Chapman’s Orthopaedic Surgery
3rd Edition

CHAPTER 52
COMPRESSION NEUROPATHIES OF THE UPPER EXTREMITY
Mark N. Halikis
Julio Taleisnik
Robert M. Szabo
M. N. Halikis: Department of Orthopaedic Surgery, Uiversity of California, Irvine, Orange, California, 92868.
J. Taleisnik: Department of Orthopaedic Surgery, Uiversity of California, Irvine, Orange, California, 92868.
R. M. Szabo: Departments of Orthopaedics and Plastic Surgery, University of California, Davis Health System, Sacramento, California, 95817.
PATHOPHYSIOLOGY
Whenever A Nerve Is Contained In A Space That Has Limited Compliance, Such As The Carpal, Cubital, Or Ulnar Tunnels, or It Lies Deep To Fibrous Bands And Tendinous Arches Of Origin, It Is Vulnerable To Compression. An Increase In The Volume Of Material Within One Of These Limited Spaces Or A Decrease In Size Of The Space Can Lead To Increased Pressures, Which In Turn Can Compress The Nerve. Other Factors That May Lead To A Mechanical Peripheral Neuropathy Include Stretching Of The Nerve And Abnormal Nerve Motion About Or Adherence To Fibrous Bands Or Fascial Edges. The Intrinsic Response Of The Nerve To This Mechanical Insult Varies Little Regardless Of The Location Of The Injury Or The
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nature of the offending agent. The sequence of pathologic changes within the median nerve and the resulting clinical progression are the same whether the entrapment is secondary to synovitis within the carpal tunnel or secondary to a bone fragment from a fracture of the distal radius. Relief of the compression, generally accomplished by releasing the confining tunnel or compressive fibrous band, reverses these changes partially or completely. If damage to the nerves is irreversible (i.e., if entrapment is chronic), release can halt progression. All three major nerves of the upper extremity, the median, ulnar, and radial, may be injured by compression in locations where they are anatomically vulnerable.
Compression of a nerve has an effect on its structure and function. The severity of the resulting lesion depends on the magnitude of the compression as well as its duration. Both direct mechanical factors causing myelin damage and alterations in blood flow to and within the nerve likely play roles of varying degrees in causing the nerve changes seen in compression neuropathies. Ischemic changes caused by blood-flow alterations play a part in acute, easily reversible nerve-function alterations (72). Experiments have shown that elevation of pressure in and about the nerve to within 40 mm Hg of diastolic blood pressure cause profound changes in sensory nerve function of the median nerve, which are reversible with restoration of blood flow. Motor dysfunction of the nerve requires higher and more sustained elevations in pressure. These changes in function are not associated with structural changes in the nerve (132). Ischemia also plays a role in chronic compression. It is believed to contribute to intraneural scarring as well as edema from prolonged loss of blood supply to the nerve. Structural changes, particularly alterations in or loss of the myelin coatings of nerve fibers, are seen in chronic, higher-pressure compressions, especially those involving an edge such as a fibrous band or tendon. These changes resolve only in some cases, after enough time has elapsed for repair of damaged myelin. Compression of the nerve has also been shown to inhibit axoplasmic flow, both antegrade and retrograde, diminishing nerve function and contributing to the bulging appearance of the nerve proximal and distal to the site of compression (72).
The mechanism whereby surgical decompression works is not entirely understood. The frequently dramatic response to treatment can be explained only by the reversal of a vascular lesion (33,34). According to this theory, the mechanical factor responsible for producing the compression obstructs venous return, followed by segmental anoxia, capillary vasodilatation, and edema (33,125). The nerve edema aggravates the compression and leads to abnormal axonal and cellular exchange (34,124,131). Surgical release at this stage is a rewarding procedure. Prolonged compression results in intraneural fibrosis, after which nerve recovery is less likely to occur despite decompression.
ASSESSMENT
Clinical evaluation of an entrapment syndrome and determination of the site of compression are greatly aided by a knowledge of the anatomic distribution of a nerve and its function. Clinical evaluation of nerve compression neuropathies includes sensory threshold testing, provocative testing, and evaluation of muscle weakness or atrophy. The most consistent and reliable way to evaluate sensibility in nerve compression is to use threshold testing (126,127,132,133,134). Threshold tests evaluate how well a single nerve fiber innervating a receptor or group of receptor cells is functioning. These include vibrometry, Semmes–Weinstein monofilaments, and vibration testing. To test with Semmes–Weinstein monofilaments, apply pressure to the fingertip with the filament until the filament bends (Fig. 52.1). The pressure required to bend the filament is directly related to its diameter. Apply filaments of successively increasing diameter to determine the sensory threshold of slowly adapting nerve fibers. Perform vibration testing with a 256 cycles-per-second (cps) tuning fork to evaluate the sensory threshold of quickly adapting nerve fibers (Fig. 52.2).
Figure 52.1. Threshold testing with Semmes–Weinstein monofilaments.
Figure 52.2. Vibration sensation testing with a 256 cps tuning fork.
Innervation density tests (i.e., two-point and moving two-point discrimination) (Fig. 52.3) measure multiple overlapping peripheral receptor fields and the density of innervation—how many nerve fibers are present and correctly represented in the cerebral cortex. Early in compression neuropathies, nerve fibers are not lost; rather, the nerve fibers that are present are not functioning well. In nerve laceration, in contrast, nerve fibers to the innervated
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area are lost. Innervation density tests are more useful for evaluating nerve laceration and recovery after repair than for evaluating compression neuropathies. These tests are abnormal in only 20% of patients with electrically proven carpal tunnel syndrome (CTS), whereas threshold tests detect more than 80% of electrically proven CTS patients (133).
Figure 52.3. Two-point discrimination testing.
Provocative tests compress, stretch, or percuss the nerve to elicit numbness and paresthesias in its sensory distribution. Provocative tests are especially important in patients with exertional compression neuropathies, where symptoms and signs may be minimal or absent at rest. [For this reason, it may also be advisable to perform sensory testing before and after activity (12).] The examiner evaluates weakness and atrophy subjectively. Muscles innervated by the nerve suspected of compression are tested for bulk and strength. Comparison to the uninvolved extremity is especially helpful.
DIAGNOSTIC STUDIES
Although not a substitute for a thorough clinical examination, electrodiagnostic studies may help to corroborate clinical impressions. They truly are the only objective test of nerve compression. Additionally, they may indicate a level of severity of nerve damage that may have prognostic implications for treatment. A detailed explanation of neurodiagnostics of the upper extremity is beyond the scope of this chapter. Here we offer a brief, basic description of methods and definitions of terms. For a more complete understanding, read review articles and book chapters published on this subject (49,51,56). The neurodiagnostic study, when used for the majority of upper extremity compression injuries, is composed of two parts: the nerve conduction or velocity (NCV) and the electromyography (EMG) needle examination. The NCV measures the speed of conduction of an impulse along a segment of nerve. The EMG measures the response of muscle fibers to conducted nerve impulses.
When stimulated, a segment of nerve conducts or propagates an electrical impulse. This impulse can be detected by a surface electrode on the skin overlying a nerve or a muscle innervated by a nerve. In an NCV test, the nerve is stimulated electrically at one point and the impulse measured at another point along its length. When the study measures an impulse traveling in a physiologic direction, it is called an orthodromic study; when it measures an impulse traveling in the opposite direction, it is called antidromic. Impulses propagated by sensory nerves or the sensory fibers of a mixed nerve are measured by surface electrodes as a waveform called the sensory nerve action potential. Motor nerves or the motor fibers of mixed nerves are measured by the electrical response of multiple muscle fibers, which produce a waveform known as the composite muscle action potential.
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The interval from stimulation of the nerve to the time at which the sensing electrode detects the waveform is known as the latency. In motor nerves, latency also encompasses the time it takes the nerve impulse to be transmitted across the neuromuscular junction and to activate the muscle fibers. Neurodiagnosticians often report latencies, especially when evaluating nerve conduction across short nerve segments at the wrist. Latencies are reported in units of time (msec). Conduction velocities are reported in units of meters per second and can be calculated from the measured latency and knowledge of the length of the nerve segment over which the latency was measured. Velocities are reported for longer lengths of nerve segments tested, such as from the midforearm to the hand. Additional measurements can be obtained by evaluating the waveforms. These include the amplitude, duration, and area of the waveform (Fig. 52.4). These parameters can aid the electromyographer in characterizing the conduction of the nerve. The amplitude and duration depend on the number of nerve fibers and the speed of conduction of the different nerve fibers transmitting the stimulated impulse, respectively.
Figure 52.4. A waveform obtained from nerve conduction testing. (From Holmlund T. Electrodiagnosis and Neurologic Evaluation. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1277, with permission.)
Electromyography employs needle electrodes placed within muscle to evaluate the activity of a single motor unit consisting of the nerve cell, its fibers, and the group of muscle fibers it innervates (Fig. 52.5). Normally, a muscle fiber at rest is essentially electrically silent. After a brief burst of electrical activity that occurs while the electrode is inserted, the needle measures only occasional background impulses. When the muscle is voluntarily contracted, the electrode senses the electrical activity of the motor unit, which is a waveform called the motor unit potential (MUP). In the pathologic state, different waveforms may be detected that give insight into the disease process affecting the muscle as well as the chronicity of the condition and whether recovery or further loss is occurring. (Some names of these waveforms and their general implications are offered here, but this information should not be considered a definitive reference.)
Figure 52.5. Electromyography (EMG). APB, abductor pollicis brevis; MUP, motor unit potential. (From Hillburn JW. General Principles and Use of Electrodiagnostic Studies in Carpal and Cubital Tunnel Syndromes. Hand Clin 1996;12:205, with permission.)
Positive sharp waves and fibrillation potentials commonly indicate recent muscle denervation (Fig. 52.6A).
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The development of small highly polyphasic MUPs (Fig. 52.6B) and decreased fibrillations is considered evidence of early reinnervation of muscle. MUPs that are of great duration and amplitude are considered evidence of chronic denervation with collateral reinnervation resulting from adjacent nerve sprouting. Many waveforms are characteristic of neuropathies, and others of myopathies. The significance of the different electrical events is subject to the clinical setting and the interpretation of the electromyographer.
Figure 52.6. Abnormal EMG motor unit potentials. A: Fibrillation potentials and positive sharp waves indicate recent muscle denervation. B: Polyphasic MUPs indicate early reinnervation of muscle. (From Hillburn JW. General Principles and Use of Electrodiagnostic Studies in Carpal and Cubital Tunnel Syndromes. Hand Clin 1996;12:205, with permission.)
When evaluating the electrodiagnostic report, it is important to understand that “normals” for particular tests are laboratory, machine, and operator dependent because of variations in how measurements are calculated, technique, and environmental factors such as skin temperature. However, rule-of-thumb normals may be useful. For the median nerve at the wrist, distal motor latencies of more than 4.5 msec and distal sensory latencies of more than 3.5 msec are considered abnormal. In a patient with unilateral involvement, a difference from one hand to the other of more than 1.0 msec for motor latency and 0.5 msec for sensory latency is also considered abnormal (Table 52.1) (126). It is helpful to develop a relationship with an electromyographer who produces reliable and
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consistent results and whose interpretations of these studies are useful in your evaluation and treatment of patients.
Table 52.1. Electrodiagnostic Tests for Carpal Tunnel Syndrome
Certain clinical and metabolic disorders can affect nerve function. Conditions commonly associated with nerve dysfunction include hypothyroidism with myxedema (98), obesity (84,85), cervical radiculopathy, diabetes mellitus, alcoholism (83), and exposure to neurotoxic chemicals or chemotherapeutic agents. These disorders in and of themselves can cause polyneuropathy, independent of compression neuropathy; they may increase the susceptibility of nerves to compression; or they may negatively affect recovery of nerves after adequate treatment. When suspected, these disorders should be investigated and managed. They are not, however, contraindications to treatment of coexisting compression neuropathies.
Recently, some members of the medical community, of the popular media, and in the medicolegal and workers’ compensation arena have included certain compressive neuropathies, most notably CTS, in a category of disorders known as cumulative trauma disorders or repetitive stress injuries. The association between repetitive stress or activity, and compression neuropathies has been described (41). It is fairly well accepted that certain activities or prolonged positioning of the extremities can incite the symptoms of compression neuropathies, but controversy exists about whether certain activities or occupations can cause them (129).
PRINCIPLES OF TREATMENT
The critical component of effective treatment of compression neuropathies of the upper extremity is an accurate diagnosis. A perfectly performed surgical procedure is likely to provide no benefit to the patient if it is not indicated for the condition causing the symptoms. Remember that each of the compression neuropathies is related to a syndrome, which is a constellation of symptoms and signs (123). Positive neurodiagnostic studies in the absence of symptoms and signs cannot make the diagnosis of any of the compression neuropathy syndromes.
Categorizing patients based on the relative severity of their compression neuropathies may be helpful in determining treatment options. Mild cases are those with a short history of symptoms that are intermittent rather than continuous, and with negative or minimally abnormal electrodiagnostic findings. Severe cases are those with histories of symptoms for more than a year, profound and persistent numbness with atrophy of involved musculature, and both very prolonged (or absent) conduction velocities and advanced EMG findings. Mild cases are likely to respond to nonoperative measures (40), whereas severe cases do not, and therefore initial treatment should be operative.
Nonoperative treatment includes splinting, medications, physiotherapy, corticosteroid injections, and correction of metabolic abnormalities. The nerve may be protected through avoidance of positions that are deleterious to nerve function. For instance, prolonged extreme positioning of the wrist in flexion in patients with CTS or of the elbow in flexion in patients with cubital tunnel syndrome aggravates symptoms and should be avoided. Splinting is employed, usually at night, to prevent this type of positioning. Therefore, nerve protection involves educating the patient about activities and postures that may lead to compression of nerves at vulnerable sites, and how to avoid them.
Oral medications, most commonly nonsteroidal anti-inflammatory drugs (NSAIDs) and diuretics, have been used in treating compression neuropathies. No medications, however, have any documented efficacy. Physiotherapy may be helpful in treating certain types of nerve compression but is most helpful in postoperative rehabilitation. Corticosteroid injection is usually employed after failure of the previously described nonoperative treatments. A powerful anti-inflammatory agent is delivered directly to the tissues about the nerve, at a specific location. Since few cases of CTS are the result of acute or chronic inflammation in the flexor tenosynovium (62,82), the mechanism whereby steroid injections relieve symptoms is unknown. In addition to their therapeutic value, injections may help in confirming a diagnosis, providing a prognostic indicator of the potential effectiveness of operative treatment (45).
Treat CTS induced by pregnancy with splints and elastic gloves at night until delivery of the child, when it will likely resolve spontaneously. For severe symptoms, local injections of steroids may help. If symptoms persist thereafter, operation may be necessary.
Indications for surgery include failure of nonsurgical management; acute, rapidly progressive involvement; severe cases; and symptom recurrence. Tourniquet control during surgery is preferred unless the site of compression is too proximal or unless specific contraindications exist. Meticulous hemostasis is imperative during the exposure, especially in patients with a coagulopathy and in those who are taking aspirin or are on anticoagulation treatment to reduce postoperative bleeding and swelling. Facilitate this by exsanguinating the extremity through elevation rather than by elastic wrapping, so that vessels remain partially filled and are easier to identify and coagulate or tie off.
Decompression is generally an outpatient procedure and may be performed under general, regional, or local anesthesia. Local anesthesia is reserved for less involved cases and can be used with tourniquet control, which is well tolerated for brief procedures. Make the incision to allow adequate visualization of the nerve and all suspected sites of compression. The choice of treatment of the nerve
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depends on its appearance under direct visualization, the location of the entrapment, and the clinical findings. If the bed in which the nerve lies is scarified or makes the nerve vulnerable to potential mechanical trauma, consider nerve transposition or flap coverage.
COMPRESSION NEUROPATHIES OF THE MEDIAN NERVE
Compression of the median nerve typically occurs within the carpal tunnel or deep to the origin of the pronator teres (PT). A third form of median nerve entrapment is isolated compression of the anterior interosseous nerve (AIN).
CARPAL TUNNEL SYNDROME
Pathophysiology and Anatomy
At the level of the wrist, the median nerve lies within the confined space of the carpal tunnel along with the long flexor tendons to the fingers and thumb. The tunnel is bounded on three sides by the bones of the carpus, which make up the floor of the canal, and on the fourth by the transverse carpal ligament (TCL), which forms the roof (Fig. 52.7). Compressive neuropathy of the median nerve within the carpal tunnel may result from any space-occupying lesion under the TCL (19,67,145). A frequent cause is flexor tenosynovitis; other causes are fractures and dislocations of the floor of the canal and distal radius, and other space-occupying lesions such as tumors and ganglia. These space-occupying lesions increase the volume of the contents of the noncompliant carpal tunnel, raising the pressure on its contents, which include the median nerve. In many cases, there are no particular identifiable causes even though the nerve is clearly compressed. Although many of these cases are attributed to “nonspecific synovitis,” pathologic examination of the synovium obtained from the carpal canal in these cases usually fails to reveal signs of inflammation. Rather, fibrosis and/or edema changes are seen, which may themselves be secondary to compression rather than the primary cause of the entrapment neuropathy (62,82).
Figure 52.7. Cross section of a wrist through the carpal canal. The median nerve and digital flexor tendons lie in the space formed by the bony carpal arch and transverse carpal ligament. (Adapted from North ER, Kaul MP. Compression Neuropathies: Median. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1307, with permission.)
Assessment
The diagnosis of CTS is strongly suggested by the patient’s history. Typically, he complains of aching or burning pain along the median nerve distribution and of numbness and tingling in the median-nerve-innervated digits (Fig. 52.8A) during the night and early morning as well as during activities. Numbness may extend into the ulnar digits in some patients. These symptoms are aggravated by elevation, repetitive activities, and prolonged flexion positioning of the wrist (130). Radiation of symptoms proximal to the wrist is not unusual. Complaints of the hand feeling fat, clumsiness in manipulation, and dropping items are also frequent. The incidence is greater in women than in men, although the difference is decreasing. In the past, postmenopausal women were the most common patients; commonly associated diagnoses were rheumatoid arthritis and distal radius malunion. Recently, a large, younger group of patients with essentially equal distribution of women and men has emerged. In this group the carpal tunnel disease has been labeled idiopathic (62).
Figure 52.8. A: Palmar sensory distributions of ulnar, median, palmar cutaneous, and radial nerves. B: Dorsal sensory distributions of radial, median, and ulnar nerves.
Examination includes sensory, provocative, sudomotor, and strength testing. Sensibility may be reduced throughout the area normally supplied by the median nerve except for the thenar eminence, the distribution of the palmar cutaneous branch (Fig. 52.8A), which does not
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enter the carpal canal (135). As noted previously, the most consistent and reliable way to evaluate sensibility in nerve compression is to use threshold testing (Semmes–Weinstein monofilaments, vibrometry, and 256 cps vibration testing) (126,127,132,133,134). Provocative tests compress or percuss the median nerve to elicit numbness and paresthesias in the distribution of the median nerve in patients with CTS. Phalen’s wrist flexion test, in which the wrist is maximally flexed with the fingers slightly curled, is sensitive (Fig. 52.9) (43). A positive test for CTS is reproduction of symptoms within 60 sec. Tinel’s nerve percussion test, in which the median nerve is percussed as it enters the carpal canal to elicit symptoms (Fig. 52.10), is specific and indicates CTS in cases in which Phalen’s test is also positive (65). Another useful test is the direct compression test, which is sensitive and specific. The examiner’s thumbs apply direct pressure to the median nerve as it enters the carpal tunnel (Fig. 52.11) (29). A positive test is reproduction of symptoms, which appear within 30 sec and disappear with release of compression. Together, these tests provide added clinical evidence of median nerve compression at the wrist (Table 52.2).
Figure 52.9. Phalen’s wrist flexion test.
Figure 52.10. Tinel’s nerve percussion test.
Figure 52.11. Durkan’s median nerve compression test.
Table 52.2. Diagnostic Tests for Carpal Tunnel Syndrome
Sudomotor activity (sweating) may be diminished. This is easy to detect clinically by sliding a metal object (e.g.,
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a pen) between the patient’s fingers, which are held together. The object slides much more easily on dry skin than on skin with normal perspiration. Strength testing is difficult and somewhat subjective. The most easily evaluated muscle of the thenar eminence is the abductor pollicis brevis (APB) muscle. Most often, this muscle is innervated solely by the median nerve, but it can also have a contribution from the radial nerve. It is the most superficial of the thenar muscles and can be palpated during active opposition or resisted palmar abduction of the thumb. Relative weakness of palmar abduction of the thumb against resistance or muscle atrophy occurs in more advanced cases.
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Flattening or concavity of the normally bulging thenar eminence indicates atrophy of the APB (Fig. 52.12A). A weak, soft, or small APB is seen in severe cases of CTS and indicates denervation of the muscle.
Figure 52.12. A: A flattened thenar eminence indicates atrophy of the abductor pollicis brevis. B: Abductor pollicis brevis (arrow). (From North ER, Kaul MP. Compression Neuropathies: Median. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1307, with permission.)
Radiographic examination is not indicated in all cases because there is a low yield of findings (9); it should be restricted to patients with a history of trauma or arthritis and those with decreased wrist range of motion on examination. One of us (JT) obtains radiographs to rule out Kienböck’s disease in younger patients and peritrapezial arthritis in older ones. Additional diagnoses uncovered by preoperative radiographs include scapholunate advanced collapse (SLAC) wrists, ununited fractures of the scaphoid, and radiopaque masses within the carpal tunnel (136). The views recommended include posteroanterior (PA), lateral, and carpal tunnel views.
Additional examinations include electrodiagnostic studies and laboratory tests. Positive nerve conduction velocities show increased latencies. In severe cases, EMG exams may show abnormalities and may give information regarding treatment prognosis. In mild or exertion-related cases, electrodiagnostic studies may be negative. This negative finding does not rule out CTS in the presence of typical signs and symptoms. Provocative nerve conduction evaluation may help to uncover these dynamic forms of CTS (14). EMG examination may be helpful when a cervical radiculopathy is suspected. Order laboratory testing to screen for metabolic disorders that may contribute to or cause CTS, (a) when there is suspicion of these disorders, (b) when there is bilateral presentation, and (c) in children who may have rare mucopolysaccharidosis or mucopolylipidosis (139). Tests include erythrocyte sedimentation rate, rheumatoid factor, serum glucose level, uric acid, thyroid panel, and renal indices. Liver function tests may be indicated if alcohol-related peripheral neuropathy is suspected. If doubt persists about the correct diagnosis, an injection of a small amount of a steroid preparation mixed with local anesthetic into the carpal
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tunnel (not into the nerve) can be a therapeutic and diagnostic aid (Fig. 52.13) (Table 52.3) (45). The entry site for the needle is slightly proximal to the distal wrist crease, ulnar to the palmaris longus (PL) to avoid impaling the median nerve, and approximately 1 cm radial to the flexor carpi ulnaris (FCU) to avoid entrance into the canal of Guyon. Insert the needle at a 45° angle, beneath the proximal margin of the TCL and directed in line with the ring finger ray. Palpation in the midpalm just distal to the TCL while injecting can help confirm proper needle placement by enabling you to feel the flush of fluid into the canal.
Figure 52.13. Injection into the carpal tunnel. A: The entry site for the needle. PL, palmaris; FCU, flexor carpi ulnaris. B: Insertion of the needle. (From Gelberman RH, Rydevik BL, Pess GM, et al. Carpal Tunnel Syndrome: A Scientific Basis for Clinical Care. Orthop Clin North Am 1988;19:117, with permission.)
Table 52.3. Carpal Tunnel Syndrome Summary
Classification
Patients with CTS may be classified into three categories. The mild group consists of patients with intermittent symptoms that have been present less than 1 year, who have normal two-point discrimination, no thenar weakness or atrophy, no denervation potentials on EMG, and mildly elevated NCV. With conservative treatment and steroid injection, 40% will be free of symptoms at 12 months. The severe group consists of those with profound, persistent symptoms that have been present longer than 1 year, thenar weakness or atrophy, and marked abnormalities on electrodiagnostic studies (40). Patients in the severe group fail to respond adequately to conservative therapy and should receive operative treatment, which may include tendon transfers concurrent with carpal tunnel release. In the moderate group, conservative treatment shows findings and gives results intermediate between those of the mild and severe groups. The presence of underlying disorders or advanced age in any of these patients diminishes the response to conservative (and possibly operative) care.
Nonoperative Treatment
Initially, institute nonoperative treatment in all patients except those with severe disease. Splint the wrist in neutral to slight extension at night and during activities that exacerbate symptoms. In exertional or dynamic cases, modification of activities that exacerbate symptoms may be helpful. Vitamin B6 has no effect on the natural history of CTS (3,4). Steroid injection offers transitory relief in 80% of patients, with only 22% being free of symptoms at 12 months. The patients in the mild group fare better than others with steroid injection (40). Treat or correct underlying disorders if possible.
Surgical Indications and Relative Results
Indications for surgery include failure of nonoperative treatment, persistent or progressive symptoms, acute onset with profound sensory loss associated with trauma, and weakness or atrophy of thenar muscles. Results of surgery vary according to severity of disease, choice of surgical treatment, and individual patient physiology and social issues. As a general rule, we believe that with adequate release of the carpal tunnel, major or complete relief of discomfort associated with CTS is likely, as is relief of transient numbness. Persistent or profound numbness may not disappear with release if it has been present for a prolonged period (over 12 months). Weak or atrophied
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muscle is not expected to recover with release, but if it is not complicated by underlying disease, its progression will likely be halted. Nolan et al. (87) showed that patients with severe disease, followed for more than 2 years after carpal tunnel release, show improvement. Therefore, surgery is indicated in these patients, especially if symptoms of discomfort are present.
Preoperative Planning
Make the decision to perform surgical release in a patient with CTS in the context of the patient’s general condition. You must be certain of the diagnosis of CTS and that its cause is compression of the median nerve at the wrist. Within reason, exclude other potential sources of the symptoms and maximally correct any contributing conditions. With these issues resolved, you must include the particular considerations of the patient in the surgical care. If malunions and carpal instabilities are severe enough to compromise results, treat them prior to or concurrently with release. In patients with severe atrophy of the thenar musculature, perform opponensplasty at the time of release. A particularly suitable procedure for restoration of thumb palmar abduction in the patient with severe CTS is the Camitz opponensplasty, in which the PL is harvested and extended with a strip of palmar fascia, then routed subcutaneously and sutured into the thumb at the level of the metacarpophalangeal (MP) joint along the APB tendon (Fig. 52.14).
Figure 52.14. The Camitz transfer for restoration of thumb palmar abduction in patients with severe atrophy of the thenar musculature. A: Harvesting of the palmaris longus. B: Rerouting of the PL. (From Imbriglia JE, Hagberg WC, Baratz ME. Median Nerve Reconstruction. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1381, with permission.)
Open Carpal Tunnel Release
  • Start the incision at the junction of the proximal and middle thirds of the palm (at the level of Kaplan’s Cardinal Line) on the radial aspect of the ring finger ray and
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    continue it proximally to a point where the interthenar crease intersects the distal wrist crease, just ulnar to the PL tendon (Fig. 52.15).
    Figure 52.15. Approach to the carpal tunnel. The more proximal porton (dashed and dotted lines) is used when a more extensive exposure is required.
  • To extend this incision for increased exposure, as is needed in flexor tenosynovectomy, carry the incision along the wrist crease ulnarly to a point just radial to the flexor carpi ulnaris tendon and, if necessary, gently curve it proximally and radially to the ulnar aspect of the PL tendon.
  • Divide the subcutaneous fat to expose the palmar fascia and divide the palmar fascia in line with the incision, which exposes the TCL. Take care to avoid injury to the ulnar nerve and artery that lie nearby, on the ulnar aspect of the field in the canal of Guyon.
  • Divide the TCL longitudinally, close to its ulnar attachments and extending distally until you reach the fatty envelope surrounding the vessels of the superficial palmar arch.
  • Proximally, with the median nerve under direct vision, elevate the skin off of the TCL where it blends into the antebrachial fascia.
  • Divide the proximal portion of the TCL and the antebrachial fascia with scissors 3–5 cm proximal to the carpal canal.
  • Elevate the entire radial flap of skin, including subcutaneous tissue, ligament, and intact palmar cutaneous branch of the median nerve and its divisions, to expose the median nerve in the canal.
  • Use blunt dissection to free the median nerve from the radial wall of the canal, where it is often tethered by synovium.
  • Sweep the contents of the canal away from first the radial and then the ulnar aspects of the canal, inspecting the floor for masses or irregularities. Also examine the digital flexor tendons for fraying and other damage.
  • Perform synovectomy (e.g., in rheumatoid patients), and reduce and fix fractures or dislocations if indicated.
  • Release the tourniquet and obtain hemostasis. Close only the skin with 5-0 nylon suture.
  • Apply a well-padded dressing with plaster reinforcement as desired to immobilize the wrist in neutral and the thumb in palmar abduction. Be sure not to splint the thumb in radial abduction because this position encourages lengthening of the thenar muscles, which results in prolonged pinch weakness.
There have been significant differences of opinion about whether internal neurolysis improves the results of carpal tunnel release in patients with severe CTS manifested by thenar atrophy or fixed sensory deficit (33,34,42,71,73). In a combined series of patients (69 hands) from San Diego and Sacramento, added benefit from internal neurolysis in the treatment of severe CTS could not be demonstrated (42). Lowry and Follender (71) confirmed this finding with a prospective, randomized, double-blind, controlled study. We therefore no longer perform or recommend internal neurolysis in the treatment of CTS. Concomitant release of the canal of Guyon in patients with evidence of compression of the ulnar nerve at the level of the wrist in conjunction with CTS is not recommended (117). Transection of the TCL during carpal tunnel release alone results in an increase in the volume of the carpal tunnel of approximately 24% and a change in the orientation and shape of the canal of Guyon (102). Clinically, this results in resolution of the symptoms referable to ulnar nerve compression at the wrist in these patients.
Endoscopic Carpal Tunnel Release
Open carpal tunnel release is considered the preferred surgical technique, especially for surgeons not doing a large volume of these surgeries, because it offers good visualization of the TCL, the superficial arch, and the carpal canal contents. It is a proven, reliable method. Nonetheless, some herald endoscopic carpal tunnel release as a step forward in the treatment of CTS (15,21,94). Proponents of the latter technique claim decreased morbidity as a result of the smaller scar, which occurs away from the base of the palm, and more rapid rehabilitation (35,142). Several systems exist for the purpose of endoscopic release; they have in common visualization of the undersurface of the TCL with an arthroscope as the ligament is divided from within the canal using special knives or a blade mechanism. Agee et al. (2) and Chow (21) developed independent systems that are available commercially.
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In a multicenter prospective randomized study, Agee et al. (2) demonstrated a decrease in early postoperative pain and morbidity using his device, but by 6 weeks, results were comparable to those of standard carpal tunnel release.
Additional studies have evaluated endoscopic release (15,35). Although scar pain has been reduced and time to recovery of preoperative grip and pinch strength minimally shortened, pillar pain and palmar tenderness have not been eliminated. In cadaver studies, incomplete release of the TCL has been demonstrated to occur in up to 50% of the specimens (111). Clinically, however, patients do obtain symptomatic relief from the endoscopic technique. As endoscopic release systems have been refined and experience with the technique gained, results have improved. The procedure remains hazardous in inexperienced hands and requires specialized training. A risk of cutting neurovascular structures or tendons exists because of limited visualization and deviations from proper technique (81,110). Recurrent or incomplete relief of symptoms from endoscopic release has been shown to be related to incomplete release of the TCL. This improves after subsequent open carpal tunnel release (36,53).
Endoscopic carpal tunnel release remains a controversial method for treatment of CTS. However, with a thorough knowledge of the pertinent anatomy and with experience, it can be a safe and effective treatment in appropriate patients if the surgeon adheres to several tenets. The surgical consent form must specify both an endoscopic and an open carpal tunnel release, because several conditions may necessitate aborting the former and proceeding with the latter. These include (a) difficulty in visualization that results from equipment problems, fogging, or the inability to clear synovium from the undersurface of the ligament, (b) presentation of atypical anatomy, and (c) difficulty in manipulating the endoscope. The surgeon must place the endoscope in the ulnar aspect of the carpal tunnel and keep it aligned with the ring finger ray to prevent injury to the median nerve and the superficial vascular arch (108). (Specific techniques are not discussed here; refer to the manufacturer’s technique manual for each system.) The surgeon must verify absolutely that the endoscope is within the carpal tunnel and not in the canal of Guyon before making any cuts. Endoscopic carpal tunnel release is inappropriate in patients with bony deformity caused by fracture or dislocation and in those with inflammatory synovitis who require synovectomy or whose synovitis may make visualization difficult. If endoscopic tunnel release is considered, preoperative radiographs are necessary to evaluate these issues.
Multiple limited- and minimal-incision methods and systems have been developed for carpal tunnel release and are commercially available (13,68,86). These differ from endoscopic techniques in that the TCL is divided by a relatively blind method rather than being visualized with an arthroscope. The benefits of this technique over open carpal tunnel release are similar to those of the endoscopic methods, as are the risks.
Figure 52.16. Endoscopic carpal tunnel release with the system developed by John M. Agee. A: Insertion of the blade assembly beneath the transverse carpal ligament. B: Division of the transverse carpal ligament. (From Gelberman RH, North ER. Carpal Tunnel Release. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991:899, with permission.)
Postoperative Care and Rehabilitation
Immediately postoperatively, encourage active, gentle finger range-of-motion exercises. Patients should also maintain
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mobility of the elbow and shoulder. Elevation is crucial, especially during sleep, to reduce edema. Remove bulky dressings and splints 5 days postoperatively. The patient then wears a removable prefabricated wrist splint for comfort only. [One of us (MNH) instructs the patient to wear the splint full time.] The wrist is put through gentle range-of-motion excercises several times a day, independently of finger motion. Continue the splint for 2–3 weeks for patient comfort only, during which time encourage progressive use of the hand. Then discontinue daytime splinting. Continue nighttime wear for an additional 3–4 weeks if desired (96). Use physiotherapy selectively for patients who are progressing poorly. Recovery takes months, so patients who are told that the carpal tunnel release is a minor operation and full recovery can be anticipated in 2 weeks are grossly misled and usually unhappy.
The patient’s return to work depends largely on the demands of his occupation. Gellman et al. (44) have shown that grip strength returns to preoperative levels 3 months after surgery, and pinch strength returns at 6 weeks. Their work provides us with an indication of when patients ought to be able to return to their previous levels of occupational activity. Many studies employ “return to work” as a measure of outcome without clearly delineating what criteria are to be met to determine when a patient should return to work. Many factors influence the actual return-to-work time. Palmar tenderness, a particularly important consideration in manual laborers, may persist for longer than 6 months. Full recovery of nerve function may not occur, depending on the severity of nerve damage. Persistent palmar pain and early recurrent symptoms in workers’ compensation cases are increasing, unsolved problems for patients, physicians, and industry. Without job modification for these patients, carpal tunnel release alone may lead to failure in returning the patient to gainful employment.
Complications
Complications are caused by misdiagnosis or technical factors. Conditions associated with peripheral neuropathies must be suspected, recognized, and treated before surgery, or concurrently with the surgical release. Upton and McComas (137) proposed a “double crush” syndrome as a hypothesis to explain the failure of distal decompressions in nerves subject to compression in multiple sites. Many patients with CTS have a cervical radiculopathy. Others may have concomitant compression at the carpal tunnel as well as under the PT. Release of the carpal tunnel in these cases may not relieve symptoms because the more proximal compression remains. Hypertrophic synovium, if not removed at the time of surgery, may cause persistent compression despite ligament release.
Complicating technical factors include improper placement of the incision (i.e., usually too far radially), which jeopardizes the median nerve and its motor branch, as well as leading to injury or entrapment of the palmar cutaneous nerve or its branches (Fig. 52.17). Poor exposure may result in incomplete division of the TCL or in injury to the superficial palmar arch. Do not use transverse incisions at the wrist crease for blind decompression of the carpal tunnel.
Figure 52.17. The palmar cutaneous branch of the median nerve and its divisions crossing a carpal tunnel incision placed too far radially.
A rare complication is a tendency of the flexor tendons to the little finger to sublux during strong gripping. This is often only a transitory problem. Bowstringing of the flexor tendons with flexion of the wrist has been noted. This complication is easily prevented by postoperatively immobilizing the wrist in slight dorsiflexion for 2–3 days (138), which additionally may prevent adherence of the nerve and tendons to palmar structures and improve grip strength (88). Reserve reconstruction of the TCL for instances where immobilization of the wrist in flexion is necessary after carpal tunnel release. Complications from deficient postoperative management usually result from swelling and edema or poor control of pain, leading to loss of finger or wrist motion (particularly if a synovectomy was performed) and to reflex sympathetic dystrophy. The benefits of a good postoperative dressing, an aggressive exercise program, and elevation cannot be emphasized enough.
Pillar pain—pain at the base of the thenar and hypothenar eminences after carpal tunnel release—is a common
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finding in patients. It varies greatly from case to case in both severity and duration of its symptoms. Its etiology is poorly understood, although many theories have been proposed. It generally subsides and resolves over time. Seradge and Seradge (113) noted ulnar-sided wrist pain in 1% of their patients after carpal tunnel release. They attributed this pain to the pisotriquetral joint, whose mechanics are altered by division of the TCL. Treatment consisted of excision of the pisiform in cases with transient response to steroid injection of the joint. We have no evidence to substantiate this theory or to recommend this approach.
PRONATOR SYNDROME
The term pronator syndrome was initially coined to describe compression of the median nerve in the proximal forearm beneath the pronator teres muscle. Since then, common usage has evolved so that it now denotes compression of the median nerve in the proximal forearm and about the elbow (59).
Pathophysiology and Anatomy
The median nerve lies anterior to the brachial artery and medial to the biceps muscle in the midarm. In the distal arm, it crosses the brachial artery to lie medial to it, coursing on the brachialis muscle. The supracondylar process is an anomalous spur arising on the anteromedial aspect of the distal humerus, 5 cm proximal to the medial epicondyle, in as many as 3% of individuals. The ligament of Struthers is a fibrous band that may arise from the supracondylar process (spur) of the humerus (7) and attaches to the medial epicondyle, forming a fibro-osseous tunnel through which the median nerve and, at times, the brachial artery pass (Fig. 52.18) (66). The median nerve enters the antecubital fossa coursing beneath the lacertus fibrosus (bicipital aponeurosis), then travels between the superficial (humeral) and deep (ulnar) heads of the PT muscle. It continues distally beneath the arch of origin of the flexor digitorum superficialis (FDS), coming to lie between it and the flexor digitorum profundus (FDP). The median nerve maintains this relationship throughout its course to the wrist. Potential sites of compression include the supracondylar process and the ligament of Struthers, the lacertus fibrosus, the arch of the origin of the PT, and the arch of the origin of the FDS (Fig. 52.26, Table 52.4).
Figure 52.18. The ligament of Struthers. (From Stern PJ, Fassler PR. Pronator Syndrome. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991:995, with permission.)
Figure 52.26. A: Division of the lacertus fibrosus. B: Exposure of the median and anterior interosseous nerves and the arch of the superficialis. C: The radial origin of the superficialis muscle elevated by subperiosteal dissection to expose the deep volar compartment and the AIN. (From Eversmann WW Jr. Entrapment and Compression Neuropathies. In: Green DP, ed. Operative Hand Surgery. New York: Churchill Livingstone, 1982:1341, with permission.)
Table 52.4. Potential Compression Sites of the Median Nerve in Pronator Syndrome
Assessment
The symptoms arising from compression of the median nerve at this level, including numbness in the radial three and one-half digits and thenar weakness, may be attributed to CTS. In pronator syndrome, unlike in CTS, paresthesias are typically absent at night. Important additional symptoms that may help differentiate this condition from CTS are pain in the anterior aspect of the proximal forearm and numbness in the thenar region—the territory of the palmar branch of the median nerve that does not travel through the carpal tunnel, having branched from the median nerve several centimeters proximal to the wrist. Sensory threshold testing detects decreased sensation in the radial three and one-half digits, as in CTS, with the addition of numbness in the thenar eminence, the area innervated by the palmar cutaneous branch (Fig. 52.8A). The findings of weakness and atrophy in the thenar musculature
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may be indistinguishable from those seen in CTS, although they are less severe and are most often absent.
The portion of the physical examination that will further differentiate pronator syndrome from CTS is provocative testing. Phalen’s test should be negative, but it may be positive (47,95). Tinel’s percussion test, in which the median nerve is percussed at the level of the pronator muscle, elicits paresthesias in the distribution of the median nerve in the proximal forearm rather than at the carpal tunnel (Fig. 52.19). To perform the pronator compression test, place direct thumb pressure just proximal and lateral to the proximal edge of the PT muscle belly (Fig. 52.20). (The brachial pulse will be palpable lateral to the nerve.) A positive test is reproduction of paresthesias in the median-nerve-innervated digits within 30 seconds, and it supports the diagnosis of pronator syndrome (38). According to Olehnik et al. (95), the pronator compression test is the most accurate diagnostic test. Several tests have been designed to give clues to the specific site of compression of the median nerve in pronator syndrome. The production of pain or aggravation of paresthesias with simultaneous resisted forearm supination and resisted elbow flexion beyond 120° indicates probable entrapment of the median nerve at the lacertus fibrosus (Fig. 52.21) (7,33,58,115,122). Entrapment of the nerve between the two heads of the PT muscle is indicated by elicitation of paresthesias in the median nerve sensory distribution with resisted forearm pronation while the elbow is slowly extended from full flexion (Fig. 52.22) (33,58,121,122). Paresthesias elicited in the radial three and one-half digits with resisted independent flexion of the proximal interphalangeal (PIP) joint of the long finger suggest entrapment beneath the superficialis arch of origin (Fig. 52.23, Table 52.5) (33,122).
Figure 52.19. Tinel’s percussion test in the proximal forearm for evaluation of pronator syndrome.
Figure 52.20. The pronator compression test.
Figure 52.21. Testing for entrapment of the median nerve at the lacertus fibrosus in pronator syndrome.
Figure 52.22. Testing for entrapment of the median nerve at the pronator in pronator syndrome.
Figure 52.23. Testing for entrapment of the median nerve at the arch of the flexor digitorum superficialis in pronator syndrome.
Table 52.5. Carpal Tunnel versus Pronator Syndrome
Special diagnostic procedures include electrodiagnostic studies and radiographs of the elbow. Median nerve conduction velocities from the elbow to the wrist are decreased in less than one third of cases (16,47,95). The value of obtaining these studies is to evaluate for the presence of CTS. A normal conduction velocity at the level of the wrist supports proximal compression of the median nerve in the presence of symptoms and signs of pronator syndrome. A study consistent with CTS indicates the necessity
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of treatment directed at the wrist but does not rule out a double crush phenomenon, with compression both at the carpal tunnel and in the proximal forearm. Failed carpal tunnel releases that respond to subsequent operative release in the proximal forearm support the occurrence of simultaneous compression of the nerve at these two sites (95). Four views of the elbow—anteroposterior (AP), lateral, and two obliques—are obtained to evaluate the presence of a supracondylar process. Although its presence is suggestive of compression of the median nerve beneath the ligament of Struthers, it is not pathognomonic; this is a very rare site of entrapment. The absence of a supracondylar process does not rule out the presence of a ligament of Struthers and entrapment at this site (Table 52.6).
Table 52.6. Pronator Syndrome Summary
Preoperative or Nonoperative Management
Nonoperative treatment consists of anti-inflammatory medications, splinting, and rest for 4–6 weeks. Modification of activities is particularly important because symptoms are often related to repetitive elbow flexion and extension and to forearm pronation and supination. Physiotherapy in the form of massage, stretching, and iontophoresis to mobilize and relax potentially tight structures may be helpful. Carefully placed steroid injections in the site of maximal tenderness and pain (but not into the nerve) may be useful for diagnostic and therapeutic purposes.
Surgical Indications and Relative Results
Surgery generally is not necessary because most patients respond to nonoperative care. Surgery is indicated in those cases where symptoms persist longer than 6 weeks to 3 months following adequate conservative management.
Improvement after surgical release is reported in approximately
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80% to 90% of cases (38,47,59,95). Complete relief of symptoms occurs in only about one third of those who improve. There appears to be no preoperative indicator of which patients will have the better results (95). As in CTS, return to work will depend in part on the demands of the patient’s particular vocation. Of the 36 patients in the series reported by Olehnik et al. (95), 25 returned to their preoperative or similar occupations and eight returned to work but had to change jobs. The final work status of the remaining three patients was unknown.
Preoperative Planning
To plan the surgical incision, you must determine whether the site of compression is above or below the elbow. If there is evidence of compression under an arcade of Struthers, center the surgical exposure at the radiographic projection of the supracondylar process. If the compression is below the elbow, extend the incision distal to the elbow flexion crease onto the forearm to expose the pronator and the arch of the FDS.
Technique for Release of Compression at the Ligament of Struthers
  • Center the incision over the supracondylar process and make it in line with the medial neurovascular bundle anterior to the medial intermuscular septum (Fig. 52.24).
    Figure 52.24. Entrapment of the median nerve (MN) under a ligament of Struthers. A: Initial appearance. B: The ligament divided and elevated (arrow). C: Supracondylar process (arrow).
  • Palpate the supracondylar process and expose the ligament of Struthers.
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  • The median nerve, brachial artery, and sometimes the ulnar nerve lie within the proximity of the supracondylar process; therefore, proceed; cautiously with dissection.
  • Divide the ligament of Struthers and excise the supracondylar process.
  • Continue distally and divide the lacertus fibrosus. This is done routinely in decompression of the median nerve for these cases and for others that do not involve compression at the supracondylar process. The lacertus fibrosus may act as a compressive band across the flexor muscle mass in supination and hence should be divided with any exploration of the median nerve.
  • If you do not find a ligament of Struthers, you must discover the area of compression by additional dissection distally.
Technique for Release of Compression Distal to the Ligament of Struthers
  • Begin the incision along the projection of the medial neurovascular bundle, 5 cm proximal to the elbow flexion crease.
  • Continue it in a gentle curve along the elbow flexure, and extend it distally past the superficialis arch (Fig. 52.25).
    Figure 52.25. Extensile approach for the exposure of the median nerve at the elbow and proximal forearm.
  • Protect the medial antebrachial cutaneous nerve from injury.
  • Raise full-thickness flaps radially and ulnarly off the forearm muscle fascia.
  • Identify the median nerve proximal to the lacertus fibrosus and the PT (Fig. 52.26A).
  • The lacertus fibrosus originates from the anteromedial aspect of the musculotendinous junction of the biceps and travels distally and medially, crossing the median nerve and brachial artery to blend into the fascia of the flexor pronator muscle mass. Divide it in line with the course of the median nerve.
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  • Follow the median nerve distally as it passes between the two heads of the PT.
  • Detach the superficial head of the pronator from its distal conjoined tendon with the deep head, using a stepcut or long oblique incision designed to allow reattachment of the superficial head with relative lengthening (122). This requires dissection distal to the midforearm level.
  • Reflect the superficial head ulnarly (Fig. 52.26B).
  • Identify the arch of the FDS, which lies in the distal portion of the wound, deep to the pronator. Expose the FDS by reflection of the superficial head of the pronator.
  • Follow the median nerve as it courses deep to the arch of the FDS.
  • Detach the radial origin of the FDS (Fig. 52.26C) or, alternatively, divide it in line with its fibers between its radial and ulnar halves to expose and decompress the median nerve.
  • Reattach the superficial pronator at a point proximal to its original insertion or in a lengthened position, using the stepcut.
  • Close the skin.
Alternative incisions that are oriented fairly transversely, with a goal of minimizing unsightly scarring, have been described (38). These have been criticized for not providing adequate exposure of the nerve and the sites of compression (58). Olehnik et al. (95) described an oblique incision centered over the point of maximal tenderness in the proximal forearm (Fig. 52.27). The fascia was then split longitudinally to allow adequate access to the soft-tissue structures in the antecubital fossa to the midforearm. Deep digital palpation and dissection were used to evaluate for compression of the nerve proximally by a ligament of Struthers. They additionally released intramuscular fascial bands of the PT and FDS that crossed the nerve. The authors of this study point out the importance of tracing the nerve along its course, releasing all fibrous bands and vascular structures that are potential sites of compression.
Figure 52.27. An oblique incision 3 months after surgery for decompression of the median nerve in pronator syndrome. (From Olehnik WK, Manske PR, Szerzinski J. Median Nerve Compression in the Proximal Forearm. J Hand Surg [Am] 1994;19:121, with permission.)
Postoperative Care and Rehabilitation
After skin closure, apply a well-padded compression dressing and a posterior plaster splint with the elbow flexed at right angles and the forearm in semipronation. Encourage shoulder and finger motion immediately after the operation. After 5 days, discontinue immobilization; allow the patient to resume elbow flexion and extension and forearm rotation and to gradually return to full activities as tolerated.
Complications
As for CTS, misdiagnosis and technical factors are responsible for most complications. The most important is failure to release constriction at one of the four sites of possible entrapment. You must also address all other potential sources of compression by visualizing the nerve along its course. Avoid accidental damage to branches of the median nerve by initially exposing and dissecting the nerve along its lateral aspect, which is free of branches.
ANTERIOR INTEROSSEOUS NERVE SYNDROME
Pathophysiology and Anatomy
The anterior interosseous nerve (AIN) is a branch of the median nerve that is essentially entirely motor except for a few terminal branches that are sensory to a portion of the carpus. The most common pattern of muscles innervated by the AIN includes the FDP to the index finger, the flexor pollicis longus (FPL), and the pronator quadratus (PQ). This innervation pattern varies significantly, which can cause confusion during clinical examination. The nerve arises from the dorsal aspect of the median nerve as it passes between the two heads of the PT. In some cases, it passes deep to the deep head of the PT. It passes beneath the arcade of the FDS and courses distally along the anterior surface of the interosseous membrane between the FDP and the FPL, accompanied by the anterior interosseous artery. The AIN gives branches to the FPL and the radial aspect of the FDP muscles approximately 4 cm distal to its origin from the median nerve (Fig. 52.28). Compression may be caused by one of many structures, including the deep head of the PT, the FDS, accessory muscles (e.g., Gantzer’s muscle, and an accessory FPL) (28,74), aberrant vessels (e.g., anomalous radial artery), and tendinous bands along the course of the nerve.
Figure 52.28. The course and innervations of the anterior interosseous nerve. (From Chidgey LK, Szabo RM. Anterior Interosseous Nerve Palsy. In: Szabo RM, ed. Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare, NJ: Slack, 1989:153, with permission.)
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Assessment
Patients initially complain of vague, aching pain in the proximal forearm and sometimes in the wrist. This occurs at rest and is exacerbated by activities. There is no sensory deficit with AIN syndrome, which is different from carpal tunnel and pronator syndromes. Patients may note difficulty with activities such as writing, or weakness in tip pinch. Frequently, there is a history of a single episode of strong contraction of elbow, wrist, and finger flexors accompanied by pain and followed shortly thereafter by motor loss.
Findings on clinical examination include weakness or paralysis of the muscles innervated by the AIN (18). Weakness of the FPL and of the radial half of the FDP makes it difficult or impossible for the patient to tip pinch with the index finger and thumb (i.e., to make the so-called OK sign). The lack of long flexors results in a hyperextension attitude of the distal joints of these two digits (Fig. 52.29) (119). You can test the weakness of the PQ by asking the patient to pronate against resistance, with the elbow flexed to neutralize the stronger PT. However, isolated paralysis of any one or a combination of these muscles has been reported (50).
Figure 52.29. Incomplete anterior interosseous nerve syndrome. A: Preoperative loss of flexion of the right thumb. B: Postoperative result.
It is important to differentiate between an FDP or FPL rupture and AIN syndrome in the patient with acute presentation. This is done best by looking for the tenodesis effect of the FPL and index FDP (79). Innervation anomalies add variability to the classic examination findings. Martin-Gruber connection (median to ulnar motor nerve connection in the forearm) occurs in 15% of individuals; 50% of these arise from the AIN. The presence of this anomaly may cause weakness of additional intrinsic muscles
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of the hand in patients with AIN syndrome. Additionally, in 50% of individuals, the FDP to the index is innervated by branches from the median nerve, not the AIN (50). The diagnosis is usually confirmed by EMG studies. Nerve conduction studies are usually not affected, although side-to-side differences may be noted (Table 52.7).
Table 52.7. Anterior Interosseous Nerve Syndrome Summary
Preoperative or Nonoperative Management
In a patient who presents acutely, obtain neurodiagnostic studies 2–3 weeks after injury, and again at 6 and 12 weeks if no clinical improvement is noted. Chronic cases, presenting after 6 weeks, should have neurodiagnostic examination performed initially and the patient should be followed clinically; if no improvement is noted, perform another study at 12 weeks after the injury. Although no specific protocols have been evaluated, nonoperative treatment may consist of avoidance of exacerbating activities, immobilization of the elbow in flexion and the forearm in pronation, and the use of NSAIDs.
Surgical Indications and Relative Results
Essentially all reported cases have gone on to spontaneous recovery, although in some instances this has taken up to 2 years. Most authors agree that recovery can be enhanced by surgical exploration when spontaneous recovery is not apparent or is slow (50). Recovery is generally complete within 6 months after surgery. Persistence of the motor symptoms without signs of significant improvement for 8–12 weeks is an indication for surgical exploration and decompression (122). Evidence of clinical motor recovery or signs of reinnervation on EMG would call for further observation.
Operative Technique
The surgical technique and postoperative management are very similar to those used in the pronator syndrome.
  • Use the same incision as for pronator syndrome.
  • Divide the lacertus fibrosus to allow access to the median nerve as it passes beneath the superficial head of the PT (Fig. 52.26A).
  • The AIN branches from the median nerve just distal to the proximal border of the superficial head of the pronator. Trace it beneath this muscle. This is a common site of entrapment.
  • If necessary for exposure, you may detach the superficial head of the pronator (Fig. 52.26B).
  • Trace the nerve distally as it passes beneath the FDS. If necessary, detach the origin of this muscle or divide its fibrous arch, as in pronator syndrome exploration, to trace the nerve distally (Fig. 52.26C).
  • Trace the nerve as it travels along the anterior interosseous membrane between the FPL and FDP muscles.
  • Terminate the distal dissection when you visualize the branches to the deep flexors.
  • Reattach the FDS muscle. (This may be done posterior to the median nerve if you feel that anterior transposition is necessary.)
  • Reattach the PT superficial head deep to the median nerve and AIN.
  • Close the skin and place a long-arm splint.
As in pronator syndrome, it is important to visualize the entire nerve and divide all suspected offending structures. The postoperative management is essentially identical to that after treatment of the pronator syndrome.
Complications
Possible complications are similar to those described for the carpal tunnel and PT syndromes. The main problem is an error in diagnosis, particularly for the patient with an incomplete syndrome involving either the thumb or the index long flexors, but not both (Fig. 52.29) (50). Such a
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presentation may lead to the erroneous diagnosis of tendon rupture and to a negative tendon exploration. Perform the tenodesis test with the wrist in maximal extension along with MP joint and PIP joint extension. This should produce slight flexion at the distal interphalangeal (DIP) joint of the index and the IP joint of the thumb with AIN syndrome but not with tendon rupture (79).
Suspect Parsonage–Turner syndrome (brachial neuritis) in cases with an acute onset of pain in the forearm followed by weakness in the muscles normally affected in AIN syndrome a few days to weeks later (at times associated with a febrile illness, vaccination, or unrelated surgery), especially in bilateral cases (149). In Parsonage–Turner syndrome, there will also be shoulder pain and involvement of the shoulder muscles at times. AIN compression syndrome generally presents after an acute injury or in conjunction with repetitive activity, whereas brachial neuritis is insidious in nature. In Parsonage–Turner syndrome there is pain not associated with an injury, which may involve more proximal areas of the upper extremity than that seen in AIN syndrome. Parsonage–Turner syndrome often produces EMG results similar to those of AIN syndrome in the FPL, FDP, and PQ. Sampling of more proximal muscles innervated by the brachial plexus, such as the deltoid, may also demonstrate EMG abnormalities, which is different from AIN entrapment (Table 52.8).
Table 52.8. AIN Syndrome versus Parsonage–Turner Syndrome
Complete recovery is seen in 90% of cases treated surgically or nonoperatively. Surgical exploration and decompression are reserved for cases associated with trauma.
COMPRESSION NEUROPATHIES OF THE ULNAR NERVE
CUBITAL TUNNEL SYNDROME
Pathophysiology and Anatomy
The most common location for entrapment of the ulnar nerve is about the elbow; this condition is known as cubital tunnel syndrome. There are five potential compression sites of the nerve that occur along its course. At the midarm level, the ulnar nerve pierces the medial intermuscular
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septum and runs distally posterior to it. Approximately 8 cm proximal to the medial epicondyle, the nerve may pass through an inconstant fibrous tunnel, the arcade of Struthers, formed by a band connecting the medial intermuscular septum to the tendon of the medial head of the triceps. This is the first potential site of compression (Fig. 52.30). The nerve continues posterior to the intermuscular septum. The edge of the septum becomes a second potential site of compression, usually after failed anterior transposition. The nerve then comes to lie in the retrocondylar groove of the medial epicondyle, the third potential site of compression, where it gives off a few articular sensory branches to the elbow joint; it then enters the cubital tunnel, the fourth potential site of compression. The cubital tunnel is a fibro-osseous canal formed by the medial epicondyle anteriorly, the ulnohumeral ligament posterolaterally, and a structure termed the cubital tunnel retinaculum (92), which is superficial and forms the roof of the tunnel. The fifth potential site of compression occurs as the nerve passes under Osborne’s fascia, a thick fascial layer that connects the heads of the FCU to the medial epicondyle and olecranon in nearly 80% of individuals and is often confluent with the cubital tunnel retinaculum (24). The nerve then courses to enter the forearm between the two heads of the FCU. At this level, it gives off several motor branches to the FCU. It comes to lie medial to the FDP, piercing the deep flexor pronator aponeurosis—a fascial structure serving as a common origin and aponeurosis of the humeral head of the FDS and the FCU—as it exits the cubital tunnel (61). This aponeurosis is the sixth and most distal potential compression site, and it, like the medial intermuscular septum, is usually a site of secondary compression after anterior transposition (Fig. 52.31, Table 52.9).
Figure 52.30. The first five potential compression sites of the ulnar nerve in cubital tunnel syndrome: (a) arcade of Struthers, (b) medial intermuscular septum (considered a secondary site of compression), (c) medial epicondyle, (d) cubital tunnel, (e) Osborne’s fascia. (From Osterman AL, Davis CA. Subcutaneous Transposition of the Ulnar Nerve for Treatment of Cubital Tunnel Syndrome. Hand Clin 1996;12:421, with permission.)
Figure 52.31. The sixth potential site of compression of the ulnar nerve in cubital tunnel syndrome, the flexor pronator aponeurosis.
Table 52.9. Potential Compression Sites of the Ulnar Nerve in Cubital Tunnel Syndrome
Compression of the nerve is often of a dynamic nature. Both constriction of the nerve and traction are implicated in its dysfunction. Flexion of the elbow has been shown to cause increased intraneural pressure in the ulnar nerve at the cubital tunnel and decreased volume in the cubital tunnel itself (92). The ulnar nerve at the elbow normally
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glides to accommodate elbow flexion (6). When tethered by scar or fibrosis, the ulnar nerve experiences traction forces, which affect nerve function.
Additional causes of compression include trauma, deformity (e.g., cubitus valgus), malunion or nonunion of the medial epicondyle, elbow instability, spurs or bone fragments within the floor of the cubital tunnel (Fig. 52.32), tumors, abnormal muscles (e.g., anconeus epitrochlearis), and a nerve that subluxates or dislocates repeatedly over the medial epicondyle.
Figure 52.32. A: Compression of the ulnar nerve at the elbow by a large osteochondral body (arrow). B: Severe nerve constriction (between arrows) after removal of the osteochondral fragment.
Assessment
The presenting complaint is usually numbness and paresthesias along the ulnar nerve distribution, the small finger, the ulnar half of the ring finger, and the ulnar aspect of the hand (Fig. 52.8). This is exacerbated by leaning on the elbow or positioning it in flexion. Aching pain may be referred to the medial aspect of the elbow. Numbness on the medial half of the forearm is not usually present.
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Weakness of grip or loss of dexterity in the fingers may accompany these symptoms.
Physical examination includes sensory evaluation, provocative testing, and motor examination. Threshold sensory evaluation, including Semmes–Weinstein monofilaments and vibratory testing, is most sensitive and is recommended. Two-point discrimination yields abnormal results in more advanced cases. Sensation is decreased in the ring and small fingers as well as in the ulnar half of the dorsum of the hand, which indicates compression proximal to the origin of the dorsal cutaneous branch of the ulnar nerve and therefore proximal to the wrist.
Employ provocative testing to help localize the site of compression, as well as uncover dynamic forms of the disorder. Tinel’s test is positive if paresthesias are elicited in the distribution of the nerve when it is gently percussed. The location of percussion with maximal elicitation of symptoms may indicate the site of compression. Tinel’s test is sensitive but not specific, giving a high rate of false positive results at the cubital tunnel (23). The elbow flexion test described by Buehler and Thayer (17) and others (101), which is flexion of the elbow beyond 90° with the forearm in supination and the wrist in extension, is positive when symptoms are produced within 1 minute, and it may localize compression to the level of the elbow. Novak et al. (90) modified this test to include direct compression of the ulnar nerve with the examiner’s finger just proximal to the cubital tunnel while the elbow is flexed maximally (Fig. 52.33). The test is considered positive when paresthesia symptoms are produced in the ulnar nerve distribution within 30 seconds. This test is reported to have 0.91 sensitivity and 0.97 specificity. Evaluate potential subluxation of the ulnar nerve over the medial epicondyle by direct palpation while the elbow is brought from full extension to full flexion. Ulnar nerve subluxation is seen in 16% of normal individuals (20) and therefore is not considered pathologic per se. If associated with neuritic symptoms, it may be the cause of injury to the nerve. Palpation may also elicit tenderness and disclose an enlarged, sensitive nerve.
Figure 52.33. The flexion compression test for cubital tunnel syndrome.
Motor examination is helpful in patients with more advanced disease. Atrophy may be seen most commonly in the hypothenar musculature and in the first dorsal interosseous muscle. When weakness is present, it involves not only the ulnar innervated intrinsic muscles but typically the FDP to the ring and small fingers. When both ulnar innervated intrinsic and extrinsic muscles are involved, the ulnar claw hand, a sign of intrinsic–extrinsic imbalance, does not appear as severe. Grip strength testing is often normal unless there is significant loss of power to the long flexors of the ring and small finger. Pinch strength, especially key position, is decreased as a result of loss of strength to the flexor pollicis brevis (FPB), the adductor pollicis, and the first dorsal interosseous muscle. Froment’s sign (hyperflexion of the IP joint) and Jeanne’s sign (hyperextension of the MP joint of the thumb) are elicited during key pinch (Fig. 52.34). Weakness or paralysis of the FPB concentrates the flexion force of the FPL at the IP joint, causing hyperflexion of this joint (11). The EPL compensates for the adductor pollicis and enhances hyperextension
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of the MP joint of the thumb because it is unopposed by the intrinsic flexor of the thumb (the EPB).
Figure 52.34. Froment’s sign and Jeanne’s sign, seen with intrinsic muscle weakness in ulnar nerve palsy.
For subjective evaluation, directly test the strength of the first dorsal interosseous muscle against resistance, and measure it by side-to-side comparison in unilateral cases. In some individuals, contribution of innervation to this muscle from the median nerve can occur (109), and therefore this test is not specific. Evaluation of the abductor digiti quinti is also subjective. Side-to-side comparison is facilitated by a confrontation test. Ask the patient to maximally abduct her fingers while holding her hands out in front, palms facing her. She brings the tips of her small fingers together and, while she resists collapse of the abducted small fingers, she brings her hands together. In unilateral cases with abductor weakness, the weak hand’s small finger collapses to the side of the ring finger (Fig. 52.35).
Figure 52.35. The confrontation test.
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Wartenberg’s sign is abduction of the small finger with extension of the fingers at the MP joint level. It indicates interosseous dysfunction. The cross finger test (30) is very useful and also evaluates function of the interossei. Ask the patient to cross his index and long fingers. Patients with ulnar nerve dysfunction often have trouble performing this task. Atrophy and weakness of intrinsic muscles innervated by the ulnar nerve indicate a moderate to severe lesion of the nerve (Table 52.10).
Table 52.10. Provocative Tests for Cubital Tunnel Syndrome
Radiographs are indicated in cases of previous trauma, deformity, and suspected arthritis, and where there is incomplete range of motion. AP, lateral, and oblique views are obtained, as well as axial views of the distal humerus and olecranon for evaluation of the ulnar groove.
Neurodiagnostic studies include NCV and EMG evaluation. These are helpful in confirming the diagnosis and in classifying the case for treatment and prognostic purposes. NCV evaluations of the segment of the ulnar nerve across the elbow are considered significant if conduction values are reduced by 33% (33). Segmental “inching” studies may be helpful in localizing the site of compression, especially in previously operated cases with recurrence of symptoms. EMG evaluation of the ulnar innervated muscles can provide information on chronicity and progression as well as severity, and it may indicate the approximate site of compression. More importantly, EMG needle examination coupled with somatosensory evoked potential (SSEP) evaluates for radiculopathies and more proximal lesions, including thoracic outlet syndrome (TOS), which is suspected especially in cases of bilateral ulnar nerve symptoms (Table 52.11).
Table 52.11. Cubital Tunnel Syndrome Summary
Classification
Dellon (26) developed a useful classification system for cubital tunnel syndrome (Table 52.12). He classified patients into mild, moderate, and severe categories depending on physical and electrodiagnostic findings. Surgical treatment options and the relative results with respect to the patient classification will be discussed.
Table 52.12. Staging of Ulnar Nerve Compression at the Elbow
Preoperative or Nonoperative Management
Neither vitamin B6 nor NSAIDs have been shown to have an effect on cubital tunnel syndrome. Injections are advocated by some. Two of us (MNH and JT) occasionally use them. Water-soluble steroid is injected at the proximal aspect of the cubital tunnel, not into the tunnel. Take great care to avoid injury to the ulnar nerve, which is at risk. Most agree, though, that injection is to be avoided because of the great risk of injury to the nerve, especially if injection is made into the cubital tunnel where the nerve is tightly confined.
The most effective nonsurgical management of cubital tunnel syndrome includes patient education and splinting. The occupational or physical therapist instructs the patient in nerve protection. This includes avoidance of repetitive flexion and extension of the elbow, of prolonged positioning of the elbow in the flexed position, and of leaning on the medial aspect of the elbow. Adjustments are made in the height of work stations and seats when indicated, so that the elbow is flexed no more than 30° during work. Elbow pads may be worn to prevent direct pressure on
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the nerve in its subcutaneous position (Fig. 52.36). Hand therapists can provide Thermoplast or pillow extension splints that hold the elbow in 30° to 45° of flexion during sleep to prevent hyperflexion (Fig. 52.37). Recheck the patient after 3 months of treatment. In mild cases and some moderate ones, patients who comply with these instructions may have a good response and be able to avoid surgery.
Figure 52.36. Commercially available elbow pads worn to protect the ulnar nerve from mechanical irritation.
Figure 52.37. Thermoplast night splints custom fabricated by a hand therapist.
Surgical Indications and Relative Results
Progression or inadequate amelioration of symptoms with nonoperative care is an indication for surgery. Inability of the patient to comply with nonsurgical care in mild or moderate cases is a relative indication. Severe involvement, including motor dysfunction, requires surgical intervention. Ulnar neuropathies associated with deformity, bony lesions, tumors, and elbow instabilities, among others, require attention to the pathology contributing to the nerve compression as well as the nerve itself.
The severity of disease, its chronicity, and the general condition of the patient all influence the outcome of treatment. Patients with intermittent symptoms, no atrophy, and mild electrodiagnostic findings respond well to nonoperative treatment (32). The choice of surgical procedure in some instances may also have an effect. In most uncomplicated cases, return of sensation and motor function occurs within 6 months. Nouhan and Kleinert (89) evaluated 33 limbs that had been followed for an average of 49 months. Preoperative nerve compression was classified as mild in 6, moderate in 7, and severe in 20. Surgical treatment consisted of submuscular transposition with Z-lengthening of the flexor pronator mass. There were 97%
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good to excellent results overall; the preoperative classification did not influence the final result.
Seradge and Willis (114) evaluated the results of 160 cases undergoing cubital tunnel release and medial epicondylectomy. Preoperative severity of compression was mild in 7%, moderate in 86%, and severe in 7%. There were 87% good, 12% fair, and 1% poor results (failure of treatment). Factors that increased the rates of symptom recurrence in their patients included female sex, the presence of concomitant CTS or TOS in the same extremity, age in the third or fourth decade, and patients who did not return to work within 3 months after surgery. Limb dominance, length of preoperative conservative care, and EMG results did not have a relationship to recurrence rate.
In a literature review by Dellon (26), patients in the mild group had excellent results from surgery no matter what technique was used. Patients in the moderate group did not improve without surgery, and decompression in situ was not effective. Medial epicondylectomy produced 50% excellent results with a high recurrence rate, whereas submuscular transposition gave 80% excellent results with the lowest recurrence rate. In severe patients, surgery resulted in less than 50% excellent results for sensory recovery and up to 25% for motor recovery. Recurrence developed in 30% of these patients. In this group, the poorest results were in those undergoing intramuscular transposition, and the best were in those receiving submuscular transposition and internal neurolysis.
Preoperative Planning
When a particular condition contributes to compression of the ulnar nerve, consider additional diagnostic studies to further delineate the pathology. Computed tomography (CT) scans can further characterize suspected bony abnormalities, including space-occupying spicules or fragments, fracture callus, and malunions or nonunions. Suspected tumors are best visualized by magnetic resonance imaging (MRI) evaluation. Progressive deformities (e.g., cubitus valgus due to nonunion of the lateral condyle) must be stabilized at the time of decompression and transposition of the nerve, or in a staged fashion. Patients with previously failed decompressions should undergo inching nerve conduction velocities to better localize the site of compression, most often in the most proximal or distal portion of the previous surgical exposure.
Better than 80% to 90% good results are obtainable with any of the commonly employed operative methods. The choice of operative technique is greatly influenced by the cause of the compression, the patient’s age, and systemic conditions such as diabetes or alcoholism. Operative techniques include simple decompression, medial epicondylectomy, subcutaneous transposition, intramuscular transposition, and submuscular transposition. The nerve may be decompressed by simple division of the arch of origin of the FCU (or the cubital tunnel) in the following cases: (a) if clinical findings (e.g., a localized nerve percussion sign) suggest isolated entrapment of the nerve beneath the arch (or cubital tunnel retinaculum), (b) if the nerve presents a constricting groove caused by this arch (or retinaculum), as visualized during operation (Fig. 52.38), or (c) if the nerve is vulnerable to manipulation (e.g., in older patients or patients with diabetic or alcoholic neuropathy) (148).
Figure 52.38. Well-defined constriction of the ulnar nerve (arrow), seen after division of the arch of origin of the flexor carpi ulnaris.
Anterior submuscular transposition is best suited for neuropathies associated with elbow deformity, abnormalities of the cubital canal, and the subluxing or dislocating ulnar nerve, particularly in the younger population and in the more severe cases with evidence of motor involvement (66,69). A particular indication for medial epicondylectomy is the ulnar neuropathy associated with nonunion of a fracture of the medial epicondyle. Routine use of this technique has been shown to be effective (48,60). Some prefer anterior subcutaneous transposition over submuscular transposition (1,31,99,104). Subcutaneous transposition is commonly employed as part of other operative procedures about the elbow, including fracture reduction, elbow arthroplasty, and neurorrhaphy of the ulnar nerve in cases where there is loss of nerve length.
Dissection of the ulnar nerve is delicate and requires patience and diligence to prevent damage to the nerve, its branches, and its accompanying blood supply. This is aided by use of magnification, fine instruments, and bipolar cautery. A trained surgical assistant is invaluable in facilitating these procedures and in adding a level of safety to prevent potential complications related to nerve injury.
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In Situ Decompression
  • Start the skin incision equidistant between the olecranon and the medial epicondyle; extend it 3–4 cm proximally and 6–8 cm distally (Fig. 52.39A).
    Figure 52.39. In situ decompression of the ulnar nerve at the cubital tunnel. A: Skin incision. B: Division of the arcuate ligament (cubital tunnel retinaculum). C: Extension of the incision into the interval between the two heads of the flexor carpi ulnaris to ensure distal decompression. (From Ferlic DC. In Situ Decompression of the Ulnar Nerve at the Elbow. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991;1063, with permission.)
  • Isolate the ulnar nerve before it enters the cubital canal.
  • Delineate the arch of origin of the FCU, elevate it from the nerve, and divide both it and Osborne’s fascia while protecting the nerve under direct visualization (Fig. 52.39B).
  • Extend this division distally between the two heads of the FCU to allow room for the nerve (Fig. 52.39C).
  • Flex and extend the elbow, and make sure the nerve does not sublux. If subluxation occurs, be prepared to transpose the nerve or perform a medial epicondylectomy.
  • Release the tourniquet for careful hemostasis.
  • Do not close the FCU heads beneath the ulnar nerve.
  • Close only the skin.
  • Apply a well-padded dressing.
Support the arm in a sling for a few days. Encourage immediate active flexion and extension of the elbow. Subluxation of the nerve after decompression is rare. On the contrary, nerves that are as tense as bow strings proximal to the constricting tendinous arch, snapping over the medial epicondyle during elbow flexion and extension, recover a normal excursion after decompression.
Medial Epicondylectomy
  • Center the incision over the medial epicondyle, and extend it proximally and distally far enough to expose all potential compression sites (Fig. 52.40).
    Figure 52.40. Skin incision for medial epicondylectomy (dark line). The dashed line represents a common position of a cutaneous nerve branch (usually from the medial antebrachial cutaneous), which must be protected during exposure. (From Heithoff SJ, Millender LH. Medial Epicondylectomy. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991:1088, with permission.)
  • Isolate the ulnar nerve as it enters the cubital tunnel.
  • Decompress the nerve in the cubital tunnel; lift the retinaculum off the nerve; protect the nerve and directly visualize it to prevent formation of a painful neuroma. Divide the retinaculum.
  • Trace the nerve into the FCU muscle. Divide the origin of the arch of the FCU.
  • Continue decompression of the nerve between the heads of the FCU; do not damage the multiple muscular branches in this area.
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  • Divide the deep flexor pronator aponeurosis until the nerve has been dissected 8 cm distal to the medial epicondyle.
  • Trace the nerve approximately 8 cm proximally.
  • Release the arcade of Struthers.
  • Excise the distal 8 cm of the intermuscular septum in the arm, taking care not to damage any of the vessels associated with the nerve. (Multiple vascular leashes exist near the insertion of the septum into the medial epicondyle.)
  • Make an incision directly over the medial epicondyle. Elevate the flexor pronator mass subperiosteally, both radially and ulnarly, while preserving the proximal attachments of the muscle mass (Fig. 52.41A).
    Figure 52.41. Medial epicondylectomy. A: Elevation of the flexor pronator mass. B: Removal of the medial epicondyle with an osteotome. C: Closure of the flexor pronator origin. (From Eversmann WW Jr. Entrapment and Compression Neuropathies. In: Green DP, ed. Operative Hand Surgery, 3rd ed. New York: Churchill Livingstone, 1993:1341, with permission.)
  • Perforate the base of the epicondyle where you will make the osteotomy with a small drill, Kirschner wire (K-wire), or osteotome.
  • Preserve the medial collateral ligament, which arises from the distal, inferior portion of the epicondyle.
  • Remove the epicondyle, cutting it in line with the medial cortex of the distal humerus (Fig. 52.41B). Perforating the planned osteotomy line with drill holes may be helpful.
  • Cover the raw bone surface with bone wax, and close the tendon of the flexor pronator mass (Fig. 52.41C). We recommend decompression of the nerve proximally and distally at all sites of potential compression.
  • Check that the ulnar nerve glides unimpeded during flexion–extension of the elbow.
  • Release the tourniquet and obtain hemostasis.
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  • Close only the skin after this.
  • Apply a well-padded dressing and a long arm posterior splint.
Postoperatively, leave the splint in place for 3–5 days. Then remove it and begin active range-of-motion exercises. Use a sling to protect the arm when it is not engaged in therapy. Full range of the elbow should be achieved by 3–4 weeks. At that time, begin progressive, gentle strengthening. Theoretically, the nerve will slowly transpose itself anteriorly and come to rest in a position without tension, anterior to or on the flexion–extension axis of the elbow. Seradge (112) demonstrated a decreased incidence of elbow contracture and a decrease in return-to-work time of 50% in patients who had mobilization of their elbows within 3 days of surgery following medial epicondylectomy versus those who were immobilized for 14 days postoperatively.
Anterior Transposition
The three methods of anterior transposition—subcutaneous, intramuscular, and submuscular—are essentially similar in their means of initial decompression and mobilization of the nerve, and this is described here. Both the way the transposition is maintained and the rehabilitation vary with the method, however, so they will be described under separate headings.
  • Center the incision between the olecranon and the medial epicondyle, and extend it along the axes of the humerus and ulna 8–10 cm proximally and distally.
  • Expose the deep fascia, and elevate the radial flap along this plane over the origin of the flexor–pronator muscles. Extend the exposure to adequately visualize the ulnar nerve along its course from the arcade of Struthers to well into the interval between the heads of the FCU and, laterally, to visualize the median nerve.
  • Isolate the ulnar nerve as it enters the cubital tunnel.
  • Decompress the nerve in the cubital tunnel; lift the retinaculum off the nerve, protect the nerve and directly visualize it, then divide the retinaculum.
  • Trace the nerve into the FCU muscle. Divide the origin of the arch of the FCU (Fig. 52.42A).
    Figure 52.42. Anterior transposition. A: Exposure of the ulnar nerve. B: Decompression carried distally and proximally. C: Excision of the distal 8 cm of the intermuscular septum. (From Spinner M, Linscheid RL. Nerve Entrapment Syndromes. In: Morrey BF, ed. The Elbow and Its Disorders, 2nd ed. Philadelphia: Saunders, 1993:813; and from Spinner M. Injuries to the Major Branches of the Forearm, 2nd ed. Philadelphia: Saunders, 1978, with permission.)
  • Continue decompression of the nerve between the heads of the FCU (do not damage the multiple muscular branches in this area), releasing Osborne’s fascia, the fascia of the two heads of the FCU, and the pronator aponeurosis.
  • Divide the deep flexor pronator aponeurosis 8 cm distal to the medial epicondyle.
  • Trace the nerve approximately 8 cm proximally.
  • Release the arcade of Struthers (Fig. 52.42B).
  • Excise the distal 8 cm of the intermuscular septum of the arm to prevent secondary impingement on the nerve after anterior transposition. Take care not to damage any of the vessels associated with the nerve. Multiple vascular leashes exist near the insertion of the septum into the medial epicondyle (Fig. 52.42C).
  • Mobilize the nerve from the cubital tunnel, preserving the small longitudinal vessels accompanying it.
  • You may need to divide small branches arising from the nerve to the joint; branches to the ulnar head of the FCU must be preserved. Carefully separate them proximally from the main trunk by interfascicular dissection, to allow mobilization of the nerve.
  • Make sure the nerve can be brought anterior to the medial epicondyle so that it lies in a relaxed course anterior to the flexion–extension axis of the elbow, none of the muscular branches to the FCU are under tension, and there is no kinking of the nerve proximally or distally.
Subcutaneous Transposition
Eaton et al. (31) described a technique (described next) that employs a fasciodermal sling fashioned from the fascia of the medial epicondyle and sutured into the dermis of the anterior skin flap (Fig. 52.43). The nerve comes to lie in the plane between the dermis and fat of the anterior flap, and the fascia of the flexor–pronator muscles, and it is maintained there by the sling. An alternative method for creation of a sling to maintain the anterior position of the nerve employs the medial intermuscular septum as described by Pribyl and Robinson (99). One of us (RMS) avoids the use of fascial slings and prefers to suture the fat of the lateral skin flap to the medial fascia to create a broad-based tunnel.
Figure 52.43. The fasciodermal sling for maintaining the ulnar nerve in its transposed position. (From Osterman AL, Davis CA. Subcutaneous Transposition of the Ulnar Nerve for Treatment of Cubital Tunnel Syndrome. Hand Clin 1996;12:421, with permission.)
  • Make a mark on the dermis of the anterior (radial) skin flap, approximately 1 cm anterior to the medial epicondyle, to indicate the site of attachment of the dermal sling.
  • Raise a strip of fascia from the flexor pronator muscles at least 1.5 cm in length, detaching it distally so that it hinges proximally from the medial epicondyle.
  • Transpose the nerve anterior to the hinge of the fascial flap.
  • Suture the fascial flap into the dermis of the anterior skin flap with nonabsorbable suture, at the mark. Take care to not damage cutaneous branches in the flap arising largely from the medial antebrachial cutaneous nerve.
  • Inspect the nerve in its position anterior to the fasciodermal sling. The nerve must not bend at the sling and may only bend at a 45° angle at the FCU hiatus with the elbow in flexion and extension. It must glide without tethering, and there must be enough space for a hemostat to be passed alongside it without difficulty.
  • Release the tourniquet and obtain hemostasis.
  • Close the skin.
Postoperative care consists of a splint and sling for approximately 5 days, followed by early active range-of-motion
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exercises. Weirich et al. (144) demonstrated average return to work and activities of daily living by 1 month in patients immediately mobilized after subcutaneous transposition, versus 2.75 months in those mobilized later than 7 days. By 2–3 weeks, the patient should regain nearly full range of motion of the elbow. Progress with strengthening thereafter, with a return to most activities by 6 weeks postoperatively.
Intramuscular Transposition
This technique was described by Adson at the turn of the century, and it was evaluated in a series published by Kleinman and Bishop in 1989 (63), from which the following description is derived. We do not use this technique as part of routine treatment for cubital tunnel syndrome.
  • Decompress and mobilize the ulnar nerve (Fig. 52.44A). Transpose it anteriorly to a position where it will lie without kinking or tension, and mark or note its position on the fascia of the flexor–pronator mass (Fig. 52.44B).
    Figure 52.44. Intramuscular transposition. A: Decompression and mobilization of the ulnar nerve. B: Transposition of the nerve to the flexor pronator fascia. C: Laying the nerve in a trough. D: Closing the fascia over the nerve. (From Kleinman WB. Anterior Intramuscular Transposition. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991:1069, with permission.)
  • Return the nerve to the ulnar groove, and make an incision in the fascia of the flexor–pronator musculature where the nerve lay in the previous step.
  • Along this incision, create a 5- to 10-mm-deep trough in the substance of the muscles. Sharply excise portions of the fibrous septae that cross the trough from within the bellies of the muscles so that the tissue contacted by the nerve will be muscle.
  • Lay the nerve in the trough. Ensure that its course is without sharp angles at the proximal and distal extents of the trough, and that it rests easily in the trough, beneath the level of the fascia (Fig. 52.44C).
  • Close the fascia over the nerve, and test the excursion of the nerve under the closure; it should glide without hindrance. Fascial closure is facilitated by placing the forearm in full pronation and the elbow in 90° of flexion (Fig. 52.44D).
  • Release the tourniquet and obtain hemostasis.
  • Close the skin.
  • Place the arm in a bulky splint that holds the forearm in 45° of pronation and the elbow in 90° of flexion.
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Postoperatively, hold the forearm in the semipronated position and the elbow in flexion for 3 weeks, then institute progressive range of motion exercises. Permit unrestricted use by 6 weeks.
Submuscular Transposition
Learmonth (66,69) provided the classical description of the technique of submuscular transposition of the ulnar nerve. He lengthened the flexor–pronator muscle mass by a stepcut, or Z-lengthening, of the common tendinous origin from the medial epicondyle to decrease the tension on the nerve in its anterior position on the fascia of the brachialis muscle and anterior capsule of the elbow (89).
  • Identify the lateral border of the flexor–pronator origin, and raise the anterior skin flap adequately to visualize it.
  • Identify the median nerve, which lies lateral to the flexor–pronator origin. The goal of the procedure is to place the ulnar nerve alongside the median nerve.
  • To gain access to the lateral margin of the muscles, cut the fascial reflection at this margin.
  • Using blunt dissection, elevate the flexor–pronator muscles from lateral to medial. This dissection begins distal to the flexor–pronator origin and proceeds between the flexor–pronator muscle group and the brachialis muscle and anterior elbow capsule.
  • The appropriate medial exit of this dissection is in the interval between the humeral and ulnar heads of the FCU. To facilitate completion of the lateral-to-medial dissection in this plane, identify the interval medially.
  • After the entire muscle mass is raised, detach it from its origin by creating a 90° stepcut in the common tendon, and turn it distally (Fig. 52.45A). Leave the posterior limb of the stepcut long and based on the epicondyle. To avoid damage to the medial collateral ligament complex of the elbow, you may use an elevator to dissect the muscle off the anterior elbow capsule. At this stage, ensure that the deep pronator aponeurosis, which forms a common intermuscular septum between the FCU and the humeral head of the FDS (Fig. 52.31), is divided adequately to avoid kinking of the nerve distally when it is transposed.
    Figure 52.45. Detachment of the flexor pronator mass from the medial epicondyle using a stepcut. A: Making the stepcut. B: Reattachment of the flexor pronator mass after transposition of the nerve. (From Rayan GM. Proximal Ulnar Nerve Compression: Cubital Tunnel Syndrome. Hand Clin 1992;8:325, with permission.)
  • Transpose the nerve anteriorly so that it lies next to the median nerve on the anterior surface of the brachialis muscle and tendon and the anterior joint capsule, where it will be deep to the flexor pronator mass.
  • Make certain there is no kinking of the nerve proximally at the arcade of Struthers (or the medial intermuscular septum) or distally at the deep pronator aponeurosis, and that the muscular branches of the nerve are not under tension (Fig. 52.46). Protect the posterior branch of the medial antebrachial cutaneous nerve.
    Figure 52.46. Anterior submuscular transposition. A: Extensile incision, allowing visualization of all potential compression sites. Note the proximity of the posterior branch of the medial antebrachial cutaneous nerve. B: Transposition of the nerve and reattachment of the muscles to the epicondyle. (From Spinner M, Linscheid RL. Nerve Entrapment Syndromes. In: Morrey BF, ed. The Elbow and Its Disorders, 2nd ed. Philadelphia: Saunders, 1993:813; and from Spinner M. Injuries to the Major Branches of the Forearm, 2nd ed. Philadelphia: Saunders, 1978, with permission.)
  • Release the tourniquet and carefully secure hemostasis.
  • Reattach the stepcut flexor–pronator origin in a lengthened position over the ulnar nerve with nonabsorbable suture, and reapproximate the heads of the FCU with absorbable suture (Fig. 52.45B) (25).
  • Close the skin.
  • Apply a well-padded dressing from the hand to the upper arm, with a posterior plaster splint.
Postoperatively, maintain the arm in plaster immobilization for 7–12 days. Then remove the immobilization, place the arm in a sling, and institute active range-of-motion exercises. The wrist can be protected from extending with a removable Velcro splint. Full elbow range is expected by 3 weeks, when the sling is removed. Restrict the patient from forceful gripping with the hand for an additional 1–3 weeks, but encourage light activities. Begin strengthening 4–6 weeks postoperatively, and have the patient return to nearly full activities at 6–9 weeks, with unrestricted use at 9–12 weeks depending on individual progress and demands.
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Complications
The most common causes of recurrent cubital tunnel syndrome are incomplete decompression and inadequate mobilization of the nerve at the time of transposition. Failure to decompress the nerve at the site of entrapment often results in failure to relieve symptoms, and this can be avoided by carefully evaluating all potential sites of compression. When initial relief of symptoms is followed by recurrence, common causes are kinking of the nerve proximally at the arcade of Struthers or on the margin of the intermuscular septum, and distally at the deep pronator aponeurosis. You can avoid this by making the incisions adequate for exposure and by examining the nerve at surgery, before closing the wound, to ensure that it is not entrapped by the procedure anywhere along its length.
Reoperation should be preceded by nonoperative care and repeat neurodiagnostics, including the inching studies previously mentioned, to evaluate for the potential site of secondary compression. When revision surgery is appropriate, the procedure of choice is submuscular transposition (26) unless this was the initial procedure. In that case, the choice of revision surgical technique is often determined at surgery, at which time the status of the nerve and its bed can be evaluated. The results of repeat decompression are poor in comparison to those of initial decompression (5,106). The medial antebrachial cutaneous nerve (particularly the posterior branch) is at risk for injury during the dissection. This injury commonly results in pain and an unhappy patient.
ULNAR TUNNEL SYNDROME
Pathophysiology and Anatomy
Ulnar tunnel syndrome is caused by the compression of the motor, sensory, or motor and sensory portions of the ulnar nerve in the canal of Guyon. The canal of Guyon is a confined fibro-osseous triangular space on the ulnar aspect of the volar wrist (Fig. 52.47). The roof of this space is formed by the volar carpal ligament proximally (the thickened distal extension of the antebrachial fascia, which becomes confluent with the tendinous insertion of the FCU onto the pisiform) and the pisohamate ligament distally (which is the extension of the FCU from the pisiform onto the hook of the hamate). The lateral wall is formed by the TCL proximally and the hook of the hamate distally. The medial wall is formed by the pisiform and its associated fibrous structures, and the abductor digiti minimi. The ulnar artery and nerve enter the canal of
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Guyon at the wrist, deep and radial to the FCU tendon, the artery lying radial to the nerve. In the proximal portion of the canal, the motor and sensory bundles of the nerve lie side by side as one nerve. Just at the distal margin of the pisiform, the nerve divides into deep and superficial branches. The deep branch, which is the motor division, dives through a fibrous arch formed by the origins of the abductor digiti minimi and flexor digiti minimi at the base of the hypothenar muscle group. It continues on to innervate the intrinsic muscles of the hand. The superficial branch continues on through the canal, beneath the pisohamate ligament, to course along the palmar surface of the hypothenar musculature and become, in its terminal branches, the proper digital nerves of the ulnar and radial small finger and the ulnar ring finger.
Figure 52.47. The anatomy of the ulnar tunnel and the course of the ulnar nerve from the forearm into the wrist as seen in a palmar view of the medial side of the wrist. ODQ, opponens digiti quinti muscle; FDQ, flexor digiti quinti muscle; ADQ, abductor digiti quinti muscle; H, hook of hamate; P, pisiform; FCU, flexor carpi ulnaris tendon. (From Eversmann WW Jr. Entrapment and Compression Neuropathies. In: Green DP, ed. Operative Hand Surgery, 3rd ed. New York: Churchill Livingstone, 1993:1341, with permission.)
Gross and Gelberman (46) described the ulnar tunnel and divided it into clinically relevant zones (Fig. 52.48). Zone I is the area of the canal from the proximal margin of the volar carpal ligament to the distal margin of the pisiform—more specifically, where the nerve bifurcates. It is defined by the presence of both the motor and the sensory divisions of the ulnar nerve. With division of the nerve into motor and sensory branches, zones II and III are defined; the former is associated with the motor and the latter with the sensory division. These last two divisions run side by side in the canal up to the level of the hypothenar fibrous arch.
Figure 52.48. Zones of the ulnar tunnel. Zone 1 is defined by the presence of both the sensory and motor divisions of the ulnar nerve, prior to the bifurcation at the level of the pisiform. Zone 2 is the zone of the motor branch only. Zone 3 is the region of the sensory branch only. H, hook of hamate; P, pisiform; FCU, flexor carpi ulnaris tendon; PL, palmaris longus tendon. (From Gelberman RH. Ulnar Tunnel Syndrome. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: Lippincott, 1991:1131, with permission.)
Entrapment of the ulnar nerve in the ulnar tunnel may be a result of space-occupying lesions. Ganglions arising from the triquetrohamate joint are the most common cause. Others include aneurysms (Fig. 52.49), lipomas, fractures of the bony walls (particularly the hook of the hamate) of the canal of Guyon, anatomic variations of the canal, and accessory or aberrant muscles. Repeated blunt trauma to the hypothenar region is the second most common cause (10,116). Compression in zones I and II is most
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often caused by ganglions and fractures of the hook of the hamate. Zone III is most often affected by a vascular lesion of the ulnar artery (116,128).
Figure 52.49. Aneurysm of the ulnar artery within the canal of Guyon (ulnar tunnel), producing an ulnar tunnel syndrome.
Classification
Entrapment at the wrist may produce pure motor, sensory, or mixed symptoms (10). Shea and McClain (116) described three ulnar nerve compression syndromes at and distal to the wrist. These correspond to the three anatomic areas of the canal. In type I, the entrapment takes place in the proximal zone, resulting in mixed motor and sensory deficit. Type II is purely motor, secondary to compression in the canal of Guyon or at the hook of the hamate in association with the origins of the abductor digiti minimi and the flexor digiti minimi and within the substrate of the opponens digiti quinti. Type III is caused by pressure on the superficial branch of the ulnar nerve, producing a sensory deficit in the ring and small fingers without associated muscle weakness or atrophy (Table 52.13).
Table 52.13. Classification of Ulnar Tunnel Syndrome
Assessment
Ulnar tunnel syndrome may be difficult to distinguish from cubital tunnel syndrome. One difference is the sparing of sensation of the dorsal ulnar half of the hand in ulnar tunnel syndrome. This area is innervated by the dorsal branch of the ulnar nerve, which arises variably from the ulnar nerve, but always proximal to the wrist crease, and does not enter the canal. Another difference is sparing of the long flexors of the ring and small fingers, leading to a more pronounced ulnar claw deformity in patients with ulnar tunnel versus cubital tunnel syndrome. Additionally, a history of repeated trauma to the hypothenar region may direct special attention to evaluation of this area in patients who present with ulnar-nerve-related symptoms (Table 52.14).
Table 52.14. Cubital versus Ulnar Tunnel
A careful examination is extremely helpful in precisely localizing the site of compression. Palpation of the deep structures within the hypothenar region may suggest a mass, not infrequently a ganglion within the canal. Allen’s test (an evaluation of the contributions made by the radial and ulnar arteries to the blood supply of the hand) is performed because thrombosis or aneurysm of the ulnar artery may be the cause of the neuropathy. Tinel’s test over the ulnar nerve at the level of the wrist and compression of the nerve over zone I may be helpful in distinguishing ulnar tunnel from cubital tunnel syndrome, although this has not been verified by studies. Phalen’s test may also be positive in ulnar tunnel syndrome.
Because of the high incidence of space-occupying lesions and fractures associated with compression of the ulnar nerve in the canal of Guyon, obtain radiographs. Plain radiographs, including PA, lateral, and carpal tunnel (ulnar tunnel) views, can be used to screen for fractures,
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dislocations, and arthritis. If a hook-of-the-hamate fracture is suspected but not proven in plain radiographs, a CT scan is the diagnostic study of choice. Mass lesions include ganglia and aneurysms and are best evaluated by MRI. In some cases of vascular lesions, arteriograms may be of additional help. Electrodiagnostic studies show slowing of the NCV across the wrist of the sensory and/or motor portions of the nerve. In theory, isolated slowing in the sensory portion is not diagnostic of isolated sensory division compression because the sensory fibers of the nerve are more susceptible to compression than are the motor fibers. If EMG evaluation shows abnormalities in the FCU and FDP muscles in addition to the intrinsics, compression of the ulnar nerve is present proximally (Table 52.15).
Table 52.15. Ulnar Tunnel Syndrome Summary
Preoperative or Nonoperative Management
Except for cases resulting from repeated blunt trauma, in which cessation of trauma may lead to complete resolution of symptoms, and for the mild type II neuropathy, the ulnar tunnel syndrome is best treated surgically. In the absence of identifiable lesions causing compression of the nerve in the ulnar tunnel, nonoperative treatment consists of splinting, NSAIDs, and avoidance of activities that aggravate or precipitate symptoms. Failure to adequately improve symptoms is an indication for surgery.
Surgical Indications and Relative Results
As noted in the preceding section, most cases of ulnar tunnel syndrome are treated operatively because there is often a mass lesion or a vascular injury or anomaly causing compression of the nerve. In cases of acute onset of ulnar tunnel syndrome in association with wrist trauma and swelling, Vance and Gelberman (140) recommend operative release and exploration if no improvement is noted within 48 hours. Alternatively, Howard (52) suggests observation for 6–8 weeks after the injury before exploration. It is reasonable to treat acute, traumatic ulnar tunnel syndrome expectantly in cases of incomplete or mild neurologic deficit, and to reserve urgent operative decompression for those cases with dense sensory deficits and/or paralysis of intrinsic muscles. Results of operative management are generally good, and recurrence is rare. Return of muscle function is adequate to avoid the need for tendon transfer. The rate and extent of recovery are likely related to the preoperative duration and severity of symptoms.
Preoperative Planning
Identification of the cause and site of compression is essential to treat the offending lesion at surgery. Plan for and inform the patient of excision of a fractured hook of the hamate or arthritic pisiform. Vascular reconstruction may
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be necessary in ulnar artery aneurysms and thrombosis. Ganglia must be identified and excised. If no particular lesion is identifiable, suspicion of a particular zone of compression will help direct particular attention to the segment of the nerve corresponding to that zone.
Operative Technique
The choice of incision and extent of exposure vary according to the particular pathology suspected as the cause of compression. The technique of exploration and decompression of the nerve through its course in the ulnar tunnel is described here.
  • Center a zigzag incision over the canal of Guyon, beginning just proximal to the proximal wrist crease at the radial border of the FCU tendon (Fig. 52.50). Or, in the case of concomitant CTS, use the incision for carpal tunnel release described earlier in this chapter and carry the dissection ulnarly to expose the canal of Guyon.
    Figure 52.50. Incision for exposure of the ulnar tunnel. H, hook of hamate; P, pisiform. (From Osterman AL, Kitay GS. Compression Neuropathies: Ulnar. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1339, with permission.)
  • Begin dissection proximally. Incise the fascia along the lateral border of the FCU.
  • Identify the ulnar artery and nerve after retracting the FCU medially; the artery lies lateral to the nerve.
  • Trace the ulnar nerve and artery distally, and incise (in order) the overlying palmaris brevis muscle, the hypothenar fat, any fibrous bands, and the palmar carpal ligament.
  • Identify the pisiform. The ulnar nerve bifurcates as it passes by the pisiform; the sensory branch continues
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    distally, and the motor branch dives toward the origin of the hypothenar muscles.
  • Trace the sensory branch onto the hypothenar muscles, dividing any crossing and potentially constrictive structures.
  • Trace the motor branch into the fibrous arch of the hypothenars and several millimeters distally, again dividing any potentially constricting fibrous structures.
  • Inspect the floor, walls, and contents of the canal, and identify any masses, aberrant muscles, fractures, or offending structures.
  • Identify and inspect the ulnar artery for any abnormalities.
  • One of us (JT) performs release of the carpal tunnel routinely at this time.
  • Close the skin.
  • Apply a padded hand dressing similar to that for carpal tunnel release.
Postoperative care is as for carpal tunnel release. If you treated other pathology simultaneously, institute specific rehabilitation and advise precautions as indicated.
Complications
Complications are similar to those associated with CTS. Incomplete release is potentially a problem if the nerve is not traced distally enough into zone III, between the pisohamate and pisometacarpal ligaments. An additional pitfall is failure to recognize the existence of a vascular component within this syndrome.
COMPRESSION NEUROPATHIES OF THE RADIAL NERVE
The radial nerve can be entrapped as it crosses the lateral intermuscular septum in the arm (most frequently in conjunction with displaced fractures of the humerus) or compressed proximal to the elbow in association with a fibrous arch from the lateral head of the triceps (a rare form of compression) (75). Evaluation of these two conditions reveals involvement of the muscles innervated by the posterior interosseous nerve as well as those by the radial nerve prior to its branching into motor and sensory divisions—typically the brachioradialis and extensor carpi radialis longus (ECRL) muscles. Additionally, sensory disturbances in the radial nerve distribution are common with these disorders. EMG evaluation is often diagnostic, and observation is the treatment of choice. If recovery is not spontaneous within 3 months, exploration and decompression are warranted.
The two more distal compressions are the posterior interosseous nerve (PIN) syndrome and the radial tunnel syndrome (RTS) (143). Additionally, the superficial, sensory branch of the radial nerve (SBR) can be compressed in the distal forearm, causing pain and sensory disturbances in the radial nerve sensory distribution.
POSTERIOR INTEROSSEOUS NERVE SYNDROME
Pathophysiology and Anatomy
The radial nerve travels along the posterior aspect of the middle third of the humerus in a diagonal course between the lateral and medial heads of the triceps. At the distal third of the humerus, the nerve pierces the lateral intermuscular septum and then travels anteriorly and distally between the brachialis and brachioradialis muscles. Just proximal to the elbow, the nerve bifurcates into superficial and deep branches. The superficial branch, the sensory division, continues distally, traveling between the brachioradialis and supinator muscles. The posterior interosseous (deep) branch, essentially a purely motor nerve, passes between the two heads of the supinator muscle under an inverted fibrous arch, the arcade of Frohse, which is formed by the thickened edge of origin of the superficial head and is seen readily (Fig. 52.51) (55). It continues beneath the supinator muscle, exiting under its
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distal edge. The PIN innervates the muscles of the posterior forearm (Fig. 52.52).
Figure 52.51. A: Composite drawing of dissections of the forearm at the level of the elbow. B: Enlarged view of the posterior interosseous nerve and its relationship to the supinator muscle. The motor supply to the extensor carpi radialis brevis arises most frequently from the superficial radial nerve. (From Spinner M. Injuries to the Major Branches of Peripheral Nerves of the Forearm. Philadelphia: Saunders, 1972, with permission.)
Figure 52.52. Innervations of the posterior interosseous nerve. Not labeled in the diagram are the distal innervations, from radial to ulnar: abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, and terminal sensory branches to the dorsal carpus. (From Spinner M, Linscheid RL. Nerve Entrapment Syndromes. In: Morrey BF, ed. The Elbow and Its Disorders, 2nd ed. Philadelphia: Saunders, 1993:813; and from Spinner M. Injuries to the Major Branches of the Forearm, 2nd ed. Philadelphia: Saunders, 1978, with permission.)
There are five classic potential compression sites of the PIN (Fig. 52.53). Just proximal to the radiocapitellar joint, after branching from the radial nerve, the PIN travels through fibrous tissue that is associated with the anterior capsule of the radiocapitellar joint. This fibrous tissue may form bands that can cause constriction of the nerve (37). The nerve continues distally and is crossed by the leash of Henry, small radial recurrent vessels that have been reported to be a source of compression (70). The fibrous leading edge of the extensor carpi radialis brevis (ECRB) muscle travels diagonally across the proximal edge of the supinator muscle and can cause compression of the PIN just prior to its entrance under the arcade of Frohse (70,107,118). The edge of the ECRB and the fibrous arcade of Frohse, the thickened proximal edge of the supinator muscle, are the most common sites of compression in PIN syndrome (Table 52.16). The nerve wraps around the proximal radius between the two heads of the supinator and may also be compressed as it exits from beneath the superficial head on its distal margin of this muscle.
Figure 52.53. The five potential compression sites of the posterior interosseous nerve: fibrous bands on the anterior radiocapitellar joint capsule, the vascular leash of Henry (radial recurrent vessels), the proximal edge of the extensor carpi radialis brevis, the arcade of Frohse (proximal edge of the supinator), and the distal edge of the supinator. (From Hynes DE, Peimer CA. Compression Neuropathies: Radial. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1291, with permission.)
Table 52.16. The Five Potential Compression Sites of the PIN from Proximal to Distal
Other causes of PIN compression include space-occupying lesions such as lipomas (103) and ganglions (77,93), radiocapitellar synovitis in patients with rheumatoid arthritis (78,147), fractures of the radial neck, and dislocations of the radial head (80). PIN compression may also be iatrogenic, as after internal fixation of fractures of the proximal radius, in which the nerve is extremely vulnerable because it may lie directly on the periosteum opposite the tuberosity of the radius (Fig. 52.54) (120).
Figure 52.54. A: In supination with a bare area of the proximal radius, the posterior interosseous nerve comes to lie against the periosteum of the radius. B: Details of the bare area. (From Spinner M. Injuries to the Major Branches of Peripheral Nerves of the Forearm. Philadelphia: Saunders, 1972, with permission.)
Assessment
The PIN syndrome is purely motor. Onset is usually insidious. There may be a history of trauma to the radial head or neck. Symptoms include weakness of the PIN-innervated muscles, and pain but not sensory dysfunction. The bra-chioradialis and the ECRL are not involved because they are innervated by the radial nerve. The ECRB may be spared because its innervation may originate more proximally, or it may appear to arise from the superficial bifurcation
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of the radial nerve (Fig. 52.51). The complete syndrome involves loss of extension of all digits and of the extensor carpi ulnaris. The patient can dorsiflex the wrist but with radial deviation. Middle and distal digital joints may still be extended through their intact intrinsics. Partial syndromes may involve just the extensor digitorum communis (EDC), with extension of the thumb and index finger preserved (Fig. 52.55). Early in the compression syndrome, a less striking clinical picture may exist, with paresis or paralysis of isolated digits. Patients with rheumatoid
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arthritis may present the same attitude of the hand whether the cause is a PIN compression or rupture or dislocation of the EDC tendons. A careful examination assists the clinician in differentiating between these two entities (76,78).
Figure 52.55. Incomplete dorsal interosseous nerve syndrome.
Diagnostic studies include routine radiographs of the elbow, especially in cases of trauma or arthritis. Soft-tissue masses may stretch or compress the PIN near the proximal radius. Functional loss of finger extension may be present, even though the patient is completely unaware of the presence of a mass. MRI examinations are extremely helpful in these patients, for preoperative evaluation of the size, shape, and location of the mass. Electrodiagnostic studies are imperative. The EMG portion of the examination is usually diagnostic (Table 52.17).
Table 52.17. Posterior Interosseous Nerve (PIN) Syndrome
Preoperative or Nonoperative Management
Patients rarely present with acute PIN syndrome except in cases of trauma. In cases of fracture or dislocation, follow management algorithms for treatment of such injuries complicated by nerve dysfunction. In the rare case of acute onset of PIN without injury, rule out the presence of a mass. In the absence of fracture, dislocation, or tumor, the patient can be evaluated with EMG studies and observed for 6–8 weeks. During this time, we recommend NSAIDs, maintaining joint mobility to prevent contracture, and avoidance of activities requiring repetitive or forceful elbow or wrist flexion and extension and forearm pronosupination. Splinting of the wrist in slight extension alone will often improve function of the hand markedly. Additional dynamic splinting for MP joint extension aids in opening the hand for grasp, but the splint itself may be cumbersome and interfere with activities. Failure to improve clinically or electromyographically in 6–8 weeks is an indication for operative treatment.
Results
Surgical decompression for the treatment of PIN syndrome produces good to excellent results in 85% of patients (54). Patients generally recover motor function, although improvement may take 18 months to complete. If the paralysis has been longstanding (more than 12–18 months), so that end organ innervation of the muscle has atrophied, there will be residual loss or inadequate recovery. These patients can be treated with appropriate tendon transfers (see Chapter 55 on radial nerve palsy) (54).
Preoperative Planning
Be prepared to address concomitant fractures and dislocations. You must delineate the sizes and locations of masses to optimize the choice of approach. This requires a preoperative MRI. In cases of suspected malignancy, perform a metastatic workup and choose a treatment appropriate for the neoplasm. In patients with rheumatoid arthritis and radiocapitellar disease, radial head excision may be indicated.
There are several approaches to the radial nerve in the proximal forearm. Use the one that allows complete visualization of the potential compression sites of the nerve and that allows treatment of any associated conditions. Three popular approaches are the anterolateral extensile, posterior, and brachioradialis muscle–splitting approaches. Perform the surgery under tourniquet control and regional or general anesthetic.
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Anterolateral Approach
  • Begin the incision 5 cm above the flexor crease on the lateral aspect of the arm, over the interval of the brachioradialis and biceps. Extend it distally, across the flexor crease, along the ulnar border of the brachioradialis muscle (Fig. 52.56).
    Figure 52.56. The anterolateral approach to the radial nerve. (From Eversmann WW Jr. Entrapment and Compression Neuropathies. In: Green DP, ed. Operative Hand Surgery, 3rd ed. New York: Churchill Livingstone, 1993:1341, with permission.)
  • Develop the skin flaps to the level of the muscle fascia. Protect the lateral brachial and lateral antebrachial cutaneous (LABC) nerves as well as the cephalic vein in the subcutaneous tissues.
  • Deepen the dissection proximally and identify the radial nerve in the interval between the brachialis and brachioradialis just proximal to the flexion crease of the elbow.
  • Trace the nerve distally onto the anterior capsule of the radiocapitellar joint, the first site of potential compression, where fibrous bands may compress the nerve. Release all substantial structures crossing the nerve.
  • Continue tracing the nerve distally. The fan-shaped leash of vessels from the radial recurrent artery cross the nerve as they travel to the brachioradialis. With bipolar cautery, coagulate the vessels and divide them.
  • While visualizing the nerve, pronate the forearm and flex the wrist. This will tighten the leading edge of the ECRB and may demonstrate its compression of the PIN. Remove a portion of the fibrous edge of the muscle in the region of the nerve.
  • Continue following the nerve as it enters the arcade of Frohse. Divide the fibrous arch while protecting the underlying PIN.
  • The superficial head of the supinator often has a tough fascial envelope. Because of this and for the benefit of exploration of the nerve as it travels through the supinator, it may be preferable to divide the superficial head of the supinator as it crosses the PIN.
  • Trace the nerve as it branches and exits the supinator. Divide the distal margin of the superficial head of the supinator.
Posterior Approach of Thompson
  • Make an incision along the line connecting the lateral epicondyle and Lister’s tubercle with the forearm in pronation. Begin it 2 cm distal to the lateral epicondyle, and extend it 8 cm.
  • Locate the interval between the ECRB and EDC muscles in the distal portion of the wound. Develop this interval and extend it proximally.
  • Identify the transverse-oblique fibers of the supinator muscle (Fig. 52.57).
    Figure 52.57. The posterior muscle-splitting approach to the radial tunnel and the arcade of Frohse. ECU, extensor carpi ulnaris; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; EDC, extensor digitorum communis. (From Eversmann WW Jr. Entrapment and Compression Neuropathies. In: Green DP, ed. Operative Hand Surgery. New York: Churchill Livingstone, 1982:1341, with permission.)
  • Increase exposure by developing the interval between the ECRB and the supinator. Avoid dissection between the EDC and the supinator, which would place the motor innervation of the EDC at risk (120).
  • Explore the nerve as previously described, beginning proximally. It may be difficult to isolate the fibrous bands of the first site of compression, which is a disadvantage of this approach. (One can extend this approach proximally by developing the interval on the medial and lateral aspects of the brachioradialis muscle.)
Brachioradialis Muscle–Splitting Approach
  • Make an incision centered over the mobile wad at the level of the radiocapitellar joint (Fig. 52.58).
    Figure 52.58. Incision for the muscle-splitting approach to the radial tunnel.
  • Develop the skin flaps to the level of the muscle fascia. Protect the lateral brachial and LABC nerves in the subcutaneous tissues.
  • Make an incision in the brachioradialis fascia in line with the muscle fibers.
  • Palpate the radial head.
  • Bluntly dissect through the substance of the muscle, separating its fibers and heading toward the radial head. Continually locate the radial head by palpation.
  • Identify the transverse-oblique fibers of the supinator. The superficial branch of the radial nerve will be on the underside of the brachioradialis (Fig. 52.59).
    Figure 52.59. The muscle-splitting approach to the radial tunnel. (From Peimer CA, Wheeler DR. Radial Tunnel Syndrome/Posterior Interosseous Nerve Compression. In: Szabo RM, ed. Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare, NJ: Slack, 1989:177, with permission.)
  • Identify the PIN as it enters the arcade of Frohse.
  • Dissect the nerve, evaluating the five potential sites of compression and dividing all potential offending structures. (Pronate the forearm and flex the wrist to evaluate ECRB compression of the nerve.) Carry decompression out to the distal margin of the supinator.
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  • If more proximal exposure is desired, extend the skin incision along the interval between the brachioradialis and the biceps on the arm. Proceed with deeper exposure as described in the anterolateral approach.
  • If more distal exposure is desired, extend the incision so that you can reach the interval between the ECRB and EDC muscles. Proceed with deeper dissection as described in the posterior approach.
  • Loosely approximate the fascia of the brachioradialis before closing the skin.
Authors’ Preferred Method
  • Start the incision 4–5 cm proximal to the elbow flexion crease, at the interval between the brachioradialis laterally and the brachialis medially.
  • Distally, continue the incision to the interval between the ECRB and the ECRL laterally and to the EDC medially (Fig. 52.60).
    Figure 52.60. Approach for the radial nerve and its bifurcation at the elbow and proximal forearm.
  • Begin deep dissection at the proximal end of the incision.
  • Identify the radial nerve and tag it with a moist, wide Penrose drain.
  • At the distal end of the incision, develop the plane between the ECRB and the EDC, exposing the oblique fibers of the supinator muscle (Fig. 52.57).
  • Accomplish wider exposure by partially detaching the ECRB from the lateral epicondyle.
  • Dissection to increase exposure is between the ECRB and the supinator, as in the posterior approach. (Do not dissect between the EDC and the supinator.)
  • Trace the nerve from proximal to distal, using the proximal and distal intervals for exposure.
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  • Divide all potential compressing structures as previously noted.
After decompression of the nerve, release the tourniquet and obtain hemostasis. Do not close any deep structures except as noted for the brachioradialis-splitting technique. Suture the skin in layers. Apply a padded dressing and a long-arm splint with the forearm in supination and with the elbow flexed 90°.
Postoperative Care and Rehabilitation
Immediately postoperatively, encourage shoulder and finger range-of-motion exercises. Because these approaches are carried out between anatomic planes, you may discontinue immobilization as early as 3–5 days and no later than 7–10 days. Depending on individual patient recovery, slings or wrist splints may be used for up to 3 weeks for comfort. Formal therapy for strengthening and range of motion is not routinely implemented but should be used when the patient is slow to progress. Return-to-work time is influenced by the severity of the syndrome and the particular job demands.
Complications
In addition to the pitfalls common to other entrapment syndromes, differentiation of the PIN syndrome from extensor tendon ruptures or dislocations in the patient with rheumatoid arthritis is important. Make this distinction by performing a tenodesis test. When the wrist is passively flexed, the fingers will not extend at the MP joints if the tendons are ruptured. If the tendons are intact, as in PIN syndrome, extension of the MP joints will occur as the wrist falls into flexion.
Avoid forceful dissection between the supinator muscle and the extensor digitorum, because this will jeopardize the innervation of the EDC muscle. Identification and resection of a portion of the fibrous leading edge of the ECRB where it crosses the PIN, as well as separate division of the arcade of Frohse, are critical because these are the common sites of compression of the nerve. “Recurrence,” or rather failure of operative treatment, is caused by incomplete decompression of the nerve at all the potential sites of entrapment.
RADIAL TUNNEL SYNDROME
Pathophysiology and Anatomy
The radial tunnel is the region along the course of the radial nerve and its posterior interosseous (deep) branch, beginning proximally where the radial nerve lies deep between the brachioradialis and the brachialis, and extending distally to the distal border of the supinator muscle (107). The five sites of compression are the same as those for PIN syndrome (97,107), easily remembered by the mnemonic FREAS (Table 52.16). Unlike in PIN syndrome, the compression of the PIN in RTS is not caused by masses, fractures, and disturbances of the radiocapitellar joint. It is associated with repetitive elbow flexion and extension and forearm rotation. It is likely a dynamic form of compression of the PIN (57).
Assessment
Radial tunnel syndrome is a painful condition, without motor deficit and usually without sensory changes. Patients present with a dull, aching or burning pain over the lateral aspect of the elbow in the region of the proximal extensor–supinator muscle mass. Symptoms may radiate distally along the course of the extensor muscles to the radial aspect of the hand or proximally to the shoulder. In some cases, there may be paresthesias in the radial nerve distribution. Symptoms are worsened by activities, especially those requiring forceful and repetitive elbow motion or wrist flexion and extension and forearm pronosupination, and are relieved by rest. The association between lateral epicondylitis, or “tennis elbow,” and RTS has been noted (107,141). Patients may present with tennis elbow symptoms and evidence of lateral epicondylitis, which may respond to local steroid injections followed by localization of discomfort several centimeters distal to the lateral epicondyle over the radial tunnel. The resultant RTS can then exist solely or concurrently with the tennis elbow; 5% of patients with lateral epicondylitis also have RTS (128). The diagnosis of RTS is differentiated from tennis elbow by examination.
Physical examination will reveal tenderness centered over the radial head and neck along the course of the radial nerve. Comparison of the opposite, unaffected side is recommended because many normal individuals find this area exquisitely tender to deep palpation. Distal radiation of symptoms can occur with manual compression of
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the nerve in this region. Limitation of elbow extension and weakness of grip further suggest RTS. Sensory deficits in the distribution of the superficial radial branch may be seen in RTS and suggest compression of the nerve in the proximal aspect of the tunnel at a point where both divisions of the main trunk are simultaneously vulnerable, such as beneath the fibrous bands proximal to the arcade of Frohse. Because of its dynamic or exertional nature, provocative testing is invaluable in detecting RTS and may give clues to the site of compression of the nerve within the radial tunnel. Described provocative tests for RTS include the elbow flexion test, the middle finger extension test (107), passive pronation of the forearm (33), and the supination test (70) (Table 52.18). In the elbow flexion test (Fig. 52.61), ask the patient to flex his elbow against resistance. Reproduction of pain with this maneuver indicates compression of the nerve by fibrous bands on the capsule of the radiocapitellar joint. In the middle finger extension test (Fig. 52.62), ask the patient to extend his middle finger against resistance applied by you over the proximal phalanx. Hold his forearm in full pronation and his elbow extended. Reproduction of pain in the radial tunnel region with this maneuver indicates entrapment of the PIN at the ECRB tendon.
Table 52.18. Provocative Tests for Radial Tunnel Syndrome (RTS)
Figure 52.61. The elbow flexion test for radial tunnel syndrome.
Figure 52.62. The middle finger extension test for radial tunnel syndrome.
Electrodiagnostic studies are not generally helpful in diagnosis of RTS. Conduction velocities are often normal, and EMG changes are present in patients with clinically evident weakness or atrophy and therefore carry the diagnosis of PIN syndrome. There may be a place for dynamic electrodiagnostic studies to detect subtle changes in nerve function (64,100). We believe that a localized injection of anesthetic, with or without steroid, into the radial tunnel, which produces a PIN palsy and relieves symptoms, is diagnostic for RTS. Localized steroid injection may also assist in differentiating RTS from tennis elbow (Table 52.19).
Table 52.19. Radial Tunnel Syndrome Summary
Preoperative or Nonoperative Management
Nonoperative management of RTS includes initially reducing inflammation in the area of the radial tunnel with
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wrist splinting, administration of NSAIDs, and avoidance of activities that involve forearm pronosupination. Prescribe formal hand therapy. Administer steroid iontophoresis over the radial tunnel three times per week for 2–3 weeks. After significant reduction in inflammation, begin soft-tissue mobilization, gentle progressive stretching, and nerve gliding exercises. Institute strengthening later, tailoring it so that it does not exacerbate symptoms.
Surgical Indications and Relative Results
Failure to improve after 2–4 months of adequate treatment, progressive symptoms, and the impracticality of permanent activity modification are all indications for surgical intervention.
The relief of aching pain in the proximal forearm often occurs within the first few weeks after surgery, although
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complete resolution of pain may take several months to a year. Lister et al. (70) noted approximately 92% good to excellent results in a review of the combined cases of three series, including their own. Jebson and Engber (57) reported 71% good results and 29% fair/poor results in their 8-year follow-up of 33 extremities in 31 patients. Ritts et al. (105) reviewed the results of 34 cases performed over the span of 10 years. They noted only 51% good results with surgery, and workers’ compensation cases often had an unsatisfactory result. There is no difference in the operative results of patients with normal preoperative electrodiagnostic studies and those with abnormal ones. Peimer and Wheeler (97) noted that the best results were in patients whose nerves appeared normal at surgery. Ritts et al. (105) noted that the best prognostic factor for operative treatment was a good response to a preoperative injection.
Operative Technique—Authors’ Preferred Method
The technique for decompression of the PIN in RTS is the same as that described for PIN syndrome. Because of its simplicity and sufficient exposure, the brachioradialis–splitting technique (107) is preferred. If the site of compression has been well localized by clinical methods to the arcade of Frohse, a limited skin incision may be employed.
  • Make an incision approximately 6 cm long, starting at the elbow crease and projected longitudinally over the radial head (Fig. 52.58).
  • Expose the brachioradialis and split its fibers by blunt dissection. Take care to not injure branches of the lateral brachial and antebrachial nerves.
  • After traversing the brachioradialis, retract the superficial branch of the radial nerve and the ECRL laterally to expose the deep branch of the radial nerve and the oblique fibers of the supinator (Fig. 52.59, Fig. 52.63).
    Figure 52.63. Superficial and deep branches of the radial nerve. A: The deep branch is seen as it passes under the arcade of Frohse (arrow). B: Compression of the deep branch (arrow) after division of the superficial head of the supinator.
  • Divide the structures at the five potential sites of compression to fully expose the PIN.
  • Loosely approximate the deep fascia.
  • Close the skin.
Apply a well-padded compression dressing from above the elbow to beyond the wrist, with the forearm and wrist in neutral.
Postoperative Care and Rehabilitation
Encourage immediate postoperative finger and shoulder range-of-motion exercises. Remove the postoperative dressing at 5 days. Place the arm in a sling and the wrist in a cock-up splint. Encourage active range-of-motion exercises of the elbow and wrist so that full range is achieved by 3 weeks postoperative. Remove the wrist splint and sling at 3 weeks and institute therapy for elbow and wrist range of motion if the patient is progressing slowly. If the patient is progressing well, encourage progressive use of the upper extremity in daily activities, but caution against forceful activities until 6 weeks after surgery. If job demands are fairly strenuous, a strengthening program may be prescribed under a therapist’s supervision. Return to work is allowed at 6–8 weeks but may not be realized until
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up to 3–4 months for patients who are manual laborers. Complete recovery can take up to a year. Job modification in conjunction with surgery may be indicated, especially in workers’ compensation cases.
Complications
Radial tunnel syndrome is identified solely by clinical examination and must not be overdiagnosed. Overdiagnosis leading to incorrect treatment or overtreatment is the main cause of failure. Lateral epicondylitis is far more common. Injections of local anesthetic over the lateral epicondyle and more distally over the radial tunnel are helpful in differentiating between these two entities and in establishing the diagnosis. When the two conditions coexist and are unresponsive to nonoperative management, treatment of the lateral epicondylitis at the time of radial tunnel release is requisite for maximal postoperative relief of symptoms. Postoperatively, transitory but distressing partial paresis of the finger extensors may occur, but it resolves spontaneously in 6–12 weeks.
SUPERFICIAL RADIAL NERVE COMPRESSION SYNDROME (CHEIRALGIA PARESTHETICA)
Compression neuropathy of the SBR was first described by Wartenberg in 1932 (143). He suggested that the condition be named cheiralgia paresthetica because of its similarity to the isolated involvement of the lateral cutaneous nerve of the thigh, which is called meralgia paresthetica.
Pathophysiology and Anatomy
The radial nerve bifurcates just proximal to the elbow, in the interval between the brachioradialis and brachialis muscles. The superficial sensory branch continues toward the wrist under cover of the brachioradialis and medial to the ECRL muscle. It courses superficially to the supinator in the proximal forearm, and then to the PT insertion in the midforearm. In the distal third of the forearm, the nerve pierces the antebrachial fascia between the tendons of the brachioradialis and ECRL muscles. The nerve passes superficially to the extensor retinaculum and divides into terminal branches to provide cutaneous innervation to the dorsoradial aspect of the hand (Fig. 52.8).
When the forearm is in supination, the sensory branch lies deep to the fascia, without compression from the tendons of the brachioradialis and ECRL muscles. As the forearm pronates, the ECRL tendon crosses beneath the brachioradialis tendon in a scissors-like fashion, pinching or compressing the nerve (Fig. 52.64A). Palmar–ulnar deviation of the wrist places traction on the nerve (Fig. 52.64B). Repetitive traumatization of the nerve causes swelling, which inhibits its normal gliding through the fascia, leading to a traction injury (27).
Figure 52.64. A: Pronation of the forearm causes a pinching of the superficial branch of the radial nerve. B: Palmar–ulnar flexion of the wrist puts the superficial radial nerve in maximal traction. (From Dellon AL, MacKinnon SE. Radial Sensory Nerve Entrapment in the Forearm. J Hand Surg [Am] 1989;11:199, with permission.)
Assessment
Usually, a history of repeated, job-related forearm pronosupination is given. Affected patients complain of pain, numbness, tingling, and dysesthesias over the dorsoradial aspect of the hand. Symptoms are brought on by wrist movement and are intensified when the patient makes a tight grip with the thumb and index finger. Nighttime awakening caused by symptoms is not common. Sensory examination reveals alterations in moving two-point and vibratory sensation. There is no motor dysfunction of radially innervated muscles, although grip and pinch strength may be decreased secondary to pain. Percussion along the course of the nerve, particularly as it emerges between the brachioradialis and ECRL tendons, produces paresthesias. Dellon and MacKinnon (27) described a provocative test for eliciting symptoms in which the patient is instructed to pronate the forearm with the elbow in extension. If within 30–60 seconds the symptoms of paresthesias or dysesthesias are evoked or exacerbated over the dorsal radial aspect of the hand, entrapment is confirmed (Fig. 52.65).
Figure 52.65. The provocative test for entrapment of the superficial branch of the radial nerve, consisting of forced pronation of the forearm. (From Dellon AL, MacKinnon SE. Radial Sensory Nerve Entrapment in the Forearm. J Hand Surg [Am] 1989;11:199, with permission.)
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The entity most commonly confused with superficial radial nerve entrapment is de Quervain’s stenosing tendovaginitis of the first dorsal wrist compartment. Finklestein’s test (i.e., pain on quick ulnar deviation of the hand with the patient’s thumb grasped in the palm) is positive in both entities. The presence or absence of swelling over the first dorsal compartment, a nerve compression test over the course of the superficial radial nerve, and careful sensory testing are used to differentiate these two entities. Electrodiagnostic testing is rarely useful, although it often shows abnormalities in conduction velocity or amplitude (27). Injury to the LABC nerve as a source of the patient’s symptoms must also be excluded because there is overlap in the innervation of the LABC and the SBR nerves in the mid and distal forearm in 75% of patients (27). Exclude it by performing serial blocks with local anesthetic. First block the LABC nerve at the lateral arm, then block the SBR at the site of suspected entrapment. Improvement in symptoms subsequent to the second injection but not the first implicates the SBR as the cause (Table 52.20).
Table 52.20. Cheiralgia Paresthetica Summary
Preoperative or Nonoperative Treatment
Nonoperative treatment includes avoidance of pronosupination and radioulnar deviation of the wrist, splinting of the wrist with or without inclusion of the thumb and forearm, and NSAIDs. Physiotherapy, including tissue mobilization and nerve gliding exercises, steroid iontophoresis, and progressive gentle stretching, may be helpful. Administer steroid injections subfascially, and use them judiciously
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because of the potential for depigmentation of the skin and subcutaneous fat atrophy. Patients with long-term symptoms or onset of symptoms associated with a fracture or crush injury tend not to improve with nonoperative treatment.
Surgical Indications and Relative Results
Failure to improve, or inadequate improvement, after prolonged nonoperative treatment is an indication for surgery.
In the series reported by Dellon and MacKinnon (27), pain relief was good or excellent in 86% of patients undergoing surgery. Of these patients, 43% returned to their regular jobs, 22% returned to modified work, and 35% remained disabled because of associated injuries. Objectively, marked improvement was noted in grip and pinch strength.
Operative Technique
  • Make an 8 cm curvilinear incision just volar to the mid-radial aspect of the radius, centered in relation to the point where the nerve pierces the antebrachial fascia (Fig. 52.66A). (The location of the positive Tinel’s sign may also be used.) To prevent scarring about the nerve, avoid placing the incision directly over the nerve.
    Figure 52.66. Decompression of the superficial branch of the radial nerve. The incision (A) is represented by the dashed line. The fascia joining the brachioradialis and extensor carpi radialis longus (B) is divided distally (C) and proximally (D). The nerve is lying loosely in its bed, and the brachioradialis and ECRL are gliding independently. (From Dellon AL, MacKinnon SE. Radial Sensory Nerve Entrapment in the Forearm. J Hand Surg [Am] 1989;11:199, with permission.)
  • Identify and protect cutaneous branches of the LABC nerve.
  • Identify the SBR and the fascia between the BR and ECRL.
  • Release the fascia joining the BR and ECRL distally out to the insertion of the BR (Fig. 52.66B).
  • Release the fascia at least 6 cm proximal to the nerve (Fig. 52.66C).
  • Ensure that the nerve lies loosely in the subcutaneous tissue and that the BR and ECRL glide independently without constriction of the SBR (Fig. 52.66D).
  • Close the wound, and apply a bulky compression dressing with a volar splint.
Postoperative Care and Rehabilitation
Remove the postoperative dressing after 7–10 days. We discourage splinting. Begin a home program of scar therapy and tissue mobilization. Encourage the patient to use the hand progressively in regular activities.
Complications
As with the majority of compression neuropathies, accurate diagnosis and good surgical technique will prevent complications. You must differentiate between SBR entrapment and de Quervain’s tendovaginitis by physical examination. If concomitant de Quervain’s exists, treat it appropriately. Exclusion of entrapment of the LABC nerve by differential anesthetic blocks is also imperative. Avoid excessive handling of the nerve at surgery to prevent neuroma formation.
LATERAL ANTEBRACHIAL CUTANEOUS NERVE COMPRESSION
Pathophysiology and Anatomy
The LABC nerve is the terminal, sensory portion of the musculocutaneous nerve. Arising from the musculocutaneous nerve in the interval between the biceps and brachialis muscles, it continues distally under cover of the biceps muscle and then the lateral border of the biceps tendon to the elbow flexion crease. At this level, the nerve lies on top of the brachialis, lateral to the biceps and medial to the brachioradialis. It pierces the brachial fascia lateral to the biceps tendon. It divides into an anterior branch and a posterior branch, the former traveling with the cephalic vein to innervate the anterior surface of the radial forearm to the thenar eminence, and the latter continuing to innervate
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the radial and posterior aspect of the distal forearm to the wrist (Fig. 52.67). The anterior branch of the LABC nerve communicates with the superficial radial nerve above the wrist (8). Compression of the LABC nerve is rare but can occur where it emerges from beneath the lateral border of the biceps tendon just medial to the brachioradialis. The nerve is compressed between the brachialis fascia and the tendon of the biceps when the elbow is extended. Compression of the nerve can be further accentuated with pronation of the forearm (8,91).
Figure 52.67. Palmar and dorsal sensory innervation of the lateral antebrachial cutaneous (musculocutaneous) nerve. (From Nunley JA, Howson P. Lateral Antebrachial Nerve Compression. In: Szabo RM, ed. Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare, NJ: Slack, 1989:201, with permission.)
Assessment
Characteristically, the history includes repetitive, forceful exercise of the elbow in a position of extension. Patients complain of pain over the lateral aspect of the elbow on active motion of the elbow, with accompanying burning or numbness in the radial forearm. Examination reveals decreased sensibility distally along the radial aspect of the forearm. Elbow extension is limited with the forearm fully pronated. Point tenderness is found lateral to the biceps tendon at the elbow crease. Compression may be confirmed with sensory NCV studies measured between the elbow flexion crease and the axilla. A nerve block with local anesthetic that produces numbness along the nerve’s cutaneous distribution and eliminates symptoms aids in the diagnosis. The nerve lies between the cephalic and median cubital veins 1.5 cm lateral to the biceps tendon, and the injection is best placed just distal to the cubital crease (Table 52.21).
Table 52.21. Lateral Antebrachial Cutaneous (LABC) Nerve Compression
Preoperative or Nonoperative Management
Conservative treatment initially consists of splinting and anti-inflammatory medication. If symptoms persist or
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worsen over the first few weeks, administer a local injection of corticosteroids around the nerve. Nonoperative treatment has limited success.
Surgical Indications and Relative Results
Consider surgical decompression if symptoms do not resolve within 3 months.
Davidson et al. (22) reviewed 15 patients with a diagnosis of LABC nerve entrapment. Average follow-up was 13.4 years, with a minimum of 2 years. Eleven of these patients underwent surgical decompression. Of these, none had recurrence of hypesthesia, and all had complete relief of pain and full range of motion. One patient subsequently underwent release of the lateral epicondyle. Of the four patients who were treated nonoperatively, one had persistent hypesthesia but full range of motion and complete pain relief.
Preoperative Planning
If surgery is planned, obtain radiographs of the elbow to rule out bony pathology. Examine the patient on more than one occasion to confirm consistent findings. Consider all extraarticular and intraarticular elbow conditions when evaluating the patient.
Operative Technique
  • Begin the incision proximal to the elbow flexion crease along the lateral border of the biceps muscle. Curve it laterally at the elbow flexion crease to head toward the radial tunnel. Do not cross the cubital flexion crease at right angles.
  • Identify the LABC nerve 1.5 cm lateral to the tendon at the level of the medial condyle (Fig. 52.68A).
    Figure 52.68. A: The lateral antebrachial nerve emerging from beneath the lateral border of the biceps tendon. B: A wedge-shaped section taken out of the overlying biceps tendon to decompress the nerve. (From Nunley JA, Howson P. Lateral Antebrachial Nerve Compression. In: Szabo RM, ed. Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare, NJ: Slack, 1989:201, with permission.)
  • Trace the nerve proximally several centimeters.
  • Demonstrate the area of entrapment by pronating the arm in extension. Look for flattening of the nerve and loss of vascular markings.
  • Excise a triangular wedge of biceps tendon (1×3 cm) where the nerve is compressed by the edge of the biceps and the brachialis (Fig. 52.68B).
  • Ensure that the decompression is complete by pronating and supinating the elbow while it is in extension.
  • Apply a bulky dressing, and splint the elbow at 90° in neutral rotation.
Postoperative Care and Rehabilitation
At 2–3 weeks postoperatively, remove the splint and allow full, unrestricted activity to tolerance.
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