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The human anterograde amnesic syndrome is a condition whereby the person can no longer learn new facts or pieces of information, and yet retains short-term memory processing, and older memories learnt before the onset of the syndrome. Both human case studies, and experimental animal models of this condition, have strongly indicated that damage to certain closely interrelated structures and cortical areas may be responsible for this failure to learn new information. Particular emphasis has been placed on the hippocampus, the mammillary bodies, certain thalamic nuclei, and those regions of cortex (particularly rhinal cortex and parts of prefrontal and cingulate cortices) that receive strong connections from the hippocampus and selective thalamic nuclei. While the evidence for the role of the hippocampus in mnemonic processing (especially regarding rats performing spatial tasks) is strong, the evidence is less certain concerning the involvement of the other structures and regions. This thesis has directly attempted to ascertain the relative contributions of certain thalamic nuclei, one region of cortex (the cingulate region), and a fibre pathway (the cingulum bundle) which connects the hippocampus and thalamus with cingulate cortex. The contribution of this fibre bundle received particularly close experimental scrutiny in this thesis as it's possible role in the neuroanatomical circuitry governing certain forms of mnemonic processing may have been underestimated. A series of five related experiments are described, each involving the DA pigmented strain of rat, whose spatial working memory processing was evaluated using a range of automated and maze-type tasks. These animals received a variety of lesions to the hippocampus, thalamus, cingulate cortex or the cingulum bundle, created by either neurotoxic or radiofrequency methods. Two forms of spatial memory processing were assessed; these consisted of egocentric and allocentric processing, and evidence is presented that they may be mediated by dissociable neuroanatomical circuits. Lesions of the mediodorsal thalamic nucleus and cingulate cortex had no effect on tasks assessing egocentric or allocentric processing. However, bilateral lesions of the cingulum bundle, whilst having no effect upon egocentric tasks, caused a severe impairment on tasks assessing allocentric processing. Lesions of the hippocampal system (the fornix) caused a severe impairment on both types of tasks. The nature of the putative neuroanatomical circuitry governing both allocentric and egocentric memory processing is discussed.

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Insomnia, the experience of poor quality or quantity of sleep, is a very common complaint. In the community estimates for the current prevalence of insomnia range from 15 to 28%. Pharmacological treatment of insomia is faster and more effective than other treatments, including psychotherapy, hypnosis, and so on. In pharmacological treatment, benzodiazepines (BZDs) and non-benzodiazepines, including zolpidem, are very common prescribing hypnotic usages because of more effectiveness and safer side-effect profiles. Our retrospective, current observational study is a chart review of 3,152 psychiatric outpatients, attempted to review adverse effects, specifically somnambulism and antegrade amnesia after these medications, to see whether or not, this is an infrequent occurrence in Taiwan population. Of a total 406 long-/intermitted-half-life BZD hypnotics users, 0.25% (1 of 406) reported incidence of somnambulism and anterograde amnesia. However, 5.1% (13 of 255) reported incidence of zolpidem-induced somnambulism and anterograde amnesia. It serves as a reminder for clinicians to inquire of spouses (bed parters) of the patients about any unusual behavior of parasomnia activities when prescribing zolpidem, specifically in Taiwan population.

The reminiscence bump is a phenomenon whereby older subjects recall a disproportionately large number of autobiographical memories from the period of adolescence. Chapter 1 provides a background to the field of autobiographical memory and Chapters 2 and 3 evaluated a claim that this was due to self-definition occuring during this period which biases subsequent recall; however the results were not conclusive. Chapter 4 showed that a reason for the lack of a bump in younger subjects' recall could be an over-reliance on recent memories - blocking this produced a reminiscence bump in their recall. Chapter 5 explored the idea that preferential recall of memories from an earlier point in life was simply due to a sampling bias but found that early memories are consistently recalled more quickly than subsequent memories and also that there is a large proportion of first-time or unique memories in this period suggesting a long-term "primacy" effect. Chapters 6 and 7 attempted to see if autobiographical recall consisted of a U-shaped curve encompassing this primacy as well as an advantage for recent memories at the expense of mid-life memories. The results showed that early and very recent memories are consistently recalled more rapidly and with greater detail implying that the underlying representations themselves are strongerChapters 8 and 9 were case studies on two patients, one diagnosed as a Korsakoff and the other as suffering from "Focal Retrograde Amnesia". These two studies used the paradigms and findings from the work on normals in an attempt to explain the patterns of recall that are classically associated with these disorders. Finally, Chapter 10 assimilates the work both with normals and with the amnesic patients and attempts to explain the findings using a number of models concerning the organisation of normal memory

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