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Two anatomic structures are of central importance in memory function: the diencephalon (speci cally the medial portions of the dorsomedial and adjacent midline nuclei of the thalamus) and the hippocampal formations of the medial temporal lobes (dentate gyrus, hippocampus, parahippocampal gyrus, subiculum, and entorhinal cortex) Discrete bilateral lesions in these regions derange memory and learning out of all proportion to other cognitive functions, and even a unilateral lesion of these structures, especially of the dominant hemisphere, can produce a lesser degree of the same effect The clinical-anatomic relationships that bear on this subject are discussed in greater detail by Aggleton and Saunders and in the monograph on Wernicke-Korsakoff syndrome by Victor, Adams, and Collins While central to memory function, these are not the only regions engaged in the formation and retrieval of memory, since a severe but less enduring defect in retentive memory has also been observed with damage of the septal gray matter; a cluster of midline nuclei at the base of the frontal lobes, just below the interventricular septum and including the septal nucleus, nucleus accumbens, diagonal band of Broca; and paraventricular hypothalamic gray matter (see the well-worked-out case of infarction of this region reported by Phillips and colleagues) These septal nuclei have connections with the hippocampus through the precommissural fornix and with the amygdala through the diagonal band The amnesic syndrome that follows ruptured anterior communicating aneurysm is due to disruption of these nuclei Again, what is most remarkable about this basal frontal amnesic syndrome is its initial severity lasting for weeks to months and the potential for almost complete recovery Experimental studies in monkeys have con rmed the importance of the diencephalic-hippocampal structures in memory function (The reviews of these studies by Zola-Morgan et al are recommended) The dif culty of evaluating memory function in monkeys has been largely overcome by use of the delayed nonmatching-to-sample task, which is essentially a re ned test of recognition memory and is impaired both in patients with the amnesic syndrome and in monkeys with lesions of the mediodorsal nuclei of the thalamus and inferomedial temporal cortical regions (Mishkin and Delacour) Using this method and several others that simulate a restricted form of human amnesia, Zola-Morgan and colleagues have shown that bilateral lesions of the hippocampal formation cause an enduring impairment of memory function Lesions con ned to the fornices or mammillary bodies and stereotaxic lesions of the amygdala that spared the adjacent cortical regions (entorhinal and perirhinal cortices) failed to produce a memory defect However, lesions that were con ned to the perirhinal and entorhinal cortex (Brodmann s areas 35 and 36) and the closely associated parahippocampal cortex did cause a persistent memory defect, presumably by interrupting the major afferent pathways conveying cortical information to the hippocampus Lesions of the anteromedial parts of the diencephalon, which receive and send bers to the amygdala and hippocampus, similarly abolished memory function A body of modern work using functional neuroimaging also addresses the anatomic representation of memory function It is found that the hippocampal formations are consistently engaged during memory acquisition and retrieval tasks, con rming the fundamental role of these structures Furthermore, as alluded to earlier,.

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