Archive for July, 2006

icon_psychoanalysis.jpgToday we received this nice email from Paul Watson at Psychology Press. They are launching a new site for cognitive neuroscience news. I’ll let the email speak for itself:

Hi Martin & Thomas

Just a quick note to say we’ve recently launched a new Cognitive Neuroscience Arena which I think might be of interest to you two.

(We = Psychology Press, publishers of the journal Social Neuroscience, which you commented on in your blog post on July 4th)

We’ve included a link to the Brain Ethics blog on our blogs page.

As well as all our relevant books and journals, we’ve included a few other features that may be of interest to you and your readers:

1. The whole of the first chapter of our textbook “The Student’s Guide to Cognitive Neuroscience” is available to read free online (we think it’s a great introduction to the subject)

2. In a similar vein, we’ve also got the introductory article from our journal Social Neuroscience, also available to read free online (this is the same one which is on the Social Neuroscience journal website which you posted about).

3. There’s also a page of links to the latest Cognitive Neuroscience blog posts (courtesy of Technorati)

4. An a nifty GoogleMap showing forthcoming Cogntitive Neuroscience conferences (only 3 we know of at time of writing) at http://www.cognitiveneurosciencearena.com/resources/conferences.asp

And numerous other features including an RSS feed of our latest Cogntive Neuroscience books.

I’ve sent the link to your blog to Rose Allet who runs the marketing for the Social Neuroscience journal here at Psychology Press, so she may also email you and will probably send the URL of your blog to the editors of Social Neuroscience so they can see your comments).

If you’ve got any questions, feel free to drop me a line.


Paul Watson

Paul Watson, Senior E-Marketing Executive
Psychology Press



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violent-child.jpgViolence and criminal behaviour is today thought to involve a series of complex interactions between heritable and environmental factors. Centuries of debate of the relative contribution of nature and nurture have not reached anything resembling a solution, and even today we can find ardent proponents and defenders of each extreme view (see Steven Pinker on this, PDF).

While violence and crime has been part of all recorded history, the society’s understanding of the underlying causes of these acts and how they should be dealt with have changed over time. In modern times, we also see a wide variety of legal practices in dealing with criminals and violators: from the death penalties and multiple life sentences in the US, Russia and other countries, to briefer treatment sentences in Europe. These different societal solutions build – explicitly or implicitly – upon what causes violence and criminal acts, and how they should, if at all possible, be treated.

It would be no understatement to claim that the biological explanation of violence and crime has not been fully implemented (nor understood) by law makers or enforcers. Just as you could say about the society in general: aside from specific demonstrations of how violent offenders have larger or smaller neural damage, little is known about the biological properties of violence. Not that the literature has been flourishing with articles demonstrating such relationships. It hasn’t. Until now, where recent studies report detailed analyses of how genes and environments alter the brain’s workings to make people more or less prone to violence, impulsive acts and criminal behaviour.

In a most interesting paper (PDF) published in PNAS, a team of researchers from Austria, Italy and USA headed by Andreas Meyer-Lindenberg have uncovered neurobiological factors that contribute significantly to violence in humans. The team studied the normal allelic variation in the X-linked monoamine oxidase A (MAOA) gene, a gene that has also been shown to be associated with impulsive aggression in humans and animals.

In the study both structural and functional MRI methods were applied. First, the researchers asked whether the low expression variant of MAOA, known to be associated with increased risk of violent behaviour, would predict differences in the size of limbic structures such as the amygdala. Indeed, what they found was that the low expression MAOA predicted limic reductions, as can be shown from the figure article


Structural reductions in limbic and paralimbic regions due to genotype. The size of both the amygdala and cingulate cortex are predicted by benotype. The low expression MAOA have significantly reduced volumes of these structures, compared to the high expression MAOA group.

Second, the team studied how these structures worked using two fMRI paradigms. The first task was a facial expression matching task, a task known to involve the amygdalae. The amygdala activation was significantly influenced by genotype: the low MAOA group displayed higher amygdala activation and at the same time lower activation in cingulate cortex subregions, as well as left orbitofrontal cortex and left insular cortex – all brain regions implied in emotion processing.


Regions involved in facial expression matching (click image for larger version). As you can see from the graphs, there is a genotype-by-gender interaction.

The second task was an emotion memory task, where subjects were asked to encode and recall aversive (compared to neutral) valenced information. Here, the results pointed to a significant genotype-by-gender interaction effect, in that men with a low MAOA version showed increased reactivity of the left amygdala and hippocampus during recall. No such relationship was found for women.

Interestingly, the researchers also found a tight relationship between gender and genotype during the first volumetric study. Here, low-MAOA males showed increased orbitofrontal volume bilaterally, while no such relationship was found in females. In this sense, the MAOA allelic variances seem to influence males most.

Finally, Meyer-Lindenberg and his co-workers draw the lines to other studies relating MAOA variance to a highened sensitivity in low-MAOA males to aversive events (e.g. abuse) during childhood. The combination of a low-MAOA genotype with such events seem to produce abnormal regulation (through the cingulate) of the amygdala and an increased predisposition to impulsivity and violence. As the authors note:

Predisposition to impulsive violence by means of abnormal activation and regulation of emotion-related amygdala function might be further enhanced by deficient neural systems for cognitive control, especially over inhibition, the capacity to suppress prepotent but inappropriate behavior that might originate from a dysregulated affective response. Although the rostral cingulate is key to the regulation of acute affective arousal and emotional learning, inhibitory control of prepotent cognitive responses is thought to be critically dependent on caudal aspects of anterior cingulate. Our study of genetic influences on cognitive impulse control revealed a sex-dependent impairment in precisely this area of cingulate, affecting men only. Our finding of a genotype-by-sex interaction in this region therefore provides a plausible neural mechanism for reduced cognitive inhibitory control in risk allele-carrying males, suggesting synergistic impairment in cognitive and emotional neural regulatory mechanisms that might render MAOA-L men at especially high risk for a neural phenotype that plausibly relates to the slightly greater probability of impulsive violence.

Endnote: it might be useful to note that this study was conducted on healthy, non-criminal volunteers. The obvious step next is to study crime offenders (different types) and the complex interplay between genes, gender and childhood events.


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pvs.jpgIt’s all in the news these days. A man who has been in a coma (or is it “coma-like”, “almost coma” or what?) since a car accident in 1984 has now regained consciousness, and cognitive abilibties such as his speech. It’s already been written so much about this topic, but little is actually addressing the science. Often, the sensationalism is only covered. You can get them all by this simple google.

So why start writing about this here at BrainEthics? The story should have been covered by now? I think there are several reasons to address this story in a bit more detail, one of them being that the science, ethics and philosophical consequences are not – or very superfluously – noted. Another good reason is that the article describing this case has come out, and it’s available for free (PDF). Before we get to it, let me briefly let you know what I’d like to mention here:

  • the diagnosis – coma, vegetative state and related mental states are still very hard to tell apart, even to specialists
  • the development – much has happened to our knowledge about these states, but this knowledge has neither reached the general public, science writers nor always professionals dealing with these patients
  • the future – in addition to developments in traditional diagnosis, neuroimaging is already having a significant impact on our understanding on the relations and distinctions between these different states
  • the ethics – should we reach a scientifically valid model about states of consciousness the next step is to determine who is conscious and who is not – but still we are likely to ask “are our judgements correct?

The Diagnosis

If you are involved in a car accident and lose consciousness, the time from when you lose consciousness until you wake up is characterized by different stages where the brain’s level of functioning changes; from improved primitive reflexes to cognitive and mental restoration. A soon as you reach a state where you become aware of your surroundings, even the feeblest sensation, you have reach a state that is called post-traumatic amnesia (PTA). The person is conscious and appears responsive and they may even be able to talk to family members and medical staff, however after a short time, the person will forget all recollection of conversations and actions. The person will be disorientated and may not know the date, where they are, or why they are there.

The important discussion here is that we are discussing whether a person is conscious, or if he has any chance of becoming conscious again. A person in a coma is not conscious – he cannot be awakened, fails to respond normally to pain or light, does not have sleep-wake cycles, and does not take voluntary action. Coma is separate from vegetative state, in which the patient still has no cognitive neurological function or awareness of the environment. However, he has noncognitive function and a preserved sleep-wake cycle. Even more perplexing, the patient may exhibit spontaneous movements and he may open his eyes in response to external stimuli, and even track moving objects (or people) with his eyes. So why is this person not conscious? We know this from the fact that 1) he does not respond to verbal commands; 2) he shows no voluntary movements, only reflexes; 2) reports from people in this stage that have awakened show that they have had no experience. This, of course, is coupled to a variety of theory-bound measures of preserved vs. non-operative reflexes, and more recently neuroimaging.

What makes the diagnosis of coma and vegetative state so hard is that there are cases where patients show almost exactly the same symptoms as these conditions, only that they are aware. Patients in a minimally conscious state are indeed conscious, they may drift in and out of awareness, but they show signs of voluntary movement and communication. Terry Wallis is thought to be in this state, not coma, nor vegetative state. Another condition is locked-in syndrome, in which the patient is aware and awake, but cannot move or communicate due to complete paralysis of all voluntary muscles in the body.

The frequency of misdiagnosis of these patients has not been reviewed in full, but the fear is that it happens more often that we would like to. The misdiagnosis goes both ways: sometimes a patient is thought to be conscious while actually being in a persistent vegetative state. Other times – and this is the most problematic error – a patient that has some level of awareness (e.g. locked-in) is diagnosed with a coma or vegetative state.

The Development

How can we be so wrong about these patients? One reason is that we have just began to explore this field at the level of detail that we do today, incorporating better diagnostic tools and multi-modal assessment tools such as EEG, SPECT and MRI. A willingness to study consciousness, that mongrel concept that we still really don’t know what means, is another reason for the recent developments in this field. In all, our ability to distinguish between conscious and unconscious states has gone from a dichotomic distinction to a range of possibilities that are sometimes hard to distinguish.

This development is often the reason to the sensational awakenings that we can hear from time to time. News about a person regaining consciousness after 20 years from a coma (!) should be taken with a grain of salt. 20 years ago the diagnosis and distinctions to other (conscious) conditions was notas developed as today. So we should maybe think of this rather as a sensational awakening of the science surrounding these patients, not the patients themselves. That’s a bit harsh, but it is true that the conceptual and diagnostic improvements in this fueld has come through the past few years only.

The Future

What can we expect to happen in this field? First of all we can expect that neuroimaging tools will be used more. Today we can record EEG to exclude ideas about brain death; we use MRI images to see where in the brain we find lesions. But studies showing differences in the brain’s activity between these different patients have been emerging – see this article (PDF). The problem with these studies are that they are group studies. As I have argued previously, going from group study mean differences to the ability to identify individual differences – and diagnosing people on this ground – is not a straightforward thing. So tools needs to be developed that makes it possible to look at an individual scan to determine whether a person is conscious or not. As Steven Laureys from the University of Liège says:

Chronically unconscious or minimally conscious patients represent unique problems for diagnosis, prognosis, treatment, and everyday management. They are vulnerable to being denied potentially life-saving therapy….. This case shows that old dogmas need to be oppugned.

It should be noted that efforts are already being made for developing a “consciousness meter“. This stems from the finding of mid-operational awakenings; people undergoing surgery that are put into anaesthesia nevertheless wake up during surgery yet without the ability to notify others about their presence, often suffering pain as their sensations are restored. In other words; an induced locked-in syndrome. However, interesting as it has been it’s been hard to find any updates on the effectiveness of this apparatus. But we should probably think along these lines. Saying that, the consciousness meter suggested is based on EEG, and any measurement of a traumatised brain is bound to show different signals. That needs to be kept in mind.

What, then, about treatment? This is bound to follow the trace of our enhanced knowledge of these conditions. But what is interestig with the case of Terry Wallis is that he showed signes of rewiring of fibres in the brain. While these findings are in no way conclusive, they suggest that new intervention tools can be developed that focus on the regeneration of fibres in the brain. Not only general restitution, but maybe more focal, to the regions in which we have seen Wallis’ brain change (see changes in cerebellum, as indicated by white arrow below).


Diffusion tensor images of a brain at the first scan (left) and 18 months later (right). Color shows direction of white matter fibers, e.g., green for anterior-posterior fiber tracts. Large red area in second scan (arrow) shows what scientists think is growth of new neural processes in a part of the brain that controls movement. (Credit: Weill Cornell Citigroup Biomedical Imaging Center/Henning U. Voss.)

The Ethics

The growing knowledge about brain function and diagnosis of these cases should make us ask whether we are using the most up to date knowledge about these stages and states. Even more troublesome, spreading the knowledge to the entire world is a problematic affair, and even within the developed world. One thing is having an operational diagnostic system; an entirely different thing is seeing it implemented throughout the world. While the diagnosis of brain death is more or less universal across regions, cultures and religions, spreading the news about differential mental state diagnosis is only now beginning to spread. Hopefully, the use of evidence based medicine will provide the tools for such a knowledge dispersal.

Understanding that there is a tight relationship between the brain and the mind has a deep impact on our self-knowledge. Knowing how the brain works and breaks is a tale about yourself. It’s a direct relationship, not only a superficial association of flesh and mind. A loss of brain function is a loss of mental life (or part of it). All in all, the scientific study of unconscious states such as coma and persistent vegetative states are one part of the story that ties the brain and mind together tightly to a coherent picture of our minds as natural, biological phenomena.


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geek.jpgWe started this blog in late November last year. From November to April we used Blogspot to host it, but then relocated to WordPress. All in all we think it has been a good move. We had some 5000 visitors in our first four months at Blogspot; in just three months at WordPress this number has rised to 10000 new visitors. Also, using WordPress’ superior options we have started adding stand-alone pages, such as our reading list, and category tags to our posts. We aim to add new pages with downloads in the future (papers, audio, video), and to introduce new types of posts – interviews, conference reports, and other nifty things. We would also love to publish more discussions with other neuroethicists, seeing as neuroethics deals in very contentious issues.

Of course, the biggest obstacle to getting content online, is to find the time to write up the content in the first place! Being two authors has proved very beneficial in that regard. We are also toying with the idea of using guest authors from time to time. Our current goal is to put up at least four or five posts every week.

Now, feel free to let us know if you have any good ideas as to how we may improve the blog or just if you feel we are doing an OK job. We are always interested in comments and suggestions.


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socneurosci1.jpgAt the forthcoming Social Neuroscience journal homepage, editors Jean Decety and Julian Paul Keenan have a nice intro to the field of social neuroscience. It contains an initial definition of the field:

Social neuroscience may be broadly defined as the exploration of the neurological underpinnings of the processes traditionally examined by, but not limited to, social psychology. This broad description provides a starting point from which we may examine the neuroscience of social behavior and cognition.

However, we see this definition as a guide, rather than as a rule and, as such, we see this field as inclusive, rather than exclusive. The behaviors and cognitions studied under the umbrella “social” are diverse. From complex human interactions to the most basic animal relationship, social research is an expansive, diverse, and complex domain. Likewise, exploring the neurological underpinnings allows for equally assorted and varied lines of research. The combination of the areas reflects such diversity, in which research is performed in domains as wide reaching as the maternal behavior of knockout mice and endocast examinations of early Australopithecus.

I guess they would accept the brief report about the empathic mouse? Furthermore, the editors pinpoint some interesting issues pertaining to this field, including the problem of relating general (folk-)psychological concepts and constructs to the macro- and microscopic data from neurobiology:

One main challenge of social neuroscience is that social psychology and its related disciplines involve psychological constructs, such as moral dilemma, empathy, or self-regulation, that are difficult to map directly onto neural processes. These constructs often need to be deconstructed. Further, given the complexity of social interaction in humans, social neuroscience research needs to combine and integrate multiple-level analysis across different domains. Social neuroscience requires a system approach rather than a single level of analysis. We strongly believe that social and biological approaches when they are bridged can achieve a more accurate understanding of human behavior.

And they even have some precautionary remarks:

One drawback of neuroimaging research is that it can be perceived as the new phrenology (see Uttal, 2003) and it may give an over-simplistic account of the neuroscience of social cognition and behavior. With neuroimaging, there are gimmicks and trends, claims that extend beyond the research, and debates that can reach fever pitch levels over seemingly mundane differences. While hardly unique to our field, we encounter the danger of labeling parts of the brain as the “love center” or the area responsible for psychopathological behavior. In this sense, we are certainly flirting with a new phrenology. Therefore, we agree with our sensible colleagues who remind us to replicate and rely on all of the tools at our disposal.

Finally, Decety and Keenan point to the emerging ethical issues that are becoming apparent through this emerging scientific field:

Beyond the clear impact of social neuroscience in various academic domains, including education, for which we are all excited, we must carefully consider how society uses research findings from social neuroscience. There is a tendency in public journals to report over simplistic interpretations of complex issues. As Wolpe put it, “history has shown us again and again that society tends to use science to reinforce the moral assumptions and biases of the cultural moment. There is clearly a role for a thoughtful social neuroscience, where findings become part of considered policymaking around controversial issues. For example, research into addiction has provided new perspectives and tools for policymakers willing to use them. But if scientists are not clear about the scope and nature of their work, eager policymakers can seize preliminary and speculative findings and implement programs unsupported by the science itself”

At the homepage you can also find a section for related books. A few books are added here, and I wonder why they, in such a small and emerging field, have not added obvious books such as The neuroscience of social interaction by Frith & Wolpert.


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iwake-up-call.gifThe Mixing Memory blog has a very nice critique of the Neuron prejudice article and hence the prejudice post I uploaded yesterday. Admitted, I feel guilty at not spotting these humongous errors in the research design! I stand corrected. Thanks MM for doing so in a gentle manner.

Hence, the issues I address at the end of the blog should be taken even more serious: we need studies replicating and doing variations on the Mitchell study. Now with the twist of doing the study right!

Saying all this, I think the follow-up post on the dehumanizing brain is a bit better regarding a critical view. Hmm, did I write that before or after the morning coffee?


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beggar.jpgHere’s a buzz — and strange conclusions based on neuroimaging data.

A forthcoming article in Psychological Science by Lasana Harris and Susan Fiske is studying how people react when they are shown images of people from social out-groups. What they find is that people react with disgust (rather than the socially correct fellow humanity). Subjects were shown images of people from different social groups, and other non-human and hoh-animal objects (from the Stereotype Content Model). The perception of a picture’s “warmth” was judged by friendliness, competence by capability. The two emotional extremes were pride and disgust; pride elicited high warmth and high perception of competence, and disgust elicited low warmth and low perception of competence.

The article is not available yet. However, from EurekAlert we can read that:

Medial prefrontal cortex (MPFC) brain imaging determined if the students accurately chose the correct emotion illustrated by the picture (according to pretest results in which a different group of students determined the emotion that best fit each photograph). The MPFC is only activated when a person thinks about him- or her-self or another human. When viewing a picture representing disgust, however, no significant MPFC brain activity was recorded,

Well, that’s interesting. If you see a picture of a person whom you have rated as less favourable (i.e. “disgusting” (huh?)), the activity of your medial prefrontal cortex is less activated. According to EurekAlert, these results indicate that the subjects:

(…) did not perceive members of social out-groups as human. The area was only activated when viewing photographs that elicited pride, envy, and pity. (However, other brain regions — the amygdala and insula — were activated when viewing photographs of “disgusting” people and nonhuman objects.)

Furthermore, citing the researchers themselves, it is claimed that “members of some social groups seem to be dehumanized.”

I have not read the article yet, but I can’t see how the results warrant this kind of conclusion. To put the argument very simple:

  • area X is activated when we look at people (of our own kin)
  • area X is not activated when we look at non-kin people
  • ergo: we don’t look at non-kin people as being human

That’s just plain bad logics to me. Did these guys ever look at other areas that are known to involve face perception? An obvious example would the fusiform gyrus, so often found to activate when we see HUMAN faces? I guess that this area would be showing activation to non-kin faces, too. That’s just a guess. I need to read the article. But there is a hint that “other brain regions — the amygdala and insula — were activated when viewing photographs of “disgusting” people and nonhuman objects”. So if we find fusiform activation, that indicates that at least part of these people’s brain (be it conscious or unconscious perception) show that they perceive these faces as human.

So the lacking medial PfC activation should probably be viewed in a different light. Maybe it rather reflects how people judge other people as in-group or out-group (or, kin vs. non-kin)? To me, that sounds much more favourable. If your medial PfC activates, you have identified a kin member. If not, and it is still a face you’re looking at, you perceive it as a human non-kin.

I guess I’ll have to wait until the article comes out. Just as everybody else. Buzz-buzz-buzz.


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