I get irritated when philosophers talk about C-fibers firing as the neural substrate of pain experience, but not because of the factual wrongness of the claim --C-fibers and A(delta) fibers are nociceptive afferent axons which (I believe) are not even present in the brain. Clearly, they are using 'C-fibers' as shorthand for 'whatever neural mechanism science discovers about pain-processing in the brain' (Kripke explictly makes this qualification in Naming and Necessity). I have no objection to such shorthand; in fact, I like it when philosophers remember their place vis-a-vis scientists.
Instead, I worry that this shorthand connotes too simple of a picture of what pains are --both in terms of experience and underlying psychology/neurology. I worry that 'C-fibers firing' suggests that there is one discrete part of the brain dedicated to processing pains. Such a picture, I think, can lead to many philosophical mistakes about what pains are.
Let me loosely distinguish between two uses of 'brain-state': (1) a state of the brain such that that the brain has many discrete brain-states at any given time; and (2) a state of the brain such that the whole brain is in one state at any given time.
Many writers --at least those working in ethics and axiology-- seem to assume that pains are essentially phenomenological (where 'phenomenology' refers to the hurting of the pain) and only accidentally associated with emotions, affect, expectation, etc. I therefore worry that when such writers say 'of course, the phenomenology supervenes on/ is identical with some brain-state' they are too close to (1) in what they are imagining pains are. They assume that there is some discrete neural phenomenon corresponding to the discrete phenomenological phenomenon --the pain.
I, of course, think this picture of what pains are is a mistake. I think that pains are best understood as having certain emotional, desiderative, conative, and affective components essentially. Hence I worry that the shorthand 'C-fibers' in discussing brain-states takes us too close to (1) rather than the more distributed and complex picture of pains of (2) (of course, we don't want to be too close to (2) either).
Now, I believe --and hopefully will be in print soon arguing-- that this mistaken picture of what pains are has great importance for how we understand and answer the axiological and normative questions about pain. Indeed, I suspect this mistake of shorthand that I'm suggesting affects the moral philosopher's view of pain, may also matter to other issues in philosophy of mind and metaphysics where pain is a central example.
(see, for example, Nancy Hardcastle's book The Myth of Pain and her When a Pain is Not J Phil 1997 94 381-409. I'm being intentionally vague here as to whether she commits these mistakes or whether her arguments are especially attuned to them; I haven't thought enough about her work to decide what exactly is going on in it)
24 May 2004
Thoughts about 'C-fibers firing'
19 May 2004
"And furthermore Susan, I wouldn't be surprised to learn that they habitually smoke marijuana cigarettes --reefer"
Check out this story on Alternet about the history of biomedical research on marijuana and its biochemical effects.
Ongoing research conducted by Mechoulam, and his counterpart at the University of Buffalo, Herbert Schuel, shows that anandamides appear to be involved in regulating and balancing the body's biochemical systems, influencing or controlling the reproductive, sleep, fight-or-flight and appetite cycles.
"It's a quirk of nature that THC works on our receptors," Mechoulam remarked. "We were lucky to be the only group in the world working on this chemical." All mammals, fish, birds and reptiles seem to have anandamide-based regulatory systems; it's even found in cacao nuts, from which chocolate is made. "It is found in substantial quantities in chocolate, and may account for the feelings of pleasure that come from chocolate," Schuel said. Other researchers have found that chocolate seems to prolong the marijuana high – as pot users have long claimed.
...
In 1988, an American research group that included Bill Devane announced they had found evidence of a cannabinoid receptor in the mammalian brain. Devane joined Mechoulam in Israel to further research this question: Did our brains evolve to receive marijuana?
"We assumed that such a receptor does not exist for the sake of a plant compound," they concluded. Other drugs, like opium, had been found to bind at the molecular level to brain receptor sites intended for endorphins, the body's natural pain reliever. Mechoulam and Devane decided to look for the natural version of THC, and in 1992 they announced finding a fatty molecule that bound naturally to the cannabinoid receptor site
...
Anandamides are produced by our brains and bodies to achieve a sort of yin-yang biochemical balance, and do not produce the extreme "high" of marijuana, Mechoulam says.
...
"They're completely different, from a chemical point of view, from THC," he said. "But they combine in the receptor sites the same way." Anandamides are quickly broken down by the body after they have served their intended purpose, and do not last as long as THC metabolites, which remain in the body for weeks.
...
Anandamides play a survival role for young mammals – their instinctive suckling behavior seems integrally tied to the presence of anandamides. "If we block the system (from receiving anandamides), there is no suckling," Mechoulam explains.
I'm not sure how exactly this fits with some of the research on cannabinoids and pain I posted about earlier. Here's two comments:
First, though this article is about a year old, the research on cannabinoids and pain seems to have been pretty well established for several years (there's a bigger body of literature than I suspected when I originally posted here). Thus its odd that the article doesn't mention the endogenous cannabinoid-mediated system. It lists many other biological-processes; why not the role in pain?
Is it because (a) the experts discussed or the reporter is unaware of this role --in big research fields, right hands often don't know what left hands are doing; (b) the focus of the article is on anandamides and the role cannabinoids play with pain involve a different set of receptors and chemicals? If so, what are the relevant differences?
Also, as far as I understand it 'cannabinoids' are defined as (roughly) 'chemicals unique to cannabus', but the pain-literature talks about 'cannabinoid-receptors' and 'endogenous cannabinoids'. Does this mean that there are two classes of chemical here --anandamindes and cannabinoids-- or am I just confused?
Second, the article mentions something I've heard in several places before --that its a mystery why THC interacts with these systems of ours-- with the implications being that we somehow evolved to smoke weed. But if all this research is correct, there's no mystery here. No more than why we evolved to have ascorbic acid from citrus interact beneficially with us. Presumably, if there is any sense to the 'mystery', it turns on the fact that cannabinoids are unique to cannabus. That raises the first set of questions.
13 May 2004
And on a different note
Sorry, I just can't resist:
Does aromatherapy massage benefit patients with cancer
attending a specialist palliative care day centre? Wilcock,et.al. Palliative Medicine 2004; 18: 287¡/290
Does aromatherapy massage benefit patients with cancer
attending a specialist palliative care day centre? Wilcock,et.al. Palliative Medicine 2004; 18: 287¡/290
A randomised controlled pilot study was carried out to examine the effects of adjunctive aromatherapy massage on mood, quality of life and physical symptoms in patients withcancer attending a specialist unit.Participants were randomised to conventional day care alone or day care plus weekly aromatherapy massage using a standardised blend of oils for four weeks....Forty-six patients were recruited to the study. Due to a large number of withdrawals, only 11 of 23 (48%) patients in the aromatherapy group and 18 of 23 (78%) in the control group completed all four weeks.
I'd bet that the same aromatherapy massage regime would lead to this result
Mood, physical symptoms and quality of life improved in both groups. There was no statistically significant difference between groups in any of the outcome measures. Despite a lack of measurable benefit, all patients were satisfied with the aromatherapy and wished to continue.
for the symptoms of graduate school
Meanings and pain intensity
Here's an abstract from Pain 109 (2004) 20-25
The meaning of pain influences its experienced intensity by Arnoud Arntz*, Lily Claassens
This experiment tested whether meaning influences the experience of pain. Thirty-one healthy students participated in a study on
evaluations of various stimuli placed against the neck. By suggesting that a very cold metal bar was either hot or cold, the potentially tissue damaging property of the stimulus was experimentally manipulated. A manipulation check revealed that participants believed the experimenter’s information, as they rated the bar as more hot in the corresponding condition than in the other condition. Confirming the hypothesis that tissue-damaging meaning influences the experience of pain, participants who were told that the bar was hot rated it as more painful than participants who were told that it was cold. Damage interpretations mediated the effect of information on pain intensity scores,which supported the theory that tissue-damage is a crucial aspect of meaning to influence the subjective intensity of pain.
(c)2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
While we have known that the perception of threat or severe injury influences the unpleasantness of pain, it would be interesting to find that such meanings also influence judgments about intensity.
On its face this sort of result does seem to tell in favor of the views of writers such as Pitcher and Nelkin who believe that the badness of pain lies in its connection with bodily injury. It may also help --though I know less about such views-- representational accounts of pain phenomenology such as Tye's.
Its also worth noting the bearing this has on the arguments concerning the hot-poker trick in Stuart Rachels' excellent 'Is Unpleasantness Intrinsic to Unpleasant Experiences'
Myself, I think that this appearance of support for Pitcher/Nelkin views is ultimately specious. But that is a subject for another post.
12 May 2004
More sex differences in pain processing
Another abstract from Pain 109 (2004) 115–123
Sex differences in temporal summation of pain and aftersensations following repetitive noxious mechanical stimulation by Eleni Sarlani, Edward G. Grace, Mark A. Reynolds, Joel D. Greenspan
Sex differences in temporal summation of pain and aftersensations following repetitive noxious mechanical stimulation by Eleni Sarlani, Edward G. Grace, Mark A. Reynolds, Joel D. Greenspan
Several studies demonstrate that women are more sensitive to experimental pain than men. In addition, women exhibit greater temporal summation of heat and mechanically evoked pain. Since temporal summation of pain is centrally mediated, its greater expression in women suggests a central nociceptive hyperexcitability relative to men. The purpose of this study was to pursue this theory, by further assessing sex differences in (1) temporal summation of mechanically evoked pain, and (2) aftersensations following repetitive noxious stimulation. Sixteen
series of 10 repetitive, mildly noxious, mechanical stimuli were applied to the fingers of 25 women and 25 age-matched men. The subjects rated the pain intensity and unpleasantness caused by the first, fifth and tenth stimulus in the series, as well as their aftersensations 15 s and 1 min following the end of stimulation...Temporal summation of pain intensity and unpleasantness ratings were more pronounced in women than men...In addition, significant temporal summation occurred only with 2 s interstimulus interval for men...but with 2 and 5 s interstimulus interval for women...Moreover, women provided greater ratings for the intensity and the unpleasantness of aftersensations...and reported painful aftersensations at greater frequency...
Greater temporal summation of pain and aftersensations in women suggests that their central processing of nociceptive input may be more easily upregulated into pathological hyperexcitability, possibly accounting for the higher prevalence of various chronic pain conditions among women.
(c) 2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
04 May 2004
Biofeedback and pain supression
This suggests we can add biofeedback to hypnotic analgesia and meditation as surprisingly effective analgesic techniques.
People can learn to suppress pain when they are shown the activity of a pain-control region of their brain, a small new study suggests. The new biofeedback technique might also turn out to be useful for treating other conditions.
Twenty years ago Rosenfeld found that he could change the pain threshold in mice by training them to alter their brainwave patterns through a process called conditioned learning, where an altered brainwave state was rewarded by direct stimulation of the reward centres in their brains. Since this meant placing an electrode into the brain, however, his team never tried the technique on people.
Now Fumiko Maeda, Christopher deCharms and their colleagues at Stanford University in California have tried showing people real-time feedback from a functional magnetic resonance imaging (fMRI) scanner.
The eight volunteers saw the activity of a pain-control region called the rostral anterior cingulate cortex represented on a screen either as a flame that varied in size, or as a simple scrolling bar graph. This brain region is known to modulate both the intensity and the emotional impact of pain.
During the scans the volunteers had to endure painful heat on the palm of their hand. They were asked to try to increase or decrease the signal from the brain scanner and to periodically rate their pain sensations.
It took just three 13-minute sessions in the scanner for the eight volunteers to learn to vary the brain activity level, and thus to develop some control over their pain sensations, the researchers reported at the Cognitive Neuroscience Society meeting in San Francisco last week.
The effect seemed to last beyond the sessions in the scanner, although the researchers have yet to determine how strongly and for how long.
The volunteers could not explain how they did it. The researchers ruled out other explanations for the effect through a series of controls. They gave people false feedback data, no feedback at all, or feedback from a part of the brain unrelated to pain control. They also sometimes asked people to pay attention to the pain or distracted their attention away from it.
People can learn to suppress pain when they are shown the activity of a pain-control region of their brain, a small new study suggests. The new biofeedback technique might also turn out to be useful for treating other conditions.
Twenty years ago Rosenfeld found that he could change the pain threshold in mice by training them to alter their brainwave patterns through a process called conditioned learning, where an altered brainwave state was rewarded by direct stimulation of the reward centres in their brains. Since this meant placing an electrode into the brain, however, his team never tried the technique on people.
Now Fumiko Maeda, Christopher deCharms and their colleagues at Stanford University in California have tried showing people real-time feedback from a functional magnetic resonance imaging (fMRI) scanner.
The eight volunteers saw the activity of a pain-control region called the rostral anterior cingulate cortex represented on a screen either as a flame that varied in size, or as a simple scrolling bar graph. This brain region is known to modulate both the intensity and the emotional impact of pain.
During the scans the volunteers had to endure painful heat on the palm of their hand. They were asked to try to increase or decrease the signal from the brain scanner and to periodically rate their pain sensations.
It took just three 13-minute sessions in the scanner for the eight volunteers to learn to vary the brain activity level, and thus to develop some control over their pain sensations, the researchers reported at the Cognitive Neuroscience Society meeting in San Francisco last week.
The effect seemed to last beyond the sessions in the scanner, although the researchers have yet to determine how strongly and for how long.
The volunteers could not explain how they did it. The researchers ruled out other explanations for the effect through a series of controls. They gave people false feedback data, no feedback at all, or feedback from a part of the brain unrelated to pain control. They also sometimes asked people to pay attention to the pain or distracted their attention away from it.
Mary Jane's palliative care
IASP Newsletter Technical Corner: Basic Mechanisms of Cannabinoid-Induced Analgesia
The paper's really technical, but if I read it right, this conclusion is pretty interesting
Taken together, these results indicate (1) that endogenous cannabinoids modulate acute nociceptive processing, (2) that this system is tonically active, and (3) that the activity of the cannabinoid receptor system increases after injury. If this is indeed the case, then the decreased nociceptive threshold that occurs in the setting of injury may partly be due to loss of a tonic cannabinoid activity. Thus, administration of exogenous cannabinoids could restore the tone of the system and presumably could alleviate the allodynia and pain that are triggered by injury.
In English: Cannabinoids (chemicals found normally in marijuana and its relatives) are involved in the suppression of acute pains. And the diminution of cannabinoids in this system that occurs with injuries may be that part of the reason why injured body parts have hyperalgesia (painful stimulation causes much more pain than normal) and allodynia (non-noxious stimuli --e.g., temperature changes or wind-- cause pains). This suggests that giving someone cannabinoids may help alleviate the lingering pains of injuries.
Categories: Legal, Marijuana
The paper's really technical, but if I read it right, this conclusion is pretty interesting
Taken together, these results indicate (1) that endogenous cannabinoids modulate acute nociceptive processing, (2) that this system is tonically active, and (3) that the activity of the cannabinoid receptor system increases after injury. If this is indeed the case, then the decreased nociceptive threshold that occurs in the setting of injury may partly be due to loss of a tonic cannabinoid activity. Thus, administration of exogenous cannabinoids could restore the tone of the system and presumably could alleviate the allodynia and pain that are triggered by injury.
In English: Cannabinoids (chemicals found normally in marijuana and its relatives) are involved in the suppression of acute pains. And the diminution of cannabinoids in this system that occurs with injuries may be that part of the reason why injured body parts have hyperalgesia (painful stimulation causes much more pain than normal) and allodynia (non-noxious stimuli --e.g., temperature changes or wind-- cause pains). This suggests that giving someone cannabinoids may help alleviate the lingering pains of injuries.
Categories: Legal, Marijuana
Botox and pain
This is a bit old, but still interesting.
Combining the most potent neurotoxin known to man and a protein from the Mediterranean coral tree could deliver a long-lasting treatment for the chronic pain that afflicts millions of people, including cancer patients.
The neurotoxin in question is botulinum toxin, perhaps better known as Botox ....The neurotoxin, whose effects can last for months, works by blocking the release of the neurotransmitters that relay the "contract now" message from nerves to muscles. The machinery that is knocked out is actually found inside most cells, but the toxin only affects the neurons that control muscles. This is because of a targeting sequence in the toxin that only permits it to bind to muscle cells.
So Keith Foster's team at the Centre for Applied Microbiology and Research near Salisbury, UK, went looking for a targeting sequence specific to the nerves that transmit pain signals. He wanted to use this sequence to turn the neurotoxin into a painkiller. They found it in the Mediterranean coral tree, Erythrina cristagalli.
It may be a complete coincidence that the coral tree protein binds to the surface of pain neurons and no other cells, but all that matters to Foster is that it does. Since pain nerves do not carry any other sort of message, the altered toxin his team has created stops pain without affecting touch, for example
Results from tests in mice have been impressive. In three experiments, Foster's painkiller performed as well as morphine at preventing pain. But it was still working nine days later, whereas morphine would have worn off after four hours.
Combining the most potent neurotoxin known to man and a protein from the Mediterranean coral tree could deliver a long-lasting treatment for the chronic pain that afflicts millions of people, including cancer patients.
The neurotoxin in question is botulinum toxin, perhaps better known as Botox ....The neurotoxin, whose effects can last for months, works by blocking the release of the neurotransmitters that relay the "contract now" message from nerves to muscles. The machinery that is knocked out is actually found inside most cells, but the toxin only affects the neurons that control muscles. This is because of a targeting sequence in the toxin that only permits it to bind to muscle cells.
So Keith Foster's team at the Centre for Applied Microbiology and Research near Salisbury, UK, went looking for a targeting sequence specific to the nerves that transmit pain signals. He wanted to use this sequence to turn the neurotoxin into a painkiller. They found it in the Mediterranean coral tree, Erythrina cristagalli.
It may be a complete coincidence that the coral tree protein binds to the surface of pain neurons and no other cells, but all that matters to Foster is that it does. Since pain nerves do not carry any other sort of message, the altered toxin his team has created stops pain without affecting touch, for example
Results from tests in mice have been impressive. In three experiments, Foster's painkiller performed as well as morphine at preventing pain. But it was still working nine days later, whereas morphine would have worn off after four hours.
01 May 2004
Talk II
---Here's a brief explanation of the dialectic of the point Adam and Denis(?) were pressing with part of my response, please leave any comments you may have---
---Other readers: This discusses without defining a bunch of theses and views; it will therefore probably be nearly unintelligible to those not at the talk.--
The ease with which the intuitively plausible Kernel View dismissed suggests that PHENOMENOLOGY, SELF CONTAINMENT and TRANSPORTABILITY, did not capture the picture underlying the Kernel View. Perhaps the Kernel View, as I have described it, was a strawman.
The obvious concern is that the Kernel View never was committed to TRANSPORTABILITY. Why should we think, the proponent of the Kernel View might ask, that just because the same stimulus is present in each of two contrast cases, the phenomenology is the same? If the essence of the Kernel View is the intuition that pains are bad because they hurt, it seems that PHENOMENOLOGY and SELF CONTAINMENT are essential. But why add the problematic TRANSPORTABILITY?
Eliminating TRANSPORTABILITY from the Kernel View permits easy rejoinders to many of my arguments. Consider the argument from attention (Section I.A) where I claimed that the Kernel View is committed to the same pain persisting between attention and distraction. But why not simply say that the pain feels different in each case? Why should the Kernel View assume that the same pain is present in each case? While TRANSPORTABILITY plausibly captures an intuitive atomistic dimension of pain, perhaps the cost of including it in the Kernel View is too high.
Abandoning TRANSPORTABILITY would help rehabilitate pain kernels as the basis of the intrinsic badness of pain. If the phenomenology associated with a particular stimulus is labile enough to vary from context to context, then the contextual elements I have identified could serve to explain why the pain feels as it does in a particular case. Differences in contextual elements would then explain why the same stimulus produces pains which feel differently in each of my contrast cases. The badness of the pain might then still depend entirely on how a pain kernel feels as described by PHENOMENOLOGY and SELF CONTAINMENT.
But in thusly revising the Kernel View, it is important to be clear about an ambiguity in what ‘how the pain feels’ and ‘phenomenology’ are referring to. A wide reading of ‘phenomenology’ takes the phenomenology of pain to include the felt components of the conative, affective, and desiderative contextual elements. In a sense, this would make the phenomenology of pain like the phenomenology of audition. Just as a heard sound has pitch, volume, timbre, and density (etc), a felt pain might be thought to have sensory, affective, conative, and doxastic (etc), qualities.
The Revised Kernel View cannot accept this wide reading of ‘phenomenology’. Since variation in these qualities of a felt pain affect its intrinsic badness, this is simply a form of the Iceberg View. It could be a form of the narrow version on which ‘pain’ refers to any phenomenological quality of the pain, or it could be the wide version as written.
Instead, this Revised Kernel View must retain the narrow reading of ‘phenomenology’ that restricts the role of non-sensory contextual elements to affecting the sensory quality of the pain. It is logically possible to claim that these other elements are present in phenomenal consciousness but are not part of the phenomenology of the pain, but that would be implausible. The Revised Kernel View must therefore claim that the other contextual elements are not themselves present in phenomenal consciousness but influence how the (sensory component of the) pain feels. It must be that the pains in each of my contrast cases simply differ in their sensory qualities (where these are those aspects of pain experience described by adjectives such as [insert from McGill Q]). The tenability of the Revised Kernel View thus rests on an empirical issue: Do the pains in my cases differ in their sensory components?
As the empirical literature suggests, there are more quantifiable aspects to the experience of pain which influence its badness than simply the sensory qualities. Thus I submit that the Revised Kernel View is false. Unfortunately, since there are some important issues lurking here about how to interpret the scientific data, the case is admittedly not air-tight.
---Other readers: This discusses without defining a bunch of theses and views; it will therefore probably be nearly unintelligible to those not at the talk.--
The ease with which the intuitively plausible Kernel View dismissed suggests that PHENOMENOLOGY, SELF CONTAINMENT and TRANSPORTABILITY, did not capture the picture underlying the Kernel View. Perhaps the Kernel View, as I have described it, was a strawman.
The obvious concern is that the Kernel View never was committed to TRANSPORTABILITY. Why should we think, the proponent of the Kernel View might ask, that just because the same stimulus is present in each of two contrast cases, the phenomenology is the same? If the essence of the Kernel View is the intuition that pains are bad because they hurt, it seems that PHENOMENOLOGY and SELF CONTAINMENT are essential. But why add the problematic TRANSPORTABILITY?
Eliminating TRANSPORTABILITY from the Kernel View permits easy rejoinders to many of my arguments. Consider the argument from attention (Section I.A) where I claimed that the Kernel View is committed to the same pain persisting between attention and distraction. But why not simply say that the pain feels different in each case? Why should the Kernel View assume that the same pain is present in each case? While TRANSPORTABILITY plausibly captures an intuitive atomistic dimension of pain, perhaps the cost of including it in the Kernel View is too high.
Abandoning TRANSPORTABILITY would help rehabilitate pain kernels as the basis of the intrinsic badness of pain. If the phenomenology associated with a particular stimulus is labile enough to vary from context to context, then the contextual elements I have identified could serve to explain why the pain feels as it does in a particular case. Differences in contextual elements would then explain why the same stimulus produces pains which feel differently in each of my contrast cases. The badness of the pain might then still depend entirely on how a pain kernel feels as described by PHENOMENOLOGY and SELF CONTAINMENT.
But in thusly revising the Kernel View, it is important to be clear about an ambiguity in what ‘how the pain feels’ and ‘phenomenology’ are referring to. A wide reading of ‘phenomenology’ takes the phenomenology of pain to include the felt components of the conative, affective, and desiderative contextual elements. In a sense, this would make the phenomenology of pain like the phenomenology of audition. Just as a heard sound has pitch, volume, timbre, and density (etc), a felt pain might be thought to have sensory, affective, conative, and doxastic (etc), qualities.
The Revised Kernel View cannot accept this wide reading of ‘phenomenology’. Since variation in these qualities of a felt pain affect its intrinsic badness, this is simply a form of the Iceberg View. It could be a form of the narrow version on which ‘pain’ refers to any phenomenological quality of the pain, or it could be the wide version as written.
Instead, this Revised Kernel View must retain the narrow reading of ‘phenomenology’ that restricts the role of non-sensory contextual elements to affecting the sensory quality of the pain. It is logically possible to claim that these other elements are present in phenomenal consciousness but are not part of the phenomenology of the pain, but that would be implausible. The Revised Kernel View must therefore claim that the other contextual elements are not themselves present in phenomenal consciousness but influence how the (sensory component of the) pain feels. It must be that the pains in each of my contrast cases simply differ in their sensory qualities (where these are those aspects of pain experience described by adjectives such as [insert from McGill Q]). The tenability of the Revised Kernel View thus rests on an empirical issue: Do the pains in my cases differ in their sensory components?
As the empirical literature suggests, there are more quantifiable aspects to the experience of pain which influence its badness than simply the sensory qualities. Thus I submit that the Revised Kernel View is false. Unfortunately, since there are some important issues lurking here about how to interpret the scientific data, the case is admittedly not air-tight.
10 April 2004
Bad but not bad for?
I've made use of the distinction between a pain being bad and a pain being bad for someone --this can be taken as roughly tracking either the subjective/objective value distinction or the agent-relative/agent-neutral distinction. While there are a lot of issues that this raises (organic unities, harmless bads, Temkin's 'Slogan', Parfit's Mere Addition Paradox, etc), I want to comment on whether a pain can be bad without being bad for anyone as the arguments below claim.
As I've implied, I think ultimately its not possible to have a pain that is bad but not bad for anyone, but there are examples which should give one pause. I've mentioned fetal pain, here's a few others:
Philosophers love the fact that people given lobotomies and leucotomies for chronic pain tend to report that the pain is still present but that it doesn't bother them. We get similar reports with various opiates and strong sedatives.
People adept at meditation and hypnotic analgesia sometimes report that they are disassociated from their pain while in these states --I seem to remember that the Buddha somewhere advises that when one gives up attachment to her pain, the pain does not go away but she no longer suffers from it.
Finally, I've at times been tempted to argue --for various technical reasons having to do with the way I think pains get their objective and subjective badness-- that certain deserved pains are neither bad nor bad for their sufferer. That is, Hitler's pain wasn't bad for Hitler --when he stubbed his toe, nothing bad for him occurred. If such a conclusion held, then it would seem plausible that there could be pains which were themselves bad but not bad for anyone.
These are, I think, prima facie plausible cases of a pain being bad but not bad for someone (in fact, if we add certain Moorean intuitions about the nature of intrinsic badness --esp., the isolation test-- they can be made even more plausible).
Myself, I think that this plausibility turns on several mistakes about what pains are (notably, identifying pain with its sensory component alone) and some related mistakes about the nature of value. Thus I do not believe that there are pains that are themselves bad but not bad for someone.
But this conclusion is harder to come by than it at first may seem.
As I've implied, I think ultimately its not possible to have a pain that is bad but not bad for anyone, but there are examples which should give one pause. I've mentioned fetal pain, here's a few others:
Philosophers love the fact that people given lobotomies and leucotomies for chronic pain tend to report that the pain is still present but that it doesn't bother them. We get similar reports with various opiates and strong sedatives.
People adept at meditation and hypnotic analgesia sometimes report that they are disassociated from their pain while in these states --I seem to remember that the Buddha somewhere advises that when one gives up attachment to her pain, the pain does not go away but she no longer suffers from it.
Finally, I've at times been tempted to argue --for various technical reasons having to do with the way I think pains get their objective and subjective badness-- that certain deserved pains are neither bad nor bad for their sufferer. That is, Hitler's pain wasn't bad for Hitler --when he stubbed his toe, nothing bad for him occurred. If such a conclusion held, then it would seem plausible that there could be pains which were themselves bad but not bad for anyone.
These are, I think, prima facie plausible cases of a pain being bad but not bad for someone (in fact, if we add certain Moorean intuitions about the nature of intrinsic badness --esp., the isolation test-- they can be made even more plausible).
Myself, I think that this plausibility turns on several mistakes about what pains are (notably, identifying pain with its sensory component alone) and some related mistakes about the nature of value. Thus I do not believe that there are pains that are themselves bad but not bad for someone.
But this conclusion is harder to come by than it at first may seem.
08 April 2004
More on fetal pain
A correspondent has kindly pressed me on whether we really would want to say that fetuses don't feel pain given that newborn's clearly evince pain-behavior. My earlier post was certainly unclear on the matter, so here's a second pass:
Its certainly the case that newborns and therefore late term fetuses experience pain in at least its sensory components (and probably in some of its other more complex affective and conative aspects as well --but this is an empirical matter). And, I agree that the fetus is connected to its body in a relevant way. In fact, its probably the case that, the fetus/newborn is more connected to its body in the experience of pain than an adult human is to hers, since it doesn't have the sense of self as something above our bodies that we seem to.
My only point (insofar as I have a clear opinion on the proper account --I meant the post to mostly bring out some of the hard issues involved) is that by lacking the higher order capacities that adult humans and even adult housecats do, fetal/newborn pain has a different normative significance than adult human and housecat pain. The extreme version of this claim (which I probably myself don't endorse) is that a fetus being in pain is bad but not bad in a way that is bad for the fetus --its a hard distinction, its roughly the same point as the claim that the fetus feels pain but doesn't suffer.
Now, if this is coherent, inflicting pain upon fetuses is still bad and therefore ought to be avoided. (and presumably this is easy to do via opiates --indeed, from some of the literature on anesthesia during surgery on newborns it seems that low-dose opiates are safe in newborns-- and I suppose safety for the fetus isn't so much a concern in an abortion). What it does deny is the presumption that if the fetus feels pain it ought to be due certain legal protections in virtue of the pain being evidence for the fetus's moral status as a person (though that might be established on other grounds). Since that's the context in which the question of fetal pain usually gets raised, in the post I suggested that the proper (short) answer to the judge's question is no.
In any event, while I've thought a lot about pain and value in general, I haven't thought too much about the specific question of fetal pain (its going to be a section in a later chapter of my dissertation which I haven't yet begun), so its entirely possible that I'm all wrong about this. Still, the topic is hard and interesting; I'll greatly appreciate any further comments.
Its certainly the case that newborns and therefore late term fetuses experience pain in at least its sensory components (and probably in some of its other more complex affective and conative aspects as well --but this is an empirical matter). And, I agree that the fetus is connected to its body in a relevant way. In fact, its probably the case that, the fetus/newborn is more connected to its body in the experience of pain than an adult human is to hers, since it doesn't have the sense of self as something above our bodies that we seem to.
My only point (insofar as I have a clear opinion on the proper account --I meant the post to mostly bring out some of the hard issues involved) is that by lacking the higher order capacities that adult humans and even adult housecats do, fetal/newborn pain has a different normative significance than adult human and housecat pain. The extreme version of this claim (which I probably myself don't endorse) is that a fetus being in pain is bad but not bad in a way that is bad for the fetus --its a hard distinction, its roughly the same point as the claim that the fetus feels pain but doesn't suffer.
Now, if this is coherent, inflicting pain upon fetuses is still bad and therefore ought to be avoided. (and presumably this is easy to do via opiates --indeed, from some of the literature on anesthesia during surgery on newborns it seems that low-dose opiates are safe in newborns-- and I suppose safety for the fetus isn't so much a concern in an abortion). What it does deny is the presumption that if the fetus feels pain it ought to be due certain legal protections in virtue of the pain being evidence for the fetus's moral status as a person (though that might be established on other grounds). Since that's the context in which the question of fetal pain usually gets raised, in the post I suggested that the proper (short) answer to the judge's question is no.
In any event, while I've thought a lot about pain and value in general, I haven't thought too much about the specific question of fetal pain (its going to be a section in a later chapter of my dissertation which I haven't yet begun), so its entirely possible that I'm all wrong about this. Still, the topic is hard and interesting; I'll greatly appreciate any further comments.
01 April 2004
Do fetuses feel pain?
Here's a place in the law where some very deep and difficult issues of science, philosophy of mind, and ethics, come out in a courtroom.
A doctor who performs abortions found himself quizzed by a federal judge about whether a fetus feels pain during a controversial abortion procedure and if the physician worries about that possibility. The inquiry, at times graphic, came in U.S. District Court on Wednesday after lawyers on both sides had finished questioning Dr. Timothy Johnson, a plaintiff in one of three lawsuits brought to try to stop enforcement of the Partial-Birth Abortion Ban Act.
"Does the fetus feel pain?" Judge Richard C. Casey asked Johnson, saying he had been told that studies of a type of abortion usually performed in the second trimester had concluded they do. Johnson said he did not know, adding he knew of no scientific research on the subject.
...
The simultaneous litigation centers on the ban of what lawmakers defined as "partial-birth" abortion and what doctors call "intact dilation and extraction" - or D&X. In the procedure, a fetus is partially delivered and its skull is punctured. An estimated 2,200 to 5,000 such abortions are performed annually in the United States, out of 1.3 million total abortions.
Government lawyers say the law protects fetuses from pain during the abortion procedures that usually involve crushing the soft skull or draining brain tissue to shrink the fetus to a size in which it can be pulled from the body.
Link
Behind the question 'does the fetus feel pain?' lies several important issues surrounding pain and the nature of value. Since these are my specialty, let me try to briefly sort out some of them.
The first is the question whether pains are necessarily (intrinsically) bad. Most people believe that this has to be true (indeed, many think it is a conceptual truth about pain). Assume it is true.
It may very well be that late-stage fetuses have the neurology necessary for processing nociception (the signals produced by painful stimuli). If so, and if phenomenological states supervene on neural states, then fetuses plausibly are capable of having the sensory component of pains (roughly, the 'hurting' of the pain). So if something is a pain by virtue of its phenomenology --how it feels--, then it would follow that (a) fetuses can have pains, and (b) the pains fetuses have are bad. (Notice that this is not yet an answer to the judge's question --having pain may be distinct from feeling pain)
The question is then whether the pain is bad for the fetus.
Some plausible interpretations of cases involving patients with leucotomies or otherwise disassociated from their pains suggest that a pain isn't bad for someone unless she identifies with it as hers. Hence a potential difference between 'having pain' and 'feeling pain'. Clearly, a fetus doesn't have the sense of self necessary for identifying with its pain, and so the fetus's pain might be bad, but not bad for the fetus. (If that sounds incoherent, good. I do think we should reject the claim that all putative pains are intrinsically bad; but I'm just trying to organize the issues here.) Thus the law would protect no interests of the fetus in protecting it from pain; no more than proscribing the infliction of pain on chairs.
Above I assumed that we could take x to be a pain in virtue of x having the sensory component of pain. Is that correct?
This again is a hard question. In the famous McGill dog study (references on request), some researchers raised puppies without seeing older dogs react to painful stimuli. When these puppies were grown, they'd do things like lick red-hot heating pipes or repeatedly nuzzle lit matches with very little adverse reaction. Since they had, ex hypothesi, roughly the same neural architecture as other dogs, we can assume that they had the sensory component of pain. This combined with everything we know about the conative and affective components of pain (emotions, disliking the pain, being motivated to escape it, etc), suggests that, if we think that pains are necessarily bad, we should think that there is more to pains than their sensory components. Since fetuses do not have the capacity for these other components of pains, it follows that they do not have pains.
So, I suggest then, that the proper answer to the judge's question is 'no'. But I've only skimmed the surface here of several very important and deeply contentious issues in pain science, philosophy of mind, and ethics, so I don't expect this brief comment to convince many. Indeed, these claims only follow from the assumption that all pains are intrinsically bad.
If readers are interested, I'll return to the issues in more depth and detail in later posts.
A doctor who performs abortions found himself quizzed by a federal judge about whether a fetus feels pain during a controversial abortion procedure and if the physician worries about that possibility. The inquiry, at times graphic, came in U.S. District Court on Wednesday after lawyers on both sides had finished questioning Dr. Timothy Johnson, a plaintiff in one of three lawsuits brought to try to stop enforcement of the Partial-Birth Abortion Ban Act.
"Does the fetus feel pain?" Judge Richard C. Casey asked Johnson, saying he had been told that studies of a type of abortion usually performed in the second trimester had concluded they do. Johnson said he did not know, adding he knew of no scientific research on the subject.
...
The simultaneous litigation centers on the ban of what lawmakers defined as "partial-birth" abortion and what doctors call "intact dilation and extraction" - or D&X. In the procedure, a fetus is partially delivered and its skull is punctured. An estimated 2,200 to 5,000 such abortions are performed annually in the United States, out of 1.3 million total abortions.
Government lawyers say the law protects fetuses from pain during the abortion procedures that usually involve crushing the soft skull or draining brain tissue to shrink the fetus to a size in which it can be pulled from the body.
Link
Behind the question 'does the fetus feel pain?' lies several important issues surrounding pain and the nature of value. Since these are my specialty, let me try to briefly sort out some of them.
The first is the question whether pains are necessarily (intrinsically) bad. Most people believe that this has to be true (indeed, many think it is a conceptual truth about pain). Assume it is true.
It may very well be that late-stage fetuses have the neurology necessary for processing nociception (the signals produced by painful stimuli). If so, and if phenomenological states supervene on neural states, then fetuses plausibly are capable of having the sensory component of pains (roughly, the 'hurting' of the pain). So if something is a pain by virtue of its phenomenology --how it feels--, then it would follow that (a) fetuses can have pains, and (b) the pains fetuses have are bad. (Notice that this is not yet an answer to the judge's question --having pain may be distinct from feeling pain)
The question is then whether the pain is bad for the fetus.
Some plausible interpretations of cases involving patients with leucotomies or otherwise disassociated from their pains suggest that a pain isn't bad for someone unless she identifies with it as hers. Hence a potential difference between 'having pain' and 'feeling pain'. Clearly, a fetus doesn't have the sense of self necessary for identifying with its pain, and so the fetus's pain might be bad, but not bad for the fetus. (If that sounds incoherent, good. I do think we should reject the claim that all putative pains are intrinsically bad; but I'm just trying to organize the issues here.) Thus the law would protect no interests of the fetus in protecting it from pain; no more than proscribing the infliction of pain on chairs.
Above I assumed that we could take x to be a pain in virtue of x having the sensory component of pain. Is that correct?
This again is a hard question. In the famous McGill dog study (references on request), some researchers raised puppies without seeing older dogs react to painful stimuli. When these puppies were grown, they'd do things like lick red-hot heating pipes or repeatedly nuzzle lit matches with very little adverse reaction. Since they had, ex hypothesi, roughly the same neural architecture as other dogs, we can assume that they had the sensory component of pain. This combined with everything we know about the conative and affective components of pain (emotions, disliking the pain, being motivated to escape it, etc), suggests that, if we think that pains are necessarily bad, we should think that there is more to pains than their sensory components. Since fetuses do not have the capacity for these other components of pains, it follows that they do not have pains.
So, I suggest then, that the proper answer to the judge's question is 'no'. But I've only skimmed the surface here of several very important and deeply contentious issues in pain science, philosophy of mind, and ethics, so I don't expect this brief comment to convince many. Indeed, these claims only follow from the assumption that all pains are intrinsically bad.
If readers are interested, I'll return to the issues in more depth and detail in later posts.
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]
Gender
Categories: Environment
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]
Gender
Categories: Environment
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
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
Bibliography
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
Abstract
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
Abstract
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
Abstract
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.
Categories: Gender, Anxiety
study with topical capsaicin
Maud Frota, Jocelyne S. Feine, M. Catherine Bushnella
Pain 108 (2004) 230–236
Abstract
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.
Categories: Gender, Anxiety
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
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
Interesting
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
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."
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?
Link
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...)
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
HYPNOSIS DOESN'T IMPROVE PAIN RELIEF STRATEGIES
Link
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.
Link
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.
Link
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.
Link
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.
Link
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.
Categories: Gender, Hormones
Link
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.
Categories: Gender, Hormones
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
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.
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
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
By DINITIA SMITH
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.
By DINITIA SMITH
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).
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.
Categories: Congenital insensitivity 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.
Categories: Congenital insensitivity to pain
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