27 March 2004

Men cause more pain than women

I've seen a report of this study in a couple of places. Though I haven't yet seen the actual study (it doesn't seem to be published yet). Here it is from New Scientist.

Participants placed a finger in a clamp which was tightened using a pressure gauge until they reported feeling pain. Both men and women appeared to feel pain more quickly if the person turning the clamp was a man.

Previous studies have shown that men report feeling less pain in front of a female experimenters - but this was put down to their wanting to appear more macho.

David Williams, who carried out the study at the University of Westminster in the UK, says his findings contradict this assumption. Williams suggests that the subjects of his study may be socially conditioned to expect men to be more likely to inflict harm. The effect, "is likely to be a result of what participants subconsciously expect, based on socially acquired gender stereotypes," he says.

The study also shows that a person's surroundings can affect their sensitivity to pain. Objects that might be associated with suffering - such as a chart showing wounds or a poster related to blood donations - were found to make the participants report feeling pain more readily

I'll admit I'm quite excited about this story; hopefully it will be in print soon and withstand scrutiny. Externalism about phenomenological content anyone?
[ed: This and the preceding post were old posts; I've moved them up because they are more interesting than some of the abstracts I had recently posted]


26 March 2004

Theory-Theory and pain

I don't know much about the theory-theory/mind-reading literature, but this study seems pretty interesting.

From: SCIENCE VOL 303 20 FEBRUARY 2004 (p.1121)

Researcher Tania Singer of the Institute of Neurology at University College London, U.K., and her team set up an experiment using 16 couples who were romantically involved and presumed to be acutely sensitive to each other’s pain. Keeping both partners in the same room, they put the female in a magnetic resonance imaging machine and watched her brain while a 1-second electric shock was delivered to the back of either her hand or her partner’s. She could not see his face but could see from an indicator which one of them was going to be zapped and whether it would be a weak shock or a sharp, stinging one. When the woman received sharp shocks, well-known pain regions in the limbic system were activated, including the anterior cingulate cortex, the insula (which is involved in relaying information from the cortex), the thalamus, and the somatosensory cortices, which relay the physical nature and location of the pain. Many of the same regions were activated in subjects when their partners got the painful shock. But empathy alone failed to activate the somatosensory cortices, for instance. The fact that the same affective brain areas respond to both experienced and imagined pain, claims Singer, is the root of empathy

23 March 2004


I just found this bibliography on pain: http://www.clas.ufl.edu/users/maydede/pain/PainBib.htm it appears to be mostly philosophical material, including stuff in journals I've never even heard of.

16 March 2004

No dear, pains are not C-fibers firing. They are not the release of cystatin C either

Before some enterprising philosopher latches onto this, another thing that pains are not

A recent subtractive cDNA cloning study in rats demonstrated an unexpected increase in expression of the proteinase inhibitor, cystatin C in the spinal cord during acute peripheral inflammation, suggesting this protein may be involved in the pathogenesis of persistent pain. A subsequent study of 10 women suggested that prolonged labor pain resulted in increased cystatin C concentrations in cerebrospinal fluid, and that this could be used as a biomarker for pain. To confirm and extend these observations, we measured cystatin C concentrations in cerebrospinal fluid in 131 subjects: 30 normal volunteers without pain, 25 women at elective cesarean section without pain, 60 women in labor with severe pain, and 16 patients with chronic neuropathic pain and tactile allodynia. The median cystatin C concentration in normal volunteers, 2.2 mg/ml, was similar to that previously reported by multiple investigators, and cystatin C concentrations were increased in women in labor (3.9 mg/ml). However, contrary to the previous report, cystatin C concentrations in laboring women with pain did not differ from those of pregnant women without pain (3.7 mg/ml). There was no relationship between duration of painful labor and cystatin C concentration. Patients with neuropathic pain had similar cystatin C concentrations (2.4 mg/ml) to controls. Logistic regression analysis indicated that cystatin C concentrations could not be used to reliably predict the presence of pain in either acute or chronic settings. These data suggest that cystatin C concentration in cerebrospinal fluid is an unreliable diagnostic marker for pain in humans.
q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Cystatin C in cerebrospinal fluid is not a diagnostic test for pain in humans
James C. Eisenach*, John A. Thomas, Richard L. Rauck, Regina Curry, Xinhui Li
Pain 107 (2004) 207–212

Sex differences in anxiety and pain perception

Sex differences in pain perception and anxiety. A psychophysical
study with topical capsaicin
Maud Frota, Jocelyne S. Feine, M. Catherine Bushnella

Pain 108 (2004) 230–236

Much evidence indicates that women experience painful stimuli as more intense than men do. Nevertheless, some data suggest that sustained low-level pain may be more disturbing to men than to women. The current experiment evaluated the hypothesis that pain is more disturbing for men than for women by comparing across genders sensory and emotional aspects of pain evoked by capsaicin. Ten men and 10 women (aged 20–46 years) received topical capsaicin for 30 min on the face in one session and on the ankle in another. The subjects rated on visual analog scales pain intensity, unpleasantness and anxiety each minute during capsaicin application and for 30 min after its removal. During capsaicin application, females rated both pain intensity ðP ¼ 0:04Þ and unpleasantness ðP ¼ 0:05Þ higher than did males. Further, subjects rated pain intensity and unpleasantness higher on the face than on the ankle, although the physical stimulus was the same. Despite their lower pain ratings, men reported more pain-related anxiety than women ðP ¼ 0:02Þ: Moreover, men showed a significant positive correlation between anxiety and pain intensity and unpleasantness, whereas women did not. After removing the capsaicin, there was no overall effect of sex on either intensity ðP ¼ 0:18Þ or unpleasantness ðP ¼ 0:37Þ of the residual sensation. However, men still showed a positive correlation between anxiety and the intensity and unpleasantness of the sensation. Our data confirm with the topical capsaicin model that women rate pain higher than men, but despite their lower pain ratings, males have more anxiety related to pain.
q 2003 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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Also Interesting

From the current issue of Pain Medicine, another (not well-fitting?) piece of the chronic pain and depression puzzle

RESEARCH PAPERS A Case-Matching Study of the Analgesic Properties of Electroconvulsive Therapy. By: Wasan, Ajay D.; Artin, Kamal; Clark, Michael R.. Pain Medicine, Mar2004, Vol. 5 Issue 1, p50, 9p; Abstract: Chronic pain improves with electroconvulsive therapy (ECT), yet few case reports account for treatment of comorbid major depression, a significant confounder of the analgesia of ECT. This study reports on the analgesia of ECT, controlling for treatment of depression. This is a case-matching study comparing outcomes of inpatients with chronic pain and major depression in a multidisciplinary pain treatment unit treated with ECT and medications (cases) with those of inpatients treated with medications only (controls). Both groups received the same behavioral and pharmacological treatments for depression and chronic pain. Outcome measures included 0–10 pain rating scales and the Montgomery-Asberg Depression Inventory. Patients were matched on sex, age within 5 years, admission date within 6 months, psychiatric diagnoses, and, as much as possible, on race and pain syndrome diagnosis. Percentage changes in depression scores and pain scores were calculated from the beginning to the end of admission. There were nonsignificant differences in demographics, except in the proportion married. Twenty-five of 28 ECT patients were matched. Depression improvements were similar between cases and controls (55.9% vs 40.5%). Despite higher initial pain (8.1 vs 6.9 on a 10-point scale), the ECT group had less final pain (3.4 vs 5.5). The ECT group had a 59.8% drop in pain versus a 15.8% drop in the control group, P > 0.01. ECT has analgesic properties independent of its improvement of depression in patients with chronic pain and major depression. Improvements in depression were similar, while there was a significantly greater improvement in pain with ECT. The lower post-ECT treatment pain scores suggest a specific analgesic effect of ECT. [ABSTRACT FROM AUTHOR]; DOI: 10.1111/j.1526-4637.2004.04006.x; (AN 12255076


This seems interesting, though I haven't had a chance to look at the actual article yet

RESEARCH PAPERS Comorbidity of Fibromyalgia and Posttraumatic Stress Disorder Symptoms in a Community Sample of Women. By: Raphael, Karen G.; Janal, Malvin N.; Nayak, Sangeetha. Pain Medicine, Mar2004, Vol. 5 Issue 1, p33, 9p; Abstract: To test alternative explanations for the comorbidity between fibromyalgia (FM), a medically unexplained syndrome involving widespread pain, and posttraumatic stress disorder (PTSD). In contrast to a default “risk factor” hypothesis, tested hypotheses were that: A) The association is due to a sampling bias introduced by the study of care-seeking individuals; B) FM is an additive burden that strains coping resources when confronting life stress; and C) Arousal symptoms of PTSD and FM are confounded. Community-dwelling women in the New York/New Jersey metropolitan area (N=1,312) completed a telephone survey regarding FM-like symptoms prior to September 11, 2001. Approximately 6 months after the World Trade Center terrorist attacks, they again completed the survey, to which questions regarding PTSD symptoms were added. The odds of probable PTSD were more than three times greater in women with FM-like symptoms, both assessed after 9/11. The odds ratio was not reduced by controlling for FM-like symptoms before 9/11 or for the potentially confounded symptoms of PTSD specifically related to arousal. These findings lead us to reject alternate explanations for the comorbidity between FM and PTSD. Speculations that FM and PTSD share psychobiological risk factors remain plausible. [ABSTRACT FROM AUTHOR]; DOI: 10.1111/j.1526-4637.2004.04003.x; (AN 12255079)

From current issue of Pain Medicine

11 March 2004

The different effects of fear and anxiety

This is kind of an old study but I came across it again in organizing my files and found the online description here.

Texas A&M University psychologist Mary W. Meagher, who has conducted pain research for 16 years, says two emotional states - fear and anxiety - have profoundly different effects on a person's ability to feel pain.

"Fear and anxiety have divergent effects on pain reactivity in humans: fear reduces pain, whereas anxiety has a sensitizing, or enhancing effect," says Meagher, who holds joint appointments in clinical psychology and behavioral neuroscience.

Her conclusions are based on her and graduate student Jamie L. Rhudy's recent work focusing on the role of human emotion on pain. Previous animal studies have suggested that fear inhibits pain and anxiety enhances it, but Meagher's results support the view that emotional states influence human pain reactivity.

"From a clinical perspective, these data suggest that a patient anticipating an unpredictable threatening event will experience enhanced pain," she says. "In contrast, a patient that has been exposed to a threatening event will experience a fear state that inhibits pain processing."

Abnormal brain pathways behind mysterious back pain?

Patients with lower back pain that can't be traced to a specific physical cause may have abnormal pain-processing pathways in their brains, according to a new study led by University of Michigan researchers.

The effect, which as yet has no explanation, is similar to an altered pain perception effect in fibromyalgia patients recently reported by the same research team.

In fact, the study finds, people with lower back pain say they feel severe pain, and have measurable pain signals in their brains, from a gentle finger squeeze that barely feels unpleasant to people without lower back pain. People with fibromyalgia felt about the same pain from a squeeze of the same intensity.

But the squeeze's force must be increased sharply to cause healthy people to feel the same level of pain - and their pain signals register p in different brain areas.

The results, which will be presented Oct. 27 at the annual meeting of the American College of Rheumatology in New Orleans, may help lead researchers to important findings on lower back pain, and on enhanced pain perception in general.

Senior authors Richard Gracely, Ph.D., and Daniel Clauw, M.D., did the study at Georgetown University Medical Center and the National Institutes of Health, but are now continuing the work at the University of Michigan Health System. In May, they and their colleagues published a paper in the journal Arthritis and Rheumatism on pain perception in fibromyalgia patients.

To correlate subjective pain sensation with objective views of brain signals, the researchers used a super-fast form of MRI brain imaging, called functional MRI or fMRI. They looked at the brains of 15 people with lower back pain whose body scans showed no mechanical cause, such as a ruptured disk, for their pain. They also looked at 15 fibromyalgia patients and 15 normal control subjects.

As a result, they say, the study offers the first objective method for corroborating what lower back pain patients report they feel, and what's going on in their brains at the precise moment they feel it. And, it continues to give researchers a road map of the areas of the brain that are most - and least - active when patients feel pain. The researchers hope that further study on larger groups of patients will yield more information on altered pain processing.

"The fMRI technology gave us a unique opportunity to look at the neurobiology underlying tenderness, which is a hallmark of both lower back pain and fibromyalgia," says Clauw. "These results, combined with other work done by our group and others, have convinced us that some pathologic process is making these patients more sensitive. For some reason, still unknown, there's a neurobiological amplification of their pain signals."

Take that Valerie Hardcastle. (Actually, I'm not sure if this is the sort of thing she has in mind for the 'mentally caused pains' she rails against since she never bothers to give them a sharp characterization despite discussing several different alleged cases. I'd appreciate it if someone could explain it to me in the comments...)

Hypnosis and pain



Techniques like relaxation and visualizing a pleasant scene can take the sting out of mild pain, but adding hypnosis to the mix does not make such techniques more effective, according to a new report in Health Psychology.

Leonard S. Milling, Ph.D., of the University of Hartford and colleagues, compared five different behavioral treatments for finger pain delivered under hypnotic and non-hypnotic conditions.

Treatments included imagining a pain-protective glove, relaxing various muscle groups, picturing a warm summer day and reciting statements like: "I'll make the pain less severe when it comes."

While all five treatments lessened the intensity of pain among participants, the hypnotic versions were no better than their non-hypnotic counterparts in reducing pain, even among participants who were highly sensitive to hypnotic suggestions, say the researchers.

The amount of pain relief experienced by all participants, regardless of treatment, was due in part to how much they expected to benefit from the therapy, according to Milling.
Shorter treatments were also just as effective as longer ones, an encouraging sign for their use in pain relief among patients who have a hard time concentrating or who suffer through multiple painful tests and therapies, like burn victims or cancer patients.

Milling and colleagues caution, however, that the study's results may be limited.

"Our results may generalize more readily to acute clinical pain that is mild to moderate in intensity, like a finger stick, and less readily to severe acute pain or to pain that is recurrent or chronic," they say.

That last qualification is pretty important given the large body of well-accepted literature on hypnotic analgesia in chronic pains or cases involving relatively severe acute pains.

Genes and pains

Oddly enough, this study on genetic dispositions in pain processing came out of studies on genes and alcoholism.


For the current study, Drs. Goldman, Zubieta, and their colleagues used positron emission tomography (PET) targeting the endogenous opioid system to examine the effects of a specific genetic variant on neurochemical brain responses to sustained pain. The researchers also used questionnaires that measure pain-related sensory and affective qualities and internal emotional state to link the neurochemical responses to participants' psychological and physical experience of the pain challenge.

The cathechol-O-methyltransferase (COMT) gene encodes a major enzyme involved in the metabolism of the neurotransmitters dopamine (a chemical messenger involved in motivation and reward) and norepinephrine (a chemical messenger involved in sympathetic nervous system stimulation and inhibition). The val158met variant of the COMT gene codes the substitution of valine (val) by methionine (met) and is associated with a three- to fourfold reduction in COMT enzyme activity. This is a common genetic variant such that the distribution of the three genotypes in the general population is approximately 1/3,1/2 and 1/6. Previous research has linked val158met genotypes to a number of behavioral diseases with complex origins, including obsessive-compulsive disease and schizophrenia.

Drs. Goldman, Zubieta, and colleagues hypothesized that variations in COMT activity conferred by the various val158met genotypes might influence functions regulated by dopamine and adrenergic/noradrenergic (epinephrine/norepinephrine) neurotransmission. One such system, the m-opioid neurotransmitter system, typically is activated in response to prolonged pain or stress. To test their hypothesis, the researchers examined 15 men and 14 women genotyped with respect to the val158met polymorphism. The participants were randomized and blinded during the infusion of painful and nonpainful saline solutions.

As anticipated, the researchers who monitored neurochemical changes observed significant effects of genotype on m-opioid receptor binding and system activation. Compared with heterozygotes (individuals with one copy of each allele), individuals with two copies of the met158 allele and lowest COMT enzyme activity showed diminished regional m-opioid system responses, higher sensory and affective ratings of pain, and a more negative internal state. Persons with two copies of the val158 allele and greater COMT enzyme activity demonstrated opposite effects. The regions of the brain showing these changes included the thalamus, a key pain sensory relay station in the pathway for pain perception, and the amygdala, a region of the brain integral for the emotions of anxiety and distress.

The sex hormones, gender and pain

More interesting stuff. (the mu-opioid system is the main anti-nociceptive system for modulating pain. Its the system that opiate drugs (morphine, heroin, etc) affect.

In July, 2001, the U-M team published a paper in the journal Science that contained the first glimpse of the brain's mu-opioid system in action, and confirmed the system's important role. Using a radioactive tracer attached to a molecule that only binds to mu-opioid receptors, they showed on PET scans that the endorphin systems became activated in the brains of 20 volunteers who were subjected to moderate levels of pain in their jaw muscle over 20 minutes.

That activation of endorphin release also corresponded with a drop in the volunteers' perceived pain and pain-related emotions - thereby linking the physical response with the emotional one.

Armed with the ability to see the brain's response to pain, Zubieta's team began looking at how that system handled pain in people of different genders, hormone levels and genetic makeup.

Study participants were scanned as they received a pain-causing but harmless injection of salt water in their jaw muscle.
They used the same double-blind, placebo-controlled jaw pain model, induced by a harmless injection of salt water into the masseter muscle, for all the studies. The injection is meant to simulate a condition called temporomandibular joint pain disorder, but is also a useful human model of sustained pain, and physical and psychological stress. Subjects rate their pain often during the PET scan, and the injection is controlled to keep the pain level the same at all times, so that unnecessary suffering is avoided. Subjects fill out standardized questionnaires after the scan, about how the pain made them feel.

In June 2002, the team reported in the Journal of Neuroscience the first findings that some of the differences between individuals in response to pain are governed by the mu-opioid system. In the study, 14 men scanned before and during jaw pain showed increases in endorphin release in certain brain areas during the painful state, as shown in the previous study. But most of the 14 women studied actually showed a reduction in endorphin release. The women also reported feeling more intense pain, and more pain-related negative emotions, than the men.

Zubieta notes that all the women were studied at a time in their menstrual cycle when levels of estrogen and progesterone were lowest.


For their latest pilot study, the team scanned healthy women once during their early follicular phase, and again during that same phase in another month - after they had been wearing an estrogen-releasing skin patch for a week. The patch made their levels of estrogen rise to levels normally seen during later parts of the menstrual cycle. This allowed the team to study estrogen's effect without the effects of other hormones, such as progesterone, that normally increase along with it.

...Scans made without the painful jaw stimulus showed that under high estrogen conditions, the number of available mu-opioid receptors, where endorphins would dock in case of pain, increased in several pain- and stress-controlling areas of the brain.

When the painful jaw injection was given, the effect of the estrogen on the capacity to activate this painkiller system was also striking. Instead of the low or absent activation of the mu-opioid system seen in women during low-estrogen conditions, the same women under high-estrogen conditions showed a marked increases in their ability to release endorphins and activate the receptors.

In other words, they had a response to pain that was more like the men in the previous study. And the effect was seen in multiple brain areas involved with the perception and regulation of pain, and of other stressful and emotionally significant stimuli

This isn't in the story, but its worth mentioning: there are actually thought to be three independent systems for pain modulation. I couldn't even begin to explain how the second one works, but the third is thought to only exist in women and, from what I've read, it is thought to be regulated by estrogen. Thus I'm not sure how the results of this study bear on the alleged third system. It might be that these results show the third system to be part of the main mu-opioid system, or that men and women lack a common mu-opioid system.
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Depression and pain

No wonder my back always hurts while grading papers...

Depression can lead to back pain

It is well documented that physical pain can lead to feelings of depression, but a new study from the University of Alberta shows the reverse can be true, as well.

Dr. Linda Carroll, a professor in the U of A Department of Public Health Sciences, led the study that shows depression is a risk factor for onset of severe neck and low back pain. The study is published in the journal Pain.

Carroll and her colleagues followed a random sample of nearly 800 adults without neck and low back pain and found that people who suffer from depression are four times as likely to develop intense or disabling neck and low back pain than those who are not depressed.

"We've known for a long time that pain can lead to depression, and now we're finding that each is a risk for the other," Carroll said. "Both conditions are recurrent, that is, they can both come and go; and both are very common--in fact, only 20 per cent of the population has not experienced any neck or low back pain in the past six months--so it's important to try to deal with these conditions before they become troublesome and lead to a vicious cycle."

Carroll is now interested to figure out why the two conditions are commonly related, and she is focusing her research on the coping methods of people with depression, a condition researchers have long known to be associated with physical ailments.

There are two broad ways people can cope with pain, Carroll said. One is to be passive, which entails such things as withdrawing from activities because of the pain or wishing for better pain medication. The other is to be active, which entails getting exercise and staying busy, for example.

"We're wondering if depression leads people to cope passively when they experience the kinds of mild pain episodes that most of us are periodically subject to. This in turn may increase the likelihood that pain will become a problem in someone's life. The next step is to answer this question," added Carroll, whose research is sponsored by the Alberta Heritage Foundation for Medical Research.

From U Alberta via Scienceblog

Cognitive factors in the placebo effect

More interesting stuff on the placebo effect in pain reduction.

From: SCIENCE VOL 303 20 FEBRUARY 2004 (p.1121)

In this study, headed by Tor Wager of the University of Michigan, Ann Arbor, subjects were given an inert salve that they were told was being tested as an analgesic cream. They were then given a shock or painful heat stimulus on the wrist. Those who showed increased activity in the prefrontal cortex prior to the stimulus also showed the biggest reduction of activity in pain-sensitive brain regions and reported the greatest pain reduction—suggesting that anticipation of pain relief is intimately tied with actual pain reduction. Co-author Richard Davidson of the University of Wisconsin, Madison, says this indicates that cognitive control may be crucial for downregulating pain circuitry. Presumably, he says, more prefrontal activity reflects “the active maintenance of a [mind]set” associated with pain relief. Mayberg, who has done brain-imaging studies on placebo effects with depressed patients, says the study supports the notion that it may be possible to predict response to medication by looking at the “expectation component” in patients’ brain scans.

To my mind, the stuff about the placebo effect is some of the most philosophically suggestive material in the pain science literature. I mean, (and this is from other studies) how can you not be curious about the fact that the analgesic effect of a placebo is almost always 50% of the actual analgesic effect of the drug the patient thinks she's getting (that is, if you tell her its asprin, her pain will be reduced 50% of what it would be with actual asprin; same thing with morphine). Of course, the phenomenon is extremely complicated: injected placebos are more effective (overall) than ingested ones which are in turn more effective than topical salves.

10 March 2004

Killer snails kill pain?

This is a bit old

A sea-snail toxin could relieve chronic pain. Tests on rats hint the chemical could be 10,000 times more potent than morphine, non-addictive and not cause side-effects.

A team from the University of Melbourne led by Bruce Livett extracted the 'conotoxin' from a cone-shell snail. They will announce their patented discovery, called ACV1, this week at the Venoms to Drugs 2002 conference on Heron Island, Australia.

"We are confident not only that ACV1 inhibits pain, but also that it accelerates the recovery of injured nerves - a unique property not previously documented for an analgesic," says one of the research team, Zeinab Khalil. Moreover, says Khalil, "the universal way in which the drug blocks pain should mean it is effective in treating all types of chronic pain".

'Venoms to Drugs' would be a good name for an album

07 March 2004

More on contextual features in pain perception

The NY Times elaborates on the study I mentioned below. Link

Published: March 6, 2004
When David Williams, a psychologist at the University of Westminster in London, was deciding how to construct a pain machine, he realized a kitchen scale would do the trick. He attached a guillotinelike device to it, though he hastens to point out that the edge was "really blunt, not as sharp as a razor." It was designed to hit at the fingernail's half moon, where one can inflict pain without doing serious bodily harm.

He was trying to figure out what influences the perception of pain. What he discovered was that both men and women were willing to take more pain from a woman than from a man.

"A person's perception of pain doesn't necessarily depend on the intensity of the stimulus," Mr. Williams said in a telephone interview from his home in Stevenage, 30 miles north of London. It depends on environmental factors, like who is inflicting it. The 40 people who were tested waited longer to say "stop" when a woman was causing the pain than when a man was.

"The stereotype we have of women is that they are nurturing, caring, sensitive, that they have empathy," said Mr. Williams, who administered the experiments for his doctoral dissertation. "We feel safer with them."

In another experiment he looked at what you could call the pre-pain conversation. First he measured a subject's pain threshold. Then he told the subject that there was no need to say "stop" because he already knew exactly how much the subject could take. "The consequence was very odd," Mr. Williams said. When people were denied control, they felt the hurt as more intense.

Next Mr. Williams told subjects that he would not say exactly how much discomfort he was going to inflict, and again there was no point in telling him to stop. "When they were denied control and information," he said, "60 percent said it was less painful, 30 percent said it was more painful."

Mr. Williams theorizes that the different responses were a consequence of people's sense of control in their lives. Those who see themselves as in control experienced less pain, while those who tend to believe their lives are controlled by others or by chance experienced more.

By saying, "This is going to hurt a bit, try to hang on," doctors may actually make the patient feel out of control, he said.

And, yes, décor matters. In another experiment he found, not surprisingly, that graphic pictures of wounds hanging on the walls made people call it quits earlier. Therefore redecorating hospitals to make them less threatening to patients makes sense, Mr. Williams said. The smell of pine disinfectant is pervasive, and machinery and medical instruments are in full view.

"Only an operating room needs to be that clinical," he said. "The smell, the look, the whole appearance, everything which says, `This is a hospital, and you have no control. You are here to suffer' — all are changeable."

Again, I think these results are extremely important to our understanding of pain and how it is bad. I'll post something later to set out some of the philosophical issues I believe they bear upon.

01 March 2004

Virtual (reality) analgesia

Add virtual reality to hypnosis and meditation on the list of surprisingly effective techniques for pain control. From the BBC story.

Dr Hunter Hoffman, research fellow at the Harborview Medical Center in Seattle, has tested his virtual worlds on victims of burns injuries who suffer excruciating pain during their daily dressing changes which conventional drug therapy fails to control.

Hoffman's virtual worlds, which he calls by names such as SnowWorld or SpiderWorld, are designed to immerse the user so deeply in the virtual experience that their attention is distracted away from the pain.
Mike Robinson, a patient who has undergone the virtual reality treatment, said it helped him to overcome the extreme discomfort he felt when his dressings were changed.

"My pain when the nurse is changing my bandages is consistently extreme," he told BBC News Online.
"But during the time I was in VR, I was pretty much unaware that the nurse was even working on my wound.

"I mean, at some level I knew she was working on me, but I wasn't thinking about it because I was inside that SnowWorld."

Virtual analgesia is founded on the principle of distracting the attentional resources of the brain.

Dr Hoffman believes pain contains a significant psychological element which is why distracting thoughts by virtual reality lends itself so well to pain control

Of course, I'm not surprised that this works since my view predicts that it would (inasmuch as a philosophical view predicts).

Congenital insensitivity to pain

A friend pointed out this story on a little girl who is congenitally insensitive to pain.

Though they didn't seem to say so in the story, the sad thing is she probably won't live past 20. Even when they get kids to avoid hurting themselves, they don't move enough when sitting and sleeping (we constantly shift our positions when they become uncomfortable to take some of the stress off the joints). That leads to some pretty horrific (and fatal) infections from the joint tissue.