The Journal of Family Practice

In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

In contrast to stable chronic obstructive pulmonary disease (COPD), acute exacerbations of COPD pose special management challenges and can significantly increase the risks of morbidity and death as well as the cost of care. This review from Cleveland Clinic Journal of Medicine, available at http://www.ccjm.org/topics/pulmonary/single-article-page/treating-and-preventing-acute-exacerbations-of-copd/8265d5ff355c3a17c96fa34564ea7465.html, provides the latest information on the definition and diagnosis of COPD exacerbations, disease burden and costs, etiology and pathogenesis, and management and prevention strategies.

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; kylemacgillis@gmail.com.

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; kylemacgillis@gmail.com.

Neuropathic hand complaints—for which patients typically seek medical attention when the pain or paresthesia starts to interfere with their daily routine—are common and diverse. The ability to assess and accurately diagnose upper extremity compression neuropathies is critical for physicians in primary care.

Assessment starts, of course, with a thorough history of the present illness and past medical history, which helps define a broad differential diagnosis and identify comorbidities. Physical examination, including judicious use of provocative testing, allows you to objectively identify the pathologic deficit, evaluate function and coordination of multiple organ systems, and detect nerve dysfunction. The results determine whether additional tools, such as electrodiagnostic testing, are needed.

We’ve created this guide, detailed in the text, tables, and figures that follow, to help you hone your ability to accurately diagnose patients who present with compression neuropathies of the hand.

The medical history: Knowing what to ask

To clearly define a patient’s symptoms and disability, start with a thorough history of the presenting complaint.

Inquire about symptom onset and chronicity. Did the pain or paresthesia begin after an injury? Are the symptoms associated with repetitive use of the extremity? Do they occur at night?

Pinpoint the location or distribution of pain or paresthesia. It is paramount to identify the affected nerve.^1,2 Ask patients to complete a hand or upper extremity profile documenting location and/or type of numbness, tingling, or decreased sensation. A diagram of the peripheral nerves responsible for sensory innervation of the hand (FIGURE 1) is an effective way to screen individuals at high risk of carpal tunnel syndrome (CTS) or ulnar tunnel syndrome (UTS).^1,2

A patient report such as, “My whole hand is numb,” calls for a follow-up question to determine whether the little finger is affected,³ which would indicate that the ulnar nerve, rather than just the median nerve, is involved. And if a patient reports feeling as if he or she is wearing gloves or mittens, it is essential to consider the possibility of a systemic neuropathy rather than a single peripheral neuropathy.³

Gather basic patient information. Inquire about hand dominance, occupation, and baseline function, any or all of which may be critical in the assessment and initiation of treatment.^4,5

Review systemic conditions and medications

A broad range of comorbidities, such as cervical radiculopathy, diabetes, hypothyroidism, and vitamin deficiencies (TABLE 1),^6,7 may be responsible for neuropathic hand complaints, and a thorough review of systemic complaints and past medical history is critical. Include a medication history and a review of prior procedures, such as post-traumatic surgeries of the hand or upper extremity or nerve decompression surgeries, which may provide additional insight into disease etiology.

Symptoms guide physical exam, provocative testing

A physical examination, including provocative testing, follows based on reported symptoms, medical history, and suspected source of nerve compression.

Carpal tunnel syndrome

CTS is the most common peripheral neuropathy.⁸ Patients often report nocturnal pain or paresthesia in the distal median nerve distribution, comprising the palmar surface of the thumb, index, middle, and radial half of the ring finger.

Researchers have identified 6 standardized clinical criteria for the diagnosis of CTS. Two criteria—numbness mostly in median nerve territory and nocturnal numbness—can be ascertained during the history of present illness.The other 4, detailed below, will be found during the physical exam.⁹

Thenar weakness or atrophy.⁹ Begin your evaluation by inspecting the thenar musculature for atrophic changes. Motor exam of intrinsic musculature innervated by the recurrent motor branch of the median nerve includes assessment of thumb abduction strength (assessed by applying resistance to the metacarpophalangeal joint [MCPJ] base towards the palm in the position of maximal abduction) and opposition strength (assessed by applying force to the MCPJ from the ulnar aspect).¹⁰

Positive Phalen’s test.⁹ Provocative testing for CTS includes Phalen’s test (sensitivity 43%-86%, specificity 48%-67%),¹¹ which is an attempt to reproduce the numbness or tingling in the median nerve territory within 60 seconds of full wrist flexion. Ask the patient to hold his or her forearms vertically with elbows resting on the table (allowing gravity to flex the wrists),¹² and to tell you if numbness or tingling occurs.

Consider the possibility of a systemic neuropathy in patients who report that they feel as though they are wearing gloves.

Positive Tinel’s sign.⁹ Tinel’s sign (sensitivity 45%-75%, specificity 48%-67%)¹¹ is performed by lightly tapping the median nerve from the proximal to distal end over the carpal tunnel. The test is positive if paresthesia results. Provocative testing may also include Durkan’s test, also known as the carpal compression test. Durkan’s test (sensitivity 49%-89%, specificity 54%-96%)¹¹ involves placing your thumb directly over the carpal tunnel and holding light compression for 60 seconds, or until paresthesia is reported.

Positive 2-point discrimination test.⁹ To assess CTS disease severity, use 2-point discrimination to evaluate the patient’s sensation qualitatively and quantitatively. Two-point discrimination can only be tested, however, if light touch sensation is intact. It is typically performed by lightly applying 2 caliper points at fixed distances sufficient to blanch the skin, but some clinicians have used other tools, such as a modified paperclip.¹³ The smallest distance at which the patient can detect 2 distinct stimuli is then recorded.

Researchers have reported an average of 3 to 5 mm for 2-point discrimination at the fingertipand a normal 2-point discrimination of 6 to 9 mm in the volar surface of the hand (TABLE 2).^14,15

The scratch collapse test (sensitivity 64%, specificity 99%) is a supplemental exam that uses a different outcome measure to diagnose CTS.¹⁶ It involves lightly scratching the skin over the compressed carpal tunnel while the patient performs sustained resisted bilateral shoulder external rotation in an adducted position. A momentary loss of muscle resistance to external rotation indicates a positive test.

Pronator syndrome

Pronator syndrome (PS) is a proximal median neuropathy that may present in isolation or in combination with CTS as a double crush syndrome. Clinical symptoms include features of CTS and sensory paresthesias in the palm and distal forearm in the distribution of the palmar cutaneous branch of the median nerve. PS is commonly associated with volar proximal forearm pain exacerbated by repetitive activities involving pronation and supination.

PS is not easy to assess. Palpatory examination of a large supracondylar process at the distal humerus proximal to the medial epicondyle on its anteromedial aspect can be difficult, especially if the patient is overweight. And motor weakness is not a prominent feature. What’s more, power assessment of the pronator teres, flexor carpi radialis, and flexor digitorum superficialis may exacerbate symptoms.

Because the symptoms of PS and CTS may be the same, PS provocation maneuvers should be performed on patients with CTS symptoms and paresthesia involving the palm. Start by testing for Tinel’s sign over the pronator teres muscle, although this has been found to be positive in less than 50% of PS cases.¹⁷ Palpate the antecubital fossa and the proximal aspect of the pronator teres muscle to assess for discomfort or tenderness.

Pronator compression test. The pronator compression test has been found to be the most sensitive way to assess PS.^18,19 This test involves direct compression of the proximal and radial edge of the pronator teres muscle belly along the proximal volar forearm with the thumb.²⁰ It is performed bilaterally on supinated upper extremities, with the clinician applying pressure on each forearm simultaneously (FIGURE 2). If the symptoms in the hand are reproduced in ≤30 seconds, the test is positive. In a study of 10 patients with surgically confirmed PS, the pronator compression test was positive in every case.^20,21

Resistance testing. You can also evaluate the pronator teres compression site by testing the patient’s ability to resist pronation with his or her elbow extended and the forearm in neutral position. To test for compression from the bicipital aponeurosis, ask the patient to flex the elbow to approximately 120° to 130° and apply active supinated resistance.²² Likewise, resistance of the long finger proximal interphalangeal joint (IPJ) to flexion—a maneuver performed with elbow fully extended—assesses compression from the fibrous arcade of the flexor digitorum superficialis (FDS).²¹ A positive resistance test will reproduce the reported symptoms.

Ulnar tunnel syndrome

Symptoms of UTS, which is much less common than CTS, include pain in the wrist and hand that is associated with paresthesia or numbness in the small finger and ulnar half of the ring finger. Patients may report difficulty with motor tasks involving grip and pinch strength or fatigue with prolonged action of the intrinsic muscles. Many also report an exacerbation of symptoms associated with increased wrist flexion or at night.

Evaluation of UTS requires a full assessment of the upper extremity, starting with observation of hand posture and muscle bulk to identify signs of chronic nerve compression. The contralateral extremity serves as a control to the neuropathic hand. Classically, chronic ulnar nerve compression leads to intrinsic muscle atrophy, evidenced by loss of topographical soft tissue bulk in the first dorsal web space, the palmar transverse metacarpal arch, and the hypothenar area.²³ Ulnar motor nerve dysfunction is limited to the intrinsic muscles of the hand. The inverted pyramid sign, signified by atrophy of the transverse head of the adductor pollicis, is another visual aberrancy,²⁴ as is clawing of the ring finger and small finger. The clawing, which involves hyperextension of the MCPJ and flexion of the proximal and distal IPJ, is commonly known as Duchenne’s sign. FIGURE 3 demonstrates hypothenar atrophy and the loss of muscle bulk in the first dorsal web space.

When you suspect UTS, palpate the wrist and hand in an attempt to locate a mass or area of tenderness. Not all patients with a volar ganglion cyst responsible for UTS present with a palpable mass, but tenderness along the radial aspect of the pisiform or an undefined fullness in this area may be noted.²⁵ Any patient with a palpable mass should be tested for Tinel’s sign over the mass and undergo a thorough vascular assessment. Fracture of the hook of the hamate is indicated by tenderness in the region approximated by the intersection of Kaplan’s line and the proximal extension line from the ring finger.

Perform 2-point discrimination testing at the palmar distal aspect of the small finger and ulnar half of the ring finger. This tests the superficial sensory division of the ulnar nerve that travels within Guyon’s canal. Testing the dorsal ulnar cutaneous nerve involves the skin of the dorso-ulnar hand and dorsum of the long finger proximal to the IPJ. If this area is spared and the palmar distal ulnar digits are affected, compression within Guyon’s canal is likely. If both areas are affected, suspect a more proximal compression site at the cubital tunnel, as the dorsal ulnar cutaneous nerve branches proximal to Guyon’s canal.²⁶

Ulnar motor nerve dysfunction in UTS is limited to the intrinsic muscles of the hand. Assessment of intrinsic muscle function is described in TABLE 3.^27-32 It is important to become familiar with the tests and maneuvers described, but also to be aware that a comprehensive evaluation of ulnar nerve motor function requires a combination of tests.

Cubital tunnel syndrome

Cubital tunnel syndrome—the second most common peripheral neuropathy⁸—involves the proximal site of ulnar nerve compression in the upper extremity. Patients typically report symptoms similar to those of UTS, with sensory paresthesia in the ulnar digits and intrinsic weakness. To learn more about the symptoms, ask if the onset of pain or paresthesia is related to a particular elbow position, such as increased elbow flexion.

Notably, pain is usually not the initial complaint, unless the disease is advanced. This may be the reason atrophic intrinsic changes are 4 times more likely to be seen in patients with cubital tunnel syndrome than in those with CTS.³³ You’re more likely to hear about vague motor problems, including hand clumsiness and difficulty with fine coordination of the fingers.³⁴ Thus, it is important to evaluate patients for concurrent UTS and/or CTS, as well as for differentiation.

Focus on the elbow. Whenever you suspect cubital tunnel syndrome, pay special attention to the elbow. Examine the carrying angle of the elbow in relation to the contralateral extremity. Deformity may provide clues to a history of trauma. Assess the ulnar nerve during active flexion and extension to identify a subluxatable nerve at the cubital tunnel. Examine the ulno-humeral joint for crepitus, and palpate the joint line for large osteophytes and/or ganglion cysts.

Motor examination of the ulnar nerve primarily focuses on the intrinsic muscles detailed in TABLE 3,^27-32 although the flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP) to the ring finger and small finger are also innervated by the ulnar nerve. The FCU mediates the power grip, and can be tested by resisted wrist flexion and ulnar deviation. Ring finger and small finger FDP strength should be examined by resistance testing at the distal IPJ.

Provocative testing of cubital tunnel syndrome includes Tinel’s sign (performed over the cubital tunnel), the elbow flexion test (performed with elbow in maximum flexion and wrist at neutral position and held for 60 seconds), and the pressure provocation test (performed by applying pressure to the ulnar nerve just proximal to the cubital tunnel with your index and long fingers for 60 seconds while the patient’s elbow is at 20° flexion with the forearm supinated). For each test, eliciting distal paresthesia in ulnar nerve territory is a positive result. The sensitivity of these tests ranges from 70% (Tinel’s sign) to 98% (combined elbow flexion and pressure); specificity ranges from 95% to 99%.³⁵

The scratch collapse test for cubital tunnel syndrome evaluation is similar to the version used to assess for CTS; the only difference is the location of the site that is scratched, in this case the cubital tunnel. The reported sensitivity and specificity are 69% and 99%, respectively.¹¹

Wartenberg’s syndrome

When you suspect ulnar tunnel syndrome, palpate the wrist and hand in an attempt to locate a mass or area of tenderness.

When a patient reports paresthesia or pain along the radial aspect of the forearm that radiates into the dorsal thumb and index and middle fingers, consider Wartenberg’s syndrome—compression of the superficial radial nerve. The condition, also known as “cheiralgia paresthetica,” may exist anywhere along the course of the nerve in the forearm,³⁶ but the compression typically occurs 9 cm proximal to the radial styloid.

Assess the skin over the forearm and hand for evidence of prior trauma, surgical scars, or external compression sources, such as a watch.^37-39 Then use palpation to identify superficial or deep masses along the nerve.⁴⁰ Perform Tinel’s sign by lightly tapping along the nerve course from proximal to distal in the forearm. The test is positive if paresthesias are provoked distally.^41,42

Motor function of the extremity is unaffected in Wartenberg’s syndrome, unless a prior traumatic injury occurred or a comorbidity exists. Comorbidities to consider include de Quervain’s tenosynovitis, cervical radiculopathy, injury to the lateral antebrachial cutaneous nerve, and CTS.

Gross sensory testing usually is negative, but 2-point discrimination may show diminished responses. Testing distribution includes the dorsal radial wrist and hand, dorsal thumb skin proximal to the IPJ, and the dorsal surface of the index, middle, and radial half of the ring finger proximal to the IPJ.

Proceed with caution. Provocative testing with a pronated forearm and a flexed and ulnar-deviated wrist may exacerbate symptoms,^12,42 and Finkelstein’s maneuver (isolated ulnar deviation at the wrist to elicit pain over the first dorsal wrist compartment) and Phalen’s test may elicit false-positive results. Upper motor neuron exams (ie, deep tendon reflexes) and Hoffman’s sign (reflexive flexion of the terminal phalanges of the thumb and index finger induced by flicking or tapping the distal phalanx of the long finger) should be symmetric to the contralateral extremity.

In patients with more than one compression injury, Spurling’s sign (neck extension and lateral rotation towards the affected extremity) may induce paresthesia when combined with axial compression, while the shoulder abduction test (shoulder 90° abduction, with external rotation) may diminish reported paresthesia. In those for whom Wartenberg’s syndrome is their only compression injury, however, these provocative maneuvers will be negative.

Anterior interosseous nerve syndrome

A rare clinical entity that affects the anterior interosseous innervated muscles in the forearm, anterior interosseous nerve syndrome (AINS)’s etiology is unclear. But it is likely related to a spontaneous neuritis rather than a compressive etiology.⁴³ Paresis or paralysis of the flexor pollicis longus (FPL) and the flexor digitorum profundus (FDP) of the index and long finger is its hallmark, but patients may report vague forearm pain associated with weakness or absence of function.

Examination begins with a visual assessment and palpation of the forearm and hand for atrophy or a space-occupying lesion. Notably, sensory function of the hand should remain at baseline despite the motor dysfunction, as the anterior interosseous is purely a motor nerve.

Motor testing should focus on the median and anterior interosseous innervated muscles.

The FPL is tested by isolated thumb IPJ flexion and the Kiloh and Nevin sign—the inability to make an “OK” sign with the thumb and index finger.⁴⁴ Assess pinch grasp with a maximally flexed thumb IPJ and distal IPJ of the index finger. Anterior interosseous nerve dysfunction results in a flattened pinch without IPJ or distal IPJ flexion, which increases the contact of the thumb and index finger pulp.⁴⁵ In a series of 14 patients, researchers reported complete paralysis of FPL and FDP index finger in 5 patients, isolated paralysis of FPL in 7 patients, and isolated paralysis of FDP index and long fingers in 2 patients. None had isolated paralysis of the FDP long finger.⁴⁶FIGURE 4 shows complete (A) and incomplete (B) paralysis.

Pain is usually not the initial complaint with cubital tunnel syndrome. You're more likely to hear about hand clumsiness and difficulty with fine coordination of the fingers.

Evaluation of AINS also includes assessment of FPL and FDP tendon integrity with passive tenodesis. The appearance of the hand at rest should reflect the natural digital cascade. In a completely relaxed or anesthetized hand, the forearm is placed in wrist supination and extension, allowing gravity to extend the wrist and placing the thumb MCPJ at 30° flexion, the index finger MCPJ at 40°, and the small finger MCPJ at 70°. The thumb IPJ should approximate the radial fingertip pulp of the index finger. The forearm is then pronated and flexed at the wrist, straightening the thumb MCPJ and producing a mild flexion cascade at the proximal and distal IPJ of the index, long, ring, and small fingers within 20° of full extension. This dynamic exercise is used to confirm that the patient has an intact tenodesis effect, thus excluding tendon lacerations or ruptures from the differential diagnosis. In one study, in 9 of 33 cases of partial or complete isolated index finger FPL or FDP, paralysis was initially diagnosed as tendon rupture.⁴⁷

When to consider electrodiagnostic testing

Electrodiagnostic testing—a combination of electromyography and nerve conduction studies to assess the status of a peripheral nerve⁴⁸—provides objective data that can help diagnose a challenging presentation, rule out a competing diagnosis, or clarify an atypical clinical picture or vague subjective history. This type of testing is also used to localize the entrapment site, identify a patient with polyneuropathy or brachial plexopathy, and assess the severity of nerve injury or presence of a double crush syndrome.^49,50 Any patient with signs and symptoms of a compression neuropathy and supportive findings on physical exam should be referred for electrodiagnostic testing and/or to a surgeon specializing in treating these conditions.

CORRESPONDENCE
Kyle J. MacGillis, MD, University of Illinois at Chicago, Department of Orthopaedic Surgery, 835 South Wolcott Avenue, M/C 844, Chicago, IL 60612; kylemacgillis@gmail.com.

The 2015-2016 flu season was less severe than the last three seasons, with a lower hospitalization rate and fewer pediatric deaths.

Cases of influenza appeared later in the season than typically seen, and activity didn’t peak until March, Stacy L. Davlin, Ph.D., wrote in the June 10 issue of the Morbidity and Mortality Weekly Report (MMWR 2016;22:567-75)

“During the most recent 18 influenza seasons, only two other seasons have peaked in March (2011-2012 and 2005-2006),” wrote Dr. Davlin, an epidemiologist at the Centers for Disease Control and Prevention, Atlanta. This serves as a reminder that influenza can and does occur outside the traditionally expected season, and that clinicians shouldn’t discount the possibility of flu when a patient presents with typical symptoms.

Cynthia Goldsmith/CDC photo #10073

“Although summer influenza activity in the United States typically is low, influenza cases and outbreaks have occurred during summer months, and clinicians should remain vigilant in considering influenza in the differential diagnosis of summer respiratory illnesses,” Dr. Davlin said.

The most common influenza virus of the last season was A(H1N1), which accounted for about half of cases in those aged 5-24 years, and about 70% of cases in those younger than 5 years and those 65 years and older.

Three novel viruses were seen as well: variants of A(H1N1), A(H1N2), and A(H3N2). The A(H1N1) variant occurred in a Minnesota resident who lived and worked in an area of swine farming, but who denied direct contact with pigs. The A(H3N2) variant occurred in a New Jersey resident who reported visiting a farm shortly before symptom onset. There was no evidence of human-to-human transmission. Both recovered fully without hospitalization. The A(H1N2) variant occurred in a Minnesota resident who was hospitalized but who recovered. This person was not interviewed so no possible source of infection was identified.

The CDC tested 2,408 viral specimens for susceptibility to antiviral medications. Among the 2,193 A(H1N1) specimens, less than 1% were resistant to oseltamivir and peramivir. All were susceptible to zanamivir. However, the testing found persistent high levels of resistance to amantadine and rimantadine in the A viruses. Amantadine is not effective on the B strains at all. Therefore, CDC does not recommend the use of amantadine as an anti-influenza medication.

Reports of influenza first exceeded the 2.1% baseline level in the week ending Dec. 26, 2015, according to the U.S. Outpatient Influenza-Like Illness Surveillance Network (ILINet). They remained elevated for the next 17 weeks, with a peak of 3.6% of all outpatient visits in the week ending March 12. From October 2015-April 2016, the overall hospitalization rate for influenza-like illness was 31 per 100,000. This was highest in those aged 65 years and older (85/100,000), and lowest in those aged 5-17 years (10/100,000). About 92% of adults hospitalized for flu-like illness had at least one underlying medical comorbidity, including obesity (42%), cardiovascular disease (40%), and metabolic disorders (38%). Almost half of children (48%) also had medical comorbidities, including asthma or other reactive airway disease (22%) and neurologic disorders (18%).

CDC’s National Center for Health Statistics Mortality Surveillance System found that the percentage of deaths attributed to pneumonia and influenza peaked at 8% during the week ending March 19. This is slightly lower than the death rate seen in the last 5 years, which ranged from 9% in 2011-2012 to 11% in 2012-2013.

Of this season’s deaths, 74 occurred in children. The mean and median ages of these patients were 7 years and 6 years, respectively; the range was 2 months-16 years. This total was lower than that recorded in any of the past three influenza seasons: 171 pediatric deaths in 2012-2013, 111 in 2013-2014, and 148 in 2014-2015.

Dr. Davlin also announced the Food and Drug Administration’s recommendations for composition of the 2016-2017 influenza vaccine.

Trivalent vaccines should contain an A/California/7/2009 (H1N1) pdm09-like virus, an A/Hong Kong/4801/2014 (H3N2)-like virus, and a B/Brisbane/60/2008-like virus (B/Victoria lineage). Quadrivalent vaccines, which have two influenza B viruses, should include the viruses recommended for the trivalent vaccines, as well as a B/Phuket/3073/2013-like virus (B/Yamagata lineage).

“The vaccine viruses recommended for inclusion in the 2016-2017 Northern Hemisphere influenza vaccines are the same vaccine viruses that were chosen for inclusion in 2016 Southern Hemisphere seasonal influenza vaccines,” Dr. Davlin noted. “These vaccine recommendations were based on a number of factors, including global influenza virologic and epidemiologic surveillance, genetic and antigenic characterization, antiviral susceptibility, and the availability of candidate vaccine viruses for production.”

As a CDC employee, Dr. Davlin had no financial disclosures.

msullivan@frontlinemedcom.com

On Twitter @Alz_Gal

The 2015-2016 flu season was less severe than the last three seasons, with a lower hospitalization rate and fewer pediatric deaths.

Cases of influenza appeared later in the season than typically seen, and activity didn’t peak until March, Stacy L. Davlin, Ph.D., wrote in the June 10 issue of the Morbidity and Mortality Weekly Report (MMWR 2016;22:567-75)

“During the most recent 18 influenza seasons, only two other seasons have peaked in March (2011-2012 and 2005-2006),” wrote Dr. Davlin, an epidemiologist at the Centers for Disease Control and Prevention, Atlanta. This serves as a reminder that influenza can and does occur outside the traditionally expected season, and that clinicians shouldn’t discount the possibility of flu when a patient presents with typical symptoms.

Cynthia Goldsmith/CDC photo #10073

“Although summer influenza activity in the United States typically is low, influenza cases and outbreaks have occurred during summer months, and clinicians should remain vigilant in considering influenza in the differential diagnosis of summer respiratory illnesses,” Dr. Davlin said.

The most common influenza virus of the last season was A(H1N1), which accounted for about half of cases in those aged 5-24 years, and about 70% of cases in those younger than 5 years and those 65 years and older.

Three novel viruses were seen as well: variants of A(H1N1), A(H1N2), and A(H3N2). The A(H1N1) variant occurred in a Minnesota resident who lived and worked in an area of swine farming, but who denied direct contact with pigs. The A(H3N2) variant occurred in a New Jersey resident who reported visiting a farm shortly before symptom onset. There was no evidence of human-to-human transmission. Both recovered fully without hospitalization. The A(H1N2) variant occurred in a Minnesota resident who was hospitalized but who recovered. This person was not interviewed so no possible source of infection was identified.

The CDC tested 2,408 viral specimens for susceptibility to antiviral medications. Among the 2,193 A(H1N1) specimens, less than 1% were resistant to oseltamivir and peramivir. All were susceptible to zanamivir. However, the testing found persistent high levels of resistance to amantadine and rimantadine in the A viruses. Amantadine is not effective on the B strains at all. Therefore, CDC does not recommend the use of amantadine as an anti-influenza medication.

Reports of influenza first exceeded the 2.1% baseline level in the week ending Dec. 26, 2015, according to the U.S. Outpatient Influenza-Like Illness Surveillance Network (ILINet). They remained elevated for the next 17 weeks, with a peak of 3.6% of all outpatient visits in the week ending March 12. From October 2015-April 2016, the overall hospitalization rate for influenza-like illness was 31 per 100,000. This was highest in those aged 65 years and older (85/100,000), and lowest in those aged 5-17 years (10/100,000). About 92% of adults hospitalized for flu-like illness had at least one underlying medical comorbidity, including obesity (42%), cardiovascular disease (40%), and metabolic disorders (38%). Almost half of children (48%) also had medical comorbidities, including asthma or other reactive airway disease (22%) and neurologic disorders (18%).

CDC’s National Center for Health Statistics Mortality Surveillance System found that the percentage of deaths attributed to pneumonia and influenza peaked at 8% during the week ending March 19. This is slightly lower than the death rate seen in the last 5 years, which ranged from 9% in 2011-2012 to 11% in 2012-2013.

Of this season’s deaths, 74 occurred in children. The mean and median ages of these patients were 7 years and 6 years, respectively; the range was 2 months-16 years. This total was lower than that recorded in any of the past three influenza seasons: 171 pediatric deaths in 2012-2013, 111 in 2013-2014, and 148 in 2014-2015.

Dr. Davlin also announced the Food and Drug Administration’s recommendations for composition of the 2016-2017 influenza vaccine.

Trivalent vaccines should contain an A/California/7/2009 (H1N1) pdm09-like virus, an A/Hong Kong/4801/2014 (H3N2)-like virus, and a B/Brisbane/60/2008-like virus (B/Victoria lineage). Quadrivalent vaccines, which have two influenza B viruses, should include the viruses recommended for the trivalent vaccines, as well as a B/Phuket/3073/2013-like virus (B/Yamagata lineage).

“The vaccine viruses recommended for inclusion in the 2016-2017 Northern Hemisphere influenza vaccines are the same vaccine viruses that were chosen for inclusion in 2016 Southern Hemisphere seasonal influenza vaccines,” Dr. Davlin noted. “These vaccine recommendations were based on a number of factors, including global influenza virologic and epidemiologic surveillance, genetic and antigenic characterization, antiviral susceptibility, and the availability of candidate vaccine viruses for production.”

As a CDC employee, Dr. Davlin had no financial disclosures.

msullivan@frontlinemedcom.com

On Twitter @Alz_Gal

The 2015-2016 flu season was less severe than the last three seasons, with a lower hospitalization rate and fewer pediatric deaths.

Cases of influenza appeared later in the season than typically seen, and activity didn’t peak until March, Stacy L. Davlin, Ph.D., wrote in the June 10 issue of the Morbidity and Mortality Weekly Report (MMWR 2016;22:567-75)

“During the most recent 18 influenza seasons, only two other seasons have peaked in March (2011-2012 and 2005-2006),” wrote Dr. Davlin, an epidemiologist at the Centers for Disease Control and Prevention, Atlanta. This serves as a reminder that influenza can and does occur outside the traditionally expected season, and that clinicians shouldn’t discount the possibility of flu when a patient presents with typical symptoms.

Cynthia Goldsmith/CDC photo #10073

“Although summer influenza activity in the United States typically is low, influenza cases and outbreaks have occurred during summer months, and clinicians should remain vigilant in considering influenza in the differential diagnosis of summer respiratory illnesses,” Dr. Davlin said.

The most common influenza virus of the last season was A(H1N1), which accounted for about half of cases in those aged 5-24 years, and about 70% of cases in those younger than 5 years and those 65 years and older.

Three novel viruses were seen as well: variants of A(H1N1), A(H1N2), and A(H3N2). The A(H1N1) variant occurred in a Minnesota resident who lived and worked in an area of swine farming, but who denied direct contact with pigs. The A(H3N2) variant occurred in a New Jersey resident who reported visiting a farm shortly before symptom onset. There was no evidence of human-to-human transmission. Both recovered fully without hospitalization. The A(H1N2) variant occurred in a Minnesota resident who was hospitalized but who recovered. This person was not interviewed so no possible source of infection was identified.

The CDC tested 2,408 viral specimens for susceptibility to antiviral medications. Among the 2,193 A(H1N1) specimens, less than 1% were resistant to oseltamivir and peramivir. All were susceptible to zanamivir. However, the testing found persistent high levels of resistance to amantadine and rimantadine in the A viruses. Amantadine is not effective on the B strains at all. Therefore, CDC does not recommend the use of amantadine as an anti-influenza medication.

Reports of influenza first exceeded the 2.1% baseline level in the week ending Dec. 26, 2015, according to the U.S. Outpatient Influenza-Like Illness Surveillance Network (ILINet). They remained elevated for the next 17 weeks, with a peak of 3.6% of all outpatient visits in the week ending March 12. From October 2015-April 2016, the overall hospitalization rate for influenza-like illness was 31 per 100,000. This was highest in those aged 65 years and older (85/100,000), and lowest in those aged 5-17 years (10/100,000). About 92% of adults hospitalized for flu-like illness had at least one underlying medical comorbidity, including obesity (42%), cardiovascular disease (40%), and metabolic disorders (38%). Almost half of children (48%) also had medical comorbidities, including asthma or other reactive airway disease (22%) and neurologic disorders (18%).

CDC’s National Center for Health Statistics Mortality Surveillance System found that the percentage of deaths attributed to pneumonia and influenza peaked at 8% during the week ending March 19. This is slightly lower than the death rate seen in the last 5 years, which ranged from 9% in 2011-2012 to 11% in 2012-2013.

Of this season’s deaths, 74 occurred in children. The mean and median ages of these patients were 7 years and 6 years, respectively; the range was 2 months-16 years. This total was lower than that recorded in any of the past three influenza seasons: 171 pediatric deaths in 2012-2013, 111 in 2013-2014, and 148 in 2014-2015.

Dr. Davlin also announced the Food and Drug Administration’s recommendations for composition of the 2016-2017 influenza vaccine.

Trivalent vaccines should contain an A/California/7/2009 (H1N1) pdm09-like virus, an A/Hong Kong/4801/2014 (H3N2)-like virus, and a B/Brisbane/60/2008-like virus (B/Victoria lineage). Quadrivalent vaccines, which have two influenza B viruses, should include the viruses recommended for the trivalent vaccines, as well as a B/Phuket/3073/2013-like virus (B/Yamagata lineage).

“The vaccine viruses recommended for inclusion in the 2016-2017 Northern Hemisphere influenza vaccines are the same vaccine viruses that were chosen for inclusion in 2016 Southern Hemisphere seasonal influenza vaccines,” Dr. Davlin noted. “These vaccine recommendations were based on a number of factors, including global influenza virologic and epidemiologic surveillance, genetic and antigenic characterization, antiviral susceptibility, and the availability of candidate vaccine viruses for production.”

As a CDC employee, Dr. Davlin had no financial disclosures.

msullivan@frontlinemedcom.com

On Twitter @Alz_Gal

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed flat warts based on their typical appearance and location. Flat warts are frequently found on the face and neck and can easily be spread when men shave their beards or women shave their legs. Flat warts can also occur on the face of young children.

The FP suggested cryotherapy for the largest warts and prescribed topical imiquimod (3 times per week) for home use. The FP suggested that the patient wait 2 weeks before starting the imiquimod to allow the cryotherapy to do its work and for any blistering or irritation to subside. A follow-up appointment was set for 6 weeks.

At the follow-up visit, there was little improvement and the patient wanted to try an alternative therapy. The risks and benefits of Candida antigen intralesional injection were discussed and the patient decided to proceed with this approach. Intralesional injections with Candida antigen induce a localized, cell-mediated, and human papillomavirus (HPV)-specific response that may target the injected wart as well as more distant warts. This method has moderate effectiveness (60% cure rates) for treatment of recalcitrant warts. The Candida antigen must be diluted before use, and 0.1 to 0.3 mL should be injected into the largest warts using a 30-gauge needle (up to 1 mL per treatment). Warn patients to expect itching in the area, burning, or peeling, and repeat the procedure every 4 weeks with up to 3 treatments or until warts are gone.

For this patient, the Candida antigen was diluted with normal saline (0.25 mL of generic Candida antigen with 0.75 mL of normal saline). The mixture was injected with a 30-gauge needle into approximately 10 of the largest flat warts. One month later, all of the flat warts were gone.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Flat warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:755-758.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed this patient with common warts. While any child can develop a large cluster of warts, the FP decided to ask more about the family’s health in case this was a sign of immunosuppression. The mother acknowledged that she was positive for human immunodeficiency virus (HIV) and that the father had passed away from acquired immune deficiency syndrome (AIDS). She consented to HIV testing for her son and he tested positive. Unfortunately, the mother did not have antiretroviral therapy during her pregnancy with this child.

While there were resources within the village for HIV treatment, there were no resources for wart treatment. Because the child could receive treatment for HIV, the warts could resolve on their own as his immune system improved. Even immunocompetent children will often see their warts completely disappear over time.

In settings with greater resources, typical treatments for common warts include: cryotherapy, topical salicylic acid, topical cantharidin, topical imiquimod, and intralesional immunotherapy. Intralesional immunotherapy can be performed with Candida antigens, the measles, mumps, and rubella vaccine, and a purified protein derivative (as used for tuberculosis testing). Other less commonly used treatments include lasers, photodynamic therapy, contact immunotherapy, hypnosis, oral cimetidine, duct tape, and surgery.

The reason there are so many treatments is that no single treatment works well enough in most cases. Based on a Cochrane review, the strongest evidence supports topical salicylic acid and cryotherapy.¹ Immunosuppressed patients can sometimes have the most recalcitrant warts, but treatment of the immune system, along with typical treatment options, can still be successful.

1. Gibbs S, Harvey I, Sterling JC, et al. Local treatments for cutaneous warts. Cochrane Database Syst Rev. 2001;(2):CD001781.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Common warts. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:749-754.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed molluscum contagiosum because a few of the papules had central umbilication. While she noticed that many papules did not have central umbilication, she was aware that not all molluscum lesions would have this feature. Pearly papules are classic for molluscum, even when central umbilication is not visible.

Children with atopic dermatitis are more prone to molluscum infections and frequently get them in areas that have been, or presently are, involved with atopic dermatitis. In this case, the child had antecubital involvement with her atopic dermatitis (although her skin was relatively normal at the time). The altered barrier function found in atopic individuals makes them more prone to various viral and bacterial super infections, including molluscum, herpes, and bacterial impetigo.

In immunocompetent patients, lesions usually spontaneously resolve within 8 to 12 months. In a minority of cases, disease persists for a few years. Children do not have to be kept out of day care or school for this condition, even though it is somewhat contagious. Like warts, keeping kids out of school or day care is not useful to prevent the spread of disease and is not practical on a societal level.

The FP discussed cryotherapy with the mother and child, but the girl was not willing to allow it due to her fear of the pain. Other options included watch and wait, topical salicylic acid, tretinoin, and imiquimod—although none of these have been approved by the Food and Drug Administration. Cantharidin had also been used previously in this office, but it was not available because regulations have made it very difficult to obtain. Imiquimod is not suggested for children younger than 12; therefore, this costly medicine would not be covered by insurance.

The mother requested a prescription for tretinoin and stated that if the insurance would not cover it, she would go with over-the-counter salicylic acid. The FP wrote a prescription for 0.025% tretinoin cream to be applied daily and said to stop using it if irritation became too bothersome. Follow-up was to be done as needed, but was not completed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux, EJ. Molluscum contagiosum. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:743-748.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com