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Reason 1: Historical Cases of Investigator-Participation in Pain Research

In the early twentieth century, scientists commonly viewed self-experimentation an essential part of medical research. Self-exposure to untested interventions was believed the most ethical way to assess human responses to those interventions, and to catalyse further research (Dresser 2013). Some of this research helped to found new scientific fields. Respiratory physiology was one such field, formed in the 1920s through self-experiments conducted by scientist John Haldane and colleagues. In 1984, physician Barry Marshall ingested Helicobacter pylori, which helped to establish the link between H. pylori and gastric pathology, and in 1992, self-experiments conducted by Mike Stroud and Ranulph Fiennes in Antarctica advanced understanding of nutrition in extreme conditions.

Self-experiments to study pain experience have been published by Sir Head (1920), Woollard and Carmichael (1933), Landau and Bishop (1953), Price (1972), Price et al. (1977), and Staud et al. (2001, 2008), to name only a few significant investigator-participants who studied pain. William Landau and George H. Bishop conducted standard psychophysical research on themselves to study the qualitative differences between “first pain” and “second pain” (i.e. “double pain”; later termed epicritic and protopathic pain) (Landau and Bishop 1953). Initially, Landau and Bishop identified through introspection the differential experiential qualities between first and second pain, followed by scientifically informed speculation about the mechanistic difference between the two types of pain. They discovered that first pain was sharp or stinging, well localized, and brief, whereas second pain was dull, aching, throbbing, or burning, and poorly localized, and longer lasting. The qualities of second pain were felt when skin C-nociceptors were stimulated.

These findings were subsequently confirmed by Price (1972) based on researcher and naïve participant introspective reports. Temporal differences between first and second pain were introspected on and mechanistically explained in terms of central temporal summation in studies by Price et al. (1977), and Staud et al. (2001, 2008), using investigator- and naïve-participants.

Conducting self-experiments to study referred pain, collaborators Herbert Woollard and Edward Carmichael observed that 300 g of weight placed on the right testicle produced slight discomfort in the right groin, while 650 g on the right testicle caused severe pain on the right side of the body. They confirmed that injury to the testicles caused pain to be referred throughout the body. For instance, as the weight on the testicle increased to over 900 g, they reported pain “of a sickening character” not only in the groin but also spreading across the back (Woollard and Carmichael 1933).

Self-experimentation on pain has on occasion led to surprising results. The psychologist B. Berthold Wolff self-experimented in his pain psychophysics laboratory, varying thermal pain which was produced at that time by briefly shining a strong light on a spot on the forearm blackened with candle black for a calibrated time and intensity of exposure (Hardy et al. 1940). On one occasion, Wolff pushed the button to deliver the noxious stimulus, but then something unexpected happened: he screamed with pain, which was brief but intense and filled his whole body. He described it as the most intense whole-body pain he had ever experienced. Wolff later discovered that the light stimulus had been knocked off its correct aim, and had missed his forearm altogether and instead diffused onto the opposite wall where it created a very strong flash of light throughout the normally dark room. Wolff speculated that, as he was expecting to feel pain, the unexpected flash of strong light had the same effect, producing an experience of pain.

It is unclear if investigators today independently conduct self-experiments or co-participate in their own pain studies. The convenience of recruiting participants from university classes and the internet may have made self-experimentation or co-participation of pain seem somewhat redundant to researchers. The Declaration of Helsinki advises on conducting ethical research using patients and healthy volunteers, although it is unclear if this is reason enough for challenging independent self-experimentation or investigator co-participation. In self-experiments, the researcher is both investigator and single participant, so the requirement for informed consent could be waived. Still, there is clear historical precedent for scientific investigators successfully observing and analyzing their own experiences of pain. The results of such published self-experiments have been integrated into the body of knowledge of pain, and replicated in numerous studies using naïve participant introspective reports and standard scientific methods.

References

Dresser R (2013) Personal knowledge and study participation. J Med Ethics. doi:10.1136/medethics-2013-101390.

Hardy JD, Wolff HG, Goodell H (1940) Studies on pain: a new method for measuring pain threshold: observations on spatial summation of pain. J Clin Investig 19(4):649–657.

Head H (1920) Studies in neurology. Oxford University Press, London.

Landau W, Bishop GH (1953) Pain from dermal, periosteal, and fascial endings and from inflammation: electrophysiological study employing differential nerve blocks. AMA Arch Neurol Psychiatry 69(4):490–504.

Price DD (1972) Characteristics of second pain and flexion reflexes indicative of prolonged central summation. Exp Neurol 37(2):371–387.

Price DD, Hu JW, Dubner R, Gracely RH (1977) Peripheral suppression of first pain and central summation of second pain evoked by noxious heat pulses. Pain 3(1):57–68.

Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD (2001) Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain 91 (1):165–175.

Staud R, Craggs JG, Perlstein WM, Robinson ME, Price DD (2008) Brain activity associated with slow temporal summation of C-fiber evoked pain in fibromyalgia patients and healthy controls. Eur J Pain 12(8):1078–1089.

Woollard HH, Carmichael EA (1933) The testis and referred pain. Brain 56(3):293–303.

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van Rysewyk S, von Baeyer CL. Should investigators introspect on their own pain experiences as study co-participants? In: van Rysewyk S (2016). Meanings of Pain. Springer International Publishing AG: Switzerland.

Abstract

The question of investigators introspecting on their own personal pain experiences in pain studies has received little attention in the literature. Study of this question may reflect ethical reservations about the many points at which self-interest may lead us to introspect on personal experiences through personal biases that in turn impair professional decision-making and perception. Despite this valid concern about research co-participation, we offer three reasons why investigators can introspect on personal pain as co-participants in their own pain studies. First, there is historical precedent for investigator participation and co-participation in scientific pain research using introspection as a study method. Second, general concerns about variability in self-report based on introspection on pain experience partly derive from true fluctuations in personal pain experience and perceived interests in self-reporting pain, not simply error in its scientific measurement. Third, the availability of the Experiential-Phenomenological Method, a mixed research method for the study of human experiences, allows investigators to co-participate with naïve participants in their own studies by encouraging passive introspection on personal pain experiences.

Download a copy of the chapter here.

 

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.

In this first post of a series, I describe and challenge several criticisms of reductive materialism, or mind-brain identity theory [5,6,7,8,9,10], made by psychologist Max Velmans. My focus in this post concerns Velmans’s arguments against mind-brain identity theory as presented in ‘What non-eliminative materialism needs to show’ in Appendix I of [4]. Future posts will address his other arguments against mind-brain identity theory as presented in the same work. My intention here is not simply negative, but also positive: using the first-person third-person distinction Velmans appeals to, I propose that the first-person point of view (introspection) and first-person methods are necessary to consciousness science. In developing this view, I focus mostly on pain.

Velmans is a long-time critic of materialist theories of phenomenal consciousness [1,2,3,4]. Following philosopher CD Broad, Velmans distinguishes three versions of materialism: radical, reductive and emergent. He writes [4]:

Radical materialism claims that the term “consciousness” does not refer to anything real (in contemporary philosophy this position is usually called “eliminativism”). Reductive materialism accepts that consciousness does refer to something real, but science will discover that real thing to be nothing more than a state (or function) of the brain. Emergentism also accepts the reality of consciousness but claims it to be a higher-order property of brains; it supervenes on neural activity, but cannot be reduced to it. [4,20]

Velmans begins his argument against mind-body identity theory:

Let us assume that, in some sense, our conscious experiences are real. To each and every one of us, our conscious experiences are observable phenomena (psychological data) which we can describe with varying degrees of accuracy in ordinary language. Other people’s experiences might be hypothetical constructs, as we cannot observe their experiences in the direct way that we can observe our own, but that does not make our own experiences similarly hypothetical. Nor are our own conscious experiences “theories” or “folk psychologies.” We may have everyday theories about what we experience, and with deeper insight, we might be able to improve them, but this would not replace, or necessarily improve the experiences themselves. [4,20-21]

In this passage, Velmans denies that our conscious experiences are ‘theories’ or ‘folk psychologies.’ However, since that is a central claim made by radical materialism (‘eliminativism’) [5,6], not reductive materialism (mind-brain identity theory), Velmans is in error to attribute it to the latter. Like mind-brain identity theory, eliminativism accepts the claim that conscious states are ‘nothing over and above’ brain states (minimal reductionism), but it rejects type identity. This is because eliminativism denies that conscious states are real, and do not exist [10]. By contrast, mind-brain identity theory is realist about mental states and experiences [10]. Mind-brain identity theory is not equivalent to eliminativism [10] (1).

The final sentence in the quote above reads: ‘We may have everyday theories about what we experience, and with deeper insight, we might be able to improve them, but this would not replace, or necessarily improve the experiences themselves.'[my italics] Critics of mind-brain identity theory, like Velmans, believe that a successful scientific reduction of consciousness would make all conscious experiences somehow unreal or even disappear [e.g., 17,18]. Using this conception of reduction, it is then reasoned that because it is observably obvious that a conscious experience like pain is real, it cannot be reduced by science to neurobiological mechanism. This misunderstanding trades on a peculiar view of reduction, where it is expected that in science, type identity claims make conscious experiences disappear. 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. Thus, a successful type identity of pain with mechanism means only that there is an explanation of pain. It is a reduction. But, scientific explanations of phenomenon do not typically make them disappear [5,6,10].

Velmans continues his argument:

In essence then, the claim that conscious experiences are nothing more than brain states is a claim about one set of phenomena (first-person experiences of love, hate, the smell of mown grass, the colour of a sunset, etc.) being nothing more than another set of phenomena (brain states, viewed from the perspective of an external observer). Given the extensive, apparent differences between conscious experiences and brain states this is a tall order. [4,21]

By characterizing mind-brain identity theory as a ‘tall order’, Velmans is in danger of begging the question. It is possible that science will never understand how brain structures such as neurons and protein channels produce pains, emotions and thoughts. The reality of the brain may be forever closed to us. Still, that the problem of consciousness is scientifically tractable or intractable, solvable or insolvable, is impossible to tell simply by noting appearances, since problems do not rank level of difficulty on their sleeves. Why should the problem of consciousness be any different?

Besides, things change. Over time, the nature of a problem may alter shape as new knowledge and understanding arrive. A problem may come to be viewed in novel ways as a result of reciprocal developments in technology, scientific methods and theory. For example, the composition of stars was regarded by scientists as an intractable problem. The problem was that it was impossible to get close enough to collect a star sample without burning up. However, with the unexpected discovery of spectral analysis, this problem proved tractable. The elements of stars were found to produce a type of fingerprint when heated to incandescence, easily observed when light produced from a source is passed through a prism.

In the early twentieth century, the copying problem in molecular genetics was thought to be intractable. This problem, however, was solved in the decades following Watson and Crick’s 1953 publication that DNA is a double helix. By contrast, the problem of how protein molecules fold into their 3D shape once made, believed by many scientists to be solvable in the mid-twentieth century, remains entirely unsolved today despite many decades of effort. Moreover, contributing solutions to twenty-first century problems can come from surprising and novel sources that may challenge conventional thinking. What seems apparently true or observably obvious during immediate experience or armchair reflection is sometimes a poor guide to reality.

Velmans again:

Instances where phenomena viewed from one perspective turned out to be one and the same as seemingly different phenomena viewed from another perspective do occur in the history of science. A classical example is the way the “morning star” and the “evening star” turned out to be identical (they were both found to be the planet Venus). But viewing consciousness from a first- versus a third-person perspective is very different to seeing the same planet in the morning or the evening. From a third-person (external observer’s) perspective one has no direct access to a subject’s conscious experience. Consequently, one has no third-person data (about the experience itself) which can be compared to or contrasted with the subject’s first-person data. [4,21]

It is unclear what Velmans means by ‘From a third-person (external observer’s) perspective one has no direct access to a subject’s conscious experience.’ I presume he intends that what I experience during a conscious episode cannot be available to you or indeed any one else in the way it is directly available to me. I occupy a uniquely privileged position concerning my experience that no one else can occupy. But if so, then he is intuitively characterizing the problem of consciousness in terms of method of access, and in terms of a privileged mode of access at that, namely, ‘direct’ personal introspection, which is question-begging.

This intuitive take on the problem of consciousness also results in a misrepresentation of what science is really up to, since the scientific enterprise relies on the intersubjective availability of its subject matter, in that no one is privileged with regard to collecting evidence about the object of the study. This means that no one has any special epistemic authority over evidence that others cannot in principle understand. In principle, must a successful reduction of pain produce a scientific explanation and pain? Obviously, no – scientific pain research aims to explain pain; it is not in the business of spontaneously concocting the phenomenon in question. To think otherwise is to misrepresent the limits and possibilities of science [5,6,10].

Now, there is a positive characterization of Velmans’s appeal to the first-person and third-person distinction I wish to show. Velmans’s description of the consciousness landscape should be taken to imply that the subject matter of consciousness research is brain mechanism as related to conscious 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). Consciousness research aims to discover the brain mechanisms subserving conscious experiences accessible only through introspection, which means that consciousness research is entirely reliant on the first-person point of view and on using first-person investigative methods. Contrary to Velmans’s view, this necessarily includes introspection together with third-person methods (e.g., neuroimaging). Since consciousness research aims to know which experience types are generated by which brain mechanism, researchers must naturally know when specific conscious experiences occur and what their personal qualities are. Which means that introspection is indispensable to consciousness research.

The history of scientific pain research clearly 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 [19].

Finally, Velmans:

Neurophysiological investigations are limited, in principle, to isolating the neural correlates or antecedent causes of given experiences. This would be a major scientific advance. But what would it tell us about the nature of consciousness itself? [4,21]

I will respond to Velmans’s question with my own: how is mind-brain identity theory positioned relative to the indispensability of introspection to consciousness research? As Velmans notes, introspection is a direct way of coming to know about personal experiences and their qualities. It is an epistemological activity. Still, despite appearances to the contrary or personal conviction, what introspection reveals to us may be utterly mechanistic. It may be that what neuroscientists study through third-person methods is type 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.

Mind-brain identity theory follows a long line of identifications that have marked progress in knowledge: water is H2O, light is electromagnetic energy, lightning is electrical discharge, influenza is a viral infection, and so on. Each of these identities is part of a larger theory that was accepted because it provided a better explanation of the evidence than rival theories. To illustrate this claim, take the conventional example of the type identity of fire and rapid oxidation. Why is this type identification descriptive (i.e., informative)? The first step is to conduct a qualitative investigation of fire. The flame is the visible part of fire, it releases heat and light, is normally sustained by a continuous supply of fuel, and so on. Some qualitative facts about fire are easily observed and others take further investigation, for instance, facts about the reactions that make fire explode. This provides a provisional description of fire. These qualitative descriptions (facts) about fire are then matched with qualitative descriptions (facts) about the operation of rapid oxidation, which is the sequence of chemical reactions between a fuel and an oxidant, such as oxygen or fluorine gas. These facts are harder to describe but essential. When sufficient information is at hand concerning the parts and operations of fire and the parts and operations of specific chemical reactions (rapid oxidation), we can describe how the structure of fire delineates its qualitative chemical properties. The multilevel mechanistic description of fire type identifies it with a specific mechanism type, rapid oxidation, and describes its behavior in terms of the behavior and composition of this mechanical operation. Fire is rapid oxidation.

The type identification of fire and rapid oxidation is only enabled if other substances are also type identified with other molecules, and if elements are type identified with chemical types, and so on. That is, the type identity of fire and rapid oxidation works because it is framed in the broader descriptive context of chemistry and physics. Those general framework theories imply the type identifications. Of course, the type identification of fire and rapid oxidation might be faulted as an incorrect description, perhaps because the physical operations involve activity in a broader range of physical processes. But that criticism merely asserts a different type identity description, and does not challenge type identity claims per se. It is conceivable to ponder whether fire is correctly type identified with rapid oxidation rather than with some other operation; but within the framework of chemistry and physics as they are understood, it is not reasonable to ponder whether fire might fail to be any type of mechanical operation at all.

In the same way, mind-brain identity theory is part of a rich theory that aims to explain conscious and unconscious mental phenomena such as perception, memory, reasoning, addiction, and disease. The personal experience of pain is multidimensional and involves specific sensory, emotional and cognitive features. I think there is a well established multilevel view of the physiological mechanisms that best describes pain qualities. This mechanistic description is framed within the context of advancing theories of the nervous, endocrine and immune systems and their complex functional interdependencies. There are also complex adaptive system-based descriptions of pain experience. Taken together, these descriptions reveal how pain is type identified with mechanism [10].

Although empirical progress in the understanding of pain is typically gradual and piecemeal, the type identification of pain with brain mechanism does not proceed in an additive manner. Pain scientists do not discover one pain type identity at a time and then add them together. Rather, what justifies claims to have type identified the mechanisms of pain is the way the entire multilevel mechanistic package coheres [10].

Endnotes

1. Briefly, the central argument for eliminativism is the idea that we use a theoretical framework to explain and predict human behavior [11], usually called the theory-theory (TT). TT views folk psychology (FP) as comprising specific theoretical claims and generalizations (and laws), described by our everyday common-sense psychological (i.e., mental) words such as ‘belief’, ‘desire’, ‘recognition’, ‘fear’, ‘anticipate’, ‘memory’ or ‘pain’. FP generalizations are thought to describe the diverse causal regularities and relations of FP claims.

TT claims that FP generalizations and claims operate in FP much like the generalizations and laws of scientific theories. However, the laws of FP are acquired more informally than scientific theories, as part of normal human development [e.g., 12,13,14,15]. For example, children who observe their parents showing fear and behavioral avoidance to back-stressing tasks, such as lifting heavy objects, may adjust their understanding of that situation (‘back-stressing tasks are dangerous and can cause pain’) and the behavioral effects (‘avoidance of back-stressing tasks generally reduces pain’) based on the generalization ‘Since back-stressing tasks can cause pain, and avoidance of these tasks generally reduces pain, it is best to avoid such tasks’ [16].

References

[1] Velmans, M. (2000). Understanding Consciousness. London: Routledge/Psychology Press.

[2] Velmans M. (2001a). A natural account of phenomenal consciousness. Consciousness and Communication, 34(1&2), 39-59.

[3] Velmans M. (2001b). Heterophenomenology versus critical phenomenology: A dialogue with Dan Dennett. http://cogprints.soton.ac.uk/documents/disk0/00/00/17/95/index.html.

[4] Velmans M. (2002). How Could Conscious Experiences Affect Brains? Journal of Consciousness Studies 9(11), 3-29.

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

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

[7] Place UT. (1956). Is Consciousness a Brain Process? British Journal of Psychology47, 44-50.

[8] Polger TW. (2004). Natural minds. Cambridge, Mass.: The MIT Press.

[9] Smart JJC. (1959).  Sensations and Brain Processes. Philosophical Review68, 141-156.

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

[11] Sellars W. (1956). Empiricism and the Philosophy of Mind. Minnesota Studies in Philosophy of Science, 1, 253-329.

[12] Churchland PM. (1981). Eliminative Materialism and the Propositional Attitudes. Journal of Philosophy, 78, 67-90.

[13] Hardcastle VG. (1999). The Myth of Pain. Cambridge, Mass.: MIT Press.

[14] Roth M. (2012). Folk psychology as science. Synthese, 189(4), 1-12.

[15] Stich S. (1983). From Folk Psychology to Cognitive Science. Cambridge Mass.: MIT Press.

[16] Goubert L, Vlaeyen JW, Crombez G, & Craig KD. (2011). Learning about pain from others: an observational learning account. The Journal of Pain, 12(2), 167-174.

[17] Chalmers D. (1996). The Conscious Mind. Oxford: Oxford University Press.

[18] Searle JR. (1992). The Rediscovery of Mind. Cambridge, Mass.: MIT Press.

[19] 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.

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

William’s reasoning for the title of his excellent article – that dualism inspired by radical skepticism can mystify and confound experimental results – conveys a truth often neglected in a majority of philosophy of mind and consciousness; namely, skepticism is an organ of doubt, but please don’t forget what we already know. Doubt is useful in philosophy; but radical doubt is self-consuming.

The intrauterine view of gender identity and sexual orientation

The intrauterine theory of gender identity proposes that gender identity is encoded in brain during intrauterine development (e.g., Savic et al. 2011; Swab, 2007). The brain is thought to develop in the male ‘direction’ through a surge of testosterone on nerve cells, likely in the bed nucleus of the stria terminalis (BSTc) in the limbic system (Chung et al. 2002; Krujiver et al. 2000; Zhou et al. 1995), whereas in the female ‘direction’ this surge is absent. This view of gender identity has been adapted to explain transsexualism: since sexual differentiation of the brain occurs in the second half of pregnancy, and sexual differentiation of the sexual organs occurs in months 1-2 of pregnancy, transsexuality is possible. Thus, the relative masculinization of the brain at birth may not reflect the relative masculinization of the genitals (e.g., Bao & Swab, 2011; Savic et al. 2011; Veale et al. 2010).

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The intrauterine theory implies that transsexualism is entirely dependent on a specific and dedicated neuroanatomical brain ‘module’, the BTSc). At a time during the second half of pregnancy, the BSTc comes ‘on-line’, and sexual  – or transsexual  – identity is thereby formed in the individual.

The intrauterine theory as a maturational theory

As a maturational brain theory, the intrauterine theory assumes functional localization of gender identity as an attribute of a specific brain structure or region (i.e., the BSTc) and its patterns of functional connectivity, rather than its patterns of functional connectivity to other structures or regions, to the whole brain and its external environment (van Rysewyk, 2010). Developmentally, a maturational view assumes establishment of intraregional connections, rather than interregional connectivity. It follows that the intrauterine view implies that transsexualism involves a process of organizing intraregional interactions within the BSTc. The bed nucleus of the STc appears to be critically involved.

Extending the maturational aspect of the intrauterine view to gender development also means that we should observe changes in the response properties of the BSTc during pregnancy as regions within the BSTc interact with each other to establish their functional gender roles. Thus, the onset of transsexual identity during intrauterine development will be associated with reliable changes in several regions in the BSTc.

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ST ‘off-line’

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ST ‘on-line’; onset of transsexual identity

The intrauterine theory and mind-brain identity theory

Philosophically, the intrauterine view is also highly compatible with mind-brain identity theory, a philosophy of mind and consciousness (van Rysewyk, 2013). Mind-brain identity theory claims that mental states are identical to brain states. This implies that a person’s indubitable sense of gender identity as manifested in real-time feelings, sensations, thoughts and reports made to others of being a woman or a man are numerically identical to specific brain states, possibly states of a single brain structure or region. Are the brain states in question states of one brain structure – the BSTc? It appears not, for Chung et al. (2002) found that significant sexual dimorphism in BSTc size and neuron number does not develop in humans until adulthood. However, most male-to-female (MTF) transsexuals self-report that their feelings of gender dysphoria began in early childhood (e.g., Lawrence, 2003).

Clearly, these important findings are not compatible with the maturation of one brain structure or region, but with inter-regional brain development, of which the BSTc may feature as merely one, but significant, contributor. Thus, following the onset of transsexual identity, there is a reorganization of interactions between different brain structures and regions. This reorganization process could change previously existing mappings between brain structures and regions and their functions. It follows that the same phenomenal sense of gender identity in a person (e.g., recurring feelings of gender dysphoria) could be supported by different neural substrates at different ages during development. This possibility doesn’t necessarily exclude a maturational theory of transsexual identity, since the BSTc may be stimulated to reorganize its intrauterine functional connectivity following appropriate stimulation during postnatal development.

Future experimental questions for the function of the BSTc in gender identity and sexual orientation

1. The extent of BSTc localization in gender identity: how diffuse or focal is BSTc activity that results from gender-identity based stimulation?

2. The extent of BSTc specialization in gender identity: How coarsely or finely-tuned is BSTc activity that results from gender-identity based stimulation?

The inter-regional interaction theory of gender identity assumes that as brain tissue becomes more specialized (i.e., finely-tuned), it will become activated by a narrow range of gender-based experiences. With increased specialization, less extensive areas of brain tissue (BSTc?) will identify with gender-based phenomenology.

References

Bao, A. M., & Swaab, D. F. (2011). Sexual differentiation of the human brain: relation to gender identity, sexual orientation and neuropsychiatric disorders.Frontiers in neuroendocrinology32(2), 214-226.

Chung, W. C., De Vries, G. J., & Swaab, D. F. (2002). Sexual differentiation of the bed nucleus of the stria terminalis in humans may extend into adulthood. Journal of Neuroscience, 22, 1027-1033.

Kruijver, F. P., Zhou, J. N., Pool, C. W., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (2000). Male-to-female transsexuals have female neuron numbers in a limbic nucleus. Journal of Clinical Endocrinology and Metabolism, 85, 2034-2041.

Lawrence, A. A. (2003). Factors associated with satisfaction or regret following male-to-female sex reassignment surgery. Archives of Sexual Behavior, 32, 299-315.

Savic, I., Garcia-Falgueras, A., & Swaab, D. F. (2010). Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Progress in Brain Research, 186, 41-65.

Swaab, D. F. (2007). Sexual differentiation of the brain and behavior. Best Practice & Research Clinical Endocrinology & Metabolism21(3), 431-444.

van Rysewyk, S. (2010). Towards the the developmental pathway of face perception abilities in the human brain. In: A. Freitas-Magalhães (Ed.), ‘Emotional Expression: The Brain and the Face’ (V. II, Second Series), University of Fernando Pessoa Press, Oporto: pp. 111-131.

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

Veale, J. F., Clarke, D. E., & Lomax, T. C. (2010). Biological and psychosocial correlates of adult gender-variant identities: a review. Personality and Individual Differences48(4), 357-366.

Zhou, J. N., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (1995). A sex difference in the human brain and its relation to transsexuality. Nature, 378, 68-70.

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.

Here.

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.

Introduction

According to an influential neuroscientific theory, gender identity is encoded in the brain during intrauterine development. The brain is thought to develop in the male ‘direction’ through a surge of testosterone on nerve cells; in the female ‘direction’, this surge is thought to be absent (e.g., Savic et al. 2011; Swab, 2007). Call this the ‘standard view of gender identity’.

The standard view of gender identity offers an explanation of transsexualism. Since sexual differentiation of the brain occurs in the second half of pregnancy, and sexual differentiation of the sexual organs occurs in months 1-2 of pregnancy, trans-sexuality may occur. The relative masculinization of the brain at birth may not reflect the relative masculinization of the genitals (e.g., Bao & Swab, 2011; Savic et al. 2011; Veale et al. 2010). According to the standard view, transsexualism is entirely dependent on, and thereby reduces to, specific neurophysiological changes that occur during intrauterine growth in two interconnected organ types (i.e., brain and genitals).

The reductive nature of the standard view of gender identity is compatible with  mind-brain identity theory in philosophy of mind and consciousness. Mind-brain identity theory claims that mental states are identical to brain states. Concerning gender identity, mind-brain identity theory claims that a person’s gender identity is identical to neurophysiological mechanism. A strong and profound implication of this view, if it is correct, is that a person’s indubitable sense of being a ‘female’ or a ‘male’ is nothing more than the operations of neurophysiology encoded during intrauterine growth. Mind-brain identity theory contrasts with philosophies of mind which propose that minds are dependent but still somehow ‘more than’ the body on which they depend.

Brain-Sex Theory of Transsexualism and Mind-Brain Identity

According to the strong version of ‘brain-sex’ theory of transsexualism,  transsexualism is nothing more than (one and the same as) a specific neuranatomical (i.e., structural) intersex type, in which one or more sexually dimorphic brain areas are incompatible with bological sex. The theory therefore assumes that the relationship between transsexualism and neurophysiology is one of identity. Gender identity reduces to neurophysiology. Thus, there is a specific neuroanatomical type for female gender identity in male-to-female (MTF) transsexuals, and a specific neuroanatomical type for male gender identity in female-to-male (FTM) transsexuals. The most compelling neuroscientific evidence in support of an identity view of transsexualism comes from Kruijver et al. (2000) and Zhou et al. (1995).

Neuroscientific Evidence for Brain-Sex Theory of Transsexualism

Zhou et al. (1995)

Zhou et al. (1995) observed that a group of neurons in the hypothalamus, the central subdivision of the bed nucleus of the stria terminalis (BSTc), was sexually dimorphic in humans. Zhou et al. found that the average volume of the BSTc in postmortem males was roughly 44% larger than in females. However, in 6 male-to-female (MTF) transsexuals who had feminizing hormone treatment, the average volume of the BSTc was within the typical female range. The authors found that the 6 transsexuals they investigated varied in their sexual orientations and inferred that there was no relationship between BSTc size and the sexual orientation of transsexuals. I assume that this assertion implies that transsexual sexual orientation and BSTc size are not type identical; that is, they are not the same type. Finally, further postmortem investigations conducted in a small number of nontranssexual patients with abnormal hormone levels, led Zhou et al. to reason that the small volume of the BSTc in MTF transsexuals cannot be explained by adult sex hormone levels (p. 70). Thus, there appears to be a relationship of identity between transsexualism and small BSTc volume. They are one and the same.

Kruijver et al. (2000)

Kruijver et al. (2000) conducted a follow-up study in which they investigated the number of neurons in the BSTc rather than its volume. The authors examined tissue from the same 6 MTF transsexuals studied by Zhou et al. (1995). They also studied nerve tissue from one female-to-male (FTM) transsexual and from an 84-yr-old man who ‘had very strong cross-gender identity feelings but was never . . . sex-reassigned or treated . . . with estrogens’ (p. 2039). The authors found that BSTc neuron number was even more sexually dimorphic than BSTc volume; namely, the average BSTc neuron number in males was 71% higher than in females. Once again, the 6 MTF transsexuals showed a sex-reversed identity pattern, with an average BSTc neuron number in the female range. BSTc neuron number was also in the female range in the untreated gender dysphoric male and was in the male range in the FtM transsexual. Again, the putative sexual orientation of the MTF transsexuals appeared to make no difference. In contrast to the claims of the standard view of gender identity, data from the few non-transsexual patients with abnormal hormone levels led Kruijver et al. (2000) to conclude that ‘hormonal changes in adulthood did not show any clear relationship with the BSTc . . . neuron number’ (p. 2039).

Neuroscientific Objections to Brain-Sex Theory of Transsexualism

Chung et al. (2002)

Brain-sex theory of transsexualism faces several neuroscientific challenges. Chung et al. (2002) found that significant sexual dimorphism in BSTc size and neuron number does not develop in humans until adulthood. However, most MTF transsexuals self-report that their feelings of gender dysphoria began in early childhood (e.g., Lawrence, 2003). Since MTF transsexuals have not yet become sexually dimorphic by the time cross-gender feelings have become obvious, it is unlikely that BSTc volume and neuron number can be a neuroanatomical signature identifiable with gender identity. However, Chung et al. (2002) speculate that foetal or neonatal hormone levels could influence gender identity and could also produce changes in BSTc synaptic density, neuronal activity, or neurochemicals that may not affect BSTc volume or neuron number immediately, but may do so during adulthood. I am not aware of any evidence in support of this hypothesis. In any event, mind-brain identity theory can agree with Chung’s et al. (2002) speculation. Mind-brain identity theory is neutral on whether ‘brain characteristics’ will be macro or micro, or both, or what their specific developmental effects will be. Gender identity might be a state of the entire brain, synapses, or multiple, interacting physiological systems. Macro/microreductionism is optional, not required. Finally, Chung et al. (2002) speculate that inconsistency between an individual’s gender identity and biological sex might likely affect adult BSTc size and neuron number by some yet unknown mechanism or mechanisms. Given that neuroscience is in a very early stage of understanding gender identity, the implication that more time is needed to understand transsexualism appears prudent.

Joel (2011)

Joel (2011) challenges an implicit assumption in the standard view of gender identity; namely, human brains are one of two types –  ‘male’ or ‘female’ – and that the differences between these two types subserve subtype differences between men and women in gender identity and transsexualism. According to Joel (2011), this assumption is true only if there is robust correspondence (i.e., high statistical correlation) between the ‘male’/’female’ type of all of the brain characteristics in a single brain. It turns out there isn’t. As Joel points out, concerning most documented sex brain differences, there is overlap between the distributions of the two sexes (e.g., Juraska, 1991; Koscik et al. 2009). Neuroanatomical data also reveal that sex interacts with other factors during the intrauterine period and throughout life to determine brain structure (e.g., prenatal exposure to psychoactive drugs, early handling, rearing conditions, maternal separation, acute and chronic postnatal stress). Human brains therefore are a dynamic heterogeneous mosaic of ‘male’ and ‘female’ brain characteristics that cannot be type identified on a simple continuum between a ‘male type brain’ and a ‘female type brain’ (Joel, 2011). Thus, brains are not type sexed, but type intersexed; sexually multi-morphic rather than dimorphic.

Joel’s theory is compatible with brain-sex theory of transsexualism since both theories claim that transsexualism is intersexual, but incompatible because it denies what brain-sex theory asserts; namely, in transsexualism, one or more sexually dimorphic brain areas are incompatible with bological sex. Thus, Joel’s view rejects the stronger claim that gender is type identical with the sexually dimorphic brain. Accordingly, we cannot predict the specific properties of ‘male/female’ brain characteristics of an individual based on her/his sex.

However, Joel’s view implies the weaker consequence that, on average, we can predict that females will have more brain characteristics with the ‘female’ type than with the ‘male’ type (vice versa for FTM transsexuals), and males will have more brain characteristics with the ‘male’ type than with the ‘female’ type (vice versa for MTF transsexuals). Whether two individuals are similar or not is dependent on the similarity in the details of their brain mosaic; not on the quantity of ‘male’ and ‘female’ characteristics. This means that two similar individuals share characteristics of the same ‘brain mosiac’ type – they have the same type. Brains of the same type must possess the characteristics and properties typical of the type, but that does not imply that they all be exactly similar to one another. This implication is compatible with mind-brain identity theory.

References

Bao, A. M., & Swaab, D. F. (2011). Sexual differentiation of the human brain: relation to gender identity, sexual orientation and neuropsychiatric disorders. Frontiers in neuroendocrinology, 32(2), 214-226.

Chung, W. C., De Vries, G. J., & Swaab, D. F. (2002). Sexual differentiation of the bed nucleus of the stria terminalis in humans may extend into adulthood. Journal of Neuroscience, 22, 1027-1033.

Hines M. (2004). Brain Gender. Oxford: Oxford University Press.

Koscik, T., O’Leary, D., Moser, D. J., Andreasen, N. C., & Nopoulos, P. (2009). Sex differences in parietal lobe morphology: relationship to mental rotation performance. Brain Cognition, 69, 451–459.

Kruijver, F. P., Zhou, J. N., Pool, C. W., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (2000). Male-to-female transsexuals have female neuron numbers in a limbic nucleus. Journal of Clinical Endocrinology and Metabolism, 85, 2034-2041.

Joel, D. (2011). Male or female? Brains are intersex. Frontiers in integrative neuroscience, 5, 57.

Juraska J. M. (1991). Sex differences in “cognitive” regions of the rat brain. Psychoneuroendocrinology 16, 105–109. doi: 10.1016/0306-4530(91)90073-3.

Lawrence, A. A. (2003). Factors associated with satisfaction or regret following male-to-female sex reassignment surgery. Archives of Sexual Behavior, 32, 299-315.

Savic, I., Garcia-Falgueras, A., & Swaab, D. F. (2010). 4 Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Progress in Brain Research, 186, 41-65.

Swaab, D. F. (2007). Sexual differentiation of the brain and behavior. Best Practice & Research Clinical Endocrinology & Metabolism, 21(3), 431-444.

Veale, J. F., Clarke, D. E., & Lomax, T. C. (2010). Biological and psychosocial correlates of adult gender-variant identities: a review. Personality and Individual Differences, 48(4), 357-366.

Zhou, J. N., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (1995). A sex difference in the human brain and its relation to transsexuality. Nature, 378, 68-70.

Is gender identity – the sense of being a man or a woman – a perception identical with the nonconscious physical brain or the conscious non-physical soul? Since people who identify as transsexual verbally self-report strong feelings of being the opposite sex and a feeling that their sexual characteristics are not constitutive of their actual gender, they are a powerful case in explaining the nature of gender identity and phenomenal consciousness.

It is possible that a person’s sense of gender identity may be subserved by an
nonconscious physical base with a specific neurophysiological or neural ‘signature’. Explaining gender identity in this direct way aims first to describe the base as a correlate of gender identity, then ultimately to achieve a reductive neurophysiological explanation of gender identity.

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

There is support for theoretical identification of gender identity with neurophysiological mechanism. According to the most influential theory, during the intrauterine period, two mechanical operations may occur: (1) in the female ‘direction’, there is no surge of testosterone on nerve cells; (2) in the male ‘direction’, there is a surge of testosterone on nerve cells. Since sexual differentiation of the brain occurs in the second half of pregnancy, and sexual differentiation of the sexual organs occurs in months 1-2 of pregnancy, transsexuality may result. Thus, the relative masculinzation of the brain at birth may not reflect the relative masculinization of the genitals (e.g., Berenbaum & Beltz, 2011; Savic et al. 2011; Veale et al. 2010).

One line of neuroscientific support for a neuroanatomical signature of gender identity derives from studies on whether gray matter volumes in (heterosexual) male-to female (MTF) transexuals before cross-sex hormonal treatment are correlated with people who share their biological sex (i.e., men), or people who share their gender identity (i.e., women). Luders et al. (2009) analyzed MRI data of 24 male-to-female (MTF) transsexuals and found that regional gray matter variation in MTF transsexuals correlates with the pattern found in men than in women. Luders et al. (2012) found thicker cortices in MTF transsexuals, both within regions of the left hemisphere (i.e., frontal and orbito-frontal cortex, central sulcus, perisylvian regions, paracentral gyrus) and right hemisphere (i.e., pre-/post-central gyrus, parietal cortex, temporal cortex, precuneus, fusiform, lingual, and orbito-frontal gyrus) than age-matched control males.

In contrast, Rametti et al. (2011) found that the white matter microstructure pattern in MTF transsexuals is halfway between the pattern of examined male and female controls. These differences may indicate that some fasciculi do not complete the masculinization mechanical operation in MTF transsexuals during foetal brain development. This implies that the social environment is co-constitutive of gender identity. Clearly, more research is needed to answer this question.

Another line of neuroscientific research has focused on intrinsic brain activity (i.e., brain resting-state) to investigate correlations between the spontaneous brain connectivity of transexuals and control groups. Santarnecchi et al. (2012) used both seed-voxel and atlas-based region-of-interest (ROI) approaches and found that brain regions sensitive to gender dimorphism (e.g., left lingual gyrus, precuneus) revealed robust correlations between the female-to-male (FTM) subject and female control group with regard to control males, with comparable extension and location of functional connectivity maps. ROI analysis supported this result, demonstrating an increased pattern of differences between the FTM subject and males and the FTM subject and females. No statistically significant difference was found between seed-voxel results in the FTM subject and females. This study supports the hypothesis that untreated FTM transgender shows a functional connectivity profile comparable to female control subjects.

Taken together, these findings provide evidence that transsexualism is correlated with a specific physical signature, in terms of neuroanatomy and brain connectivity, which supports the claim of mind-brain identity theory that neurophysiological mechanism is constitutive of gender identity. Thus, the most reasonable explanation of transsexualism and gender identity is that it is entirely physical in nature.

References

Berenbaum, S. A., & Beltz, A. M. (2011). Sexual differentiation of human behavior: Effects of prenatal and pubertal organizational hormones. Frontiers in Neuroendocrinology, 32(2), 183-200.

Luders, E., Sánchez, F. J., Gaser, C., Toga, A. W., Narr, K. L., Hamilton, L. S., & Vilain, E. (2009). Regional gray matter variation in male-to-female transsexualism. Neuroimage, 46(4), 904-907.

Luders, E., Sánchez, F. J., Tosun, D., Shattuck, D. W., Gaser, C., Vilain, E., & Toga, A. W. (2012). Increased Cortical Thickness in Male-to-Female Transsexualism. Journal of Behavioral and Brain Science, 2, 357-362.

Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Segovia, S., Gomez, Á., & Guillamon, A. (2011). White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study. Journal of psychiatric research, 45(2), 199-204.

Santarnecchi, E., Vatti, G., Déttore, D., & Rossi, A. (2012). Intrinsic Cerebral Connectivity Analysis in an Untreated Female-to-Male Transsexual Subject: A First Attempt Using Resting-State fMRI. Neuroendocrinology, 96(3), 188-193.

Savic, I., Garcia-Falgueras, A., & Swaab, D. F. (2010). 4 Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Progress in Brain Research, 186, 41-65.

Veale, J. F., Clarke, D. E., & Lomax, T. C. (2010). Biological and psychosocial correlates of adult gender-variant identities: a review. Personality and Individual Differences, 48(4), 357-366.

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