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.

FIGURE 28-1. Spurling examination. Rotation and lateral flexion to the involved side with mild extension and axial load reproduces upper extremity radicular symptoms.

FIGURE 28-2. The Neer impingement test causes rotator cuff impingement against the anterior edge of the acromion with shoulder flexion.

FIGURE 28-3. The Hawkins impingement test causes rotator cuff impingement against the coracoacromial ligament in this position.

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.

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).

FIGURE 28-4. Radiograph demonstrating hip osteoarthritis. Note the joint space narrowing, osteophytes, subchondral sclerosis, and subchondral cysts, which are the hallmark radiographic signs of osteoarthritis.

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 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.

Upper Extremity Compression Neuropathies