title: Novelty preference in patients with developmental amnesia.
abstract: To re-examine whether or not selective hippocampal damage reduces novelty preference in visual paired comparison (VPC), we presented two different versions of the task to a group of patients with developmental amnesia (DA), each of whom sustained this form of pathology early in life. Compared with normal control participants, the DA group showed a delay-dependent reduction in novelty preference on one version of the task and an overall reduction on both versions combined. Because VPC is widely considered to be a measure of incidental recognition, the results appear to support the view that the hippocampus contributes to recognition memory. A difficulty for this conclusion, however, is that according to one current view the hippocampal contribution to recognition is limited to task conditions that encourage recollection of an item in some associated context, and according to another current view, to recognition of an item with the high confidence judgment that reflects a strong memory. By contrast, VPC, throughout which the participant remains entirely uninstructed other than to view the stimuli, would seem to lack such task conditions and so would likely lead to recognition based on familiarity rather than recollection or, alternatively, weak memories rather than strong. However, before concluding that the VPC impairment therefore contradicts both current views regarding the role of the hippocampus in recognition memory, two possibilities that would resolve this issue need to be investigated. One is that some variable in VPC, such as the extended period of stimulus encoding during familiarization, overrides its incidental nature, and, because this condition promotes either recollection- or strength-based recognition, renders the task hippocampal-dependent. The other possibility is that VPC, rather than providing a measure of incidental recognition, actually assesses an implicit, information-gathering process modulated by habituation, for which the hippocampus is also partly responsible, independent of its role in recognition.
authors.affiliation: Developmental Cognitive Neuroscience Unit, UCL Institute of Child Health, 30 Guilford St., WC1N 1EH London, UK. Monica.munoz@ich.ucl.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Munoz
authors.forename: M
authors.initials: M
authors.lastname: Chadwick
authors.forename: E
authors.initials: E
authors.lastname: Perez-Hernandez
authors.forename: F
authors.initials: F
authors.lastname: Vargha-Khadem
authors.forename: M
authors.initials: M
authors.lastname: Mishkin
mesh_terms: D000328:Adult; D017668:Age of Onset; D000647:Amnesia / Q000503:physiopathology*; D001238:Asphyxia Neonatorum / Q000150:complications; D001284:Atrophy; D001925:Brain Damage, Chronic / Q000209:etiology; D005106:Exploratory Behavior; D005260:Female; D006185:Habituation, Psychophysiologic; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007003:Hypoglycemia / Q000150:complications; D020925:Hypoxia-Ischemia, Brain / Q000150:complications; D007231:Infant, Newborn; D008297:Male; D061212:Memory, Episodic; D010364:Pattern Recognition, Visual / Q000502:physiology; D010775:Photic Stimulation; D012640:Seizures / Q000150:complications; D055815:Young Adult