Is the emergence of speech errors in chronic post-stroke aphasia a result of ongoing compensatory brain plasticity mechanisms?

Abstract

Traditional descriptions of aphasia have ascribed language disturbances to tissue damage but symptoms expressed as repetitive verbal behaviors such as echolalia, perseverations and so forth, cannot emanate from fully dysfunctional. We propose that in aphasia, repetitive verbal behaviors (such as conduite d’approche (CdA) and mitigated echolalia (ME)) may be compensatory behaviors emerging from ongoing plastic changes occurring in the preserved tissue. CdA is the repetitive and self-initiated approximation to a target word during spontaneous speech or naming tasks. ME refers to the echoing of a just heard sentence introducing a subtle change. At brain level, language deficits usually result from lesions affecting the dorsal and the ventral streams. Damage to the main dorsal pathway is related to deficits in verbal repetition and fluency, while lesions affecting the ventral pathway are related to comprehension deficits. Thus, we propose that ME may emerge from spared dorsal stream when the ventral system is compromised, while CdA may result as an attemp of the ventral stream to compensate dorsal damage. In this study we analysed three cases of aphasia at linguistic and structural (MRI and PET) levels. In patient 1, speech was predominantly characterized by instances of CdA, patient 2 presented predominantly ME instances, and patient 3 had both CdA and ME. Results showed that patient 1 had a disconnection pattern that greatly overlapped with the dorsal language pathway, while patient 2 ́s lesion location bisected the ventral pathway discontinuing the projection of fibers that run through it. Patient 3 presented a disconnection pattern in-between the two previous ones. These findings suggest that symptoms as CdA and ME, that frequently appear in the chronic stage of aphasia may represent the behavioral expression of plastic changes occurring within the preserved language network in an attempt to compensate the linguistic functions associated to the damaged pathway.