Carpal tunnel syndrome, or compression of the median nerve at the wrist, is the most prevalent compression neuropathy of the upper extremity. It more commonly affects the middle-aged and older population with a mean age at diagnosis of 50 years, and it is more common in women than men (approximately 4:1). Other risk factors for the development of carpal tunnel syndrome include pregnancy, menopause, obesity, hypothyroidism, diabetes mellitus, renal failure, alcoholism, inflammatory arthritis, amyloidosis, and high hand/wrist repetition rate.¹,² Despite identifying these risk factors, there is still no uniform consensus on the precise mechanism by which carpal tunnel syndrome develops.

The diagnosis of carpal tunnel syndrome is made with a clinical history and physical examination, as well as adjunct diagnostic testing. The classic patient will describe nocturnal paresthesias in the median nerve distribution (thumb, index finger, long finger, and radial side of the ring finger), although this can be variable. Patients may also describe a burning, painful sensation in the hand and wrist as well as loss of hand dexterity and muscle atrophy, particularly in more severe cases. These symptoms gradually worsen as nerve compression continues and injury progresses. Abnormal sensibility testing and positive provocative examination maneuvers such as the Phalen test, Tinel sign, and Durkin compression test are supportive of the diagnosis but should not be used in isolation to make the diagnosis.

Nerve conduction studies (NCS) and needle electromyography (EMG) can be useful diagnostic tools to help confirm carpal tunnel syndrome. Focal demyelination of the median nerve is manifested by delayed conduction velocities across the wrist on NCS and may assist in ruling out other possible sites of nerve compression. The presence of thenar atrophy and/or muscle fibrillations on needle EMG can help determine the severity of disease and therefore influence prognosis.

There have been more recent advances in and support of ultrasonography as a reproducible, rapid, and painless alternative to electrodiagnostics. Diagnosis is made by the identification of an enlarged, hypoechoic median nerve at the carpal tunnel inlet (Figure 1). The cross-sectional area (CSA) of the nerve is measured with a diagnostic cut-off value of 11 mm².³,⁴ When compared with electrodiagnostics, one study found a positive correlation (r = 0.81) between increased nerve CSA and
distal motor and distal sensory latency values on NCS.⁵ Additional studies have reported on the inter-rater and intrarater reliability among examiners when measuring nerve CSA as well as suggested superiority of ultrasonography over NCS/EMG, promoting its use as a reliable and accurate diagnostic tool. Another study⁶ found moderate agreement among examiners of varying levels of experience when measuring the CSA of the median nerve (Lin concordance correlation coefficient of 0.59), with experienced examiners having excellent intra-rater reliability. Additionally, a 2019 prospective cohort series demonstrated that ultrasonography had a lower false-positive rate than NCS (23% compared with 43%) in asymptomatic patients as measured by the six-item carpal tunnel symptoms scale (CTS-6), which relies on history and physical examination alone to make the diagnosis⁷ (Table 1).

There also has been recent controversy regarding the necessity of adjunct diagnostic testing, particularly electrodiagnostics, given the reliability of the CTS-6 scoring system. One study prospectively compared CTS-6 (as well as other clinical diagnostic questionnaires) with NCS in 408 wrists in 250 patients and reported that although NCS had a high sensitivity (94%), CTS-6 had the highest specificity (99% compared with 50% for NCSs), suggesting that electrodiagnostics are actually not ideal confirmatory tests.⁸ Further research is needed in this area, which is challenging given the current lack of an objective gold standard diagnostic tool.

Nonsurgical management in the form of therapy, bracing the wrist in a neutral position particularly at nighttime, and corticosteroid injection should be considered as initial treatment options for mild to moderate symptoms.² A 2021 double-blind randomized clinical trial reported on the efficacy of corticosteroid injection.⁹ A total of 111 patients with idiopathic carpal tunnel syndrome were randomized to one of two steroid injection groups (40 and 80 mg of methylprednisolone) or a saline placebo group. Ultimately, 90% of the trial participants went on to have carpal tunnel surgery within 5 years of injection; however, there were some notable findings. Surgical treatment was less likely in the higher dose steroid group compared with placebo (84% versus 97%) and time from injection to surgical treatment was significantly longer after steroid injection compared with saline (6 months versus 3 months).

Surgical treatment involves releasing the transverse carpal ligament, decompressing the median nerve. Historically this procedure is performed via a standard, open approach; however, other techniques have been developed including endoscopic and ultrasonography-guided carpal tunnel release, facilitated by a retractable blade or a thread device, respectively. Patients undergoing endoscopic carpal tunnel release have been shown to return to work faster, with less postoperative pain and pain medication use; however, this technique has been reported to have a higher procedural cost as well as an increased risk for iatrogenic nerve injury.¹⁰,¹¹,¹² However, a 2021 study evaluated the cost-effectiveness of endoscopic versus open techniques in patients undergoing unilateral carpal tunnel release and determined that endoscopic carpal tunnel release is actually more cost-effective if performed under local anesthesia when considering earlier return-to-work parameters.¹³ Conversely, a 2020 study reported that patients who underwent endoscopic carpal tunnel release had a higher rate of
revision surgery within 1 year after the index procedure compared with those who had an open release (6.5% versus 4.4%).¹⁴ There has also been recent advocacy of “wide awake, local anesthesia, no tourniquet,” or WALANT, surgical release, which spares the patient the possible complications of intravenous anesthesia as well as tourniquet pain, whereas others claim that there is no difference in outcomes or patient satisfaction when compared with monitored anesthesia care and a local anesthetic.¹⁵,¹⁶,¹⁷ Cost-effectiveness by setting and surgical technique continues to be evaluated in the literature.¹⁸

Although studies including large randomized controlled trials continue to question the superiority of the different techniques, there has been no definitive evidence to suggest a best approach when considering long-term outcomes. Postoperative complications of all surgical techniques include a 0.5% incidence of nerve, arterial, or tendon injury; complex regional pain syndrome; and infection (<1%).¹⁹

Recurrent carpal tunnel syndrome after surgical release can occur from a number of causes including improper diagnosis, incomplete release, secondary nerve compression, scar formation, and adhesions. A thorough history and examination as well as a diagnostic workup are indicated to determine the most likely etiology and therefore treatment. The authors of a 2020 study looked at risk factors for and rate of revision carpal tunnel release.¹⁴ They reported a revision rate of 1.5% and a median time to secondary surgery of 1.23 years, with risk factors being older age, male sex, bilateral release, and endoscopic release. Revision median nerve neurolysis can be performed alone or in combination with local soft-tissue flaps or allograft wraps, although, similar to primary release techniques, there does not appear to be a superior method.²⁰

Cubital tunnel syndrome, or compression of the ulnar nerve at the elbow, is the second most common compression neuropathy, with an incidence of approximately 30 per 100,000 person-years.²¹ It is more common in the older and male population. Patients will typically present with progressive paresthesias in the ulnar digits of the hand (small finger and ulnar aspect of the ring finger) and eventual motor weakness and atrophy of the hypothenar and intrinsic muscles. Vague elbow pain can be an additional presenting symptom. Patients also tend to present with a more severe presentation than with carpal tunnel syndrome.

Cubital tunnel syndrome is similarly diagnosed by clinical history and examination with diagnostic testing as adjuncts. Careful examination of sensation in the ulnar nerve distribution, specifically the dorsal ulnar cutaneous nerve, is paramount. Given its anatomic origin, branching from the ulnar nerve proper 6 cm proximal to the wrist, preservation of sensation indicates a more distal compression site (Guyon canal), whereas absence of sensation is more likely to indicate compression at the level of the elbow. Positive provocative examination maneuvers such as symptom exacerbation by prolonged elbow flexion, Tinel sign at the elbow, Wartenberg sign (weakness in small finger active adduction), Froment sign (obligate thumb interphalangeal flexion with pinch from a weak adductor pollicis), and the scratch collapse test (obligate shoulder internal rotation after lightly scratching the area of compression coupled with resisted shoulder external rotation) also support the diagnosis of cubital tunnel syndrome, though the latter has been reported to be very operator dependent.²² NCS and EMG can be helpful to confirm the diagnosis, demonstrating delayed conduction velocities across the elbow and possible muscle atrophy and fibrillations in distal ulnarly innervated muscles; however, their reported sensitivity in the literature is only 60% to 80%. As with carpal tunnel syndrome, ultrasonography and uniquely MRI are being increasingly recognized as diagnostic aids in lieu of electrophysiologic studies. Diagnosis is made by measuring the CSA of the ulnar nerve 1 cm proximal to the medial epicondyle, with a cutoff value of 11.0 mm².²³,²⁴ Ultrasonography also can be helpful in determining ulnar nerve instability because physical examination assessment has been found to be poorly correlated with intraoperative findings of instability (12% compared with 88% with ultrasonography).²⁵

Patients without atrophy or dense sensory loss should initially be treated with nonsurgical modalities including therapy, extension bracing at nighttime and elbow padding, and anti-inflammatory medication. If these interventions fail in these patients, surgical treatment can be considered. The most appropriate surgical intervention is still debated, ranging from simple in situ decompression to ulnar nerve transposition. There are various degrees of in situ decompression from simply unroofing the cubital tunnel to circumferential neurolysis extending from the proximal arcade of Struthers to the distal Osborne fascia. If nerve subluxation or dislocation is present or affects a younger patient, many surgeons advocate for transposition of the ulnar nerve.²⁶ Similarly with in situ decompression, an anterior transposition of the ulnar nerve can be performed by various techniques including subcutaneous, intramuscular, or submuscular, with a multitude of different methods to secure the nerve anteriorly. Transposition typically
requires a more extensive dissection to prevent tethering of the nerve. Potential tethering structures include branches of the medial antebrachial cutaneous nerve and ulnar artery, the medial intermuscular septum, the flexor-pronator muscle origin, and flexor digitorum superficialis fascia.

A recent Cochrane review²⁷ reported 70% of patients with good or excellent results after both in situ and anterior transposition techniques but with insufficient evidence to recommend one method over the other, although many studies have compared the rates of reoperation and complication rates between the two methods.²⁸,²⁹ Some studies have reported higher rates of secondary surgery and complications in patients undergoing anterior transposition.³⁰,³¹ Endoscopic techniques are also increasingly being used, the benefits of which can include better scar satisfaction and reduced early postoperative pain among patients; however, symptom relief and return-to-work parameters have been similar when compared with in situ decompression.³²,³³ Complications of surgical intervention include incomplete release, nerve injury (ulnar nerve or branches of the medial antebrachial cutaneous nerve), nerve instability, and infection.

In patients with weakness and atrophy from long-standing cubital tunnel syndrome, attention has been given to nerve transfer procedures to improve recovery of intrinsic function. Patients with severe cubital tunnel syndrome with significant intrinsic weakness and atrophy (as well as electrodiagnostic evidence of axonal loss) may benefit from a supercharge end-to-side anterior interosseous nerve to ulnar motor nerve transfer.³⁴,³⁵ A 2020 study reported outcomes in the first cohort of patients undergoing this procedure.³⁴ The study authors evaluated improvement in first dorsal interosseous Medical Research Council grade and time to reinnervation, changes in pinch and grip strength, as well as Disabilities of the Arm, Shoulder and Hand (DASH) scores. Thirty-nine of the included 42 patients had successful improvement of intrinsic function from baseline, 33 of whom improved to a Medical Research Council grade of three or higher. First dorsal interosseous, pinch, and grip strength as well as DASH scores were significantly improved from baseline at a mean follow-up of 11.2 months. Age was the only identified risk factor for failure. This study also noted that additional research is needed to better understand ideal standard outcome measures (objective intrinsic function) as well as more clearly delineate indications for the procedure.

Recurrent cubital tunnel syndrome can occur for the same stated reasons as recurrent carpal tunnel syndrome, which can be challenging to diagnose and treat. Recent literature suggests, however, that a significant percentage of patients (77%) can experience symptom improvement after revision cubital tunnel decompression. This procedure should therefore be considered in patients with recurrent disease, but with appropriate counseling that outcomes have been shown to be inferior compared with primary surgery.³⁶,³⁷ If an obvious area of compression cannot be identified, submuscular transposition is recommended.³⁸

Radial tunnel syndrome is a controversial diagnosis that involves the compression of the posterior interosseous nerve in the proximal forearm. It is a much rarer compression neuropathy, occurring in approximately 0.03% of the general population, although some think that it is more common than this. The mean age at diagnosis is 30 to 50 years, and it occurs more frequently in women than men in some studies.

The most common symptom on initial presentation is a deep aching, often nocturnal pain in the proximal forearm overlying the mobile wad, but distal to the lateral humeral epicondyle (approximately 5 cm distal). Patients will have focal tenderness to palpation in this area, but with preserved muscle strength and intact sensation in the posterior interosseous innervated muscles and superficial radial sensory nerve distribution, respectively. Pain may be worsened with resisted supination of the forearm and/or resisted wrist hyperextension. Electrodiagnostic studies are almost always normal unless the nerve is injured, making the diagnosis a clinical one. However, adjunct studies such as ultrasonography or MRI can be used if a space-occupying lesion or mass that could be compressing the nerve is suspected. Caution should be used when implementing ultrasonography as a diagnostic tool because the posterior interosseous nerve can normally appear flattened as it enters the supinator.³⁹ Corticosteroid injection can be diagnostic as well as therapeutic. Radial tunnel syndrome is a diagnosis of exclusion, as other more common diagnoses should be ruled out first, most notably lateral epicondylitis, which often is a concurrent diagnosis.