Although athletes at all levels of participation may experience the same entrapment neuropathies as the general population, some sport-specific peripheral nerve factors must be considered with regard to the wrist and hand. Neuropathies may occur as a result of chronic repetitive motion or acute isolated trauma experienced during athletic activities. Just as with other pathologies that may have an effect on, or be affected by, sports participation, the type and timing of treatment will vary depending on severity and “sport season” considerations. Although “playing with pain” may be an acceptable choice in the presence of some repetitive traumatic injuries, hand and wrist neuropathies often necessitate careful and timely treatment to prevent irreversible damage. Although a multitude of potential upper extremity neuropathies exist, this chapter focuses on the ones that are most typical and/or cause the most concern. Acute traumatic nerve laceration injuries are not addressed because these injuries may be treated in a standard manner, although return-to-play issues may not be standard and require the case-specific input of the operating surgeon, therapist, trainer, and athlete.
Some wrist and hand neuropathies are more common with certain athletic activities. Median neuropathy at the wrist may result from activities that (1) apply prolonged direct compression, such as bicycling or wheelchair events, (2) elicit vibratory stimuli, such as motocross racing, or (3) require repetitive power gripping, such as in weight lifting and ice hockey. In addition to similar mechanisms of injury for the ulnar nerve at the wrist, secondary extrinsic causes of compression dominate, including a high prevalence of hamate hook fractures as a result of using a stick in certain sports and ulnar artery aneurysm/thrombosis (hypothenar hammer syndrome) that occurs as a result of the repetitive blunt palmar trauma commonly experienced by baseball catchers and martial arts practitioners. The superficial sensory radial nerve is susceptible to either direct blunt trauma, which is most commonly associated with football, lacrosse, and ice hockey, or repetitive traction forces, which are often experienced by competitive rock climbers and powerlifters. Furthermore, the perpetual use of compressive wrist bands or athletic tape, which is frequently seen in athletes whose sport entails use of a racquet, may cause local irritation of the radial nerve at the wrist. The ulnar digital nerve of the thumb is vulnerable in bowlers, and the radial digital nerve of the index finger may be affected in tennis, racquetball, or squash players.
The symptoms of sports-related wrist and hand neuropathies may include subjective paresthesias and weakness in the affected nerve’s distribution, loss of coordination, and a variable level of pain. Depending on the reported distribution of symptoms, further questioning should focus on potential areas of nerve compression or repetitive trauma precipitated by the athlete’s activity requirements. Direct questioning of the athlete will also reveal if the symptoms worsen or improve in certain positions or occur while the athlete is sleeping. Determining the onset, frequency, and intensity of nerve symptoms may be helpful in deciding how aggressive an approach to take with further workup and treatment. The benefit or futility of prior treatment should be elicited. The practitioner should also remember that although symptoms and signs may be present in the wrist and hand, the true site of pathology may be more proximal, and therefore an inventory of proximally generated symptoms should be conducted. As with most pathologies, the patient’s history typically directs one to the diagnosis. I try to avoid asking patients leading questions. Instead, allowing athletes to describe their own symptoms, exacerbating and remitting factors, and prior treatments often leads to the correct diagnosis and determines the course of further management.
The athlete’s subjective complaints direct the focus of the physical examination. Rating light touch sensation in the distribution of the symptomatic nerve relative to the asymptomatic wrist and hand is fast, easy, and helpful. This determination of light touch sensation should include the dorsal sensory branch of the ulnar nerve, the palmar cutaneous branch of the median nerve, and the dorsal sensory branch of the radial nerve. Involvement of these terminal cutaneous nerve components is helpful in confirming the site of peripheral nerve compression or disease. For example, normal findings of a sensory examination over the dorsal ulnar hand in the setting of other ulnar nerve symptoms and signs typically indicates ulnar nerve pathology in the wrist or hand rather than at the elbow. Altered sensation in the central palmar aspect of the hand indicates median nerve pathology proximal to the level of the carpal tunnel due to involvement of the palmar cutaneous branch of the median nerve. For digital neuropathies, such as bowler’s thumb, altered sensation in the digital nerve is expected, and a palpable mass may be present. More advanced sensory examinations, such as static and moving two-point discrimination, vibratory sense, and Semmes-Weinstein monofilament testing, may provide good objective and standardized data points that are monitored for the progression or resolution of neuropathy.
Expeditious assessment of peripheral nerve motor function may be performed by having the athlete make the “OK” sign (median nerve), cross the index and long fingers (ulnar nerve), and extend the index finger and thumb (radial nerve). When making the OK sign, it is important for the patient to make a rounded circle with the thumb and index finger; flattening of the circle into a more oval shape is an abnormal result that indicates proximal involvement of the anterior interosseous nerve. Other nerve-specific maneuvers include having the athlete oppose the thumb to the base of the small finger (distal median and ulnar innervated thenar muscles), pinch a piece of paper between the thumb and index finger (ulnar innervated adductor pollicis), and abduct the small finger against resistance (ulnar innervated abductor digiti minimi). Clawing of the ring and small finger indicates significant ulnar neuropathy distal to the digital flexor muscles in the forearm. Formal tip-pinch, key-pinch, and grip strength measurements with dynamometers provide objective results that are tracked over time.
Hoffman-Tinel testing along the course of the symptomatic peripheral nerve may help determine a specific site of chronic trauma or compressive neuropathy. It is usually helpful to initially tap lightly for this test to get a sense of the hypersensitivity/reactivity of the symptomatic nerve. The Finkelstein test (i.e., ulnar deviation of the athlete’s wrist by the examiner) may cause dorsal radial sensory nerve symptoms ( Fig. 78-1 ). These symptoms should be differentiated from symptoms caused by De Quervain first extensor compartment tenosynovitis by checking for the presence of nerve symptoms and a positive Hoffman-Tinel sign proximal to the radial styloid at the level where the brachioradialis and extensor carpi radialis longus meet and the dorsal radial sensory nerve exits. Direct compression and/or flexion/extension tests along the course of the symptomatic nerve may also be helpful in localizing the site of compression. These tests are typically performed for 30 to 60 seconds or until symptoms occur, whichever comes first. For ulnar nerve symptoms at the wrist and hand, the practitioner should also consider a vascular examination because of possible associated ulnar artery aneurysm and/or thrombosis. This examination typically entails looking at the athlete’s nails for streaking (splinter hemorrhages) that could indicate thrombotic/embolic events, checking for ulcerations or skin breakdown due to ischemia, especially in the palmar fingertips, and Allen testing ( Fig. 78-2 ).
Examination of hand and wrist neuropathies should always prompt consideration of more proximal nerve disorders that could manifest symptoms distally in the hand and wrist. Again, symptoms and signs dictate whether the cervical spine, brachial plexus, arm, or proximal forearm should be scrutinized for the source of the problem. Cervical radiculopathy and brachial plexopathy are not uncommon conditions in athletes who participate in contact sports.
In general, radiographic and advanced imaging is not necessary for evaluation of hand and wrist neuropathies, although special circumstances may spur the examiner to pursue imaging. For example, ulnar nerve symptoms in an athlete who sustains acute and/or chronic trauma to the ulnar-palmar aspect of the hand may be a sign of hamate hook fracture or nonunion. If other symptoms or signs are suggestive of hamate hook pathology, then radiographic views and/or a computed tomography or magnetic resonance imaging (MRI) scan is helpful ( Fig. 78-3 ). Although the carpal tunnel view is an often-cited special view for assessing the hamate hook, an alternative view is much easier to perform reproducibly, especially with use of fluoroscopy. To achieve this view, start with the wrist in radial deviation and the thumb abducted, as if the patient were holding a cup. The wrist is then slightly supinated from a lateral x-ray view position to generate a slightly oblique view. In this position, the x-ray beam is directed between the thumb and finger metacarpals and the hamate hook is seen projecting palmarly.
Unexplained masses in the region of symptomatic digit, hand, or wrist nerves also warrant advanced imaging. In patients with apparent ulnar nerve compression at the Guyon canal, I prefer to obtain an MRI scan before performing surgery because of the relatively high incidence of associated pathology such as a lipoma, a ganglion, hamate hook nonunion, anomalous muscle, and ulnar artery thrombosis or aneurysm, even though idiopathic compression is still plausible. A high index of clinical suspicion for ulnar artery aneurysm and/or thrombosis may require noninvasive vascular studies and/or an arteriogram for further information, especially if surgical intervention is imminently necessary to restore adequate perfusion to the hand ( Fig. 78-4 ). For athletes with symptoms and signs of proximal median nerve compression, elbow or humerus radiographs may reveal a supracondylar process. In the absence of a supracondylar process, MRI may be justified to evaluate for an occult forearm mass causing extrinsic compression on the median nerve.
As with any other athletic injury, decision making is be based on the nature and extent of the pathology and sport-specific considerations for the athlete. I typically present a spectrum of reasonable treatment and timing options that vary from conservative to aggressive and early to late. I try to convey to the athlete and his or her support staff how these options fit into their specific sport, along with the relative risks and benefits of the alternatives. It is often helpful to present options as they relate to the athlete’s season, career, and remainder of his or her life, which helps the athlete put the different choices into perspective. Certainly with hand and wrist nerve pathologies, progressive motor and/or sensory deficits that are nonresponsive to conservative options lead to stronger recommendations for aggressive and early treatment to try to limit and potentially reverse nerve impairment. Most of the decision-making principles for specific peripheral nerve issues are addressed in the next section.
Treatment options for the various peripheral nerve pathologies depend on the particular nerve involved, the severity of the involvement, and the type and timing of the patient’s athletic activities. With regard to carpal tunnel syndrome, neurodiagnostic studies are ordered for athletes who demonstrate either gross motor involvement or constant sensory dysfunction. Otherwise, I have the patient start wrist-neutral nighttime bracing at a minimum and attempt daytime and/or athletic-activity wrist-neutral bracing as much as possible. Although the use of oral antiinflammatory drugs along with bracing may be beneficial, using these drugs in isolation has not been shown to be effective. Modification of activities that worsen symptoms is helpful and may be facilitated by therapists and athletic trainers. If the signs and symptoms persist or progress during the next 6 to 8 weeks despite use of these measures, I order formal neurodiagnostic tests, writing the referral for “PM&R or Neurology evaluate & treat including neurodiagnostics as indicated” and also include my presumptive diagnosis. I also specify if I am concerned about any other particular diagnoses, such as peripheral neuropathy, cervical radiculopathy, or brachial plexopathy. Writing the prescription in this way allows the neurodiagnostician to perform the nerve conduction study with or without the electromyography as needed. It also indicates that they may proceed with further evaluation and treatment as warranted, such as by obtaining cervical spine imaging or ordering physical therapy rather than just performing the neurodiagnostic tests.
At this stage in the treatment of carpal tunnel syndrome I typically offer a corticosteroid injection or surgical release. The decision about which option to choose is often based on the patient’s immediate, short-term, and long-term athletic schedule. For example, if it is off-season, the athlete may elect to proceed with surgical release as the most definitive treatment so he or she will not have persistent or worsening issues during the season. However, if the athlete is in the middle of a playoff run or a similar competitive scenario and taking time off for surgery is impossible, a corticosteroid injection is potentially helpful to improve symptoms over the course of several weeks to months. A corticosteroid injection may also be helpful from a diagnostic standpoint in differentiating between carpal tunnel syndrome and more proximal nerve compression issues when the history, examination, and neurodiagnostic tests are equivocal or inconclusive. I use a 1.5-inch 25-gauge needle and inject 40 mg of Kenalog with 1 mL of lidocaine, entering just ulnar to the palmaris longus at the distal volar wrist crease. The needle is directed distal and slightly radial and is buried to the hub to ensure that it is within the carpal canal and deep to the median nerve. Transient median nerve paresthesias may signal initial penetration of the median nerve, but once the needle is advanced and the paresthesias resolve, the medication may be safely administered without risk of intraneural dispersion. Although intraneural injection of medication does not necessarily cause iatrogenic pressure necrosis of nerves and its role in causing permanent neuropathy is controversial, most practitioners strive to avoid it. If the needle strikes the floor of the carpal canal, I withdraw it just enough to allow the injection to flow easily. I warn the patient that transient paresthesias may recur as the needle is withdrawn. The entire injection process should take only 5 to 10 seconds. Some persons may question this method because of the theoretical risk of direct median nerve injury from needle penetration, but no evidence of permanent adverse sequelae has been reported with use of this technique when a small-gauge needle is used. I have used this method at least 200 times, and none of my patients has experienced iatrogenic median neuropathy.
Some practitioners prefer to inject the drug superficially in an attempt to inject the medication into the potential space between the antebrachial fascia and the median nerve. Other practitioners opt to inject the medication through the flexor carpi radialis tendon sheath, directing the needle ulnarly, which places the palmar cutaneous branch of the median nerve at greater risk than the median nerve proper. The use of ultrasound-guided nerve blocks in the office and operating room setting is rapidly expanding, and applications in the diagnosis and treatment of carpal tunnel syndrome continue to evolve.
For ulnar neuropathies of the wrist and hand, I also order neurodiagnostic tests if symptoms are constant or if motor involvement is apparent. False-negative results are more common for ulnar tunnel syndrome than for carpal tunnel syndrome. Again, activity modification and intermittent bracing may be helpful. One difference in the treatment of ulnar neuropathy at the wrist involves the presence of motor involvement. Intrinsic muscle weakness or atrophy resulting from identifiable secondary pathology, such as a hamate hook fracture, ulnar artery thrombosis, or other mass, should prompt the surgeon to address the offending source of compression sooner rather than later. A period of observation and activity modification is reasonable if secondary pathology is absent and the onset of motor changes has occurred recently. Situations typically occur in which a single acute trauma (e.g., a direct blow) or a few episodes of direct compression (e.g., from cycling) cause the ulnar nerve palsy. Although witnessing overt clawing or intrinsic muscle atrophy is discouraging, I typically monitor the athlete closely with monthly visits during the ensuing 4 months. Steady clinical improvement warrants further observation without repeat neurodiagnostic tests, and many palsies resolve completely within this time frame. Neurodiagnostic tests precede surgical intervention for cases that fail to resolve after the observation period. In my practice, the need for surgical intervention for ulnar neuropathy at the wrist is relatively rare without a laceration or secondary extrinsic cause of the neuropathy.
Although proximal radial neuropathy may cause both motor and sensory loss, involvement at the level of the wrist and hand is purely sensory in nature. Idiopathic neuropathy originating between the brachioradialis and extensor carpi radialis longus is called Wartenberg syndrome, or cheiralgia paresthetica. The main goals of treatment for this condition are to improve symptoms and prevent worsening, which may lead to complex regional pain syndrome type II, also known as causalgia . The most common nonoperative treatment for radial neuropathy at the wrist is removal of any constrictive external devices, wraps, or bands. Avoiding power pronosupination may have a limited benefit. Rehabilitative efforts focus on gentle stretching and nerve traction exercises, albeit with modest success. These activities must be undertaken with caution because careless actions may exacerbate the symptoms and be counterproductive. For recalcitrant cases, injection of a corticosteroid and/or a local anesthetic may be attempted, more for diagnostic than therapeutic purposes. If symptoms persist despite several (usually at least 4) months of conservative management and the athlete has at least temporary resolution of symptoms from injection of a local anesthetic, I offer surgical treatment.
Digital neuropathies that result from bowling, baseball, or racquet sports typically respond to nonoperative measures such as grip modification, padding, or other equipment changes. Again, several months of nonoperative trials are warranted before considering surgery. Although it is uncommon to treat idiopathic digital neuropathy surgically, procedures such as neurolysis and/or transposition have been described. For example, the ulnar digital nerve of the bowler’s thumb is usually released and transposed to prevent continued local mechanical trauma.
The list of medications that may reduce the severity of neurogenic pain and paresthesias is short. I usually reserve these medications for occasions when other nonoperative measures have failed and the athlete either declines surgery at the time or I believe surgery is unlikely to provide a benefit. I usually consider prescribing these medications only if the symptoms interfere with sleep or cause functional limitations during activities of daily living or athletic events. I have the most experience with gabapentin (Neurontin) and pregabalin (Lyrica) and typically start with the lowest dose at bedtime and titrate accordingly. Common adverse effects include dizziness and somnolence, which may limit the prescriber’s ability to increase the dosage for further symptom resolution. Questions regarding medication interactions or contraindications are deferred to a primary care physician to determine if these regimens are viable and safe options for the athlete.