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While awareness of qualitative research of lived pain is slowly increasing in the field of pain, it is far from established and needs cultivating from within the field by pain researchers (Mitchell & MacDonald, 2009; Osborn & Rodham, 2010; Price & Barrell, 2012). Pain research has traditionally been dominated by quantitative research methods, which have their roots in physiology, physics, biology, and psychophysics, arising from mathematics, statistics, and psychometrics (Price et al. 2002; Price & Aydede, 2005; Price & Barrell, 2012). This trend continues unabated today, and perhaps explains why Osborn and Rodham (2010) found that many individual pain researchers have not yet accumulated a significant body of qualitative pain research. A body of qualitative pain research would enable researchers to develop their arguments in more depth concerning the nature and types of personal meanings apparent in pain experience, especially clinical pain experiences across the lifespan. The rationale for conducting qualitative pain research is likely not clear to many in the field of pain, and researchers are probably unaware of the potential richness of qualitative pain data to uniquely describe lived pain or the diverse tools available for analyzing qualitative data. In line with this, Osborn & Rodham (2010) found that many of the qualitative pain studies they reviewed used only one type of analysis (i.e., data analysis was not triangulated), description rather than interpretation prevailed in discussion of data meaning, and research methods were not thoroughly described.

A powerful reason to conduct more qualitative pain research is the common complaint from clinical pain patients that they feel they have never had an opportunity to fully explore their lived pain experiences with health care professionals, that no one has ever fully understood what is wrong with them and, most importantly, that no one appears to be listening (e.g., Melzack, 1990; Hoffmann & Tarzian, 2001; Hansson et al. 2011; McGee et al. 2011; Thacker & Moseley, 2012; De Ruddere et al. 2014). Clinical failure to sufficiently appreciate patient pain and its felt meanings can result in profound patient dissatisfaction, exacerbation of feelings of isolation and confusion, among other negative existential appreciations, and cause up-regulation of nociception (Butler et al. 2003). Despite this significant problem in the treatment and management of clinical pain, some pain researchers (e.g., Apkarian et al. 2011; Wortolowska, 2011) and government agencies (e.g., National Research Council of the National Academies, 2008; National Institutes of Health, 2011) have argued for replacing first-person patient experiential pain data with brain-imaging data.

Although qualitative research alone cannot solve these challenges, because of its exploratory nature, it can complement quantitative clinical pain research to describe lived pain and the psychosocial factors that improve or worsen the efficacy of pain interventions, as well as core intervention components that are associated with desired or undesired patient outcomes (Price et al. 2002; Price & Aydede, 2005; Price & Barrell, 2012; Thacker & Moseley, 2012).

References

Apkarian, A. V., Hashmi, J. A., & Baliki, M. N. (2011). Pain and the brain: specificity and plasticity of the brain in clinical chronic pain. Pain, 152(3 Suppl), S49–64.

De Ruddere, L., Goubert, L., Stevens, M. A. L., Deveugele, M., Craig, K. D., & Crombez, G. (2014). Health Care Professionals” Reactions to Patient Pain: Impact of Knowledge About Medical Evidence and Psychosocial Influences. The Journal of Pain, 15(3), 262–270.

Hoffmann, D. E., & Tarzian, A. J. (2001). The girl who cried pain: a bias against women in the treatment of pain. The Journal of Law, Medicine & Ethics, 28(s4), 13–27.

McGee, S. J., Kaylor, B. D., Emmott H., & Christopher, M. J. (2011). Defining chronic pain ethics. Pain Medicine, 12, 1376–1384.

Melzack, R. (1990). The tragedy of needless pain. Scientific American, 262(2), 27–33.

National Institutes of Health. (2011). Biomarkers for chronic pain using functional brain connectivity. Common Fund NIH Government.

National Research Council of the National Academies. Emerging cognitive neuroscience and related technologies. (2008). Washington, DC: National Academies Press.

Price, D. D., & Aydede, M. (2005). The experimental use of introspection in the scientific study of pain and its integration with third-person methodologies: The experiential-phenomenological approach. In M. Aydede (Ed.), Pain: New Essays on its Nature and the Methodology of its Study (pp. 243–273). Cambridge, Mass.: MIT Press.

Price, D. D., & Barrell, J. J. (2012). Inner Experiences and Neuroscience. Merging the two perspectives. Cambridge, Mass.: MIT Press.

Price, D. D., Barrell, J. J., & Rainville, P. (2002). Integrating experiential-phenomenological methods and neuroscience to study neural mechanisms of pain and consciousness.

Thacker, M. A., & Moseley, G. L. (2012). First-person neuroscience and the understanding of pain. The Medical Journal of Australia, 196(6), 410–411.

Wortolowska, K. (2011). How neuroimaging can help us to visualise and quantify pain? European Journal of Pain, 5, 323–327.

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The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” The IASP definition of pain includes in its notes, “Pain is always subjective”. The term “subjective” emphasizes that pain is a conscious experience rather than simply a causal result of unconscious nociceptive processing. The intuition underlying the IASP definition of pain is that if a pain is not being consciously felt by its owner then it does not exist.

Up until the late twentieth century, it was widely believed by pain researchers that conscious pain could not be felt by humans in sleep because sleep is an unconscious state. This pre-scientific intuition about pain has since been undermined by numerous scientific studies showing that both stimulus-induced and non-stimulus induced pain reported during rapid eye movement (REM) sleep does not always result in subject wakefulness and that pain can also feature in dreams (e.g., Nielsen et al. 1993; Zadra et al. 1998; Raymond et al. 2002; Knoth & Schredl, 2011). Concerning dream pain, Zadra et al. (1998) found that 48.2% of subjects reported that they have had at least one pain dream in their lives, although only 0.62% of recorded dreams in home diary studies contain clear reference to pain feelings and meanings. In some subjects, dream pain continues to be felt following wakefulness; in other subjects, it is rapidly terminated after awakening. These divergent findings prompt the causal question: Why does dream pain exist and have the nature it does?

To explain dream pain, Schredl (2003) proposed that there is continuity between wakeful and dream pain such that pain regularly felt when awake is causally efficacious concerning its occurrence in dreams. Raymond et al. (2002) investigated Schredl’s “continuity hypothesis” in hospitalized burn patients and healthy control subjects and found that patients reported a significantly higher rate of dreamed pain than controls. The burn patients also reported marginally more intense pain during wakeful medical procedures, a finding which was interpreted by Raymond et al. (2002) to support the continuity hypothesis. The patients reported constant pain during wakefulness, which further supports the continuity hypothesis. However, there are three further competing interpretations of the data presented in Raymond et al. (2002). Since dreamed pain was not always reported as located in injured body regions or in bodily areas patients reported pain in during the night and following awakening, Raymond et al. (2002) speculated that dream pain might not be causally continuous with wakeful pain experiences, but with a personal pain memory trace formed after wakeful pain experiences. In support of this interpretation of the data, Jantsch et al. (2009) showed the existence of a reliable long-term memory trace for experimentally induced pain sensations. This finding would explain the rarity of reported dream pain in controls since pain is rare in their everyday experience. A competing causal explanation of the data in Raymond et al. (2002) is that some dreamers report pain they had never experienced in real life (e.g., dream pain in a fictional fight situation) (Schredl, 2011). In support of this view, Danziger et al. (2009) found that people with congenital insensitivity to pain show patterns of brain activation in shared-circuits for “self” and “other” pain while observing pain in other persons. This finding leads to the proposal that pain observed externally in others or in electronic media might also explain dream pain (Borsook & Beccera, 2009).

Thus, the three explanations on offer to explain why dream pain occurs are: (1) Dream pain is causally continuous with wakeful pain experiences; (2) Dream pain is causally continuous with personal pain memories formed after wakeful pain experiences; and (3) Dream pain is causally continuous with pain observed externally in others or in electronic media during wakefulness. These competing explanations show that the task of explaining why dream pain occurs is still very much an open question in the field, and more research on the topic is needed.

References

  1. Borsook D, Becerra L. Emotional Pain without Sensory Pain-Dream On? Neuron 2009; 61(2):153–155.
  2. Danziger N, Faillenot I, Peyron R. Can We Share a Pain We Never Felt? Neural Correlates of Empathy in Patients with Congenital Insensitivity to Pain. Neuron 2009; 61(2):203–212.
  3. Jantsch HHF, Gawlitza M, Geber C, Baumgärtner U, et al. Explicit episodic memory for sensory discriminative components of capsaicin–induced pain: Immediate and delayed ratings. Pain 2009; 143(1–2):97–105.
  4. Nielsen TA, McGregor DL, Zadra A, et al. Pain in dreams. Sleep 1993; 16: 490–498.
  5. Raymond I, Nielsen TA, Lavigne G, et al. Incorporation of pain in dreams of hospitalized burn victims. Sleep 2002; 25: 765–770.
  6. Schredl M, Erlacher, D. Lucid dreaming frequency and personality. Personality and Individual Differences 2004; 37(7): 1463–1473.
  7. Schredl M. Continuity between waking and dreaming: a proposal for a mathematical model. Sleep and Hypnosis 2003; 5: 38–52.
  8. Zadra AL, Nielsen TA, Germain A, et al. The nature and prevalence of pain in dreams. Pain Research and Management 1998; 3: 155–161.
  9. Zappaterra M, Jim L, and Pangarkar, S. Chronic pain resolution after a lucid dream: A case for neural plasticity? Medical hypotheses 2014; 82(3): 286–290.
Philosophical Thesis  Type Identity
Theory 
Eliminative
Materialism
Realism – Pain is real. Yes No
Materialism – Pain is neurophysiological. Yes Yes
Minimal Reductionism – Pain is nothing more than neurophysiological mechanism. Yes Yes
Identity – Pain is identical to a
neurophysiological mechanism.
Yes No
Naturalistic – Philosophies of pain are both metaphysical and scientific theories. Yes Yes
Theoretical – Metaphysical theories of pain can
be assessed according to their theoretical virtues (e.g., simplicity), and competing empirical predictions.
Yes Yes

 

Polger, T. W. (2011). Are sensations still brain processes? Philosophical Psychology, 24(1), 1-21.

 

The personal experience of pain produces a reliable effect on facial behavior in humans and in nonhuman mammals. Why should pain have a face? What is it for? I will attempt to head towards answering this question by invoking a theoretical framework: polyvagal theory (Porges, 2001, 2006).

1 Polyvagal Theory

According to polyvagal theory (Porges, 2001, 2006), evolution of neural control within the autonomic nervous system (ANS) has tracked three stages, each revealing a specific behavior, and a specific function:

In the first stage, the ancient unmyelinated visceral vagus nerve that enables digestion could respond to danger and pain only by reducing metabolic output and producing immobilization behaviors.

In the second stage, the sympathetic nervous system (SNS) made it possible to increase metabolic activity and inhibit the visceral vagus nerve, thus allowing fight/flight behaviors following perceived threat or pain.

The third stage, which is uniquely mammalian, involves a myelinated vagus that can rapidly control cardiac and bronchi output to enable spontaneous interaction (i.e., engagement or disengagement) with the environment. The interaction of the autonomic nervous system (ANS) with the hypothalamo-pituitary-adrenal (HPA) axis, nervous and immune systems change to maximize response to stressors such as nociception. During nociception, the ANS operates together with nervous, endocrine and immune systems to produce stress (Chapman et al. 2008; Porges, 2001, 2006). In terms of polyvagal theory, pain facial expression is a dynamic autonomic response caused by noxious signaling. In terms of polyvagal-type identity mechanistic theory pain facial expression is a type of behavior that is identical to a type of neurophysiological mechanism; namely, the phylogenetically recent brain-heart-face mechanism.

The expansion of cortex in the third stage increased innervation and neural control of the mammalian face: upper face innervation is bilateral and arises from the supplementary motor area (M2) and the rostral cingulate motor area (M3). Lower face innervation is contralateral and arises from primary motor cortex (M1), ventral lateral premotor cortex, and the caudal cingulate motor cortex (M4) (Morecraft et al. 2004). Human pain facial movements of the eyebrows and upper lip are type identical with negative emotional aspects of pain and activation of M1, M2, M3, whereas facial movements around the eyes are type identical with somatosensory aspects of pain, and activation of M2 and M3 (Kunz et al. 2011). Thus, evolution of cranial anatomy enabled a highly integrated facial representation of the multidimensional experience of pain.

2 Why Pain Should Have a Face

In clinical and experimental settings, the pain face is observed to rapidly appear following noxious stimulation, and diminish concurrent with cessation of the noxious stimulus, or when analgesics are administered (e.g., Craig & Patrick, 1985). The brain-heart-face mechanism is an integrated system with both a somatomotor part controlling the striated facial muscles and a visceromotor part controlling the heart through a myelinated vagus nerve (Porges, 2001, 2006). When the vagal tone to the cardiac pacemaker is high, the myelinated vagus acts as a brake or restraint limiting heart rate. Rapid inhibition and disinhibition of vagal tone to the heart supports the rapid mobilization of facial muscles and formation of the pain face concurrent with pain onset. In humans and nonhuman mammals, the main vagal inhibitory pathways in the myelinated vagus originate in the nucleus ambiguus.

The vagal brake supports the low-metabolic requirements involved in the rapidly appearing and disappearing pain face. Withdrawal of the vagal brake is strongly correlated with the rapid appearance of the pain face; reinstatement of the vagal brake is strongly correlated with the rapid diminishing of the pain face. These correlations are not unique to pain facial expression; similar relationships hold with regard to the vagal brake and the timing and duration of aversive, but non-noxious emotional facial expressions (e.g., Pu et al. 2010), and positive emotional facial expressions (e.g., Kok & Fredrickson, 2010).

In terms of the function of rapid pain face onset and offset, the vagal brake makes it possible for the individual in pain to quickly disengage from source of wounding and pain, concurrent with the rapid appearance or diminishing of pain facial expression, which may offer temporary access to additional metabolic resources to aid healing, recovery and self-soothing behaviors, with likely involvement from care givers.

Concerning aid from others, the vagal brake reliably maps onto specific interaction types observed in mammalian pain events. In pain events comprising the individual in pain and care givers, mammalian behavior is typed according to interpersonal communication through facial expressions, vocalizations, head and hand gestures (Hadjistavropoulos et al. 2011; Porges, 2001, 2006; Williams, 2002). A relevant feature is the rapid ‘switching’ of temporary engagement to temporary disengagement behaviors between the individual in pain and care givers. This interaction type may involve care givers speaking to the one in pain, and then quickly switching to listening; for the one in pain, looking into the face of the care giver, and then quickly switching to vocalizing (Craig et al. 2011; Hadjistavropoulos et al. 2011; Porges, 2001, 2006; Williams, 2002). The brain-heart-face mechanism thus allows the one in pain and the care giver to get the timing right. Some philosophers and neuroscientists claim that evolutionary neurobehavioral solutions to timing problems such as these are implicated in the origin of empathy and ultimately consciousness itself (Churchland, 2002; Cole, 1998; Engen & Singer, 2012; van Rysewyk, 2011).

However, if pain is severe or chronic and the vagal brake is withdrawn (or dysfunctional), the concurrency of increased pain facial expression, cardiac output, and other mobilization behaviors (i.e., increased SNS and HPA output), means that, if care giving is to succeed in promoting healing and recovery, the care giver’s vagal brake must be dynamically reinstated. By applying their own vagal brake, care givers may regulate their own visceral distress and thereby succeed in allocating valuable metabolic resources to communicate safety to the one in pain (and themselves) through calming facial and head behaviors, eye gaze, and prosodic vocalizations (i.e., increasing the vagal brake decreases SNS and HPA output). Since the vagal brake of the person in pain has been provisionally withdrawn, the care giver is effectively an integrated external brain-heart-face mechanism (cf. Tantam, 2009, the ‘interbrain’).

Thus, the pain facial muscles function as neural timekeepers detecting and expressing features of safety and danger that cue the one in pain to quickly disengage from the source of wounding and pain, simultaneous with the rapid appearance or attenuation of pain facial activity, and also cue others who can help.

References

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. Journal of Pain, 9(2), 122-145.

Churchland, P. S. (1989). Neurophilosophy: Toward a Unified Science of the Mind-Brain. Cambridge, Mass.: MIT Press.

Cole, J. (1998) About face. Cambridge, Mass.: The MIT Press.

Craig, K. D., & Patrick, C. J. (1985). Facial expression during induced pain. Journal of Personality and Social Psychology, 48(4), 1080-1091.

Craig, K. D., Prkachin, K. M., & Grunau, R. E. (2011). .The facial expression of pain. In D. C. Turk, & R. Melzack, Handbook of Pain Assessment, 2nd Edition (pp. 117-133). New York: The Guilford Press.

Engen, H. G., & Singer, T. (2012). Empathy circuits. Current Opinion in Neurobiology, 23, 1-8.

Hadjistavropoulos, T., Craig, K. D., Duck, S., Cano, A., Goubert, L., Jackson, P. L., Mogil, J. S., Rainville, P., Sullivan, M. J. L., de C. Williams, Amanda C., Vervoort, T., & Fitzgerald, T. D. (2011). A biopsychosocial formulation of pain communication. Psychological Bulletin, 137(6), 910-939.

Kok, B. E., & Fredrickson, B. L. (2010). Upward spirals of the heart: Autonomic flexibility, as indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social connectedness. Biological Psychology, 85(3), 432-436.

Kunz, M., Lautenbacher, S., LeBlanc, N., & Rainville, P. (2011). Are both the sensory and the affective dimensions of pain encoded in the face? Pain, 153(2), 350-358.

Morecraft, R. J., Stilwell-Morecraft, K. S., & Rossing, W. R. (2004). The Motor Cortex and Facial Expression: New Insights From Neuroscience. The Neurologist, 10(5), 235-249.

Porges, S. W. (2001). The polyvagal theory: phylogenetic substrates of a social nervous system. International Journal of Psychophysiology, 42(2), 123-146.

Porges, S. W. (2006). Emotion: An Evolutionary By‐Product of the Neural Regulation of the Autonomic Nervous System. Annals of the New York Academy of Sciences, 807(1), 62-77.

Pu, J., Schmeichel, B. J., & Demaree, H. A. (2010). Cardiac vagal control predicts spontaneous regulation of negative emotional expression and subsequent cognitive performance. Biological Psychology, 84(3), 531-540.

van Rysewyk, S. (2011). Beyond faces: The relevance of Moebius Syndrome to emotion recognition and empathy. In: A. Freitas-Magalhães (Ed.), ‘Emotional Expression: The Brain and the Face’ (V. III, Second Series), University of Fernando Pessoa Press, Oporto: pp. 75-97.

Williams, A. C. D. C. (2002). Facial expression of pain: an evolutionary account. Behavioral and Brain Sciences, 25(4), 439-455.

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The official scientific definition of pain was initially formulated in the 1980s by a committee organized by the International Association for the Study of Pain (IASP). This definition was updated in the 1990s by the IASP to reflect advancements in pain science and has since been widely accepted by the scientific community:

Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Note:The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain. Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report. If they regard their experience as pain, and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause (IASP-Task-Force-On-Taxonomy, 1994: 207-213).

An apparent immediate and inconvenient fact facing pain reductionism is that pain stubbornly resists identification with only the brain. The original pain identity statement, ‘Pain = C-fibre activation’ (Place, 1956), neglects two essential features of pain observed in contemporary pain science: (1) Conscious awareness of wounding is multimodal and is correlated with integrated visual, kinaesthetic, and enteric sensory modalities in addition to noxious signalling (e.g., Chapman et al. 2008); (2) Wounding is typically part of overall bodily awareness that is correlated with multiple reciprocal nervous, endocrine and immune states (e.g., Chapman et al. 2008; Lyon et al. 2011; van Rysewyk, 2013; Vierck et al. 2010). Convergent lines of evidence demonstrate that wounding followed by pain is strongly correlated with endocrine and immune operations as well as sensory signaling that together exert an extensive non-neural impact. These operations interact and comprise a defensive stress response to wounding [1].

A consideration of the higher structures of the central nervous system (CNS) alone reveals an extraordinarily complex picture of pain. Unimodal functional brain imaging studies of nociceptive transmission, projection and processing show that signals of wounding reach higher CNS levels via the spinothalamic, spinohypothalamic, spinoreticularpathways (i.e., the paleospinothalamic tract) including the locus caeruleus (LC) and the solitary nucleus, spinopontoamygdaloid pathways, the periaqueductal gray (PAG), and the cerebellum (e.g., Burstein et al. 1991; Price, 2000). The thalamus (THA) projects to limbic areas including the insula and anterior cingulate, which have been identified with the integration of the emotional and motivational features of pain (Craig, 2002, 2003a, 2003b). Noradrenergic pathways from the LC project to these and other limbic structures. Accordingly, pain reveals extensive limbic, prefrontal and somatosensory cortical components. A meta-analysis of the literature described brain operations during pain as a complex network involving THA, primary and secondary somatosensory cortices (S1, S2), insula (INS), anterior cingulate (ACC), and prefrontal cortices (Apkarian et al. 2005). Thus, the brain engages in massive, distributed, parallel processing in response to noxious signaling.

The mechanisms of multimodal integration pose a formidable challenge for pain scientists. Hollis et al. (2004) examined how catecholaminergic neurons in the solitary nucleus integrate visceral and somatosensory information when peripheral inflammation is present. Pre-existing fatigue, nausea, intense physiological arousal, and a systemic inflammatory response induced by proinflammatory cytokines (e.g., Anderson, 2005; Eskandari et al. 2003) are all correlated with sensory signalling in the experience of pain. In addition to Craig (2002, 2003a, 2003b), an increasing number of studies have investigated the integration of information from multiple sensory modalities and central operations correlated with emotion and cognition in pain (e.g., Bie et al. 2011; Liu et al. 2011; Neugebauer et al. 2009). The more we are able to delineate the qualia of pain and map these experiences onto specific multimodal physical operations, the closer we come to identifying pain with those operations.

So, why has Place’s (1956) original pain identity statement survived in philosophy of mind? One reason is that the use of ‘C-fibre activation’ by identity philosophers is merely a placeholder for whatever the eventual mechanisms of nervous systems prove to be. We now know that wounding is identical to specific endocrine and immune operations in addition to sensory signaling. These operations interact and in concert comprise a defensive stress response to wounding. However, the purpose of calling it the identity theory of mind is to separate it from philosophical theories that identify mental states with states of immaterial souls or minds (dualism), abstract machine systems (functionalism), or those theories that reject the reality of mental states (eliminativism). It is not to make any substantive assumption about the sensory modality. This is why Place’s (1956) pain identity claim of C-fibre activation has survived, despite being explanatorily incomplete.

[1]In clinical settings, problems of acute and chronic pain do not easily conform to pain-brain type identities. The persistence of chronic pain as a major problem in medicine may indicate that identifying pain with the brain (‘pain in the brain’) has failed to inform clinicians toward curative interventions (e.g., Chapman et al. 2008).

References

Anderson, J. (2005). The inflammatory reflex-introduction. Journal of Internal Medicine, 257(2), 122-125.

Apkarian, A. V., Bushnell, M. C., Treede, R. D., & Zubieta, J. K. (2005). Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain, 9(4), 463-463.

Bie, B., Brown, D. L., & Naguib, M. (2011). Synaptic plasticity and pain aversion. European Journal of Pharmacology, 667(1), 26-31.

Burstein, R., Dado, R. J., Cliffer, K. D., & Giesler, G. J. (1991). Physiological characterization of spinohypothalamic tract neurons in the lumbar enlargement of rats. Journal of Neurophysiology, 66(1), 261-284.

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. The Journal of Pain, 9(2), 122-145.

Craig, A. D. (2002). How do you feel? Interoception: the sense of the physiological condition of the body. Nature Reviews Neuroscience, 3(8), 655-666.

Craig, A. D. (2003a). A new view of pain as a homeostatic emotion. Trends in Neurosciences, 26(6), 303-307.

Craig, A. D. (2003b). Pain mechanisms: labeled lines versus convergence in central processing. Annual Review of Neuroscience, 26, 1-30.

Eskandari, F., Webster, J. I., & Sternberg, E. M. (2003). Neural immune pathways and their connection to inflammatory diseases. Arthritis Research and Therapy, 5(6), 251-265.

IASP-Task-Force-On-Taxonomy (1994). IASP Pain Terminology. In H. Merskey & N. Bogduk (Eds.), Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms (pp. 209-214). Seattle: IASP Press.

Liu, C. C., Shi, C. Q., Franaszczuk, P. J., Crone, N. E., Schretlen, D., Ohara, S., & Lenz, F. A. (2011). Painful laser stimuli induce directed functional interactions within and between the human amygdala and hippocampus. Neuroscience, 178, 208-217.

Lyon, P., Cohen, M., & Quintner, J. (2011). An Evolutionary Stress‐Response Hypothesis for Chronic Widespread Pain (Fibromyalgia Syndrome). Pain Medicine, 12(8), 1167-1178.

Neugebauer, V., Galhardo, V., Maione, S., & Mackey, S. C. (2009). Forebrain pain mechanisms. Brain Research Reviews, 60(1), 226.

Place, U. T. (1956). Is consciousness a brain process? British Journal of Psychology, 47, 44-50.

Price, D. D. (2000). Psychological and neural mechanisms of the affective dimension of pain. Science, 288(5472), 1769-1772.

van Rysewyk, S. (2013). Pain is Mechanism. Doctoral Dissertation, University of Tasmania.

Vierck, C. J., Green, M., & Yezierski, R. P. (2010). Pain as a stressor: effects of prior nociceptive stimulation on escape responding of rats to thermal stimulation. European Journal of Pain, 14(1), 11-16.

The International Association for the Study of Pain (IASP) defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’ (Merskey & Bogduk, 1994). The IASP definition of pain is unique in that it explicitly recognizes that pain is an experience that can be understood in itself, in an internal way, in contrast to prior definitions (Sternbach, 1968; Mountcastle, 1974) that defined pain in terms of external causal stimuli that are correlated in some way with pain feelings and sensations.

External characterizations of pain based on neuroscientific findings remain influential in the pain literature. For example, according to a leading theory, pain feelings and sensations are externally related to a brain image of the ‘afferent representation of the physiological condition of the body’ (Craig, 2003). Interpreted philosophically, this view of pain is analogous to the traditional rational-metaphysical presupposition that feelings are but ‘sensations or emotions of the soul which are related especially to it,’ as Descartes put it, and thus are features only of the self and not of the world.

But pain is not only a personal feeling adhering to the self but that through my pain I am connected to a felt reality of the world. This world is not a world of causal reasons but a world that tonally flows in a certain direction and manner (Smith, 1986). When a sharp object is painfully cutting me, I experience a feeling of wincing back and away from the object, and in correlation with this feeling-flow the sharp object is felt to have a tonal-flow of flowing forwards, towards and into me in a piercing manner. When pain makes me fearful, I experience a feeling-flow of retreating backwards and away from the existent that is threatening me. The feeling flows backwards in a shrinking and cringing manner; I have the sensation of ‘shrinking and cringing back from’ the threatening existent. When my pain presents the quality of anxiety, my experience does not flow backwards as a ‘retreat from’, but has the directional sense of being suspended over an inner bottomlessness. The feeling flow of anxiety during pain is a flow that hovers before the possibility of flowing in a downward direction. When pain presents angry retaliation, I feel an angry ‘striking back’ towards the pain-affected body-part, and as such flows forwards, towards the limb at which I am angry. It flows forwards in a violently attacking manner. By virtue of correlated tonal and painful flows, the world and I are joined together in an extrarational and sensuously appreciative way.

Instead of only describing the external things to which pain is externally related, it is also possible to describe pain internally by noting other internal determinations of the feelings and sensations with which it is united. Joint internal-external characterizations of pain very roughly map onto neuroscientific evidence showing that our cutaneous nociceptive system differentiates into interoceptive and exteroceptive causal features, such that our interoceptive nociceptive system signals tissue disorders that are inescapable, and causes homeostatic responses, and our exteroceptive nociceptive system extracts meaningful information about events in the world in order to effect behaviors that protect the organism from external threats (Price et al. 2003).

References
Craig AD (2003). A new view of pain as a homeostatic emotion. Trends in neurosciences 26(6): 303–307.

Merskey H, Bogduk N (Eds) (1994). Classification of Chronic Pain (Second Ed.). IASP Press: Seattle, pp 209–214.

Mountcastle VB (1974). Pain and temperature sensibilities. Medical Physiology 13(1): 348–391.

Price DD, Greenspan JD, Dubner R (2003). Neurons involved in the exteroceptive function of pain. Pain, 106(3), 215–219.

Smith Q (1986).The felt meanings of the world: A metaphysics of feeling. Purdue University Press.

Sternbach RA (1968). Pain: A psychophysiological analysis. Academic Press: New York.

Pentti Haikonen

How does the physical growth of the fetal brain relate to pain function? Addressing this question is not just of research interest, but has profound consequences in guiding clinical use of analgesic and anesthetic intervention for in utero surgery. Adult brains appear structurally and functionally specialized for types of pain; for example, acute pain preferentially engages medial prefrontal cortical and subcortical limbic regions [1,2]. However, the question of the relationship between such specializations and pain is still controversial in the debate concerning fetal pain [3, for review]. One ‘maturational’ perspective is that brain growth and pain function co-develop through innate genetic and molecular mechanisms, and that postnatal experience merely has a role in the final ‘fine tuning’ [4,5,6,7]. Evidence concerning the differential neuroanatomical development of brain regions is used to determine a lower gestational age when particular regions likely become functional for pain. Several authors claim that maturation within subcortical brain regions enables pain function as early as 20 weeks gestation [6,7], others claim expansion of thalamocortical regions at 24 weeks is necessary and sufficient. An alternative ‘expertise’ view is that brain development and pain function involve a prolonged process of co-specialization that is shaped by postnatal experience [3,8,9,10]. Based on this approach, some authors argue that the fetal brain is not functional for pain at any gestational stage because skills such as sense of self and mind-reading learnt in postnatal life are necessary for pain [3,8,9,10].

Maturational views of functional brain development assume that brain growth and the appearance of functions are equivalent or the same thing, in the way that water and H2O are equivalent or the same thing, which implies that concerning the question of fetal pain, the sequential coming ‘on-line’ of specific brain regions during fetal development is identical with the appearance of pain function. That is, pain function numerically shares all its properties or qualities with the brain. Things with qualitative identity share properties, so things can be more or less qualitatively identical. Apples and oranges are qualitatively identical because they share the quality of being a fruit, but two apples have greater qualitative identity. Maturational views of fetal pain demand more than this, however, since they imply numerical identity. Numerical identity implies total qualitative identity, and can only hold between a thing and itself. This means that a maturational view of fetal pain makes a very strong demand about pain capacity: specific brain regions and pain function co-develop in the fetus because they are numerically identical, one and the very same thing. Pain is in the brain.

Expertise views of fetal pain challenge the core maturational commitment of brain-pain numerical identity and present philosophical arguments and data which claim instead to show the non-identity of brain-pain relationships in the fetus and the necessity of postnatal experience and learning [3,8,9,10]. A representative philosophical argument driving expertise views of fetal pain is the following: All pains are personal experiences and therefore entirely subjective; All brains are physical objects and therefore entirely objective; There is a fundamental divergence between pain and the brain. Therefore, pain cannot be numerically identical to the brain. Thus, the argument:

1. Pains are subjective.

2. Brains are objective.

Therefore, since pains and brains fundamentally diverge,

3. Pain is not numerically identical to the brain.

I will now critically examine and discuss this argument. Take the first premise: ‘pains are subjective.’ On a reasonable interpretation of its meaning, to say that ‘pains are subjective’ is to say that pains are knowable by direct personal experience. However, since brain events such as brain growth are not knowable by direct personal experience, pains cannot be one and the same thing as brain events. Here is the argument:

1. Pains are knowable to me by direct personal experience.

2. Brain events are not knowable to me by direct personal experience.

Therefore, since pains and brains fundamentally diverge,

3. My pain is not numerically identical to my brain.

Once the argument is represented in this form, it is clear that it is fallacious. This can be observed if we compare the argument with the following example:

1. Ibuprofen is known by me to relieve pain.

2. Iso-butyl-propanoic-phenolic acid is not known by me to relieve pain.

Therefore, since ibuprofen and iso-butyl-propanoic-phenolic acid fundamentally diverge,

3. Ibuprofen cannot be identical to iso-butyl-propanoic-phenolic acid.

The premises in the example are true, but the conclusion is known to be false. The argument is fallacious because its core assumption – ‘fundamental divergence’ – is mistaken: it mistakenly assumes that a thing must be known by somebody somewhere. But the property ‘being known by somebody’ is not a necessary feature of anything, much less a property that might establish its identity or non-identity with something otherwise known. The truth of the premises may be due to nothing else but my ignorance of what turns out to be identical with what. This point entails that ‘being known by somebody’ is not a necessary feature of pain that might explain its identity or non-identity with the brain. The non-identity of fetal brain development and pain function cannot be established by this argument.

The argument needs to produce independent evidence for the idea of ‘fundamental divergence’, since it is not self-evident. To illustrate this point, consider the argument for pain-brain numerical identity that personal pain would have no influence on mammalian behaviour were it not numerically identical with brain events [11]. This apparently simple argument wasn’t established until fairly recently because a crucial premise was not available. This is the premise that physical effects like pain are determined by prior physical causes. This is an empirical premise, and one which scientific theories of pain didn’t take to be fully evidenced until the middle and late twentieth century [12, for review]. It is this evidential shift, and not the apparently obvious, which is responsible for the argument’s persuasive power. It remains to be seen if stronger evidence for pain-brain identity in the fetus is forthcoming.

Of course, the failure of this particular argument to establish its conclusion does not thereby abolish the expertise perspective and self-guarantee its opposite, the maturational perspective, or even prove that the two perspectives are mutually exclusive. Rather, what the failure of the argument shows is that apparently obvious logic is sometimes a poor guide to reality. Whether pain-brain identity is true or false is impossible to tell simply by arguing personal appearances.

References

[1] Apkarian AV, Hashmi JA, Baliki MN. Pain and the brain: specificity and plasticity of the brain in clinical chronic pain. Pain 2011; 152(3 Suppl): S49–S64.

[2] Wager TD, Atlas LY, Lindquist MA, Roy M, Woo CW, Kross E. An fMRI-based neurologic signature of physical pain. New England Journal of Medicine 2013; 368(15): 1388–1397.

[3] Derbyshire SWG, Raja A. On the development of painful experience. Journal of Consciousness Studies 2011; 18: 9–10.

[4] Anand KJ, Hickey PR. Pain and its effects in the human neonate and fetus. New England Journal of Medicine 1987; 317(21): 1321–1329.

[5] Anand KJ. Consciousness, cortical function, and pain perception in nonverbal humans. Behavioral and Brain Sciences 2007; 30(1): 82–83.

[6] Lowery CL, Hardman MP, Manning N, Clancy B, Whit Hall R, Anand KJS. Neurodevelopmental changes of fetal pain. Seminars in Perinatology 2007; 31(5): 275–282.

[7] Brusseau RR, Mashour GA. Subcortical consciousness: Implications for fetal anesthesia and analgesia. Behavioral and Brain Sciences 2007; 30(01): 86–87.

[8] Derbyshire SWG. Controversy: Can fetuses feel pain? BMJ: British Medical Journal 2006; 332(7546): 909–912.

[9] Derbyshire SWG. Fetal analgesia: where are we now? Future Neurology 2012; 7(4): 367–369.

[10] Szawarski Z. Do fetuses feel pain? Probably no pain in the absence of “self”. BMJ: British Medical Journal 1996; 313(7060): 796–797.

[11] Papineau D. Thinking about consciousness. Oxford: Oxford University Press; 2002.

[12] Perl ER. Pain mechanisms: a commentary on concepts and issues. Progress in Neurobiology 2011; 94(1): 20–38.

Abstract. Functionalism of robot pain claims that what is definitive of robot pain is functional role, defined as the causal relations pain has to noxious stimuli, behavior and other subjective states. Here, I propose that the only way to theorize role-functionalism of robot pain is in terms of type-identity theory. I argue that what makes a state pain for a neuro-robot at a time is the functional role it has in the robot at the time, and this state is type identical to a specific circuit state. Support from an experimental study shows that if the neural network that controls a robot includes a specific ’emotion circuit’, physical damage to the robot will cause the disposition to avoid movement, thereby enhancing fitness, compared to robots without the circuit. Thus, pain for a robot at a time is type identical to a specific circuit state.

Here.

UC Berkeley psychologist Tania Lombrozo has responded to the Annual Edge Question for 2014, ‘What scientific idea is ready for retirement?’, with a piece entitled ‘The Mind is Just the Brain’, in which she argues for the rejection (‘retirement’) of mind-brain identity theory.

Using a baking analogy to illustrate her case against reductionism, she writes:

But a theory of baking wouldn’t be very useful if it were formulated in terms of molecules and atoms. As bakers, we want to understand the relationship between—for example—mixing and texture, not between kinetic energy and protein hydration. The relationships between the variables we can tweak and the outcomes that we care about happen to be mediated by chemistry and physics, but it would be a mistake to adopt “cake reductionism” and replace the study of baking with the study of physical and chemical interactions among cake components.

But if you are interested in the project of explaining, predicting, and controlling the quality of your baked goods, then you’ll need something like a baking theory to work with.

Rejecting the mind in an effort to achieve scientific legitimacy—a trend we’ve seen with both behaviorism and some popular manifestations of neuroscience—is unnecessary and unresponsive to the aims of scientific psychology. 

In these passages, Lombrozo makes a common anti-reductionistic mistake of thinking that mind-brain identity makes mental experiences somehow unreal or even disappear. Her reasoning implies that a correct explanation of mental phenomena cannot involve scientific reduction of mental phenomenon to neurobiological mechanism. This misunderstanding trades on a peculiar view of reduction, where it is expected that in neuroscience, mind-brain identities eliminate mental experiences. I think this expectation is incorrect.

Temperature was ontologically reduced to mean molecular kinetic energy, but no person expects that temperature therefore ceased to be real or became scientifically disrespectable or redundant. Visible light was ontologically reduced to electromagnetic radiation, but light did not disappear. Instead, scientists understand more about the real nature of light than they did before 1873. Light is real, no doubt; and so is temperature. Some expectations about the nature of temperature and light did change, and scientific progress does occasionally require rethinking what was believed about phenomenon. In certain instances, previously respectable states and substances sometimes did prove to be unreal. The caloric theory of heat did not survive rigorous experimental testing; caloric fluid thus proved to be unreal. A successful mind-brain identity of mental phenomenon such as pain means only that there is an explanation of pain. It is a reduction. Scientific explanations of phenomenon do not typically make them disappear [1,2,3].

It is critical to clear-up a further common misconception about mind-brain identity theory. This is the misconception that mind-brain identity theory is equivalent to reductionism. The truth is that whereas identity theory is compatible with a wide range of reductionistic philosophies, it is not equivalent to all of them. Here are some illustrative examples [4]:

1) Identity theory is reductionistic in the sense that it denies minds are ontologically independent of brains and uniquely self-guaranteeing, in line with functionalist and realization (physicalist) philosophies of mind. But functionalism and realization physicalism are not equivalent to the identity theory, so identity theory is not uniquely reductionist in the sense of (1).

2) Identity theory is reductionistic in the minimal sense that it claims, in line with functionalist and realization (physicalist) philosophies, that mind is ‘nothing over and above’ the brain, but since identity theory and functionalist and realization philosophies are not equivalent, identity theory is not equivalent to reductionism. A philosopher could be a reductionist without being an identity theorist.

3) Identity theory is not reductionistic in the sense that it asserts ‘micro-reductionism’. Mental phenomena might be identified with innate genetic or molecular mechanisms (John Bickle), but this is optional, not required. The core metaphysical commitment of identity theory is that mental states are numerically identical to brain states. Nothing is expected in this core claim about the precise mechanistic nature of brain states, which is a scientific question, anyway.

4) Identity theory is not reductionistic in the sense that it asserts that (e.g.) psychology reduces to neuroscience, cognitive neuroscience reduces to molecular neuroscience, or philosophy of mind reduces to quantum mechanics. One can assert identity theory without asserting epistemic reductionism.

Positively, I entirely agree with Lombrozo when she says:

But if we want to know—for instance—how to influence minds to achieve particular behaviors, it would be a mistake to look for explanations solely at the level of the brain.

Understanding the mind isn’t the same as understanding the brain.

Understanding the mind requires first-person descriptions of mental states and experiences, and third-person scientific descriptions of associated brain states, and a method to integrate them, such as the experiential-phenomenological method [5]. So, Lombrozo is right: ‘Understanding the mind isn’t the same as understanding the brain.’ More precisely, I argue that her correct thesis implies that the subject matter of psychology is brain mechanism as related to mental phenomena. For example, the subject of pain science is brain mechanism as related to pain phenomena (e.g., acute pain, chronic pain, fetal pain, empathy for pain, dreamed pain, near-death pain, and so on). Pain research aims to discover the brain mechanisms subserving conscious pain experiences accessible only through introspection, which means that pain research is entirely reliant on the first-person point of view and on using first-person investigative methods. This necessarily includes introspection together with third-person methods (e.g., neuroimaging). Since pain research aims to know which experience types are generated by which brain mechanism, researchers must naturally know when specific pain experiences occur and what their personal qualities are.

The history of scientific pain research shows that introspection has been extensively used. For example, pain psychophysics typically uses subject pain verbal-report or non-verbal behavior (e.g., facial expressions) to infer the presence of pain. That is, pain psychophysics is committed to subject introspection. It is also important to remember that the validity of pain-related neuroimaging was established by the correlation of brain images with self-report of pain [6]. Pain psychophysics, like psychology, preserves an epistemological dualism in its subject matter while rejecting metaphysical dualism.

How then is mind-brain identity theory positioned relative to the indispensability of introspection in mind science? Personal introspection is a direct way of coming to know about personal experiences and their qualities. It is epistemological. Still, despite appearances to the contrary, what introspection reveals to us may be utterly mechanistic. It may be that what scientists study through third-person methods is numerically identical with what is personally experienced through introspection, that is, brain mechanisms of the appropriate type. There is only one type of activity in question: the brain mechanism with all and only physical properties. Thus, mind-brain identity theory is preserved in the study of the mind.

References

[1] Churchland PM (2007). Neurophilosophy at work. Cambridge, UK: Cambridge University Press.

[2] Churchland PS (1989). Neurophilosophy: Toward a unified science of the mind-brain. Cambridge, Mass.: The MIT Press.

[3] van Rysewyk S (2013). Pain is Mechanism. PhD Dissertation, University of Tasmania.

[4] Polger TW (2009). Identity Theories. Philosophy Compass4(5), 822-834.

[5] Price DD, Aydede M (2006). The Experimental Use of Introspection in the Scientific Study of Pain and its Integration with Third-Person Methodologies: The Experiential-Phenomenological Approach. In M Aydede (ed.), Pain: New Essays on Its Nature and the Methodology of Its Study, pp. 243-275. Cambridge, Mass.: MIT Press.

[6] Coghill RC, McHaffie JG, Yen YF (2003). Neural correlates of interindividual differences in the subjective experience of pain. Proceedings of the National Academy of Science USA, 100, 8538-8542.

The trend in the literature on fetal pain is to approach the question of consciousness in the fetus in terms of conscious states of pain. That is, first define what makes a pain a conscious mental state, and then determine being a conscious fetus in terms of having such a state. Thus, the possibility of a conscious fetus is thought to rely on theories of conscious pain states. Call this the state approach to fetal pain. 

Two state approaches to fetal pain are present in the literature. One approach looks at the brain structure(s), pathways and circuits necessary for conscious pain states and then seeks to establish whether this substrate is present and functional in the fetus. There is broad agreement among researchers that the minimal necessary neural pathways for pain are in the human fetus by 24 weeks gestation [1, for review]. Some researchers argue that the fetus can feel pain earlier than 24 weeks because pain is enabled by subcortical brain structures [4,5,6].

Another phenomenal approach is to consider the subjective content of a conscious experience of pain, and to ask whether that content might be available to the fetus [1,2,3]. Based on this approach, some researchers argue that the fetus cannot feel pain at any stage because it lacks developmental abilities and concepts such as sense of self necessary for pain [1,2,3].

Although both state approaches are presented as opposites in the literature, they share the determination of fetal pain based on specific levels or degrees of complexity, whether of the brain structures and the relationship they have to the conscious state of pain, or of the subjective contents that constitute that state.

An alternate approach to understanding fetal consciousness that has not been explored in the literature on fetal pain is the extent to which pain is based on the arrangement of certain brain structures (or experiential contents), rather than a result of maturation or increase in complexity achieved by growth of the brain substrate which below a certain size does not enable consciousness [7,8]. Thus, whether the fetus is excluded in this regard is not due to its simplicity, but because its lack of certain brain arrangements necessary to enable consciousness.

According to this alternate view of fetal pain, a living creature’s subjective contents may differ greatly in complexity. To convey the range of conscious possibilities, consider the Indian ‘scale of sentience’ (cited in [8]):

‘This.’
‘This is so.’
‘I am affected by this which is so.’
‘So this is I who am affected by this which is so.’

The possibilities in this consciousness scale range from simply experienced sensation (‘This’; ‘This is so’) to self-consciousness (‘I am affected by this which is so’; ‘So this is I who am affected by this which is so’). Each stage in this scale presupposes consciousness. Any experience, whatever its degree of complexity, is conscious. It follows that to see, to hear, and to feel is to be conscious, irrespective of whether in addition a creature is self-conscious that it is seeing, hearing, and feeling [7]. To feel pain is to be conscious of that experience regardless of whether in addition one is self-conscious of being in pain. Self-consciousness is just one of many contents of consciousness available to big-brained living creatures with complex capacities: it is not definitive of consciousness [7,8]. The point of saying this is that it circumvents the logical mistake of misidentifying attributes unique to a specialized form of consciousness (e.g., self-consciousness) as general features of consciousness itself.

With this alternate view of consciousness now sketched in, we should determine where the fetus and where pain fall in the Indian scale of sentience. The possibilities in the scale extend from mere sensation to self-consciousness–where does the fetus fall in?

References

[1] Derbyshire S, Raja A. (2011). On the development of painful experience.Journal of Consciousness Studies18, 9–10.

[2] Derbyshire SW. (2006). Controversy: Can fetuses feel pain?. BMJ: British Medical Journal332(7546), 909.

[3] Szawarski Z. (1996). Do fetuses feel pain? Probably no pain in the absence of “self”. BMJ: British Medical Journal313(7060), 796–797.

[4] Anand KJ, Hickey PR. (1987). Pain and its effects in the human neonate and fetus. New England Journal of Medicine317(21), 1321–1329.

[5] Anand KJ. (2007). Consciousness, cortical function, and pain perception in nonverbal humans. Behavioral and Brain Sciences30(01), 82–83.

[6] Lowery CL, Hardman MP, Manning N, Clancy B, Whit Hall R, Anand KJS. (2007). Neurodevelopmental changes of fetal pain. In Seminars in perinatology (Vol. 31, No. 5, pp. 275–282).

[7] Merker B. (1997). The common denominator of conscious states: Implications for the biology of consciousness. Available at: http://cogprints.soton.ac.uk.

[8] Merker B. (2007). Consciousness without a cerebral cortex, a challenge
for neuroscience and medicine. Target article with peer commentary and author’s response. Behavioral and Brain Sciences, 30, 63–134.

The University of Tokyo Center for Philosophy, Uehiro Research Division,
Philosophy of Disability & Co-existence Project (UTCP/PhDC):

3rd International Conference ‘Phenomenology of Pain’

20140104_poster_ver4

There is broad agreement among researchers that the minimal necessary neural pathways for pain are in the human fetus by 24 weeks gestation [1, for review]. However, some argue that the fetus can feel pain earlier than 24 weeks because pain can be enabled by subcortical brain structures [2,3,4,5]. Other researchers argue that the fetus cannot feel pain at any stage of gestation because the fetus is sustained in a state of unconsciousness [6]. Finally, others argue that the fetus cannot feel pain at any stage because the fetus lacks the conceptual postnatal development necessary for pain [7,8,9]. If a behavioral and neural reaction to a noxious stimulus is considered sufficient for pain then pain is possible from 24 weeks and probably much earlier. If a conceptual subjectivity is considered necessary for pain, however, then pain is not possible at any gestational age. According to [1], much of the disagreement concerning fetal pain rests on the understanding of key terms such as ‘wakefulness’, ‘conscious’ and ‘pain’.

A motivation for thinking conceptual subjectivity is necessary for pain is the idea that subjective experiences such as pain cannot be reduced to or identified with the objective features of the brain [7,8,9]. All pains are personal experiences and therefore entirely subjective; all brain states are physical events and therefore entirely objective. There is a fundamental divergence between pain and the brain. Thus, pain cannot be in the brain. The basic argument:

1. Pain experiences are subjective.

2. Brain events are objective.

Therefore, since pain experiences and brain events fundamentally diverge,

3. Pain experiences are not identical to brain events.

Is this a good argument? Let’s examine its first premise – ‘pain experiences are subjective.’ On a reasonable interpretation of its meaning, to state that ‘pain experiences are subjective’ is to state that pain experiences are knowable by introspection. However, since brain events are not knowable by introspection, pain experiences cannot be identical to brain events. Here is the argument:

1. Pain experiences are knowable to me by introspection.

2. Brain events are not knowable to me by introspection.

Therefore, since pain experiences and brain events fundamentally diverge,

3. My pain experiences are not identical to any of my brain events.

Once the argument is represented in this form, it is clear that it is fallacious. This can be clearly observed if we compare the argument with the following example:

1. Ibuprofen is known to me to relieve pain.

2. Iso-butyl-propanoic-phenolic acid is not known by me to relieve pain.

Therefore, since ibuprofen and iso-butyl-propanoic-phenolic acid fundamentally diverge,

3. Ibuprofen cannot be identical to iso-butyl-propanoic-phenolic acid.

The premises in the example are true, but the conclusion is known to be false. The argument is fallacious because the core idea of the argument – ‘fundamental divergence’ – makes an erroneous assumption; namely, it assumes that a thing must be known by somebody. But the property ‘being known by somebody’ is not a necessary feature of any thing, much less a property that might establish its identity or non-identity with some thing otherwise known. The truth of the premises may be due to nothing else but my ignorance of what turns out to be identical with what. These considerations challenge the assumed epistemology in the conceptual subjectivity view of pain.

They also challenge the related claim made by proponents of conceptual subjectivity that any description of a pain given in objective scientific terms will necessarily always exclude the personal experience of that pain [7,8,9]. The argument made here is by now familiar: since descriptions of pain in personal subjective terms are different from scientific descriptions of pain, it follows that a pain and its private subjectivity cannot be identical with a brain event and its public objectivity. Only persons can feel pain – brain cells and protein channels can’t. Clearly, the argument begs the issue in question: whether or not the subjective features of a pain I personally experience are identical with some objective features of my brain that might be discovered by neuroscience is precisely the question at issue [10,11].

Besides, in order to understand a scientific explanation of pain, neuroscience does not require of a person that he both understands the explanation and feels pain as a condition of understanding. Neuroscience aims to explain pain, that is its main purpose. Too much is demanded of neuroscience if, in addition to formulating an explanation of pain, it is meant to re-create pain in somebody as a requirement of understanding [10,11]. This expectation is therefore much too strong.

References

[1] Derbyshire SWG, Raja A. (2011). On the development of painful experience.Journal of Consciousness Studies18, 9–10.

[2] Anand KJ, Hickey PR. (1987). Pain and its effects in the human neonate and fetus. New England Journal of Medicine, 317(21), 1321–1329.

[3] Anand KJ. (2007). Consciousness, cortical function, and pain perception in nonverbal humans. Behavioral and Brain Sciences30(1), 82–83.

[4] Lowery CL, Hardman MP, Manning N, Clancy B, Whit Hall R, Anand KJS. (2007). Neurodevelopmental changes of fetal pain. In Seminars in perinatology, 31(5), 275–282.

[5] Merker B. (2007). Consciousness without a cerebral cortex, a challenge
for neuroscience and medicine. Target article with peer commentary and author’s response. Behavioral and Brain Sciences, 30, 63–134.

[6] Mellor DJ, Diesch TJ, Gunn AJ, Bennet L. (2005). The importance of ‘awareness’ for understanding fetal pain. Brain research reviews49(3), 455-471.

[7] Derbyshire SWG. (2012). Fetal analgesia: where are we now? Future Neurology7(4), 367-369.

[8] Derbyshire SWG. (2006). Controversy: Can fetuses feel pain? BMJ: British Medical Journal332(7546), 909.

[9] Szawarski Z. (1996). Do fetuses feel pain? Probably no pain in the absence of “self”. BMJ: British Medical Journal313(7060), 796–797. 

[10] Churchland PS. (2002). Brain-wise: V: Studies in Neurophilosophy. MIT press.

[11] van Rysewyk S. (2013). Pain is Mechanism. PhD Dissertation, University of Tasmania.

Conscious pain is always personal. It is experienced from the view of oneself, and is not real or meaningful apart from this perspective.

All pains cluster around one’s personal aperture as around a single point or origin from which they are all perceived, irrespective of where in the body pain is felt. The sensation of a pain in a hand is sensed as located in the hand, but that pain sensation in the hand is not felt from the hand, but from about the same spatial location from which that hand is personally seen, even if pain is felt in complete darkness or in a dream. It is the ‘here’ with regard to which any pain is ‘there.’

It may intuitively feel that this single experiential point is located at the mid-point between the centers of rotation of the two eyes. Mach’s drawing above shows a monocular view of this point given in peripheral vision. In fact, the empirically determined location of the point is deeper inside the head, in the midsagittal plane, roughly 4–5 cm behind the bridge of the nose. Initially developed by Herring (1879/1942), this determination identifies the intersection of a few lines of sight obtained by fixating certain locations in the environment and aligning pins with them along each of the lines of sight or attention.

The self thus located is the origin of all lines of sight/attention and so cannot be any kind of self-representation (Merker, 2007, 2013). It defines the view point from which any and all representations of sensory experience are perceived, including personal pain. It is the point from which attention is directed and relative to which percepts are located in the space whose origin it defines (Merker, 2007, 2013).

To think that self must involve a kind of self-representation is to transfer sensory experience from the sensory state to one of its sub-domains (the self), which I think motivates viewing the self as a kind of cartesian homunculus. On this cartesian view, pain is interpreted in presence of the self. To my mind, it seems the other way round: the self in pain finds itself in the presence of pain (the ‘content’ of pain). The self of any conscious pain is not inherently conscious. Pain is intruder, not self. That is why pain is an aversion.

From this single experiential point we look out upon the world along straight and uninterrupted lines of sight. This orientation is dramatically reversed in the experience of pain. During pain, attentional focus is rapidly and involuntarily moved backwards along these same lines toward their most proximal origin. I believe this reverse direction helps to characterize the meaning of conscious pain as intrusion or threat to oneself.

References

Hering, E. (1879/1942). Spatial Sense and Movements of the Eye. Trans. C. A. Radde. Baltimore, MD: American Academy of Optometry (Original work published in 1879).

Mach, E. (1897). Contributions to the Analysis of the Sensations. La Salle, IL: Open Court.

Merker, B. (2007). Consciousness without a cerebral cortex, a challenge
for neuroscience and medicine. Target article with peer commentary and author’s response. Behavioral and Brain Sciences, 30, 63–134.

Merker, B. (2013). The efference cascade, consciousness, and its self: naturalizing the first person pivot of action control. Frontiers in Psychology, doi:10.3389/fpsyg.2013.00501.

Call for Chapters: ‘Pain Experience and Neuroscience’, Edited Collection, 2014 

You are warmly invited to submit your research chapter for possible inclusion in an edited collection entitled ‘Pain Experience and Neuroscience’. The collection editor is Dr. Simon van Rysewyk. The target publication date is December 2014. Target publisher: MIT Press.

According to the International Association of the Study of Pain, pain is ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage’. Nociceptor activity induced by a noxious stimulus is not pain even though pain most typically has a peripheral physical cause. Pain is always personal. Many laboratory and clinical studies support the IASP pain definition, and it is widely endorsed in the international pain community. Not all pain is associated with tissue damage (stomach and head ache). Pains present in countless varieties associated with different sensations, imbued with different meanings and strong emotions and cognitions. Pain can have intense, complex features that need to be explained. The discovery of how such varied dimensions of pain experience relate to each other and to the pain-related neural pathways, neurotransmitters, and integrative centers of the brain that support them is a major scientific challenge in the study of pain. How can it be done?

The way to meet this challenge is to integrate knowledge from current models of pain with knowledge and insights from neuroscience, psychology, and humanities. A history of experiential pain investigations does exist. For example, early in the twentieth century, Sir Henry Head, William Landau and George H. Bishop conducted psychophysical studies on qualitative differences between ‘first pain’ and ‘second pain’ and neurophysiological studies on the relationship of these pain sub-types to brain activity. Later, temporal differences between first and second pain were explained in terms of central temporal summation in psychophysiological studies by Donald D. Price and others and Roland Staud. These integrative studies use well-known psychophysical scaling methods (e.g., ratio scales) or, the ‘experiential-phenomenological method’, in studies by Price and colleagues. Other experiential methods that form productive research programs should be considered to model pain experience, such as descriptive experience sampling (DES) (to analyze very brief episodes of experience in natural settings) developed by Russell T. Hurlburt and his colleagues, or the explication interview method to analyze the fine grain of chronic experiences, exemplified in the works of Francisco Varella, Claire Petitmengin, and Pierre Vermersch.

Without a detailed experiential analysis of the qualities of pain, or the qualitative differences between pain sub-types, it is extremely challenging to establish a detailed examination of the neural systems that support such features. Experiential analyses are also essential for the advancement of psychological pain theory and clinical practice. The aim of this edited collection is to contribute towards integrating pain psychology and neuroscience with the humanities in the study of pain.

Target audiences of ‘Pain Experience and Neuroscience’

The expected target audiences of ‘Pain Experience and Neuroscience’ are scientists, researchers, authors, and practitioners currently active in pain science, including the neurosciences and clinical neurosciences, psychology, and the humanities. The target audience will also include various stakeholders, like academic scientists and humanists, research institutes, and individuals interested in pain, including pain patients, their families and significant others, and the huge audience in the public sector comprising health service providers, government agencies, ministries, education institutions, social service providers and other types of government, commercial and not-for-profit agencies.

Intent to submit your chapter

Please indicate your intention to submit a manuscript to Simon with the title of the chapter, and author(s). He will approach a publisher once he has accepted 25 intents to submit.

Please feel free to contact Simon if you have any questions or concerns. Many thanks!

IMPORTANT DATES:

Intent to Submit: December 31, 2013
Full Version: May 31, 2014
Decision Date: July 31, 2014
Final Version: August 31, 2014 

Editor 

Dr. Simon van Rysewyk

Post-Doctoral Fellow, Graduate Institute of Medical Humanities, Taipei Medical University, 250 Wu-Hsing Street, Xin-yi District, Taipei City, Taiwan 110.

email: vanrysewyk@tmu.edu.tw

mobile: +886 916 608 88

Email: vanrysewyk@tmu.edu.tw
http://simonvanrysewyk@wordpress.com
http://utas.academia.edu/SimonvanRysewyk

A flash of lightning produces a single sound. Pain in the brain is not like that. Neurons in the brain can excite or inhibit many other neurons, to which they are connected. Pain is not controlled by a single neuron.

A flash of lightning has no intended direction. But pain in the brain is not like that. The synaptic connections between neurons enable coordinated patterns of activation between millions of interconnected neurons. A type of pain is just a type of activation pattern.

Pain in the brain is not conducted like a symphony orchestra by a single individual. It is more like a free-jazz ensemble whose music is produced by loose and coordinated effort among the ensemble members.

‘Do you try to find the real artichoke by stripping it of its leaves?’ Wittgenstein once said. The same can be said of pain in the brain.

The brain is a causal mechanism to convey pain as a sensation. Pain also conveys to us itself. Pain in the brain is like a melody in music. When we feel a pain, the pain doesn’t convey something else that compounds with the activation patterns in the brain. We get the feeling of a pain because pain just is an activation pattern.

In the absence of a general theory of pain or brain function, metaphor and philosophy serve useful placeholder roles.

It is not obvious that experiences of pain are identical to brain activation patterns. In reply, it is not obvious that an ensemble of human beings could produce exciting jazz music, either.

Here, I briefly respond to Robinson, Staud and Price6 concerning what constitutes the ‘neural signature’ of pain (p. 325), note a logical mistake in their article, and highlight a reason why explaining pain is difficult. It is probable that conscious pain may be subserved by an unconscious physical base with a specific neurophysiological signature. Explaining pain in this direct way aims first to describe the base as a correlate of pain, then ultimately to achieve a reductive neurophysiological explanation of pain. Multiple evidential lines demonstrate that the neurophysiological base of pain need not be limited to one physical location, as Robinson, Staud and Price rightly note (p. 325). Since the hypothetical pain base is probably distributed, and therefore is more akin to the immune system than the liver, it is mistaken to expect that if it is not confined to a single neural region, or a single pattern of functional interaction, then there cannot be a physical signature of pain, as Robinson, Staud and Price appear to think (p. 325). Instead of a region-based view of the hypothetical pain base, it may be more accurate to think of it as a distributed mechanism.5, 8

The mechanism of pain could involve any number of neurophysiological systems (nervous, endocrine, immune), or reciprocal interactions between them, or any number of neurophysiological levels (pathway, network, single cell, molecular), or reciprocal interactions between them.1, 7, 8 The probability of a distributed mechanism, combined with the open-ended probability concerning the systems and level at which the mechanism exists, explains why current hypotheses and theories of pain in the literature, including those made in the article by Robinson, Staud and Price, are relatively unconstrained. However, the absence of constraints is not indicative of the likely truth of Cartesian dualism, the futility of searching for neurophysiological pain correlates, or the unreliability of verbal pain self-report. Rather, it indicates that pain science has much to do.

Neurophysiological mechanism and pain experiences can be correlated for a variety of reasons: the mechanism is part of the cause of pain; the mechanism is part of the effect of pain; the mechanism indirectly parallels pain; the mechanism is what pain can be identified with.2, 8 Discovering the neurophysiological signature of pain requires the identification of some neurophysiological mechanism with pain. The correlation of mechanism x with pain is informative because x may be the one for identifying pain. Correspondingly, mechanism y that does not correlate with pain indicates that y may not be the one. If there is a pain mechanism with a neurophysiological signature identifiable with pain experiences, the scientific and clinical benefits could be huge. Thus, investigating pain directly is worth a try.

Now, it is quite possible that a scientist may be looking at an instance of the pain signature without comprehending that it is an instance. This will occur if the physical base of pain does not possess an identifying property that is obvious to naïve researchers, but is comprehensible only through the availability of a more complete general theory of brain function.2, 3, 4, 8 The limitations in explaining pain are not simply technological. After all, how would a person know, independently of Antoine Lavoisier’s studies on oxygen, that metabolizing, burning and rusting are identical with the same mechanism, but that lightning and sunlight are not? Thus, Robinson, Staud and Price are right in asserting that it is misconceived to replace pain ratings with neuroimaging data, especially at this early stage of pain investigations.

References

Chapman CR, Tuckett RP, & Song CW: Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. J Pain 9: 122-145, 2008.

Churchland PS: A neurophilosophical slant on consciousness research. Progress in brain research 149: 285-293, 2005.

Frith CD, Perry R, Lumer E: The neural correlates of conscious experience: an experimental framework. Trends in Cognitive Science 3: 105-114, 1999.

Northoff, G: Philosophy of the brain: The brain problem (Vol. 52). Amsterdam, John Benjamins Publishing Company, 2004.

Northoff, G: Region-Based Approach versus Mechanism-Based Approach to the Brain. Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences 12: 167-170, 2010.

Robinson ME, Staud R, & Price DD: Pain Measurement and Brain Activity: Will Neuroimages Replace Pain Ratings? J Pain 14: 323-327, 2013.

Tracey I, Mantyh PW: The Cerebral Signature for Pain Perception and Its Modulation. Neuron 55: 377-391, 2007.

van Rysewyk S: Pain is Mechanism. PhD Thesis, University of Tasmania, 2013.

Variations in response to pain have been reported in clinical settings (e.g., Bates et al. 1996; Cherkin et al. 1994; Jensen et al. 1986; Unruh, 1996; Wormslev et al. 1994). Patients with similar types and degrees of wounds vary from showing no pain to showing severe and disabling pain. Many chronic pain patients show disabling chronic pain despite showing no observable wound. Other patients show severe wounds but do not show pain. Why is it that two persons with identical lesions do not show the same pain or no pain at all? Why are all pain patients unique?

I propose that mind-brain identity theory may offer an answer to this difficult question. There are two main versions of identity theory: type and token identity. A sample type identical property is to identify “Being in pain” (X) with “Being the operation of the nervous-endocrine-immune mechanism” (Y) (i.e., X iff Y) (Chapman et al. 2008; van Rysewyk, 2013). For any person in pain the nervous-endocrine-immune mechanism (NEIM) must be active, and when NEIM is active in a person, he or she is in pain. Thus, type identity theory strongly limits the pattern of covariation across persons. According to token identity theory, for a person in mental state X at time t, X is identical to some neurophysiological state Y. However, in the same person at time t1, the same mental state X may be identical to a different neurophysiological state Y2. Token identity theory doesn’t limit the pattern of covariation across persons; it only claims that, at any given time, some mind-brain identity must be true.

In response to the topic question, I propose a hybrid version of identity theory – ‘type-token mind-brain identity theory’. Accordingly, for every person, there is a type identity between a mental state X and some neurophysiological state Y. So, when I am in pain, I am in NEIM state Y (and vice versa), but this NEIM state Y may be quite different across persons. Type-token identity theory therefore proposes a type identity model at the level of every person (i.e., it may vary across persons). A type-token identity theory implies that group-level type identities (i.e., type-type) cannot fully explain the pattern of covariation in pain responses across persons. Measuring changes of a pattern of psychological and neurophysiological indicators over time may then support a unidimensional model of chronic pain for each pain patient. Thus, being in chronic pain for me is identical with a specific pattern of NEIM activity (Chapman et al. 2008; van Rysewyk, 2013), but for a different patient, the same state of pain may be identical to a different pattern of NEIM activity. In preventing and alleviating chronic pain, it is therefore essential to best fit the intervention to the type-token pain identity profile of the patient.

References

Bates, M. S., Edwards, W. T., & Anderson, K. O. (1993). Ethnocultural influences on variation in chronic pain perception. Pain, 52(1), 101-112.

Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. Journal of Pain 9: 122-145.

Cherkin, D. C., Deyo, R. A., Wheeler, K., & Ciol, M. A. (1994). Physician variation in diagnostic testing for low back pain. Who you see is what you get. Arthritis & Rheumatism, 37(1), 15-22.

Jensen, M. P., Karoly, P., & Braver, S. (1986). The measurement of clinical pain intensity: a comparison of six methods. Pain, 27(1), 117-126.

Unruh, A. M. (1996). Gender variations in clinical pain experience. Pain, 65(2), 123-167.

van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.

Wormslev, M., Juul, A. M., Marques, B., Minck, H., Bentzen, L., & Hansen, T. M. (1994). Clinical examination of pelvic insufficiency during pregnancy: an evaluation of the interobserver variation, the relation between clinical signs and pain and the relation between clinical signs and physical disability. Scandinavian journal of rheumatology, 23(2), 96-102.

Some philosophers worry that neuroscience will make painfulness disappear. Broadly, the objection is that if a science reduces a macro phenomenon to a micro phenomenon, then the macro phenomenon is not real or disappears (e.g., Searle, 1992). Using this conception of ‘reduction’, it is then reasoned that because it is observably obvious that a pain is real, it cannot be reduced to neuroscience. This misunderstanding trades on an idiosyncratic understanding of reduction, where it is expected that in science, reductions make macro phenomenon disappear. This expectation is confused.

Temperature was reduced to mean molecular kinetic energy, as recounted above, but no person expects that temperature therefore ceased to be real or became scientifically disrespectable or redundant. Visible light was reduced to electromagnetic radiation, but light did not disappear. Instead, scientists understand more about the real nature of light than they did before 1873. Light is real, no doubt; and so is temperature. Some expectations about the nature of temperature and light did change, and scientific progress does occasionally require rethinking what was believed about phenomenon. In certain instances, previously respectable properties and substances sometimes did prove to be unreal. The caloric theory of heat did not survive rigorous experimental testing; caloric fluid thus proved to be unreal. While no one expects that painfulness will cease to be real or become scientifically disrespectable if it is successfully explained by neuroscience, everyone believes that debilitating chronic pain will be controlled and eventually disappear as a result of scientific reduction. But this belief may turn out to be quite wrong. Simple prudence suggests that we wait and see.

Thus, the reduction of a macro phenomenon means only that there is an explanation of the phenomenon. Scientific explanations of phenomenon do not typically make them disappear. As neuroscience matures, the future of current conceptions of painfulness and sensory experience generally will rely on the empirical facts, and the enduring accuracy of current macro level theories (Churchland, 1993).

Churchland, P.M. (1993). Evaluating our self-conception. Mind and Language, 8, 211-222.
Searle, J.R. (1992). The Rediscovery of Mind. Cambridge, Mass.: MIT Press.

Fetal pain perception is often modelled on the same neural structures as in the adult.

However –

(1 The neural structures involved in pain processing in early development are unique and different from adults.

(2 Some of these structures and mechanisms are not maintained beyond specific developmental periods.

The immature pain system plays a signalling role during each stage of development, and fulfils this role using different neural resources available at specific developmental times.

Thus, the error here is reading the adult into the fetus.

To improve your life, identify all recurring pain and sufferings which are self-chosen, and eliminate them. What pain remains is necessary, and thus unavoidable.

If a science reduces a macro phenomenon to a micro phenomenon, then the macro phenomenon either is not real or ‘goes away’. Is this true? Does science make things disappear?

Obstetrics is true, and babies are born every day. Or, are babies born in spite of obstetrics? Does understanding gynecology make women sterile?

At the same time, a science of pain will hopefully reduce – or eliminate – much pain (mammalian and non-mammalian). Science makes pain ‘go away’. Surely a good thing.

How would you explain to a person who could never experience pain, what pain is?

Do the following:

1. Get a dairy food that is extremely spoiled.

2. Get the person to fill his or her mouth with this delightful food.

(ESSENTIAL: The food has to remain in the person’s mouth! Under no circumstances can the person spit out the food and clean his her mouth.)

3. Chew the food.

This test is a good model for the nature of pain.

Pain is aversive. We want to avoid pain. Eating spoiled food is the same: we want to avoid at all costs putting, much less chewing and swallowing, bad food.

Having a really bad taste in your mouth is like having a pain in your body.

My #SciFund video is finally complete!

Quite a mission to do (first time), but I am happy with the finished product.

Click on the image:

 

 

 

 

 

 

 

 

Here is a map showing the global distribution of participating scientists in Round 1 (2011) and Round 2 (May, 2012) of the #SciFund Challenge:

SciFunders Standing Tall and Talented

Come tomorrow, my #SciFund project will go online with other projects in Round 2 of the #SciFund Challenge!
 
 
What is the #SciFund Challenge?
#SciFund Challenge is about raising funds for important and interesting science projects.
It’s called crowdfunding.
In 2011, Round 1 of the #SciFund Challenge raised over US$76,000 for science projects!
The participating scientists included students, professors and independent researchers.
 
How does it work?
Each participating scientist creates a project, and a fundraising target.
Next, each scientist promotes their project online through social media, personal blogs,
YouTube, #Scifund blogs and #Scifund website, from May 1 to May 31, 2012.
A big part of a crowdfunding campaign is a 2-3 minute video advertising the project.
I’ll wrap-up my video tomorrow, and post it on RocketHub (the online host of #SciFund Round 2).
Next, I’ll invite you all to have a look at my excellent project page on RocketHub.
Then, you can decide whether I have convinced you or not!
 
What is my #SciFund project?
It is my PhD project: ‘The face of pain’. Intrigued yet?
Some of the questions I am looking at are:
What differentiates pain faces from emotion faces?
What facial features communicate the most information in a pain face?
How do observers fixate on, react to, and interpret faces of pain?
These aren’t merely interesting questions.
There is potential for direct clinical application.
How? The more clearly we define the attributes that make pain a unique expression,
the better equipped we are to assess and manage pain in patients.
This is especially critical in patients who lack verbal expressions or language
(e.g., patients with verbal disorders, dementia, autism, neonates, infants).
Clinicians rely heavily on non-verbal expressions of pain (e.g., facial expression) in such cases.
 
What is my fundraising target?
My target is US$1000. 
This target is very achievable given a bit of work on my part during May,
and your outstanding generosity and vision!
This target will fund costs related to conducting my experiments online (it ain’t cheap!).
Oh, and did I mention there are rewards for donators?
I’m not kidding around.
I’ll reveal my rewards when my project is online tomorrow!
Now, if you don’t wish to support my project, that’s completely OK.
But, I do ask of you one small thing: spread the word about my #SciFund project 
through your social network.
How is that? 
Muchas gracias, mi buen amigo!
 
What happens next?
I will post the link to my project-page on Rocket Hub on this blog!
Thanks!

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