Conduction aphasia and optic ataxia are both "dorsal stream" sensory-motor integration syndromes. The only difference is they affect distinct motor effector systems. At least that is the view I'd like to promote.
For those who aren't familiar with these syndromes, conduction aphasia is a language disorder characterized by phonemic paraphasias (speech production errors), difficulty with verbatim repetition of speech, but with preserved auditory comprehension. Optic ataxia is a "motor" disorder which affects the patient's ability to perform visually guided reaching/grasping actions. For example, "such patients demonstrate an exaggerated and poorly scaled grip aperture" (p. 172)(Rossetti et al. 2003). Visual recognition is unimpaired.
Let's consider the parallels between these syndromes. First, in both cases, "ventral stream functions" are preserved. Conduction aphasics can comprehend speech (even speech they can't repeat) and optic ataxics can recognize visually presented objects. Second, sensory-guided action is disrupted. Conduction aphasics have difficulty transforming auditory speech input into motor gestures that will reproduce what was heard. Optic ataxics have difficulty using visual information to guide reaching and grasping actions. Third, both syndromes exhibit familiarity effects. Conduction aphasics have more trouble repeating longer, lower-frequency phrases than shorter familiar phrases. Optic ataxics "exhibit far less visuomotor deficits when they reach and grasp familiar objects" (p.173) (Rossetti et al. 2003). The lesion location for both syndromes is in the same relative vicinity. Conduction aphasics have lesions that involve the inferior parietal lobe/superior temporal lobe (area Spt, I would argue). Optic ataxics have lesions that involve the superior posterior parietal lobe.
Optic ataxia is the poster child of "dorsal stream deficits". I have been arguing for some time that conduction aphasia is also best conceptualized as a dorsal stream deficit, but affecting a different output modality, the vocal tract (e.g., Hickok et al. 2003). The functional parallels between conduction aphasia and optic ataxia provide further evidence for this proposal.
One interesting consequence of this situation is that opens up the possibility of cross-fertilization between these rather disparate domains of research. What can we learn about conduction aphasia from research on optic ataxia and vise versa?
References
Hickok, G., Buchsbaum, B., Humphries, C., & Muftuler, T. (2003). Auditory–Motor Interaction Revealed by fMRI: Speech, Music, and Working Memory in Area Spt Journal of Cognitive Neuroscience, 15 (5), 673-682 DOI: 10.1162/089892903322307393
Rossetti, Y., Pisella, L., & Vighetto, A. (2003). Optic ataxia revisited: Experimental Brain Research, 153 (2), 171-179 DOI: 10.1007/s00221-003-1590-6
2 comments:
Hi,
there is a more recent paper in Neuropsychologia 44 (2006, p. 2734) by Pisella et al. in which they argue for "far more complex organisation with multiple parallel visual-to-motor connections" of at least three pathways. I have yet to read the paper, though.
There is some work on the interaction of the pathways, either explicitly or implicitly addressed. In the field of repetition of verbal stimuli, Jefferies et al. (2005, Cognitive Neuropsychology, 22, p. 183) demonstrated that repetition of nonwords in semantic dementia was affected by a subject's comprehension skills. This suggests interactions of long-term conceptual representations (ventral pathway?) with nonword repetition which may be viewed as a task using the dorsal pathway. I wonder whether the evidence of interactive processing generated in cognitive neuropsychological studies contradict the MRI-based neat distinction of dorsal and ventral pathways? The issue of how these interact, at least, needs to be tackled eventually.
Best wishes,
Tobias Bormann, Freiburg
Hi Tobias,
I haven't read the Pisella paper yet either, but similar arguments (that the dissociation between dorsal and ventral is not absolute) were made eloquently in the Rossetti et al. paper that I cited in my original post. This has to be the case right? That is, we generally reach for things we recognize and desire so there HAS to be interaction.
In the speech domain, an interaction between the dorsal and ventral streams has been a part of our model from the beginning: the same auditory-phonological system (STS) that is part of the ventral stream recognition network interfaces with the motor system via the Spt/dorsal stream circuit. So interaction is built in to the proposed architecture.
Another point made by Rossetti et al. is that the ventral route can engage frontal action systems, but perhaps on a slower timescale. This general idea has been part of the language neuroscience world since Wernicke (the original dorsal-ventral theorist!) who proposed that there is not only a direct auditory-motor pathway, but also a route via conceptual systems, a claim we have endorsed. Of course, conceptually-mediated sensory-motor interaction is going to be slower than "direct" interaction, so this is consistent with Rossetti et al.'s suggestion.
All in all, the parallels between conduction aphasia and optic ataxia, and between dorsal and ventral streams as they are studies in vision and language are pretty compelling in my view.
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