Entrapment neuropathies refers to isolated peripheral nerve injuries occurring at specific locations where a nerve is mechanically constricted in a fibrous or fibro-osseous tunnel or deformed by a fibrous band. In some instances the nerve is injured by chronic direct compression, and in other instances angulation or stretching forces cause mechanical damage to the nerve. Common examples of nerve compression in a fibro-osseous tunnel are the carpal tunnel syndrome and ulnar neuropathy at the cubital tunnel (Stewart, 2000).
PATHOPHYSIOLOGY, HISTOLOGY AND BIOCHEMISTRY OF NERVE COMPRESSION:
A peripheral nerve consists of myelinated and unmyelinated axons originating in the dorsal root ganglion (in case of sensory fibres) and the grey matter of the anterior horn (in case of motor fibres) to form a mixed peripheral nerve. Some autonomic fibers too are carried by the nerve (Mackinnon, 2002).
Compression of a nerve in a given area can lead to a cascade of physiological changes resulting in pathological situations and then anatomical changes in the later stages. Eventually there is severe compromise of nerve function if left untreated (Hirata, et al.,2004).
Each axon is covered by endoneurium, a group of axons is surrounded by perineurium which is the most critical layer in neurophysiology as it represents the ‘Blood–Nerve Barrier’ (Mackinnon SE, 2002).
Between the fascicles there is the internal epineurium, and the whole nerve is covered by the epineurium, the connective tissue around the nerve is called mesoneurium and often carries the segmental blood supply of the nerve (Hirata, et al., 2005).
Nerves have both axial (e.g. the median artery) and segmental vasculature (e.g. the Superior Ulnar colateral artery) all along its course and compression results in altered pressure in the vessels on and within the nerve creating an internal compartment syndrome and/or a breakdown of the blood–nerve barrier with consequent leakages (Olsson Y, 1990).
The inner layers of the perineurium and the endothelial cells of the endoneurial microvessels create the blood–nerve barrier. These cells have tight junctions that are impermeable to many substances (Shimizu, et al., 2013).
Thus, the blood–nerve barrier provides a privileged environment within the endoneurial space. There are no lymphatic vessels within the endoneurial or perineurial spaces (Floris, et al., 2004).
Breakdown in the blood–nerve barrier will result in the accumulation of proteins and the ingress of lymphocytes, fibroblasts and macrophages as a reaction to previously shielded antigens contained within the perineurial space (Banerjee, et al., 2006).
This will initiate inflammation and eventually there is scar formation. If the barrier site at the inner layers of the perineurium remains relatively intact, this will then result in increased endoneurial fluid pressure and a mini compartment syndrome within the fascicle (Sukriti Nag, 2011).