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Home > Research > Publications & Outputs > Broca's area and inflectional morphology
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Broca's area and inflectional morphology: evidence from Broca's aphasia and computer modeling

Research output: Contribution to journalJournal article

Published

Journal publication date05/2006
JournalCortex
Journal number4
Volume42
Number of pages14
Pages563-576
Original languageEnglish

Abstract

In a series of articles Ullman (2001, 2004; Ullman et al., 1997) has proposed that regular inflection is critically subserved by Broca's area. This suggestion is motivated by the finding that English speaking Broca's aphasics show selective deficits with regular inflection. Here we argue that this proposal does not hold cross-linguistically but is based on a confound between inflectional suffix and regularity that is specific to the English language. We present data from two experimental studies of participle inflection with 13 German and 12 Dutch Broca's aphasics. None of these aphasic speakers are selectively impaired for regular inflection but instead most of them show selective deficits with irregular inflection. These data suggest that a selective regular deficit is not a characteristic of Broca's aphasia across languages, and that Broca's area is not critically involved in regular inflection. To investigate the nature and localization of the processes underlying inflection we present a connectionist neural network model that accounts for the deficits of the German aphasic speakers. The model implements the view that the inflection of all verb types is based on a single mechanism with multiple representations that emerge from experience-dependent brain development. We show that global damage to this model results in a selective deficit for irregular inflection that is comparable to that of the German aphasic speakers. This finding suggests that a selective impairment of irregular participles as observed by German and Dutch aphasic speakers does not presuppose two distinctly localized mechanisms or processes that can be selectively affected by brain damage.

Bibliographic note

The final, definitive version of this article has been published in the Journal, Cortex 42 (4), 2006, © ELSEVIER.