Walsh has identified three causative factors for TOS that could be interrelated or exist separately: compressive neuropathy, faulty posture, and entrapment.

• Compressive neuropathy. Compression of the neurovascular structures can occur if there is a decrease in the size of the area through which the brachial plexus and subclavian vessels pass. Compression can result from muscle hypertrophy in the scalenes or pectoralis minor, anatomical anomalies such as cervical rib or fractured clavicle, adaptive shortening of fascia, or a space-occupying lesion.

• Faulty posture. Changes in posture, particularly forward head with increased thoracic kyphosis, protracted scapulae, and forward shoulders narrow the spaces through which the neurovascular structures pass. Specifically, adaptive shortening of the scaleni and pectoralis minor muscles can potentially compress the neurovascular tissues or can cause repetitive trauma and adhesions with overuse. If the angle of the clavicle falls below the level of the sternoclavicular joint, the shoulder girdle causes traction on the plexus. In addition, the clavicle can compress the neurovascular structures against the first rib.

Other contributing factors to postural stresses include hypertrophy of breast tissue leading to postural fatigue or pressure from undergarment support straps, and carrying a heavy briefcase, suitcase, or shoulder purse that causes pressure across the shoulder girdle, fatigue in the scapular stabilizers, or traction across the shoulder girdle tissues.
A surgical study reported findings that pathological adhesions of the brachial plexus to the scalenus muscle led to nerve fiber distraction as the mechanism behind the symptoms and suggested that the restrictive adhesions were directly related to long-standing postural deviations and myofascial pain syndrome.

• Entrapment of the neural tissue from scar tissue or pressure. Entrapment affects the ability of nerve tissue of the brachial plexus to tolerate tension as it courses through the various tissues in the thoracic outlet. A possible explanation was offered in a review article by Carotti wherein the pain-immobility-fibrosis loop that occurs after trauma (e.g., following an acceleration-extension motor vehicle injury) leads to the development of adhesions, which cause or perpetuate TOS symptoms. The Halstead test and the upper limb tension test for the median nerve place the brachial plexus and median nerve on a stretch and with symptoms may indicate restricted nerve gliding. The Halstead test also may obliterate the radial pulse indicating vascular entrapment. Wilson et al.described a cadaver study that demonstrated tension placed on the subclavian artery with either ipsilateral or contralateral side-bending of the cervical spine during the TOS testing maneuvers. They suggested that this could be the source of pain or tension symptoms even prior to signs of vascular pathology (decreased pulse, pallor, skin temperature).

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