Slide Slam H2
Damage to Broca’s area does not contribute to long-term speech production outcome after stroke
Andrea Gajardo-Vidal1,2,3, Diego Lorca-Puls1,2,4, Holly Warner1, Bawan Pshdary1, Jennifer T. Crinion5, Alexander P. Leff5, Thomas M. H. Hope1, Sharon Geva1, Mohamed L. Seghier6, David W. Green7, Howard Bowman8,9, Cathy J. Price1; 1Wellcome Centre for Human Neuroimaging, University College London, 2Memory and Aging Center, University of California San Francisco, 3Faculty of Health Sciences, Universidad del Desarrollo, Chile, 4Department of Speech, Language and Hearing Sciences, Faculty of Medicine, Universidad de Concepcion, 5Institute of Cognitive Neuroscience, University College London, 6Cognitive Neuroimaging Unit, Emirates College for Advanced Education, 7Department of Experimental Psychology, University College London, 8Centre for Cognitive Neuroscience and Cognitive Systems and the School of Computing, University of Kent, Canterbury, 9School of Psychology, University of Birmingham
Broca’s area in the posterior half of the left inferior frontal gyrus has long been thought to be critical for speech production. The current view is that long-term speech production outcome in patients with damage in and around Broca’s area is best explained by the combination of damage to Broca’s area and neighbouring brain regions including the underlying white matter, which was affected in Paul Broca’s two historic cases. Here, we dissociate the effect of damage to Broca’s area from the effect of damage to neighbouring brain regions by studying long-term speech production outcome in 134 stroke survivors with relatively circumscribed left frontal lobe lesions that spared posterior speech production areas in lateral inferior parietal and superior temporal association cortices. Collectively, these patients sustained varying degrees of damage to one or more of nine atlas-based grey or white matter regions: Brodmann areas 44 and 45 (together known as Broca’s area), ventral premotor cortex, primary motor cortex, insula, putamen, the anterior segment of the arcuate fasciculus, uncinate fasciculus and frontal aslant tract. Spoken picture description scores from the Comprehensive Aphasia Test were used as the outcome measure. Multiple regression analyses allowed us to tease apart the contribution of other variables influencing speech production abilities such as total lesion volume and time post-stroke. We found that, in our sample of patients with left frontal damage, persistent speech production impairments were solely predicted by the degree of damage to the white matter, directly above the insula, in the vicinity of the anterior part of the arcuate fasciculus, with no contribution from the degree of damage to Broca’s area (as confirmed with Bayesian statistics). The effect of white matter damage cannot be explained by a disconnection of Broca’s area, because the speech production abilities of patients with direct damage to Broca’s area and relative sparing of the white matter in the vicinity of the anterior part of the arcuate fasciculus were, on average, within the normal range and significantly better than those of patients with damage to the white matter in the vicinity of the anterior part of the arcuate fasciculus and relative sparing of Broca’s area. Our findings therefore provide evidence for three novel conclusions: (i) Broca’s area damage does not contribute to long-term speech production outcome, irrespective of the extent of the stroke lesion; (ii) persistent speech production impairments after white matter damage in the vicinity of the anterior part of the arcuate fasciculus cannot be explained by a disconnection of Broca’s area; and (iii) the prior association between persistent speech production impairments and Broca’s area damage can be explained by co-occurring white matter damage, above the insula, in the vicinity of the anterior part of the arcuate fasciculus.