The neurovascular bundle from the neck and chest, including the brachial plexus, the subclavian artery, and the subclavian vein, passes through three anatomic compartments to reach the upper extremity on each side (Figure 1, Page 4). From medial to lateral, the brachial plexus and subclavian artery pass through the scalene triangle (bounded by the anterior and middle scalene muscles), the costoclavicular interval (bounded by the clavicle and the first rib), and the retropectoralis space (bounded by the posterior margin of the pectoralis minor muscle and the anterior chest wall ). The subclavian vein takes a slightly different course, first passing anterior to the anterior scalene muscle, then joining the brachial plexus and subclavian artery to pass through the costoclavicular interval and retropectoralis space(5, 46-52).
Each of these three compartments may be narrowed by a number of processes that result in compression of the vital structures that pass through them (Figure 2, Page 5). The scalene triangle may be narrowed by abnormal size, tension, origins or insertions of the scalene muscles. The costoclavicular interval may be narrowed by congenital bony anomalies of the vertebrae, clavicle, or ribs, by healed fractures of the clavicle or ribs, or by abnormal positions of the shoulder girdle or clavicle. The retropectoralis space may be narrowed by abnormal positions of the scapula or clavicle, or by enlargement of the pectoralis minor muscle. These processes may cause isolated compression or entrapment of the brachial plexus(3, 23, 26, 53-56), the subclavian artery, or the subclavian vein. However, there is most often predominant compression of one structure, with lesser degrees of compression of the other structures.
The processes that narrow the anatomic compartments may be classified as structural, functional, or post-traumatic. Structural processes include congenital muscle anomalies, fibrous bands and variant ligaments at the thoracic outlet, variant courses of the brachial plexus components, and bony abnormalities such as the cervical rib. These have been extensively documented and categorized by surgeons, anatomists and pathologists (7, 10-12, 19, 20, 23, 28, 38, 42-44, 53, 57-64). These anomalies, bands and ligaments, or the less common bony abnormalities, decrease the baseline dimensions of the three anatomic compartments. Narrowing of any of these compartments at baseline predisposes the patient to nerve or vascular compression after an episode of trauma, or after overuse or non-physiologic use of the upper extremities.
Functional abnormalities include overuse or non-physiologic use of the muscles of the shoulder girdle in occupational or recreational settings, resulting in hypertrophy of the scalene muscles or imbalance of the extensive shoulder girdle musculature. These functional abnormalities may result in direct narrowing of the anatomic compartments by the hypertrophied muscles, or in secondary narrowing of the anatomic compartments through abnormal positions of the clavicle and shoulder girdle relative to the chest wall. It should also be noted that the position of the shoulder girdle is highly dynamic, and that the clavicle undergoes a complex three-dimensional motion with flexion or abduction at the shoulder joint. In particular, the clavicle moves to the greatest extent in a posterior direction, to a lesser extent in a superior direction, and rotates along its long axis. Since the first rib is relatively static, clavicular motion on flexion or abduction of the shoulder narrows the costoclavicular interval.
Post-traumatic abnormalities include direct trauma or stretching of the brachial plexus in motor vehicle accidents, fractures of the clavicle or ribs, and soft tissue injuries of the scalene muscles or other supporting structures of the neck (10-12, 19, 20, 28, 38, 42-44, 53, 57, 59-61, 65, 66).
Any congenital anatomic abnormality, functional change in the shoulder girdle, or post-traumatic alteration of the soft tissue or bony structures in the thoracic outlet can predispose the patient to compression of the brachial plexus as it passes through the thoracic outlet, especially with use of the affected upper extremity.
Thoracic outlet syndrome is divided clinically into three forms, based on which of the vital structures is compressed:
1. Neurogenic TOS-compression of the brachial plexus.
2. Arterial TOS-compression of the subclavian or axillary arteries.
3. Venous TOS-compression of the subclavian or axillary veins.
Neurogenic TOS is by far the most common form of TOS, accounting for 95 to 98% of all TOS cases. Unfortunately, this form of TOS has the most confusing clinical presentation of all the forms, and it is the form most likely to present in a subtle and insidious manner, and to follow a chronic and progressive course. No "gold standard" test has been accepted by the medical community for the diagnosis of neurogenic TOS.
Arterial and venous TOS are very uncommon, accounting for 5% or less of cases of TOS. These forms of TOS have dramatic clinical presentations, and are readily and accurately diagnosed with objective vascular imaging tests. Arterial TOS typically presents with upper extremity arterial insufficiency symptoms or embolic episodes, and ultrasound or arteriography demonstrates subclavian artery aneurysm, arterial thrombosis, or distal emboli. Venous TOS (Paget-Schroetter syndrome) typically presents with arm swelling and cyanosis, and ultrasound demonstrates thrombosis in the subclavian-axillary venous system.
The remainder of this white paper focuses on neurogenic TOS, because of its anatomic complexity, its diagnostic dilemma, and the past history of controversy regarding neurogenic TOS.