Introduction to Thoracic Outlet Syndrome
Pathology of Chronic Nerve Compression
There are histopathological changes that occur to a nerve undergoing chronic compression which takes place in thoracic outlet syndrome (TOS). The compression causes injury which progresses as follows:
Symptoms begin with aching in the limb, then progress to weakness and muscle atrophy; from passing paresthesia (abnormal sensations in the absence of a stimulus) to constant numbness.
Based on current research, it appears that following the beginning stages of compression, there is a malfunctioning or breakdown of the blood-nerve barrier. This barrier is made of cells that protect the nervous system from being damaged by compounds or toxins which may be circulating in the blood. The malfunctioning of this protective barrier renders the nerves in the brachial plexus vulnerable to damage.
With continued compression, there is a thickening of the perineurum (the sheath surrounding a bundle of peripheral nerve fibers).
Demyelination (loss of the fatty cover, called myelin, from nerve fibers) of segments of the neurons develops which becomes more diffuse with time and ultimately results in injury to the nerve sheath (axon).
Electrodiagnostic studies are typically normal until demyelination commences. Nerve changes occur slowly and are related to the duration and degree of compression.
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