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Worsening of Partially Recovered Aphasia After a Right Occipital Stroke

Department of Neurology, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA

J. Sullivan

Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA

J. Kaplan

Department of Neurology, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA

W. Klein

Department of Neurology, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA

R. Calvanio

Department of Neurology, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA

We present the first case of deterioration of aphasia associated with a nondominant (right) hemisphere lesion in an area that is nonhomotopic to left hemisphere language zones. A 70-year-old right-handed woman, who had partially recovered from Wer nicke's aphasia after a left posterior temporal and occipital lobe ischemic infarct, pre sented with sudden deterioration of aphasia. Imaging studies of the brain showed a new intraparenchymal hemorrhage in the right occipital lobe. Speech evaluation demonstrated worsening of comprehension, repetition, writing, and verbal expression. During a 4-month follow-up period, a small improvement in the ability to repeat was made, but no gains in functional language skills were achieved. This study provides evidence for participation of the right hemisphere in recovery from aphasia after left hemisphere damage. It also suggests that the subsequent lesions in the right hemi sphere cortex may not necessarily have to be located within an area that is homotopic to left hemisphere cortical language zones. The possible mechanisms for this deteri oration include diaschisis, disruption of interhemispheric fibers descending from the cortical parieto-temporo-occipital junction area, and synergistic effects. Key Words: Language—Recovery—Right hemisphere—Occipital lobe—Homotopic areas.

Neurorehabilitation and Neural Repair, Vol. 12, No. 3, 105-110 (1998)
DOI: 10.1177/154596839801200305


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