Thesis (M.S.)--University of Wisconsin--Madison, 1971. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.) in Psychology--University of Maine, 2001. / Includes vita. Advisory Committee: Sandra T. Sigmon, Assoc. Prof. of Psychology, Advisor; Jeffrey E. Heckler, Assoc. Prof. of Psychology; Mark Jackson, Director, Student Health Services; Michael A. Robbins, Cooperating Assoc. Prof. of Psychology; Geoffrey L. Thorpe, Prof. of Psychology. Bibliography: leaves 140-157.

Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Thesis (M.A.)--Kutztown University of Pennsylvania, 1993. / Source: Masters Abstracts International, Volume: 45-06, page: 3306. Typescript. Includes bibliographical references (leaves 16-18).

The successful reduction of fear is the aim of clinicians treating people with anxiety disorders such as post-traumatic stress disorder or phobias. Existing treatments for these conditions, however, require many treatment sessions and are prone to relapse. A new technique, first demonstrated in rats by Monfils, Cowansage, Klann, & LeDoux (2009) and later shown to be effective in humans (Schiller et al., 2010), provides a method of efficiently reducing fear in a manner which is resistant to various known triggers of relapse. This procedure involves a single presentation of the fear-inducing stimulus one hour prior to extinction training. This procedure produces extinction learning that is resistant to the return of fear resulting from a change of context, the passage of time, exposure to the unconditioned stimulus, and even further conditioning of the stimulus with an aversive stimulus. This dissertation focuses on one particular property of this procedure: that a stimulus extinguished using this procedure is resistant to subsequent retraining of the fear association. The first four experiments presented here are aimed at replicating this phenomenon and determining whether prediction error at retrieval is necessary for the effect to occur. Following on from these studies, the next chapter presents three experiments which investigate whether trial spacing effects could explain the enhanced extinction and highlights conditions under which the effect is weakened, or possibly reversed. The next three experiments compare the properties of a stimulus extinguished under these conditions with a stimulus extinguished under normal conditions. These studies focus on explanations involving inhibition, inattention and the disruption of stimulus representations. In the final three experiments, the possibility of reversing the effect is investigated. These studies look at the effect of memory retrieval prior to retraining of the stimulus to determine the conditions under which the stimulus can again come to elicit a fear response.

Thesis (Ph. D.)--Ohio State University, 2005. / Title from first page of PDF file. Document formatted into pages; contains xii, 103 p.; also includes graphics (some col.). Includes bibliographical references (p. 90-103). Available online via OhioLINK's ETD Center

Thesis (M.A.)--Baylor University, 2009. / Includes bibliographical references (p. 44-55).

Thesis (DPhil (SW Play Therapy))--University of Pretoria, 2004. / Includes bibliographical references.

Situações ameaçadoras (p.ex., exposição ao labirinto em cruz elevado LCE) induzem respostas comportamentais e neurovegetativas, geralmente acompanhadas por antinocicepção e da ativação do eixo hipotálamo-pituitária-adrenais (HPA). Além disso, é conhecido que a matéria cinzenta periaquedutal (MCP) faz parte do substrato neural para a expressão de alterações comportamentais e neurovegetativas em resposta a estímulos aversivos e que essa estrutura mesencefálica é longitudinalmente dividida em quatro colunas (dorsomedial, dorsolateral, lateral e ventrolateral) que estão envolvidas em coordenar estratégias distintas para o animal lidar com diferentes tipos de estresse, ameaça e dor. No presente estudo foram analisados os níveis plasmáticos de corticosterona em camundongos expostos a 3 tipos de LCE, o fechado (LCEf: 4 braços fechados - situação não aversiva), o padrão (LCEp: 2 braços abertos e 2 braços fechados - situação aversiva com a possibilidade de esquiva/fuga) ou o aberto (LCEa: 4 braços abertos - situação aversiva sem a possibilidade de esquiva/fuga). O perfil da resposta hormonal foi também avaliado em animais concomitantemente submetidos à injeção de formalina 2,5% no dorso da pata traseira direita (teste de nocicepção). O estudo também avaliou a duração da antinocicepção induzida pela exposição ao LCEa em animais mantidos ou não neste ambiente aversivo. A caracterização da participação da MCP neste tipo de antinocicepção foi avaliada pela lesão irreversível (produzida pela injeção de NMDA) uni ou bilateral da porção dorsal (MCPd: colunas dorsolateral e dorsomedial) e bilateral da porção ventrolateral (MCPvl) desta estrutura mesencefálica sobre a resposta nociceptiva induzida pela injeção de formalina na pata traseira direita em camundongos expostos ao LCEf ou ao LCEa. Finalmente, os efeitos da lesão da MCPd ou da MCPvl nos índices de ansiedade foram avaliados no labirinto em cruz elevado padrão (LCEp) em camundongos com ou sem a injeção prévia de formalina. Os resultados mostraram que a exposição aos três tipos de LCE aumentou a secreção plasmática de corticosterona (CORT), porém os níveis foram superiores nos animais expostos ao LCEp ou LCEa quando comparados ao LCEf. Além disso, quando os animais foram submetidos ao teste de formalina níveis elevados, porém semelhantes, de CORT foram verificados após a exposição aos diferentes LCE, sugerindo que o estímulo nociceptivo elevou as concentrações plasmáticas desse glicocorticóide para valores máximos. Na avaliação da duração da antinocicepção induzida pela exposição ao LCEa, verificou-se que esta reação defensiva cessou imediatamente após a retirada do animal deste ambiente, mas perdurou por até 20 minutos quando o animal foi mantido nesta condição ameaçadora. Por fim, a lesão das diferentes porções da MCP mostrou que tanto a MCPd como a MCPvl parecem não estar envolvidas na antinocicepção induzida pela exposição ao LCEa. Curiosamente, a lesão da MCPvl reduziu a resposta nociceptiva de animais submetidos ao LCEf e aumentou a locomoção durante a exposição ao LCEf e LCEa. Além disso, a lesão bilateral da MCPd reduziu seletivamente os índices de ansiedade (% de entradas e de tempo nos braços abertos do LCEp) somente em camundongos que não foram submetidos ao teste da formalina, o que sugere que a nocicepção prejudicou o efeito ansiolítico produzido pela lesão desta porção da MCP. No entanto, é importante destacar que a lesão da MCPvl não alterou os índices de ansiedade e a locomoção de camundongos não submetidos a estimulação sensorial nociceptiva concomitante. / Threatening situations (e.g., exposure to an elevated plus-maze with four open arms oEPM) induce behavioral and neurovegetative responses generally accompanied by antinociception and activation of the hypothalamus-pituitary-adrenal (HPA) axis. Furthermore, it is known that the midbrain periaqueductal gray (PAG) is part of the neural substrate for the expression of behaviorally and neurovegetative alterations in response to aversive stimuli. In addition, the PAG is longitudinally divided into four columns (dorsomedial, dorsolateral, lateral and ventrolateral) that are involved in coordinating distinct strategies for animals coping with different types of stress, threat and pain. The present study analyzed the plasmatic levels of corticosterone when mice with or without prior 2.5% formalin injection into the right hind paw (nociception test) were exposed in one of the 3 types of EPM, the enclosed (eEPM: 4 enclosed arms - non-aversive situation), the standard (sEPM: two open and two closed arms - aversive situation with the possibility of avoidance/flight) or the open (oEPM: 4 open arms - aversive situation without the possibility of avoidance/flight) EPM. The study also investigated the temporal evaluation of the oEPM-induced antinociception when mice were kepted in (for 30 min) or removed from (after 10 min of exposure) that aversive environment (i.e., the oEPM). The characterization of the PAG participation in this type of antinociception was evaluated by irreversible (produced by NMDA injection) uni or bilateral lesion of dorsal PAG portion (dPAG: dorsolateral and dorsomedial columns) and bilateral ventrolateral PAG lesion (vlPAG). Finally, the effects of dPAG or vlPAG lesion on the anxiety indices were investigated in mice with or without prior formalin injection during the exposure to the sEPM. Results showed that the eEPM exposure increased the plasmatic concentration of corticosterone (CORT), however sEPM or oEPM exposure animals showed higher levels of CORT than eEPM-exposed mice. Moreover, when animals were submitted to the formalin test high, but similar levels of this glucocorticoid were verified after the exposure to the different EPM, suggesting that nociception also has provoked a ceiling effect on plasma corticosterone concentration. Results also showed that the oEPM-induced antinociception ceased immediately after mice withdrawal from the aversive situation. However, this pain inhibition response remained unchanged for approximately 20 min in animals that were kept in the threatening condition. Finally, the lesions of different portions of PAG showed that neither dPAG nor vlPAG appear to be involved in the modulation of the oEPM-induced antinociception. Curiously, vlPAG lesion reduced the nociceptive response in animals submitted to the eEPM and increased the locomotion during eEPM and oEPM exposure. Moreover, bilateral dPAG lesion reduced anxiety indices (% of open arm entries and % of open arm time) only in mice that had not received prior injection of formalin, suggesting that nociception impaired the anxiolytic-like effect produced by dPAG lesion. It is important to highlight that vlPAG lesion did not alter the anxiety-like indices and the locomotion in mice not submitted to the concurrent nociceptive stimulation.

Diploma thesis deals with the psychological care and psychological guidance and their potentialities and availability for people or their close ones, who need help in period of diseases or disease effects. There is only psychiatrist-consultation care of psychic condition of patients in most of medical centres, but all diseases affect the psychic condition, even for patient´s close ones. Good psychic condition linked up with changed social condition is very important for successful cure. If the patients have low stress tolerance there is a risk, that every disease causes the hard life situation. Psychological care and cooperation with the doctor, medical staff, rehabilitation and social workers also as the communication competence can highly increase the quality of life of patients and their relatives.