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“If you can force your nerve, heart and sinew to serve you long after they are gone, and so hold on when there is nothing in you except the will which says to them: ‘Hold on!’”

Rudyard Kipling (1865–1936)


On completion of this chapter, the student/practitioner will be able to:

  • Describe the anatomical course of each upper extremity peripheral nerve.

  • Identify common nerve entrapment sites in the upper extremity.

  • Discuss the signs and symptoms of common tunnel syndromes of the upper extremity.

  • Discuss the possible functional loss attributed to each neuropathy.

Key Terms

  • Compressive neuropathy

  • Entrapment

  • Tensile neuropathy

  • Tunnel syndrome


With the undulating course of peripheral nerves from the central nervous system distally to the end organs, nerves pass through bony, fibrous, osteofibrous, and fibromuscular tunnels risking injury from compression, entrapment, and tensile forces. Because most peripheral nerves carry motor, sensory, and autonomic fibers, the potential spectrum of impairment is impressive. Careful linking of the presenting signs and symptoms assists the clinician in identifying a list of differential diagnoses that, through examination and testing, can be confirmed, disproved, or added to.

The nomenclature of the etiology of entrapment, compressive, and tensile neuropathies is diverse. Some syndromes are named after the describing author, such as Kiloh-Nevin syndrome. Some are named after an anatomical area, such as metatarsalgia and thoracic outlet syndrome. The movement producing the symptoms may provide the name, such as glenohumeral hyperabduction syndrome. “Tunnel” is often in the name, such as carpal tunnel syndrome (CTS) or tarsal tunnel syndrome. The nerve may be the descriptor, such as ilioinguinal syndrome. Lastly, the etiological structure may be the descriptor, such as pronator teres syndrome.

Although the diagnostic names may vary, all entrapment, compressive, and tensile neuropathies originate from a lesion to the peripheral nerve and associated structural elements in a narrow anatomical space. Neuropathy may be compressive, such as from a hypertrophied muscle, aberrant bone or bone formation, or tumor. Traumatic neuropathy may occur from a missile, laceration, repetitive use, or blunt contact. Metabolic etiologies include diabetes mellitus or hyperthyroidism. Toxic neuropathies occur with lead and mercury intoxication or with some prescriptive medications. Infections may produce space-occupying lesions or neural necrosis via bacteria and viruses. Tensile causes include stretching over or around aberrant anatomy. Anatomical variations may affect nerves, such as a post-fixed brachial plexus or a cervical rib. In this chapter, we concentrate on entrapment, compressive, and tensile neuropathic sites of injury. Other chapters provide more detailed descriptions of the etiology of the neuropathy.

For this chapter, the term “tunnel syndromes” indicates all entrapment, compressive, and tensile neuropathies. Although there are a large number of tunnel syndromes in the upper extremity, this chapter focuses only on the more common syndromes in the upper extremity. This text also includes ...

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