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PATHOLOGY
In the first stage the spinal nerves are inflamed (radiculitis) and the adjacent blood vessels distended (hyperaemia). The subarachnoid space disappears. Deposition of collagen fibrils (scar tissue) begins. In the second stage, (arachnoiditis) the scar tissue increases, and the nerves become adherent to each other and the dura. The third stage, (adhesive arachnoiditis), involves complete encapsulation of the nerve roots. The subsequent compression causes them to atrophy. The scarring prevents the arachnoid from producing spinal fluid in that area. These stages were described by Burton in 1978. In some cases, the scar tissue calcifies (arachnoiditis ossificans). Benini and Blanco ([8]) described arachnoiditis as cystic and adhesive in nature. The cysts are collections of spinal fluid walled off by the meningeal adhesions. Arachnoid cysts are seen in some cases, especially if there is a foreign body present. They are particularly seen after Pantopaque myelography. An animal study ([9]) showed that there was proliferation of fibrous tissue, lymphocyte infiltration and that the pial blood vessels were obliterated. In the spinal cord adjacent, there were multiple small areas of demyelination. Cavitation of the cord was observed in areas where there was ischaemia (poor blood supply). Syringomyelia (cavity) is a complication of arachnoiditis, probably arising due to the pressure dissociation between the subarachnoid space and the central canal. It must be stressed that it does not occur in all cases of arachnoiditis. A further, uncommon, complication is communicating hydrocephalus. This is thought to be due to alterations in the cerebrospinal fluid dynamics, due to the effects of the scarring in the subarachnoid space. Arachnoiditis may, in a minority of cases, involve the brain as well as the spinal cord. There are also subdivisions of the condition called rhinosinugenic arachnoiditis and optochiasmic arachnoiditis, which are rare forms principally affecting the brain.
Introduction
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