Sunday, September 25, 2011

Hyperbole and a Half: Boyfriend Doesn't Have Ebola. Probably.

I took Boyfriend to the Emergency Room last night because he was vomiting up vast quantities of what I thought was blood but actually it was just Craisins. You guys, if you feel like you may become violently ill in the near future, stay away from red food. Failure to do so may create an atmosphere of unnecessary panic and chaos.

Anyway, the doctor wanted to make sure that Boyfriend didn't have SARS or stomach AIDS or something, so he had to poke him a lot. While he was doing this to Boyfriend, he pointed to a little reference chart on the wall and asked Boyfriend to rate his pain::

You've probably seen some version of that chart before.  You may also have noticed how inadequate it is at helping you.  Based on the faces, this is my interpretation of the chart.

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Saturday, September 17, 2011

From Pain to Suffering - Marvin Minsky, MIT

This is a draft (July 27, 2005) of Chapter III of The Emotion Machine by Marvin Minsky (MIT).

What happens when you stub your toe? You've scarcely felt the impact yet, but you catch your breath and start to sweat—because you know what's coming next: a dreadful ache will tear at your gut and all other goals will be brushed away, replaced by your wish to escape from that pain.


Why does the sensation called pain sometimes lead to what we call suffering? How could such a simple event distort all your other thoughts so much? This chapter proposes a theory of this: if a pain is intense and persistent enough, it will stir up a certain set of resources, and then these, in turn, arouse some more. Then, if this process continues to grow, your mind becomes a victim of the kind of spreading, large-scale "cascade" that overcomes the rest of the mind.

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Audio lecture from The Society of Mind course at MIT

Friday, September 16, 2011

Tell Me Where It Hurts by Heather Kovich - Guernica

A former examiner of Social Security disability applicants had forty minutes to determine a claimant's fate.

Doug Stanton enjoyed cooking as much as he enjoyed anything. Late in his life, he made dinner most nights with his ex-wife Laurel, who lived in an identical apartment one floor below his at their motel-style complex in a working-class suburb of Seattle. He told me his favorite dish was Tuna Helper. "We put in two cans of albacore tuna—the good stuff—and then we put in a half a cup of frozen peas and some onions, all the while trying to keep the noodles al dente." At the time, Doug didn't have any teeth. He liked to add "three-quarters of a cup of sour cream to make it, you know, good and fatty, but it makes it really tasty." He said this with a self-deprecating smile. He weighed 345 pounds. "We don't usually have leftovers with that."

I was Doug's doctor when I was a resident in family medicine at the University of Washington and I looked forward to chatting for a few minutes at each visit. He had wide ranging interests: the Large Hadron Collider, the Seahawks, and whatever hot topic there was in national politics. Doug's medical problems were complex, and frustrating to both of us, but we always enjoyed the conversation. (This story alters several names and identifying details.)

I called Doug again about a year after I'd graduated from residency. He was no longer my patient but he agreed to meet me for a series of interviews about his life before disability and his experience with the disability system. I'd taken a job doing physical examinations for Social Security disability applicants. The job had a flexible schedule, which, at the time, was worth its low prestige. There is a stereotype of people who apply for disability: they don't take care of themselves and don't want to work, exaggerating their maladies for a meager check. There is also a stereotype of the doctors who do this work: lazy and disinterested. I found the job fascinating. The more I learned about the disability system, the more I pondered its complexities: it provides a safety net but keeps people mired in poverty. Helpful services, including job retraining, are available, but aren't advertised. And the system rests on a deeply flawed premise—that there is a way to objectively determine who is able to work and who is not. The claimants I met through the job were certain that obtaining disability benefits was going to improve their lives, and they were desperate to tell me their stories. Doug had been subsisting on Social Security Disability Income (SSDI) since 2002, before I met him, and I wanted to hear his. 

Payments to the disabled and their families make up about 20 percent of new Social Security awards every year, with retirement benefits constituting most of the rest. Even though Social Security remains in surplus, with the amounts taken in from taxpayers exceeding the amount owed to them, American politicians fret about the impending bankruptcy of Social Security and blame the aging baby boomer generation. Annual awards to disabled workers, however, are increasing. According to the Wall Street Journal, in 2010 one of the two Social Security programs paid out $124 billion in benefits to 10.2 million people.
In the 1980s, before Doug's life unraveled, he was making a good salary at an engineering firm in Seattle. His work was complex: he helped build a crane for NASA that assembled orbiters at Kennedy Space Center and an underwater crane for nuclear submarines. He and Laurel married in 1983 and she brought three children into the marriage. Doug quickly came to consider them his own. They owned a house in the working-class suburbs south of Seattle. But in the winter of 1996, when the tingling started, Doug's life started to fall apart.

He felt it first in his right arm: little electrical pinpricks in the tips of his fingers that shot up to his elbow, causing an aching heaviness at his shoulder. After months of physical therapy the pain had only worsened and spread. An MRI showed the cause of the problem: his spine was collapsing around his spinal cord, crushing many of the nerves, and strangling the cord itself: cervical spinal stenosis. It was bad luck—there was no injury that caused it, no family history that would have predicted it. A neurosurgeon operated to stabilize the vertebrae and take pressure off the spinal cord, but the cord had suffered permanent damage and the pain never lessened. He started drinking to dull it, the drinking affected his work. Eventually he lost his job.

He spent his severance on a drafting table so that he could continue to do part-time work from home. Then, too disabled to support himself completely, he applied for Social Security Disability Insurance.
Before 1956, when Social Security expanded to include disability benefits, disabled workers had to rely on their families or on state welfare for financial subsistence. The 1956 federal bill was controversial—it was expensive, and many politicians thought that paying the disabled not to work would lead to laziness. But Henry Jackson, a senator from Washington, passionately argued for the benefit: "It should be clear to all of us that no matter at what age a person becomes totally and permanently disabled, he needs Social Security payments worse than a person who retires at sixty-five in good health. The worker who is disabled early in life usually has accumulated less savings than has an older person. He has more dependents to care for than has an older worker whose family has grown up and left home… Retirement after one's working years can be planned for. Disability strikes without warning." President Eisenhower signed the bill, giving rise to SSDI, which allowed workers to collect their Social Security prior to age sixty-five if they became disabled. In 1974 the program added Supplemental Security Income, or SSI, which provided minimal payments to the disabled, including children, who had not contributed enough to Social Security to qualify for SSDI.

Doctors were leery of the bill. They worried that they would be put in the uncomfortable position of deciding whether their patients, people they may have known for years, were eligible for this income. To deal with this concern, applicants are now often sent to doctors who work for private staffing firms that contract with the government. This was my job, "independent medical examiner." On the basis of a forty-minute interview and examination, I was supposed to determine how disabled an applicant or "claimant" was. 

My first day was a Saturday, in Spokane, Washington. The receptionist showed me around the office, and pointed out where I could discreetly watch the claimants walk back out to their cars. This was so I could see if a limp disappeared, or a wheelchair went unused, once the claimant had left the office. "I'm sorry to say it but you'll meet the scum of the earth doing this job," she explained.
I did hundreds of disability exams over the next year, and while I did meet two people who were obviously faking, for the most part the stories I heard were heartbreaking: car accidents, massive strokes, lost jobs, dead spouses. Many people who apply for disability have lived through a tragedy. But the stories also told of the inefficiencies of the disability system. That first day in Spokane I met a man who had worked in manual labor his whole life, but for years had been getting crushing chest pain after walking a few blocks. His blood pressure was dangerously high. His condition was obviously treatable, but he did not have insurance so he had not been to a doctor in years. He knew that if he qualified for permanent disability he would eventually get Medicare or Medicaid and get proper treatment. He had no idea he could go to a community health center, a federally financed clinic where he could pay on a sliding-scale basis. With the right treatment and a less strenuous job, he would probably have not needed disability.

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Wednesday, September 14, 2011

NIH Common Fund Strategic Planning | Chronic Pain Conditions: A Transformative Classification for Stimulating Research, Improving Diagnosis, and Personalizing Treatment

Major obstacle/challenge to overcomeChronic pain conditions afflict as many as one-third of the US population and incur $560-635 billion per year in incremental healthcare costs and lost productivity (IOM Report June 29, 2011). The long term clinical goal in alleviating chronic pain is to develop targeted therapies and identify patients responsive to these therapies, both of which are supported by etiological- and mechanism-based case definitions and diagnostic criteria of disease. A major challenge in the field is the lack of a mechanism-based case definition and diagnostic criteria for multiple chronic pain conditions. Common Fund investments could facilitate the development of a new objective, biopsychosocial classification system for chronic pain disorders to overcome this major obstacle. This new system will accelerate research by standardizing research diagnoses used across laboratories, enhance clinical diagnoses by developing more objective, mechanism-based measures of disease, and identify subjects responsive to new therapies by developing novel biomarkers of disease and clinical outcomes.


Emerging scientific opportunity ripe for Common Fund investment:    We propose a research program to develop a new, comprehensive, mechanism-based, biopsychosocial classification of chronic pain conditions. Three opportunities are ready for Common fund investment. This proposal endorses the ideas and sharpens the focus of "Molecular Classification of Disease", a topic that emerged from the Innovation Brainstorm meeting, and takes on sophisticated data management and analysis elements of the topics on "Beyond GWAS" and "Cross-Cutting Issues in Computation and Informatics".

Common Fund investment that could accelerate scientific progress in this field:   This program would create a centralized data bank/repository containing information from a large chronic pain cohort to include study subjects with Temporomandibular Joint Disorders, Fibromyalgia, Chronic Fatigue Syndrome, Vulvodynia, Endometriosis, Irritable Bowel Syndrome, Interstitial Cystitis, Headache, Low Back Pain, Arthritis, etc., recruited and identified using today's best diagnostic criteria.  Many of these subjects will have multiple, comorbid chronic pain conditions. This cohort would be genotyped as well as phenotyped extensively using molecular, imaging and psychosocial methodologies.  All data would be agnostically analyzed via pathway analyses and new algorithms for lumping and splitting in order to subtype and re-classify these chronic pain patients.  Results emerging from the Common Fund incubator space would lead to a breakdown in the current "walls" separating these disorders (and researchers) and a transformation of diagnostic criteria based on a completely new classification of chronic pain conditions. After an intense 5 year effort, the data bank/repository and analytical tool set would become self sustaining with support from Pharma, the genotyping industry, and the NIH Pain Consortium.


Potential impact of Common Fund investment: The outcome of this project will be a completely new way of discovery and management of chronic pain conditions: researchers currently housed in different laboratories collaborating in multidisciplinary teams to study pain, rapid discovery of therapeutic targets, development of novel analgesic therapies based on common mechanisms of disease, introduction of individualized medical treatments and identification of those likely to respond to therapy. Ultimately, results from this project will lead to an overall reduction in the burden of chronic pain, currently $560-$635 billion/year in the US in incremental healthcare costs and lost productivity.

Chronic pain should be thought of as a disease unto itself like other chronic conditions such as diabetes and heart disease, and not merely a symptom of disease.  Research approaches to and management of chronic pain conditions must consider that, like other chronic conditions, disease progression and complexity, early identification and intervention, and effective therapies, all influence patient burden and economic costs of disease. A transformative classification of chronic pain conditions will ultimately reduce long-term morbidity and decrease the economic impact of these wide-spread conditions.

NIH Common Fund Strategic Planning | Biomarkers for chronic pain using functional brain connectivity

Major obstacle/challenge to overcome:  Chronic pain is a debilitating condition affecting at least 116 million American adults, resulting in significantly reduced quality of life and an estimated annual cost of $560 – 635 billion 1. Unfortunately, its assessment is based solely on subjective self-report, using limited scales or measures, which are unsuitable for elucidating the different types and causes of pain (i.e., pain endophenotypes) and for rigorously evaluating the impact of targeted interventions. Self-report measures also hamper progress in the monitoring required to precisely dose a medication and then evaluate its comparative effectiveness among different individuals.  Also, importantly, the field of pain management has been long challenged by the twin fears of undertreating pain in those who are suffering vs. triggering or facilitating a drug problem.  Because of all these obstacles, there is a pressing need for a standardized, brief and simple measurement that can translate, or at least reproducibly correlate, subjective pain experience into objective and quantitative readings for both clinical and research purposes. 


Emerging scientific opportunity ripe for Common Fund investment:  In functional neuroimaging, there has been a recent explosion of findings on functional connectivity (FC) between brain regions, especially in the resting-state (RSFC), which is defined as the signal coherence between discrete brain regions in the absence of a cognitive task. RSFC has uncovered discrete functional networks, where the strength or activity coherence can be quantified. Based on recent reports of differences in intrinsic brain network connectivity between patients with chronic pain and controls, it has been suggested that RSFC could be a suitable platform to develop objective biomarkers of pain.  Moreover, recent expansion of neuroimage data-sharing, especially of RSFC data in the 1000 Functional Connectomes Project, has demonstrated that data from different sources can be pooled to define subtypes of populations stratified by age, gender, medical conditions, and other variables, to enhance statistical power for discovery. If this level of between-labs consistency turns out to also apply to pain related measurements, RSFC could revolutionize the field of pain research and management.


Common Fund investment that could accelerate scientific progress in this field: Chronic pain is a clinical condition characteristic of a wide range of physical syndromes that collectively span the programmatic purview of many different ICs.  A request for applications (RFA) on this topic to fund five or six research project grants would enable multi-disciplinary teams (comprised of pain clinicians, functional neuroimagers, and computational/network neuroscientists) to 1) develop techniques for image time-series analysis to identify brain RSFC signatures of different types of chronic pain, and 2) test the value of said signatures in a clinical context.  For example, R21/R33 phased-innovation awards would enable initial collaborations to assess basic cross-sectional differences between controls and patients with different syndromes of chronic pain, and to develop and optimize new analytical tools for better identification of sensitive and specific RSFC biomarkers of pain.  The common fund program concept would also enable comparative effectiveness research, data harmonization across funded projects, foster a consortium on pain RSFC biomarkers, and inform prospective evidence-based, personalized care of pain.


Potential impact of Common Fund investment: Advances in image acquisition and data analytic approaches could yield a level of objectivity, sensitivity, and specificity that would be unprecedented for chronic pain.  In theory, a single resting-state functional MRI scan could serve as a diagnostic procedure akin to a head MRI for brain cancer or other neurological diagnoses.  Data derived from that scan may not only provide an objective and reliable marker, but also help identify optimum therapeutic approaches, lowering the costs and loss of productivity associated with ineffective pain treatments.  Validation of pain biomarkers is critical in the development of pain medications and for the adequate use of prescription analgesics matched to the needs of individuals.  When the proposed program achieves its objectives, the collaborative effort among funded projects will complete the characterization and validation phase of functional brain connectivity as biomarkers for chronic pain, helping to bring evidence-based, personalized management of pain closer to reality.

Does that hurt? Objective way to measure pain being developed at Stanford - Stanford University School of Medicine

Researchers from the Stanford University School of Medicine have taken a first step toward developing a diagnostic tool that could eliminate a major hurdle in pain medicine — the dependency on self-reporting to measure the presence or absence of pain. The new tool would use patterns of brain activity to give an objective physiologic assessment of whether someone is in pain.

The scientists used functional magnetic resonance imaging scans of the brain combined with advanced computer algorithms to accurately predict thermal pain 81 percent of the time in healthy subjects, according to a study that will be published Sept. 13 in the online journal PLoS ONE.

"People have been looking for a pain detector for a very long time," said Sean Mackey, MD, PhD, chief of the Division of Pain Management and associate professor of anesthesiology. "We're hopeful we can eventually use this technology for better detection and better treatment of chronic pain."

Researchers stressed that future studies are needed to determine whether these methods will work to measure various kinds of pain, such as chronic pain, and whether they can distinguish accurately between pain and other emotionally arousing states, such as anxiety or depression.

"A key thing to remember is that this approach objectively measured thermal pain in a controlled lab setting," Mackey said. "We should take care not to extrapolate these findings to say we can measure and detect pain in all circumstances."

The need for a better way to objectively measure pain instead of relying on the current method of self-reporting has long been acknowledged. But the highly subjective nature of pain has made this an elusive goal.

Advances in neuroimaging techniques have re-invigorated the debate over whether it might be possible to measure pain physiologically, and, in fact, led to this current study.

"We rely on patient self-reporting for pain, and that remains the gold standard," said Mackey, senior author of the study. "That's what I, as a physician, rely on when I take care of a patient with chronic pain. But there are a large number of patients, particularly among the very young and the very old, who can't communicate their pain levels. Wouldn't it be great if we had a technique that could measure pain physiologically?"

A study released by the Institute of Medicine in June reported that more than 100 million Americans suffer chronic pain, costing around $600 billion each year in medical expenses and lost productivity. (Mackey was a member of the committee that produced the report.) What's more, it found that cultural bias against chronic pain sufferers as being weak or even worse — they are often perceived as lying about their pain — complicates the delivery of appropriate treatment. Similar biases crop up in the legal field, with hundreds of thousands of cases each year that hinge on the existence of pain, said Stanford law professor Hank Greely, an expert on the legal, ethical and social issues surrounding the biosciences.

"A robust, accurate way to determine whether someone is in pain or not would be a godsend for the legal system," said Greely, who did not participate in the study.

The idea for this study germinated at a 2009 Stanford Law School event organized by Greely that brought together neuroscientists and legal scholars to discuss how the neuroimaging of pain could be used and abused in the legal system. Mackey and two of his lab assistants attended.

"At the end of the symposium, there was discussion about the challenges of creating a 'painometer.' I discussed hypothetically how we could do this in the future," Mackey said. "These two young scientists in my lab came up to me after and said, 'We think we can do this. We would like to try.' I was skeptical."

The two scientists — Neil Chatterjee, currently a MD/PhD student at Northwestern University, and first author of the study Justin Brown, PhD, now an assistant professor of biology at Simpson College — came up with the concept in a discussion after the symposium.

"It was very much on a whim," said co-author Chatterjee. "We thought, maybe we can't make the perfect tool, but has anyone ever really tried doing this on a very, very basic level? It turned out to be surprisingly simple to do this."

Researchers took eight subjects, and put them in the brain-scanning machine. A heat probe was then applied to their forearms, causing moderate pain. The brain patterns both with and without pain were then recorded and interpreted by advanced computer algorithms to create a model of what pain looks like. The process was repeated with a second group of eight subjects.

The idea was to train a linear support vector machine — a computer algorithm invented in 1995 — on one set of individuals, and then use that computer model to accurately classify pain in a completely new set of individuals.

The computer was then asked to consider the brain scans of eight new subjects and determine whether they had thermal pain.

"We asked the computer to come up with what it thinks pain looks like," Chatterjee said. "Then we could measure how well the computer did." And it did amazingly well. The computer was successful 81 percent of the time.

"I was definitely surprised," Chatterjee said.

Tuesday, September 13, 2011

Laughter Produces Endorphins, Study Finds -

Laughter is regularly promoted as a source of health and well being, but it has been hard to pin down exactly why laughing until it hurts feels so good.

The answer, reports Robin Dunbar, an evolutionary psychologist at Oxford, is not the intellectual pleasure of cerebral humor, but the physical act of laughing. The simple muscular exertions involved in producing the familiar ha, ha, ha, he said, trigger an increase in endorphins, the brain chemicals known for their feel-good effect.

His results build on a long history of scientific attempts to understand a deceptively simple and universal behavior. "Laughter is very weird stuff, actually," Dr. Dunbar said. "That's why we got interested in it." And the findings fit well with a growing sense that laughter contributes to group bonding and may have been important in the evolution of highly social humans.

Social laughter, Dr. Dunbar suggests, relaxed and contagious, is "grooming at a distance," an activity that fosters closeness in a group the way one-on-one grooming, patting and delousing promote and maintain bonds between individual primates of all sorts.

In five sets of studies in the laboratory and one field study at comedy performances, Dr. Dunbar and colleagues tested resistance to pain both before and after bouts of social laughter. The pain came from a freezing wine sleeve slipped over a forearm, an ever tightening blood pressure cuff or an excruciating ski exercise.

The findings, published in the Proceedings of the Royal Society B: Biological Sciences, eliminated the possibility that the pain resistance measured was the result of a general sense of well being rather than actual laughter. And, Dr. Dunbar said, they also provided a partial answer to the ageless conundrum of whether we laugh because we feel giddy or feel giddy because we laugh.

"The causal sequence is laughter triggers endorphin activation," he said. What triggers laughter is a question that leads into a different labyrinth.

Robert R. Provine, a neuroscientist at the University of Maryland, Baltimore County, and the author of "Laughter: A Scientific Investigation," said he thought the study was "a significant contribution" to a field of study that dates back 2,000 years or so.

It has not always focused on the benefits of laughter. Both Plato and Aristotle, Dr. Provine said, were concerned with the power of laughter to undermine authority. And he noted that the ancients were very aware that laughter could accompany raping and pillaging as well as a comic tale told by the hearth.

Dr. Dunbar, however, was concerned with relaxed, contagious social laughter, not the tyrant's cackle or the "polite titter" of awkward conversation. He said a classic example would be the dinner at which everyone else speaks a different language and someone makes an apparently hilarious but incomprehensible comment. "Everybody falls about laughing, and you look a little puzzled for about three seconds, but really you just can't help falling about laughing yourself."

To test the relationship of laughter of this sort to pain resistance, Dr. Dunbar did a series of six experiments. In five, participants watched excerpts of comedy videos, neutral videos or videos meant to promote good feeling but not laughter.

Among the comedy videos were excerpts from "The Simpsons," "Friends" and "South Park," as well as from performances by standup comedians like Eddie Izzard. The neutral videos included "Barking Mad," a documentary on pet training, and a golfing program. The positive but unfunny videos included excerpts from shows about nature, like the "Jungles" episode of "Planet Earth."

In the lab experiments, the participants were tested before and after seeing different combinations of videos. They suffered the frozen wine sleeve or the blood pressure cuff in different experiments and were asked to say when the pain reached a point they could not stand. They wore recorders during the videos so that the time they spent laughing could be established. In the one real-world experiment, similar tests were conducted at performances of an improvisational comedy group, the Oxford Imps.

The results, when analyzed, showed that laughing increased pain resistance, whereas simple good feeling in a group setting did not. Pain resistance is used as an indicator of endorphin levels because their presence in the brain is difficult to test; the molecules would not appear in blood samples because they are among the brain chemicals that are prevented from entering circulating blood by the so-called blood brain barrier.

Dr. Dunbar thinks laughter may have been favored by evolution because it helped bring human groups together, the way other activities like dancing and singing do. Those activities also produce endorphins, he said, and physical activity is important in them as well. "Laughter is an early mechanism to bond social groups," he said. "Primates use it."

Indeed, apes are known to laugh, although in a different way than humans. They pant. "Panting is the sound of rough-and-tumble play," Dr. Provine said. It becomes a "ritualization" of the sound of play. And in the course of the evolution of human beings, he suggests, "Pant, pant becomes ha, ha."

Gene that controls chronic pain identified - Research - University of Cambridge

A gene responsible for regulating chronic pain, called HCN2, has been identified by scientists at the University of Cambridge.

The Biotechnology and Biological Sciences Research Council (BBSRC) and EU funded research, published last week (09 September) in the journal Science, opens up the possibility of targeting drugs to block the protein produced by the gene in order to combat chronic pain.

Approximately one person in seven in the UK suffers from chronic, or long-lasting, pain of some kind, the commonest being arthritis, back pain and headaches. Chronic pain comes in two main varieties. The first, inflammatory pain, occurs when a persistent injury (e.g. a burn or arthritis) results in an enhanced sensitivity of pain-sensitive nerve endings, thus increasing the sensation of pain.

More intractable is a second variety of chronic pain, neuropathic pain, in which nerve damage causes on-going pain and a hypersensitivity to stimuli. Neuropathic pain, which is often lifelong, is a surprisingly common condition and is poorly treated by current drugs. Neuropathic pain is seen in patients with diabetes (affecting 3.7m patients in Europe, USA and Japan) and as a painful after-effect of shingles, as well as often being a consequence of cancer chemotherapy. Neuropathic pain is also a common component of lower back pain and other chronic painful conditions.

Professor Peter McNaughton, lead author of the study and Head of the Department of Pharmacology at the University of Cambridge, said: "Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications. Our research lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2."

The HCN2 gene, which is expressed in pain-sensitive nerve endings, has been known for several years, but its role in regulating pain was not understood. Because a related gene, HCN4, plays a critical role in controlling the frequency of electrical activity in the heart, the scientists suspected that HCN2 might in a similar way regulate the frequency of electrical activity in pain-sensitive nerves.

For the study, the researchers engineered the removal of the HCN2 gene from pain-sensitive nerves. They then carried out studies using electrical stimuli on these nerves in cell cultures to determine how their properties were altered by the removal of HCN2.

Following promising results from the in vitro studies in cell cultures, the researchers studied genetically modified mice in which the HCN2 gene had been deleted. By measuring the speed the mice withdrew from different types of painful stimuli, the scientists were able to determine that deleting the HCN2 gene abolished neuropathic pain. Interestingly, they found that deleting HCN2 does not affect normal acute pain (the type of pain produced by a sudden injury– such as biting one's tongue).

Professor McNaughton added: "Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation. What is exciting about the work on the HCN2 gene is that removing it – or blocking it pharmacologically- eliminates neuropathic pain without affecting normal acute pain. This finding could be very valuable clinically because normal pain sensation is essential for avoiding accidental damage."

The Schmidt Sting Pain Index

The Schmidt Sting Pain Index (a.k.a. the Justin O. Schmidt Pain Index) is a pain scale rating the relative pain caused by different Hymenopteran stings. It is mainly the work of Justin O. Schmidt, an entomologist at the Carl Hayden Bee Research Center in Arizona. Schmidt has published a number of papers on the subject and claims to have been stung by the majority of stinging Hymenoptera.

Wednesday, September 07, 2011

Maldynia: pathophysiology and management of neuropa... [Pain Med. 2010] - PubMed - NCBI

Maldynia: pathophysiology and management of neuropathic and maladaptive pain--a report of the AMA Council on Science and Public Health.



Because of disparate taxonomic arrays for classification, the American Academy of Pain Medicine has proposed categorizing pain on a neurobiologic basis as eudynia (nociceptive pain), Greek for "good pain," or maldynia (maladaptive pain), Greek for "bad pain." The latter has been viewed as maladaptive because it may occur in the absence of ongoing noxious stimuli and does not promote healing and repair.


To address recent findings on the pathogenesis of pain following neural injury and consider whether the development of maladaptive pain justifies its classification as a disease and to briefly discuss the scope of pharmacologic and non-pharmacologic approaches employed in patients with such pain.


English language reports on studies using human subjects were selected from a PubMed search of the literature from 1995 to August 2010 and from the Cochrane Library. Further information was obtained from Internet sites of medical specialty and other societies devoted to pain management.


Neural damage to either the peripheral or central nervous system provokes multiple processes including peripheral and central sensitization, ectopic activity, neuronal cell death, disinhibition, altered gene expression, and abnormal sprouting and cellular connectivity. A series of neuro-immune interactions underlie many of these mechanisms. Imaging studies have shown that such damage is characterized by functional, structural, and chemical changes in the brain. Such pain is maladaptive in the sense that it occurs in the absence of ongoing noxious stimuli and does not promote healing and repair.


As defined, maldynia is a multidimensional process that may warrant consideration as a chronic disease not only affecting sensory and emotional processing but also producing an altered brain state based on both functional imaging and macroscopic measurements. However, the absolute clinical value of this definition is not established.