Prior evidence has shown a reduction of neglect on line bisection tasks as a function of altered hemispace presentation and left cueing. The present study was conducted to examine the effect of these factors in reducing symptoms of neglect on measures of general cognitive functioning. To examine proposed changes, revised versions of the Raven's Coloured Progressive Matrices and the Memory-for-Designs (MFD) Test were constructed by placing the target stimuli in the right hemifield. Two experimental presentations, a right hemispace condition and a right hemispace plus left cue prompt condition, were compared to the standard presentation format. The primary hypotheses predicted that RBD neglect patients would reveal enhanced performance on the criterion measures as a result of these manipulations. Significant correlations were predicted between the neglect measures and between the two scoring systems for the MFD. The sample was comprised of 54 hospitalized patients, assigned to either a RBD neglect group (N = 18), a RBD nonneglect group (N = 18) , or an orthopedic control group (N = 18) . Both RBD groups were administered the Mini Inventory of Right Brain Injury, to document the presence and severity of right brain injury. Presence of neglect was assessed via the Schenkenberg Line Bisection Task and the Bells Test for Visual Neglect. Subjects were examined under all three conditions by administering one third of the items for each condition. Neglect subjects demonstrated significantly poorer performance on both criterion measures than the two comparison groups. However, no significant improvement in performance was revealed with right hemispace presentation of stimuli or left cue prompts combined with the right hemispace version. Ancillary predictions concerning correlations for the neglect measures and MFD scoring systems were confirmed. Results are interpreted in terms of increased attentional demands and task complexity. These results suggest that, despite the frequent clinical use of these manipulations in the cognitive assessment of this population, support for the efficacy of these procedures is lacking.

Orientador: Alfredo Pereira Júnior / Banca: Lauro Frederico Barbosa da Silveira / Banca: Maria Rita Marques de Oliveira / Banca: Ana Maria Guimarães Jorge / Banca: Jorge Luiz Vargas Prudêncio de Barros Pires / Resumo: Consideramos processos nutricionais como processos psicobiosociais de significação e interpretação que ocorrem em várias dimensões que se correlacionam de modo sistêmico, incluindo inter-relações entre dimensões micro e macro celulares que se estendem às correlações entre pessoas e o nosso planeta entre outros possíveis no cosmos. Apoiados na teoria semiótica de Peirce, elaboramos um diagrama (inicialmente uma tríade de elementos correlatos que formam um signo) e a partir de alguns desdobramentos do diagrama abordamos algumas correlações entre processos cognitivos corporais, a aquisição e a mudança de hábitos nutricionais. Consideramos que há uma Mente Instintiva que atua na formação de hábitos metabólicos que se expressam em termos de um instinto nutricional adquirido e modificado ao longo do tempo em vivencias de nossa espécie. Argumentamos que a partir de uma quebra de hábito, vivenciada como desprazer corporal, como por exemplo, pela fome, se desencadeia uma consciência corporal pensada na perspectiva peirceana em diferentes graus de exigência de autocontrole. Partindo da hipótese de que o conhecimento corporal se produz por meio de uma consciência imediata, ou seja, uma consciência instintiva que não necessita da mediação de uma racionalidade consciente ou de uma subjetividade individual para que os processos cognitivos aconteçam, investigamos algumas correlações entre processos nutricionais e a produção de um conhecimento corporal afetivo / Abstract: We consider nutritional processes as psychobiosocial processes of meaning and interpretation which occur in various systematically correlate dimensions, including the correlations between micro and macro cellular dimensions as well as those between men and not only the planet where they live but all the cosmos. Supported in the semiotic theory of Peirce, we prepared a diagram (originally a triad of related elements that form a sign) and from some unfolding of the diagram we covered some correlations between bodily cognitive processes, and the acquisition and change in nutritional habits. We believe that there is an Instinctive Mind that operates in the formation of metabolic habits that are expressed in terms of a nutritional instinct acquired and modified over time in the living experiences of our species. We claim that from a habit break, experienced as corporal displeasure, such as hunger, the body consciousness considered under the Peircean theoretical perspective, is unleashed in different degrees of self-control requirement. Considering the hypothesis that the bodily knowledge is produced through an immediate consciousness, that is, through an instinctive consciousness does not requiring the mediation of a conscious rationality or an individual subjectivity in order to cognitive processes happen, we investigate some correlations between nutritional processes and the production of an affective bodily knowledge / Mestre

The hippocampus is a brain structure involved in memory as well as anxiety and depression-related behavior. One unique property of the hippocampus is that adult neurogenesis occurs in this region. Rodent studies in which adult hippocampal neurogenesis is ablated have shown a role for this process in the cognitive domain, specifically in pattern separation tasks, as well as in mediating the behavioral effects of antidepressants. These studies have furnished the intriguing hypothesis that increasing adult hippocampal neurogenesis may improve these functions and therefore serve as a target for novel treatments for cognitive impairments as well as depression and anxiety disorders. Here, we use both genetic and pharmacological models to increase adult neurogenesis in mice. Under baseline conditions, we find that increasing adult hippocampal neurogenesis is sufficient to improve performance in a fear-based pattern separation task, but has no effect on exploratory, anxiety or depression-related behavior. In mice exposed to voluntary exercise, increasing adult hippocampal neurogenesis increases exploration, without affecting anxiety or depression-related behavior. Finally, in mice treated with chronic corticosterone, a model of anxiety and depression, increasing adult hippocampal neurogenesis is sufficient to prevent the behavioral effect of CORT on anxiety and depression-related behavior. Here, we therefore describe dissociations between the effects of increasing adult hippocampal neurogenesis under baseline, voluntary exercise and chronic stress conditions. Together, our results suggest that increasing adult hippocampal neurogenesis has therapeutic potential for both cognitive, and anxiety and depression-related disorders.

BACKGROUND: The human immunodeficiency virus (HIV) epidemic has been growing in China over the past few years. Extensive investigations on the neurocognitive impact of HIV have been carried out in the West, where clade B is the predominant HIV subtype. There are only a few studies on the neurocognitive pattern of Chinese in Hong Kong, where clade E and clade B HIV was equally distributed in the population. The objective of the present study was to examine the prevalence and the patterns of neurocognitive impairment of Hong Kong Chinese. / CONCLUSIONS: Among HIV+ Hong Kong Chinese, there is a pattern of subtle and variable neurocognitive deficits. The present findings has highlighted its compatibility with research on the neurocognitive profiles in clade B HIV+ individuals in the West and the impact of cART on the presentations of HAND. / METHOD: Participants include 119 HIV+ Chinese patients between the age of 18 to 50 recruited from a major tertiary specialist centre offering and territory-wide comprehensive treatment. For the comparison group, 153 age and years of education matched HIV- controls were recruited from the Hong Kong Red Cross Blood Transfusion Service. A neuropsychological test battery consisted of 12 test measures agreed to be sensitive in detecting the effects of HIV on the brain was administered to the participants. / RESULTS: Factor analysis was used to evaluate the factorial validity of the test battery and 6 neurocognitive domains were identified. A total of 24% of HIV+ participants were classified to suffer from global neurocognitive deficits. No clade-specific difference was observed in terms of prevalence of neurocognitive impairment and pattern of neurocognitive performance. Two-stage cluster analysis identified 5 clusters in both HIV+ and HIV- groups respectively. There was an overall taxonomy of 3 groupings, which are HIV+ patients who are globally impaired, who are neurocognitively intact, and who are subclinical. Neurocognitive impairment was found to have no association with depressed mood and medical indices of CD4 cell count and plasma viral load. Nevertheless, the group of globally impaired group was significantly older than the neurocognitively intact group. / Chan, Wing Sze Iris. / Adviser: Patrick Wing-Leung Leung. / Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 145-170). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Cognitive impairment after stroke or transient ischemic attack (TIA) is a prototype of vascular cognitive impairment (VCI). 30% of subjects with poststroke cognitive impairment are detected Alzheimer’s disease (AD)-like amyloid-beta (Aβ) retention with reference to ¹¹C-Pittsburgh compound B (PiB) positron emission tomography (PET). Therefore, poststroke cognitive impairment provides a good clinical context for the study about contribution of comorbid Alzheimer’s and cerebrovascular disease (CVD) pathologies to cognition. In this thesis, there are four studies addressing the effect of Aβ on poststroke cognitive impairment. / The first study investigated the accuracy of diagnosing cognitive impairment subtype in subjects with stroke/TIA using current clinical diagnostic criteria with reference to ¹¹C-PiB PET. We found the agreement between the pre and the post-PET diagnoses was poor (Kappa=0.194). The overall accuracy of clinical diagnosis of pure VCI (pVCI) was 66.7%, while that of mixed (i.e., AD with CVD) VCI (mVCI) was 68.0%. / Dementia may occur after stroke/TIA within 3-6 months (early poststroke dementia [PSD]) or from 3-6 months onward (delayed PSD). In the second study, apart from age and history of diabetes mellitus, chronic small vessel disease (SVD) lesions including lacunes and white matter changes (WMC) predicted delayed PSD as they did for early PSD. With comparable levels of SVD, the presence of acute infarcts and AD-like Aβ retention were associated with the early dementia after stroke/ TIA. / So far, there is a lack of research on the long-term effect of Alzheimer’s pathology on cognitive impairment in the context of stroke/TIA. We hypothesized that comorbid AD-like Aβ deposition played a key role in progressive cognitive decline after stroke/TIA. To test this hypothesis, we conducted a 3-year longitudinal study as study 3. Over 3 years, there was significant difference between mVCI and pVCI on the changes of the Mini-Mental State Examination (MMSE) score over time. We observed a significant decline in MMSE in the mVCI group but not the pVCI group. The annual rates of decline in MMSE and Montreal Cognitive Assessment (MoCA) score were greater in the mVCI group compared to the pVCI group. Of all MoCA domains measured, memory, executive and visuospatial functions were related to Aβ deposition. / In study 4, we investigated the relative contribution of Aβ deposition and CVD lesions to neuropsychological profiles in subjects with cognitive impairment after stroke/TIA. We found that in mVCI, Aβ retention in deep region or parietal lobe was predominantly associated with memory or executive function, respectively. In pVCI, frontal WMC and global large acute infarcts could affect memory or executive function via brain atrophy. / The conclusion of these studies reported herein can be summarized as follows: First, the overall accuracy of clinical diagnosis for cognitive impairment subtypes after stroke/TIA was low. Second, subjects with AD-like Aβ deposition tended to have dementia early after stroke/TIA, and they were more likely to experience a continuous and more severe cognitive decline 3 years later. Finally, Aβ deposition could affect both memory and executive function directly as a predominant factor in subjects with mixed Alzheimer’s and CVD pathologies. / 中風或短暫性腦缺血發作後的認知障礙被普遍視為血管性認知障礙的一種原型。通過澱粉樣蛋白正電子發射計算機斷層掃描技術（¹¹C-PiB PET），30%的中風或短暫性腦缺血發作後認知障礙患者具有阿爾茲海默氏病型的澱粉樣蛋白(Aβ)沈積。因此，中風或短暫性腦缺血發作後認知障礙是一種研究共存的阿爾茲海默氏病和腦血管疾病對認知功能的影響的良好模型。該論文通過四個研究，闡述了Aβ對中風或短暫性腦缺血發作後認知功能的影響。 / 第一個研究通過藉助¹¹C-PiB PET,調查了臨床診斷中對中風或短暫性腦缺血發作後認知障礙的分型的準確性。我們發現，對不同認知障礙類型的臨床診斷準確率較低（Kappa=0.194）。其中，對血管性認知障礙的臨床診斷準確率為66.7％，對混合性(阿爾茲海默氏病和腦血管疾病混合型)認知障礙的臨床診斷準確率為68.0％。 / 通常，我們把於中風或短暫性腦缺血發作後3至6個月內發生的癡呆定義為早髮型中風或短暫性腦缺血發作後癡呆，3至6個月后發生的癡呆定義為晚髮型中風或短暫性腦缺血發作後癡呆。在第二個研究中，我們發現，慢性小血管病（腔隙性梗塞和腦白質病變）不僅可以導致早髮型中風或短暫性腦缺血發作後癡呆，而且和晚髮型中風或短暫性腦缺血發作後癡呆也有關聯。然而，如果在相同程度的小血管病損傷的情況下，具有急性缺血性損傷和阿爾茲海默氏型Aβ沈積的患者更易提早發生中風或短暫性腦缺血發作後癡呆。 / 迄今，尚無關於共存的阿爾茲海默氏病和腦血管疾病對認知功能的長期影響的研究。我們假設合併的阿爾茲海默氏病可以導致患者中風或短暫性腦缺血發作後認知功能持續下降。為了驗證這一假設，我們進行了一個為期3年的長期隨訪研究（研究三）。在三年的隨訪中，混合性認知障礙患者和血管性認知障礙患者的簡短認知檢測（MMSE）評分變化有著顯著不同：混合性認知障礙患者的MMSE評分顯著下降，而血管性認知障礙患者的MMSE評分則無明顯改變。而且，混合性認知障礙患者的MMSE和蒙特利爾認知評估量表（MoCA）評分每年下降的平均速度皆高於血管性認知障礙患者。此外，藉助MoCA，我們發現中風或短暫性腦缺血發作後認知障礙患者的記憶、執行能力和視覺空間能力的損傷都和Aβ沉積有關。 / 在第四個研究中，我們研究了Aβ和腦血管病損傷對中風或短暫性腦缺血發作後患者不同認知功能的影響。我們發現，在混合性認知障礙患者中，腦深部的Aβ沉積和記憶功能損害直接相關，腦頂葉的Aβ沉積則和執行功能損害直接相關。在血管性認知障礙患者中，額葉腦白質病變和全腦大型腦梗病灶則可通過腦萎縮的介導，影響記憶或執行功能。 / 總之，我們的研究發現: 1.目前關於中風或短暫性腦缺血發作後患者認知障礙分型的臨床診斷的準確性較低。2.具有阿爾茲海默氏型Aβ沉積的患者不僅易於在中風或短暫性腦缺血發作後早期發生認知障礙，而且其認知水平在長期隨訪中也會不斷下降。3. Aβ沉積可以作為主導因素直接影響混合性認知障礙患者的記憶和執行功能。 / Liu, Wenyan. / Thesis Ph.D. Chinese University of Hong Kong 2015. / Includes bibliographical references (leaves 164-187). / Abstracts also in Chinese; appendixes in Chinese. / Title from PDF title page (viewed on 12, October, 2016). / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only.

Thesis (M.A.)--York University, 2002. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves 68-73). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ75382

Thesis (M.A.)--Miami University, Dept. of Speech Pathology and Audiology, 2003. / Title from first page of PDF document. Document formatted into pages; contains vii, 66 p. Includes bibliographical references (p. 53-59).

Thesis (Ph. D.)--Florida State University, 2003. / Advisor: Dr. Michelle Bourgeois, Florida State University, College of Communication, Dept. of Communication Disorders. Title and description from dissertation home page (viewed Oct. 6, 2003). Includes bibliographical references.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences