Abstract
Word learning requires learners to bind together arbitrarily-related phonological, visual, and conceptual information. Prior work suggests that this binding can be robustly achieved via incidental cross-situational statistical exposure to words and referents. When cross-situational statistical learning (CSSL) is tested in the laboratory, there is no information on any given trial to identify the referent of a novel word. However, by tracking which objects co-occur with each word across trials, learners may acquire mappings through statistical association. While CSSL behavior is well-characterized, its brain correlates are not. The arbitrary nature of CSSL mappings suggests hippocampal involvement, but the incremental, statistical nature of the learning raises the possibility of neocortical or procedural learning systems. Prior studies have shown that neurological patients with hippocampal pathology have word-learning impairments, but this has not been tested in a statistical learning paradigm. Here, we used a neuropsychological approach to test whether patients with bilateral hippocampal pathology (N = 3) could learn new words in a CSSL paradigm. In the task, patients and healthy comparison participants completed a CSSL word-learning task in which they acquired eight word/object mappings. During each trial of the CSSL task, participants saw two objects on a computer display, heard one novel word, and selected the most likely referent. Across trials, words were 100% likely to co-occur with their referent, but only 14.3% likely with non-referents. Two of three amnesic patients learned the associations between objects and word forms, although performance was impaired relative to healthy comparison participants. Our findings show that the hippocampus is not strictly necessary for CSSL for words, although it may facilitate such learning. This is consistent with a hybrid account of CSSL supported by implicit and explicit memory systems, and may have translational applications for remediation of (word-) learning deficits in neurological populations with hippocampal pathology.