A new electrophysiological study just published in Neuron, based on a VERY unusual type of data, provides support for the view articulated by Crosson (1985) and Nadeau & Crosson (1997) (of all the subcortical regions that could matter, it's the thalamus that actually matters for sentence processing) and not such good news for Michael Ullman (declarative/procedural model: of the subcortical regions, the basal ganglia matter the mostest).
A clinical group from Berlin (the Charité Hospital), led by Fabian Klostermann, and a bunch of collaborators (including psycholinguists Angela Friederici, Anja Hahne, and Doug Saddy) studied patients (22 of them) with implanted electrodes for Deep Brain Stimulation (DBS). In DBS, electrodes are implanted to manage, for example, severe tremor, Parkinson's disease, and dystonic diseases. Although these electrodes are placed to deliver electrical stimulation in specific locations, they can also be used for recording.
Electrophysiological data were acquired in these subjects both from the DBS electrodes and scalp electrodes. The DBS placement was in the ventral intermediate nucleus (thalamus); the subthalamic nucleus, and the globus pallidus internus (basal ganglia). Subjects were presented with "the usual", namely syntactic violations eliciting ELAN/LAN and P600 patterns and semantic violations eliciting N400 responses.
All three patient groups showed the standard pattern of ERP responses for the scalp recordings, i.e. ELAN from the left front (F7) and early, N400 and P600 from posterior electrodes, typically Pz. OK, so far so good. What about the subcortical recordings?
The data from VIM show vigorous responses for both syntactic and semantic experimental conditions. However, the recordings from STN and GPi show nothing ... So that's not so great for the model that argued for a central role for the basal ganglia. The authors go pretty directly against Michael Ullman's declarative/procedural model. A large chunk of the discussion is devoted to arguing against Michael's position. I'd be curious to hear his response -- i.e. how do you defend the DP model in light of such findings?
I find the most interesting part of the data the timing between the cortical and thalamic responses. The thalamic responses must be driven by cortical (or other top-down) inputs), because they occur later than the cortical ones ... So what is being fed down to the thalamus? And why?? The authors have some speculations about this, but the story is undeveloped. In any case, since the thalamus receives an enormous number of cortical inputs, the phenomenon merits some attention.
The paper is certainly worth taking a look at because:
-- it's a very unusual source of data
-- the problematic data for the declarative/procedural model merit some thought
-- the timing between the cortical and the thalamic responses point to an interesting relation between these regions. since it can be bottom-up mediated .... what's going on? Attentional gating? Perceptual re-evaluation? Enhancement of those parts of the input that violate local expectations/predictions?
5 comments:
If the subjects are patients (for example, severe tremor, Parkinson's disease, and dystonic diseases.), can we make inference to the normal population? Even the ERP results from the scalp recordings are normal.
It's a fascinating paper. This sort of data is so rare. I'm also particularly drawn to the possible top down influence of cortical sources on the thalamus. It's impossible to guess what exactly is happening here based solely on the timelag in the ERP peaks - all we have is a temporal correlation - but causative influences within the system could probably be explicitly modelled from the data already collected using a modification of something like DCM. I'd be very interested to see, for example, if there are recurrent dynamics between the operculum and the thalamus, or if a "operculum to thalamus to temporo-parietal" model explained the data better than a "operculum to temporo-parietal" one.
Hmmm, yeah, sure, the extent to which we can generalize based on patient data is -- and always has been -- problematic ... The fact that they recorded from the scalp and found the canonical response patterns is helpful, of course. But fair enough: patient data of this type always has interpretive limitations. (That being said: comparison to putatively 'normal' subjects is itself pretty sketchy ... I have yet to meet a so-called normal)
Tom's idea to use dynamic causal modeling is nice -- but where will you get the right data? I'd certainly be curious to see whether an operculum-thalamus-temporoparietal link can be established
I bet I could do it with the data they already have, if only I could get access to it (fat chance!). It's a shame I don't know any of the people involved. Maybe I'll start asking around to see if there's anyone in my neck of the woods doing anything similar (even fatter chance!).
Tom:
send me email, and I will connect you to the people. I have talked to two of the coauthors, and I suspect that it would be possible to get your hands on these data.
If you are genuinely interested, let me know, and I will facilitate the contact/data exchange. I'm sure they would be excited to see their data analyzed in innovative ways.
--David
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