Entrapment neuropathies are common of chronic pain, often resulting in severe pain and significant loss of function. This chapter highlights six of the most common neuropathies that can be associated with pain: carpal tunnel syndrome (CTS), ulnar neuropathy at the elbow, thoracic outlet syndrome, meralgia paresthetica, tarsal tunnel syndrome, and Morton’s neuroma. However, many other neuropathies can also be seen although most may be more associated with dysfunction than pain. In most cases, symptoms and physical exam provide important initial clues that may further guide diagnostic testing. Treatments often begin with conservative medical management followed by injections in some cases and ultimately managed with surgery if indicated.
Keywordscarpal tunnel syndrome, entrapment neuropathy, meralgia paresthetica, Morton’s neuroma, tarsal tunnel syndrome, thoracic outlet syndrome, ulnar neuropathy
Drs. Michael M. Minieka, Takashi Nishida, and Hubert A. Benzon wrote the previous version.
Nerve entrapments can be a common cause of chronic pain, causing debilitating symptoms and loss of function. We discuss six of the most common entrapment neuropathies in detail: carpal tunnel syndrome (CTS), ulnar neuropathy at the elbow, thoracic outlet syndrome (TOC), meralgia paresthetica (MP), tarsal tunnel syndrome (TTS), and Morton’s neuroma. Other entrapment neuropathies, such as peroneal palsy at the fibular head, may result in weakness or paresthesia but not pain. These and other neuropathies are summarized in Table 33.1 .
|Nerve||Site of Entrapment||Syndrome|
|Brachial plexus||Anterior and medial scalene muscle||Anterior scalene syndrome|
|Subclavius muscle||Costoclavicular syndrome|
|Pectoralis minor and coracoid process||Hyperabduction syndrome|
|Cervical rib or band, medial antebrachial cutaneous nerve||Thoracic outlet syndrome|
|Long thoracic||“Rucksack” palsy|
|Suprascapular||Transverse scapular ligament, scapular notch or foramen|
|Spinoglenoid ligament or notch|
|Brachial fascia, lateral antebrachial cutaneous nerve|
|Axillary||Quadrangular foramen or lateral axillary hiatus (long head of triceps, teres major and minor)||Quadrilateral space syndrome|
|Radial||Lateral intermuscular septum||“Saturday night” palsy, “honeymooners’” palsy|
|Arcade of Frohse (supinator), leash of Henry (brachioradialis, extensor carpi radialis brevis), Monteggia lesion||Supinator syndrome, posterior interosseous syndrome, radial tunnel syndrome, tardy radial palsy, “tennis elbow,” “Frisbee flinging”|
|Superficial branch||Cheiralgia paresthetica, Wartenberg’s disease, “handcuff” or “wristwatch” neuropathy|
|Median||Ligament of Struthers (supracondylar process: medial epicondyle)|
|Pronator teres muscle, sublimis bridge (flexor digitorum sublimis), lacertus fibrosis||Pronator syndrome, flexor digitorum sublimis syndrome|
|Gantzer’s muscle (flexor pollicis longus)||Anterior interosseous syndrome, Kiloh-Nevin syndrome|
|Transverse carpal ligament||Carpal tunnel syndrome|
|Transverse metacarpal ligament||Intermetacarpal tunnel syndrome, “bowlers’ thumb”|
|Ulnar||Arcade of Struthers (internal brachial ligament, medial head of triceps, medial intermuscular septum)|
|Epicondylo-olecranon ligament, cubital tunnel retinaculum, arcuate ligament of Osborne||Cubital tunnel syndrome|
|Humeroulnar aponeurosis (flexor carpi ulnaris)||“Tardy” ulnar palsy|
|Deep flexor-pronator aponeurosis||—|
|Guyon’s canal (piso-hamate ligament, volar and transverse carpal ligament)||Ulnar tunnel syndrome, “cyclists’” palsy (Radfahrerlahung)|
|Deep branch||Piso-hamate hiatus syndrome|
|Transverse and oblique heads of adductor pollicis|
|T2–6 posterior rami||Notalgia paresthetica|
|L5 spinal||Iliolumbar ligament (fifth lumbar: wing of the ilium)||Lumbosacral tunnel syndrome|
|Ilioinguinal||Transverse abdominis muscle|
|Lateral femoral cutaneous||Inguinal ligament at anterior superior iliac spine||Meralgia paresthetica, Roth’s meralgia, Bernhardt’s syndrome|
|Femoral||Iliopectineal arch||Iliacus tunnel syndrome|
|Hunter’s canal (vastus medialis, adductor longus, sartorius), subsartorial canal|
|Infrapatellar branch of saphenous nerve||Gonyalgia paresthetica, “housemaid’s knee”|
|Obturator||Obturator canal||Howship-Romberg syndrome|
|Sciatic||Pyriformis muscle||Pyriformis syndrome|
|Greater and lesser sciatic foramens, sciatic notch, Gibraltar of the gluteus|
|Common peroneal||Fibular neck, peroneus longus muscle||“Cross leg” palsy|
|Crural fascia, superficial branch|
|Inferior external retinaculum (ligamentum cruciforme)||(Anterior) tarsal tunnel syndrome|
|Posterior tibial||Canal calcaneen de Richet (ligamentum laciniatum)||(Posterior) tarsal tunnel syndrome|
|Medial plantar nerve||“Jogger’s foot,” abductor hallucis tunnel syndrome|
|Medial plantar proper digital nerve||Joplin’s neuroma|
|Transverse metatarsal ligament||Morton’s neuroma (metatarsalgia)|
Entrapment neuropathies frequently involve a specific nerve distribution, thus, a thorough understanding of anatomic location and function of the nerve is important for diagnosis. A careful history and physical examination will reveal specific sensory and motor deficits that help localize the site of entrapment. Further, electrodiagnostic (EDX) testing can be helpful to confirm diagnosis as well as characterize its severity and chronicity, lending insight to its prognosis. An EDX study has two components: a nerve conduction study (NCS) and electromyography (EMG). NCS is performed by stimulating a sensory or motor nerve and recording conduction velocity and evoked response amplitude as well as, for motor nerves, the distal motor latency. The degree of deficit also helps to gauge severity of the disease. EMG assesses the integrity of the muscle unit by evaluating its firing pattern with and without activation to further confirm neurologic deficit. The usefulness of EDX is variable depending on the specific entrapment discussed. In recent years, imaging has played an increasing role in diagnosis as well. Ultrasound, magnetic resonance imaging (MRI), as well as x-ray and computed tomography (CT) can help to visualize the lesion and identify external causes of entrapment.
Despite advances in diagnosis and increasing recognition of entrapment neuropathies, treatments have largely remained either conservative care or surgery. Conservative care includes a combination of activity modification, physical therapy, and oral analgesics, whereas surgical options are often resorted to in severe or refractory cases. Recently, localized steroid injection at the site of entrapment is now often tried before proceeding with surgery, providing increasing evidence to its efficacy. Our discussion here highlights some of the most common diagnoses and treatments for each of the six entrapment neuropathies. However, there is large variability in presentation and response to treatment. Both diagnosis and treatment must be individualized to achieve optimal results.
Carpal Tunnel Syndrome
Carpal tunnel syndrome (CTS) is the most common and the most studied entrapment neuropathy. It may occur in as many as 1 in 10 people at some point in their lives and even more frequently in high-risk groups.
The syndrome refers to compression of the median nerve as it passes through a fibrous canal, called the carpal tunnel, located at the base of the hand. The tunnel is composed of the carpal or wrist bones at its base, the flexor retinaculum at the roof, the transverse carpal ligament, median nerve, and nine flexor tendons ( Fig. 33.1 ). Because of this crowded arrangement, any tenosynovial proliferation, fluid collection, or arthritic deformity can lead to median nerve compression. In controlled external compression of healthy volunteers, critical compression between 30 mm Hg and 60 mm Hg acutely affected nerve viability. This pressure may double with passive wrist flexion and triple with passive wrist extension of 90 degrees, especially in the proximal aspect of the wrist. Functional experiments have suggested that ischemic injury also play a significant role by impeding blood flow and causing epineural ischemia. At lower pressures, venous return may be reduced, resulting in venous stasis and intraneural edema.
Occupations involving both increased impact and repetitive motion—such as food processing, carpentry, and roofing—pose the largest risks, with odds ratios greater than 4. The risk from typing and computer work is also seen with a long exposure, or at least 12–20 hours a week of intensive work. Similarly, patients with osteoarthritis or rheumatoid arthritis are about twice as likely to get CTS than those without. However, there is an association between physiologic states such as pregnancy, menopause, and CTS, which can sometimes be acute, suggesting that hormonal components may play a role in altering the degree of edema in the tunnel. Similarly, abnormal hormonal states such as hypothyroidism, diabetes mellitus, and obesity also pose a risk (up to 1.5–2 times greater) of developing CTS, correlating positively with the severity of disease. The shape of the wrist can also be a risk factor for CTS. Square wrists—that is, those whose dorsal-volar distance is close to the mediolateral distance with a ratio greater than 0.7—are at increased risk for developing CTS. Perhaps this is why CTS is often present in both hands. It may also be the reason why many patients have a positive family history of CTS.
Classically, patients report numbness or pain on the palmar surface of the thumb and on the index, middle, and half of the ring finger along distribution of the median nerve. However, in practice, reports of numbness often involve only a portion of the median distribution, especially the middle or index finger. The patient may initially report numbness of the entire hand, but when specifically asked to observe which fingers are involved, will observe that the fifth finger is spared. Pain can occur both distal and proximal to the site of compression, including the hand, wrist, elbow, and even shoulder. Symptoms initially present as paresthesia mostly at night or with activities that involve frequent flexion or extension of the hand, as while driving. As the syndrome progresses, patients can have increasing symptoms during the daytime and later weakness expressed by dropping items and difficulty in closing buttons or opening jar lids.
The median nerve supplies sensation to the palmar surface of the thumb and index, middle, and half of the ring finger. It also supplies the dorsal tips of these same fingers. However, sensation covered by the palmar branch of the median nerve, including proximal portion of the palm and thenar eminence, is preserved in CTS since it does not go through the carpal tunnel. Two-point discrimination and pinprick testing will often elicit sensory deficits in parts of the median sensory territory. Often, these deficits are noted only when direct comparisons are made with the unaffected hand.
Motor function affected by the median nerve includes five intrinsic hand muscles, as well as the abductor pollicis brevis, one of the easiest to test. To test the strength of the abductor pollicis brevis, the patient should place the thumb perpendicular to the plane of the hand and then resist as the examiner attempts to push the thumb into the plane of the hand. In most patients, weakness will be appreciated only when the result is compared with the unaffected hand or to the flexor pollicis longus muscle of the affected side.
Several provocative tests can further confirm CTS. Two of the most common of these are Phalen’s and Tinel’s tests. Phalen’s test is carried out by placing the patient’s wrist in hyperflexion or extension to elicit paresthesia or pain within 60 seconds. This test has sensitivity of 42%–85% and specificity of 55%–98% in various studies. Tinel’s test is done with the examiner’s middle and index fingers or a reflex hammer gently percussing over the flexor retinaculum 6 times to elicit symptoms. This test has a sensitivity of 38%–100% and a specificity of 55%–100%. However, in one controlled comparison with healthy volunteers, Phalen’s test was shown to have sensitivity and specificity of 88% and 89%, respectively, as opposed to 67% and 68% for Tinel’s test. The carpal compression test can further confirm CTS. With the patient’s affected arm supinated, force is applied over the flexor retinaculum to elicit symptoms within 30 seconds. The tourniquet test can easily be done by applying a pneumatic compression cuff around the arm and inflating it to the patient’s systolic blood pressure to elicit symptoms within 60 seconds. Lastly, the hand elevation test can easily compare symptoms on the affected versus unaffected hand by elevating both arms above the head to look for symptoms within 60 seconds. In one comparison study of the five maneuvers discussed, the combination of tourniquet test, carpal compression, and Phalen’s test has the highest predictive value, whereas hand elevation provides the best means to rule out CTS.
Electrodiagnostic (EDX) testing is very sensitive for confirming the diagnosis of CTS. Nerve conductions are especially helpful, having sensitivity and specificity reaching 80%–90% and 95%, respectively. The hallmark of NCS includes decreased conduction velocity especially in digital nerves and across the wrist, with sensory fibers disproportionately affected more than motor fibers. EMG is more useful for excluding concurrent causes of pain, such as cervical radiculopathy or proximal median neuropathies, than in confirming the diagnosis of CTS.
With advances in imaging technology, ultrasonography has grown in popularity as an additional aid in the diagnosis of CTS. Using a high-frequency probe, ultrasound can identify sites of compression with high accuracy. In a recent meta-analysis, ultrasonography was found to have a sensitivity of 78% and specificity of 87% for the diagnosis of CTS compared with clinical presentation. It may be a helpful screening tool that may complement but not replace EDX studies.
The first line of treatment for CTS is splinting to maintain the wrist in a neutral position along with lifestyle modifications. Splints should be worn both day and night. Oral antiinflammatory treatments may provide relief for select patients. Steroid injection, especially done with ultrasound guidance, has been shown to be more effective than placebo, as well as antiinflammatory medications for reducing symptom severity and rate of surgery at 1 year. However, the majority of patients eventually proceed to surgery. In refractory cases, surgical release is the next step. Surgical procedures can be done via traditional open techniques or endoscopically with no significant difference in outcome between the two methods.
Ulnar Neuropathy at the Elbow
Ulnar nerve entrapment at the elbow is the second most common neuropathy in the upper extremity. Entrapment can occur either at several locations within the elbow, with the classic compression occurring at the cubital tunnel.
Ulnar nerve compression may be a result of intrinsic or extrinsic factors. Intrinsic factors contributing to compression include inherent anatomic structural abnormalities, pathologic lesions such as perineuroma, and congenital anomalies such as hamartoma of the nerve itself. External compression by muscle hypertrophy, hematoma or vascular lesions, or tendon proliferation often seen in inflammatory fibrosis are just some examples of extrinsic factors. The ulnar nerve is particularly vulnerable to compression or stretch at the elbow owing to its complex course around multiple aponeuroses, at five common locations ( Fig. 33.2 ). The nerve separates from the axillary artery in the distal arm to emerge on top of the medial head of the triceps. In 70% of the population, a thickened fascia called the arcade of Struthers lies over the nerve and is one source of compression. The nerve then pierces the medial intermuscular septum, another source of compression, to course in the condylar groove between the medial epicondyle and olecranon. When the elbow is in the flexed position, the groove shallows, exposing the more superficial ulnar nerve to injury and creating the “the funny bone” sensation. Nonunion from previous lateral condylar fracture may result in cubitus varus or inward deviation of the forearm, causing “tardy ulnar palsy” or delayed ulnar compression. The nerve then enters the cubital tunnel, a space surrounded medially by the medial epicondyle, laterally by the olecranon, and roofed by the arcuate (Osborne’s) ligament, which extends distally to connect the ulnar and humeral heads of the flexor carpi ulnaris. Flexion commonly causes increased pressure in the tunnel, resulting in compression. Deficit in the hand occurs before deficit in the forearm muscle because, topographically, they are in the outer circumference of the nerve bundle. As the nerve leaves the elbow, it pierces through the deep flexor pronator aponeurosis, the fifth potential point of compression.
Ulnar neuropathy at the elbow is aggravated by flexion of the elbow, which can result in both compression and traction of the nerve, leading to injury. This may occur with flexion of the elbow at night while sleeping, prolonged surgical procedures with poor positioning, bed-bound patients with limited mobility, or long flights during which a flexed elbow is pushed against the armrest for extended periods. Certain activities—such as intense gripping while driving, frequent throwing motions by athletes, or work involving repetitive motion—may predispose to ulnar neuropathy either by direct compression or via joint or ligamentous inflammation. Some patients are predisposed to injury. In one study, approximately 37% of the healthy volunteers exhibited hypermobility of the nerve within the condylar groove, increasing the risk of ulnar nerve irritation. Acute elbow fracture or dislocation can also cause acute or delayed ulnar neuropathy.
Symptoms of ulnar nerve entrapment typically start with numbness, tingling, and weakness in the hand in the distribution of the nerve covering the entire fifth digit and ulnar half of the fourth digit. Pain frequently occurs at night, when the elbow is flexed with or without pain radiating to the medial aspect of the elbow. Cramping of the hypothenar eminence may also be felt. In more severe cases, hand weakness, as loss of dexterity or general difficulty with good grip, may be reported. However, weakness without any paresthesia or pain should require further workup to rule out concurrent cervical radiculitis with myelopathy or signs of upper motor neuron disease. Nerve compression can occur at a number of other locations, including the brachial plexus and the ulnar nerve at the wrist, to produce similar symptoms, the exact location can be differentiated based on the position that elicits symptoms. Entrapment at the elbow causes symptoms with elbow flexion, whereas entrapment at Guyon’s canal results in symptoms with wrist flexion. Compression more proximally at the thoracic outlet results in symptoms with arm elevation. Thus a careful history can be helpful in distinguishing the source of compression.
On inspection, atrophy of the hypothenar eminence and first dorsal interosseous muscle may be seen in severe cases. The ulnar nerve supplies sensory fibers to the fifth finger, both palmar and dorsal surfaces, and usually half of the ring finger. Sensory deficits that split the ring finger are classic for an ulnar nerve injury. Abnormal sensation limited only to the palmar surface may suggest a more distal compression of the nerve at Guyon’s canal at the wrist, since the dorsal sensory branch typically separates 5–6 cm proximal to the ulnar styloid. However, in some individuals the ulnar nerve may supply the whole ring finger and even part of the long finger, making it difficult to distinguish from a C8–T1 radiculopathy. Extension of sensory deficit to medial edge of the forearm, above the wrist, indicates a lesion proximal to the elbow, such as a cervical radiculopathy or brachial plexopathy, since the ulnar sensory distribution ends at the base of the hand whereas the medial edge of the forearm is innervated by the medial antebrachial cutaneous (MABC) nerve, which is supplied by C8–T1 via an independent branch of the medial cord of the brachial plexus.
The ulnar nerve is primarily responsible for all intrinsic motor function of the hand. Entrapment can be seen when pinching with the index finger and thumb or adducting the thumb ( Fig. 33.3A ). There are five muscles of the hand, however, that are innervated by the median nerve: abductor pollicis brevis, flexor pollicis brevis, opponens pollicis, and the lateral two lumbricals ( Fig. 33.3B –D ). A positive Jeanne’s sign is seen when a flexed interphalangeal joint of the thumb is accompanied by hyperextended metacarpophalangeal joint. It can also be tested by having the patient pinch a paper against resistance with a fully adducted straight thumb and first metacarpophalangeal joint. A positive Froment’s test occurs when the patient cannot hold on to the paper and compensate by bending the distal interphalangeal joint of the thumb. The patient may also present with Wartenberg’s sign or spontaneous abduction of the little finger in attempting to extend all five fingers. More severe compressions may show “claw hand” or “hand of benediction,” for which the fourth and fifth digits are extended in the metacarpophalangeal joints and flexed at the interphalangeal joints while the patient is trying to extend all five fingers. Note that the same sign may be seen in median nerve compression, but with the patient attempting to form a fist rather than to extend the hand.
EDX testing may be helpful in confirming the diagnosis of ulnar compression, location of compression, and chronicity of disease. Compression neuropathy may present early as dynamic ischemia for which temporary ischemia has been restored. EDX studies are likely normal initially. For more severe compression, demyelination may occur, demonstrating slowing of fastest conducting fibers and associated with recovery 3–4 months after decompression surgery. In long-standing or severe cases of compression, axonal loss is present and nerve conduction studies will show a decrease in amplitude of the compound motor action potential, reflective of an overall decrease in the number of functioning nerves. EMG also demonstrates fibrillations and positive sharp waves at rest as well as long-duration motor unit action potentials and reduced recruitment with maximal effort. Although there are case reports of ultrasound successfully identifying the source of ulnar compression, it remains difficult to visualize the difference between abnormal and normal nerve on imaging. At least one study showed no significant difference in the ultrasound imaging of the nerve as compared with imaging from asymptomatic healthy volunteers. Thus clinical history and EDX testing remain the main sources for diagnosis.
Mild to moderate cases of ulnar nerve entrapment—as indicated by intermittent symptoms, motor conduction greater than 40 m/s, and no evidence of atrophy—can be successfully managed with nonsurgical options. This includes reducing elbow flexion, especially at night, with soft towel or padding; extensive postural education; activity modification; and steroid injection. Improvements are usually seen within 3–6 months and, in one study, 50% of the patients reported improved symptoms with conservative care. For those who fail conservative treatment or in severe cases as indicated by decreased amplitudes on nerve conduction, surgery is the next step. One of three major surgical methods is commonly used for surgical correction: decompression, epicondylectomy, or transposition. Decompression involves a simple incision and quick postoperative mobilization but poses the risk of incomplete decompression and ulnar subluxation. Epicondylectomy, or resection of the medial epicondyle, involves less dissection than transposition, poses a low risk for ulnar injury, but leads to greater postoperative pain and the potential for elbow instability. Transposition, most commonly an anterior approach, moves the ulnar nerve anterior to the axis of the elbow and thus releases all potential sources for compression and reduces the risk of nerve injury, but it does require extensive dissection and prolonged postoperative immobilization; it is also a technically more demanding procedure. Although there are many studies comparing the results of each approach, the procedure chosen must be tailored to the patient, mechanism of entrapment, and severity of the compression.
Thoracic Outlet Syndrome
Thoracic outlet syndrome (TOS) comprises a group of disorders that result from the compression of one or more of the neurovascular structures as they exit the thoracic outlet. There are three major types of TOS: neurogenic, arterial, and venous. Neurogenic TOS (nTOS) is the most common type, accounting for greater than 90% of cases, and is the primary focus of our discussion. Venous and arterial TOSs are much rarer, accounting for 3% and less than 1%, respectively. Neurologic TOS is further categorized as true nTOS, which accounts for only 1% of all cases, which is about 1 per million persons, and the disputed type, which accounts for 99% of the cases. Although true neurologic TOS is relatively rare, there are extensive publications on the topic, ranking it second to CTS in nerve entrapment syndromes. There is growing interest in TOS as well as controversy on its pathophysiology and management approach.
The thoracic outlet is a large space, extending from the base of the neck to the axilla, that can be divided into three portions as it travels superomedial to inferolateral: the interscalene triangle, the costoclavicular space, and the subcoracoid space. Compression of the neurovascular structures—namely the brachial plexus, subclavian or axillary artery, and their veins—is the primary cause of symptoms. The interscalene triangle, bounded by the anterior and middle scalene muscle and the first rib, contains the exiting brachial plexus and subclavian artery. Hyperextension injuries may cause local hematoma, inflammation, and subsequent fibrosis of the scalene muscles.
The brachial plexus, subclavian artery, and vein exit the costoclavicular space, which comprises the middle third of the clavicle anteriorly, the first rib posteriorly, and the upper border of the scapula at its posterolateral edge. The space can be narrowed by prolonged shoulder abduction or extension such as seen in archery or in poor posture. In one case-controlled study, patients with TOS were more likely to have a low shoulder girdle (complex of clavicle, coracoid, and scapula), as measured by radiography, than those in the control group. This suggests that inherent anatomic differences play a role as well.
The subclavian vessels are renamed the axillary vessels as they cross the lateral border of the first rib. They then enter the subcoracoid space, which is surrounded by the coracoid process superiorly; the pectoralis minor muscle (PMM) overlies the space. Shortening of the PMM in contractures causes abduction of the scapula and shoulder girdle protraction, narrowing the space. Similarly, hypertrophy of the PMM with repeated use in overhead sports may create hypertrophy, swelling, and fibrosis, causing nTOS.
Like many other entrapment neuropathies, the risk factors for TOS include anatomic predisposition, repeated activities, and various anatomic anomalies. TOS is more frequently seen in women, especially in the third and fourth decades. An anatomically lower shoulder girdle position, which results in compression of neurovascular structures by the clavicle, has been hypothesized to be a cause. The presence of a cervical rib, which is quite common in the general population, accounts for 20% of nTOS, although not all patients with a cervical rib have nTOS. Abnormal position of the first rib or a supernumerary scalene muscle may increase risk by decreasing the size of the interscalene triangle. Repeated activities that involve unnatural shoulder postures, as sometimes seen in computer users or players of string instruments, can further aggravate symptoms. Acquired conditions such as local trauma, tumor, infection, or inflammatory procedure can further predispose individuals to the development of TOS.
Symptoms of TOS depend, in part, on whether the impingement affects the brachial plexus, the artery, or the vein. True nTOS presents with predominantly motor deficits, including loss of dexterity, weakness, and atrophy. Upon further inquiry, some patients may also have sensory symptoms, such as pain or paresthesia. In contrast, the disputed type of nTOS presents with predominantly sensory deficits, including pain and myalgia of the neck, shoulder, medial arm, or forearm with paresthesia of the hand usually in a C8–T1 distribution. This is because compression typically affects the lower trunk of the brachial plexus. In both cases, symptoms are often exacerbated with arm elevation. Also, anterior flexion of the shoulder or frequent abduction and supination of the arm can further trigger symptoms. Unlike the other forms of TOS, disputed nTOS is frequently bilateral.
Similarly, arterial TOS may also present with pain in the neck, shoulder, or arm triggered by increasing activity, but hand or arm ischemia is also seen if arterial embolization occurs. A subset of patients will also present with symptoms of neurologic TOS from simultaneous compression of the brachial plexus. Venous TOS, sometimes referred to as Paget-Schroetter syndrome, was shown in a large series to present with visible collateral circulation (99% of cases) in the shoulder and arm, upper extremity edema (96%), and bluish discoloration of the distal extremity (94%). Relatively fewer patients present with pain, which usually occurs with exercise (33%).
General inspection and palpation is the best initial exam for identifying TOS, especially when compared with the unaffected limb. Palpation for presence of a cervical rib, asymmetry, or mass may indicate the cause of compression. In true nTOS, inspection often leads to motor findings such as atrophy of the thenar eminence muscles with or without patchy sensory deficit in the forearm and medial arm, while disputed nTOS has a relatively unremarkable neurologic exam. Tenderness to palpation of the anterior chest wall and the scalene, pectoralis, and trapezius muscles may be seen in both subtypes of nTOS. Vascular compression can be evident from a discrepancy in blood pressure between the affected and unaffected upper extremity as well as evidence of bruit or digital ischemia more distally. A palpable mass in the location of the thoracic outlet would suggest a vascular type of TOS. Several provocative tests can further confirm pathology, although most have limited sensitivity and specificity. The specific maneuvers are listed in Table 33.2 .