Neurogenic thoracic outlet syndrome is a chronic compressive and entrapment neuropathy of the brachial plexus. Chronic nerve compression in rodents and primates has been well studied, and these histopathologic changes occur as a predictable and progressive continuum of changes.  The clinical changes seen in neurogenic thoracic outlet syndrome parallel these histopathologic changes.

Initial disturbance of intraneural blood flow leads to early breakdown of the blood-nerve barrier, which is followed by edema within the affected nerve fascicles.  Fibrosis and thickening of connective tissue structures within and around the fascicles then develops.  With continued compression, segmental demyelination occurs, eventually progressing to diffuse demyelination.  Finally, the underlying axons undergo Wallerian degeneration.  The degree and rapidity of these changes is related to the degree and duration of nerve compression, and within any one nerve, certain fascicles are affected more than others.  Thus, sensory and motor symptoms and signs may take different courses.

The clinical symptoms and signs of neurogenic TOS parallel this temporal pattern.  Initial sensory nerve compression occurs only with specific postures or maneuvers, resulting in pain, paresthesias, or vascular disturbances of the neck, shoulder, and upper extremity.  These symptoms often occur hours after the compressive episodes, often waking the patient at night or being noted by the patient after waking from sleep.  The patient may be completely asymptomatic at rest. In many cases, the patient learns to avoid these postures or maneuvers, either limiting or stabilizing the symptoms.  If the patient is unable to limit or avoid these postures or maneuvers, the sensory symptoms may become persistent, even after the patient returns to a normal posture.  Without resolution of the causative compression, the sensory symptoms can progress to anesthesia in some or all of the affected areas.

Initial motor nerve compression causes poorly localized pain or a cramping sensation in the muscles of the upper extremity.  If the nerve compression persists, damage to the larger and more centrally located motor axons will occur, and weakness will gradually appear.  Finally, in the most severe and persistent nerve compression syndromes, the large motor axons will degenerate, neurotrophic changes in the subtended muscles will occur, and atrophy of these muscles will be clinically detectable.  These motor changes are the first objective clinical signs of TOS, but they occur late in the course of the disease process, and often represent permanent and irreversible nerve damage, with accompanying functional disability.