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?
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