Mechanisms of aphasia recovery and brain imaging.

Aphasia recovery may depend on right hemisphere or non-lesioned left hemisp here structures, pre-morbid brain language organization, and de novo learni ng of language. Here we review the brain imaging evidence supporting these different hypotheses. CT-scan studies have investigated the prognosis value of size and site of left hemisphere lesions. The size of the lesion is a g lobal but not an individual predictor of the initial severity and subsequen t recovery of aphasia. Studies on the site of the lesion have given differe nt results for verbal expression and comprehension. There is no consensus o n a single critical site for recovery of verbal expression in non-fluent ap hasia, which may depend on sub-cortical more than cortical extend of the le sion. Conversely the extend of the lesion in the superior temporal gyrus em erges as a critical negative factor for comprehension recovery. Rest measur ements of brain metabolism have consistently shown that aphasia severity de pends much more on the degree of dysfunction of language-related areas in t he left hemisphere than on the site of the lesion it-self This suggests tha t aphasia recovery may depend on metabolic dysfunction recovery in peri-les ional structures. More recently, activation studies have shown consistent r ight hemisphere activation during language tasks in aphasic subjects, but t heir role in recovery remains debated. it is likely limited, and may depend on atypical pre-morbid language lateralization. Left hemisphere activation s are also found in aphasic patients. They are often relocalized in peri-le sional areas, and emerge in most studies as the main factor of aphasia reco very.