Low back pain (LBP) is the most common cause of pain and disability in modern society, and costs related to disorders that cause LBP amount to billions of dollars each year. Pathologic conditions responsible for LBP are protean, and their precise diagnosis remains elusive. Pain can originate not only from the various components of the spinal column, such as the intervertebral disks (IVDs), vertebral bodies, facet joints, spinal nerve roots (NRs), and surrounding muscles and ligaments, but also from adjacent structures such as abdominal and pelvic viscera. The list of conditions that can produce LBP is exhaustive and includes causes as diverse as degenerative conditions, spinal metastasis, vertebral body fractures, abdominal aortic aneurysm, and chronic pancreatitis. Furthermore, the various disorders causing LBP are often present concomitantly, and their symptoms and signs are frequently analogous. The problem is further confounded by the fact that the tests currently used for diagnosis of these disorders are nonspecific and may show abnormalities in asymptomatic individuals. It is therefore crucial that a thorough clinical evaluation be accompanied by appropriate diagnostic testing to elucidate the cause of the LBP. In this chapter we will discuss the causes of chronic LBP that are pertinent to the practice of pain medicine. The clinical conditions discussed here include lumbar radicular syndrome (LRS), herniated lumbar disk (HD), lumbar spinal stenosis (LSS), internal disk disruption (IDD), and lumbar facet syndrome (LFS). Other significant causes of chronic LBP such as myofascial pain syndrome, spondylosis, spondylolisthesis, spinal instability, and sacroiliac joint dysfunction are discussed elsewhere in this book. Notable but less common causes of LBP such as spinal fractures, malignancies, osteomyelitis, and inflammatory and metabolic conditions such as ankylosing spondylitis and Paget’s disease are usually excluded before a patient is evaluated by a pain medicine physician and are beyond the scope of this chapter.
Lumbar Radicular Syndrome
Definition and Terminology
Pain, paresthesias, and numbness in a typical dermatomal distribution, with or without the accompanying signs of weakness, diminished reflexes, and a positive straight-leg raise (SLR) test, are typically due to pathology or dysfunction of the sensory spinal nerve roots (SSNRs) or dorsal root ganglia (DRGs). Although radicular signs and symptoms are often present in conjunction with axial LBP, LRS is distinctive in its etiology and treatment. The term lumbar radiculopathy is frequently used to describe this clinical entity; however, it inappropriately implies the obligatory occurrence of objective signs of NR damage—loss of sensation, muscle weakness, and diminished reflexes. Lumbar radiculitis is another term commonly used, although it incorrectly proposes that an inflammatory process is primarily responsible for the radicular signs and symptoms. Another term used, lumbar radicular pain , mistakenly assumes pain as being the predominant symptom. Hence, the descriptive term lumbar radicular syndrome may be the most accurate in that it correctly suggests a constellation of clinical signs and symptoms of variable etiology secondary to pathology or dysfunction of the SSNRs or DRGs. Although the term sciatica is often used synonymously for LRS, this term is more suited to describe pain in the distribution of the sciatic nerve.
Prevalence
Epidemiologic studies of low back and lower extremity pain are often inexact in that the conditions producing these symptoms are frequently nonhomogeneous and poorly defined. Although the prevalence and lifetime incidence of LBP are reported variably, its overall occurrence ranges from 13.8% to 31%, and the related health care costs amount to billions of dollars each year. The incidence of radicular symptoms in patients with LBP has been reported to range from 12% to 40%.
Etiology and Differential Diagnosis
Pathologic involvement of SSNRs and DRGs generates ectopic impulses at these locations that are perceived as pain, numbness, and tingling in areas innervated by the affected axons (i.e., a dermatomal distribution) ( Fig. 21.1 ). Pathologic processes that can affect SSNRs and DRGs are diverse, with lesions of the IVDs and degenerative spinal disorders being most prevalent. Neoplastic, infectious, traumatic, metabolic, and vascular lesions involving SSNRs, DRGs, the spine itself, and lumbosacral plexuses can also produce radicular signs and symptoms. Pathologic lesions and entrapment neuropathies involving the sciatic nerve (e.g., piriformis muscle and ischial tunnel syndromes) can generate pain and paresthesias in its distribution and often affect multiple dermatomes. Pain originating in the IVDs and in the sacroiliac and facet joints and pain of myofascial origin can also be referred to the lower extremities. This somatic referred pain is due to interneuronal convergence within the spinal cord. It is nondermatomal, has a deep aching quality, rarely radiates below the knees, and lacks the objective signs of NR involvement. In this chapter we review the two most common causes of radicular pain in the lower extremities, HDs and LSS.
Clinical Features
Although pain is the predominant symptom, other symptoms of radicular involvement include paresthesias, numbness, and weakness in the territory of the involved NR. Radicular pain typically travels along a narrow band and has a sharp, shooting, and lancinating quality. Objective signs of gait disturbances, loss of sensation, reduced muscle strength, and diminished reflexes involve the appropriate dermatome. HDs and the degenerative conditions commonly involve the lower lumbar NRs, whereas other, often more sinister causes of LRS involve higher NRs with greater frequency. The following are characteristic features of various lumbar and sacral NR involvement:
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S1: Pain, paresthesia, and numbness of the posterior part of the thigh, calf, and plantar surface of the foot; there may be associated difficulty in toe walking, weakness of plantar flexion, and loss of the plantar reflex.
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L5: Similar symptoms involving the buttock, anterolateral aspect of the leg, dorsal surface of the foot, and great toe, with possible difficulty heel walking (steppage gait) and weakness of ankle and toe extension.
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L4: Radicular symptoms involving the anterior part of the thigh, knee, and upper to medial portion of the leg with weakness of knee extension and a diminished patellar tendon reflex.
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L3 and L2 NRs: Tend to produce symptoms and sensory alterations involving the groin and inner thigh areas.
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Lower sacral NRs: Involvement produces decreased sensation in the buttock and perineal areas (i.e., saddle anesthesia) and autonomic dysfunction, as indicated by bowel and bladder dysfunction, typically urinary retention and constipation followed by incontinence, and sexual dysfunction manifested as loss of erection in men and vaginal anesthesia in women.
Clinical Tests of Nerve Root Irritation
Several tests can be used to confirm the presence of NR irritation ( Box 21.1 ). Passive SLR with ankle dorsiflexion of the extended lower extremity causes traction on the lower lumbar NRs by pulling them caudally between 1.4 and 4 mm. The radicular nature of the pain is suggested by worsening pain in the radicular distribution caused by such a maneuver. A positive SLR or Lasègue test is therefore suggestive of radicular pathology of the lower lumbar NRs (L4, L5, and S1). Radicular pain in the affected leg when the contralateral asymptomatic leg is similarly raised constitutes a positive crossed straight-leg raise (X-SLR) test. Although a positive SLR test is highly sensitive, X-SLR is more specific for lumbar NR irritation. An increase in back pain during an SLR is typically attributed to lumbar spinal movement and indicates the mechanical nature of the LBP. One exception noted is that centrally, HDs can generate LBP with an SLR because of strain on the anterior theca. The tripod test is a maneuver to confirm a positive SLR test when the patient is sitting—extending the knee and dorsiflexion of the foot with the patient seated. The femoral stretch test places the L2 and L3 NRs under tension and indicates irritation of these NRs; this is tested by bending the knee and extending the hip with the patient in the prone position.
Straight-leg raise
Straight-leg raise and ankle dorsiflexion of the extended lower extremity
Crossed straight-leg raise
Tripod test
Femoral stretch test
“Red Flags” in the Medical History of a Patient with Low Back and Radicular Pain
As previously stressed, the list of conditions causing LBP, with or without radicular symptoms, is intimidating. Fortunately, in the vast majority of patients the pain is due to benign, self-limited musculoskeletal conditions, such as muscular sprain or ligamentous strain, and the symptoms typically resolve in 4 to 6 weeks. Indiscriminate diagnostic workup in these patients can be expensive and may produce findings that are unrelated and could be misleading. Hence, the Agency for Health Care Policy and Research (AHCPR) developed guidelines to help identify signs and symptoms—red flags—that indicate the presence of conditions that pose significant threat to life or neurologic function and would require further diagnostic testing ( Table 21.1 ). These conditions include malignancies, infections, fractures, and cauda equina syndrome (CES). The following is the list of “red flags” proposed in the AHCPR Publication 95-0643, published in 1994.
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Age younger than 20 or older than 50 years : Patients younger than 20 years have a higher incidence of congenital and developmental anomalies, and those older than 50 years are prone to neoplasms, pathologic fractures, serious infections, and life-threatening extraspinal processes as a cause of their low back and radicular symptoms.
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Duration of symptoms : The AHCPR guidelines consider symptoms of less than 3 months’ duration as acute and subacute LBP. Chronic pain, or pain greater than 3 months’ duration, indicates symptoms of a less serious etiology.
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History of trauma : A history of trauma in older patients and those with serious medical conditions may result in bony injury and require further workup.
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Constitutional symptoms : A history of fever, chills, malaise, night sweats, and unexplained weight loss should make one suspect a serious underlying disorder such as malignancy or infection.
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Systemic illness : A history of cancer, recent bacterial infections such as serious respiratory or urinary tract infections, intravenous drug abuse, immunosuppression (e.g., infection with human immunodeficiency virus), organ transplantation, and chronic corticosteroid use increase the likelihood of pathologic fractures, epidural and vertebral body abscesses, and metastasis.
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Unrelenting pain : Pain of benign etiology is typically relieved with rest and in supine position, especially at night. Unrelenting pain from serious pathologic conditions is often worse at night and is unresponsive to rest and analgesics.
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Cauda equina syndrome : CES is caused by acute compression of the spinal NRs comprising the cauda equina in the lumbosacral spine. In approximately 10% of patients with symptoms similar to CES, however, the cause is spinal cord compression at higher levels—the thoracic and even the cervical spinal cord. Although CES is rare, with a prevalence of approximately 4 in 10,000 patients with LBP, it is a neurosurgical emergency that requires emergency spinal decompressive surgery. Massive midline disk herniation or smaller disk herniation in a previous stenotic spine is the most frequent cause of CES. Rare causes of CES include spinal metastases, hematoma, epidural abscess, traumatic compression, acute transverse myelitis, and abdominal aortic dissection. Almost 70% of patients with CES relate a history of chronic LBP, whereas the rest of the patients have CES as their primary compliant. These patients are typically seen within 24 hours of the onset of their symptoms ( Box 21.2 ), usually with bilateral radicular pain, although pain in one leg is often worse than pain in the other, and less frequently with back pain. The pain is often accompanied by weakness in both feet, gait disturbances secondary to pain and weakness, and abdominal discomfort as a result of urinary retention, which may be followed by overflow urinary incontinence. Objective signs include motor and sensory deficits, diminished reflexes, and a positive SLR test, often in both lower extremities. Of particular importance is diminished sensation in the buttocks and perineum (saddle anesthesia), diminished sphincter tone, and evidence of urinary bladder retention. Imaging of the entire spine, with magnetic resonance imaging (MRI) being the “gold standard,” is indicated because of the possibility of spinal cord compression at higher levels. Once the diagnosis is made, treatment involves high-dose intravenous steroids and urgent decompressive surgery to reduce permanent neurologic disability.
Box 21.2
Features in the Clinical History
Radicular pain in both lower extremities; pain in one leg may be greater
Isolated low back pain is rare
Complaint of weakness in one or both legs and feet
Gait disturbances because of pain and weakness
Abdominal discomfort as a result of urinary retention
Features in the Clinical Examination
Motor and sensory deficits in the lower extremities
Diminished lower extremity reflexes
Positive straight-leg raise and crossed straight-leg raise tests
Saddle anesthesia
Diminished sphincter tone
Evidence of urinary bladder retention
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