Had a nice visit with Richard Wise yesterday. We are long time fans of Richard's work and share a number of theoretical views with him, such as bilateral organization of speech recognition and sensory-motor integration in the auditory dorsal stream. We have friendly disagreements on a few points as well, specifically the relative role of anterior vs. posterior temporal lobe areas in lexical-semantic aspects of language processing.
Richard views the anterior temporal lobe as a critical site for lexical-semantic processing, based largely on evidence from semantic dementia, whereas we are more impressed by the stroke data showing impairments of auditory comprehension and production following left posterior temporal lesions as is often found in Wernicke's aphasia. We have discounted semantic dementia data because the disease, while most severe in ATL areas, is nonetheless quite diffuse and therefore one cannot link ATL damage to lexical-semantic impairments with confidence. Richard has discounted the stroke data by (correctly) pointing out that strokes can disrupt function not only at the site of tissue loss, but also in distal sites by disrupting functional connectivity.
Of course we discussed this issue yesterday, and here was the outcome:
1. We agree on the data, and each acknowledge the feasibility of the counterarguments (diffuse damage in semantic dementia and remote effects of stroke).
2. We still disagree on the relative importance of these sources of data.
3. But, as Richard put it nicely, when reasonable people have legitimate disagreements it probably means both are right to some extent. So I suppose the disagreement has weakened into one of degrees: I would argue that while both anterior and posterior areas are involved, the posterior regions are more important, whereas Richard would view the anterior areas as more important. Of course, both of us are ignoring the likely contributions of frontal areas...
4. We both agree strongly that whatever the ATL is doing, it's doing it bilaterally. Unilateral resection of the left or right ATL does not produce semantic dementia, and while atrophy in semantic dementia is often greater on the left, the disease affects the ATL in both hemispheres (as well as several other areas including medial temporal lobe). The best explanation of these data is that bilateral disruption is accounting for the severity of the deficit in semantic dementia. The rumor is that another group has done a TMS study disrupting function in the ATL bilaterally. Could be interesting.
More on Richard's visit to follow...