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September 30th, 2003 · 3 Comments

So Bhisma has requested a few long posts on the cognitive neuroscience conference I’m currently attending in Oxford (that’s my life – one long, endless round of conferences…). The conference, properly named the Autumn School in Cognitive Neuroscience, began on Monday at the Department of Experimental Psychology. Some thoughts on the sessions:

First talk was by Heidi Johansen-Berg from Oxford on ‘Plasticity of movement representations in disease’. Basically about the problems of investigating remapping of function to different brain areas (elicited by brain trauma), monitored by fMRI. The problem is that of correlation and causation; is the remapping a direct consequence of the trauma, or merely epiphenomenal? Heidi advocates using transcranial magnetic stimulation to tease out of the causation to test the functional relevance of the areas in question in human subjects. Seemed interesting to me, but nothing world-shattering.

Oh, and she mentioned something called DTI – diffusion tensor imaging, which is a way of using fMRI to map out neurones and blood vessels in the brain. Very neat stuff. It works by tracking the self-diffusion of protons, and from that you can infer fibre direction. Check Catani et al, Neuroimage, 2002.

Next talk was by Roger Lemon of UCL. I know this guy because he’s a collaborator with a guy who worked down the corridor in Cambridge. I have serious issues with his use of multi-unit neuronal recording in brains. That’s about it – he did talk about the importance of oscillations in neurones that might serve as a ’sensorimotor working memory’ to ensure a constant and appropriate level of force while grasping objects.

Nothing hugely interesting for the rest of the day until Daniel Wolpert’s talk (UCL) in the afternoon. Wolpert is an excellent speaker and he talked about his theory of how all human movement is governed by a requirement to reduce the uncertainity of final limb position, given the fact that there is inevitably noise generated when moving limbs in the first place. Touched on the difficulty of tickling yourself, and Bayesian estimates for the uncertainty of the body’s own sensors.

Today started off with a talk about Janette Atkinson on kids suffering from Williams’ Syndrome. A good talk, except for the fact that it was identical to the one given by her at the Festival of Science last year in Leicester. Oh well.

Kate Watkins (formerly of McGill, now Oxford) talked about using a new technique of ‘Brain morphometry’ to help map out the brain and investigate differences in brain morphology between patients with brain trauma and controls. Not so bad, but I have concerns about the methodology of exactly how ‘morphometry’ works. I imagine I will have to read a paper or two on this to make an informed comment.

Kate Plaisted (Cambridge) discussed her theory of ‘reduced generalisation’ to explain both the social and non-social aspects of autism. We all know that autists are very good at distinguishing very small differences in objects or things that most normal people wouldn’t even notice – this is why autists can solve jigsaw puzzles by simply looking at the shape of the pieces, rather than the pictures on them. Kate argues that the downside of this is that they aren’t good at generalising the similarities between objects and things, which leads to lots of problems down the road – including social deficits.

An interesting theory, that again I will have to read up on. I asked a question at the end, about whether she feels her theory is in conflict with Baron-Cohen’s Theory of Mind (that she briefly mentioned). She basically thinks that it is. I am a bit worried about this because I feel that Baron-Cohen’s theory is awfully convincing as well. She also doesn’t like his idea that ‘autism is an extreme form of the male mind’ – but then, neither do most people.

The last talk today was by John Stein, on ‘The magnocellular theory of dyslexia’. This was great stuff, if very controversial. Stein basically thinks that a great deal of dyslexia, and similar cognitive deficits, can be explained by problems in the magnocellular component of the visual system (the retinal ganglion cells, remember?) – and the putative ‘magnocellular auditory system’ which most people don’t think even exists.

Apparently dyslexics generally have a very reduced magnocellular system which means that they aren’t good at all at stablising their vision, resulting in blurry vision – and blurry text when reading. Why is this so? Several reasons. Dyslexics have an uncommonly high number of auto-immune problems that could explain the reason for an impaired magnocellular system (the growth of which is, appropriately enough, governed by the immune system) and they are also lacking in essential fish oils. By this, he means HUFAs – highly unsaturated fatty acids – that make up an essential component of cell membranes that accelerate the action of ion channels.

Some interesting factoids from his talk: 3/4 of people in jail are illiterate. Half of those in jail are dyslexics. Dyslexia is one of the biggest causes of family strife and misery. Furthermore, the state of literacy in the western world is such that 20% of people in the UK and USA are unable to find the word ‘plumber’ in the Yellow Pages.

All in all, the conference has been interesting. There have been some boring talks, to be sure, but there have been some interesting ones. I have fallen asleep for roughly the average amount of time I normally do during lecture (maybe 10-15% of the time). I’ve met a lot of interesting people in neuroscience, and amazingly enough, despite the fact that this is the sixth conference I’ve been to, it’s the very first academic conference related to my actual line of research.

Tags: bio · conference · neuro · oxford · science

3 responses so far ↓

  • bhisma // Oct 1, 2003 at 5:04 pm

    Thanks a ton, adrian!A few observations: Plaisted’s views are interesting, though I don’t think I understand how it conflicts with SB-C’s theory-of-mind story.’Reduced generalisation’ is perhaps more of an umbrella term for explaining certain symptoms,but seems unlikely to be the causal mechanism.In any case, both ‘categorisation/generalisation’ and ‘theory-of-mind’ tasks are subserved largely by the pfc:so no matter what the psychological explanation is,we should hopefully be able to pin down the associated neural abnormality/dysfunction soon.
    On a diff note,the HUFA hypothesis for dyslexia seems almost scarily simplistic: what do you think?

  • Adrian // Oct 1, 2003 at 11:24 pm

    Agreed about how ToM and ‘reduced generalisation’ are, after all, simply terms for something that is going wrong in the PFC.

    Well, I have to admit that I simplified the HUFA/dyslexia thing somewhat; he didn’t say that lack of HUFAs was the main cause of dyslexia. He basically said that there were about five different causes that could all interact, including low IQ, bad nutrition, bad environment, bad genetics and bad something else…

    But I do find the HUFA argument quite convincing. Here’s an article about a study investigating the use of fatty acid supplements to improve kids’ intelligence: – I recall reading a related article suggesting there were drastic improvements. Needless to say, I have started taking fish oil supplements myself now… :)

  • Alexander Van Ingen // Oct 4, 2003 at 12:21 am

    While this all takes me out of my depth, the above link to a BBC article reminds me of a similar recent news story concerning similar (if not identical?) supplements and dietary changes (more veg). These were give to / forced upon the residents of HM Prisons. A fairly drastic change in the behaviour of those detained at Her Majesty’s Pleasure who received the supplements / altered diet was noted: their behaviour became remarkably more civilised and generally “better”.

    I apologise for not providing you with a link to the appropriate research (or at least news article) – sorry chaps (and chapesses, naturally).


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