Thesis (M.A.) University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on August 28, 2007) Includes bibliographical references.

Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2009. / Title from first page of PDF file (viewed July 22, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 115-137).

M.A. / Himmehoch (1984, 1987) in discussion of major mood disorders related to epilepsy, describes an affective condition termed subictal mood disorder. Patients with subictal mood disorder are divided into manic-depressive and dysthymic subtypes, the former resembling an atypical, usually rapid-cycling bipolar mood disorder. The latter dysthymic group, are characterised by a baseline dysthymia, severe recurrent depressive episodes, and transient euphorias. In addition, these dysthymic patients are described as being especially prone to impulsive suicide attempts, extreme irritability, rage outbursts and deliberate self-harm. Himmelhoch (1984, 1987) postulates temporolimbic dysfunction with both ictal and subictal (subclinical) changes as the underlying aetiology. Temporolimbic phenomena such as anamnesic, dissociative and perceptive distortions are important aspects of neuropsychiatric phenomenology. Clinical evidence, however, suggests that these occurrences are not routinely sought for or uncovered during the clinical evaluation of patients and their relevance for atypical affective presentations not clearly understood. The aim of this clinical survey was to evaluate the presence and nature of both temporolimbic dysfunction and subictal mood disorder among a subpopulation of private psychiatric patients. Furthermore in order to explicate a possible association between the above, the electroencephalographic records of these patients were examined. Records of 761 patients who attended a private practice over a two-year period were retrospectively reviewed. 546 patients had been questioned in sufficient detail and were deemed reliable in their responses. Of the 546 patients reviewed 128 (23,4%) were found to have experienced significant temporolimbic phenomena. The most common features were dissociative states, deja vu, premonitions, jamais vu and tactile hallucinations. 150 (27,5%) patients met Himmelhoch's criteria for the presence of subictal mood disorder. Of those 150, 100 (66,7%) demonstrated significant temporolimbic phenomena. EEG results, with the exclusion of 16 patients (the appropriate records not being available), highlighted 64 iY (76,2%) ofthe probands as having met the criteria for significant temporolimbic phenomena and subictal mood disorder and demonstrating unequivocal abnormality onEEG. Taking into account the sample bias of this particular private practice, and the obvious flaws of a retrospective, naturalistic survey of this nature, the concept of sub ictal mood disorder is discussed. Case vignettes are used to illustrate the phenomenological presentation ofthese patients and the potential benefits of the addition of anticonvulsants in their management.

Recent studies have indicated stronger mood dependent memory (MDM) effects when subjects generate both the to-be-remembered events and the cues used in their retrieval, and when subjects who experience similar moods are compared to subjects who report a change in both pleasure and arousal, rather than others who report a change in pleasure alone. The first study was undertaken to experimentally evaluate the relationship between mood change and memory performance. Specifically, four mood manipulations were developed to compare memory performance in subjects assigned to no mood change, change in pleasure, change in arousal, or change in both pleasure and arousal. Subjects generated autobiographical events in response to neutral nouns, and were tested for free recall and recognition of these events two days later. Results demonstrated greater memory disruption after change in both pleasure and arousal than after change in pleasure alone. However, one-dimensional change in arousal led to as much memory disruption as did change in both dimensions. Separate ANOVAs compared each mood in combination with each other mood and indicated that MDM was more strongly supported in some combinations than others. Further, the pattern in free recall was different from the pattern in recognition indicating that MDM effects may vary interactively across moods and tasks. The second study was undertaken to validate prior research by employing subjects who experience large, but naturally occurring, changes in mood. Patients with rapid-cycling Bipolar Disorder performed a variety of tasks during study sessions and were tested for implicit and explicit memory during test sessions. Significant MDM effects were supported in free recall of autobiographical events and inkblot recognition, but not in implicit category production of autobiographical event probes, picture fragment completion, explicit nor implicit memory for letter associates. Results validate MDM as a real world phenomenon that impacts on explicit memory performance in subjects whose moods are not manipulated. Discussion centers on prospects for future studies that consider a wider range of manipulated moods and tasks, theories of emotion, and other clinical groups in the investigation of MDM. / Arts, Faculty of / Psychology, Department of / Graduate

The purpose of this exploratory study was to investigate the differences between dependent personality characteristics and clinical symptomology as measured by the MCMI-II, in three major psychiatric syndromes in inpatient and outpatient treatment settings. Results show differences in profile in all groups. Treatment setting differences show higher scores on alcohol and drug dependence and major depression for inpatients. The affective group exhibited higher scores on dependent personality, dysthymic and major depression, confirming previous research on depressive disorders and dependent personality.

The biological mechanisms proposed to underlie primary mood disorder do not usually include a neuropathological component. Over recent years, a significant imaging literature attests to structural abnormalities in various brain regions in mood disorder, and has encouraged neuropathological investigations. Although the neuropathological understanding of mood disorder is still rudimentary, structural correlates have begun to emerge. The studies described in this thesis investigate the neuropathology of the anterior cingulate cortex in mood disorder. The anterior cingulate cortex is extremely diverse and complex, particularly in respect to its cytoarchitecture and functional organisation. These details are important when considering the precise localisation and clinical correlates of the neuropathological changes of this region in disease. Accordingly, I performed a detailed analysis of the cytoarchitecture of the human anterior cingulate cortex, as a prelude to investigations of this region in mood disorder. I measured several morphometric parameters within different anatomical levels and both hemispheres of the anterior cingulate cortex. Overall I found a clear distinction in the cellular composition of the supragenual and subgenual regions of the anterior cingulate cortex. The subgenual region demonstrated a lower glial density and smaller neurons in comparison to the supragenual region. A modest difference in neuronal density was also observed, with a higher density in the deep layers of the subgenual cortex compared to the deep layers of the supragenual cortex. Total cortical depth was also thinner in the subgenual region. This work may have important implications for the interpretation of imaging and pathological data in mood disorder. To assess the cytoarchitecture of this brain region in mood disorder, I examined several morphometric indices in addition to various parameters of gene expression in post mortem brains. I found a range of cytoarchitectural abnormalities in the supragenual anterior cingulate cortex in mood disorder. The most prominent change included a reduction in glial density, which was evident in all layers of the cortex. Glial fibrillary acidic protein was also reduced, providing some evidence for astrocyte involvement. Various neuronal changes were also observed in the mood disorder group. These included layer-specific reductions in pyramidal neuron density and a modest change in the density of cairetinin-immunoreactive neurons. I did not find any evidence supporting synaptic pathology in the anterior cingulate cortex in mood disorder. These findings extend previous evidence of cytoarchitectural alterations in the anterior cingulate cortex in mood disorder and in particular emphasise the prominent involvement of glial cells in the neuropathology of this disease. The origins of the glial (and neuronal) deficits in mood disorder remain to be established, but they are likely to have pathophysiological consequences.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 227-244).

Thesis (M.D.)--University of Adelaide, 1986. / Includes bibliographical references (leaves 317-350).

Thesis (Ph. D.)--University of Wyoming, 2005. / Title from PDF title page (viewed on Nov. 5, 2007). Includes bibliographical references (p. 60-70).

Thesis (Ph. D.)--University of Missouri-Columbia, 1997. / Typescript. Vita. Includes bibliographical references (leaves 124-136). Also available on the Internet.