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Thoracic outlet syndrome (TOS) consists of a group of distinct disorders that affect the brachial plexus (nerves that pass into the arms from the neck), and/or the subclavian artery and vein (blood vessels that pass between the chest and upper extremity).
For the most part, these disorders are produced by compression of the components of the brachial plexus (the large cluster of nerves that pass from the neck to the arm), the subclavian artery, or the subclavian vein. These subtypes are referred to as neurogenic TOS, arterial TOS, and venous TOS, respectively. The compression may be positional (caused by movement of the clavicle (collarbone) and shoulder girdle on arm movement) or static (caused by abnormalities or enlargement of the various muscles surrounding the arteries, veins and brachial plexus).
The neurogenic form of TOS accounts for 95 to 98% of all cases of TOS.
It is known from pathological studies of cadavers, and from surgical studies of patients with TOS, that there are numerous anomalies of the scalene muscles and the other muscles that surround the arteries, veins and brachial plexus. TOS may result from these anomalies of the scalene muscles or from enlargement (hypertrophy) of the scalene muscles. One common cause of hypertrophy is trauma, as may occur in motor vehicle accidents.
The two groups of people most likely to develop TOS are those suffering neck injuries in motor vehicle accidents and those who use computers in non-ergonomic postures for extended periods of time. Young overhead athletes (such as swimmers, volleyball players and baseball pitchers) and musicians may also develop thoracic outlet syndrome, but significantly less frequently than the two large groups above.
The following taxonomy of TOS is used in ICD-9-CM and older sources:
A more modern system of classification is provided on the website of the National Institute of Neurological Disorders and Stroke (NINDS).[1]
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