The clinical signs of CTS may be quite variable on neurologic examination; early, there are often no specific findings. In this instance, sometimes typical CTS symptoms can be precipitated by tapping over the nerve at the wrist. This maneuver is known as the Tinel sign; parenthetically, this is not specific to CTS but rather to any site of focal nerve damage where percussion produces sensory symptoms distal to the site of clinical involvement. This is also particularly useful with ulnar lesions at the elbow, radial nerve lesions in the mid–upper arm, and fibular (peroneal) nerve lesions below and just lateral to the knee.
Early, when clinically defined CTS deficits develop, these are usually confined to loss of sensation in the median-innervated finger tips, sparing the palm because the palmar branch of the median nerve leads off from the primary median trunk proximal to the carpal tunnel and thus passes superficial to the same and is not subject to entrapment. Two-point discrimination, light touch, and pinprick sensory modalities may be affected with early sensory loss. As the degree of entrapment increases, the motor branches become affected. This leads to weakness and atrophy of the thenar eminence, particularly affecting thumb abduction and opposition. Atrophy of these muscles leads to a hollowing out of the most lateral (radial) portion of the thumb.
Differential diagnosis is usually straightforward. Cervical radiculopathies, particularly at C6 or C7, are the most common consideration. These patients often first experience unilateral intrascapular pain and/or develop significant cervical radicular pain and persistent sensory paresthesias unrelated to time of day, in contrast to nocturnal expression with early CTS. Cervical spine and spinal cord magnetic resonance imaging (MRI) is useful in making this differential diagnosis.
Other considerations in the differential diagnosis, particularly when there is thenar atrophy, include proximal median nerve lesions, motor neuron disease, multifocal motor neuropathy, and the rare thoracic outlet syndrome. The last condition is related to compression of the upper medial portion of the brachial plexus, affecting the T1 root. In contrast to involvement in a median nerve distribution with feelings of numbness in the thumb, index, and middle fingers, patients with the thoracic outlet have sensory loss in an ulnar nerve distribution. Before the development of electrodiagnostic techniques, many patients with ulnar nerve lesions were incorrectly presumed to have thoracic outlet lesions and were surgically decompressed without any improvement.
In addition, when the clinical and electrodiagnostic findings do not support a CTS diagnosis, the outside chance of a central nervous system lesion always needs to be considered. Syringomyelia or other intramedullary spinal disorders may lead to an atrophic thumb. However, observing the classic cape-type sensory loss and obtaining a cervical spine MRI allow for this diagnosis. Lastly, especially with intermittent symptoms, carotid atherosclerosis producing transient ischemic attacks or a slow-growing intracranial tumor, such as meningioma or glioma, may initially mimic CTS.
DIAGNOSIS AND THERAPY
Nerve conduction studies (NCS) are the primary means for confirming a CTS diagnosis. These demonstrate delayed conduction across the carpal tunnel; the sensory components are most sensitive to early change. Although conservative therapy with wrist splints (used while sleeping), are helpful early, most patients with significant CTS changes require simple outpatient surgical decompression. This is successful in the vast majority of patients.

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