Lumbar radiculopathy refers to pain in the back or buttocks that radiates down the leg in a dermatomal distribution. The prevalence of true lumbar radiculopathy in the general population is approximately 3% to 5%.1 Although the two most common causes for these symptoms are a herniated disk or, less commonly, spinal stenosis, many other potential causes mimic lumbar radiculopathy. If the diagnosis of radiculopathy is presumed, this action may result in misdiagnosis, leading to unnecessary tests and treatment and ultimately a delay in delivery of appropriate care.
Although the simultaneous presence of low back pain may increase the likelihood of these symptoms originating in the lumbar spine, low back pain is common in the general population. This symptom may create a bias toward inappropriately attributing lower extremity symptoms to lumbar spine pathology. Furthermore, because an asymptomatic lumbar disk bulge or herniation is a common finding on MRI, the presence of such changes must be correlated with the patient’s symptoms. These issues highlight the importance of the clinician’s working from a broad list of differential diagnoses, especially when the signs and symptoms are atypical for radicular pain.2,3 Potential mimickers include musculoskeletal, neurogenic, immunogenic, and iatrogenic conditions (Table 1). A careful history and physical examination are the first and most important steps in distinguishing these conditions from one another.
Lumbar Disk Herniation
Lumbar disk herniation most frequently occurs in patients younger than 50 years. Symptom onset may be acute, may or may not be associated with an inciting event, and begins with a tear in the posterior annulus. The annulus is richly innervated by sensory pain fibers; therefore, a common initial presenting symptom may be severe low back pain. As the pathology progresses, pressure within the disk forces a portion of the nucleus pulposus through the tear into the spinal canal, where it compresses and possibly chemically irritates the nerve root, causing radicular pain.4 This process is often associated with a transition of the patient’s symptoms from the low back to the buttock and down the leg, accompanied by pain, numbness, tingling, and weakness. Symptoms usually have a mechanical component that are intensified by activity and ameliorated with rest. Any action that increases intradiscal pressure, such as sneezing or bending forward, tends to exacerbate the pain. An important physical examination finding is nerve root tension; a positive straight leg raise test is present in 60% of patients5 with disk herniation at L4-5 and L5-S1. A femoral stretch test may be positive for disk herniation at L2-3, L3-4, and occasionally L4-5. Asymmetric reflexes of the patellar tendon (ie, L4) or Achilles tendon (ie, S1) may be noted.
The presence of saddle anesthesia, bowel or bladder dysfunction, and lower extremity weakness are consistent with cauda equina syndrome, a potential consequence of a large disk herniation. It is crucial to identify this condition because it may require urgent surgical decompression.
Neurogenic claudication secondary to lumbar spinal stenosis, first described by Verbiest,6 is the most common indication for spine surgery in patients older than 65 years.7 It is caused by narrowing of the spinal canal that is the result of age-related changes of the facet joints, the ligamentum flavum, and the disk.8 Whereas a history of chronic low back pain is common, patients experience symptoms mainly in the buttocks and legs either as bilateral neurogenic claudication or, less commonly, as unilateral radicular pain that may indicate the presence of a synovial facet cyst.9,10 Neurologic deficits, such as asymmetric reflexes, sensory changes, and motor weakness, are found in >50% of patients with lumbar spinal stenosis; however, these findings are nonspecific. Approximately 20% of patients present with a positive straight leg raise test or femoral stretch test.9
Mimickers of Lumbar Radiculopathy
The most common group of mimickers of lumbar spine pathology originate in the musculoskeletal structures around the pelvis, hip joint, and femur.11 This group includes hip joint conditions (eg, osteoarthritis, osteonecrosis, femoral acetabular impingement), femoral neck stress fractures, pelvic insufficiency fractures, bursitis, and sacroiliac joint pain.
Hip joint pathology usually may be differentiated from lumbar pathology by the presence of groin pain with activity. The pain is most evident during day-to-day activities that require hip movements, such as turning in bed, getting in or out of a car, climbing stairs, and putting on shoes and socks. Pain may also be present in the buttock and radiate to the anterior thigh and knee (Figures 1 and 2). Passive range of motion of the hip, particularly flexion and internal rotation, may be diminished and may reproduce the patient’s symptoms; this is strongly suggestive of a pathologic hip joint.12 Brown et al13 noted that patients who walk with a limp are seven times more likely to have hip joint pathology with or without coexisting spinal stenosis as the etiology of their pain rather than spinal stenosis alone (Table 2).
Osteoarthritis of the hip is the most common hip joint condition in patients older than 65 years, with a prevalence of 5% to 10% of the population.14 Hip radiographs show joint space narrowing, osteophyte formation, subchondral cysts, and sclerosis. For patients who have coexisting lumbar stenosis and osteoarthritis of the hip, an injection of local anesthetic into the hip joint may help differentiate the patient’s primary pain generator.15
Osteonecrosis, caused by a disruption of blood flow to the femoral head, may progress to femoral head collapse and hip arthritis. Patients aged 20 to 50 years who have risk factors for osteonecrosis (eg, history of excessive alcohol intake, chronic steroid use, sickle cell disease) and groin or buttock pain should be evaluated with hip radiographs; MRI may be done if osteonecrosis is suspected but radiographs are normal or inconclusive.16 In early osteonecrosis, a lucency may be seen on AP hip or pelvic radiographs; a crescent sign (Figure 3) represents subchondral collapse of the femoral head. Coronal T1- and T2-weighted MRI of the pelvis may show an area of decreased signal intensity in the weight-bearing dome of the femoral head.
Femoral acetabular impingement, a pathologic contact of the femoral neck against the acetabulum, is a cause of hip joint pain in younger patients. Two morphologic mechanisms have been proposed. In cam impingement, an abnormally shaped femoral head contacts the acetabulum; in pincer impingement, the femoral neck makes contact with a relatively retroverted acetabular rim during terminal motion. These mechanisms lead to labral tears and cartilage damage to the hip joint, followed by pain and possible progression to arthritis. During physical examination, the pain may be reproduced by flexion, adduction, and internal rotation. An AP radiograph of the hip may identify a crossover sign, whereby the radiographic shadows of the lateral edges of the anterior and posterior walls intersect, crossing over each other and indicating a retroverted acetabulum17 (Figure 4). A lateral hip radiograph may show an abnormal bony prominence at the femoral head-neck junction that is responsible for the impingement. An MRI arthrogram is the test of choice to evaluate labral pathology and cartilage defects.18
Stress fractures of the femoral neck, also known as fatigue fractures, should be suspected in avid runners and military trainees who report insidious onset of groin pain that worsens with running/marching and improves with rest. An amenorrheic adolescent female runner is particularly at risk because of decreased bone mineral density secondary to an associated eating disorder.19 These fractures occur as a result of repetitive submaximal stress that exceeds the bone’s ability to remodel itself in response to that stress. In a young patient, it is critical to consider this diagnosis because of the risk of displacement and the resultant potential for femoral head osteonecrosis; significant disability is likely, and joint arthroplasty may be required. AP and lateral radiographs of the hip are the initial imaging choices; MRI is used for confirmation. Lateral or tension-sided femoral neck fractures are at high risk for displacement and are treated with surgical stabilization; fractures on the medial or compression side of the femoral neck may be managed symptomatically with protected weight bearing and cessation of the offending activity.20 Stress fractures of the tibia and the metatarsals are also common in these populations and should be considered in the differential diagnosis.
Greater trochanteric bursitis, commonly found in middle-age aged patients, presents as peritrochanteric pain that occasionally radiates down the thigh to the lateral knee. It affects 10% to 25% of the population and has the clinical findings of tenderness to palpation over the lateral hip and pain on resting on the ipsilateral side, particularly at night.21 In a retrospective review, Tortolani et al22 diagnosed trochanteric bursitis in 20.2% of patients who presented to the authors’ spine clinic for presumed lumbar spine pathology. Women are affected twice as much as men. Other pelvic bursa, such as the ischial, iliopectineal, and iliopsoas, may more rarely be a cause of pelvic or thigh pain.23,24
Sacral insufficiency fractures occur as a result of normal stresses across abnormal, weakened bone and are most commonly seen in elderly women with osteoporosis. Chronic steroid use and a history of pelvic irradiation are also risk factors. Weber et al25 estimate an annual incidence rate of 2%. Patients report vague low back and occasionally radicular pain, often with no history of antecedent trauma. The pain may be so debilitating that patients use a wheelchair because they are unable to ambulate. Physical examination may reveal sacral tenderness. Lumbar and pelvis radiographs may be negative for a fracture. A dedicated pelvis MRI shows edema around an acute fracture on fat-suppressed T2-weighted images or short tau inversion recovery sequences (Figure 5). Nondisplaced fractures may be missed on CT;26 therefore, MRI is indicated if an insufficiency fracture is suspected. A technetium bone scan may be ordered if the patient is unable to undergo MRI.
Sacroiliac joint pain presents as nonradiating buttock pain over the posterior superior iliac spine that is worse with activity. It is a diagnosis of exclusion. Physical examination findings include a positive FABER test (flexion, abduction, and external rotation), Gaenslen test (extension of the affected leg by hanging it off the examination table using a downward force while holding the contralateral hip in flexion), sacral compression, thigh thrust, and anterior superior iliac spine distraction. Van der Wurff et al27 found that performing three or more positive stress maneuvers is 85% sensitive and 79% specific for sacroiliac pain.
Intermittent vascular claudication refers to lower extremity pain secondary to arterial insufficiency in patients with peripheral arterial disease (PAD). Risk factors include smoking (ie, 80% to 90% of affected patients are current or former smokers),28 diabetes, hyperlipidemia, and hypertension. Buildup of atherosclerotic plaque leads to arterial stenosis, precipitating a mismatch between oxygen supply and demand in the leg muscles. Pain from vascular claudication classically radiates from distal to proximal during ambulation and may be bilateral or unilateral; the latter may closely mimic lumbar radiculopathy. Walking distance before the onset of pain tends to be more predictable with PAD compared with that in neurogenic claudication. In addition, patients with vascular claudication may relieve their symptoms with cessation of walking; patients with neurogenic claudication must lean forward or sit down for pain relief. Careful physical examination should include evaluation for diminished, asymmetric, or absent pedal pulses and for the presence of shiny, hairless, or dystrophic skin. Redness of the lower extremity that is alleviated by elevation (ie, dependent rubor) is common. Noninvasive ankle-brachial indices (ABIs) are considered positive when the ABI ratio is <0.9. In patients unaffected by PAD, the lower extremities should show a pressure differential between 30 to 40 mm Hg compared with the brachial pressure.29 Jeon et al30 reported a sensitivity and specificity of 85.3% and 85.7%, respectively, of ABI testing in patients presenting with claudication symptoms of uncertain vascular or neurogenic origin.
Both benign and malignant extraspinal tumors involving the pelvis and femur may produce symptoms and signs of lumbar radiculopathy (Figure 6). Important elements in the history that may distinguish these patients include (1) insidious onset of symptoms without antecedent trauma; (2) crescendo pain pattern, particularly at night; (3) no change in pain pattern with position or activity; (4) presence of constitutional symptoms; and (5) identified cancer risk factors such as prior diagnosis of cancer, tobacco use, and prior irradiation to the pelvis (Table 3). Physical examination features that may be revealing include point localization of pain or mass effect along the course of the sciatic nerve. A high index of suspicion is required, particularly if pain is out of proportion to or anatomically inconsistent with spine imaging studies. The key diagnostic steps are to obtain an accurate history and to perform a careful physical examination. Based on these considerations, further workup of the pelvis, hip, and femur should include radiographs, supplemented with more advanced imaging (ie, bone scan, MRI, CT) as indicated.
Metabolic disorders represent the predominant etiology of extremity pain arising from peripheral neurogenic origin. Although several causes of peripheral neuropathy exist, diabetes mellitus is the most common cause; peripheral neuropathy affects up to 66% of patients with diabetes.31 In distal sensory peripheral neuropathy, which is present in 80% of patients with diabetic peripheral neuropathy, demyelination of large myelinated nerve fibers that are responsible for vibration, touch, and proprioception leads to a sensation of pins and needles bilaterally in the lower extremities in a stocking distribution.32,33 Patients reporting these sensations often falsely attribute their symptoms to a spinal etiology.34 Proximal diabetic neuropathy, also known as diabetic amyotrophy, presents as unilateral or bilateral buttock, thigh, and/or leg pain. Other common signs and symptoms include burning anterior thigh pain at night and weakness and atrophy of the proximal muscle girdles. As a result, patients report difficulty with ambulation and climbing stairs. Men older than 50 years with poorly controlled type 2 diabetes are most commonly affected; many report a history of weight loss around the time of the onset of symptoms.35 The pain usually subsides within 3 to 6 months; therefore, the prognosis for these patients is good.
Peroneal neuropathy most commonly arises from trauma about the knee and ankle. Between 30% to 60% of nontrauma patients experience compression of the common peroneal nerve by ganglion cysts originating from the proximal tibiofibular joint.36,37 Tibialis anterior weakness may result from a common peroneal neuropathy or from an L4 or L5 radiculopathy. Clinical distinction between the two etiologies may be made by assessment of the strength of the ipsilateral hip abductor muscle and the tibialis anterior muscle; both of these muscles receive primary innervation from the L5 nerve root. Jeon et al38 reported ipsilateral hip abductor weakness in 85.6% of patients with a foot drop caused by an L5 radiculopathy, but only 3% of patients with foot drop caused by a peroneal neuropathy had concomitant hip abductor weakness. A palpable mass and a positive Tinel sign at the lateral proximal fibula may be present in 97% of patients with peroneal nerve compression.39 MRI of the lumbar spine is indicated in a patient with a foot drop. Electrodiagnostic studies can help distinguish proximal etiologies from distal etiologies if the MRI is equivocal. If the MRI of the lumbar spine is normal and/or electrodiagnostic studies are consistent with compressive peroneal neuropathy at the knee, then MRI of the knee should be performed to rule out a ganglion cyst of the proximal tibiofibular joint.
Anterolateral thigh paresthesia, secondary to compression of the lateral femoral cutaneous nerve (LFCN), is known as meralgia paresthetica (MP); it most commonly occurs in middle-aged men with an incidence of 0.43 per 10,000 persons.40 The LFCN, a purely sensory nerve, originates in the lumbar plexus from any combination of the L1, L2, or L3 nerve roots; therefore, it may be confused with radiculopathy from these levels.41 It courses underneath or over the inguinal ligament along an aponeurotic fascial tunnel in which compression of the nerve may occur. Symptoms, often described as numbness or burning along the anterior thigh, are usually improved with sitting.42 External sources that may compress the LFCN include tight-fitting pants, belts, or girdles. Obesity, diabetes, and pregnancy are risk factors for MP. Iatrogenic injury may occur with prone positioning during surgery. The presence of hip flexor weakness is more consistent with an L2 or L3 radiculopathy than with MP. A positive Tinel sign over the lateral aspect of the inguinal ligament supports the diagnosis of MP. Nouraei et al43 described a pelvic compression test in which the patient lies in the contralateral decubitus position while downward pressure is applied to the pelvis, relaxing the inguinal ligament and putting pressure on the LFCN. The authors reported sensitivity and specificity of 95% and 93%, respectively, for the relief of discomfort caused by MP in patients with a positive pelvic compression test and surgical release.
Several other lower extremity compressive neuropathies have been reported. Examples include entrapment of the peroneal nerve in the anterior compartment of the lower leg and entrapment of the tibial nerve in the tarsal tunnel. Piriformis syndrome, irritation of the sciatic nerve by an aberrant piriformis muscle, trauma, or overuse cause symptoms very similar to those of lumbar radiculopathy.44,45 In a systematic review of 55 studies with a total of 126 patients, Hopayian et al45 identified three common symptoms that patients experienced, including buttock pain (50% to 95% of patients), aggravation of pain with sitting (39% to 97% of patients), and point tenderness over the greater sciatic notch (59% to 92% of patients); these symptoms were present together with a 22% frequency. A positive straight leg raise was present 42% to 62% of the time. The authors suggest that the diagnosis be considered when a lumbar MRI is negative for evidence of nerve root compression and when patients have atypical histories.
Infectious and Autoimmune Disorders
Infectious etiologies, such as osteomyelitis, spondylodiscitis, and epidural abscess should be considered in the differential diagnosis of lumbar radiculopathy, particularly in immunocompromised patients who report unremitting low back pain, fever, chills, and/or pain that is worse at night. Osteomyelitis and discitis are likely causes of axial nonradiating back pain with fever, but they also may produce radiculopathy with epidural extension of the infection.46,47 In addition to axial pain (89% of patients), radiculopathy and neurologic deficit (80% of patients) are the most common presenting symptoms of epidural abscess, followed by fevers and chills (67% of patients).48 The most commonly identified organism in spinal pyogenic infections is Staphylococcus aureus. Laboratory studies, including erythrocyte sedimentation rate, C-reactive protein level, and white blood cell count with differential, and MRI with contrast should be ordered when infection is suspected.
Shingles (ie, herpes zoster) occurs when the dormant varicella-zoster virus in nerve cell bodies of the dorsal root ganglia reactivates and causes a painful, vesicular rash in a dermatomal pattern. Therefore, it is important to inquire about the presence of a skin rash or blisters and inspect the patient’s skin from the back and buttock down the leg. Patients older than 60 years and immunosuppressed patients (ie, patients with cancer, human immunodeficiency virus [HIV], diabetes) are particularly susceptible. Lumbar radiculitis occurs in 20% of patients and can cause burning dysesthesias and even motor weakness.49,50 Sprenger DeRover et al51 described two patients with L5 radiculitis with foot drop caused by a herpes zoster infection.
HIV can cause a distal symmetric polyneuropathy similar to diabetic neuropathy; it is typically found in patients with profound immunosuppression manifested by CD4+ counts of <200 cells/μL and high viral levels.52 Whereas this is the most common neuropathy associated with HIV, several other neuropathic disorders exist. Rapidly progressive lumbosacral polyneuropathy presents as cauda equina syndrome that is characterized by saddle anesthesia, lower extremity weakness, and loss of bowel or bladder function; it occurs in patients with severe immunosuppression and a history of cytomegalovirus infection.53,54 This presentation warrants a lumbar MRI or CT myelogram to rule out a compressive spinal etiology. The diagnosis is made by examination of the cerebrospinal fluid and a positive polymerase chain reaction test for cytomegalovirus infection.
HIV-associated radiculitis and myelopathy have also been reported from co-infection by herpes zoster, herpes simplex virus, syphilis, and tuberculosis.52 Other neuropathic entities associated with HIV infection include Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy.55,56
GBS (incidence = 1:100,000) is characterized by demyelination of peripheral nerves, and transverse myelitis (TM) (incidence = 1 to 5/1,000,000) is characterized by demyelinating myelopathy involving the spinal cord, most commonly at the thoracic level.56,57 GBS presents as the acute onset of paresthesia in the hands and/or feet that ascends symmetrically to involve the proximal muscle girdles; it may rapidly worsen to affect the diaphragm with the potential for respiratory failure. Flaccid paralysis, areflexia, and autonomic dysfunction also may be present. The pathogenesis is believed to arise from an autoimmune mechanism because GBS commonly follows a viral illness such as herpes simplex and cytomegalovirus infections; however, it has also been associated with Borrelia burgdorferi and Campylobacter jejuni infections.58,59 These infections stimulate antigenic mimicry that leads to cross reactivity of native tissue; this produces an immune response against myelinated peripheral nerves and results in the slowing of nerve conduction velocities. The diagnosis is made by clinical presentation, cerebrospinal fluid analysis (ie, protein count >0.4 g/L and cell count <10/mL), electrodiagnostic studies, and blood laboratory studies to exclude chemical toxicities.1,57
An idiopathic or a peri-infectious autoimmune etiology is most likely responsible for GBS and TM.57 Symptoms include back pain, weakness, sensory loss, dysesthesias of the lower extremities, and bladder and possibly bowel dysfunction. Hyperreflexia is often present below the level of the lesion when TM symptoms develop over several weeks, but patients may be areflexic when symptoms are rapid in onset.57,60
MRI of the whole spinal cord should be obtained to rule out a compressive etiology in both GBS and TM. MRI findings in GBS are usually negative, whereas in TM they may show focal or multilevel increased spinal cord signal on T2-weighted images (Figure 7). When the diagnosis of GBS or TM is suspected, urgent neurology referral and access to intensive critical care is indicated because respiratory failure and paralysis may ensue.
Iatrogenic causes of lower extremity pain that may be misdiagnosed as lumbar radiculopathy may be divided into two categories: myogenic and neuropathic. Systemic medications prescribed for a variety of acute and chronic medical conditions constitute most iatrogenic neuropathies and myopathies (Table 3).
According to the IMS Institute for Healthcare Informatics, lipid regulators are the most commonly prescribed class of medication in the United States, with simvastatin being the single most commonly prescribed medication after hydrocodone/acetaminophen.61 A common adverse effect of the statin class of drugs is myopathy, occurring in 5% to 10% of patients.62 According to the Prediction of Muscular Risk in Observational Conditions (PRIMO) study involving 7,924 French patients, those taking simvastatin reported the highest incidence of myopathy (18%), whereas those taking fluvastatin had the lowest incidence (5.1%). Weakness and cramping pain in the thighs or calves was reported in 75% of affected patients, whereas another 25% reported diffuse myalgias.63 Onset of symptoms occurs at a mean of 6.3 months after initiation of statin therapy; however, symptoms may occur as early as 1 week or as late as 4 years.64 Symptoms usually resolve once the statins are stopped, helping to support the diagnosis.
Modern treatment regimens for patients infected with HIV have markedly reduced morbidity and mortality associated with the disease; however, potent antiretrovirals have neuropathic adverse effects that patients may attribute to a spinal origin. The nucleoside analogues zalcitabine, didanosine, and stavudine have been shown to have a dose-dependent effect on the incidence and time to onset of distal symmetric polyneuropathy.54 Chemotherapeutic agents used to treat cancer, especially platinum-containing compounds (eg, cisplatin, carboplatin, oxaliplatin), are also well-known potential causes of sensory neuropathy; this can be a dose-limiting adverse effect. Thalidomide used in the treatment of multiple myeloma may have the adverse effect of both a distal sensory and a motor neuropathy.65,66 A distal sensory polyneuropathy may be an adverse effect from chronic use of amiodarone as a treatment of atrial fibrillation; however, a rapid form of neuropathy with lower extremity weakness, areflexia, and ataxia has been reported.67
The most common cause of lumbar radiculopathy is a herniated disk, which tends to follow a predictable onset and pattern. However, there are several other diagnoses that may cause lumbar radiculopathy-type symptoms and are therefore mimickers of lumbar radiculopathy. These mimickers each have a different onset and pattern of symptoms. Performing a thorough history and physical examination, supplemented when needed with additional diagnostic tests, and/or referral to appropriate specialists, can help differentiate them. Providing high-quality, cost-effective medical care requires identifying these mimickers when they are the cause of a patient’s symptoms.
References printed in bold type are those published within the past 5 years.
1. Tarulli AW, Raynor EM: Lumbosacral radiculopathy. Neurol Clin 2007;25(2):387–405.
2. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS: Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994;331(2):69–73.
3. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW: Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation. J Bone Joint Surg Am 1990;72(3):403–408.
4. Kawakami M, Tamaki T, Hayashi N, Hashizume H, Nishi H: Possible mechanism of painful radiculopathy in lumbar disc herniation. Clin Orthop Relat Res 1998;351:241–251.
5. Weinstein JN, Tosteson TD, Lurie JD, et al.: Surgical vs nonoperative treatment for lumbar disk herniation: The Spine Patient Outcomes Research Trial (SPORT): A randomized trial. JAMA 2006;296(20):2441–2450.
6. Verbiest H: A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg Br 1954;36(2):230–237.
7. Turner JA, Ersek M, Herron L, Deyo R: Surgery for lumbar spinal stenosis: Attempted meta-analysis of the literature. Spine (Phila Pa 1976) 1992;17(1):1–8.
8. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J: Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine (Phila Pa 1976) 1978;3(4):319–328.
9. Weinstein JN, Tosteson TD, Lurie JD, et al.; SPORT Investigators: Surgical versus nonsurgical therapy for lumbar spinal stenosis. N Engl J Med 2008;358(8):794–810.
10. Genevay S, Atlas SJ: Lumbar spinal stenosis. Best Pract Res Clin Rheumatol 2010;24(2):253–265.
11. Swezey RL: Overdiagnosed sciatica and stenosis, underdiagnosed hip arthritis. Orthopedics 2003;26(2):173–174, discussion 174.
12. Devin CJ, McCullough KA, Morris BJ, Yates AJ, Kang JD: Hip-spine syndrome. J Am Acad Orthop Surg 2012;20(7):434–442.
13. Brown MD, Gomez-Marin O, Brookfield KF, Li PS: Differential diagnosis of hip disease versus spine disease. Clin Orthop Relat Res 2004;419:280–284.
14. Dagenais S, Garbedian S, Wai EK: Systematic review of the prevalence of radiographic primary hip osteoarthritis. Clin Orthop Relat Res 2009;467(3):623–637.
15. Crawford RW, Gie GA, Ling RS, Murray DW: Diagnostic value of intra-articular anaesthetic in primary osteoarthritis of the hip. J Bone Joint Surg Br 1998;80(2):279–281.
16. Seamon J, Keller T, Saleh J, Cui Q: The pathogenesis of nontraumatic osteonecrosis. Arthritis 2012;(2012):601763.
17. Kassarjian A, Belzile E: Femoroacetabular impingement: Presentation, diagnosis, and management. Semin Musculoskelet Radiol 2008;12(2):136–145.
18. Leunig M, Podeszwa D, Beck M, Werlen S, Ganz R: Magnetic resonance arthrography of labral disorders in hips with dysplasia and impingement. Clin Orthop Relat Res 2004;418:74–80.
19. Hutchinson PH, Stieber J, Flynn J, Ganley T: Complete and incomplete femoral stress fractures in the adolescent athlete. Orthopedics 2008;31(6):604.
20. Shin AY, Gillingham BL: Fatigue fractures of the femoral neck in athletes. J Am Acad Orthop Surg 1997;5(6):293–302.
21. Collée G, Dijkmans BA, Vandenbroucke JP, Cats A: Greater trochanteric pain syndrome (trochanteric bursitis) in low back pain. Scand J Rheumatol 1991;20(4):262–266.
22. Tortolani PJ, Carbone JJ, Quartararo LG: Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2002;2(4):251–254.
23. Schapira D, Nahir M, Scharf Y: Trochanteric bursitis: A common clinical problem. Arch Phys Med Rehabil 1986;67(11):815–817.
24. Lauder TD: Musculoskeletal disorders that frequently mimic radiculopathy. Phys Med Rehabil Clin N Am 2002;13(3):469–485.
25. Weber M, Hasler P, Gerber H: Insufficiency fractures of the sacrum: Twenty cases and review of the literature. Spine (Phila Pa 1976) 1993;18(16):2507–2512.
26. Murthy NS: Imaging of stress fractures of the spine. Radiol Clin North Am 2012;50(4):799–821.
27. van der Wurff P, Buijs EJ, Groen GJ: A multitest regimen of pain provocation tests as an aid to reduce unnecessary minimally invasive sacroiliac joint procedures. Arch Phys Med Rehabil 2006;87(1):10–14.
28. Smith GD, Shipley MJ, Rose G: Intermittent claudication, heart disease risk factors, and mortality: The Whitehall Study. Circulation 1990;82(6):1925–1931.
29. Lipetz JS, Beer JR, Silber JS: Atypical proximal limb pain of suspected high lumbar stenotic origin arising from severe aortoiliac disease: Leriche’s syndrome. Pain Physician 2004;7(1):123–128.
30. Jeon CH, Han SH, Chung NS, Hyun HS: The validity of ankle-brachial index for the differential diagnosis of peripheral arterial disease and lumbar spinal stenosis in patients with atypical claudication. Eur Spine J 2012;21(6):1165–1170.
31. Dyck PJ, Kratz KM, Karnes JL, et al.: The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: The Rochester Diabetic Neuropathy Study. Neurology 1993;43(4):817–824.
32. Said G: Diabetic neuropathy: A review. Nat Clin Pract Neurol 2007;3(6):331–340.
33. Feng Y, Schlösser FJ, Sumpio BE: The Semmes Weinstein monofilament examination as a screening tool for diabetic peripheral neuropathy. J Vasc Surg 2009;50(3):675–682, 682.e1.
34. Walcott BP, Coumans JV, Kahle KT: Diagnostic pitfalls in spine surgery: Masqueraders of surgical spine disease. Neurosurg Focus 2011;31(4):E1.
35. Said G, Elgrably F, Lacroix C, et al.: Painful proximal diabetic neuropathy: Inflammatory nerve lesions and spontaneous favorable outcome. Ann Neurol 1997;41(6):762–770.
36. Van Langenhove M, Pollefliet A, Vanderstraeten G: A retrospective electrodiagnostic evaluation of footdrop in 303 patients. Electromyogr Clin Neurophysiol 1989;29(3):145–152.
37. Kim JY, Ihn YK, Kim JS, Chun KA, Sung MS, Cho KH: Non-traumatic peroneal nerve palsy: MRI findings. Clin Radiol 2007;62(1):58–64.
38. Jeon CH, Chung NS, Lee YS, Son KH, Kim JH: Assessment of hip abductor power in patients with foot drop: A simple and useful test to differentiate lumbar radiculopathy and peroneal neuropathy. Spine (Phila Pa 1976) 2013;38(3):257–263.
39. Flanigan RM, DiGiovanni BF: Peripheral nerve entrapments of the lower leg, ankle, and foot. Foot Ankle Clin 2011;16(2):255–274.
40. van Slobbe AM, Bohnen AM, Bernsen RM, Koes BW, Bierma-Zeinstra SM: Incidence rates and determinants in meralgia paresthetica in general practice. J Neurol 2004;251(3):294–297.
41. Dias Filho LC, Valença MM, Guimarães Filho FA, et al.: Lateral femoral cutaneous neuralgia: An anatomical insight. Clin Anat 2003;16(4):309–316.
42. Harney D, Patijn J: Meralgia paresthetica: Diagnosis and management strategies. Pain Med 2007;8(8):669–677.
43. Nouraei SA, Anand B, Spink G, O’Neill KS: A novel approach to the diagnosis and management of meralgia paresthetica. Neurosurgery 2007;60(4):696–700, discussion 700.
44. Halpin RJ, Ganju A: Piriformis syndrome: A real pain in the buttock? Neurosurgery 2009;65(suppl 4)A197–A202.
45. Hopayian K, Song F, Riera R, Sambandan S: The clinical features of the piriformis syndrome: A systematic review. Eur Spine J 2010;19(12):2095–2109.
46. Carragee EJ: Pyogenic vertebral osteomyelitis. J Bone Joint Surg Am 1997;79(6):874–880.
47. Skaf GS, Domloj NT, Fehlings MG, et al.: Pyogenic spondylodiscitis: An overview. J Infect Public Health 2010;3(1):5–16.
48. Tang HJ, Lin HJ, Liu YC, Li CM: Spinal epidural abscess: Experience with 46 patients and evaluation of prognostic factors. J Infect 2002;45(2):76–81.
49. Shapiro M: Herpes zoster related lumbar radiculopathy. Orthopedics 1996;19(11):976–977.
50. Thomas JE, Howard FM Jr: Segmental zoster paresis: A disease profile. Neurology 1972;22(5):459–466.
51. Sprenger De Rover WB, Alazzawi S, Hallam PJ, Hutchinson R, Di Mascio L: Herpes zoster virus: An unusual but potentially treatable cause of sciatica and foot drop. Orthopedics 2011;34(12):e965–e968.
52. Kamerman PR, Wadley AL, Cherry CL: HIV-associated sensory neuropathy: Risk factors and genetics. Curr Pain Headache Rep 2012;16(3):226–236.
53. Robinson-Papp J, Simpson DM: Neuromuscular diseases associated with HIV-1 infection. Muscle Nerve 2009;40(6):1043–1053.
54. Pardo CA, McArthur JC, Griffin JW: HIV neuropathy: Insights in the pathology of HIV peripheral nerve disease. J Peripher Nerv Syst 2001;6(1):21–27.
55. Brannagan TH III, Zhou Y: HIV-associated Guillain-Barré syndrome. J Neurol Sci 2003;208(1-2):39–42.
56. Viegas GV: Guillain-Barré syndrome. Review and presentation of a case with pedal manifestations. J Am Podiatr Med Assoc 1997;87(5):209–218.
57. Awad A, Stüve O: Idiopathic transverse myelitis and neuromyelitis optica: Clinical profiles, pathophysiology and therapeutic choices. Curr Neuropharmacol 2011;9(3):417–428.
58. Halperin JJ, Little BW, Coyle PK, Dattwyler RJ: Lyme disease: Cause of a treatable peripheral neuropathy. Neurology 1987;37(11):1700–1706.
59. Louwen R, Horst-Kreft D, de Boer AG, et al.: A novel link between Campylobacter jejuni bacteriophage defence, virulence and Guillain-Barré syndrome. Eur J Clin Microbiol Infect Dis 2013;32(2):207–226.
60. Ropper AH, Poskanzer DC: The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. Ann Neurol 1978;4(1):51–59.
62. Joy TR, Hegele RA: Narrative review: Statin-related myopathy. Ann Intern Med 2009;150(12):858–868.
63. Bruckert E, Hayem G, Dejager S, Yau C, Bégaud B: Mild to moderate muscular symptoms with high-dosage statin therapy in hyperlipidemic patients: The PRIMO study. Cardiovasc Drugs Ther 2005;19(6):403–414.
64. Hansen KE, Hildebrand JP, Ferguson EE, Stein JH: Outcomes in 45 patients with statin-associated myopathy. Arch Intern Med 2005;165(22):2671–2676.
65. Peltier AC, Russell JW: Recent advances in drug-induced neuropathies. Curr Opin Neurol 2002;15(5):633–638.
66. Manji H: Toxic neuropathy. Curr Opin Neurol 2011;24(5):484–490.
67. Orr CF, Ahlskog JE: Frequency, characteristics, and risk factors for amiodarone neurotoxicity. Arch Neurol 2009;66(7):865–869.