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This digital document is a journal article from Neuropsychologia, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

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Human anterograde amnesia can develop following bilateral damage to the hippocampus and medial temporal lobes, as in hypoxic brain injury, or following damage to the basal forebrain, as following anterior communicating artery (ACoA) aneurysm rupture. In both cases, the mnestic deficit may be similar when assessed by standard neuropsychological measures. However, animal and computational models suggest that there are qualitative differences in the pattern of impaired and spared memory abilities following damage to hippocampus versus basal forebrain. Here, we show such a dissociation in human amnesia using a single two-stage task, involving conditional discrimination and reversal. Consistent with a prior study, 10 individuals with anterograde amnesia subsequent to hypoxic brain injury were spared on acquisition but impaired at reversal. However, 10 individuals with amnesia subsequent to ACoA aneurysm showed the opposite pattern of impaired acquisition but spared reversal. The differences between groups cannot be easily ascribed to severity of mnestic or cognitive deficit, since the two amnesic groups performed similarly on neuropsychological tests of memory, intelligence and attention. The results illustrate qualitative differences in memory impairments in hypoxic and ACoA amnesics and highlight the importance of considering etiology in evaluating mnemonic deficits in amnesic populations.

Conditional discrimination and reversal in amnesia subsequent to hypoxic brain injury or anterior communicating artery aneurysm rupture

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From the Preface

At the present time, physicians and scientists are working feverishly to find novel strategies for neuroprotection in human preterm and term hypoxic newborns. Cerebral hypoxia-ischemia and asphyxia present a great challenge to all of us concerned with the deleterious consequences that manifest as cerebral dysfunction, mental retardation, and cerebral palsy. This book entitled Mechanisms of Hypoxic Brain Injury in the Newborn and Potential Strategies for Neuroprotection will be of great interest to physicians, clinician-scientists, and researchers in a number of disciplines including Pediatrics, Neonatal-Perinatal Medicine, Developmental Biology, Neurology, Pediatric Neurology, Obstetrics and Gynecology, Neuroscience, Developmental Neuroscience, Developmental Neurochemistry, and to everyone interested in the developing brain . The information presented in this book will be appropriate to residents, clinical fellows, pre- and post-doctoral fellows, faculty of basic science departments, faculty of clinical departments, and to the most advanced researchers in the field of hypoxic ischemic brain injury in the fetus and the newborn. I would like to thank sincerely my colleagues and contributors to this book for their excellent efforts and extremely valuable time. Each contributor to this book is a pioneer in his or her field: the contributions are superb. As a reader, you will find that the authors of this book are from different parts of the world and that this book presents the forefront of cutting-edge global research and developments in the field of hypoxic brain injury in newborns.

MEchanisms of Hypoxic Brain Injury in the Newborn and Potential Strategies for Neuroprotection 2007

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