A neurobehavioral-polyvagal theory of pain facial expression

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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Challenges facing pain reductionism

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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.

Pain in the brain? The question of fetal pain

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.

Links between the intrauterine theory of gender identity, transsexualism and mind-brain-body identity

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).

fp4-5.jpg (836×591)

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.

Gray691

 

 

 

 

 

 

 

 

 

 

ST ‘off-line’

Gray691 (1)

         

 

 

 

 

 

 

 

 

 

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.

Eben Alexander: ‘Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife’ (2012) – is consciousness cortical?

Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife‘ (2012), by neurosurgeon Eben Alexander, presents a narration and interpretation of the near-death experience (NDE) of its author. Alexander developed bacterial meningitis, and was hospitalized. During hospitalization, he became deeply comatose, a condition which lasted seven days. Alexander was fortunate to come out of his coma state and retain full wakeful consciousness. Following wakefulness, Alexander reported remarkably clear visions, sensations and thoughts he claims to have had during his near-death coma. In his book, Alexander interprets this NDE as proof that life follows death, death is not the end, there exists an extremely pleasant and serene afterlife, and that consciousness is independent of the cortical brain. It is the last claim of Alexander’s that I will consider in this post. Specifically, is consciousness independent of cortex?

According to Alexander, his coma-induced NDE occured when his cerebral cortex was ‘completely shut down’, ‘inactivated’, and ‘totally offline’. In the article he wrote for Newsweek, Alexander writes that the absence of cortical activity in his brain was ‘clear from the severity and duration of my meningitis, and from the global cortical involvement documented by CT scans and neurological examinations.’ The problem with Alexander’s view of coma is that it is not supported by evidence. First, ‘global’ (complete) cortical ‘shut down’ does not result in coma, as Alexander believes. Complete cortical ‘shut down’ is fatal, and results in brain death (e.g., Cavanna et al. 2010; Charland-Verville et al. 2012; Laureys et al. 2004a; Laureys et al. 2004b). Second, ‘flat’ EEG recordings concurrent with high alpha cortical brain activity are frequently observed in comatose patients; this event is termed ‘event-related desynchronization’. There is a vast and well-established scientific literature on this topic (e.g., Pfurtscheller & Aranibar, 1979; Pfurtscheller, 1992; Pfurtscheller et al. 1999). Thus, coma does not require complete cortical deactivation.

Alexdander’s claim that NDEs require complete cortical shut down carries the implication that fully (wakeful) sensory consciousness must involve only cortex. Alexander’s argument is in line with a trend in consciousness studies research to investigate cortical regions, pathways, and activity guided by the slogan ‘seeking the neural correlates of consciousness.’ Clinical studies of cortical lesions have motivated this approach, largely due to robust correlations such as fusiform lesions leading to prosopagnosia, or ventral stream lesions leading to the visual inability to percieve shapes. The convenience of neuroimaging cortical activity with MEG, EEG, PET and fMRI has likely also played a part in the focus on cortex.

However, viewing (wakeful) sensory consciousness as purely cortical neglects essential subcortical-cortical behavioural aspects (e.g., Churchland, 2002; Damasio, 1999; Guillery & Sherman, 2002; Llinas, 2001; van Rysewyk, 2013). Put very simply (and briefly), a basic function of mammalian and non-mammalian nervous systems is to enable and regulate movements necessary to evolutionary goals such as feeding and reproducing. Peripheral axons that carry sensory information have collateral branches that project both to subcortical motor structures (primarily, thalamus) and cortical motor structures (primary motor cortex, M1). According to Guillery and Sherman (2002), all peripheral sensory input communicates information about ongoing instructions to such subcortical-cortical motor stuctures, which implies that a sensory signal can become a prediction about what movement will happen next. Thus, as an organism learns the effects of a specific movement, it learns about what in the world will likely occur next (planning), and thus what it might do following that event (deciding, acting). Temporality emerges as central to the nature of consciousness. In order to keep the body alive, nervous systems face numerous complex challenges in learning, continuous effective prediction, attention to different sensorimotor events, and calling up stored (timing) information. Neuroanatomical loops between thalamocortico structures are a plausible physical substrate involved in (identical to?) the temporal and causal aspects of the world, and of one’s own body (e.g., Damasio, 1999; Guillery & Sherman, 2002; Llinas, 2001). This leads to the empirical prediction that in a near-death event, normal functioning of thalamocortico loops is compromised.

References

Cavanna, A. E., Cavanna, S. L., Servo, S., & Monaco, F. (2010). The neural correlates of impaired consciousness in coma and unresponsive states. Discovery medicine, 9(48), 431.

Charland-Verville, V., Habbal, D., Laureys, S., & Gosseries, O. (2012). Coma and related disorders. Swiss archives of neurology and psychiatry, 163(8): 265-72.

Churchland, P. M. (2007). Neurophilosophy at work. Cambridge, UK: Cambridge University Press.

Churchland, P. S. (1989). Neurophilosophy: Toward a unified science of the mind-brain. Cambridge, Mass.: The MIT Press.

Churchland, P. S. (2002). Brain-wise: Studies in neurophilosophy. Cambridge, Mass.: The MIT Press.

Churchland, P. S. (2011). Braintrust: What neuroscience tells us about morality. Princeton: Princeton University Press.

Damasio, A. R. (1999). The Feeling of What Happens. New York: Harcourt Brace.

Guillery, R. W., & Sherman, S. M. (2002). The thalamus as a monitor of motor outputs. Philos. Trans. R Soc. Lond. B Biol. Sci., 357: 1809-1821.

Laureys, S., Owen, A. M., & Schiff, N. D. (2004a). Brain function in coma, vegetative state, and related disorders. The Lancet Neurology, 3(9), 537-546.

Laureys, S., Perrin, F., Faymonville, M. E., Schnakers, C., Boly, M., Bartsch, V., Majerus, S., Moonen, G., & Maquet, P. (2004b). Cerebral processing in the minimally conscious state. Neurology, 63(5), 916-918.

Llinas, R. R. (2001). I of the Vortex: From Neurons to Self. Cambridge, Mass.: MIT Press.

Pfurtscheller, G., & Aranibar, A. (1979). Evaluation of event-related desynchronization (ERD) preceding and following voluntary self-paced movement. Electroencephalography and clinical neurophysiology, 46(2), 138-146.

Pfurtscheller, G. (1992). Event-related synchronization (ERS): an electrophysiological correlate of cortical areas at rest. Electroencephalography and clinical neurophysiology, 83(1), 62-69.

Pfurtscheller, G., & Lopes da Silva, F. H. (1999). Event-related EEG/MEG synchronization and desynchronization: basic principles. Clinical neurophysiology, 110(11), 1842-1857.

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