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Editors Memo

Back-and-forth on back pain

Back-and-forth on back pain

By Leo Robert

In the popular cable TV series The Sopranos, a mobster complained of back pain as an excuse to avoid work—hardly a novel concept—so a colleague referred him to a specialist whose diagnostic skills had earned him the unofficial title “the Jonas Salk of backs.”The doctor gave him “the works, MRIs, cat scans, dog scans, you name it” but concluded there was nothing wrong with his back. This finding upset the skeptical colleague, but he acknowledged the difficulty of assessing back pain by noting, “When it comes to backs, nobody knows anything really.”

Clearly the know-it-all colleague had no medical training, but never has the dilemma of low back pain diagnosis been more eloquently stated.

Complaints of back pain—the most common physical condition for which patients see a doctor—result in physician visits of 12% to 15% of the U.S. population in a given year, according to the U.S. Bone and Joint Decade (USBJD). Back pain also is reported more frequently than any other form of musculoskeletal pain, including pain in the arms, shoulders, hips, or knees.

It might be surmised that diagnosis of a condition seen as frequently as back pain would be relatively simple because affected patients would be reporting similar sets of symptoms seen many times before. But that’s hardly the case. Back pain often results from complex conditions that are not easily understood.

Backache traditionally was considered a rheumatologic condition. Now it is recognized that possible causative factors include advanced age, poor fitness,obesity, poor dietary habits, heredity, race, and cigarette smoking.

Many diseases can cause or contribute to back pain, including osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and cancer. Mechanical problems maybe responsible, particularly intervertebral disk degeneration but also spasms, muscle tension, and herniated disks. Sports and work injuries can cause acute orchronic back pain. Scoliosis and spondylolisthesis are possible causes.

Even pregnancy, fibromyalgia, and infections may contribute to back pain, and emotional stress can play a role in its severity and duration.

It’s no wonder then that diagnosis of back pain presents practitioners with such a major challenge. But patients face a similar challenge as they try to obtain an accurate diagnosis. Who do they see first when they experience symptoms?

Back pain traditionally was managed by orthopedists and chiropractors. Now many other professionals are involved, including primary care physicians,rheumatologists, pain management specialists, physiatrists, neurologists, physical therapists, trainers, psychologists, and practitioners of complementary and alternative medicine.

It’s generally recommended that persons with back pain see their primary care physician first. But if a patient comes to you with complaints of back pain, are you equipped to manage the problem or make an appropriate referral?

The USBJD used an objective scientific research design to measure the incidence and prevalence of musculoskeletal conditions and to project trends. The goal in reporting the key facts about back pain, as well as other musculoskeletal conditions, was to provide better understanding of the underlying mechanisms and to develop novel approaches to therapy and prevention.

That’s also the goal in this month’s cover story (“Low back pain poses diagnostic challenge to clinicians,” page 20.) This first part of a two-part article by Features Editor Kristen Light provides an overview of basic principles of patient evaluation, including recommendations from the American College of Physicians and the American Pain Society.

We hope this discussion will answer your questions about back pain so you can help patients achieve thebest possible outcome.

  

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Pain Management

Deciding fibromyalgia treatment revolves around key issues

Five main points can guide clinicians in decision making during interactions with patients.

By David S. Hallegua, MD, and Daniel J.Wallace, MD

Primary care physicians are the first line of triage for patients who have fibromyalgia syndrome (FMS). They are responsible for ruling out coexisting disorders and establishing possible inducing factors that may warrant specific management. Once these goals are accomplished, they can steer patients in a positive direction toward addressing their symptoms without becoming stigmatized. Providing patient education, instilling a sense of self worth, advising avoidance of disability and narcotic medications, offering instruction in optimal sleep hygiene, establishing anxiety reduction measures, and recommending a comprehensive exercise and stretching program all may help this effort. Involving patients in management decisions has the potential to improve physician-patient interaction and, as a result, improve outcomes.1

Patients with early FMS that is diagnosed and managed in the primary care setting have a very good prognosis; more than half no longer meet the American College of Rheumatology criteria within two years.2 Those who have special needs (e.g., counseling and local injections) and refractory cases may benefit from referral to a musculoskeletal specialist (e.g., rheumatologist, neurologist, orthopedist, osteopath, or physical medicine and rehabilitation physician). The specialist can confirm the diagnosis in a single encounter or work with the primary care physician to treat the patient. Patients with longstanding FMS who have psychological issues (e.g., bipolar illness or posttraumatic stress disorder [PTSD]) have a poorer prognosis, but the family physician or internist should remain the “captain of the ship” in directing treatment.

Primary care physicians can best manage FMS, and thereby improve patients’ prognosis and quality of life, by addressing five key issues. In this article, we describe several cases of FMS that demonstrate the issues that frequently arise and how primary care physicians can address them with enhanced communication techniques to improve outcomes.

Basic science

FMS is a syndrome, or group of symptoms that occur together, rather than a disease. It is characterized by chronic widespread musculoskeletal pain of at least three months’ duration in all four quadrants of the body and is thought to be a central sensitization syndrome3 (afferent sensory inputs into the dorsal root ganglion of the spinal column overwhelm the “gated” protective mechanism). A “wind-up” phenomenon (hyperexcitability with a low discharge threshold that worsens with each sensory input) creates greater discomfort than is seen in most persons. Thin unmyelinated C fibers and large myelinated A fibers and autonomic B fibers carry signals that result in amplified pain, hypervigilance, and discomfort from sensations that most persons would find pleasurable (e.g., gentle stroking). Other central sensitization syndromes include irritable bowel syndrome (IBS), irritable bladder syndrome, chronic pelvic pain, chronic fatigue syndrome, tension headache, and temporomandibular joint dysfunction syndrome.

The primary manifestations of FMS include altered sleep architecture, aching, and fatigue (Table 1). FMS affects 2% to 3% of the U.S. population4; most patients are women, and the syndrome often develops during their reproductive years.

Two clinical cases are presented here and are followed by a discussion of the key issues that they illustrate.

Clinical case I

A 36-year-old woman with a history of postpartum depression and hypothyroidism presents in a primary care physician’s office with a complaint of pain all over her body. The symptoms appeared to start three months earlier after the patient slipped and fell while shopping in a department store. The fall aggravated the low back pain that had started during her pregnancy 18 months earlier. During the following week, the pain had spread from her lower back up her spine and down into her legs. Her sleep became progressively disturbed, and the pain spread to her shoulders, neck, and arms.

The patient’s current medications include fluoxetine, 20 mg/d, and levothyroxine, 100 μg/d. Results of laboratory tests performed within the last three months showed a normal complete blood cell count, erythrocyte sedimentation rate, and thyroid-stimulating hormone level; results for rheumatoid factor and antinuclear antibodies were negative.

The patient admits to feeling upset because the pain prevents her from adequately taking care of her child and her home. She denies having feelings of hopelessness and episodes of crying that made her isolated and unable to care for her child in the early postpartum period. She believes that she is constantly behind in her housework and often blames herself for her condition. She fears that her symptoms are the result of an undiagnosed serious condition that the tests performed so far have failed to detect.1. Is FMS primary or secondary?

The many factors associated with the onset of FMS include motor vehicle accidents, infections, continuous work-related overuse of some muscles (e.g., heavy lifting or pulling), and psychosocial stressors.5 In addition, well-defined medical conditions are known to involve an increased prevalence of FMS. Patients who have inflammatory disorders, metabolic disturbances, or underlying malignancies frequently have a reactive FMS when undertreated inflammation or tissue insults result in muscle spasm. Chronic use of corticosteroids induces cutaneous hyperesthesia and an acute FMSlike syndrome when the dose is reduced. In addition, some patients are told that they have FMS when there are other explanations for their symptoms.

When a diagnosis of FMS is made, the primary care physician may play an important role in assessing what other conditions are present and ruling out those that could stigmatize a patient given a diagnosis for a disorder that he or she does not have. The physician should explain to the patient that FMS is simply a set of symptoms and physical findings that can be nonspecific and provide important clues toward understanding why the patient feels unwell. Managing comorbid conditions goes a long way toward ameliorating FMS symptoms.

2. Are there underlying psychosocial stressors?

Although many patients with FMS have a history of depression, only 15% to 20% are depressed at any given physician visit.6 Primary care physicians may be able to handle many FMS flares in a crisis intervention mode by addressing a patient’s divorce, death of a loved one, or job loss.

The most common behavioral conditions associated with FMS are generalized anxiety disorder, PTSD, and mood disorders. 6,7 Anxiety may be related to a patient’s perception that he has a serious medical condition, psychosocial stressors, or discomfort at not feeling well. Anxious patients with FMS often have perfectionistic tendencies, tend to make lists, exhibit hypervigilance, and sleep poorly; however, they tend to hide their discomfort in social settings.

Anxious patients are the most responsive to FMS-related interventions, counseling, biofeedback, reassurance, cognitive-behavioral therapy, and complementary regimens that promote relaxation. Most remain under the care of their primary care physician except for an occasional musculoskeletal specialist visit.

However, when PTSD is associated with a personal or family history of alcoholism, substance abuse, domestic violence, emotional or sexual abuse, or military service, simply injecting tender points and prescribing a tricyclic antidepressant and physical therapy has a very low improvement rate. The physician needs to query the patient in a sensitive but methodical way. Persons with such a history who have ongoing psychosocial stressors tend to cope poorly and usually benefit from ongoing counseling and long-term psychotropic interventions.

Mood disorders range from bipolar illness to alexithymia. Bipolar illness is 150 more times common in patients with FMS than in healthy controls and does not respond to most interventions.8 However, primary care physicians may have a significant impact on dysthymic states, catastrophizing, and depression by prescribing tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), duloxetine, benzodiazepines, or anticonvulsants (e.g., pregabalin).

Patient expectations need to be addressed. For example, make sure that patients understand that pharmacotherapy is adjunctive to other interventions and that there are some things that the physician cannot do to help them.

3. Is the pain regional or widespread?

The pain associated with FMS may be myofascial or widespread (involving all four quadrants of the body and the spine). The widespread pain may be provoked by light touch (allodynia). Myofascial pain may be the primary problem in a muscle or may be associated with a pain trigger, such as a bulging disk or costochondritis. It may be considered significant when it accounts for at least 50% of the patient’s total pain experience at a given visit.

The most common triggers that can worsen and contribute significantly to FMS pain are headaches, including migraines, degenerative disk disease, and IBS. Conversely, a patient, such as the one described in the second clinical case, may present with chronic regional pain syndrome when a diagnosis of myofascial pain syndrome should be considered.

Regardless of the presentation, the primary care physician needs to be cognizant of the contribution of a local process to the total pain experience; all factors need to be managed. Therapy for the local process— physical therapy, bracing, exercise, trigger point injection, acupuncture, and local heat—can have a dramatic effect on the patient’s pain level and leads to improvement in the therapeutic response of baseline medications (e.g., sleep and pain medications used to manage FMS).9,10

Attention must be paid to finding not only the regional distribution of myofascial pain but also the appropriate trigger points for therapy and local predisposing factors (e.g., regional arthritis, limb length discrepancy, and unusual loading of a skeletal muscle). Functional disturbances (e.g., IBS and restless legs syndrome) tend to be less prevalent in patients with regional myofascial pain syndrome.Clinical case II

A 52-year-old male store owner presents with a complaint of pain over the right shoulder blade and base of the neck on the right side that has lasted for three years. The pain appeared to be intermittent at its onset and to worsen with excessive bending or twisting of the neck and carrying of heavy weights in his right arm. One year before, the patient was evaluated for cervical radiculopathy with MRI of the cervical spine and electromyography. The results showed normal neuromuscular function by examination and on needle EMG. The MR scan showed moderate degenerative disk disease and slight disk bulging at the C5-6 level. The worst pain now appears to be triggered by pressure over the base of the neck lateral to the seventh cervical spinous process on the right side.

A diagnosis of regional myofascial pain syndrome is made, and trigger point therapy is started. The pain persists even though the patient receives two sequential local trigger point injections with 1% lidocaine and 20 mg of triamcinolone.

The patient is referred for physical therapy and acupuncture and receives these therapies once a week. Physical therapy consists of muscle mobilization and strengthening, modalities, and massage three times a week.

An overzealous therapist rapidly increases the free-weight lifting above the shoulder from a 10-pound to a 30-pound weight with 20 to 30 isotonic repetitions. The patient experiences a pain flare-up the day after the first strenuous workout; he notices that the pain has crossed over to the left side of the neck.

The patient’s pain spreads and in two weeks involves the neck, shoulders, and upper back on both sides, even though he is using analgesic medications (e.g., ibuprofen) around the clock and muscle relaxants (e.g., cyclobenzaprine) at bedtime. The patient reports disturbed sleep, with an inability to fall asleep because of pain and frequent awakening at night because of pain felt when he lies in one position for more than an hour.

Physical examination reveals tender points in the trapezius muscle at the occiput, the base of the neck, and the midpoint of the trapezius between the shoulder and neck. The trigger points radiate pain into the upper arms bilaterally. Myofascial pain is present between the shoulder blades and over the subscapularis muscle in the axillary areas bilaterally. Pain with light touch is present over the upper chest wall at the site of attachment of the pectoral muscles and over both subacromial bursa areas.

The ibuprofen is substituted with tramadol in an extended-release formulation to manage the around-the-clock pain. The dose is gradually titrated up to achieve pain levels of three to four on a zero-to-10 pain scale. Intermittent spiking of pain lasting a few hours continues to occur in the late afternoon, after aquatherapy, and at night. Pain on light touch continues to be present over the chest wall. The breakthrough pain is managed with immediate-release hydrocodone twice a day, before aquatherapy and at bedtime.

Cyclobenzaprine is discontinued and pregabalin is started in low doses twice a day and titrated to a total daily dose of 300 mg; there is improvement of the pain on light touch and of sleep. A persistent trigger point in the left trapezius is injected with a combination of 20 mg of methylprednisolone acetate and 1 cc of lidocaine. The patient continues to receive these medications at six months and has achieved good pain control, improved sleep function, and has returned to work full time.

4. How to approach exercise?

Exercise is a major component of managing FMS, regional myofascial pain syndrome, and other “chronically painful” syndromes. There is ample evidence of decreased endurance, fatigue, and muscle pain in FMS with exercise. Most is attributed to muscle deconditioning, but some studies show that anabolic hormones (e.g., dihydroepiandrostenedione and testosterone) are reduced in FMS.

Growth hormone (GH) secretion— which occurs predominantly at night during nonrapid eye movement delta wave sleep—is suppressed in FMS, leading to a lack of muscle repair at night and poor muscle endurance and pain during the day. An enhanced somatostatin tone that limits GH release is thought to be present in the brain. Inhibiting the somatostatin tone with exercise and use of pyridostigmine corrects the impaired secretion of GH.

In a double-blind trial of several months’ duration, GH administration decreased patients’ overall level of pain and tender points on examination.11 However, the effects were short-lived and the cost of the GH medication is prohibitive. Therefore, treatment is directed at improving sleep and encouraging exercise to improve muscle endurance.

The ability to exercise is quite variable in patients with FMS. Some can barely walk a few blocks because of an increase in myalgia that occurs postexercise. Therefore, exercise should be tailored to the specific patient’s ability.

Some forms appear to work better than others in patients with FMS. Evidencebased approaches suggest that aquatherapy holds the most promise.

5. How to determine medication approaches?

A fundamental approach to treating any patient who has chronic pain is to ascertain whether the pain is around-the-clock or intermittent. The history and physical examination should determine whether the pain is regional or widespread and whether an underlying condition (e.g., myelopathy or a metabolic illness) could be the cause. If the pain has been determined to be the result of central sensitization of the dorsal neuron in the spinal cord by the presence of allodynia, widespread trigger points, or more than 11 out of the 18 designated tender points for FMS, treatment should be directed at improving sleep architecture and decreasing spinal neuron excitation.12

Approach to improving sleep efficiency and sleep architecture. Sleep efficiency is the ratio of time spent sleeping in bed versus total time spent in bed. Sleep may be improved by decreasing the pain present at the time of sleep onset and using a rapid-acting sleep medication (e.g., zolpidem).13 Sleep maintenance may be achieved by combining longer-acting sleep medications (e.g., amitriptyline, trazodone, and clonazepam). The need to manage comorbidities, such as migraines and anxiety, should be considered.

Alterations in sleep architecture in FMS include a lack of stage-four delta wave sleep. Some improvement in delta wave sleep may be obtained by using a medication, such as amitriptyline, tiagabine, or sodium oxybate. A sleep study may be useful in detecting restless legs syndrome, sleep-associated myoclonic jerks, or obstructive sleep apnea, 40 BIOMECHANICS which may be managed with pramipexole, clonazepam, or continuous positive airway pressure, respectively. Daytime naps may not provide sufficient stage-four sleep; patients should be advised to make every effort to avoid sleeping during the day.

Decreasing spinal neuron activation. A variety of approaches are used to decrease pain that results from central sensitization of neurons. They can be divided broadly into nonpharmacological and pharmacological methods. Nonpharmacological methods include the use of appropriate exercise to improve endurance, muscle strength, and endorphin levels in the brain.14 Acupuncture may be used to manage localized myofascial pain, and cognitive-behavioral methods may alter thought processes that are unconducive to proper healing.

Medications may be used to target various pathways that have been identified as important in reducing sensitization of neurons (Table 2). They may improve the function of descending inhibitory tracts on spinal neurons (e.g., duloxetine, venlafaxine, and tizanidine) or decrease the activity and wind-up of pain-sensing neurons (e.g., pregabalin, dextromethorphan, and ketamine).

Adjunctive medications also may help decrease spinal nerve sensitization; they improve coping mechanisms by decreasing anxiety and depression. Decreases in overall levels of pain in FMS may be achieved by targeting pain triggers—managing a bulging disk with an epidural corticosteroid injection, reducing knee osteoarthritis with local hyaluronic acid injections, preventing migraines with topiramate, and relieving a nagging trigger point with a local corticosteroid/ lidocaine combination injection.

Use of long-acting medications to control around-the-clock pain is essential. The least potent yet effective narcotic medication (e.g., tramadol extended-release or oxycodone sustained-release preparations) may be needed to control pain that persists in spite of all other attempts to address it. Short-acting pain medications must be used to control breakthrough pain.

David S. Hallegua, MD, is an assistant clinical professor of medicine and Daniel J. Wallace, MD, is a clinical professor of medicine at Cedars-Sinai Medical Center, David Geffen School of Medicine, at the University of California, Los Angeles.

A version of this article originally appeared in our sister publication, the Journal of Musculoskeletal Medicine, in April.

References

1. Bieber C, Müller KG, Blumenstiel K, et al. A shared decisionmaking communication training program for physicians treating fibromyalgia patients: effects of a randomized controlled trial. J Psychosom Res 2008;64(1):13-20.

2. MacFarlane GJ, Thomas E, Papageorgiou AC, et al. The natural history of chronic pain in the community: a better prognosis than in the clinic? J Rheumatol 1996;23(9):1617-1620.

3. Yunus MB. Fibromyalgia syndrome: clinical features and spectrum. J Musculoskel Pain 1994;2:5-21.

4. Wolfe F, Ross K, Anderson J, et al. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum 1995;38(1):19-28.

5. Wallace DJ, Clauw DJ, eds. Fibromyalgia and other central pain systems Philadelphia: Lippincott Williams & Wilkins; 2005.

6. Wallace DJ, Clauw DJ, Hallegua DS. Addressing behavioral abnormalities in fibromyalgia. J Musculoskel Med 2005;22:562- 579.

7. Aaron LA, Bradley LA, Alarcon GS, et al. Psychiatric diagnoses in patients with fibromyalgia are related to health care-seeking behavior rather than to illness. Arthritis Rheum 1996;39(3):436-445.

8. Wallace DJ, Gotto J. Hypothesis: bipolar illness with complaints of chronic musculoskeletal pain is a form of pseudofibromyalgia. Semin Arthritis Rheum 2008;37(4):256-259.

9. Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Vol 1: the upper extremities. Baltimore: Lippincott Williams & Wilkins; 1983.

10. Ready LB, Kozody R, Barsa JE, Murphy TM. Trigger point injections vs. jet injection in the treatment of myofascial pain. Pain 1983;15(2):201-206.

11. Jones KD, Deodhar P, Lorentzen A, et al. Growth hormone perturbations in fibromyalgia: a review. Semin Arthritis Rheum 2007;36(6):357-379.

12. Hallegua DS, Wallace DJ. Comprehensive management of fibromyalgia. J Musculoskel Med 2005;22:382-391.

13. Burckhardt CS. Nonpharmacologic management strategies in fibromyalgia. Rheum Dis Clin North Am 2002;28(2):291-304.

14. Barkhuizen A. Rational and targeted pharmacologic treatment of fibromyalgia. Rheum Dis Clin North Am 2002;28(2):261-290.

  

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Sports Medicine

Elbow instability injuries require evaluation strategy

Elbow instability injuries require evaluation strategy

Elbow stability involves complex interactions among the bony articulation of the elbow joint, capsular ligamentous structures, and dynamic muscle restraints. Elbow instability may result in injuries. They often are chronic overuse injuries that occur with overhead throwing in athletes. Instability may affect the lateral or medial aspect of the elbow.

Understanding the functional anatomy of the elbow and the relative contributions to instability of the various structures is crucial to developing a strategy for diagnosis and management of injuries and recognizing the patient’s activity level requirements.

Anatomy and biomechanics

The anatomy of the elbow features several prominent characteristics.

Bony articulation. The radiohumeral and proximal radioulnar articulations allow for rotation or pivoting motion or both. The ulnohumeral articulation functions more as a hinge in forward flexion and extension. The greater sigmoid notch of the ulna articulates with the spool-shaped trochlea of the distal humerus to form a highly conforming articulation. The capitellum is aspheroidal; it is separated from the trochlea by a groove in which the radial head articulates. The radial head is concave and usually is more elliptical than circular; it is slightly offset from the neck.

Bony stability. The ulnohumeral articulation provides the elbow with a significant amount of inherent stability because of its congruent nature. As a result, the elbow has been considered primarily a hinge-type joint. The ulnohumeral joint may be assumed to move in a uniaxial articulation except when it is in extreme flexion-extension.

With the elbow in full extension, valgus instability is divided equally among the medial collateral ligament (MCL), anterior capsule, and bony articulation. The joint articulation provides about 55% of stability in extension and up to 75% in 90º of stability in flexion.1 At 90º of flexion, valgus instability does not change with the contribution of the articulation. These values represent a pure varus and valgus instability and do not take into account any rotational forces that usually are present with instability.

After a simple elbow dislocation, the olecranon process provides a significant amount of varus and valgus instability. Studies have shown that excision of the olecranon process leads to a decrease in combined stability in extension and at 90º of flexion.2

Posterior-directed forces are resisted by the coronoid process, which provides an anterior bony buttress. A correlation between coronoid fracture or fragment size and the tendency toward dislocation is particularly evident in the absence of a radial head.3

The importance of the radial head in elbow stability has received increasing recognition in recent years. Studies have shown that the radial head can provide as much as 30% of valgus stability, even when the MCL is intact. If the MCL is disrupted, the radial head becomes a crucial secondary elbow stabilizer and provides up to 75% of the resistance to valgus stress. In addition, about 60% of longitudinally applied force normally is transmitted through the radial head.

Capsule. When taut in extension, fibrous bands within the elbow joint provide significant strength and an important stabilizing effect. The anterior capsule may be a significant stabilizing element to pure varus and valgus stress in extension but not in flexion.

Medial collateral ligament. The MCL complex, also known as the medial ulnar collateral ligament (MUCL), consists of three bundles: anterior, posterior, and transverse (Figure 1). The anterior bundle is the strongest component of the MUCL. It originates in the anteroinferior aspect of the medial epicondyle and inserts onto the medial aspect of the coronoid process at the sublime tubercle, with an average distance of 18 mm distal to the coronoid tip.

The anterior bundle is functionally composed of an anterior band and a posterior band that provide resistance in valgus stress throughout the range of flexion and extension motion. The posterior bundle is a fan-shaped thickening of the capsule that originates on the medial epicondyle and forms the floor of the cubital tunnel. The transverse ligament connects the inferomedial coronoid process with the medial tip of the olecranon. It is thought to make little or no contribution to valgus stability.4

Lateral collateral ligament. The lateral collateral ligament (LCL) complex has four components: annular ligament, radial collateral ligament (RCL), lateral UCL (LUCL), and accessory LCL (Figure 2). This complex originates from the lateral epicondyle at a point through which the center of rotation passes; therefore, it is isometric throughout the normal range of flexion-extension. The RCL terminates in the annular ligament, which stabilizes the proximal radioulnar joint. The LUCL, which is superficial and distal, inserts onto the tubercle of the supinator crest of the ulna.

O’Driscoll and associates5 first described posterolateral instability of the elbow in 1991. The cause was thought to be LUCL laxity, which allows for rotatory subluxation of the ulnohumeral joint and, subsequently, a secondary dislocation of the radiocapitellar joint. The LCL complex maintains these joints in a reduced position when the elbow is loaded in supination. However, a mechanism for elbow subluxation and dislocation has been described in which there is increased ligamentous and capsular damage, progressing from lateral to medial across the joint. Elbow dislocation is the final of the three sequential stages of instability from posterolateral rotation. The lateral complex also resists varus forces.

Dynamic stability. The flexor and extensor muscles achieve compression across the elbow joint and, in turn, provide dynamic stability. In addition, the extent of instability after a simple elbow dislocation appears to be directly associated with the amount of muscle damage on both the medial and lateral epicondyles. The brachialis and triceps also provide stability, particularly because they have broad cross-sectional areas and also because their insertion is closer to the joints and pivot of joint rotation. Overall, muscle instability is likely, but the magnitude and effect are uncertain.

Medial instability

Recurrent medial instability usually is associated with chronic overuse from sports activities, such as those that involve overload throwing. Valgus stress is applied during throwing, resulting in repetitive microtrauma, attenuation, and even possible rupture to the MCL.6 Acute MCL ruptures may occur with elbow dislocations. They usually heal well, but in athletes there is a greater amount of valgus stress imposed on the elbow than in patients who have a dislocation and use the elbow for activities of daily living.

During the overhead throwing motion, valgus stress occurs primarily during the late arm-cocking and early acceleration phases. A significant amount of force may be generated but is dissipated through a combination of the MCL, flexor pronator mass, and ulnohumeral articulations. Acute ruptures of the MCL usually cause a “popping” sensation and pain and swelling over the medial aspect of the elbow.6

Presentation. Patients who have medial elbow instability usually present with pain and tenderness over the medial aspect of the elbow that is aggravated during and after throwing. If there is a ligament tear, pain may not occur until as much as 70% to 80% of the throwing effort has been made.7

Ulnar nerve symptoms also may occur with medial instability because of compression caused by inflammation of ligaments within the cubital tunnel or because of traction resulting from repeated valgus loading. Up to 40% of patients with medial instability have ulnar nerve symptoms.8, 9

Patients may have point tenderness over the insertion of the anterior bundle of the MCL, which is 2 cm distal to the medial epicondyle. Elbow motion usually is not compromised and elbow instability may be difficult to demonstrate.

Testing. Norwood and colleagues6 described an abduction stress test as a means of evaluating MCL integrity. The test is performed with the forearm supinated and in 15º to 20º of elbow flexion to unlock the olecranon from its fossa. Any reproduction of the athlete’s symptoms is a positive test result. It is currently recommended that the test be performed with the patient’s forearm in full pronation-supination, because a pseudovalgus instability may occur as a result of unrecognized posterolateral instability.10

The moving valgus stress test may be more sensitive in the evaluation of injury to the MUCL. The shoulder is abducted to 90º and fully externally rotated to recreate the throwing position. The elbow is then flexed and extended with a valgus force applied. Pain directly over the MUCL is considered a positive test result. This is the most useful clinical examination in our hands.

The milking maneuver requires the patient to reach under the affected arm, grab the thumb, and pull the elbow into valgus. Pain over the MUCL is considered a positive result. Very few of our patients can perform this maneuver.

These tests apply a valgus stress to the elbow during extension and flexion in an attempt to elicit pain and demonstrate joint line opening. Deficiency of the anterior bundle of the MCL during these tests has been shown to be significantly greater at 70º of flexion than at 30º. Therefore, clinical testing should be performed at these higher degrees of flexion. Detection of partial ruptures of the anterior bundle based on medial joint line opening and increased valgus movement usually is not possible.

Imaging. Recurrent medial instability is primarily a clinical diagnosis, but a stress radiograph may help confirm the diagnosis. However, a normal x-ray film result does not rule out symptomatic ligament attenuation. Stress radiography may be performed with gravity or manually. Plain radiographs also may demonstrate abnormalities associated with recurrent MCL instability, including medial olecranon osteophytes, loose bodies, ligamentous calcification, and formation of heterotopic bone.

Stress radiography results should be compared with those from the contralateral side, because significant ulnohumeral gapping may occur in persons who have normal elbows. For overhead throwers, a side-to-side difference greater than 2 mm is a good standard for making the diagnosis of MCL insufficiency.

MRI is the modality of choice for evaluating MCL insufficiency. Diagnosis of partial tears on MRI is more difficult. Because these partial tears usually occur in the under surface of the ulnar attachment of the MCL, use of MRI with intra-articular gadolinium may provide information for making a diagnosis of partial MCL tears. The role of ultrasonography in evaluation remains to be determined.

Lateral instability

Patients who have lateral instability usually present with symptoms after an elbow dislocation. In some cases, there may be a history of lateral-side surgery.

Presentation. The clinical presentation varies, but typically the patient has a history of painful clicking, catching, or snapping of the elbow; there may be a sensation that the elbow is slipping in and out of the joint. Symptoms typically occur in the extension portion of the motion arc with the forearm in supination. Those that occur with flexion and pronation probably are related to reduction of the subluxation. The classic activity that patients report that will reproduce their symptoms is rising from a chair while pushing down on the arm rest. Motion usually is normal, but patients may be apprehensive in full supination and extension.

Testing. The test reported to be most sensitive is a lateral pivot shift apprehension test.8 The test is performed with the patient prone or supine. The forearm is fully supinated, and valgus force is applied while it is moved back to full extension. The radial head and proximal lateral forearm are noted to shift posterolaterally and then reduced similar to the same test in the anterior cruciate ligament–deficient knee. Posterolateral instability is best detected between 70º and 110º of flexion.

Two other clinical tests described by Regan involve having the patient push up from a chair but with the palms facing inward, and having the patient push up from a prone position first with the forearms maximally pronated and the thumbs pointing toward each other. Repeating the test with the thumbs pointed outward and the forearms maximally supinated elicits symptoms that were not present with the forearms pronated. This test may be performed with the patient standing and performing a wall push-up.11

Imaging. Plain radiography results usually are normal, but stress radiographs may help the diagnosis. MRI also may help in the diagnosis of posterolateral instability, and adding gadolinium may allow for clear depiction of the undersurface tears, which are poorly demonstrated on a conventional MRI scan.

Manish A. Patel, MD, practices orthopedic surgery and sports medicine at Southampton Orthopaedic and Sports Medicine Center in Franklin, VA. Felix H. Savoie III, MD, is the Lee Schlesinger professor of shoulder, elbow, and sports surgery at Tulane University School of Medicine in New Orleans.A version of this article originally appeared in our sister publication, the Journal of Musculoskeletal Medicine, in May.

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