Abstract

One of the features of both adult-onset and developmental forms of amnesia resulting from bilateral medial temporal lobe damage, or even from relatively selective damage to the hippocampus, is the sparing of working memory. Recently, however, a number of studies have reported deficits on working memory tasks in patients with damage to the hippocampus and in macaque monkeys with neonatal hippocampal lesions. These studies suggest that successful performance on working memory tasks with high memory load require the contribution of the hippocampus. Here we compared performance on a working memory task (the Self-ordered Pointing Task), between patients with early onset hippocampal damage and a group of healthy controls. Consistent with the findings in the monkeys with neonatal lesions, we found that the patients were impaired on the task, but only on blocks of trials with intermediate memory load. Importantly, only intermediate to high memory load blocks yielded significant correlations between task performance and hippocampal volume. Additionally, we found no evidence of proactive interference in either group, and no evidence of an effect of time since injury on performance. We discuss the role of the hippocampus and its interactions with the prefrontal cortex in serving working memory.

Highlights

  • One of the striking features of both adult- and developmentalonset amnesia produced by damage to the hippocampus is the sparing of working memory (e.g. Milner, 1966; Cave and Squire, 1992)

  • Independent samples t-tests confirmed that the two groups did not differ in age (t = 0.12, p = 0.909), Full Scale IQ (FSIQ) (t = 0.61, p = 0.55) or in various components of verbal working memory

  • The control group performed significantly better than the patient group on conditions with intermediate memory load, but the two groups did not differ in reaction time in most conditions and neither group showed evidence of proactive interference from one trial to the

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Summary

Introduction

One of the striking features of both adult- and developmentalonset amnesia produced by damage to the hippocampus is the sparing of working memory (e.g. Milner, 1966; Cave and Squire, 1992). Often display normal working memory on such standard tasks as digit span and block span (but see Rose et al, 2012) Given this profile, it might be surmised that the hippocampus makes no contribution to working memory, an ability that is often assumed to be served instead by neocortical regions, especially the prefrontal areas implicated in the maintenance and manipulation of on-line information (Brahmbhatt et al, 2008; Molteni et al, 2008; Vuontela et al, 2009). The results further suggest that the deficits may relate to an alteration of hippocampal-prefrontal interactions” (Heuer and Bachevalier, 2013, p. 11)

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