We model word substitution errors made by normal and phasic speakers with an interactive activation model of lexicalization. This comprises a three-layer architecture of semantic, lexical, and phonological units. W e test four hypotheses about the origin of aphasic word substitutions: that they result from pathological decay, loss of within-level inhibitory connections, increased initial random noise, or reduced flow of activation from the semantic to the lexical level. W e conclude that a version of the flnal hypothesis best explains the aphasic data, but with random fluctuations in connection strength rather than a uniform decrement This model accounts for aspects of recovery in aphasia, and frequency and imageability effects in paraphasias. Pathological lexical access is related to transient lexical access difficulties in normal speakers to provide an account of normal word substitution errors. W e argue that similar constraints operate in each case. This model predicts imageability and frequency effects which are verified by analysis of our normal speech error data.

The fragmentation model of associative memory has the attraction of specifying neither a spatial metaphor nor a symbolic representation for remembering. It was used in order to compare the recall of groups of unrelated words by amnesic and normal people. Similarly, a schema model was used in order to compare their recall of groups of related words. It was found that the impairment in remembering with amnesia revealed by these models was remarkably uniform rather than selective. This suggests that the level at which the memory storage system is damaged in amnesia is a relatively low one. In a connectionist formulation, this would presumably correspond to widespread random damage to units and the connections between them.