Exploring the impact of plasticity-related recovery after brain damage in a connectionist model of single-word reading.
The effect of retraining a damaged connectionist model of single-word reading was investigated with the aim of establishing whether plasticity-related changes occurring during the recovery process can contribute to our understanding of the pattern of dissociations found in brain-damaged patients. In particular, we sought to reproduce the strong frequency x consistency interactions found in surface dyslexia. A replication of Plaut, McClelland, Seidenberg, and Patterson's (1996) model of word reading was damaged and then retrained, using a standard backpropagation algorithm. Immediately after damage, there was only a small frequency x consistency interaction. Retraining the damaged model crystallized out these small differences into a strong dissociation, very similar to the pattern found in surface dyslexic patients. What is more, the percentage of regularization errors, always high in surface dyslexics, increased greatly over the retraining period, moving from under 10% to over 80% in some simulations. These results suggest that the performance patterns of brain-damaged patients can owe as much to the substantial changes in the pattern of connectivity occurring during recovery as to the original premorbid structure. This finding is discussed in relation to the traditional cognitive neuropsychological assumptions of subtractivity and transparency.
Welbourne
Stephen R
SR
Department of Psychology, University of Manchester, Oxford Road, Manchester M13 9PL, England. stephen.r.welbourne@man.ac.uk
Ralph
Matthew A Lambon
MA
D000465:Algorithms; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D003198:Computer Simulation; D006801:Humans; D007802:Language; D007806:Language Disorders / Q000503:physiopathology; D007858:Learning / Q000502:physiology; D016571:Neural Networks, Computer; D009473:Neuronal Plasticity / Q000502:physiology*; D009483:Neuropsychological Tests; D011932:Reading; D020127:Recovery of Function / Q000502:physiology*