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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.
- Borsook D, Becerra L. Emotional Pain without Sensory Pain-Dream On? Neuron 2009; 61(2):153–155.
- 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.
- 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.
- Nielsen TA, McGregor DL, Zadra A, et al. Pain in dreams. Sleep 1993; 16: 490–498.
- Raymond I, Nielsen TA, Lavigne G, et al. Incorporation of pain in dreams of hospitalized burn victims. Sleep 2002; 25: 765–770.
- Schredl M, Erlacher, D. Lucid dreaming frequency and personality. Personality and Individual Differences 2004; 37(7): 1463–1473.
- Schredl M. Continuity between waking and dreaming: a proposal for a mathematical model. Sleep and Hypnosis 2003; 5: 38–52.
- Zadra AL, Nielsen TA, Germain A, et al. The nature and prevalence of pain in dreams. Pain Research and Management 1998; 3: 155–161.
- 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
|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
|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.
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.
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.
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 .
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.
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).
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).
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.
I invite you to complete a 5 minute survey to assess the status of the mind-brain identity theory in current professional philosophy. It is open to philosophy faculty members and philosophy graduate and undergraduate students.
In the survey, the mind-brain identity theory is represented as a list of 9 philosophical claims adapted with permission from Thomas W Polger’s paper ‘Are Sensations Still Brain Processes?’ (2011), and which correspond to claims philosopher Jack Smart defended over fifty years ago in his paper ‘Sensations are Brain Processes’ (1959).
In the survey, each claim in the list is a binary ‘yes/no’ question. There are 9 questions. I will publish the results on my webblog and in an article.
Simon van Rysewyk
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 . 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.
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