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B.P.A.A. News Letter - Spring 1996
Volume 4, Number 2 (Page 2)

Margaret A. Hill

Dr. Charles V. Burton, medical director of the Institute for Low Back Care in Minneapolis, Minnesota (and the honorary chairman of BPAA), describes arachnoiditis in three stages: (4) arachnoidal adhesions, adhesive arachnoiditis, and calcified arachnoiditis. The spectrum of arachnoiditis is shown in figure 1 on page 4 (Figure 1-a shows the normal anatomy.) The initial phase, Figure 1-b, reflects swelling and hyperemia (increased flow of blood to the area) of the nerve roots of the cauda equina as a response to infection, irritation, or the presence of a foreign body substance. If this response is greater, the subarachnoid space is often obliterated by the swollen nerve roots such that, if the dura is surgically opened, its contents may herniate through the dural opening. Fibroblast proliferation is initiated by the inflammatory response, and collagen deposition occurs.

 

In the next phase, Figure 1-c, the process has become less acute, and the nerve swelling and hyperemia have subsided. This phase is characterized by more extensive collagen deposition (hence the term “adhesive”), which serves to attach the nerves to each other as well as to the meninges. It is probably at this point that autoimmune response factors determine whether the process abates or progresses in intensity and scope.

Those rare cases in which fulminating arachnoiditis travels up the neuraxis to involve the brain stem and brain (capable then of producing hydrocephalus and death) most likely represent extreme examples of the autoimmune reaction to foreign body insult.

 

Figure 1-d shows nerves that have become atrophic, more adherent, and enmeshed in dense scar tissue. The nerves may become so completely covered with collagen that an observer, on opening the dura, is presented with what typically appears to be an empty tube devoid of identifiable nerve fibers. Because they have become an integral part of the dural membrane, it is possible to section these spinal nerves by a single lumbar puncture or by surgically opening the dural sac. In advanced lumbosacral adhesive arachnoiditis, residual iophendylate is the only foreign body commonly seen to cause this type of reaction.

 

 

The re-absorption of free postmyelographic residual iophendylate by the body is estimated to be about 1 ml per year, but after it becomes encysted, it may remain present and unchanged for many years. Diagnostic radiography, imaging studies, and operative visualization have also demonstrated that it is not unusual for cicatrix of adhesive arachnoiditis to completely block the spinal canal in a focal manner. (4)

 

According to Burton, in a very small percentage of patients, the dense scar tissue of adhesive arachnoiditis may progressively calcify. This appears to be a very slow change, and it is sometimes seen in association with a progressive sacral nerve root syndrome that produces bowel and bladder impairment.

 

 

It is estimated that at least 1 million people world wide have arachnoiditis, and approximately 412,500 of those people reside in the United States. (4) It is believed by many medical professionals that the number of people with arachnoiditis is much higher, but too many physicians are still saying clinically significant adhesive arachnoiditis is [Continued on Next Page]

 

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