Here's a few random highlights from our second meeting. I'll try to post more throughout the week.
Hodges & Patterson, 2007. Semantic dementia: a unique clincopathological syndrome. Lancet, 6: 1004-14. This is an excellent overview of semantic dementia. Start here if you are interested in learning about SD.
Patterson, et al., 2007. Where do you know what you know? The representation of semantic knowledge in the human brain. Nature Reviews Neuroscience, 8: 976-987. An clear, informative paper that makes the best argument I've seen for the anterior temporal lobe being critically involved in the representation of conceptual semantic knowledge. They argue that the anterior temporal lobe is an amodal "hub" that binds together modality specific bits of semantic information. They refer to this as the "distributed-plus-hub" view. This is a reasonable hypothesis, but I'm not yet convinced the data supports this view, particularly the anatomical claim.
The crux of the claim boils down to this, stated succinctly by Patterson et al.,
"The cognitive and neuroanatomical abnormalities in SD, provide trenchant [nice adjective!] evidence for the distributed-plus-hub view... The strength of this evidence hinges, however, on claims about the relatively focal nature of the pathology in SD." p. 980.
This is what I'm not so sure about, whether we can really tie the semantic deficits in SD to ATL dysfunction. I'm not opposed to the idea, in fact, it makes a lot of intuitive sense, but with so many people so unquestioningly enthusiastic about the association between SD and ATL dysfunction, it is worthwhile taking a very critical look at the data.
Here's a couple of reasons to remain cautious:
1. Herpes simplex virus encephalitis (HSVE). Patients present primarily with episodic memory impairment, not the characteristic semantic memory impairment found in SD, and when semantic memory impairment occurs in HSVE it is relatively mild. Yet, the ATL bilaterally is implicated in both SD and HSVE. In fact, according to at least one study (Noppeney et al. 2007, Brain, 130:1138-47), ATL dysfunction appears more prominent (more of the ATL involved) in HSVE than SD generally, except for a small more posterior region that was more affected in SD than HSVE. This seems problematic.
2. Pathology in SD extends beyond the ATL according to most studies. This is a bit of a complicated issue because it likely depends on how much the disease has progressed at the time of the anatomical or metabolic scan, but it is certainly NOT the case that SD involves the ATL and only the ATL. We will be looking into this issue in more depth for next week.
One thing I am sure about, though, is that the kind of "semantic" processing that David and I talk about in our papers, and that we associated with posterior temporal systems, and the kind of semantic processing that the SD folks are talking about are very different. Our claims are modality specific: a mapping between sound and meaning. Claims from the SD literature are modality independent: the deficit is thought to affect semantic knowledge at some central level. So our position, that posterior temporal regions are involved in mapping sound to meaning, is not at all incompatible with the possibility that the ATL is functioning as some sort of semantic hub.