Impairment on a self-ordered working memory task in patients with early-acquired hippocampal atrophy.
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.
Cognitive Neuroscience and Neuropsychiatry Section, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. Electronic address: s.geva@ucl.ac.uk.
Sharon
S
Geva
Cognitive Neuroscience and Neuropsychiatry Section, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. Electronic address: janine.cooper@mcri.edu.au.
Janine M
JM
Cooper
Developmental Imaging and Biophysics Section, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. Electronic address: d.gadian@ucl.ac.uk.
David G
DG
Gadian
Cognitive Neuroscience and Neuropsychiatry Section, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom; Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, MD 20892, USA. Electronic address: mishkinm@mail.nih.gov.
Mortimer
M
Mishkin
Cognitive Neuroscience and Neuropsychiatry Section, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. Electronic address: f.vargha-khadem@ucl.ac.uk.
Faraneh
F
Vargha-Khadem
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D001284:Atrophy / Q000473:pathology; D002648:Child; D005260:Female; D006624:Hippocampus / Q000473:pathology*; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000473:pathology* / Q000523:psychology; D008297:Male; D008570:Memory, Short-Term / Q000502:physiology*; D010775:Photic Stimulation / Q000379:methods*; D017397:Prefrontal Cortex / Q000473:pathology; D011597:Psychomotor Performance / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D013702:Temporal Lobe / Q000473:pathology; D055815:Young Adult
Hippocampus; Working memory