ADHESIVE ARACHNOIDITIS (AA) REQUIRES MULTIPLE CAUSES
Our studies over the past five years have concluded that AA is almost always caused by more than one causative factor. Simply put, to get AA you have to have more than one adverse condition. We have reached our conclusions after reviewing over a thousand magnetic resonance imaging (MRIs) of persons with AA, conducted inflammation and hormone studies, and analyzed clinical symptom and histories of several hundred cases.
MAJOR CAUSES OF AA:
- Infections (e.g., Lyme)
- Anatomic defects (e.g., scoliosis, tethered cord, rheumatoid spondylitis);
- Toxins (e.g., Pantopaque®, epidural solutions);
- Trauma including (e.g., surgery, electrocution, accident, spinal tap);
- Autoimmune disorder (e.g., psoriasis, Lupus, rheumatoid arthritis, Epstein Barr);
- Genetic connective tissue disease (e.g., Ehlers-Danlos, Marfan syndromes)
HOW AA DEVELOPS: AA is an unusual disease that requires two anatomical tissues (arachnoid membrane and cauda equina nerve roots) to glue together by inflammation and adhesions. To cause such “gluing”, inflammation must be generated by an infection, toxin, friction, electricity, trauma, or autoimmunity. Inflammation will produce a sticky substance that can form adhesions and merge the two tissues together.
OTHER CAUSATIVE FACTORS: In addition to the above, a hormone, genetic, or dietary inadequacy may contribute to causative factors and/or accelerate the development and/or worsening of the disease.
CONCLUSIONS: AA is a multifactorial disease that requires potent inflammation to develop in the spinal canal and cause cauda equina and arachnoid lining to form adhesions that “glue” the two tissues together. Since there is not a single cause, no single treatment will suffice. Only a protocol that targets two or more of the causes of AA will bring relief and restoration.
IDENTIFICATION OF PRECURSORS
A precursor is a forerunner or predecessor of things to come. In the past year (2022) we reviewed about 250 cases and MRIs of persons who had or believed they had AA. The most striking finding in these reviews is that EVERY person had precursor conditions, and that proper treatment at the precursor stage may have prevented AA.
PRECURSOR INFLAMMATION CONDITIONS: At least one of these lumbar-sacral conditions is found on every person who has AA:
- Multiple protruding discs
- Cauda equina inflammation
- Tarlov cysts
- Non-adhesive arachnoiditis
PRECURSOR DISEASES AND ACCIDENTS: Review of these 250 cases revealed that there were one or more precursor diseases or accidents that preceded or caused AA.
- Epstein Barr Virus Autoimmunity
- Epidural Injection
- Ehlers-Danlos Syndromes (EDS)
- Autoimmune Disease (Lupus, Psoriasis, Rheumatoid Spondylitis)
- Trauma Including Surgery, Motor Vehicle Accidents, and Spinal Taps
- Scoliosis and/or Spondylolisthesis
BASIC PATHOLOGIC MECHANISMS: Inflammation is initiated by one or more precursor diseases or accidents. It may begin in intervertebral discs, cauda equina, or spinal canal covering (dura and arachnoid layers) and then spread throughout spinal canal tissues just like cellulitis in the skin. Inflammation may then form sticky adhesions that glue cauda equina nerve roots together (clumping) and to the arachnoid lining of the spinal canal cover.
SYMPTOMS MAY BE SIMILAR: Many persons at the precursor stage have pain and neurologic impairments that are similar to AA.
RECOMMENDATION: The 3-component treatment protocol for AA should be initiated if a precursor condition or disease is present and not wait until AA has formed; (1) suppress inflammation and autoimmunity, (2) restore and heal damaged tissue, (3) pain control.
CHRONIC PROTRUDING (HERNIATED, BULGING, OR SLIPPED) DISCS ARE A CAUSE OF AA
Intervertebral discs are the cushions between the large, structural bones of the spine called vertebrae. The discs are soft, pliable and are the tissues that allow us to bend, stretch, and even walk. Discs are soft tissues that have a blood supply and are primarily composed of collagen which is derived from protein and amino acids.
PROBLEM: Millions of persons suffer from what is commonly called a “herniated”, “bulging”, or “slipped” disc in their neck or lower back. They have this name because the disc partially protrudes out from its natural setting between 2 vertebrae against the dura-arachnoid spinal canal covering and any nerve roots that are exiting or leaving the spinal canal. Injuries from lifting, trauma, or from an accident are common causes. They may also degenerate or deteriorate due to metabolic, genetic, or infectious causes. Persons with collagen disorders of the Ehlers-Danlos type commonly have this issue.
BREAKTHROUGH RESEARCH: Discs that protrude in the neck or lower back are now known to be inflamed. This is “breakthrough” knowledge since protruding discs have been thought to produce pain and neurologic defects only by exerting pressure or compression on nerve roots. Inflammation can spread as anyone who has had a “pimple”, “boil”, or “insect bite” can testify. The newest basic science research with disc inflammation shows that it can migrate and infiltrate adjoining tissues which may include nerve roots and the arachnoid-dural covering of the spinal canal.
OUR RESEARCH: Our Arachnoiditis Research Project has reviewed the MRI’s of over 1000 persons with the typical neck and lumbar-sacral symptoms of ARC/AA. All neck cases and the majority (80-90%) of persons with lumbar-sacral AA have had chronic protruding discs.
OUR CONCLUSIONS:
1. We believe that there is a spectrum or class of intraspinal canal inflammatory disorders that may simultaneously involve multiple tissues: chronic protruding discs, cauda equina nerve roots, and arachnoid-dural covering of the spinal canal.
2. Chronic protruding discs not only compress nerve roots but also may initiate a cascade of migrating inflammation that can produce severe pain and ARC, Tarlov cysts, cauda equina inflammation, and AA.
CONSEQUENCES AND COMPLICATIONS
AA has some serious consequences and complication that may cause immense suffering, impairments, and shortened lifespan.
