7 Search Results for "leads"

• Bevie

  • Views: 11
  • Since: 5 days ago

• congestive heart failure disab

  • From: verger
  • Description:

    Hi,

    I'm new to this group and want to introduce myself.  i'm 51, had a heart attack in 2005, went into cardiac arrest and now suffer with congestive heart failure.  i'm on disability but only receive $463 a month from SS, i've been able to manage up until now and find myself not being able to pay bills and some medicines because of lack of funds.  i'd love to work ( i was in carpentry before) but find it a bit impossible to find the right job.  i'm a liability in most cases and often find myself dizzy and faint, needless to say out of breath is a common companion.  i don't think i'd be able to manage a full 8 hr day at the ofice type deal for reason of fatigue and the obvious health reasons.  i've tried to get medicaid, but was denied, you need to be broke broke to qualify, i think in the range of $759 per month.  my wife makes more than that, but so much goes to my meds that rent is impossible.  dire situation to say the least.

    i want to know if anyone has found suitable jobs which can be performed at home, especially internet oriented.  if anyone could lead me in the right direction, i'd be grateful.  i'm definately not into any scam type work, i.e. mlm and the likes.  also any advice on obtaining grants to live or how to get more to live on from our great government would be appreciated.  i'm desperate and open to anything, i've tried so many different leads that i've run out of steam of where to proceed next. please help me to get by.

    thank you

    david 

  • Blog post
  • 1 month ago
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• hair2c

  • Views: 40
  • Since: 5 months ago

• CyndyWhiteDisabiltyDigst

  • Views: 140
  • Since: 1 year ago

• RA Morbidity, Mortality, Clini

  • From: geekygranny
  • Description:

    Posted : 2/17/2008 1:21 AM

    Author: Michele Calleja, MD, Specialist Registrar, Musculoskeletal Radiology, Freeman Hospital
    
    Michele Calleja is a member of the following medical societies: Royal College of Radiologists
    
    Coauthor(s): Geoff Hide, MBBS, MRCP, FRCR, Consultant Musculoskeletal Radiologist, Department of Radiology, Freeman Hospital; Honorary Clinical Lecturer, Faculty of Medical Sciences, University of Newcastle upon Tyne
    
    Editors: Amilcare Gentili, MD, Clinical Professor of Radiology, University of California at San Diego; Consulting Staff, Department of Radiology, Thornton Hospital; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Lynne S Steinbach, MD, Chief of Musculoskeletal Radiology, Professor, Department of Radiology, University of California at San Francisco; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Felix S Chew, MD, MBA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington
    
    
    Rheumatoid Arthritis Resource Center
    
    
    ........ Approximately 10% of patients with RA have an affected first-degree relative. The role of genetic influences in the etiology of RA was established by the demonstration of an association with HLA-DR4. As many as 70% of patients with classic or definite RA express HLA-DR4 compared with 28% of control subjects.
    
    Frequency
    United States
    The prevalence of RA is approximately 1% of the adult population in Europe and North America (range, 0.3-2.1%). Some Native American groups have a higher prevalence, with lower rates in the Caribbean. The worldwide incidence is around 3 cases per 10,000 population.
    
    International
    See data for the United States above.
    
    Mortality/Morbidity
    RA is usually associated with significant morbidity, disability, and mortality.
    
    
    Spontaneous clinical remission is uncommon. After 5 years with the disease, about 33% of patients are unable to work, and after 10 years, around 50% of patients have substantial physical disability.
    Oostveen et al reported an overall mortality rate of 17% in patients with RA and radiographic evidence of cervical subluxation. This rate is similar to that found in other series of patients with severe RA and no cervical involvement.
    Poor prognostic factors include persistent synovitis, early erosive disease, extra-articular features, positive serum RhF results, male sex, family history, and advanced age.
    
    Race
    RA occurs throughout the world and affects persons of all races. Disease severity differs based on ethnic and geographical variation. For example, studies have shown that RA in Greece is milder, with less radiological joint destruction and fewer extra-articular manifestations compared with Northern European countries. The incidence and severity also seem to be lower in rural sub-Saharan Africa than in other areas.
    
    Sex
    Women are affected approximately 3 times more often than men. The prevalence increases with age, and sex differences diminish in the older age group.
    
    Age
    The onset is more frequent during the fourth and fifth decades of life, with 80% of all patients developing disease from age 35-50 years. The incidence of RA is more than 6 times as great in 60- to 64-year-old women compared with 29-year-old women.
    
    Anatomy
    Various phases of joint destruction are seen in RA: early RA, erosion formation, pseudocyst formation, and advanced RA.
    
    In early RA, inflammation leads to synovial hyperemia and swelling. Synovial processes adhere to cartilage surfaces at joint periphery.
    
    In the stage of erosion formation, marginal destruction of cartilage, granulation tissue formation, and osteoclastic resorption of nearby bone leads to tissue loss, which is radiologically depicted as erosion.
    
    With pseudocyst formation, granulation tissue formed in continuity with the inflamed synovial membrane continues to replace bone and cartilage at circumference of articular surfaces. This tissue extends through the surfaces to form radiolucent zones called pseudocysts.
    
    In advanced RA, the extent of synovitis and fasciitis, tendonitis, and cellulitis becomes greater than before. Adhesions between joint surfaces cause ligament and capsule laxity. This, in addition to muscle atrophy and tendonitis, allows joint subluxation to occur. Little normal articular cartilage remains. Secondary osteoarthrosis develops with osteoporosis. Fibrous ankylosis is likely with joint shortening and destruction.
    
    Clinical Details
    
    Clinical course
    
    There are now believed to be 3 characteristic clinical courses of RA: course I, monocyclic; course II, polycyclic; and course III, progressive.
    
    Course I, monocyclic
    
    Approximately one third of all patients who develop RA undergo complete and permanent remission within 2 years of disease onset, with or without treatment. The course is benign and self-limiting.
    
    Course II, polycyclic
    
    This is a slow, progressive course with moderate activity interspersed with short episodes of acute arthritis. Periods of acute activity become more sustained with the passage of time. This is also known as the palindromic type of RA, and it affects around 40% of patients.
    
    Course III, progressive
    
    This course affects approximately 20% of patients. It represents an unrelenting, progressive, and destructive form of RA with deformity, disfigurement, and even death.
    
    In a given patient, it is not possible to predict the future course of the disease at its outset. However, in the presence of subcutaneous nodules, high titer of RhF, and erosive x-ray changes, rapid progression and destructive changes are inevitable.
    
    
    posted to discussion for educational purposes.

    Get the benefits of Social Security Disability survival experience! Join The Disability Digest

    

    Be peace,

    Mary :o) aka GG

    
    

    ~*~*~*~*~*~*~*~*~ *~*~*~*~*~*~*~*~*~*~*~* ~*~*~*~*~*~*~*~*~
    Earth is my home and animals are my family. Life is my religion and love is my example. Peace and freedom belong to us all.

  • Blog post
  • 1 year ago
  • Views: 136
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• How to Build a Successful On-l

  • From: bluetribe
  • Description:

    So you think you want to build a business on-line? That’s great, but do you know how to go about selecting the kind of business that will succeed on the Internet? And, do you know where and how to start?

    I now have a successful business on-line, but when I got started I knew nothing about how to begin. I floundered for a while until I found the right way to go about it.

    The first thing I learned was that the most important principle you need to understand is WHAT DRIVES THE INTERNET. You may think you know, after all you have searched a ton of successful sites and it all looks fairly simple. But building a business on the Internet has its own set of rules and principles.

    What then is the best way to build the kind of business that will succeed on-line? Well, success on the Internet all begins with a critical mind-set shift. This means replacing that well known off-line strategy of location, location, location with.....INFORMATION, INFORMATION, INFORMATION.

    That’s right, Information. Most of us use the Internet as a searching tool. We search for credible, high value information or solutions, anything that can fulfill a wish that we hold dear or solve a troublesome problem that we are experiencing. So, then, it is clear that we are all searching the Internet for information and solutions. Well, guess what, that is exactly what you are going to give them!

    With that in mind, here is your first guiding principle: “GIVE THEM WHAT THEY WANT” How do you go about fulfilling this principle? Simple. You will accomplish this by building a THEME-BASED CONTENT WEB SITE. What does that mean? It means building a simple site that contains information based upon a MAIN SUBJECT. Where each page focuses upon a single topic that is related to the overall theme or subject.

    By providing your visitors with high-value content, over delivering on the information they were seeking, visitors start to like and trust you. Your content-rich site builds trust and credibility.......which leads to an OPEN-TO-BUY MINDSET. Good content encourages your visitor to think about you as a friend or expert rather than as a stranger. People buy from those they know and like. They resist sales efforts from everyone else.

    So it's clear that by creating a relationship with your readers and giving them the solutions or information they are seeking leads to MONETIZATION opportunities, which of course translates to MONEY!

    Easy enough to understand, but what type of web site should YOU build? What will be PROFITABLE to YOU and how do YOU get started?

    Good Questions.... Download Ken Evoy's Free e-book, Make Your Site Sell it will provide you with the basic principles and steps that will help guide you to your goal of building a successful business on-line.

    You can check out my web site at Healthy Holistic Living. Curious about the tools I used to create a successful on-line business? Go to Site Build It

    If you have questions about how to start your own on-line business you can contact my via my Bio Page or you can contact me via my web site

    Keep in mind when starting a business it's important to understand how much money you can make and keep your benefits, knowledge is power! Stay up-to-date and on top of the latest information listen to Brian's audio How to Supplement your Income without Reducing Your Monthly Check!

  • Blog post
  • 1 year ago
  • Views: 351

• Fibromyalgia - Ultimately a Di

  • From: geekygranny
  • Description:

    by Mark J. Pellegrino, MD
    ImmuneSupport.com>
    
    05-26-2008 Excerpted with permission from Chapter 9 of Dr. Mark Pellegrino’s very popular book, Fibromyalgia: Up Close and Personal .* Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center, and has been a Fibromyalgia patient himself since childhood.

    Many conditions can lead to permanent changes in the pain transmission mechanism and result in chronic pain that overwhelms the body’s pain defense mechanisms. One such condition is Fibromyalgia.

    Fibromyalgia may not cause destruction along the pain pathways as other conditions I have mentioned can [rheumatoid arthritis, carpal tunnel syndrome, shingles, multiple sclerosis, for example]. However, Fibromyalgia does cause chronic abnormal changes along all the pathway components and this results in chronic pain via both peripheral (from skin, muscles and nerves) and central (from spinal cord and brain) neurological mechanisms.

    The end result of Fibromyalgia’s abnormal changes appears to be a state of pain amplification that cause severe generalized pain. Fibromyalgia is ultimately a disease of amplified pain.

    Dr. Robert Bennett has written and presented excellent information that explains why we hurt with Fibromyalgia (e.g., “Emerging Concepts in the Neurobiology of Chronic Pain: Evidence of Abnormal Sensory Processing in Fibromyalgia,” Mayo Clinic Proceedings ). If we trace the pain signals through the various parts of the pain pathway (from the nociceptors - or specialized pain nerve endings – to the nerves to the spinal cord to the brain) in people with Fibromyalgia, we find various abnormalities along the way. Many studies have shed light on different points along the complete pain pathway.

    I want to briefly summarize some of these different abnormalities and possible problems encountered by Fibromyalgia pain signals on the path to the brain.

    NOCICEPTORS - Pain originates from the nociceptors

    Trauma is a common trigger of Fibromyalgia. Tissue injury - damage to the muscles and soft tissues – activates the nociceptors. Some studies have suggested that microscopic injury occurs in specific parts of the muscles (for those who want the medical names: muscle spindles, intrafusal fibers, and calcium pumps).

    Localized tissue injury probably activates arachidonic acid (a biological protein), which turns into “bad” prostaglandans (called Cox-II prostaglandins), and cause inflammation and pain.

    In addition to trauma, autoimmune factors may be another pain nerve activator. Perhaps autoimmune processes create compounds which act as irritants and activate the nociceptors chronically to the point where they become “permanently” sensitized and irritated. As a result, biochemical, hormonal, and red blood cell changes occur that interfere with the cells’ ability to receive adequate supplies of oxygen, glucose, and other nutrients. Blood flow, energy formation, and the cells’ electrical and neurological harmonies are all disrupted.

    Since the nociceptors remain “faulty,” the electrical and neurological balance remains abnormal, and nociceptors continue to be activated. Pain-producing neurotransmitters are released and accumulate as long as the nociceptors stay activated at the peripheral level (skin and muscles, especially).

    These persistent pain signals we experience may be interpreted as an itching, burning, swelling, or tingling at one end of the spectrum, or – at the other end – knife-stabbing, burning, or throbbing. One nociceptor can signal different pain signals and sensations depending on its level of irritation – the more irritated it is, the more severe the pain.

    These changes can become permanent and cause the nerves to become sensitized to the point where they are easily activated to send pain, even in the absence of any noxious stimulus.

    In other words, persistent pain signals can spontaneously arise from peripheral nerve endings and bombard the rest of the pain pathway. So, instead of waiting for outside stimulation such as trauma, pressure, temperature, or touch to signal the nociceptors, these nociceptors send pain signals on their own, without any outside help. This “spontaneous” pain is what we complain about the most!

    NERVES

    The nerves, especially the sensory nerves and the autonomic nerves, “wonder what is happening” because they are getting bombarded by all of these signals from the nociceptors. At first, they try to diminish these painful signals by using accommodation and gate mechanisms.

    However, the signals persist and they, too, undergo a sensitization process. They become hypersensitized and react with an exaggerated response instead of a normal or diminishing response (accommodation). Now we get even more pain, numbness, swelling, burning, and other sensations.

    Some of the hypersensitization may be mediated by nerve growth factor, which has been found in higher levels in Fibromyalgia. A high nerve growth factor may indicate the nerves are trying to regenerate or repair themselves. But instead of repairing the nerves so they act normal again, the opposite seems to happen. Nerve growth factor is probably enhancing the nerves’ abilities to transmit pain to the spinal cord. More pain results, not less.

    SPINAL CORD – Amplification, wind-up, allodynia, Substance P, generalization

    At the spinal cord level, the Fibromyalgia begins to take control.

    It is here that additional changes occur to perpetuate the pain and spread it to different levels. When pain generators first start firing, the spinal cord pain processing centers may act at first like a dry sponge and easily soak up all the signals. Our bodies may have many pain generators at any given time, but if they are slowly and intermittently firing, drug sponges can soak up the signals and not cause any bothersome symptoms.

    From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated, and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain.

    In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more. The additional oncoming continuous signals will spill over the wet sponge, and this leads to persistent pain.

    The two main changes that occur at the spinal cord include:

    • Pain amplification (by specialized nerves called NMDA receptors)
    • And loss of pain filtering (by the diffuse noxious inhibitory control system).

    Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain. This phenomenon is called “ wind-up ,” and is the neurological mechanism for the amplification of pain.

    Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified, and be sent to the brain as pain. The spinal cord becomes more sensitized to sending pain, lots of it. Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals.

    As a result, different sensory signals such as touch, pressure, temperature, and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature, or joint motion signals.

    This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia . Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain! We can still appreciate touch, pressure, temperature, joint movement, and other non-pain signals, but pain contaminates these signals, and we feel the pain.

    Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters.

    Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain. When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal. As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “ generalization ” of the Fibromyalgia.

    This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain. A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured. Over time, the pain begins to involve the mid-back, low back, and ultimately the whole body, even though these areas were never injured. The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body.

    BRAIN

    Our poor brains have no chance, do they? Any pain memory stored in the past will be re-awakened by this process. Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops. This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive. Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated.

    The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord. Changes occur:

    • Serotonin levels decrease,
    • Brain waves change,
    • Sleep stages are affected,
    • Blood flow and glucose [blood sugar] metabolism are affected.

    The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain. Fibrofog occurs. Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness, and helplessness, which can further amplify the pain.

    In patients with Fibromyalgia, functional reorganization ( brain plasticity ) in both sensory and motor portions of the brain has been observed, and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003). These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses. The brain makes these changes to enhance its ability to perceive pain – brain amplified pain.

    This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw, et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs. This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain.

    FIBROMYALGIA PAIN SUMMARY

    To summarize, Fibromyalgia changes our pain pathways. It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain. The main problem, in a nutshell, is amplified pain.

    The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain. What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia. Our pain signal of a “1” gets amplified and magnified, and by the time it reaches our brain, it is a “10”!

    Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals. Even tiny subconscious pain signals can get amplified, or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain.

    These are not your everyday aches and pains, these are severe pains that cannot be ignored. This severe, chronic pain can completely disrupt one’s life. And by the way, while all of this is happening, we continue to look completely normal on the outside.

    ___
    * Reproduced with permission from Fibromyalgia: Up Close & Personal by Mark J. Pellegrino, MD. © Anadem Publishing, Inc. (www.anadem.com) and Mark Pellegrino, MD, 2005, all rights reserved. This book may be purchased for $24.50 plus S&H from Dr. Mark J. Pellegrino at the Ohio Rehab Center (phone 330/498-9865 or fax 330/498-9869).

    Note: This information has not been evaluated by the FDA. It is not meant to prevent, diagnose, treat, or cure any illness or disease. It is very important that you make no change in your personal healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

  • Blog post
  • 1 year ago
  • Views: 199