Objectives: Education, enhance physician awareness, raise public consciousness, encourage pharmaceutical and biotechnology companies to develop new therapies and devices for the diagnosis and treatment of neuropathies, advocate with government, support research, and increase national and international awareness and information exchange.
The next step was that the six founders found themselves sitting on the stage of the Lighthouse hosting a group of 125 people who had spotted a tiny ad in the New York Times at the first Support Group Meeting. (4/96). By the end of 1996 there were 1,500 members and five support groups. The web site www.neuropathy.org was launched and "Explaining Peripheral Neuropathy" was published. The following year the first issue of "The Neuropathy News" was distributed and an Executive Director, Eileen Kellner was hired. "Exercising With Neuropathy" was written and formal office space in the Lincoln Building was leased.
In 1998 the first affiliate chapter in St. Louis, MO was established and the 1st International continuing medical education conference was co-sponsored in Greece about the treatment of neuropathy. There were already more then 10,000 members, 110 support groups and TNA awarded its first research grants. The Association commissioned the Roper Starch Survey, which revealed that 22 million Americans suffered from neuropathy and "A Guide to the Peripheral Neuropathies", was released. This continues to be an outstanding resource for both members and providers. Membership grew to almost 37,000 in 2000 and "The First National Neuropathy Get Together" was held under the direction of our support groups in Branson, MO. Andy Griffith’s battle with Guillian Barre was publicized in "The Neuropathy News" and professional composer, lyricist and performer, Ernie Sheldon, a member of TNA wrote and recorded "The Neuropathy Blues". The following year affiliates were formed in Denver and Northern CA and the first East coast Symposium was held in Lehigh Valley, PA. A grant from Pfizer funded research by Muse & Associates, which demonstrated that 8.6% of Medicare beneficiaries have neuropathy as a primary or secondary diagnosis at an annual cost $3.5 billion dollars. The Association now numbers over 70,000 members with well over 200 support groups in all 50 states. Annual CME conferences are held to educate neurologists and other physicians and the first national neuropathy symposium sponsored by The Neuropathy Association for members and support group leaders will be held November 2003 in Denver, CO.
Our mission, to provide patient support and education, advocate for patient’s interests and most importantly to promote research into the causes and cure of peripheral neuropathy remain unchanged from its inception. The Association is housed in a small suite of offices at 60 East 42nd Street in New York City across from Grand Central Station. It houses the President, Mary Ann Donovan, Catherine Law, the Chief Financial Officer, 3 support staff and myself. There are 4.2 salaried FTE employees. The Board of Directors meets monthly with the exception of the summer. There are approximately 10 volunteers who serve in various capacities and there is National Advisory Council of high profile individuals.
My initial experience with peripheral neuropathy began in 1983. I was living through a highly stressful period during which I found myself being heavily recruited to be the New York State Mental Health Commissioner. I contracted two virulent upper respiratory viruses and 6 months later I was having trouble walking. I was treated and recovered and only became symptomatic again after a hiatus of more than 15 years. I was lucky. I was accurately diagnosed and treated on both occasions.
Subsequently, I started my postgraduate career specializing in consultation - liaison Psychiatry, the specialty closest to internal medicine. Ironically, I seem to have come full circle in my current professional life. Subsequently, I had a rich academic/administrative path including being Professor of Psychiatry and having served as New York State Commissioner of Mental Health and Director and Medical Director of the Department Of Psychiatry at Bellevue Hospital Center, New York, NY. I have also had experience as a medical director in managed care and the for-profit healthcare sector.
(B) Requests: Nat. Meeting, increased number of Newsletters, Research, and advocacy
on the nat. level.
(E) Affiliates - St. Louis, Northern California, Denver, Minneapolis
Day 1 - Support Group Leaders - Pfizer will provide support for the support group meeting in the form of an unrestricted educational grant Keynote Speaker: Paula Cummins, world-renowned trainer of trainers
Days 2-3 - Formal presentations by national experts and small group breakout sessions including, immune neuropathies, diabetic neuropathies, entrapment neuropathies etc. Breakout sessions will cover: Disability, Physical therapy, Insurance, balance, alternative medicine, nutrition etc.
The Association has funded 6 grants at $25,000/year for two or more years with outstanding results. There is a Scientific Advisory Committee; Norman Latov, MD, Ph.D. is the Scientific & Medical Advisor of TNA. Two of the 6 studies have already yielded remarkably promising results.
(A)Dr. Frank Denaro, University of Maryland Biotechnology Institute "The Neuropathology and Mechanisms of HIV-PN Disease". This study focuses on the mechanisms by which HIV-1 and possibly other retroviruses can cause PN. Retro viruses integrate DNA into cells and use the cells machinery to produce proteins. If the toxic proteins are identified their mechanisms can be investigated and we can develop tests to detect their presence and drugs to block their effects.
(B) Phillip Chance, M.D., The University of Seattle, "Hereditary Neuralgic Amyotrophy: (HNA) Identification of the Causal Gene". HNA produces episodes of weakness, primarily in the arms. The cause is unknown The project attempts to identify the gene and investigate the mechanism by which it works.
(C) Dr. Robert H. Brown Jr., Harvard University, His group has made a breakthrough discovery of a gene responsible for a type of hereditary sensory neuropathy (HSN-1). The project is entitled “Positional Cloning of the eredyHereditary Sensory Neuropathy Type-1 Gene”. Dr. Brown Initially reported the discovery in Nature Genetics November 2001.
(D) Dr. K. Bejaoui is the primary author of the team led by Dr. Brown. The paper was published in the Dec. 02 issue of “The Journal of Clinical Investigation”. The investigators are now recruiting subjects for a clinical trial. “HSN-1 is a disease caused by loss of sensory neurons. The clinical characteristics include loss of pain and temperature sensations in the legs and hands. As a consequence, minor injuries go unnoticed and therefore untreated. Repeated injuries evolve into ulcerations of the skin and infections of the bones leading ultimately to amputations of the toes and fingers. The next phase will be to develop a molecular diagnostic test for HSN-1, which will allow the detection of the disease before the symptoms begin, making it possible to take preventive measures. The gene is SPTLC-1, which is involved in the synthesis of sphingolipids, a component of peripheral nerve membranes.
(E) Zarife Sahenk, M..D., Ohio State University, "Effects of BDNF and NT3 Treatment on CMTIA Xenographs," A new drug being studied for its potential to protect and regenerate peripheral nerves (Neurotropin-3). Neurotrophin-3, which is made by the Schwann cells or myelin forming cells in peripheral nerves, can help to maintain axons and allow them to regenerate. In mice, treatment with NT-3 resulted in significant regeneration in nerve fibers. Dr. Sahenk believes that in demyelinating neuropathies like CMT, CIDP, MAG Neuropathy and Guillain-Barre syndrome there is a deficiency of NT-3 resulting in breakdown of the axons. They found that normal axons surrounded by sick Schwann cells degenerate and fail to regenerate, whereas they can regenerate if surrounded by normal Schwann cells or given NT-3.
(F) Arthur Hays, M.D., Columbia Univ., “Investigations of Diabetic Neuropathy”. This project studies the mechanisms responsible for diabetic neuropathy characterized by the pathological changes in the peripheral nerves to determine whether there are advanced glycation products (AGEs) formed in the nerves, which could do damage. Understanding this could lead to the development of better therapies.
(G) Angelica Hahn, M.D., FRCP, Director, The Neuromuscular Clinic, The University of Western Ontario, “Tolerance Induction in An Experimental Model of CIDP”. In CIDP (Chronic Inflammatory Demyelinating Polyneuropathy), the immune cells (T lymphocytes and proteins (antibodies) attack the myelin sheaths covering the peripheral nerves. This produces weakness, loss of sensation and pain. The study will look at how the myelin is being attacked and whether the process can be suppressed with oral myelin.
(A) Center for Medicare Rights
(B) Partners in Understanding Pain (American Chronic Pain Foundation)
(C) NIH - Non-political, advocate congress, arduous task, Wash. presence, Scheumer, Nadler.
(D) House of Representatives Sub-Committee on Health, the Environment, & Human Services and Ed.
Senate Sub-committee on Health, and The Environment (AKA Labor, Health
Human Services and Education).
House Committee on Appropriations.
Senate Committee on Appropriations.
(E) FDA - TNA is committed to promoting the approval of drugs and devices for the
treatment of neuropathies.
“A Conversation with Neurological Disease Patient Advocates” and "FDA leadership”
Advocacy for IVIg in Guillian Barre Syndrome.
When confronted with physical illness it is normal and adaptive to regress to earlier patterns of behavior that are characteristic of prior phases of emotional development. Being somewhat dependent, going to bed and allowing yourself to be taken care of when you are sick is appropriate and facilitates your medical professional’s making accurate diagnoses and instituting appropriate treatment.
Everyone has his or her own character and coping style that a person has developed as a result of heredity (genetic predisposition), and development. This includes education, learning, role modeling, training and other life and developmental experiences. An individual’s coping style or adaptation changes as a person matures and is somewhat different at different times in a person's life. Regardless, illness is a significant life stress and each individual reacts in his or her own characteristic manner.
It has long been known that medical illness can have psychological consequences such as depression, anxiety, hopelessness and despair. It is also generally accepted that an Individual’s emotional state can have a profound effect on the course of a medical illness, its healing and outcome. In the early 1970’s I was one of the investigators on a project at Columbia Presbyterian Medical Center which demonstrated that patients who had open heart surgery when they were depressed had poorer outcomes and a higher death rate after surgery then those who were not depressed when they entered surgery. This has now been demonstrated for several other illnesses.
What is relatively new is that there is a growing body of evidence that for some illnesses psychiatric symptoms (i.e. depression) can be independent risk factors that increase a person's predisposition to develop certain physical illnesses (i.e. coronary artery heart disease). This obviously has significant potential implications for better understanding the causative factors responsible for some neuropathies, especially those of unknown etiology and those attributed to autoimmune causes (i.e. CIDP, GBS etc.)
To return to styles of adaptation in health and disease, we know that illness, especially chronic illness is a significant life stress and that the individual mobilizes his or her emotional resources to cope with that stress. When psychoanalytic thinking was more prevalent in the training of psychiatrists, psychologists and other mental health professionals, it was understood that every person had personality or character and that an individual’s coping style under stress was predictable and repetitive over time for that person. In other words an individual reacts to illness with an array of behaviors that are characteristic for that person. Examples of personality styles are obsessive, passive-dependent, passive-aggressive, histrionic, schizoid, narcissistic, and paranoid. These are not abnormal and are not indications that the person has a disorder or illness. They are in fact labels, which describe a person's typical pattern of reactions to life’s demands including illness. The development of personality is probably a result of genetic predisposition and life experience.
As psychiatry came of age it became clear that as the other medical sciences, psychiatry had an end organ, the brain and that its basic science was neuroscience. As these concepts became accepted, scientific investigators demanded a naming system or nomenclature for mental illnesses that would allow them to be certain that everyone would be studying the same condition when conducting scientific research on a given condition. "The Diagnostic and Statistical Manual of Mental Disorders - IV of the American Psychiatric Association was developed. It made diagnoses of mental illnesses on the basis of strictly observable criteria (i.e. hallucinations, delusions, repetitive movements, agitation etc.). Diagnostic criteria and states that were made by inference or based on a theoretical hypothesis (i. e. character or personality) were eliminated. There is a section in the current diagnostic nomenclature on "Personality Disorders", but these are now classified as disorders and not considered to be part of normal behavior. Examples include Paranoid Personality Disorder, Schizoid Personality Disorder, and Antisocial Personality etc. However, the more we learn, especially from the human genome project, the more we understand that nothing is as simple as it seems and that we were in danger of throwing out the baby with the bath water. The mind is in fact in the brain and science has begun to identify the biological location of personality traits. Character style, personality traits and coping style almost certainly have their origins in the brain and are important in understanding a person’s emotional and physiological responses in health and disease.
The understanding and acceptance of these concepts has been afforded enormous credibility with the awarding of the 2002 Noble Prize in Medicine and Physiology to Eric Kandel, M.D. for his ground breaking work in Aplasia which demonstrates that every stimulus to the brain has a permanent effect on it. Interestingly, Dr. Kandel had postulated many years earlier that psychotherapy changed the brain and that this explained its ultimate mechanism of action. His work supported this hypothesis.
As stated above, people with chronic medical conditions virtually all develop emotional and psychological consequences as a result of their illnesses. Among the initial responses are those called defense mechanisms. The individual is not consciously aware when these defenses come into play, since they attempt to help the individual adapt to or cope with the anxiety that accompanies the stress of illness or the fear, which the awareness of being ill engenders. These defense mechanisms include repression, denial, rationalization, sublimation, reaction formation, isolation, projection, identification etc. They are normal reactions to stress, which help the individual deal with the anxiety associated with a situation so that the person can better deal with the stress. As stated above, in this case the stressor is a symptom of an illness or the awareness of having an illness. Although these mechanisms are adaptive, when invoked to an extreme they become maladaptive and can interfere with timely diagnosis and treatment. Examples include my own experience with peripheral neuropathy and the all too common situations in which people have obviously rapidly growing tumors and deny their existence or those situations in which women well into the late stages of pregnancy who that they are not pregnant.
Next, there are a panoply of responses to neuropathy and other chronic illnesses that while not considered diagnostic of psychiatric disorders in themselves, are maladaptive and may be symptoms of psychiatric disorders. Examples include decreased social interaction, avoidance of spouse and children, marital discord, decreased interest in sex, decreased involvement in work or leisure time activities, withdrawal, isolation, fatigue, hopelessness, despair, demoralization, anger and sleep disturbances. These reactions are very prevalent in neuropathies because of the condition's chronicity, unpredictability, uncertainty of diagnosis and treatment and at times an intermittent, relapsing course of the illness. Nobody does very well with the anticipation of loss of control, especially when life or limb is at stake. The individual must deal with loss of function, body part, quality of life and on rare occasion life itself. In some ways worst of all is that it is a highly disabling "unknown" condition that is misunderstood, under diagnosed and under treated. According to psychiatrist Scott Berman, M.D, “Neuropathy is little stigmatized, because no one has ever heard about it.”
Many individuals with neuropathy also have pain as a symptom of their peripheral neuropathies. This can vary from mild and intermittent to severe and constant. It takes many forms and many individuals including myself experience several different kinds of pain. Pain in neuropathy may be described as lancinating, squeezing, clamping, aching, electric shock like, stingers, burning, increased/uncomfortable sensitivity to stimuli that would normally not be experienced as unpleasant and misinterpretation of stimuli. Living with pain is one of the most challenging experiences a person will ever confront. Chronic pain can instantaneously change ones self-image and lead to severe emotional and psychological consequences, which can in themselves be disabling. The issue of pain in neuropathy is very complex at least in part because there are numerous pathways to the brain from the spinal cord that are experienced by the individual as painful or uncomfortable. This is the probably why people with neuropathy not uncommonly experience a number of subjectively different feelings that they describe as painful. Pain is a symptom, suffering is what one experiences.
Finally, I would be sorely remiss if I did not mention the formal psychiatric disorders, which can be the result of peripheral neuropathy. Certainly, most people with neuropathy experience periods of anxiety related to their illnesses. Anxiety Disorders, Major Depression and Dysthymia are common in people with neuropathy. It is also important to note that it is now understood that any period of sustained anxiety in itself can lead to a clinical depression. In addition, it is now suspected that some chronic medical illnesses cause specific depressions related to the primary illnesses that are in some why different than the Major Depression we are familiar with and that these are somewhat more difficult to treat. The good news is that these conditions are treatable and should be treated. Treatment of a co-occurring psychiatric disorder can influence the course and treatment of a peripheral neuropathy in a very positive way.
The foregoing is a speech given by Steven E. Katz, M.D., FACP, DLFAPA. This speech was given on May 5, 2003, at a Houston Neuropathy Support Group meeting.