OFFICIAL DEFINITION OF IPS: IPS is a complication of an underlying painful injury or disease that causes inflammation and tissue destruction inside the central nervous system which results in constant pain and physiologic and pathologic dysfunction of the neurologic, cardiovascular, endocrine, and immunologic systems.
Recent years have revealed that many persons who have what is called multisystem collagen diseases, the most common is Ehlers-Danlos Syndrome (hereafter EDS), commonly develop neurologic complications including AA. Due to this occurrence, this website will feature information on EDS and AA.
EDS belongs to a group of inherited disorders known as “Genetic Connective Tissue/Collagen Diseases”. Besides EDS, the best known, related syndrome is probably Marfan Syndrome. Hypermobility with such physiologic abnormalities as double jointed and hyperextension of fingers, toes, arms, and legs characterize most persons with these disorders. The physiologic change that causes AA and other tissue complications is dissolution of collagen in connective tissue which results in micro-tears and inflammation. The arachnoid layer of the spinal canal covering is a fragile, connective tissue that may deteriorate in EDS and develop AA. We call the simultaneous occurrence of EDS and AA the “dual disease problem”. To date we believe the “dual disease problem” requires treatment for AA plus special anabolic (tissue growth) measures. This website will publicize information for understanding and dealing with the “dual disease” issue.
IPS is defined as constant pain with cardiovascular, metabolic, and endocrine (hormone) complications. In this past year we have discovered that spinal canal inflammatory diseases are the underlying causes of the vast majority of cases of IPS. Adhesive arachnoiditis (AA) is probably No.1.
SPINAL CANAL INFLAMMATORY DISORDERS: We have identified these specific diseases as spinal canal inflammatory diseases which can lead to IPS: adhesive arachnoiditis, non-adhesive arachnoiditis, chronic cauda equina inflammation, epidural fibrosis, Tarlov cysts, rheumatoid spondylitis, multiple sclerosis, protruding discs.
Reflex sympathetic dystrophy (CRPS) is known to be caused by an inflammatory process inside the spinal cord. Collagen diseases, either genetic such as Ehlers-Danlos or acquired (viral/toxins), may initiate a number of spinal canal inflammatory disorders. Diabetes is a significant potentiator of these diseases. Sugar or glucose is “fertilizer” for inflammation.
CONSTANT PAIN IS A RESULT OF INFLAMMATION: Constant pain results when inflammation inside the spinal cord or brain damages tissues that normally shut down pain.
PREVENTION AND CONTROL OF IPS: It is clear that both prevention and control of IPS is incumbent on proper diagnosis and treatment of the initiating spinal canal inflammatory disease. To date, IPS has been treated principally with symptomatic opioids, neuropathic agents, and antidepressants. Although in early stages, protocols for AA have shown ability to halt progression of the disease and, in some cases, bring about some permanent healing.
GOAL OF THE RESEARCH AND EDUCATION PROJECT: Our overall goal is to bring diagnosis and treatment of AA to every community. When we started this project, we were oblivious to the fact that AA is usually preceded by other spinal canal inflammatory diseases. A major objective of the project is to prevent the development of IPS.
TAKE HOME MESSAGE: Persons with constant pain and IPS must know if a specific spinal canal inflammatory disease is the basic cause of their condition. They must also fully understand that suppression and control of spinal canal inflammation will likely have to be a major component of their treatment.
HOW CONSTANT PAIN CAUSES BRAIN TISSUE LOSS
Beginning in 2004, brain scan studies began to document brain tissue loss caused by intractable pain. Today, almost 20 years later, this important fact appears to be either unknown or a mystery to both the public and medical professionals. Tissue loss obviously causes the brain to malfunction. Basic science researchers have unraveled the complex process of how and why this pathological phenomenon may occur. A good understanding of how this pathology develops is critical to properly care for and treat persons who develop intractable pain whether due to a disease or an injury.
WHAT CAUSES TISSUE LOSS? Tissue loss anywhere in the body is caused by inflammation, autoimmunity, or loss of blood supply due to trauma or disease. The brain scan studies done since 2004 that documented brain tissue loss were not done in persons who had a stroke or head trauma, so the two choices to produce brain tissue loss in pain patients are inflammation and autoimmunity (i.e., collagen deterioration). It turns out that both biologic mechanisms may operate to cause brain tissue loss in intractable pain patients.
THE BRAIN HAS AN IMMUNE PROTECTION CELL: In the pursuit of understanding brain tissue loss and its accompanying malfunctions, it has been discovered that the brain and spinal cord (central nervous system-hereafter CNS) contain cells called microglia. They are closely akin to the immune protective cell in the blood stream with is called a “lymphocyte.” The microglia in the CNS lay dormant until a harmful infection, toxin, or bioelectric magnetic signal enters its domain at which time it activates to capture and encapsulate the danger or produce inflammation to destroy the offender. If microglia are overwhelmed by some danger such as a painful disease that isn’t cured, it produces excess inflammation that destroys some brain tissue which can be seen on special brain scans. Some viruses such as Epstein Barr may hibernate in microglia cells and create an autoimmune response which magnifies inflammation and brain tissue loss.
PAIN GENERATORS: Intractable pain diseases such as adhesive arachnoiditis, reflex sympathetic dystrophy (CRPS/RSD), and genetic connective tissue diseases (e.g., Ehlers-Danlos) may incessantly produce toxic tissue particles and/or bioelectromagnetic signals that perpetuate microglial inflammation, tissue loss, and CNS malfunctions. This is the reason why proper pain management must have two targets: (1) pain generator, (2) CNS inflammation.
SUMMARY: The brain not only controls pain but the endocrine, cardiovascular, metabolic, respiratory, and gastrointestinal systems. Any or all of these biologic systems may malfunction if there is brain tissue loss.
NEUROPATHIC PAIN IN AA
“Neuropathic” is a new term that has recently been adopted in pain treatment circles to classify a specific type of pain and a class of drugs that control it. The term “neuropathic” simply means nerve-damage or impairment. With nerve damage or impairment, the normal flow of electricity is interrupted. When electricity cannot normally flow, it accumulates in one spot and may cause great pain and inflammation. AA is an inflammatory disease that causes “neuropathic” pain. Consequently, the following complications may occur: partial paralysis (legs, feet) – urinary, intestine, sex dysfunction – intractable pain syndrome. The common AA symptoms and sensations of water dripping, insects crawling, burning feet, jerking, stabbing pains, and restless legs are a result of interrupted and abnormal electricity flow.
DRUGS THAT REDUCE NEUROPATHIC PAIN:
The natural chemical in nerves that conducts the flow of electricity is called “gamma amino butyric acid” (hereafter GABA). Drugs classified as “neuropathic” are synthetic derivatives of GABA to either substitute for GABA or complement its natural function which is to conduct electricity in nerves. Some of the most popular neuropathic drugs are gabapentin, carisoprodol (Soma®), baclofen, diazepam (Valium®), pregabalin (Lyrica®), topiramate (Topamax®). Natural non-prescription neuropathic agents are valerian root, glutamine, ashwagandha, and pure GABA (taken under the tongue).
RECOMMENDATIION FOR PERSONS WITH AA:
We believe one or more neuropathic drugs are essential with AA to keep electricity flowing. The natural neuropathic agents can be combined with a prescription agent. To suppress pain and some symptoms you may have to experiment with combinations of the drugs listed here.
PAIN RELIEF MAY REQUIRE A STIMULANT
Pain in adhesive arachnoiditis (AA) is arguably the worst of all pain, because both the cauda equina nerve roots and arachnoid-covering (meninges) of the spinal canal become inflamed, glued together, and cause permanent damage to microscopic nerve fibers.
WHO SHOULD TAKE A STIMULANT? Although a concept which may create some denial and controversy, we firmly believe that every patient with MRI-documented AA and who requires daily opioids for pain control, should also take a dopamine replacement-substitute drug commonly known as a stimulant. We believe that clinical experience and research supports this recommendation. The benefits over risks are justified if AA is documented by history, symptoms, physical examination, and contrast MRI.
NEW RESEARCH SHOWS NECESSITY OF STIMULANTS: Severe intractable pain results when neurotransmitters in the spinal cord and brain become deficient. The three most important neurotransmitters are: endorphin, gamma amino butyric acid (GABA), and dopamine. Pain in AA may be so severe that each of these neurotransmitters must be substituted with synthetic drugs. To date, the medical profession is knowledgeable that endorphin and GABA need replacement, but there is considerable reticence to replace dopamine. Our experience is clear: if an AA patient has developed constant, severe pain, it may not be well controlled only by an opioid, and a GABA substitute, but also require a dopamine substitute.