Sheila k. Singh and Rajiv Midha

Case Presentation

A 51-year-old, left-handed homemaker presented with a 2- to 3-year history of progressively worsening paresthesias, numbness, and tingling in the lateral three digits and radial palm of both hands, with the left hand more severely affected. She described complete left-hand numbness after peeling potatoes, and shaking the hand relieved it to some extent. She also described nocturnal numbness and burning, particularly when sleeping with her left hand flexed under her cheek, that often awakened her from sleep. These nocturnal symptoms improved slightly after she began to use wrist splints. She had recently noted difficulty in opening jars with her left hand.

She denied any neck pain or radicular symptoms in the arms. Her past medical history was significant only for hypothyroidism, and her only current medication was levothyroxine.

Physical examination showed a slight decrease in muscle power in the left abductor pollicis brevis. Reflexes were normal and symmetric. Sensory examination revealed decreased sensation to light touch and pinprick in the lateral three digits of both hands. Tinel sign was positive at both wrists, and a positive Phalen sign was present on the left. The remainder of the neurological examination was normal.

Bilateral median nerve conduction studies revealed prolonged distal sensory and motor latencies, compatible with severe left-sided and moderate right-sided carpal tunnel syndrome (CTS).

Because the patient’s paresthesias and pain failed to resolve with conservative therapy consisting of splinting and oral nonsteroidal anti-infl ammatory drugs (NSAIDs), she decided to undergo carpal tunnel release. A left carpal tunnel release was performed under local anesthesia. Operative findings included a thickened transverse carpal ligament and a swollen, indurated, and erythematous median nerve at the point of compression under the ligament.

Five weeks postoperatively, the incision was well healed, and the patient described a decrease in pain, numbness, and paresthesias in her left hand. Neurological examination was normal. She continued to experience numbness and burning pain in the right hand, which did not respond to local corticosteroid injection. She agreed to consider a right carpal tunnel release in the near future.

Diagnosis

Carpal tunnel syndrome

Anatomy

The median nerve originates from the medial and lateral cords of the brachial plexus. Coupled with the brachial artery, it runs along the medial intermuscular septum to enter the antecubital fossa medial to the biceps tendon. It enters the forearm between the two heads of the pronator teres muscle and courses along the inferior flexor digitorum sublimis (FDS) muscle belly, giving branches to the pronator teres, flexor carpi radialis, flexor digitorum superficialis, and palmaris longus. At the level of the elbow, the anterior interosseous nerve forms to innervate the flexor digitorum profundus of digits two and three, the flexor pollicis longus, and the pronator quadratus. In the distal forearm, the median nerve travels under the tendon of the palmaris longus and under the transverse carpal ligament (TCL) to enter the wrist.

The TCL, an annular pulley of the flexor mechanism, is a thick fibrous band arching over the carpal bones, attaching radially to the trapezium and scaphoid tuberosity and ulnarly to the pisiform and hook of the hamate. The floor of the tunnel is composed of the volar radiocarpal ligament, as well as the bridging ligaments between the carpal bones. In addition to the median nerve, the carpal tunnel contains nine long flexor tendons, the synovium beneath the TCL, and a median nerve vascular bundle. The nerve emerges at the distal border of the TCL, where the recurrent motor branch arises to innervate the thenar muscles. To protect this structure during exposure and division of the TCL, the surgeon must be aware of the anatomical variations of the motor branch. Lanz has provided a classification of the branching variants as extraligamentous and recurrent (50%), subligamentous (30%), and transligamentous (20%). Multiple accessory motor branches may also occur as a separate variant.

Characteristic Clinical Presentation

The classically described presentation of CTS consists of tingling, aching, burning, or numbness of the radial half of the hand and the lateral three digits, although often the entire hand is involved. Nocturnal hypesthesias are common, often awakening the patient from sleep, when the numb hand must be shaken for the patient to obtain relief. Clumsiness or weakness of the involved hand can occur, and along with the sensory disturbances, is usually aggravated by activity or use of the hand. The onset of symptoms is usually slow and insidious, although it may be acute following a traumatic injury. Patients may occasionally present with shoulder or upper arm pain, or radiation of dysesthesias from the wrist to the proximal forearm.

Most authors describe a female preponderance for CTS, with a female to male ratio of more than 2:1. Palmer has estimated an incidence of 1% in the general population, and a greater than 5% incidence among workers in industries that require repetitive use of the hands or wrists. Repetitive strain injuries represented 48% of all reported workplace illnesses in 1990, compared with 18% in 1980, with CTS ranked as the most prevalent of these disorders. More than 50% of all cases occur between the ages of 40 and 60.

Early signs of the syndrome include those described by Phalen and Tinel, in which lancinating paresthesias in the median nerve distribution are reproduced by forced wrist flexion, or percussion over the median nerve at the wrist, respectively. Caveats with these supposedly pathognomonic signs include a high false-positive rate of Tinel sign and the absence of Phalen sign in patients with profound sensory loss. As the entrapment neuropathy advances, the patient develops decreased sensation to pain or light touch in the radial half of the hand and the first, second, and third digits as well as the radial half of the fourth digit. Thenar muscle atrophy and muscle weakness, especially involving the abductor pollicis brevis, occur in advanced cases of CTS. Positive Tinel and Phalen signs and objective sensory findings in the median nerve distribution confer an 85% diagnostic certainty for CTS.

AVM, arteriovenous malformation.

Management Options

Not all patients with CTS require surgical care; indeed, one indication for operative intervention is failure to respond to conservative therapy. Conservative treatment includes splinting, corticosteroid injections into the carpal tunnel, and oral NSAIDs or steroids.

Surgical treatment is most effective when offered early in the course of the neuropathy, before significant axonal loss has occurred. A recent retrospective study of 425 patients with CTS demonstrated that patients who had surgery were six times more likely to have resolution of symptoms than were patients who did not have surgery. Furthermore, patients who underwent surgery less than 3 years from the time of initial diagnosis of CTS were more than twice as likely to have symptom resolution than patients who underwent late surgery (more than 3 years after diagnosis). The authors conclude that surgery is a highly effective treatment, but duration of CTS was a key determinant of surgical outcome.

Surgical Treatment

The TCL release is an established and well-proven therapy for CTS, the goal of which is to adequately divide the TCL while preserving the recurrent motor and palmar cutaneous branches of the median nerve, as well as other neuro-vascular structures. Open release can be done with locally injected anesthesia; our preference is to use 1% lidocaine supplemented with epinephrine.