Masqueraders of Spinal Pathology

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Chapter 28 Masqueraders of Spinal Pathology

It is not rare for spinal pathology to refer various symptoms to other parts of the body. In fact, conditions of the spine can present with a multitude of signs and symptoms masquerading as any number of pathologic conditions. A classic example is a C5 radiculopathy from a disc herniation that presents as shoulder pain. Conversely, nonspinal disorders may present with pain thought to be of spinal origin. For example, trochanteric bursitis commonly presents with symptoms that may appear to be originating from the lumbar spine. This chapter will review a number of nonspinal conditions that produce symptoms seemingly of spinal origin despite actually originating from a structure or process outside of the spine. These conditions mimicking spine pathology range from the relatively benign to the serious and life threatening, and they may mimic axial spine pain, radiculopathy, or myelopathy.

Musculoskeletal System

A variety of conditions involving the musculoskeletal system are known to mimic spine pathology.16 Typically, degenerative conditions in the upper and lower extremities such as arthritis, tendonitis, and bursitis are the primary culprits that bring the patient to the spine specialist, suspecting that their complaints are of spinal origin (Box 28-1). Many musculoskeletal structures in the extremities can present with signs and symptoms that seem to be originating from the spine; however, the most common extraspinal musculoskeletal masqueraders of spine disease are the shoulder, hip, and sacroiliac joint.


The term shoulder describes a region of the body and not a specific joint. In fact, the shoulder complex includes four separate articulations: the glenohumeral, scapulothoracic, sternoclavicular, and acromioclavicular joints. Any of these joints are subject to trauma and degenerative changes and can therefore cause pain and dysfunction that can be confused with cervical spine pathology. Two of the more common conditions involving the shoulder are impingement syndrome and osteoarthritis. The presenting signs and symptoms often overlap with those of cervical radiculopathy and neck pain. A thorough history and physical examination are often required to differentiate between cervical spine and shoulder pathology. It is necessary to recall that pain coming from shoulder pathology typically does not radiate distal to the elbow and that shoulder and cervical spine disease may coexist.

Impingement Syndrome

Impingement syndrome is a condition caused by repeated mechanical insult to the rotator cuff, with the tendons forced against the overlying coracoacromial arch as the arm is elevated overhead. A variety of anatomic, biomechanical, and neurologic factors either narrow the space available for the rotator cuff or cause abnormal arthrokinematics, leading to impingement of the tendons. Classically, there are three stages of impingement (described by Neer). Stage 1 is characterized by subacromial edema and hemorrhage; stage 2 progresses to tendonitis and fibrosis; and, ultimately, stage 3 results in tearing of the rotator cuff, either partially or completely.7

The patient with impingement syndrome generally complains of activity-related shoulder pain that extends from the top of the shoulder into the arm laterally—to the level of the deltoid tuberosity. This is especially true with overhead activities. Night pain and the inability to lie on the affected side may be additional complaints, particularly if a rotator cuff tear is present. Ultimately, the patient develops movement compensation patterns that place abnormal stresses on associated structures, leading to symptoms such as scapular and cervical muscle strain. Although cervical spine provocative maneuvers such as the Spurling test are negative8 (Fig. 28-1), a variety of physical examination maneuvers have been developed to diagnose shoulder impingement and are designed to reproduce the patient’s symptoms by compressing the rotator cuff under the subacromial arch.7 The Neer impingement sign and the Hawkins sign are two such tests (Figs. 28-2 and 28-3). The Neer impingement sign can be particularly useful; this overhead position is not well tolerated in the patient with impingement syndrome but may bring relief to the patient with cervical radiculopathy, because it decreases neural tension (shoulder abduction relief sign).9 Palpation may elicit tenderness over the rotator cuff tendons or the acromioclavicular joint. This joint can be a source of impingement due to degenerative changes, such as spurring and synovitis. In the presence of a rotator cuff tear, weakness of abduction (supraspinatus) and external rotation (infraspinatus) may be noted. However, other structures innervated by C5 and C6, such as the deltoid and bicep muscles, remain intact. In addition, impingement syndrome is not typically associated with sensory loss or reflex changes that may be found with cervical radiculopathy.

A subacromial injection of local anesthetic can implicate or rule out impingement as the cause of the patient’s symptoms. Plain radiographs, including anterior-posterior, lateral, axillary, and scapular outlet views, as well as advanced imaging techniques such as MRI, can be helpful. Care must be taken in interpreting the MRI scans in the absence of a quality physical examination because the prevalence of abnormal studies in asymptomatic subjects ranges from 15% to 60% for the cervical spine and from 4% to 54% for rotator cuff tears, depending on the age of the patient.10,11

Glenohumeral Osteoarthritis

Osteoarthritis (OA), also known as degenerative joint disease of the glenohumeral joint, is not as common as knee or hip OA but is by no means rare. Causes of glenohumeral OA may be primary (idiopathic) or secondary. Examples of secondary causes are posttraumatic, infectious, metabolic, and inflammatory. The patient with early glenohumeral OA presents with activity-related pain that is relieved by rest. The pain is generally located about the shoulder, and there may be mild range of motion (ROM) restrictions. The distribution of pain is similar to that which a patient with a C5 or C6 radiculopathy might present.12 As the disease progresses, pain may persist at rest, and night pain may become a complaint. ROM becomes more restricted, particularly external rotation, due to anterior capsular and subscapularis contracture. Motion restrictions are similar for active and passive ROM. Rotator cuff strength is usually maintained but may seem limited secondary to pain. Palpation may demonstrate tenderness, especially about the posterior glenohumeral joint line, and crepitus may be noted with ROM activities. Plain radiographs (anteroposterior [AP], lateral, and axillary views) of the shoulder are usually conclusive in the case of glenohumeral OA. Diagnostic intra-articular injections can help differentiate shoulder OA from cervical spine disease.


The hip joint is the articulation between the head of the femur and the acetabulum. However, when patients refer to the hip, they may be referring to any number of associated and neighboring structures. Due to the proximity of the hip to the lumbar spine, conditions about the hip are often confused with lumbar spine pathology, particularly radiculopathy. When discussing pathology around the hip, it is sometimes useful to separate the conditions into intra-articular and extra-articular processes. Examples of intra-articular pathology include OA and a torn acetabular labrum, whereas extra-articular examples are greater trochanteric bursitis, hamstring muscle strain, and piriformis syndrome.

Hip Osteoarthritis

OA of the hip, as in the shoulder, can be primary or secondary. It can be unilateral or bilateral. When systemic or inflammatory disease processes are responsible for the condition, involvement is more likely to be bilateral. Primary OA is by far the most common form of hip OA. It increases in frequency with increasing age, although the precise interrelationship between aging and arthritis is not clear. Patients with primary hip arthritis complain of activity-related pain that is relieved by rest. Those with severe degenerative changes may even have pain at rest. Their ambulation distance is decreased due to pain, and they may develop an antalgic gait pattern. As the disease progresses, patients may complain of difficulty with tasks such as donning shoes and socks due to limitation in hip ROM. As with any intra-articular hip pathology, OA causes groin pain that typically radiates down the ventromedial thigh to the knee. However, hip arthritis may refer pain distal to the knee in more than 40% of patients.13 In addition to mimicking lumbar radiculopathy, hip arthritis can mimic somatically referred pain from the intervertebral disc, lower lumbar facet joints, and sacroiliac joints. Secondary involvement of the gluteus musculature and trochanteric bursa due to an altered gait pattern may cause lateral hip and thigh pain as well.

Physical examination may demonstrate gait abnormalities such as a trunk lean over the affected hip during weight-bearing (to decrease the abductor moment about the hip, thus reducing compressive load across the joint). Patients may display apparent and/or true leg length discrepancy due to hip flexor/adductor contractures and/or hip joint cartilage loss, respectively. There may be weakness of the hip abductors, and they may be tender to palpation. ROM tends to be limited, primarily in hip internal rotation. The most provocative maneuver with hip OA is to flex the hip of the supine patient to at least 90 degrees and then apply adduction and internal rotation. In the case of unilateral disease, this motion is restricted and painful on the involved side. Patients with OA of the hip do not typically have sensory or reflex changes as part of their clinical picture unless there is coexisting neuropathy or spinal pathology. Occasionally, a diagnostic, intra-articular hip injection with local anesthetic is required to differentiate hip and spine symptomatology with a calculated sensitivity of 88% and specificity of 100%.14 The standard radiographic workup for primary hip OA is an AP pelvis radiograph and AP and lateral radiographs of the involved hip. This is usually confirmatory (Fig. 28-4).

Greater Trochanteric Pain Syndrome

Greater trochanteric pain syndrome (GTPS) is a term that has been used to describe lateral hip pain of soft tissue origin in the region of the greater trochanter. Trochanteric bursitis is the most common etiology of this syndrome. However, other conditions have been described such as tendonitis or tears of the gluteus medius and iliotibial band irritation.2,15 These conditions are likely related to overuse, abnormal biomechanics, or local trauma. Patients with GTPS complain of pain about the hip laterally that may radiate proximally to the buttock and distally along the lateral aspect of the thigh to the lateral knee. Several lumbar dermatomes share this distribution, allowing GTPS to mimic lumbar radiculopathy. It has been reported that up to 20% to 25% of patients being evaluated for lumbar spine pathology have GTPS as the source of their complaints. In addition, greater trochanteric bursitis has been found in 25% to 35% of patients with low back pain.2,5

Physical examination of the patient with GTPS reveals local tenderness to palpation of the involved structure (tendon or bursa). Tenderness may be ventral, dorsal, rostral, or directly over the greater trochanter, depending on the structure involved. Similarly, patients complain of increased symptoms when sleeping on the involved side due to direct pressure on the inflamed structures. Resisted hip abduction or external rotation also compresses or stresses the tissues in GTPS, reproducing the symptoms. Once the physical examination has implicated a particular structure but lumbar radiculopathy has not been ruled out, an injection of a local anesthetic can help in the differentiation between local pathology and referred pain. Some authors suggest the use of fluoroscopy for the injection to ensure that the anesthetic reaches the site of pathology.15 Plain radiographs are useful to help to rule out hip arthritis and other local pathology such as a fracture of the greater trochanter. Often, patients complain of tenderness on palpation in this region, even when this is not the presenting complaint. Recognizing the existence of the various conditions under the umbrella of GTPS, coupled with a careful history and physical examination, is usually sufficient to differentiate between hip and lumbar spine disease. One must realize, however, that these conditions can coexist.

Sacroiliac Joint

The sacroiliac joint (SIJ) is certainly capable of producing pain locally. SIJ pain is also in the differential diagnosis as an extraspinal cause of low back and lower extremity pain. A variety of pathologic processes can affect the SIJ, including SIJ pain syndrome, OA, sacroiliitis (as in ankylosing spondylitis and Reiter syndrome), septic arthritis, and traumatic SIJ instability or dislocation. Many of these conditions have an obvious history as well as objective radiographic findings, implicating the SIJ as a pain generator. However, in the absence of “hard” findings on examination or radiographs, attributing a patient’s pain to the SIJ has in recent decades been met with skepticism due to the controversy over the joint’s ability to be a source of pain and the thought that the SIJ does not move in most individuals. Recent injection studies have demonstrated the SIJ to be a potential source of pain in the low back, buttock, and lower extremity, and studies involving radiostereometric analyses have shown small but definite motion at the SIJ.4,16

Sacroiliac Joint Dysfunction

The clinical presentation of the patient with SIJ dysfunction can be highly variable. In patients with a diagnosis of low back pain, the prevalence of this condition has been reported to range from 13% to 30%. Injection studies of the SIJs of asymptomatic volunteers produced pain in the low back, posterior superior iliac spine (PSIS) area, buttock, and thigh. Further studies on symptomatic subjects demonstrated that SIJ injection with a local anesthetic relieved a variety of pain patterns, including pain in the low back, PSIS region, abdomen, buttock, groin, thigh, leg, and foot.4 Clearly, SIJ dysfunction can mimic lumbar spine pathology, including discogenic pain, lumbosacral facet joint arthropathy, and radiculopathy.

Patients with SIJ dysfunction typically present with pain in the lateral low back, in the parasacral region with radiation to the buttock and posterolateral proximal thigh. They may complain of tenderness in the area of the sacral sulcus. Some authors have suggested that a painful SIJ can refer pain into the calf and foot, although much less commonly. There are many tests described in the literature to test for SIJ dysfunction; to review all of these is not within the scope of this chapter. Two categories of SIJ testing include tests designed to stress the SIJ and reproduce the patient’s symptoms and those designed to detect abnormal or asymmetrical motion by palpation of certain anatomic landmarks about the pelvis.17 Some tests used to stress the SIJ include the Gaenslen and Faber tests and SIJ compression/distraction maneuvers. Motion palpation tests include the standing flexion test and Gillet test. However, using physical examination tests to provoke SIJ pain through manually stressing the joint, detecting motion abnormalities by palpation, or relying on features of the patient history have traditionally all correlated poorly with the response of fluoroscopically guided intra-articular SIJ injections.4 However, more recent data suggest that by using a composite of manual tests, a practitioner can reliably implicate or rule out the SIJ as a source of low back pain.18 Even with these new data, the diagnostic test of choice for SIJ dysfunction seems to be a fluoroscopically guided intra-articular SIJ injection of a local anesthetic.

Nervous System

Conditions of both the central and peripheral nervous systems can mimic spine disease. Pathology of the peripheral nervous system is more likely than that of the central nervous system to mimic spine pathology, but occasionally, an intracranial condition will do so. Intracranial conditions known to have signs and symptoms overlapping those of spine pathology include intracranial neoplasms, Chiari malformation, cerebrovascular accidents, normal pressure hydrocephalus, and spontaneous intracranial hypotension.1921

As previously stated, peripheral neuropathy is one of the more common masqueraders of spinal pathology, particularly radiculopathy and myelopathy. There are many etiologies of peripheral neuropathy, including compression or entrapment; metabolic, nutritional, toxic, hereditary, autoimmune, neoplastic disorders; and disorders associated with neuromuscular disease2227 (Box 28-2). Even in the face of an extensive workup, the etiology of peripheral neuropathy is frequently not identified. When this is the case, the initial serologic studies should include vitamin B12, folate, hemoglobin A1C, erythrocyte sedimentation rate, and thyroid-stimulating hormone. The following section will concentrate on the more common peripheral nervous system conditions mimicking spine disease. There are certainly many more causes of peripheral neuropathy than are discussed in this section. The list is too exhaustive to review in this chapter, and the authors suggest a neurology text for further detail.

Compression Neuropathy

Compression or entrapment neuropathy is a type of mononeuropathy resulting from local compression on a peripheral nerve. One well-known example is carpal tunnel syndrome. Compression neuropathies can present with varying degrees of motor, sensory, and autonomic disturbances and can be confused with myelopathy and radiculopathy. However, a careful history, physical examination, and special studies such as electromyography and nerve conduction velocity (EMG/NCV) help localize the site of compression. Injections of local anesthetics at the suspected site of compression can be performed easily in the office and can often help differentiate between several diagnoses. There are numerous peripheral nerve compression syndromes of the upper and lower extremities. Therefore, only a select few are discussed in detail, with others represented in table format (Tables 28-1 and 28-2).

TABLE 28-1 Compression Syndromes of the Upper Extremity

Compressive Syndrome Anatomy Masquerading As
Thoracic outlet syndrome Brachial plexus compression at the level of the scalenes, clavicle, first rib, or coracoid process Cervical radiculopathy, primarily C8, T1
Suprascapular nerve compression Suprascapular nerve compression at the transverse scapular ligament or at the spinoglenoid notch C5, (C6) radiculopathy
Carpal tunnel syndrome Median nerve compression at the wrist C6 radiculopathy
Pronator syndrome Median nerve compression about the anteromedial elbow C6 radiculopathy
Anterior interosseous nerve (AIN) syndrome AIN compression in the proximal volar forearm Not commonly confused with cervical radiculopathy because there are no sensory disturbances, only motor abnormalities (weakness of the flexor digitorum profundus to the index finger, flexor pollicis longus, and pronator quadratus)
Cubital tunnel syndrome Ulnar nerve compression about the medial elbow C8, T1 radiculopathy
Ulnar tunnel syndrome Ulnar nerve compression in the canal of Guyon at the wrist C8, T1 radiculopathy
Wartenberg syndrome Superficial radial nerve compression between the brachioradialis and extensor carpi radialis longus in forearm C6 radiculopathy
Posterior interosseous nerve (PIN) syndrome PIN compression in the proximal forearm C6, C7 radiculopathy
Radial tunnel syndrome Radial nerve compression at or distal to the elbow C6 radiculopathy

TABLE 28-2 Compression Syndromes of Lower Extremity

Compressive Syndrome Anatomy Masquerading As
Lumbosacral plexopathy Compression of the lumbosacral plexus, (e.g., tumor, hematoma) L1 through S4 radiculopathy
Piriformis syndrome Sciatic nerve compression at the level of the piriformis muscle S1 radiculopathy
Meralgia paresthetica (LFCN) LFCN compression at the level of the inguinal ligament L2, L3 radiculopathy
Obturator neuropathy Compression due to many intrapelvic and hip pathologies L1, L2, L3 radiculopathy
Saphenous neuropathy Saphenous nerve compression at Hunter’s canal or from direct trauma L4 (L3, L5) radiculopathy
Peroneal neuropathy Common peroneal nerve compression at the level of the fibular head L4, L5 radiculopathy
Tarsal tunnel syndrome (tibial nerve) Tibial nerve compression at the posteromedial ankle L5, S1 radiculopathy

LFCN, lateral femoral cutaneous nerve.