Thoughts about 'C-fibers firing'

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)

"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.

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

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.

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

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.

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.

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

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.

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.