Hello, Phonologists! A quick introduction—I’m Peter Richtsmeier. I have a Ph.D. in Linguistics from the University of Arizona, with expertise in phonological acquisition and learning theory, and I’m currently working as a postdoctoral fellow in the Speech, Language, and Hearing Sciences Department at Purdue.
I’m posting some scattered notes from last week’s Neurobiology of Language Conference (Thurs, Oct 15 – Fri, Oct 16, 2009; Chicago, IL). These are largely idiosyncratic as I’m not a neuroscientist and, for many presentations and almost all posters, I didn’t take detailed notes. If there are others out there that attended, you may want to supplement this posting. Well, here we go!
Summary: The panel discussions were essentially debates with additional input from moderators and the audience. This panel discussion was in many ways a discussion about the Motor Theory of speech perception (Liberman & Mattingly, 1985) and the revival this theory has seen following the discovery of mirror neurons. Luciano argued for something like an updated Motor Theory: “Our hypothesis is that the motor system [specifically, the motor cortex and mirror neurons therein] provides fundamental information to perceptual processing of speech sounds and that this contribution becomes fundamental to focus attention on others’ speech” (from the abstract, prose in brackets was added by me). Greg argued that neuroscientific data does not support Motor Theory. In particular, the fact that lesions to the motor cortex do not prevent accurate speech perception fundamentally undermines any claim about the “necessity” of motor areas for speech perception and, by extension, the lesion data undermines Motor Theory.
My personal bias here is in opposition to Motor Theory. Rather than belaboring the point, I will refer you to Greg’s blog, Talking Brains (co-managed by David Poeppel), where he has posted extensively over the past few months about the shortcomings of both Motor Theory and claims about the importance of mirror neurons in speech perception. In fact, it’s worth noting that everyone at the conference was in agreement that there is relatively poor documentation regarding the mere existence of mirror neurons in humans (cf. recent polemic article by Caramazza and colleagues). They also agreed that mirror neurons are probably there, but it seems premature to make a very strong claim about how these neurons might affect speech perception at this time, especially when auditory models of speech perception are, well, kind of obvious. And good.
A final personal note: Phonology is constructed from perception in many ways.
Panel Discussion Highlights:
- Luciano distances himself from what he calls mirror neuron “trash”, including the Magical Tapping Bears (40£ a bear!!! omg!!!)
- Attendee Tom Bever claims that, contrary to popular belief, he and moderator Michael Arbib are not old enough to have known William James. Michael responds that he knew William James.
- Luciano makes to end the session by saying that he really needs a cigarette. Moderator Michael Arbib concludes the session by saying, “Well folks, I guess it’s all been a lot of smoke and mirrors.”
Keynote Lecture: What can Brain Imaging Tell Us about Developmental Disorders of Speech and Language?
Speaker: Kate Watkins (U Oxford, UK)
Summary: Kate gave the only developmental keynote address, so naturally I was most engaged here. She’s fairly well known for her work with the KE family (Note that the KE family provided us with evidence that some language functioning depends on the FOXP2 gene. Some of the seminal research on this gene was done by Simon Fisher, another keynote speaker at the conference). Recently, Kate has branched out to neuroimaging studies of children with Specific Language Impairment (SLI) and developmental stuttering. This was not entirely clear to me before I heard her talk, but just in case anyone else out there is confused, developmental disorders such as SLI and stuttering rarely arise from lesions. Rather, they appear to result from myriad issues of neuronal size and number, as well as myelination. Kate’s research has shown that there are some interesting neurological correlates to these disorders, however. For example, children with SLI, like members of the KE family, have less gray matter in the caudate nucleus, a subcortical region implicating a motor deficit. Siblings of children with SLI also have diminutive caudate nuclei, suggesting that the size of this region primarily reflects a risk factor, and that many of the disorder’s sequelae must arise from something more complicated than a lone impaired region.
The other finding I thought worth mentioning is that children with SLI also show cortical areas with greater gray matter mass than their normally developing peers (but also reduced neural activity), including in the left frontal opercular cortex (posterior half of Broca’s area). Kate didn’t really discuss the behavioral outcomes of increased gray matter, but she suggested that the increase was likely the result of abnormal gyrification, or brain folding. Cool.
Personal note: One of my advisors here at Purdue, Larry Leonard, wrote the book on SLI.
- Kate is the only female keynote speaker, bringing some relief to what often felt like a boy’s-only club
- The presentation starts with Kate appearing to be a pleasant but disorganized British academic type who can’t seem to figure out how to get her slides to project. Oops! Turns out that the A/V staff hadn’t turned the projector on!
I’m finding that just covering these two sections has exhausted me, so this’ll be all for now. I may review some of the posters I liked sometime in the coming week, but some enouragement might be helpful to make it happen.