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.

Sound the Alarm: Fraud in Neuroscience – Dana Foundation

Here.

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.

Call for Chapters: Machine Medical Ethics, Edited Collection

You are warmly invited to submit your research chapter for possible inclusion in an edited collection entitled Machine Medical Ethics. Target publication date: 2014.

The new field of Artificial Intelligence called Machine Ethics is concerned with ensuring that the behaviour of machines towards human users and other machines is ethical. This unique edited collection aims to provide an interdisciplinary platform for researchers in this field to present new research and developments in Machine Medical Ethics. Areas of interest for this edited collection include, but are not limited to, the following topics:

Foundational Concepts

What is medical ethics?

What is machine medical ethics?

What are the consequences of creating or not creating ethical medical machines?

Can medical machines be autonomous?

Ought medical machines to operate autonomously, or under (complete or partial) human physician control?

Theories of Machine Medical Ethics

What theories of machine medical ethics are most theoretically plausible and most empirically supported?

Ought machine medical ethics be rule-based (top-down), case- based (bottom-up), or a hybrid view of both top-down and bottom-up?

Is an interdisciplinary approach suited to designing a machine medical ethical theory? (e.g., collaboration between philosophy, psychology, AI, computational neuroscience…)

Medical Machine Training

What does ethical training for medical machines consist in: ethical principles, ethical theories, or ethical skills? Is a hybrid approach best?

What training regimes currently tested and/or used are most successful?

Can ethically trained medical machines become unethical?

Can a medical machine learn empathy (caring) and skills relevant to the patient-physician relationship?

Can a medical machine learn to give an apology for a medical error?

Ought medical machines to be trained to detect and respond to patient embarrassment and/or issues of patient privacy? What social norms are relevant for training?

Ought medical machines to be trained to show sensitivity to gender, cultural and age-differences?

Ought machines to teach medicine and medical ethics to human medical students?

Patient-Machine-Physician Relationship

What role ought imitation or mimicry to play in the patient-machine-physician relationship?

What role ought empathy or caring to play in the patient-machine-physician relationship?

What skills are necessary to maintain a good patient-machine-physician relationship?

Ought medical machines be able to detect patient fakery and malingering?

Under what conditions ought medical machines to operate with a nurse?

In what circumstances should a machine physician consult with human or other machine physicians regarding patient assessment or diagnosis?

Medical Machine Physical Appearance

Is there a correlation between physical appearance and physician trustworthiness?

Ought medical machines to appear human or non-human?

Is a highly plastic human-like face essential to medical machines? Or, is a static face sufficient?

What specific morphological facial features ought medical machines to have?

Ought medical machines to be gendered or androgynous?

Ought medical machines to possess a human-like body with mobile limbs?

What vocal characteristics ought medical machines to have?

As a new field, the target audiences are expected to be from the scientists, researchers, and practitioners working in the field of machine ethics and medical ethics. The target audience will also include various stakeholders, like academics, research institutes, and individuals interested in this field, 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.

Please indicate your intention to submit your full paper by email to the editor who emails you with the title of the paper, authors, and abstract. The full manuscript, as PDF file, should be emailed to that same editor by the deadline indicated below. Authoring guidelines will be mailed to you after we receive your letter of intent.

Please feel free to contact the editors, Simon van Rysewyk or Dr. Matthijs Pontier, if you have any questions or concerns. Many thanks!

IMPORTANT DATES:

Intent to Submit: June 10, 2013

Full Version: October 20, 2013

Decision Date: November 10, 2013

Final Version: December 31, 2013

Editors:

Simon van Rysewyk

School of Humanities
University of Tasmania
Private Bag 41
Hobart
Tasmania 7001
Australia

Email: simonvanrysewyk@utas.edu.au

Dr. Matthijs Pontier

Post-Doctoral Researcher
The Centre for Advanced Media Research (CAMeRA)
Vrije Universiteit Amsterdam
Buitenveldertselaan 3
1081 HV Amsterdam
The Netherlands

Email: matthijspon@gmail.com

Ali’s excellent and revealing article is here.

‘Brain String Theory’, 2012. Jeremy Strain

InNeuroaesthetics is killing your soul(MUSE, March 2013), science writer Philip Ball argues that our artistic experience and understanding cannot ever be understood in terms of neurophysiological structure and function (i.e., mechanism). Ball claims that neuroscientific research on aesthetics (‘neuroaesthetics’) is wasteful, uninformative, and impossible.

Ball’s article on neuroaesthetics received two thoughtful and critical comments from Brad Foley and Dhalia Zaidel, with whom I entirely agree. In this post, I consider the thoughts that Ball expresses in this passage of the article:

“And what will a neuroaesthetic ‘explanation’ consist of anyway? Indications so far are that it may be along these lines: “Listening to music activates reward and pleasure circuits in brain regions such as the nucleus accumbens, ventral tegmental area and amygdala”. Thanks, but no, thanks. Although it is worth knowing that musical ‘chills’ are neurologically akin to the responses invoked by sex or drugs, an approach that cannot distinguish Bach from barbiturates is surely limited.

There are certain to be generalities in art and our response to it, and they can inform our artistic understanding and experience. But they will never wholly define or explain it”.

In the first paragraph of this passage, Ball objects to the alleged utility of neuroaesthetic explanations of artistic experience. By ‘utility’, I assume Ball means ‘being informative’. The sample neuroaesthetic explanation he gives is: “Listening to music activates reward and pleasure circuits in brain regions such as the nucleus accumbens, ventral tegmental area and amygdala”. Ball denies the utility of this type of explanation because it fails to inform of the actual difference, at the level of the brain, between equally pleasurable experiences as listening to Bach, taking barbiturates or having sex.

I want to make clear here two observations that are (implicitly, I think) backgrounded in Ball’s article. First, it is conceivable that stimulus-driven (external or internal) sensory experience may be subserved by an unconscious physical base with a specific neurophysiological signature. Explaining sensory experience in this direct way aims first to describe the base as a correlate of sensory experience, then ultimately to achieve a reductive neurophysiological explanation of sensory experience (Churchland, 2007; Churchland, 1989, 2002, 2011). Second, brain mechanism responses to stimuli can be correlated for a variety of reasons: (1) the mechanism is part of the cause of the stimulus-induced experience; (2) the mechanism is part of the effect of the experience; (3) the mechanism indirectly parallels the experience; (4) the mechanism is what the experience can be identified with (i.e., x = y) (Churchland, 2007; Churchland, 1989, 2002, 2011). Discovering the neurophysiological signature of aesthetic experience as a type of experience requires the identification of some neurophysiological mechanism with aesthetic experience.

Now, Ball’s sample neuroaesthetic explanation describes a correlation between listening to music and brain response, such as we typically find reported in neuroimaging studies in neuroscience using functional magnetic resonance imaging (fMRI). But, it is not clear which one of the four neuroscientific correlation types he designates in his sample. It would be ironic if the physical signature of aesthetic experience proves to be the very one Ball now denies as even being sufficiently informative. This is possible, but highly unlikely, since the signature will probably reveal a highly complex and interdependent nervous-endocrine-immune ensemble (compare Chapman et al. 2008). In any event, and to challenge Ball’s assertion to the contrary, the correlation of brain response x (e.g., concurrent activation in nucleus accumbens, ventral tegmental area, amygdala) with pleasure in music-listening is informative because x may be the one for identifying musical pleasure. Correspondingly, a brain response y hypothesized by neuroscientists that does not correlate with musical pleasure indicates that y may not be the one. It may turn out that listening to Bach and receiving fellatio do not share the same neural signature. At the end of the day, the implicit target in Ball’s article, and the hidden target of all those people who think as he, is the theoretical identification of aesthetic experience with mechanism (i.e., mind-brain identity theory). Mind-brain identity theory is a philosophy of mind. The identity theory of mind claims that states and processes of the mind are identical to states and processes of the brain (Place, 1956; Polger, 2004; Smart, 1959; van Rysewyk, 2013). If Ball and others surely wish to engage with neuroaesthetics at the intended level, they should acquire some expertise in philosophy of mind and philosophy of art.

In the second paragraph, Ball objects to the very possibility of a neuroaesthetic definition or explanation of artistic experience (“But they will never wholly define or explain it”). This is much stronger than the claim that neuroaesthetics is uninformative. According to Ball, a complete neuroaesethetics of artistic experience is impossible. My interpretation of Ball is speculative, since the reasons for his radical conclusion are not given in the article. And it is unclear exactly what he means by ‘wholly’. Presumably, by ‘wholly’, he means a complete and final neuroaesthetics of all aesthetic experience, irrespective of whether neuroaesthetists can formulate it. A significant casualty of Ball’s view is objective scientific explanation. Since Ball thinks a final scientific explanation of aesthetics is impossible, he is thereby commited to the view that there can be no final explanation of aesthetics which does not involve essential reference to personal opinions, experiences or points of view (i.e., a subjective explanation).

Ball does not explain why he thinks neuroaesthetics cannot ever explain or define aesthetics. I invite him to explain why. Otherwise, his article will come across as little more than a negative argument to the effect that the neuroaesthetic project will not succeed. In the meantime, I hope the following is helpful. As Churchland (1989, 2002, 2011) makes clear, explicit definitions and explanations of things tend to co-evolve in science, and emerge only quite late in the course of protracted scientific and philosophical investigations. Because neuroaesthetics is an extremely young subdiscipline of neuroscience (itself barely 60 years old), I think the prudent hope is for correlations of types (1), (2), (3), described above, to lead to novel hypothetical identities and more advanced experimental and philosophical investigation. Already, we know much more about aesthetic experience than even 5 years ago (Conway & Rehding, 2013). Ultimately, neuroaesthetics wants to produce fundamental scientific aesthetic identities; that is, robust correlations of type (4). Proximately, it is reasonable to set achievable aims. Still, the reality of the brain and body may yet thwart our best investigative attempts to identify artistic experience with neurophysiology.

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: 122-145.

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.

Conway, B. R., & Rehding, A. (2013). Neuroaesthetics and the Trouble with Beauty. PLoS Biol 11(3): e1001504. doi:10.1371/journal.pbio.1001504.

Place, U. T. (1956). Is Consciousness a Brain Process? British Journal of Psychology, 47: 44-50.

Polger, T. W. (2004). Natural minds. Cambridge, Mass.: The MIT Press.

Smart, J. J. C. (1959).  Sensations and Brain Processes. Philosophical Review, 68: 141-156.

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

Martijn D. Steenwijk’s video was a winner in the category of Best Video Illustration of the Brain in the 2012 Brain Art Competition 2012, run by The Neuro Bureau.

Martijn’s description of ‘The Brain at Rest’ video:

“By visualizing both diffusion tensor and resting-state functional MR data, this movie illustrates different concepts of image processing, connectivity and activity in a real human brain at rest. Background music was composed by assigning a musical instrument to the ten strongest functional patterns in the brain. The intensities of these patterns vary over time while the person is at rest in the scanner – these are “spontaneous” brain fluctuations that receive much attention in fMRI research now. By linking the intensity of each pattern to the pitch of its respective instrument a melody is generated, thereby making brain activity audible. The first part of the movie illustrates the source of the melody by showing functional patterns and their varying strengths. The second part shows the major fiber bundles which were obtained by running deterministic tractography from atlas seeds. In the third part, the seeds were replaced by spherical objects ‘running’ around the cortical surface. The last part combines structural connectivity with functional connectivity. Here, functional connectivity is visualized using volume rendering of the voxelwise functional correlation matrix. Together with its structural counterpart, this last part illustrates that structural and functional connectivity are quite different”.

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 absent (e.g., Savic et al. 2011; Swab, 2007). Call this the ‘standard view of gender identity’. The standard view of gender identity offers a plausible 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, transsexuality may occur. The relative masculinzation 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 is that a person’s indubitable sense of being a woman or a man 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 nontranssexual 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.

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