What Is The Common Link In Most Neuropathies

Today's post from neuropathydr.com (see links below) is a two part article from Dr John Hayes Jr, who is a very well respected practitioner with a vast experience of neuropathy treatment. He maintains that the common link between neuropathies is a loss of oxygen at neuronal junctions and it is not enough to simply categorise neuropathy as either peripheral, autonomic or idiopathic. More study is needed into the true etiology of the condition thus leading to much needed new approaches to treatment. Well worth a read and an inspiration for further research.

What’s the Common Link in the Neuropathies? – Parts 1 & 2
Posted by john on September 23, 2010

The common link in all of these peripheral neuropathies, regardless of the cause, appears to be hypoxia.

Hypoxia is simply a word that describes loss of oxygen. This occurs at what are called the neuronal junctions. That is, the areas in the human body where one nerve cell communicates to another.

At a simplistic level, nerve cells communicate electrochemically across a gap. In neuropathy caused by hypoxia, this neuronal gap widens, which is theorized to be responsible for the symptoms that include not only the burning and the tingling but the shooting pains as well.

Neuropathy and chronic pain is characterized by pain, numbness, loss of tactile feedback, and poor tissue perfusion. These symptoms may indicate that oxygen is not getting to all the cells causing dysfunction.

Because the patient’s quality of life is decreased, these results are often devastating. Pain medications do not cure the condition; it only helps mask it and, eventually, leads to complications with adverse side effects such as mental confusion and intestinal problems.

As a result of conducting our own research and reviewing published studies from around the world, we have been led to new models concerning the causes of neuropathy and chronic pain. We have concluded that it is not reasonable to merely label neuropathy and chronic pain symptoms as diabetic, peripheral, vascular, or “idiopathic”. What is needed is a more full understanding of the etiology of the condition so new technology can be brought to bear with both ameliorative and therapeutic benefits.

What is the Common Link in Neuropathies? – Part 2

Posted by john on September 24, 2010

Neuropathy and chronic pain results when nerve signal propagation is reduced between adjacent nerve cells due to insufficient oxygen being available to support nerve cell metabolism. This is responsible for 90% of all neuropathy and chronic pain cases. The remaining 10% is caused by physical trauma. Thus it appears that the main precipitating factor for neuropathy and chronic pain is hypoxia and demineralization of the synaptic fluid which creates shrinkage of the nerve cells which widens the gap between these cells making it more difficult for normal sensations to propagate, and loss of electrical conductivity in the synaptic fluid itself.

A temporary hypoxia of nerve tissue can be traced to most causes of neuropathy and chronic pain. The primary negative effects of this hypoxia are as follows:
A defensive contraction of the nerve cell resulting in oversize synaptic junctions
A loss of electrical conductivity of the synaptic fluid between nerve cells
A defensive change in the electrical potentials of the cell membrane resulting in a higher resting state of the trigger level which effectively limits the sensitivity to incoming signals

For example, when the lumbar area experiences a muscle spasm, blood flow is restricted through that muscle resulting in reduced oxygen availability to the surrounding tissue, including nerve cells. Because muscles can use either oxygen or glucose metabolic pathways, they can recover quickly from a temporary reduction in the level of available oxygen. Nerve cells, on the other hand, are limited to the Krebs oxidative reductive metabolic system and must take immediate defensive steps to assure survival during this hypo oxygen state. One of the ways they accomplish this is to contract along their longitudinal axis like a rubber band, reducing their surface area and thus lowering their need for oxygen. (This also occurs when these cells are attacked by a harsh agent in the blood such as chemotherapeutic drugs, Agent Orange, environmental toxins, insecticides, etc.) The synaptic junctions between the axons of one nerve cell and the dendrites of the next nerve cell widen. Normal nerve transmission is now compromised because a nerve signal of normal intensity cannot jump this newly widened gap. The synaptic fluid between the nerve cells must be electrically conductive. Pure water does not conduct electricity, so this conductivity relies on minerals and specific neurotransmitters such as serotonin in the synaptic fluid to enable the propagation of the nerve signal. These minerals are delivered via the perfusion of adjacent tissues with fresh blood and kept in suspension by the periodic ionization of successfully transmitted nerve signals across the junction. When nerve signals are reduced because of these larger dimensions of the synaptic junction, necessary minerals are no longer held in place by electrical tension and are slowly leeched out. This adds to the impairment of effective nerve transmission.

Common short term remedies with prescription drugs only ameliorate the pain temporarily and do little or nothing to mitigate or cure the underlying condition. They may provide some level of temporary relief, but as the disease progresses, the effective dosage of the drug needed to continue suppressing the pain increases concurrently. The side effects of these types of drugs are difficult to deal with and add to the patient’s discomfort. When the increased drug dosage reaches a threshold level, the patient can become confused, ataxic, constipated, confined to a wheelchair or may become bedridden. Symptoms similar to Alzheimer’s may soon follow.
 
When nerve signals can no longer jump the enlarged synaptic gap, the electrical tension that normally holds these minerals in place is absent, causing the synaptic fluid to leach out its mineral content. Electrical conductivity is reduced, thereby inhibiting the transmission of the normal nerves’ electrical signals across this gap.

http://neuropathydr.com/what%E2%80%99s-the-common-link-in-the-neuropathies-part-1/

http://neuropathydr.com/common-link-neuropathies-part-2/

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What a day

FINALLY............... some sunshine. After consistently rainy Fridays, today was a blessing to be at Great Hollow, both teaching (aka learning) and participating. I knew something was up after seeing that double rainbow yesterday. As you can see below, my daughter caught a barn swallow with her bare hands. It was in one of the buildings, looking for a window out. I didn't get to witness the catching, all I saw was her walking out the door holding the bird.

"Hey Mom, I caught a bird! It was trapped in the house."

It stayed patiently right in her hand long enough to show the other hikers and to set it free.

On our venture through the woods, we saw incredible huge Solomon's Seal, along with Showy pink lady's slipper flowers and patches of wintergreen, both of which I was too engrossed in talking with the kids about to remember to take photos. grrr.
Below is a captured moment of our lesson this morning which included collecting flowers and replicating their patterns.

What is Sciatica

Sciatica is the term used to describe nerve pain in the buttocks, legs and feet. It is caused when the sciatic nerve – the longest nerve in the body – becomes compressed or irritated. If you’re suffering with pain that radiates down the back of your leg and into your feet, it could be sciatica.

What is the Sciatic Nerve?

The sciatic nerve starts at the lower spine before running through the buttock, down the back of the thigh and into the foot. It’s an important nerve that sends signals from the spinal cord to the entire lower body.

Because of its location and length, the sciatic nerve has a variety of functions. That’s why sciatica can result in pain throughout the entire lower body, and can even lead to coughing, sneezing and muscle contractions.

What Causes Sciatica?

There are a number of potential causes for a compressed or irritated sciatic nerve. Some of the most common include:

• Slipped disc. If the outer casing of a disc in your spine becomes herniated, the interior of the disc bulges more than it should. This can lead to compression of the sciatic nerve, resulting in pain and discomfort.
•  Spinal injury. If you injure your spine, or the muscles that support the spine, inflammation can press on the sciatic nerve.
• Spinal stenosis. Sometimes the passage holding the spinal cord can become narrowed – often due to large ligaments. In some cases, this can cause compression on the sciatic nerve. Spinal stenosis often results in pain in the lower back.
• Spondylolisthesis. This is a condition where a vertebra moves more than it should. It can either be caused by ageing or repeatedly bending the spine in an unnatural way.
• Spinal infection. This is less common, but is a potential cause of sciatic pain.

The amount of pain, loss of sensation or tingling can vary depending on how much the nerve has been compressed or irritated. The location of the nerve compression can also affect where the pain radiates.

How is Sciatica Treated?

Each cause of sciatica requires a specific treatment plan to effectively reduce compression on the sciatic nerve and eliminate pain.

Traditional treatment for sciatica usually involves a combination of pain-killing medications and rest. This can sometimes be effective at reducing pain in the short-term. The problem is that it only treats the symptoms of sciatica, meaning the pain often returns at a later date.

Physiotherapy exercises are another common treatment. Unlike pain-killing medication, these exercises treat the underlying problem – but it’s vital that the right exercises are performed for a specific cause of sciatica. The wrong exercises can worsen pain and increase the time taken for recovery.

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What Will Help Tracking Genetic Reasons For Neuropathic Pain

Today's post from sciencedaily.com (see link below) looks at a problem scientists have faced when confronted with the question: is neuropathy genetic? The problem is the lack of a standard approach to assessing its clinical characteristics (otherwise known as a 'phenotype'). However, recently there seems to have been a breakthrough and they have developed criteria which categorise what neuropathy 'looks like' genetically and clinically. It's thought that this will help in understanding how neuropathic pain develops, leading to new approaches to treatment and prevention. Hopefully this is the case and we can look forward to effective treatments reaching our doctors' prescription pads sooner rather than later.
 

Standard phenotypes will aid in genetic research on neuropathic pain 
Date:October 26, 2015 Source:Wolters Kluwer HealthSummary:

Research on the genetic factors contributing to neuropathic pain has been hindered by the lack of a standard approach to assessing its clinical characteristics or "phenotype." Now, a report from an expert panel published in the journal PAIN® presents a consensus approach to assessing the phenotype of neuropathic pain. The journal is the official publication of the Wolters Kluwer.

Standardized "entry level" criteria for defining the phenotype of neuropathic pain were developed by an international panel of experts assembled by the IASP's Special Interest Group on Neuropathic Pain (NeuPSIG). Along with other recommendations for research reporting, the consensus criteria will achieve "greater consistency and transparency in studies of neuropathic pain in adult humans." Dr. Blair H. Smith of the University of Dundee, Scotland, is lead author of the expert panel report.

Setting Standard Criteria to Define Neuropathic Pain Phenotypes

Neuropathic pain is a common and complex pain condition caused by damage or diseases of the sensory nerves. Patients may experience shooting or burning pain, numbness, or exaggerated pain responses. Neuropathic pain can be caused by diabetes, trauma, shingles, and a wide range of other conditions.

Information on genetic factors may help in understanding how neuropathic pain develops, leading to new approaches to treatment and prevention. But so far, genetic studies have produced inconsistent results that are difficult to confirm. This is partly because of differing approaches used to identify and classify the clinical expression and characteristics of this condition, which can vary widely.

To address this problem, the expert panel "aimed to provide guidelines on collecting and reporting phenotypes" of neuropathic pain. After a thorough review of previous research evidence, panel members followed a formal consensus process to develop a set of "entry level" phenotype data to identify and classify patients with neuropathic pain, as well as appropriate comparison (control) groups.

Following this process, the NeuPSIG panel identified three basic elements:
Pain with neuropathic characteristics (described as "hot/burning" or "evoked by light touch") or assessed using a validated screening tool
Pain distributed or located in a pattern that is anatomically consistent with underlying nerve damage or disease (in other words, the pain is consistent with the anatomy of the affected sensory nerves)
Additional information on pain history and characteristics and other factors relevant to the disease or group of patients being studied

Reflecting the challenges of diagnosing neuropathic pain, the report emphasizes that these "entry level" criteria identify only "possible" cases of neuropathic pain. Depending on the situation, additional criteria could be used to identify "probable" or "definite" cases, or additional sensory or psychological assessments could be conducted to further characterize the phenotype.

The new criteria are published as IASP concludes its 2014-2015 Global Year Against Neuropathic Pain campaign. By improving awareness among patients and health-care providers, IASP hopes to improve recognition and management of this disabling and difficult-to-treat condition.

The consensus phenotype criteria will be an important step toward a more productive approach to studying the genetic factors contributing to neuropathic pain, the NeuPSIG panel members believe. They conclude, "These improvements will facilitate advancements in the field by enabling collaboration between research groups, replication of discoveries of contributing genetic variants, meta-analyses, and translation from the laboratory to the general population, and back again."

Story Source:

The above post is reprinted from materials provided by Wolters Kluwer Health. Note: Materials may be edited for content and length.

Journal Reference:
Oliver van Hecke, Peter R. Kamerman, Nadine Attal, Ralf Baron, Gyda Bjornsdottir, David L.H. Bennett, Michael I. Bennett, Didier Bouhassira, Luda Diatchenko, Roy Freeman, Rainer Freynhagen, Maija Haanpää, Troels S. Jensen, Srinivasa N. Raja, Andrew S.C. Rice, Zeʼev Seltzer, Thorgeir E. Thorgeirsson, David Yarnitsky, Blair H. Smith. Neuropathic pain phenotyping by international consensus (NeuroPPIC) for genetic studies. PAIN, 2015; 156 (11): 2337 DOI: 10.1097/j.pain.0000000000000335

http://www.sciencedaily.com/releases/2015/10/151026132144.htm

What Pain Is PART 2

Today's post is PART TWO of a two part article about pain: the introduction below is the same as that for yesterday.

I very seldom recommend an article, or advise people strongly to read it. I generally let the reader make up his or her mind if the subject interests them or not. However, today's and tomorrow's two-part post from the National Institute of Neurological Disorders and Stroke (see link below) seems to me to be extremely useful for most people living with HIV and/or Neuropathy. It was written in 2001 but as you will see, very little has changed since then (an indictment of how far we've advanced treatment of our disease!)
Sooner or later, it is possible that you will experience some HIV-related complaint which gives you pain. If it's not HIV-related then it's very helpful to be able to identify what it is. HIV-patients are constantly excluding possiblities before getting to the source of their problem. That applies even more to people with neuropathy. It is so complex; with so many causes and forms, that getting to the root of your pain problem is liking walking through a minefield.
This article provides a sort of easily-understandable breakdown of the various forms of pain and how they're treated (including 'alternative' treatments). It's long (had to be split up over two days) but absolutely worth reading, even if you're not in pain yourself. It will help to calm the inbuilt hypochondria that people with HIV acquire through experience and enable them to rule out many of their worries.

Pain: Hope Through Research
Prepared by:
Office of Communications and Public Liaison
National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892

What is the Role of Age and Gender in Pain?
Gender and Pain

It is now widely believed that pain affects men and women differently. While the sex hormones estrogen and testosterone certainly play a role in this phenomenon, psychology and culture, too, may account at least in part for differences in how men and women receive pain signals. For example, young children may learn to respond to pain based on how they are treated when they experience pain. Some children may be cuddled and comforted, while others may be encouraged to tough it out and to dismiss their pain.

Many investigators are turning their attention to the study of gender differences and pain. Women, many experts now agree, recover more quickly from pain, seek help more quickly for their pain, and are less likely to allow pain to control their lives. They also are more likely to marshal a variety of resources-coping skills, support, and distraction-with which to deal with their pain.

Research in this area is yielding fascinating results. For example, male experimental animals injected with estrogen, a female sex hormone, appear to have a lower tolerance for pain-that is, the addition of estrogen appears to lower the pain threshold. Similarly, the presence of testosterone, a male hormone, appears to elevate tolerance for pain in female mice: the animals are simply able to withstand pain better. Female mice deprived of estrogen during experiments react to stress similarly to male animals. Estrogen, therefore, may act as a sort of pain switch, turning on the ability to recognize pain.

Investigators know that males and females both have strong natural pain-killing systems, but these systems operate differently. For example, a class of painkillers called kappa-opioids is named after one of several opioid receptors to which they bind, the kappa-opioid receptor, and they include the compounds nalbuphine (Nubain®) and butorphanol (Stadol®). Research suggests that kappa-opioids provide better pain relief in women.

Though not prescribed widely, kappa-opioids are currently used for relief of labor pain and in general work best for short-term pain. Investigators are not certain why kappa-opioids work better in women than men. Is it because a woman's estrogen makes them work, or because a man's testosterone prevents them from working? Or is there another explanation, such as differences between men and women in their perception of pain? Continued research may result in a better understanding of how pain affects women differently from men, enabling new and better pain medications to be designed with gender in mind.

Pain in Aging and Pediatric Populations: Special Needs and Concerns

Pain is the number one complaint of older Americans, and one in five older Americans takes a painkiller regularly. In 1998, the American Geriatrics Society (AGS) issued guidelines* for the management of pain in older people. The AGS panel addressed the incorporation of several non-drug approaches in patients' treatment plans, including exercise. AGS panel members recommend that, whenever possible, patients use alternatives to aspirin, ibuprofen, and other NSAIDs because of the drugs' side effects, including stomach irritation and gastrointestinal bleeding. For older adults, acetaminophen is the first-line treatment for mild-to-moderate pain, according to the guidelines. More serious chronic pain conditions may require opioid drugs (narcotics), including codeine or morphine, for relief of pain.

Pain in younger patients also requires special attention, particularly because young children are not always able to describe the degree of pain they are experiencing. Although treating pain in pediatric patients poses a special challenge to physicians and parents alike, pediatric patients should never be undertreated. Recently, special tools for measuring pain in children have been developed that, when combined with cues used by parents, help physicians select the most effective treatments.

Nonsteroidal agents, and especially acetaminophen, are most often prescribed for control of pain in children. In the case of severe pain or pain following surgery, acetaminophen may be combined with codeine.

* Journal of the American Geriatrics Society (1998; 46:635-651).

A Pain Primer: What Do We Know About Pain?

We may experience pain as a prick, tingle, sting, burn, or ache. Receptors on the skin trigger a series of events, beginning with an electrical impulse that travels from the skin to the spinal cord. The spinal cord acts as a sort of relay center where the pain signal can be blocked, enhanced, or otherwise modified before it is relayed to the brain. One area of the spinal cord in particular, called the dorsal horn (see section on Spine Basics in the Appendix), is important in the reception of pain signals.

The most common destination in the brain for pain signals is the thalamus and from there to the cortex, the headquarters for complex thoughts. The thalamus also serves as the brain's storage area for images of the body and plays a key role in relaying messages between the brain and various parts of the body. In people who undergo an amputation, the representation of the amputated limb is stored in the thalamus. (For a discussion of the thalamus and its role in this phenomenon, called phantom pain, see section on Phantom Pain in the Appendix.)

Pain is a complicated process that involves an intricate interplay between a number of important chemicals found naturally in the brain and spinal cord. In general, these chemicals, called neurotransmitters, transmit nerve impulses from one cell to another.

There are many different neurotransmitters in the human body; some play a role in human disease and, in the case of pain, act in various combinations to produce painful sensations in the body. Some chemicals govern mild pain sensations; others control intense or severe pain.

The body's chemicals act in the transmission of pain messages by stimulating neurotransmitter receptors found on the surface of cells; each receptor has a corresponding neurotransmitter. Receptors function much like gates or ports and enable pain messages to pass through and on to neighboring cells. One brain chemical of special interest to neuroscientists is glutamate. During experiments, mice with blocked glutamate receptors show a reduction in their responses to pain. Other important receptors in pain transmission are opiate-like receptors. Morphine and other opioid drugs work by locking on to these opioid receptors, switching on pain-inhibiting pathways or circuits, and thereby blocking pain.

Another type of receptor that responds to painful stimuli is called a nociceptor. Nociceptors are thin nerve fibers in the skin, muscle, and other body tissues, that, when stimulated, carry pain signals to the spinal cord and brain. Normally, nociceptors only respond to strong stimuli such as a pinch. However, when tissues become injured or inflamed, as with a sunburn or infection, they release chemicals that make nociceptors much more sensitive and cause them to transmit pain signals in response to even gentle stimuli such as breeze or a caress. This condition is called allodynia -a state in which pain is produced by innocuous stimuli.

The body's natural painkillers may yet prove to be the most promising pain relievers, pointing to one of the most important new avenues in drug development. The brain may signal the release of painkillers found in the spinal cord, including serotonin, norepinephrine, and opioid-like chemicals. Many pharmaceutical companies are working to synthesize these substances in laboratories as future medications.

Endorphins and enkephalins are other natural painkillers. Endorphins may be responsible for the "feel good" effects experienced by many people after rigorous exercise; they are also implicated in the pleasurable effects of smoking.

Similarly, peptides, compounds that make up proteins in the body, play a role in pain responses. Mice bred experimentally to lack a gene for two peptides called tachykinins-neurokinin A and substance P-have a reduced response to severe pain. When exposed to mild pain, these mice react in the same way as mice that carry the missing gene. But when exposed to more severe pain, the mice exhibit a reduced pain response. This suggests that the two peptides are involved in the production of pain sensations, especially moderate-to-severe pain. Continued research on tachykinins, conducted with support from the NINDS, may pave the way for drugs tailored to treat different severities of pain.

Scientists are working to develop potent pain-killing drugs that act on receptors for the chemical acetylcholine. For example, a type of frog native to Ecuador has been found to have a chemical in its skin called epibatidine, derived from the frog's scientific name, Epipedobates tricolor. Although highly toxic, epibatidine is a potent analgesic and, surprisingly, resembles the chemical nicotine found in cigarettes. Also under development are other less toxic compounds that act on acetylcholine receptors and may prove to be more potent than morphine but without its addictive properties.

The idea of using receptors as gateways for pain drugs is a novel idea, supported by experiments involving substance P. Investigators have been able to isolate a tiny population of neurons, located in the spinal cord, that together form a major portion of the pathway responsible for carrying persistent pain signals to the brain. When animals were given injections of a lethal cocktail containing substance P linked to the chemical saporin, this group of cells, whose sole function is to communicate pain, were killed. Receptors for substance P served as a portal or point of entry for the compound. Within days of the injections, the targeted neurons, located in the outer layer of the spinal cord along its entire length, absorbed the compound and were neutralized. The animals' behavior was completely normal; they no longer exhibited signs of pain following injury or had an exaggerated pain response. Importantly, the animals still responded to acute, that is, normal, pain. This is a critical finding as it is important to retain the body's ability to detect potentially injurious stimuli. The protective, early warning signal that pain provides is essential for normal functioning. If this work can be translated clinically, humans might be able to benefit from similar compounds introduced, for example, through lumbar (spinal) puncture.

Another promising area of research using the body's natural pain-killing abilities is the transplantation of chromaffin cells into the spinal cords of animals bred experimentally to develop arthritis. Chromaffin cells produce several of the body's pain-killing substances and are part of the adrenal medulla, which sits on top of the kidney. Within a week or so, rats receiving these transplants cease to exhibit telltale signs of pain. Scientists, working with support from the NINDS, believe the transplants help the animals recover from pain-related cellular damage. Extensive animal studies will be required to learn if this technique might be of value to humans with severe pain.

One way to control pain outside of the brain, that is, peripherally, is by inhibiting hormones called prostaglandins. Prostaglandins stimulate nerves at the site of injury and cause inflammation and fever. Certain drugs, including NSAIDs, act against such hormones by blocking the enzyme that is required for their synthesis.

Blood vessel walls stretch or dilate during a migraine attack and it is thought that serotonin plays a complicated role in this process. For example, before a migraine headache, serotonin levels fall. Drugs for migraine include the triptans: sumatriptan (Imitrix®), naratriptan (Amerge®), and zolmitriptan (Zomig®). They are called serotonin agonists because they mimic the action of endogenous (natural) serotonin and bind to specific subtypes of serotonin receptors.

Ongoing pain research, much of it supported by the NINDS, continues to reveal at an unprecedented pace fascinating insights into how genetics, the immune system, and the skin contribute to pain responses.

The explosion of knowledge about human genetics is helping scientists who work in the field of drug development. We know, for example, that the pain-killing properties of codeine rely heavily on a liver enzyme, CYP2D6, which helps convert codeine into morphine. A small number of people genetically lack the enzyme CYP2D6; when given codeine, these individuals do not get pain relief. CYP2D6 also helps break down certain other drugs. People who genetically lack CYP2D6 may not be able to cleanse their systems of these drugs and may be vulnerable to drug toxicity. CYP2D6 is currently under investigation for its role in pain.

In his research, the late John C. Liebeskind, a renowned pain expert and a professor of psychology at UCLA, found that pain can kill by delaying healing and causing cancer to spread. In his pioneering research on the immune system and pain, Dr. Liebeskind studied the effects of stress-such as surgery-on the immune system and in particular on cells called natural killer or NK cells. These cells are thought to help protect the body against tumors. In one study conducted with rats, Dr. Liebeskind found that, following experimental surgery, NK cell activity was suppressed, causing the cancer to spread more rapidly. When the animals were treated with morphine, however, they were able to avoid this reaction to stress.

The link between the nervous and immune systems is an important one. Cytokines, a type of protein found in the nervous system, are also part of the body's immune system, the body's shield for fighting off disease. Cytokines can trigger pain by promoting inflammation, even in the absence of injury or damage. Certain types of cytokines have been linked to nervous system injury. After trauma, cytokine levels rise in the brain and spinal cord and at the site in the peripheral nervous system where the injury occurred. Improvements in our understanding of the precise role of cytokines in producing pain, especially pain resulting from injury, may lead to new classes of drugs that can block the action of these substances.

What is the Future of Pain Research?

In the forefront of pain research are scientists supported by the National Institutes of Health (NIH), including the NINDS. Other institutes at NIH that support pain research include the National Institute of Dental and Craniofacial Research, the National Cancer Institute, the National Institute of Nursing Research, the National Institute on Drug Abuse, and the National Institute of Mental Health. Developing better pain treatments is the primary goal of all pain research being conducted by these institutes.

Some pain medications dull the patient's perception of pain. Morphine is one such drug. It works through the body's natural pain-killing machinery, preventing pain messages from reaching the brain. Scientists are working toward the development of a morphine-like drug that will have the pain-deadening qualities of morphine but without the drug's negative side effects, such as sedation and the potential for addiction. Patients receiving morphine also face the problem of morphine tolerance, meaning that over time they require higher doses of the drug to achieve the same pain relief. Studies have identified factors that contribute to the development of tolerance; continued progress in this line of research should eventually allow patients to take lower doses of morphine.

One objective of investigators working to develop the future generation of pain medications is to take full advantage of the body's pain "switching center" by formulating compounds that will prevent pain signals from being amplified or stop them altogether. Blocking or interrupting pain signals, especially when there is no injury or trauma to tissue, is an important goal in the development of pain medications. An increased understanding of the basic mechanisms of pain will have profound implications for the development of future medicines. The following areas of research are bringing us closer to an ideal pain drug.

Systems and Imaging: The idea of mapping cognitive functions to precise areas of the brain dates back to phrenology, the now archaic practice of studying bumps on the head. Positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and other imaging technologies offer a vivid picture of what is happening in the brain as it processes pain. Using imaging, investigators can now see that pain activates at least three or four key areas of the brain's cortex-the layer of tissue that covers the brain. Interestingly, when patients undergo hypnosis so that the unpleasantness of a painful stimulus is not experienced, activity in some, but not all, brain areas is reduced. This emphasizes that the experience of pain involves a strong emotional component as well as the sensory experience, namely the intensity of the stimulus.

Channels: The frontier in the search for new drug targets is represented by channels. Channels are gate-like passages found along the membranes of cells that allow electrically charged chemical particles called ions to pass into the cells. Ion channels are important for transmitting signals through the nerve's membrane. The possibility now exists for developing new classes of drugs, including pain cocktails that would act at the site of channel activity.

Trophic Factors: A class of "rescuer" or "restorer" drugs may emerge from our growing knowledge of trophic factors, natural chemical substances found in the human body that affect the survival and function of cells. Trophic factors also promote cell death, but little is known about how something beneficial can become harmful. Investigators have observed that an over-accumulation of certain trophic factors in the nerve cells of animals results in heightened pain sensitivity, and that some receptors found on cells respond to trophic factors and interact with each other. These receptors may provide targets for new pain therapies.

Molecular Genetics: Certain genetic mutations can change pain sensitivity and behavioral responses to pain. People born genetically insensate to pain-that is, individuals who cannot feel pain-have a mutation in part of a gene that plays a role in cell survival. Using "knockout" animal models-animals genetically engineered to lack a certain gene-scientists are able to visualize how mutations in genes cause animals to become anxious, make noise, rear, freeze, or become hypervigilant. These genetic mutations cause a disruption or alteration in the processing of pain information as it leaves the spinal cord and travels to the brain. Knockout animals can be used to complement efforts aimed at developing new drugs.

Plasticity: Following injury, the nervous system undergoes a tremendous reorganization. This phenomenon is known as plasticity. For example, the spinal cord is "rewired" following trauma as nerve cell axons make new contacts, a phenomenon known as "sprouting." This in turn disrupts the cells' supply of trophic factors. Scientists can now identify and study the changes that occur during the processing of pain. For example, using a technique called polymerase chain reaction, abbreviated PCR, scientists can study the genes that are induced by injury and persistent pain. There is evidence that the proteins that are ultimately synthesized by these genes may be targets for new therapies. The dramatic changes that occur with injury and persistent pain underscore that chronic pain should be considered a disease of the nervous system, not just prolonged acute pain or a symptom of an injury. Thus, scientists hope that therapies directed at preventing the long-term changes that occur in the nervous system will prevent the development of chronic pain conditions.

Neurotransmitters: Just as mutations in genes may affect behavior, they may also affect a number of neurotransmitters involved in the control of pain. Using sophisticated imaging technologies, investigators can now visualize what is happening chemically in the spinal cord. From this work, new therapies may emerge, therapies that can help reduce or obliterate severe or chronic pain.

Hope for the Future
Thousands of years ago, ancient peoples attributed pain to spirits and treated it with mysticism and incantations. Over the centuries, science has provided us with a remarkable ability to understand and control pain with medications, surgery, and other treatments. Today, scientists understand a great deal about the causes and mechanisms of pain, and research has produced dramatic improvements in the diagnosis and treatment of a number of painful disorders. For people who fight every day against the limitations imposed by pain, the work of NINDS-supported scientists holds the promise of an even greater understanding of pain in the coming years. Their research offers a powerful weapon in the battle to prolong and improve the lives of people with pain: hope.

Appendix

Spine Basics: The Vertebrae, Discs, and Spinal Cord

Stacked on top of one another in the spine are more than 30 bones, the vertebrae, which together form the spine. They are divided into four regions:

the seven cervical or neck vertebrae (labeled C1-C7),
the 12 thoracic or upper back vertebrae (labeled T1-T12),
the five lumbar vertebrae (labeled L1-L5), which we know as the lower back, and
the sacrum and coccyx, a group of bones fused together at the base of the spine.
The vertebrae are linked by ligaments, tendons, and muscles. Back pain can occur when, for example, someone lifts something too heavy, causing a sprain, pull, strain, or spasm in one of these muscles or ligaments in the back.

Between the vertebrae are round, spongy pads of cartilage called discs that act much like shock absorbers. In many cases, degeneration or pressure from overexertion can cause a disc to shift or protrude and bulge, causing pressure on a nerve and resultant pain. When this happens, the condition is called a slipped, bulging, herniated, or ruptured disc, and it sometimes results in permanent nerve damage.

The column-like spinal cord is divided into segments similar to the corresponding vertebrae: cervical, thoracic, lumbar, sacral, and coccygeal. The cord also has nerve roots and rootlets which form branch-like appendages leading from its ventral side (that is, the front of the body) and from its dorsal side (that is, the back of the body). Along the dorsal root are the cells of the dorsal root ganglia, which are critical in the transmission of "pain" messages from the cord to the brain. It is here where injury, damage, and trauma become pain.

The Nervous Systems

The central nervous system (CNS) refers to the brain and spinal cord together. The peripheral nervous system refers to the cervical, thoracic, lumbar, and sacral nerve trunks leading away from the spine to the limbs. Messages related to function (such as movement) or dysfunction (such as pain) travel from the brain to the spinal cord and from there to other regions in the body and back to the brain again. The autonomic nervous system controls involuntary functions in the body, like perspiration, blood pressure, heart rate, or heart beat. It is divided into the sympathetic and parasympathetic nervous systems. The sympathetic and parasympathetic nervous systems have links to important organs and systems in the body; for example, the sympathetic nervous system controls the heart, blood vessels, and respiratory system, while the parasympathetic nervous system controls our ability to sleep, eat, and digest food.

The peripheral nervous system also includes 12 pairs of cranial nerves located on the underside of the brain. Most relay messages of a sensory nature. They include the olfactory (I), optic (II), oculomotor (III), trochlear (IV), trigeminal (V), abducens (VI), facial (VII), vestibulocochlear (VIII), glossopharyngeal (IX), vagus (X), accessory (XI), and hypoglossal (XII) nerves. Neuralgia, as in trigeminal neuralgia, is a term that refers to pain that arises from abnormal activity of a nerve trunk or its branches. The type and severity of pain associated with neuralgia vary widely.

Phantom Pain: How Does the Brain Feel?

Sometimes, when a limb is removed during an amputation, an individual will continue to have an internal sense of the lost limb. This phenomenon is known as phantom limb and accounts describing it date back to the 1800s. Similarly, many amputees are frequently aware of severe pain in the absent limb. Their pain is real and is often accompanied by other health problems, such as depression.

What causes this phenomenon? Scientists believe that following amputation, nerve cells "rewire" themselves and continue to receive messages, resulting in a remapping of the brain's circuitry. The brain's ability to restructure itself, to change and adapt following injury, is called plasticity (see section on Plasticity).

Our understanding of phantom pain has improved tremendously in recent years. Investigators previously believed that brain cells affected by amputation simply died off. They attributed sensations of pain at the site of the amputation to irritation of nerves located near the limb stump. Now, using imaging techniques such as positron emission tomography (PET) and magnetic resonance imaging (MRI), scientists can actually visualize increased activity in the brain's cortex when an individual feels phantom pain. When study participants move the stump of an amputated limb, neurons in the brain remain dynamic and excitable. Surprisingly, the brain's cells can be stimulated by other body parts, often those located closest to the missing limb.

Treatments for phantom pain may include analgesics, anticonvulsants, and other types of drugs; nerve blocks; electrical stimulation; psychological counseling, biofeedback, hypnosis, and acupuncture; and, in rare instances, surgery.

Chili Peppers, Capsaicin, and Pain

The hot feeling, red face, and watery eyes you experience when you bite into a red chili pepper may make you reach for a cold drink, but that reaction has also given scientists important information about pain. The chemical found in chili peppers that causes those feelings is capsaicin (pronounced cap-SAY-sin), and it works its unique magic by grabbing onto receptors scattered along the surface of sensitive nerve cells in the mouth.

In 1997, scientists at the University of California at San Francisco discovered a gene for a capsaicin receptor, called the vanilloid receptor. Once in contact with capsaicin, vanilloid receptors open and pain signals are sent from the peripheral nociceptor and through central nervous system circuits to the brain. Investigators have also learned that this receptor plays a role in the burning type of pain commonly associated with heat, such as the kind you experience when you touch your finger to a hot stove. The vanilloid receptor functions as a sort of "ouch gateway," enabling us to detect burning hot pain, whether it originates from a 3-alarm habanera chili or from a stove burner.

Capsaicin is currently available as a prescription or over-the-counter cream for the treatment of a number of pain conditions, such as shingles. It works by reducing the amount of substance P found in nerve endings and interferes with the transmission of pain signals to the brain. Individuals can become desensitized to the compound, however, perhaps because of long-term damage to nerve tissue. Some individuals find the burning sensation they experience when using capsaicin cream to be intolerable, especially when they are already suffering from a painful condition, such as postherpetic neuralgia. Soon, however, better treatments that relieve pain by blocking vanilloid receptors may arrive in drugstores.

Marijuana

As a painkiller, marijuana or, by its Latin name, cannabis, continues to remain highly controversial. In the eyes of many individuals campaigning on its behalf, marijuana rightfully belongs with other pain remedies. In fact, for many years, it was sold under highly controlled conditions in cigarette form by the Federal government for just that purpose.

In 1997, the National Institutes of Health held a workshop to discuss research on the possible therapeutic uses for smoked marijuana. Panel members from a number of fields reviewed published research and heard presentations from pain experts. The panel members concluded that, because there are too few scientific studies to prove marijuana's therapeutic utility for certain conditions, additional research is needed. There is evidence, however, that receptors to which marijuana binds are found in many brain regions that process information that can produce pain.

Nerve Blocks

Nerve blocks may involve local anesthesia, regional anesthesia or analgesia, or surgery; dentists routinely use them for traditional dental procedures. Nerve blocks can also be used to prevent or even diagnose pain.

In the case of a local nerve block, any one of a number of local anesthetics may be used; the names of these compounds, such as lidocaine or novocaine, usually have an aine ending. Regional blocks affect a larger area of the body. Nerve blocks may also take the form of what is commonly called an epidural, in which a drug is administered into the space between the spine's protective covering (the dura) and the spinal column. This procedure is most well known for its use during childbirth. Morphine and methadone are opioid narcotics (such drugs end in ine or one) that are sometimes used for regional analgesia and are administered as an injection.

Neurolytic blocks employ injection of chemical agents such as alcohol, phenol, or glycerol to block pain messages and are most often used to treat cancer pain or to block pain in the cranial nerves (see The Nervous Systems). In some cases, a drug called guanethidine is administered intravenously in order to accomplish the block.

Surgical blocks are performed on cranial, peripheral, or sympathetic nerves. They are most often done to relieve the pain of cancer and extreme facial pain, such as that experienced with trigeminal neuralgia. There are several different types of surgical nerve blocks and they are not without problems and complications. Nerve blocks can cause muscle paralysis and, in many cases, result in at least partial numbness. For that reason, the procedure should be reserved for a select group of patients and should only be performed by skilled surgeons. Types of surgical nerve blocks include:

Neurectomy (including peripheral neurectomy) in which a damaged peripheral nerve is destroyed.
Spinal dorsal rhizotomy in which the surgeon cuts the root or rootlets of one or more of the nerves radiating from the spine. Other rhizotomy procedures include cranial rhizotomy and trigeminal rhizotomy, performed as a treatment for extreme facial pain or for the pain of cancer.
Sympathectomy, also called sympathetic blockade, in which a drug or an agent such as guanethidine is used to eliminate pain in a specific area (a limb, for example). The procedure is also done for cardiac pain, vascular disease pain, the pain of reflex sympathetic dystrophy syndrome, and other conditions. The term takes its name from the sympathetic nervous system (see The Nervous Systems) and may involve, for example, cutting a nerve that controls contraction of one or more arteries.

"Pain: Hope Through Research," NINDS. Publication date December 2001.

http://www.ninds.nih.gov/disorders/chronic_pain/detail_chronic_pain.htm

You Wont Believe What Goes On In Neuropathy Patients Shoes!

Today's light-hearted post from totalfootcare.ca (see link below) should carry a government health warning because it's pretty much a wake-up call for people living with neuropathy in their feet. Because of that dratted numbness that fools you into thinking you know what's going on under your feet (because you can still feel the burning and tingling that goes on in other layers), you can so easily miss sharp objects that lurk inside your shoes. Read this article: you'll know why this is important!!
 

The Funniest Things I’ve Found in Patients’ Shoes… That Demonstrate Why Neuropathy is No Laughing Matter
Written by: HealthyFeet

Web Feet is a quarterly blog posted by Registered Chiropodist David Murphy. Dave has ten years’ experience in his field and works at Kawartha Total Foot Care Centre’s main clinic in Bobcaygeon, Ontario as well as the practice’s sites at Lakefield Physiotherapy & Foot Health Clinic and the Curve Lake First Nation Health Centre.

There’s a moment of wonder for every chiropodist before reaching into a patient’s shoes at what discoveries might be revealed. From pennies to pins and everything in between, I’ve seen my share of “shoe treasures” over the years. The sheer oddness of some of them may bring a smile to one’s face, but for people with diabetes and diminished sensation caused by peripheral neuropathy, the result can be anything but amusing – skin ulcers, serious infections, even amputations.

Here are a few examples of some shoe finds this year, and they make clear just how important it is for people with reduced sensation to check the insides of their footwear regularly.

1. Tacky Tricks
Shortly into back-to-school season, I removed the insole of one particular teacher’s shoes to reveal a bevy of thumb tacks! Unbeknownst to her, it seems she was the subject of some classroom pranksters. This “joke” could have become decidedly not funny very quickly had the tacks remained undiscovered.

2. Ho, Ho, Hold on a Minute!
The holidays are such a wonderful time full of tradition. Last season, a patient visited me shortly after the family’s annual Christmas tree cutting adventure. Just as he finished telling me that his work boots are the most comfortable boots he has ever owned, I reached in and pulled out a branch with an entire clump of pine needles that would rival any of Charlie Brown’s Christmas trees. Needless to say we went on to further sensation testing.

3. One Piña Colada Please… Hold the Cocktail Umbrella
A patient returned last winter from some fun in the sun with what I thought was a sliver embedded in his sole, perhaps picked up on a long walk on the beach. On closer examination of his deck shoes, I realized that I was right about the sliver but wrong about its origin. It was from an umbrella – a cocktail umbrella to be precise. Perhaps the next time the customs agent asks you to remove your footwear on return from your favorite all-inclusive winter destination you may also want to use this opportunity to check the insides of your shoes for unwanted stowaways!

4. Dog Gone It!
Attention pet owners… knick, knack, paddy whack give a dog a bone? This four legged member of the family used its owner’s shoe as a cozy hiding spot for a favourite bone. Unfortunately for the pet owner who was unaware of what was hiding in his Hush Puppies, the shards of fragmented bone had caused a severe infection by the time I discovered them.

5. Automatic Toe-nition
My last recollection is one that was quite remarkable and humorous to everyone involved… initially. This particular patient could not understand why on earth he could still start his car (push button ignition) when his keys had been missing for days, even leaving him to wonder perhaps about artificial intelligence or some sort of electromagnetic disturbance. He had even involved his mechanic who was also very puzzled. It was only when his wife noticed the bleeding in his socks that she checked his shoes and the mystery was solved. There they were – his full set of keys pushed into the end of his shoe. The patient was completely unaware, felt nothing, not even the bottle opener also attached to his key collection. The sad ending to this story is that complications developed and progressed to the point that his great toe required amputation.

These examples illustrate the severity and potentially life-changing impact of neuropathy. It’s something we see and treat regularly at Kawartha Total Foot Care Centre.

Know the Warning Signs and Your Risks for Neuropathy

Neuropathy can range from a mild tingling or a “pins and needles sensation,” to sharp stabbing pain, and complete numbness. This occurs when the nerves in the feet that supply the brain with sensory information are damaged. Neuropathy can result from a variety of factors such as chemical toxicity, alcoholism, and chemotherapy. However, the most common cause by far of neuropathy and neuropathic changes in feet is diabetes.

In diabetics, the neuropathic changes are caused by the fluctuating blood sugar levels. The inconsistent blood sugar levels, over time, erode the insulating layers that cover the nerves, leading to altered or complete loss of sensation.

Prevention is the Best Medicine

Don’t let a nail in your shoe be the wake-up call to give your neuropathy proper consideration.

1. If you have been previously diagnosed with neuropathy, are diabetic, or have a family history of diabetes, it’s critical to have your feet examined and cared for regularly by a Registered Chiropodist. This assessment should include a full clinical vascular and neurological exam, dermatological exam, biomechanical evaluation, and a footwear assessment, along with ongoing foot medical care.

2. If you are a diabetic, controlling your blood sugar is crucial, having a healthy balanced diet and active lifestyle is a necessity, and getting enough restful sleep is essential in preventing or delaying neuropathic changes.

3. Self Examinations – use your hand and a mirror to check your feet as well as the inside of your footwear daily. This will become habitual and will likely prevent any close calls from becoming a more serious matter later on.

4. For those individuals who have diabetes and/or neuropathy and find their symptoms progressing or find they are having a big impact on daily life, then certain medications may provide benefit. Be sure to measure your blood sugar regularly – you can’t manage what you don’t measure! Bring these results to your family doctors and/or endocrinologist regularly and work with them to manage your condition.

5. At Kawartha Total Foot Care Centre, we have had success with weekly infrared light therapy sessions. This form of treatment helps treat the symptoms of neuropathy and although results are very specific to the individual, it may be the difference between keeping up with your normal daily activities or not.

My earlier stories might be a dose of lighthearted humour, but I know first-hand that neuropathy is no laughing matter. Remember that while we may not be able to reverse nerve damage, chiropodists can certainly help patients to better manage symptoms, prevent impacts from neuropathic foot changes, and improve quality of life.

http://www.totalfootcare.ca/the-funniest-things-ive-found-in-patients-shoes-that-demonstrate-why-neuropathy-is-no-laughing-matter-2/

CIDP What Is The Path Study

Today's post from neuropathy.org (see link below) invites people to join a 'Path' study in their area. This sort of study looks at the effectiveness of immunoglobulin being injected to treat CIDP (chronic inflammatory demyelinating neuropathy. Chronic CIDP is a lesser known form of neuropathy the main symptoms of which are weakness in the arms, legs, hands and feet. Normally this is treated with corticosteroids which are administered in pill form but they are looking into the effectiveness of injected immunoglobulin as an alternative. Now many people with neuropathy (peripheral or otherwise) suffer to some extent from weakness in the limbs and this is often accompanied (or even caused by) muscle decrease. If you feel that the weakness you are feeling is more than could reasonably be expected, it may be worth talking it over with your doctor or neurologist, to see if CIDP is playing a part.

Understanding the "PATH" Study, Assessing Subcutaneous Immunoglobulin, for CIDP  
Neuropathy Association June 18, 2014

Learn more about this clinical
research study...

If you are looking to volunteer or want
information about a study site near you,
please contact the study team at
clinicaltrials@cslbehring.com.

Chronic inflammatory demyelinating polyradiculoneuropathy, or CIDP, is a rare disorder of the peripheral nerves occurring at any age. Although the exact cause is not known, CIDP is considered an autoimmune disorder. It is twice as common in males as in females. The prevalence of CIDP is unclear, but in studies performed worldwide, it has been estimated to range from 1.9 per 100,000 to 7.7 per 100,000.

CIDP is characterized by weakness in the arms and legs which gradually worsens over a period of months. A patient with CIDP may find walking difficult due to weakness, or have difficulty using their arms and hands and/or legs and feet. Children are often diagnosed because of a disturbance in the way they walk, potentially causing them to fall, or by muscle weakness and loss of tendon reflexes. The course of the disease in children may be variable, showing a pattern that changes from worsening (relapsing) of symptoms to improvement (remitting).

1. How is CIDP treated?

Clinical studies in CIDP patients have shown that effective treatments include immunoglobulins or corticosteroids. In the event that neither of these options is effective, plasma exchange may be considered.Patients with CIDP can be treated with immunoglobulins or corticosteroids as first-line therapy. Immunoglobulins can be administered intravenously (IVIg), while corticosteroids may be administered by mouth (orally) or intravenously. A third option, plasma exchange or plasmapheresis (PE) can also be effective. PE is a blood purification procedure used to treat several autoimmune diseases, including CIDP.

It is important to discuss the advantages and disadvantages of these treatment options, as recommended by the guidelines, with your doctor. To ensure the most effective treatment is being used, all patients will have an individualized assessment of their treatment response.

2. What is IgPro20?

IgPro20 is a 20%, ready-to-use, liquid formulation of purified human immunoglobulin for subcutaneous (SCIg) administration. It is manufactured by the same advanced process that is used in the manufacture of 10% intravenous immunoglobulin (IVIg), Privigen. IgPro20 contains a higher immunoglobulin concentration than other SCIg immunoglobulins and IVIg products, giving the potential for a low infusion volume and short infusion time.

SCIg administration involves injection of immunoglobulin under the surface of the skin, and does not require access to a vein. This method of administration provides a convenient alternative to the intravenous route, and is often administered under medical supervision.

CSL Behring is recruiting patients for the Polyneuropathy And Treatment with Hizentra (PATH) study to evaluate the effectiveness of IgPro20 compared with placebo in the treatment of CIDP.

3. What are the potential benefits of subcutaneous administration vs. intravenous?

Although SCIg is not yet labeled for use in CIDP, IVIg is a well-established treatment for CIDP. SCIg products are already widely used in the treatment of primary and secondary immune deficiencies, and the subcutaneous route has a number of proven advantages over intravenous administration.

The IVIg route of administration can produce high Ig levels that may trigger side effects such as headache. With SCIg -- which is administered at lower, more frequent doses -- the headaches are less frequent.

SCIg’s frequent dosing schedule also means that there are less fluctuations in the patients’ Ig levels. Typically, after IVIg treatment, Ig levels rise sharply then decline, tailing off and wearing off, as 3 to 4 weeks elapse. However, with weekly SCIg, a more consistent steady-state Ig levels are seen in patients. The wear-off effects, such as weakness, which some patients experience in between doses of IVIg may therefore be reduced in patients receiving SCIg.

In addition, the SCIg route provides the potential for patients to self-administer. After appropriate training, patients can receive their treatment wherever and whenever it suits, such as in the home, for example while reading or watching television. SCIg may also be administered by a parent or a caregiver. The result is that, compared with IVIg treatment, CIDP patients may have more independence and convenience with SCIg. E.g., Patients do not have to take time off from work or school to receive SCIg.

4. What is the PATH study and what does it involve?

The Polyneuropathy And Treatment with Hizentra (PATH) study is an international clinical trial designed to assess the use of SCIg in the treatment of CIDP. The safety and effectiveness of two different dosages of IgPro20 are evaluated by comparison with placebo.

To be eligible to take part in the study, participants must:

a) have been diagnosed with definite or probable CIDP as defined by the European Federation of Neurological Societies and Peripheral Nerve Society (EFNS/PNS) guidelines;

b) have had repeated treatment with IVIg (four or more infusions) in the previous nine months;

c) have had IVIg treatment in the previous eight weeks; and

d) be at least 18 years old.

The study lasts up to 52 weeks and is divided into four parts:

- Screening Period: During the screening period, medical assessments and a blood draw may be carried out to decide whether the patient is eligible to participate.

- Immunoglobulin Dependency Test Period: During the immunoglobulin dependency test period, the purpose is to test the patient’s dependence on immunoglobulin therapy—to be certain that immunoglobulin treatment is still needed—before the study drug is administered. The patient will be trained and asked to look for signs and symptoms of immunoglobulin dependency, for example, by monitoring ability to perform certain everyday activities.

- Re-Stabilization Period: If a patient experiences a relapse in symptoms during the 12-week dependency test period, they will be asked to visit the clinic to be re-stabilized on IVIg treatment. If symptoms do not worsen, then IVIg may not be needed or a reduced dose may be appropriate. For patients who require re-stabilization, treatment will continue for 10-13 weeks before entering the final SCIg treatment period of the study.

- SCIg Treatment Period: During the SCIg treatment period, study participants will receive weekly infusions of either placebo or the study drug for 25 weeks. The first two SCIg infusions will be performed at the clinic, where a member of the study team will teach patients how to administer the treatment. After that, patients may carry out the infusions themselves at home.

To assist in measuring the effectiveness of IgPro20 in CIDP, the study is carried out double-blinded, meaning that neither the patient nor the doctor will know which treatment is being given. Patients’ symptoms will be closely monitored throughout the study, and any worsening of symptoms will result in IVIg treatment being restarted.

5. How can I find out about taking part in the PATH study?

We are always looking for volunteers to participate in our studies. If you are looking to volunteer or want information about a study site near you, please contact the study team at clinicaltrials@cslbehring.com.

http://www.neuropathy.org/site/News2?page=NewsArticle&id=8699&news_iv_ctrl=1101

What To Do If You Dont Look Sick

Today's post from baronandbudd.com (see link below) is a heartfelt appeal for recognition that just because you don't look ill, doesn't mean to say that you're perfectly healthy. People living with neuropathy will easily identify with this article because it's a well-known invisible illness and the shame is that even doctors and health professionals, who are so used to looking for clues in faces and body language, can be influenced by the fact that the patient doesn't look to be at death's door! The natural reaction to chronic pain and illness is to present yourself in the best light possible. You don't want the rest of the world to see the extent of your suffering, so you put your best face forward. The problem is that people find it hard to believe you're suffering when you do tell them. Nobody wants to be seen as a 'moaning minnie' but at the same time, you want your condition to be taken seriously. You're damned if you do and you're damned if you don't.

Invisible Illness: Fluoroquinolone Toxicity, Peripheral Neuropathy, and Silent Suffering
By Rachel Brummert|January 28th, 2015|Fluoroquinolone Antibiotic 

As I was scrolling through my Facebook news feed, I came across a post from my friend Cheri:

"I was just told I need to take down my Facebook profile picture because I don’t look sick and people might not think I’m actually sick."

It is a sad fact that when you suffer from an invisible illness, people make judgments about your appearance and capabilities based on how you look. In their minds, if you don’t look sick, you’re not sick. That is a damaging assumption to make.

When you "don’t look sick", it’s hard to explain invisible illness and Fluoroquinolone Toxicity to someone. Even when you explain it, you’re still viewed with skepticism or a blank stare. The lack of understanding can lead to feeling isolated. Not only do you deal with an invisible illness, you start to feel invisible too because those around you can’t- or won’t- understand.

My friend Cheri Haddon, 26, from Conyers, Georgia took Cipro in 2011 for a urinary tract infection. She suffered immediate adverse reactions to it and has been disabled since then. When holidays come around, she cannot enjoy being with her family because she is so food and chemically sensitive. She can’t eat the food that her healthy relatives can eat. She becomes sick for months just smelling someone’s perfume or shampoo. She has endured insensitive comments from people around her because on the outside, Cheri "looks fine", while inside, her body is screaming in pain and rebelling against her environment.

Looking at Cheri’s photos, as well as mine, you’ll see us smiling, being social with friends and family. But those photos don’t tell the complete story. Hidden behind the smiles is body-wide pain, brain fog, nausea, dizziness, neuropathy, flaring tendons, fluctuating heart rate, and much more that you can’t see. For the one second it took to take the picture, we manage to paint a smile on our face, masking what is really going on behind those smiles. A photo cannot possibly open a window into what we are feeling like on the inside, and what you don’t see afterward is that it could take us days, weeks, or longer to recover from whatever was going on in that photo.
There is a photo of me on Facebook and in it my husband and I are having lunch with 3 other friends.

What you see:

I am smiling.
My hair is done.
I am wearing makeup.
I am wearing a nice sweater.
I’m just another diner in a restaurant out with her friends, cracking jokes, listening to what her friends have been up to.

What you don’t see:

I am wearing enough concealer under my eyes that would rival Tammy Faye Baker to cover the dark circles under my eyes because insomnia has kept me up for 3 consecutive nights.
The tremors in my hands made me drop my fork 6 times since I arrived.
All of my joints are screaming in pain and the morphine I took before I left the house isn’t touching the pain.
My left foot is numb and my right foot feels like I stepped on hot thumbtacks.
My cognitive function is poor and when I ordered my lunch, I switched words and the waitress didn’t understand what I was trying to say.
I am taking slow deep breaths in an attempt to calm my heart rate from arrhythmia.
I am in panic mode because I couldn’t remember if I took my seizure medicine that morning.
Our table is near the table of the elderly gentleman who made a snide comment to me as I walked up the ramp to the restaurant because I can’t do steps and he could.
I would be bed-ridden for close to a week after the photo was taken. 

There is a photo of Cheri on Facebook with her mom and her dog on her mother’s birthday.

What you see:

She is smiling.
She is wearing a pretty sweater.
She looks happy. 

What you don’t see:

She is in pain.
She is nauseous.
She took her sunglasses off in the house long enough to take the photo and her eyes hurt because she is sensitive to light.
She is having brain fog.
This was the first time she was able to wear "real clothes" in 3 weeks because daily activities can be difficult for her.
She was bed-ridden after the photo was taken.

Cheri’s post about someone telling her to take down her profile picture because people won’t believe that she is sick sums up what we face, even from people in our close circles. It shouldn’t take a photo of us looking like we are on our death bed to convince people that we are, in fact, suffering from a terrible illness.

They say that a picture speaks a thousand words. I think it depends on who is reading it.

To someone who isn’t chronically ill, Cheri’s picture tells the story of a healthy-looking young woman bonding with her mother. A healthy person might say "Cheri, you look great, I’m glad you’re all better".

When I look at it, I can see the hallmark squint in her eyes which speak of pain from light sensitivity. I see that she is swallowing her pain. I see that it took a lot for her to get dressed and smile and participate so her mother could have a nice birthday. I see that she feels alone because she can’t eat the same foods that her family can, and I see that she can’t be in an environment that non-sick people can be in because she is so sensitive to chemicals, new furniture smells, perfume, etc. I see in the one second it took to take that photo that she is silently suffering. I see it because my smile in my own photos tell the same story of being chronically ill with an invisible illness.

In the one second it took to take the photographs of us, we got to look just like normal people, with normal lives, who are not sick with an invisible illness.

That’s the difficult part of invisible illness. By outward appearances, you can’t tell how much someone is suffering. Asking someone to take down a photo because it makes it look like you’re not sick negates what we are going through. It implies that we should be posting pictures of ourselves crying, screaming, vomiting, gasping for breath, in the throes of a seizure, or limping so people believe that we have an illness and that we are struggling.

You can’t see air, yet we believe you are breathing. You can’t see pain, yet we believe you are hurting. So why is it so hard to believe that we are chronically ill with an invisible illness and we are just trying to survive the only way we know how?

The conversation about chronic and invisible illness needs to change.

About the Author: Rachel Brummert Rachell Brummert is the Executive Director of the Quinolone Vigilance Foundation- www.saferpills.org. In her position, she guides strategic planning for the foundation and acts as its spokesperson. As someone who has been personally impacted by quinolone toxicity, she oversees the implementation and evaluation of the organization’s programs, and promotes collaboration with researchers, donors, politicians, community groups, and others to further the organization’s mission.
The views expressed herein reflect the opinions of the author and do not necessarily reflect the views of Baron & Budd, P.C., its affiliates or its employees.

http://baronandbudd.com/protecting-whats-right/2015/01/invisible-illness-fluoroquinolone-toxicity-peripheral-neuropathy/

What Is Neuropathic Pain Exactly

Today's post from neuropathyjournal.org (see link below) is another well-written and easy to absorb article about neuropathic problems by LtCol Eugene B Richardson, who has probably as much experience as a neuropathy patient than anyone else on the Net at the moment. This article looks at the nature of the pain of neuropathy and explains why it happens, what it is and why the medical authorities often dismiss it through their ignorance and not yours. Many neuropathy patients find it difficult to find information that explains the unique pain that neuropathy can bring - this article helps!

What is Neuropathic Pain?
By LtCol Eugene B Richardson, USA (Retired) BA, MDiv, EdM, MS

The physical cause of neuropathic pain is damaged peripheral nerves and as one medical expert notes, may also be due to the attempt of damaged nerves to fire across damaged sections of the peripheral nerve. See: References #1 to #3

It is illegal to torture prisoners in our country. So why do neuropathy patients too often live with a torture known as ‘neuropathic pain’ caused by Peripheral Neuropathy while being ignored by too many doctors?

Just recently a neuropathy patient was visiting a neuropathy center in the central part of the United States only to have some of the neurologists in this center of experts diagnose the pain as a “somatization’ disorder! 

Somatization Disorders

Somatization disorder is a long-term (chronic) condition in which a person has physical symptoms that involve more than one part of the body, but no physical cause can be found.

This concept cost me my military career in the 1970’s and 80’s. It sets up the neuropathy patient while they seek help for the horror of neuropathic pain. It is important to understand that the pain and other symptoms of patients with this disorder are real and are not created or faked on purpose (malingering). It is time to stop calling patient’s crazy and ignoring this pain or the other symptoms of a neuropathy.

In 2015 we finally have a growing understanding of neuropathic pain yet with limited medication options and sometimes treatment fails the patient due to lack of adequate clinical training of doctors in the diagnosis and treatment of the neuropathies especially training in the use of what we now do know. 

Testing

Too many doctors use the tests for large fiber damage and if they find no recordable damage, dismiss the patient! These tests measure damage and do not diagnose neuropathy. Patients wish it was that simple once they learn the limits of medicine.

The patient can have symptoms and neuropathic pain for years before damage will show in these tests. Testing for small fiber neuropathy is often not done (skin biopsy) for this is the only test to show small fiber damage.. After I was diagnosed with an immune mediated neuropathy, doctor after doctor, asked, ‘Why did they not do the spinal tap?” 

Severity of pain

Dr. Norman Latov, MD, PhD of Cornell University notes that while for some patients neuropathic pain is a nuisance, but for millions of other patients, they are in fact living with constant torture at one level or another with untreated conditions that do many times lead to severe disabilities at a greater cost to society.

So as a patient, are you experiencing neuropathic pains and sometimes people and medical staff will look at you like you are crazy reporting such strange pains with no obvious visible cause! You are not crazy unless of course you ask your spouse and they may or may not agree!

Neuropathic pain can involve a wide variety of strange sensations, such as violent sudden electric shocks, stabbing, shooting, burning, tingling, pins and needles, severe muscle cramps, bone pain, sense of strange numbness, cement legs, heavy legs, strange feelings of socks on the feet or gloves on the hands, severe skin pain due to touch, no feeling on touch, digestive problems, urinary problems, problems with lack of sweating, and the list goes on, in addition to other known symptoms of neuropathy?

While only a trained doctor can determine the cause of your symptoms, you may have peripheral neuropathy and you are experiencing neuropathic pain from damaged nerves sending inappropriate but real signals to the brain.

Like many types of neurological pain, neuropathic pain does remit and relapse making it sometimes difficult to understand both for the doctor and the patient. I even had a doctor state to me on a visit, ‘well you are not hurting now,” as if this was supposed to mean something to me.

Unfortunately, doctors and patients note that these neuropathic symptoms are often worse at night. Experts theorize that this may be due to the brains relaxed state and the fact the brain is not ‘busy’ processing other data. This is why pain is sometimes perceived to be worse at night, as the brain is not as busy working on other information.

Did you know that research has shown that patients with ‘tightly wrapped” neurons in the brain will experience more intense pain than other patients! Ref: #4

While not completely understood, often how a patient experiences neuropathic pain and symptoms is related to their genetic makeup, physical and emotional resources or inappropriate exercise or physical activity in which damaged nerves are forced to work.

Exercise

Did you know that the wrong type of exercise (click to see article) will force damaged nerves to work and increase the pain!

How should a neuropathy patient exercise? Consider ordering a copy of the brand new DVD from Matt Hansen the expert as his perspective on exercise for neuropathy is perfect and understands what we can and cannot do. Yet Matt makes it possible for us to exercise WITHOUT the increase in neuropathic pain, keeping muscles as strong and flexible as possible. To see article on (click on link) Exercise for Neuropathy DVD: When ordering enter the special code NSN 10 and Matt will give 10% of your purchase price back to support the work of the NSN! 

Slow progress in Medicine

For many years, doctors who did not understand the strange manifestations of neuropathic pain would dismiss the patient, noting that the complaint is subjective and with no observable proof of the cause, it must be ‘all in the patients head’.

Disability lawyers love this statement and use this against the patient to deny help when they need it most.

Thank heavens; we are slowly moving away from such a primitive view of neuropathic pain and because of great doctors who report in books and medical journals, especially Dr. Latov in his book for patients and “The Journal of the Peripheral Nervous System” (Ref #3). Since the decades of the 60’s to the 90’’s, we have made great strides toward understanding and attempts to treat neuropathic pain, but we still have a long way to go.

Even with this progress, the most critical aspect beyond the treatment of neuropathic pain, is the absolute requirement for the patient and physician to establish a partnership in which they work together to find out what may work among the options for each individual patient.

Patient systems are different and each patient must be seen as unique when it comes to discovering what works and what does not work for each patient presenting with neuropathic pain.

Diagnosis

Conversely, it is not enough to treat these symptoms of a neuropathy. The physician must be willing to conduct the testing necessary in attempts to find and perhaps treat the cause and to identify the TYPE of the neuropathy.

If the cause is unknown, the worst possible diagnosis is to leave the patient with is a diagnosis of ‘Idiopathic’ Neuropathy. (click on link to read article)

The other important goal is to identify the TYPE of neuropathy as according to Dr. Latov this often points to s suggested cause!

Too many physicians even in 2015 have the attitude, you have neuropathy, there is nothing that can be done, go home and live with it. This attitude must cease, yesterday.

To see How Neuropathic Pain is treated.

References:

#1 Norman Latov, MD, PhD, FAAN Peripheral Neuropathy: When the Numbness, Weakness and Pain Won’t Stop, ANN Press, 2007

#2 Mims Cushing, You Can Cope With Peripheral Neuropathy (Ideas from neuropathy patients), with Dr. Norman Latov, DEMOS Publishing, 2009

#3 “Journal of the Peripheral Nervous System” published by the Peripheral Nerve Society.

http://neuropathyjournal.org/neuropathic-pain-2/

What IS the Nervous System

Today's short post from sciencedaily.com (see link below) gives a relatively simple description of what the nervous system actually is. When people are told that they have neuropathy and that it involves damage to the nerves and an interruption to the normal working of the nervous system, they often just accept it and leave the consultation with a prescription. It's only when they get home that they wonder what the nervous system actually is and what's happened to it to cause such unpleasant symptoms. This article explains it technically but in terms that most won't have difficulty understanding. More detailed information can be found by following the link.

Nervous system

The nervous system of an animal coordinates the activity of the muscles, monitors the organs, constructs and also stops input from the senses, and initiates actions.

The nervous system of vertebrate animals is often divided into the central nervous system (CNS) and the peripheral nervous system (PNS).

The CNS consists of the brain and spinal cord.

The PNS consists of all other nerves and neurons that do not lie within the CNS.

The large majority of what are commonly called nerves (which are actually axonal processes of nerve cells) are considered to be PNS.

The peripheral nervous system is divided into the somatic nervous system and the autonomic nervous system.

The somatic nervous system is responsible for coordinating the body's movements, and also for receiving external stimuli.

It is the system that regulates activities that are under conscious control. The autonomic nervous system is then split into the sympathetic division, parasympathetic division, and enteric division.

The sympathetic nervous system responds to impending danger or stress, and is responsible for the increase of one's heartbeat and blood pressure, among other physiological changes, along with the sense of excitement one feels due to the increase of adrenaline in the system.

The parasympathetic nervous system, on the other hand, is evident when a person is resting and feels relaxed, and is responsible for such things as the constriction of the pupil, the slowing of the heart, the dilation of the blood vessels, and the stimulation of the digestive and genitourinary systems.

The role of the enteric nervous system is to manage every aspect of digestion, from the esophagus to the stomach, small intestine and colon.

http://www.sciencedaily.com/articles/n/nervous_system.htm