Gluten Correlated with Neuropathic Pain

Gluten Correlated with Neuropathic Pain

Researchers observed people who were following a gluten-free diet were dramatically more likely to be free of pain

Gluten Neuropathy: Prevalence of Pain and the Role of Gluten-Free Diet. To be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018.

MSG Correlated with Chronic Pain

MSG Correlated with Chronic Pain

In a new pilot study in chronic pain sufferers, hydration in combination with replacing MSG as a spice resulted in an equal to or greater than a 30% reduction of pain in two weeks outperforming   acetaminophen.
Dietary correlates of chronic widespread pain in Meru, Kenya. Nutrition, 2018; DOI: 10.1016/j.nut.2018.01.016

Total Pain Remission with Cold Open Water Swim

Total Pain Remission with Cold Open Water Swim

A short, sharp, cold water swim may offer an alternative to strong painkillers and physiotherapy to relieve severe persistent pain after surgery, suggest doctors in the journal BMJ Case Reports.

Cold forced open-water swimming: a natural intervention to improve postoperative pain and mobilisation outcomes? BMJ Case Reports 2018; doi:10.1136/bcr-2017-222236

The brain may feel other people’s pain

2009 study posted for filing

 

By Amy Norton Amy Norton

 

NEW YORK (Reuters Health) – If you’ve ever thought that you literally feel other people’s pain, you may be right. A brain-imaging study suggests that some people have true physical reactions to others’ injuries.

 

Using an imaging technique called functional MRI, UK researchers found evidence that people who say they feel vicarious pain do, in fact, have heightened activity in pain-sensing brain regions upon witnessing another person being hurt.

 

The findings, published in the journal Pain, could have implications for understanding, and possibly treating, cases of unexplained “functional” pain.

 

“Patients with functional pain experience pain in the absence of an obvious disease or injury to explain their pain,” explained Dr. Stuart W. G. Derbyshire of the University of Birmingham, one of the researchers on the new study.

 

“Consequently,” he told Reuters Health in an email, “there is considerable effort to uncover other ways in which the pain might be generated.”

 

Derbyshire said he now wants to study whether the brains of patients with functional pain respond to images of injury in the same way that the current study participants’ did.

 

For the study, Derbyshire and colleague Jody Osborn first had 108 college students view several images of painful situations — including athletes suffering sports injuries and patients receiving an injection. Close to one-third of the students said that, for at least one image, they not only had an emotional reaction, but also fleetingly felt pain in the same site as the injury in the image.

 

Derbyshire and Osborn then took functional MRI scans of 10 of these “responders,” along with 10 “non-responders” who reported no pain while viewing the images.

 

Functional MRI charts changes in brain blood flow, allowing researchers to see which brain areas become more active in response to a particular stimulus. Here, the researchers scanned participants’ brains as they viewed either images of people in pain, images that were emotional but not painful, or neutral images.

 

The investigators found that while viewing the painful images, both responders and non-responders showed activity in the emotional centers of the brain. But responders showed greater activity in pain-related brain regions compared with non-responders, and as compared with their own brain responses to the emotional images.

 

“We think this confirms that at least some people have an actual physical reaction when observing others being injured or expressing pain,” Derbyshire said.

 

He noted that the responders also tended to say that they avoided horror movies and disturbing images on the news “so as to avoid being in pain” — which, the researcher said, is more than just an empathetic response.

 

As far as the potential practical implications of the findings, Derbyshire said it would be a “reach” to think that such brain mechanisms might be behind all functional pain. But, he added, “they might explain some of it.”

Rich people don’t need friends

2009 study posted for filing
Contact: Steve Pogonowski
steve.pogonowski@f1000.com
Faculty of 1000: Biology and Medicine

In a paper evaluated by f1000 Medicine, six studies tested relationships between reminders of money, social exclusion and physical pain.

In The symbolic power of money: reminders of money alter social distress and physical pain published in the journal Psychological Science, Xinyue Zhou, Kathleen Vohs and Roy Baumeister explored how money could reduce a person’s feeling of pain and also negate their need for social popularity.

Harriet de Wit, Faculty Member for f1000 Medicine, said: “This research extends our understanding of relationships between social pain and physical pain, and remarkably, shows how acquired symbolic value of money, perhaps because of associations with power or control, can influence responses to both emotional and physical pain.”

She also noted: “These findings have great importance for a social system such as ours that is characterized by wide disparities in financial wellbeing.”

Zhou, Vohs and Baumeister determined that interpersonal rejection and physical pain caused desire for money to increase. They said: “Money can possibly substitute for social acceptance in conferring the ability to obtain benefits from the social system. Moreover, past work has suggested that responses to physical pain and social distress share common underlying mechanisms.”

“Handling money (compared with handling paper) reduced distress over social exclusion and diminished the physical pain of immersion in hot water. Being reminded of having spent money, however, intensified both social distress and physical pain,” the authors said.

###

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Faculty of 1000
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Notes to Editors

1 Professor de Wit is Director of the Human Behavioral Pharmacology Laboratory at the University of Chicago. Her profile can be viewed at http://f1000medicine.com/member/8764194356909390

2 The full text of the evaluation of “The Symbolic Power of Money: Reminders of Money Alter Social Distress and Physical Pain” is available free for 90 days at http://www.f1000medicine.com/article/r2111rwty080l4q/id/1163818DOI: 10.1111/j.1467-9280.2009.02353.x

3 Please name Faculty of 1000 Medicine in any story you write. If you are writing for the web, please link to the website.

4 Faculty of 1000 Medicine, http://f1000medicine.com, is a unique online service that helps you stay informed of high impact articles and access the opinions of global leaders in medicine. Our distinguished international faculty select and evaluate key articles across medicine, providing a rapidly updated, authoritative guide to the medical literature that matters.

5 Please contact Steve Pogonowski, PR Manager, for a complimentary journalist subscription to Faculty of 1000 http://f1000.com.

Active ingredients in marijuana found to spread and prolong pain : Transforms transient normal pain into persistent chronic pain

2009 study posted for filing

Contact: Jim Kelly
jpkelly@utmb.edu
409-772-8791
University of Texas Medical Branch at Galveston

Research has implications for medical use of drug and concepts of chronic pain

GALVESTON, Texas — Imagine that you’re working on your back porch, hammering in a nail. Suddenly you slip and hit your thumb instead — hard. The pain is incredibly intense, but it only lasts a moment. After a few seconds (and a few unprintable words) you’re ready to start hammering again.

How can such severe pain vanish so quickly? And why is it that other kinds of equally terrible pain refuse to go away, and instead torment their victims for years?

University of Texas Medical Branch at Galveston researchers think they’ve found at least part of the answer—and believe it or not, it’s in a group of compounds that includes the active ingredients in marijuana, the cannabinoids. Interestingly enough, given recent interest in the medical use of marijuana for pain relief, experiments with rodents and humans described in a paper published in the current issue of Science suggest these “endocannabinoids,” which are made within the human body, can actually amplify and prolong pain rather than damping it down.

“In the spinal cord there’s a balance of systems that control what information, including information about pain, is transmitted to the brain,” said UTMB professor Volker Neugebauer, one of the authors of the Science article, along with UTMB senior research scientist Guangchen Ji and collaborators from Switzerland, Hungary, Japan, Germany, France and Venezuela. “Excitatory systems act like a car’s accelerator, and inhibitory ones act like the brakes. What we found is that in the spinal cord endocannabinoids can disable the brakes.”

To get to this conclusion, the researchers began by studying what happened when they applied a biochemical mimic of an endocannabinoid to inhibitory neurons (the brakes, in Neugebauer’s analogy) on slices of mouse spinal cord. Electrical signals that would ordinarily have elicited an inhibitory response were ignored. They then repeated the procedure using slices of spinal cord from mice genetically engineered to lack receptors where the endocannabinoid molecules could dock, and found that in that case, the “brakes” worked. Finally, using electron microscopy, they confirmed that the receptors were in fact on inhibitory, not excitatory neurons. Endocannabinoids docking with them would suppress the inhibitor neurons, and leave pain signals with a straight shot to the brain.

“The next step was to make the leap from spinal slices to test whether this really had anything to do with pain,” Neugebauer said. Using anesthetized rats, he recorded the spinal cord electrical activity produced by an injection in the hindpaw of capsaicin– a chemical found in hot peppers that produces a level of pain he compared to a severe toothache. Although the rats were unconscious, pain impulses could be detected racing up their spinal cords. What’s more, formerly benign stimuli now generated a significant pain response — a response that stopped when the rats were treated with an endocannabinoid receptor blocker.

“Why was this non-painful information now gaining access to the spinal “pain” neurons?” Neugebauer said. “The capsaicin produced an overstimulation that led to the peripheral nerves releasing endocannabinoids, which activated receptors that shut down the inhibitor neurons, leaving the gates wide open.”

Finally, the researchers recruited human volunteers to determine whether a compound that blocked endocannabinoid receptors would have an effect on the increased sensitivity to pain (hyperalgesia) and tendency for normally non-painful stimuli to induce pain (allodynia) often reported in areas of the body near where acute pain had been inflicted. In this case, the researchers induced pain by passing electricity through the volunteers’ left forearms, with the intensity of the current set by each volunteer to a 6 on a scale of 1 to 10. At a second session a month later, the volunteers who had received the receptor blocker showed no reduction in perceived acute pain, but had significantly less hyperalgesia and allodynia — a result that matched up well with the endocannabinoid hypothesis.

“To sum up, we’ve discovered a novel mechanism that can transform transient normal pain into persistent chronic pain,” Neugebauer said. “Persistent pain is notoriously difficult to treat, and this study offers insight into new mechanisms and possibly a new target in the spinal cord.”

It also raises questions about the efficacy of marijuana in relieving acute pain, given that endocannabinoids and the cannabinoids found in marijuana are so biochemically similar. “If you had a toothache, you probably wouldn’t want to treat it with marijuana, because you could actually make it worse,” Neugebauer said. “Now, for more pathological conditions like neuropathic pain, where the problem is a dysfunction within the nerves themselves and a subsequent disturbance throughout the nervous system that’s not confined to the pain system, marijuana may be beneficial. There are studies that seem to show that. But our model shows cannabinoids over-activating the pain system, and it just doesn’t seem like a good idea to further increase this effect.”

New study proves that pain is not a symptom of arthritis, pain causes arthritis

2008 study posted for filing

Contact: Greg Williams
Greg_Williams@urmc.rochester.edu
585-273-1757
University of Rochester Medical Center

New treatments will seek to interrupt ‘crosstalk’ between joints and the spinal cord

Pain is more than a symptom of osteoarthritis, it is an inherent and damaging part of the disease itself, according to a study published today in journal Arthritis and Rheumatism. More specifically, the study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends.

Technically, pain is a patient’s conscious realization of discomfort. Before that can happen, however, information must be carried along nerve cell pathways from say an injured knee to the pain processing centers in dorsal horns of the spinal cord, a process called nociception. The current study provides strong evidence that two-way, nociceptive “crosstalk” may first enable joint arthritis to transmit inflammation into the spinal cord and brain, and then to spread through the central nervous system (CNS) from one joint to another.

Furthermore, if joint arthritis can cause neuro-inflammation, it could have a role in conditions like Alzheimer’s disease, dementia and multiple sclerosis. Armed with the results, researchers have identified likely drug targets that could interfere with key inflammatory receptors on sensory nerve cells as a new way to treat osteoarthritis (OA), which destroys joint cartilage in 21 million Americans. The most common form of arthritis, OA eventually brings deformity and severe pain as patients loose the protective cushion between bones in weight-bearing joints like knees and hips.

“Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging,” said Stephanos Kyrkanides, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Center. “Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect,” said Kyrkanides, whose work on genetics in dentistry led to broader applications. The common ground between arthritis and dentistry: the jaw joint is a common site of arthritic pain.

Study Details

Past studies have shown that specific nerve pathways along which pain signals travel repeatedly become more sensitive to pain signals with each use. This may be a part of ancient survival skill (if that hurt once, don’t do it again). Secondly, pain has long been associated with inflammation (swelling and fever).

In fact, past research has shown that the same chemicals that cause inflammation also cause the sensation of pain and hyper-sensitivity to pain if injected. Kyrkanides’ work centers around one such pro-inflammatory, signaling chemical called Interleukin 1-beta (IL-1β), which helps to ramp up the bodies attack on an infection.

Specifically, Kyrkanides’ team genetically engineered a mouse where they could turn up on command the production of IL-1β in the jaw joint, a common site of arthritis. Experiments showed for the first time that turning up IL-1β in a peripheral joint caused higher levels of IL-1β to be produced in the dorsal horns of the spinal cord as well.

Using a second, even more elaborately engineered mouse model, the team also demonstrated for the first time that creating higher levels of IL-1β in cells called astrocytes in the spinal cord caused more osteoarthritic symptoms in joints. Past studies had shown astrocytes, non-nerve cells (glia) in the central nervous system that provide support for the spinal cord and brain, also serve as the immune cells of CNS organs. Among other things, they release cytokines like IL-1β to fight disease when triggered. The same cytokines released from CNS glia may also be released from neurons in joints, possibly explaining how crosstalk carries pain, inflammation and hyper-sensitivity back and forth.

In both mouse models, experimental techniques that shut down IL-1β signaling reversed the crosstalk effects. Specifically, researchers used a molecule, IL-1RA, known to inhibit the ability of IL-1β to link up with its receptors on nerve cells. Existing drugs (e.g. Kineret® (anakinra), made by Amgen and indicated for rheumatoid arthritis) act like IL-1RA to block the ability IL-1β to send a pain signal through its specific nerve cell receptor, and Kyrkanides’ group is exploring a new use for them as osteoarthritis treatment.

The implications of this process go further, however, because the cells surrounding sensory nerve cell pathways too can be affected by crosstalk. If 10 astrocytes secrete IL-1β in response to a pain impulse, Kyrkanides said, perhaps 1,000 adjacent cells will be affected, greatly expanding the field of inflammation. Spinal cord astrocytes are surrounded by sensory nerve cells that connect to other areas of the periphery, further expanding the effect. According to Kyrkanides’ model, increased inflammation by in the central nervous system can then send signals back down the nerve pathways to the joints, causing the release of inflammatory factors there.

Among the proposed, inflammatory factors is calcitonin gene related peptide (CGRP). The team observed higher levels calcitonin-gene related peptide (CGRP) production in primary sensory fibers in the same regions where IL-1β levels rose, and the release of IL-1β by sensory neurons may cause the release of CGRP in joints. Past studies in Kyrkanides reveal that CGRP can also cause cartilage-producing cells (chondrocytes) to mature too quickly and die, a hallmark of osteoarthritis.

Joining Kyrkanides in the publication from the University of Rochester School of Medicine and Dentistry were co-authors M. Kerry O’Banion, M.D., Ph.D., Ross Tallents, D.D.S., J. Edward Puzas, Ph.D. and Sabine M. Brouxhon, M.D. Paolo Fiorentino was a student contributor and Jennie Miller was involved as Kyrkanides’ technical associate. Maria Piancino, led a collaborative effort at the University of Torino, Italy. This work was supported in part by grants from the National Institutes of Health.

“Our study results confirm that joints can export inflammation in the form of higher IL-1β along sensory nerve pathways to the spinal cord, and that higher IL-1β inflammation in the spinal cord is sufficient in itself to create osteoarthritis in peripheral joints,” Kyrkanides said. “We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor.”