Abstract

Assessment of brain-damaged subjects presenting with dissociated repetition deficits after selective injury to either the left dorsal or ventral auditory pathways can provide further insight on their respective roles in verbal repetition. We evaluated repetition performance and its neural correlates using multimodal imaging (anatomical MRI, DTI, fMRI, and18FDG-PET) in a female patient with transcortical motor aphasia (TCMA) and in a male patient with conduction aphasia (CA) who had small contiguous but non-overlapping left perisylvian infarctions. Repetition in the TCMA patient was fully preserved except for a mild impairment in nonwords and digits, whereas the CA patient had impaired repetition of nonwords, digits and word triplet lists. Sentence repetition was impaired, but he repeated novel sentences significantly better than clichés. The TCMA patient had tissue damage and reduced metabolism in the left sensorimotor cortex and insula. DTI showed damage to the left temporo-frontal and parieto-frontal segments of the arcuate fasciculus (AF) and part of the left ventral stream together with well-developed right dorsal and ventral streams, as has been reported in more than one-third of females. The CA patient had tissue damage and reduced metabolic activity in the left temporoparietal cortex with additional metabolic decrements in the left frontal lobe. DTI showed damage to the left temporo-parietal and temporo-frontal segments of the AF, but the ventral stream was spared. The direct segment of the AF in the right hemisphere was also absent with only vestigial remains of the other dorsal subcomponents present, as is often found in males. fMRI during word and nonword repetition revealed bilateral perisylvian activation in the TCMA patient suggesting recruitment of spared segments of the left dorsal stream and right dorsal stream with propagation of signals to temporal lobe structures suggesting a compensatory reallocation of resources via the ventral streams. The CA patient showed a greater activation of these cortical areas than the TCMA patient, but these changes did not result in normal performance. Repetition of word triplet lists activated bilateral perisylvian cortices in both patients, but activation in the CA patient with very poor performance was restricted to small frontal and posterior temporal foci bilaterally. These findings suggest that dissociated repetition deficits in our cases are probably reliant on flexible interactions between left dorsal stream (spared segments, short tracts remains) and left ventral stream and on gender-dimorphic architecture of the right dorsal stream.

Highlights

  • In their pioneering studies on aphasia Broca (1861, 1863) and Wernicke (1874, 1906, 1977) described distinct syndromes associated with involvement of anterior and posterior cortical areas of the left hemisphere, respectively

  • Early described by Wernicke is what nowadays is known as conduction aphasia (CA) (Benson et al, 1973; Henderson, 1992), whereas the other, termed by Lichtheim “inner commissural aphasia,” is currently known as transcortical motor aphasia (TCMA) or dynamic aphasia (Luria and Tsvetkova, 1968; Albert et al, 1981; Berthier, 1999; Robinson et al, 2008)

  • The Naming × Frequency subtest of the Psycholinguistic Assessments of Language Processing in Aphasia (PALPA 54) (Kay et al, 1992; Valle and Cuetos, 1995) was administered. Both patients obtained Western Aphasia Battery (WAB)-Aphasia Quotient (AQ) below the cut-off score for diagnosis of clinically significant aphasia (Kertesz, 1982)

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Summary

Introduction

In their pioneering studies on aphasia Broca (1861, 1863) and Wernicke (1874, 1906, 1977) described distinct syndromes associated with involvement of anterior and posterior cortical areas of the left hemisphere, respectively. A relative preservation of repetition in the face of nonfluent verbal output and preserved auditory comprehension defines TCMA (Albert et al, 1981; Freedman et al, 1984; Berthier, 1999) These two syndromes result from the involvement of different structures. Left temporoparietal or inferior parietal lesions with variable involvement of the AF and insular cortex induce CA (Benson et al, 1973; Damasio and Damasio, 1980)

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