more investigation is required to determine why patients with instrumentation may be more prone to serious complications of opioid analgesia, this finding should caution the physician to be careful when prescribing analgesics for FBSS and to undertake close monitoring of patients on chronic opioids for pain.

FBSS patients are often pushed aside and told that their surgeons have little to offer them after their surgeries were unsuccessful. These patients are generally managed by community-based physicians, including primary care physicians, anesthesiologists, physiatrists, and neurologists. Scope of practice and the limits of a patient’s third party coverage influence the pharmacologic management, interventional therapies, and physical therapy treatments that are offered. Once treatment options are expended, FBSS patients are often told to seek out a physician who will prescribe pain medications chronically.

Treatment of FBSS demands recognition that it is a chronic pain syndrome. One reason that FBSS is a difficult-to-treat syndrome and a public health problem is that the antecedent back pain did not respond to intervention and was often augmented with additional pain complaints caused by the surgery. The psychosocial burden for individuals is huge, especially if there is job loss or loss of function physically. Many of the immediate postoperative pharmacologic strategies complicate the situation further by altering the patient sensorium, mood, affect, and even libido. Opioid-induced hyperalgesia is probably under-recognized and under-reported.

Prescription opioid abuse is now considered a major public health problem in itself. Ten years after pain was recognized as the fifth vital sign, primary care physicians and specialists alike are being placed under scrutiny for excessive opioid prescribing. As of the time of this writing, states, including Washington, Utah, Ohio, Indiana, Kentucky, and New York, all regulate and monitor opioid prescribing carefully and this trend can be expected to continue.

Patients often become chronically habituated to opioids and underinsured after job loss, leading to further marginalization by institutions and practitioners, who of necessity are becoming more focused on competitive cost containment and the potential for clinical censure. These patients are often viewed as doctor shopping when they are unable to obtain adequate relief and most do not have good insight into the nature of their problem. Despite high doses of opioids, many patients still report 10/10 pain during clinical interviews. This clinical observation has been corroborated by a study from 2007 where opioids did not give patients a significant reduction in pain from baseline.

Therapeutic encounters need to emphasize that complete pain relief may not be reasonable, but pain control allowing increased activity and enjoyment may be attainable. In general, long-acting opioids should be preferred to short-acting opioids to decrease peaks and troughs that stimulate craving, and patients need to be monitored for aberrant drug behavior, including secondary financial gains from diversion. Patient education addressing the deleterious effects of prolonged immobility and deconditioning is essential if the vicious cycle of pain and deactivation is to be interrupted.