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Showing entries tagged pain disorders.  Show all entries

December 4, 2011

Phantom Limb Pain and Cortex Reorganization

Feeling pain in the arm that you lost in an accident? Does your arm you lost in the war itch terribly? This sensation of feeling like a lost limb is still attached to the body is known as a phantom limb pain (PLP). The purpose of this study was to identify plastic changes in the somatosensory and motor cortex in patients with and without phantom limb pain. Most sensations regarding these phantom limbs are painful as if the limb was contorted into an awkward position. Although in many cases the complaint is pain, some patients experiencing a phantom limb experience sensations such as itching, burning, or feeling as though the limb is too short. Although PLP is more common in the early stages following an amputation, some have reported pain for years after. It was previously discovered that PLP had a strong correlation with representational plasticity in the somatosensory cortex; however, its correlation with the plasticity in the motor cortex was unknown. This experiment used methods such as Transcranial Magnetic Stimulation (TMS) of the motor cortex, and neuroelectric source imaging of the somatosensory cortex to study the correlation of plasticity in these cortices.

In this study, participants included five upper-limp amputees experiencing PLP and five upper-limb amputees experiencing no PLP. A German version of the West Haven- Yale Multidimensional Pain Inventory was used to evaluate each patient's stump and limb pain. To test for motor reorganization, focal TMS was delivered from a magnetic stimulator through an 8-shaped magnetic coil. The leads were positioned to cause currents to flow approximately perpendicular to the central sulcus, optimally causing the largest peak-to-peak motor evoked potential in each muscle. In patients experiencing PLP, a map of outputs determined by neuroelectric source imaging of EEGs done showed significantly larger motor-evoked outputs on the side lacking the arm than the side with the remaining arm, whereas excitability in the motor neurons of amputees remained unchanged. Since it was previously known that motor reorganization in amputees takes place at a cortical level, the leap was made that. "It is likely that cortical mechanisms are also responsible for the differences in reorganization observed in both patient groups (Karl, Anke et. al., 2011)."

While these findings support the notion that increased plasticity is present in the motor cortex of PLP patients, the evidence used to support this main point is presented in a very odd fashion. Immediately following this claim about cortical mechanisms and presenting supporting evidence, they state that their results "do not rule out the possibility of additional subcortical reorganization." This statement is saying that other factors could be causing or contributing to the claims being made by their research, thus making the research inconclusive as a whole. Another problem with the research methods is that the patient's amputations all occurred at different times. Some more recent than others, which could have a profound effect on the plasticity levels reached at the time of testing.
All in all the research conducted further supports already claimed notions, while having no real additions of any validity or originality. These limitations could be reduced by choosing patients who's amputations occurred within the same month. The potential that could be reached through studies similar to this are immense, but further research needs to be conducted in order to draw on more valuable conclusions.

The Journal of Neuroscience, 15 May 2001, 21(10): 3609-3618;
Posted by      Madelyn K. at 8:29 PM MST
displaying most recent comments (5 ommitted) | Comments (8)
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October 23, 2011

Jalapenos...a treatment for arthritis?

We've all bitten into a jalapeno and experienced the slow burning pain that is associated with it. And whether you love it or hate it you've probably wondered why some people have a higher tolerance for spicy foods than others. The answer to that is two-fold.

To understand why we must first understand the mechanism through which capsaicin (the oily substance found in peppers which gives them their signature 'kick') works. Capsaicin targets a subgroup of sensory neurons called nociceptors. Prior research has shown that capsaicin excites these neurons by increasing the permeability of the plasma membrane to cations (K+, Na+ and Ca++ in particular) although it was unknown whether this was through direct disruption of the plasma membrane (capsaicin is hydrophobic and could thus perturb the phospholipids of the membrane)or though a ligand-system in which the molecule binds to specific receptors on the surface of the cell. The latter possibility was ruled more likely as capsaicin derivatives operate in dose-dependent manners highly characteristic of receptor activation via ligand binding. This was further supported through the use of resiniferatoxin, an extremely potent capsaicin analog derived from the plant genus Eurphorbia. This neurotoxin's extreme potency, eliciting responses at nanomolar concentrations, allowed scientists to assume that it bound with great affinity to the proposed capsaicin receptor. Using this, the molecule was radio labeled and researchers were able to visualize its binding to cell-surface receptors.

This provides the first the leg of the answer. The density of these receptors on an individual's nociceptors can influence the affect spicy food has. More receptors, more binding, greater response evoked.
An interesting side note...why do spicy foods produce a burning sensation? The specific receptors that capsaicin binds to are heat-gated receptors. These are analogous to our very well known voltage-gated channels but open is response to changes in ambient temperature and apparently capsaicin binding. This produces pain and the burning sensation that I for one love.

The second leg to our answer comes with a remarkably interesting point of immense pharmacological importance. Exposure to capsaicin initially excites a neuron leading to the pain response. However prolonged exposure (in this paper just a few hours) can cause cell death. Examination of dead cells revealed no evidence of DNA fragmentation meaning that no apoptotic events occurred. The actual cause of death was cytotoxicity caused by excessive ion influx, similar to the excitiotoxicity observed in TBI.
So as you can imagine eating spicy foods can actually kill these neurons, desensitizing your mouth to the pain a jalapeno can produce.

I did mention a pharmacological importance that is briefly covered by the authors, although they do not go into any sort of detail about it. In the opening paragraph they say that this nociceptor desensitization has lead to use of capsaicin as an analgesic agent in the treatment of n analgesic agent in the treatment of disorders ranging from viral and diabetic neuropathies to rheumatoid arthritis. While they do not elaborate on the mechanisms of this we can assume that these diseases cause pain through stimulation of these same nociceptors.
Posted by      Zach I. at 2:03 PM MDT
  Christina Uhlir  says:

I am curious as to whether or not there was a discussion about the clinical uses of different peppers based on their Scoville scale heat, and the fact that they could induce excitotoxicity.
Posted on Sun, 23 Oct 2011 6:04 PM MDT by Christina U.
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October 22, 2011

Meditation: New Discoveries of Old Traditions

It isn't often in science that old methods of treatment are re-centered from their otherwise un-scientific past, to present as one of the more progressively favored treatments in modern society. However, it seems as though the old practice of meditation is working to accomplish just that. Chronic pain sufferers have endlessly struggled to find methods of treatment that they are not resistant to, or that their pain does not overcome at some point. Perhaps in favor of a reduction of cost and a more "natural" method of healing, meditation was further studied--and these studies are proving most beneficial. Research has shown that by practicing a state of "mindfulness", one can achieve decreased overall pain, as well as pain intensity.

Such mindful "interventions" have aided our understanding of pain disorders (both acute and chronic). With extensive training of one's mind (meditation), it is found that one's cortical regions that are associated with pain are thickened, perhaps enhancing that persons perception of their pain. This results in changes in their normal evaluation and perception of pain. These effects of mental training can result in a more beneficial method of neuroplasticity.

But how exactly does one measure pain? Surely we do not expose trial studies of non-pain sufferers to painful stimulus in order to further science! Why of course not--in fact, what is generally used in pain studies is not in fact 'pain' at all. Experiments with temperature extremes (hot and cold) are used to test the participant's perception, durability, and sensation of a 'painful' stimulus. In a particular experiment adhering to the purpose at hand, they tested the unpleasantness of the stimulus (hot water) before and after a series of meditative exercises. However, rather than test the person's personal opinion of the pain, they tested the person's brain's perception of the pain through measurements of Cerebral Spinal Fluid, through a method called ASL. ASL is an "MRI pulse sequence that provides a measure of CBF using water as a flow tracer". Using ASL, they found OFC (orbitofrontal cortex) activation, and deactivation of the thalamus. During painful stimulus, usually the opposite occurs--a decrease in OFC and an increase in thalamus activation are seen. This study concluded that short term mediation can decrease the affect pain, and the experience that goes along with it.

It is important to take this discussion with a grain of salt. Even though these studies did work, I believe it is essential to define the term "meditation". Perhaps all it encompasses is distraction from temporary pain, having your mind focused on other things, thus rendering it less activated in the pain 'areas' of the brain. This type of treatment would not necessarily work for those who are suffering chronic pain. However, I feel more work in the field of long term mindful trainings may prove beneficial to act as a sole treatment or a combination treatment to pain disorders.

Another limitation to this experiment is the role of an adequate control group. I felt that they had no data to argue their finding against. The perception of the irritating stimulus may have simply decreased because they had already experience it once, and could therefore were more comfortable experiencing it again. It is crucial to create a group that simply received both tests without any meditation, to see what the conclusion of diminished pain was really measuring. Nevertheless, to whatever degree this breakthrough is effective, one conclusion is for sure--studying mediation and perception of pain enables us to further understand just how our brain handles painful or noxious stimulus. Hopefully we are able to use such methods of research (such as ASL) in order to provide helpful, more affordable treatment for the individuals suffering from pain disorders.

Posted by      Amber S. at 5:15 PM MDT
  Christina Uhlir  says:

This is lovely! My mom had postherpetic neuralgia and japanese accupuncture actually worked wonders for her.
Posted on Sun, 23 Oct 2011 7:46 PM MDT by Christina U.
  Emily Nelson  says:
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Posted on Tue, 18 Feb 2020 3:44 AM MST by Emily N.
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