Wednesday, February 4, 2009

Naming difficulties in conduction aphasia

This is a follow up to a previous post on naming difficulties in conduction aphasia. In short, I was pointing out that I believe conduction aphasia results from damage to a sensory-motor integration circuit that is critical to speech, particularly under high phonological load conditions. I noted a problem for this idea in connection with the naming deficit often seen in conduction aphasia:

One problem, raised by Alfonso Caramazza in the form of a question after a talk I gave, is that sometimes conduction aphasics get stuck on the simplest of words. Case in point, in my talk, I showed an example of such an aphasic who was trying to come up with the word cup. He showed the typical conduit d'approche, "its a tup, no it isn't... it's a top... no..." etc. Alfonso justifiably noted that conduction aphasics shouldn't have trouble with such simple words if the damaged sensory-motor circuit wasn't needed as critically in these cases.

My suggestion in the previous post was that this may be explained in terms of a difference in the processes involved in naming versus repetition. I further speculated that part of the problem might be related to neighborhood density issues. Several very interesting and useful comments on that post, e.g., by Matt Goldrick, convinced me that my idea may not be all that solid.

Ok, enough back story. Here is another possible solution to the problem raised by Alfonso. It is actually one that I used to discuss in my talks, and may have even written about in print, but (duh) I seemed to have forgotten it until now (getting older sucks):

It seems likely that the lesion/deficit in conduction aphasia is not restricted to the sensory-motor network (i.e., area Spt), but also involves phonological processing/representation systems in the STG/STS. The lesions clearly involve these regions:

patients with conduction aphasia generally had more posterior lesion that overlapped in the superior temporal gyrus and inferior parietal cortex (Baldo et al., 2008, Brain and Language, 105, 134-140)

So perhaps the naming deficit in at least some conduction aphasics reflects damage to phonological systems in the left hemisphere (in addition to the load-dependent deficits caused by damage to Spt). The idea is that partial damage to phonological systems in the left hemisphere will disrupt phonological access during naming (which is harder and may be left dominant) more than recognition (which is easier and more bilaterally organized).



Matt Goldrick said...

Let me see if I follow you. The conduction aphasia syndrome reflects a combination of two deficits, one to phonological systems involved in both naming and repetition, the other to a sensory-motor system involved in repetition.

Under this scenario, you would see a repetition deficit (in the absence of any load) only when the phonological system, subserving both tasks, is damaged. If the sensory-motor system is damaged by itself, there shouldn't be any repetition deficit (it can simply rely on lexical processes). If your criteria for conduction aphasia is a repetition deficit, it's therefore not surprising that both deficits would go together.

Greg Hickok said...

The details of how this might fall out need to be assessed empirically, but here's the idea: the lesion distribution of conduction aphasia falls across two functional regions in the left posterior superior temporal lobe. One is area Spt in the planum region which I believe is involved in supporting sensory motor integration for vocal tract/speech functions, the other is the posterior STS which appears to be part of a (bilateral) network supporting phonological processing. The symptoms of conduction aphasia are predominately phonological in nature (phonemic paraphasias, tip of the tongue states in naming failure, and phonological STM/repetition problems). I suspect that the constellation of symptoms can be explained by damage to some combination of area Spt and posterior STS, and maybe that variation in the syndrome might follow from relative involvement of these two systems. For example, I can imagine that deficits that look like working memory problems with a less prominent naming or phonemic paraphasia component may result from damage mostly to area Spt whereas patients with significant naming deficits may have more STS involvement. I'm not sure I can make more specific predictions based on the currently available evidence.

Unknown said...

Thanks, I am using this in writing a paper and will attribute it. I was already using your FMRI article and came across this. Love the clear, straight forward language. Interesting stuff.