Cognitive behavioral therapy (CBT) is efficacious for panic disorder with agoraphobia (PD/A). Nevertheless, the active ingredients of treatment and the mechanisms through which CBT achieves its effects remain largely unknown. The mechanisms of action in CBT (MAC) study was established to investigate these questions in 369 patients diagnosed with PD/A. The MAC study utilized a multi-center, randomized controlled design, with two active treatment conditions in which the administration of exposure was varied, and a wait-list control group. The special feature of MAC is the way in which imbedded experimental, psychophysiological, and neurobiological paradigms were included to elucidate therapeutic and psychopathological processes. This paper describes the aims and goals of the MAC study and the methods utilized to achieve them. All aspects of the research design (e.g., assessments, treatment, experimental procedures) were implemented so as to facilitate the detection of active therapeutic components, and the mediators and moderators of therapeutic change. To this end, clinical, behavioral, physiological, experimental, and genetic data were collected and will be integrated.

Although functional magnetic resonance imaging (fMRI) has gained increasing importance in investigating neural substrates of anxiety disorders, less is known about the stress eliciting properties of the scanner environment itself. The aim of the study was to investigate feasibility, self-reported distress and anxiety management strategies during an fMRI experiment in a comprehensive sample of patients with panic disorder and agoraphobia (PD/AG). Within the national research network PANIC-NET, n = 89 patients and n = 90 controls participated in a multicenter fMRI study. Subjects completed a retrospective questionnaire on self-reported distress, including a habituation profile and exploratory questions about helpful strategies. Drop-out rates and fMRI quality parameters were employed as markers of study feasibility. Different anxiety measures were used to identify patients particularly vulnerable to increased scanner anxiety and impaired data quality. Three (3.5%) patients terminated the session prematurely. While drop-out rates were comparable for patients and controls, data quality was moderately impaired in patients. Distress was significantly elevated in patients compared to controls; claustrophobic anxiety was furthermore associated with pronounced distress and lower fMRI data quality in patients. Patients reported helpful strategies, including motivational factors and cognitive coping strategies. The feasibility of large-scale fMRI studies on PD/AG patients could be proved. Study designs should nevertheless acknowledge that the MRI setting may enhance stress reactions. Future studies are needed to investigate the relationship between self-reported distress and fMRI data in patient groups that are subject to neuroimaging research.

Title from PDF of title page. / Document formatted into pages; contains 90 pages. / Thesis (M.A.)--University of South Florida, 2001. / Includes bibliographical references. / Text (Electronic thesis) in PDF format. / ABSTRACT: My thesis explores how discourse and material practices have created agoraphobia, the fear of public places. This psychological disorder predominates among women. Throughout much of Western history, women have been encouraged to stay home for their safety and for the safety of society. I argue that agoraphobic women have internalized this discourse, expressing fears of being in public or being alone without a companion to support and protect them; losing control over their minds or their bodies; and endangering or humiliating themselves. Therapeutic discourse also has created agoraphobia by naming it, categorizing the emotions and behaviors associated with it, and describing the characteristics of agoraphobics. / The material practice of therapy reinforces this discourse. Meanwhile, practices such as rape and harassment reinforce the dominant discourse on women&softsign;s safety. I survey psychological literature, beginning with the naming of agoraphobia in 1871, to explain why the disorder is now diagnosed primarily in women. I examine nineteenth-century discourse that told women they belonged at home while men controlled the public domain. In 1871, the Paris Commune revolt epitomized the fear of women publicly out of control. I return to Paris a century later for a reading of the novel Certificate of Absence, in which Sylvia Molloy explores identity through the eyes of a woman who might be labeled agoraphobic. / I ask whether homebound women are resisting or retreating from a hostile world. Instead of seeing agoraphobia only as a personal problem, people should question why so many women fear themselves and the world outside their home.My methodology includes an analysis of nineteenth-century texts as well as current media, prose, and poetry. I also support my arguments with material from professional journals and nonfiction books in different disciplines. Common to feminist research, an interdisciplinary approach was needed to situate a psychological disorder within a social context. / System requirements: World Wide Web browser and PDF reader. / Mode of access: World Wide Web.

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Background: Learning by conditioning is a key ability of animals and humans for acquiring novel behavior necessary for survival in a changing environment. Aberrant conditioning has been considered a crucial factor in the etiology and maintenance of panic disorder with agoraphobia (PD/A). Cognitive-behavioral therapy (CBT) is an effective treatment for PD/A. However, the neural mechanisms underlying the effects of CBT on conditioning processes in PD/A are unknown. Methods: In a randomized, controlled, multicenter clinical trial in medication-free patients with PD/A who were treated with 12 sessions of manualized CBT, functional magnetic resonance imaging (fMRI) was used during fear conditioning before and after CBT. Quality-controlled fMRI data from 42 patients and 42 healthy subjects were obtained. Results: After CBT, patients compared to control subjects revealed reduced activation for the conditioned response (CS+ > CS–) in the left inferior frontal gyrus (IFG). This activation reduction was correlated with reduction in agoraphobic symptoms from t1 to t2. Patients compared to control subjects also demonstrated increased connectivity between the IFG and regions of the “fear network” (amygdalae, insulae, anterior cingulate cortex) across time. Conclusions: This study demonstrates the link between cerebral correlates of cognitive (IFG) and emotional (“fear network”) processing during symptom improvement across time in PD/A. Further research along this line has promising potential to support the development and further optimization of targeted treatments.

Submitted by VINICIUS DIAS KUMPEL null (vinicius.biotec.assis@gmail.com) on 2016-05-10T13:33:15Z No. of bitstreams: 1 Dissertação_Repositório Institucional Unesp.pdf: 6874433 bytes, checksum: 343f11878b45b778f98411f90032c73f (MD5) / Approved for entry into archive by Felipe Augusto Arakaki (arakaki@reitoria.unesp.br) on 2016-05-13T11:50:11Z (GMT) No. of bitstreams: 1 kumpel_vd_me_assis.pdf: 6874433 bytes, checksum: 343f11878b45b778f98411f90032c73f (MD5) / Made available in DSpace on 2016-05-13T11:50:11Z (GMT). No. of bitstreams: 1 kumpel_vd_me_assis.pdf: 6874433 bytes, checksum: 343f11878b45b778f98411f90032c73f (MD5) Previous issue date: 2016-03-17 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Ainda pouco se conhece a respeito da atividade serotonérgica sobre receptores 5-HT1A no hipocampo ventral na regulação de diferentes tipos de ansiedade. O Labirinto em T elevado (LTE) é um teste que avalia separadamente dois subtipos de ansiedade: a ansiedade generalizada e o pânico, respectivamente através da avaliação dos comportamentos defensivos de esquivas inibitórias e das fugas. Assim, este estudo teve por objetivo investigar o envolvimento de receptores 5-HT1A no HV sobre a manifestação dos transtornos de ansiedade generalizada (TAG) e pânico (TP) no LTE, tendo como parâmetro a ativação de receptores gabaérgicos (GABAA) nessa área do hipocampo. Foram conduzidos dois experimentos em ratos Wistar: o Experimento 1, visando avaliar o efeito do midazolam (10, 20 ou 40nmol) - um benzodiazepínico que potencializa a ação do GABA em receptores GABAA; e o Experimento 2, para avaliar o efeito de 8-OH-DPAT (0,6, 3 ou 15nmol) – um agonista de receptores 5-HT1A. Animais dos grupos controles nos dois experimentos foram tratados com salina. Dez minutos após as microinjeções foram submetidos ao LTE para avaliação das latências (em segundos) para esquivas e fugas. Imediatamente após, os animais foram colocados no centro da arena para avaliação da atividade motora (número de quadrados percorridos). Os resultados apontaram que a maior dose de midazolam microinjetada no hipocampo ventral causou ansiólise, comprovada pela diminuição na latência das esquivas em relação aos animais controles e àqueles tratados com 10nmol do mesmo fármaco. Resultado semelhante foi constatado nas três doses de 8-OH-DPAT. Não se observou qualquer alteração nas fugas, e nem na atividade motora dos animais tratados com qualquer um dos fármacos testados. Essas evidências comportamentais indicam que a ativação de receptores 5-HT1A no HV diminuiu o comportamento de esquiva dos animais, sem afetar as respostas de fugas, semelhantemente ao que se observou em decorrência da ação do midazolam sobre receptores GABAA. Esses resultados indicam um envolvimento desses receptores na regulação do TAG, mas não do TP. / The little is known about the serotoninergic activity on 5-HT1A receptors in the ventral hippocampus in the regulation of different types of anxiety. The Elevated T Maze (ETM) is a test that evaluates separately two subtypes of anxiety: generalized anxiety and panic, respectively by evaluating the defensive behaviors of inhibitory avoidance and escapes. Therefore this study aimed to investigate the involvement of 5-HT1A receptors in VH on the manifestation of generalized anxiety disorder (GAD) and Panic (PD) in ETM, having as parameter the activation of gabaergic receptors (GABAA) in that area of the hippocampus. Two experiments were conducted in rats: Experiment 1, to evaluate the effect of midazolam (10, 20 or 40nmol) – a benzodiazepine that potentiates the action of the GABA on GABAA receptors; and Experiment 2 to evaluate the effect of 8-OH-DPAT (0.6, 3 or 15nmol) - an agonist of 5-HT1A receptors. Animal control groups in both experiments were treated with saline. Ten minutes after microinjection, the animals were submitted for evaluation to the ETM latencies (in seconds) for avoidances and escapes. Immediately after, the animals were placed in the center of the arena to eavaluation of motor activity (number of covered squares). The results showed that the highest dose of midazolam microinjected in the ventral hippocampus caused anxiolysis, evidenced by the decrease in latency of avoidances compared to controls and those treated animals 10nmol of the same drug. A similar result was observed at all three doses of 8-OH-DPAT. There was no change in the escapes, nor the motor activity of animals treated with any of the drugs tested. These behavioral evidence indicates that activation of 5-HT1A receptors in VH decreases the behavior of avoidance of the animals without affecting the escape response, similar to what was observed due to the action of midazolam on the GABAA receptors. These results indicate an involvement of these receptors in the regulation of GAD, but not of PD.

Submitted by JOSIMARÍ CRISTIANE TIEMANN ARAÚJO (marietiemannpharma@gmail.com) on 2018-07-30T15:47:21Z No. of bitstreams: 1 Disssertação_Josy PDF.pdf: 1879909 bytes, checksum: b868bf7a67063f92000e7e3e22b828b0 (MD5) / Approved for entry into archive by Laura Akie Saito Inafuko (linafuko@assis.unesp.br) on 2018-07-30T18:58:11Z (GMT) No. of bitstreams: 1 tiemann-araujo_jc_me_assis.pdf: 1879909 bytes, checksum: b868bf7a67063f92000e7e3e22b828b0 (MD5) / Made available in DSpace on 2018-07-30T18:58:11Z (GMT). No. of bitstreams: 1 tiemann-araujo_jc_me_assis.pdf: 1879909 bytes, checksum: b868bf7a67063f92000e7e3e22b828b0 (MD5) Previous issue date: 2018-03-04 / Fármacos antidepressivos como os inibidores seletivos de recaptação de serotonina são utilizados no tratamento da ansiedade, pânico e outros transtornos mentais. Os efeitos desejados ocorrem somente após administração crônica, em torno de 3 a 4 semanas após o início do tratamento, com aumento dos sintomas de ansiedade no início da terapia farmacológica, ocasionando a descontinuidade do uso desses fármacos. Além disso, há relatos de resistência a esse tipo de tratamento. Visando encontrar soluções para tais problemas, fundamentados em estudos que mostraram que mecanismos opioides favorecem a atividade inibitória da serotonina em neurônios da Substância Cinzenta Pereiaquedutal Dorsal que modulam a fuga/pânico, o presente estudo teve por objetivo investigar o efeito da Buprenorfina, um agonista parcial de receptores µ-opioide e antagonista de receptores κ-opioide, como agente ansiolítico e anti-pânico, como também avaliar se o efeito ansiolítico e antipânico da Fluoxetina seriam antecipados pela associação com a Buprenorfina. Foram realizados 3 experimentos utilizando ratos machos Wistar com peso médio de 200g no início das sessões experimentais: 1. Tratamento agudo com Buprenorfina IP nas doses (0,015mg/Kg, 0,03mg/Kg 0,3mg/Kg), tendo como controle positivo o Alprazolam IP (4mg/Kg); 2. Tratamento subcrônico 3 dias com Buprenorfina IP (0,3mg/Kg); 3. Tratamento agudo com Buprenorfina (0,3mg/Kg) - associado ao tratamento subcrônico com Fluoxetina 3 dias IP, (10mg/Kg). Após os tratamentos, os animais foram submetidos à avaliação comportamental no Labirinto em T Elevado (LTE) e, subsequentemente, ao Campo Aberto e no Teste de Transição Claro-Escuro. No experimento 1 o teste comportamental foi repetido 24 horas após a primeira avaliação comportamental. Os resultados mostraram que a Buprenorfina nas doses maiores diminuiu a latência das esquivas, sem alteração das fugas no LTE, diferentemente do que se constatou no tratamento agudo com o Alprazolam, o qual diminuiu também as esquivas, mas aumentou a latência nas fugas, efeitos esses interpretados respectivamente como, ansiolítico e panicolítico. Vinte e quatro horas depois não se constatou mais efeito do Alprazolam, e o efeito da Buprenorfina sobre as esquivas só foi identificado na maior dose e apenas na LB. Em nenhuma das duas situações houve aumento de atividade motora. No teste de Transição Claro-Escuro não se constatou efeito expressivo nas condições estudadas, apenas possibilitou a escolha da maior dose para a continuidade do estudo, já que a intermediária aumentou a atividade motora nesse teste 24h após a injeção. A Buprenorfina administrada subcronicamente também diminuiu as esquivas, sem afetar a latência das fugas e o comportamento motor no campo aberto. Também não se identificou alterações no Teste de Transição Claro-escuro. A Buprenorfina antecipou o efeito ansiolítico da Fluoxetina, sem afetar as respostas relacionadas com a manifestação do pânico. Entretanto não houve confirmação dos achados no outro teste de ansiedade. Conclui-se que a Buprenorfina, administrada de forma aguda e subcrônica, diminuiu os comportamentos defensivos relacionados com a ansiedade generalizada, e antecipou o efeito ansiolítico da Fluoxetina, podendo se constituir em uma opção relevante no tratamento dos transtornos de ansiedade na clínica, devido à sua baixa capacidade de causar efeitos adversos e também diante da possibilidade de antecipar os efeitos benéficos da fluoxetina, apenas com uma injeção / Antidepressant drugs such as selective serotonin reuptake inhibitors are used in the treatment of anxiety, panic and other mental disorders. The desired effects occur only after chronic administration, around 3 to 4 weeks after starting treatment, with increased anxiety symptoms at the beginning of pharmacological therapy, causing the discontinuation of the use of these drugs. In addition, there are reports of resistance to this type of treatment. Aiming to find solutions for such problems, based on studies that showed that opioid mechanisms favor the serotonin inhibitory activity in SCPD neurons that modulate scape / panic, the present study aimed to investigate the effect of Buprenorphine, a partial agonist of μ receptors - opioid and antagonist κ receptor - opioid as anxiolytic and anti-panic agents as well as assessing whether the anxiolytic and antipanic effect of Fluoxetine would be anticipated by association with Buprenorphine.Three experiments were performed using male Wistar rats weighing 200g at the beginning of the experimental sessions: 1. Acute treatment with Buprenorphine IP at doses (0,015mg / kg, 0,03mg / kg 0,3mg / kg) or Alprazolam IP (4mg / kg); 2. Subchronic treatment 3 days with Buprenorphine IP (0,3mg / kg); 3. Acute treatment with Buprenorphine (0,3mg / kg) - associated to the subchronic treatment with Fluoxetine 3 days IP, (10mg / kg). After the treatments, the animals were submitted to behavioral evaluation in the elevated T maze (LTE) and subsequently to the Open Field and the Light-Dark Transition Test. In experiment 1 the behavioral test was repeated 24 hours after the first behavioral evaluation. The results showed that Buprenorphine in the larger doses decreased the manifestation of the elusions, without alterations of the scapes in the LTE, differently from what was observed in the acute treatment with Alprazolam, which also reduced the elusive ones, but increased the latency in the scapes, interpreted respectively as anxiolytic and panicolitic. Twenty-four hours later no effect of Alprazolam was found, and the effect of Buprenorphine on the avoidance was only identified at the highest dose and only at LB. There was no increase in motor activity in either of the two situations. In the Light-Dark Transition test, no significant effect was observed in the conditions studied, it only allowed the choice of the highest dose for the continuity of the study, since the intermediary increased the motor activity in this test 24 hours after the injection.Subchronic administration of buprenorphine also decreased the avoidances without affecting the scapes and motor behavior in the open field. Also, no changes were identified in the Light-Dark Transition Test. Buprenorphine anticipated the anxiolytic effect of Fluoxetine, without affecting the responses related to the manifestation of panic. However, there was no confirmation of the findings in the other anxiety test. It was concluded that acute and subchronic administration of Buprenorphine decreased the defensive behaviors related to generalized anxiety, and anticipated the anxiolytic effect of Fluoxetine, which may constitute a relevant option in the treatment of anxiety disorders in the clinic due to the its low ability to cause adverse effects and also the possibility of anticipating the beneficial effects of fluoxetine with an injection alone

O transtorno de pânico (TP) é uma condição crônica e recorrente que prejudica a qualidade de vida e o funcionamento psicossocial dos pacientes. O tratamento com medicamentos e a terapia cognitivo-comportamental (TCC) tem evidências comprovadas de eficácia. Entretanto, a recaída é frequente e a falha nas estratégias de enfrentamento (coping), ao lidar com eventos estressores, tem sido apontada como um gatilho deste desfecho. O protocolo de 12 sessões de TCC em grupo (TCCG), atualmente utilizado, é específico para sintomas do TP. Estudos que avaliam os efeitos de intervenções com técnicas cognitivas de estratégias de coping ainda não foram testados. Pretende-se, neste estudo, verificar se a TCCG padrão modifica as estratégias de coping dos pacientes com TP comparados a um grupo sem transtorno mental (artigo 1) e avaliar o efeito ao acréscimo de quatro sessões de reforço com técnicas cognitivas de estratégias de coping após a TCCG (artigo 2). Trata-se de um ensaio clínico com pacientes (n=48) que participaram das 12 sessões de TCCG para TP de 2006 a 2009, chamados novamente em 2010 e sorteados para o grupo de intervenção (4 sessões de reforço) ou para o grupo controle (2 reuniões educativas). A gravidade dos sintomas foi mensurada pelas escalas: Impressão Clínica Global (CGI), Escala de Gravidade do TP (PDSS), Inventário do Pânico, Hamilton-Ansiedade (HAM-A) e Inventário de Depressão de Beck (BDI). Para identificar as estratégias de coping e a resiliência foram aplicados o Inventário de Estratégias de Coping (IEC) e a Escala de Resiliência, respectivamente. A qualidade de vida (QV) foi avaliada pela WHOQOL-bref. Para o primeiro objetivo de avaliar a mudança das estratégias de coping, os instrumentos foram aplicados antes e após a TCCG e o grupo sem transtorno mental (n=75) respondeu o IEC. Para verificar o efeito das sessões de reforço, os instrumentos foram aplicados antes da intervenção e após o término (1, 6 e 12 meses) por avaliadores independentes. A TCCG padrão foi efetiva na redução dos sintomas do TP em todas as medidas de desfecho. No artigo 1, foi observado que os pacientes diminuíram significativamente o uso da estratégia de coping de confronto (p=0,039) e de fuga e esquiva (p=0,026) quando comparada com o início do tratamento. Porém, a fuga e esquiva após a TCCG não foi mais significativamente diferente (p=0,146) que o grupo sem transtorno mental. Também foi encontrado que o uso de estratégias mais adaptativas estava correlacionado à diminuição da ansiedade antecipatória e dos ataques de pânico. No Artigo 2, os resultados do efeito das quatro sessões de reforço demonstraram melhora significativa dos sintomas do TP, da ansiedade e de depressão em ambos os grupos, considerando desfecho tempo. Ocorreu aumento significativo no domínio de relações sociais da QV no grupo de intervenção, considerando a interação tempo*grupo, independentemente da melhora dos sintomas. Entretanto, não houve diferença significativa nas estratégias de coping e nos demais domínios da QV. As mudanças nos níveis de resiliência foram dependentes dos sintomas do TP, ansiedade e depressão, isto é, quanto menor a intensidade dos sintomas, maior foram os níveis de resiliência. Concluindo, as técnicas da TCCG padrão podem modificar as estratégias de coping, porém com exceção da fuga e esquiva, as estratégias continuam diferentes do grupo sem transtorno mental. A resposta ao acréscimo de sessões de reforço com técnicas específicas de coping melhora o domínio das relações sociais da QV ao longo do tempo, independentemente da diminuição dos sintomas. Por outro lado, o aumento dos níveis de resiliência foi dependente da melhora da intensidade dos sintomas do TP, ansiedade e depressão e a melhora destes sintomas foi significativa, porém não foi diferente entre os grupos intervenção e controle. A hipótese é que este resultado pode estar relacionado a fatores terapêuticos do formato de grupo tanto das sessões de intervenção quanto do controle. Portanto, estudos que investiguem a adição de técnicas cognitivas de coping durante a TCCG padrão e o efeito de fatores terapêuticos do formato de grupo ainda precisam ser realizados. / Panic disorder (PD) is a chronic and recurrent condition that impairs patients’ quality of life and psychosocial functioning. Treatment with medication and cognitive-behavioral therapy (CBT) has confirmatory evidence of efficacy. Nonetheless, relapse is frequent and failure on coping strategies, when dealing with stressful events, has been suggested as being the trigger of this outcome. The protocol of 12 cognitive-behavioral group therapy (CBGT) sessions, as currently used, is specific for PD symptoms. Studies assessing the effects of interventions with cognitive techniques of coping strategies have not been tested yet. The present study aims to verify if the standard CBGT changes PD patients’ coping strategies, when compared to the ones used by the group of individuals without mental disorders (Article 1), and to evaluate the effect of adding 4 booster sessions with cognitive techniques of coping strategies after CBGT (Article 2). This study is a controlled clinical trial with patients (n=48) who participated in the 12 CBGT sessions for PD from 2006 to 2009, who were assessed again in 2010 and assigned either for the intervention group (4 booster sessions) or the control group (2 educational sessions). Symptoms severity was measured by the following scales: Clinical Global Impression (CGI), PD Severity Scale (PDSS), Panic Inventory, Hamilton-Anxiety (HAM-A), and Beck Depression Inventory (BDI). To identify coping strategies and resilience, Coping Strategies Inventory (CSI) and Resilience Scale were applied. Quality of life (QoL) was assessed by WHOQoL-bref. For the first objective of assessing the change on coping strategies, the instruments were applied before and after CBGT, while the group of individuals without mental disorders (n=75) answered CSI. To analyze the impact of booster sessions, the instruments were applied before the intervention and after it was concluded (1, 6, and 12 months) by independent interviewers. Standard CBGT was effective in reducing PD symptoms in all outcome measures. In the Article 1, it was observed that the patients reduced significantly the use of confrontive (p=0.039) and escape and avoidance (p=0.026) coping strategies in comparison to the treatment onset. However, the escape and avoidance strategy after CBGT was not more significantly different (p=0.146) than the strategy used by the control group without mental disorders. It was also observed that the use of more adaptive strategies correlated to the reduction of anticipatory anxiety and panic attacks. In the Article 2, the results of the effect of 4 booster sessions showed significant improvement of PD, anxiety and depression symptoms in both groups, considering the outcome time. A significant increase on social relations domain of QoL was observed in the intervention group, considering interaction time*group, regardless of symptom improvement. However, there was no significant difference on coping strategies and other domains of QoL. Changes on resilience levels depended on PD, anxiety, and depression symptoms, that is, the smaller the symptoms intensity the higher the resilience levels were. In conclusion, standard CBGT techniques might change coping strategies, but, except for escape and avoidance ones, other strategies are still different from the ones used by the group without mental disorders. The response to adding booster sessions with specific coping techniques improves the social relations domain of QoL over time, regardless of the reduction of symptoms. On the other hand, the increase of resilience levels depended on the improvement of PD, anxiety, and depression symptoms intensity. The improvement of these symptoms was significant, but not different for intervention and control groups. The hypothesis is that this result may be related to therapeutic factors of the group therapy both in intervention and control sessions. Therefore, research investigating the addition of cognitive coping techniques during standard CBGT and the effect of therapeutic factors of group therapy is yet to be carried out.

[pt] A interface entre a neuropsicologia e a psicopatologia vem sendo muito estudada. No entanto, há ainda uma grande demanda de caracterização de processamento de cada função cognitiva em pacientes com transtorno de pânico (TP). Neste trabalho, visou-se verificar se há diferenças de desempenho neuropsicológico entre adultos com TP e controles saudáveis. Participaram deste estudo 30 adultos, 15 com TP diagnosticado pelo MINI (versão 5.0) e 15 controles saudáveis emparelhados por escolaridade, idade, nível sociodemográfico e habilidades intelectuais. Administraram-se os instrumentos NEUPSILIN, discurso narrativo e fluências verbais da Bateria MAC, subtestes do WAIS-III, Wisconsin, Hayling, Teste das Trilhas, Teste dos Sinos, Teste Stroop, RAVLT e Buschke. Os escores médios foram comparados pelo teste não-paramétrico Mann-Whitney (p é menor ou igual a 0,05). Encontraram-se diferenças significativas no processamento de componentes executivos: velocidade de processamento, iniciação, inibição, assim como nas memórias episódica e de trabalho. Mais estudos são necessários com amostras clínicas maiores e mais homogêneas, controlando-se depressão e agorafobia. / [en] Nevertheless there is still a great demand of process characterization of each cognitive function on patients with panic disorder (PD). In this study we tried to verify if there are differences in the neuropsychological performance between adults with PD and a healthy control group. 30 adults took part on this study, 15 with diagnosed PD and 15 healthy control subjects, matched by school years, age, sociodemographic level and intellectual abilities. A neuropsychological test battery was administered including the NEUPSILIN, narrative speech and verbal fluency of MAC battery, WAIS-III subtests, Wisconsin, Hayling, Trail-Making test, Stroop, RAVLT, Buschke and Bells Cancellation Test. The median scores were compared using the non-parametric Mann-Whitney (p less than or equal to 0,05). We found significant differences on executive components: processing speed, initiation, inhibition, episodic and working memory. Further enquires are necessary, with a larger and more homogeneous samples, and controls for depression and agoraphobia.

O transtorno de pânico é uma das questões preocupantes em termos de saúde coletiva. Pensamos que tal transtorno se configura como uma nova forma de adoecimento psíquico, categoria que tem penetrado em diferentes espaços sociais, e suas descrições vêm sendo incorporadas ao arcabouço identitário dos sujeitos. Problematizar as matrizes culturais da emergência e difusão deste transtorno, no campo da construção de subjetividade e de identidade, é o objetivo deste estudo. Na pós-modernidade, por um lado, nos centramos nas características do que se denomina sociedade de risco, (BECK, 1998) a qual gera sentimentos de imprevisibilidade, desenraizamento e desfiliação; por outro, juntamente com o desprestígio do ideal da interioridade, observa-se um recurso a se recorrer ao registro do corpo e da biologia como âncora subjetiva. (COSTA, 2005). Com a predominância de um cenário de incerteza e de risco permanente, cria-se uma atmosfera em que a previsibilidade e a confiabilidade são constantemente ameaçadas, Ou seja, o valor da confiança no registro da ontologia refere-se à existência de um ambiente suficientemente confiável e previsível para que os sujeitos experienciem uma constância dos ambientes de ação social e material circundante (WINNICOTT, 1963). Verificaremos, em meio a um cenário de risco ambiente, como o pânico emerge e é difundido com base em matrizes desviantes. O transtorno de pânico, pretensamente radicado no cérebro e determinado pela genética, parece ser uma das entidades às quais as pessoas aderem e ao redor das quais se agregam. Nesse sentido, defendendo que os tipos de patologia, nos quais se inclui o transtorno de pânico, podem servir também como redes de pertencimento, formas de sociabilidade que se organizam em torno de predicados físicos, tanto na esfera da normalidade quanto da patologia, entre as quais o corpo anatomofisiológico se destaca como fenômeno identitário, denominado por alguns autores de bioidentidade (ORTEGA, 2000). Humanizar o conceito transtorno de pânico, portanto, é afirmar que tais sintomas já conheceram outras utilizações. Entendendo o sujeito como um conjunto de crenças podem ser alteradas, revistas, repensadas, redimensionadas (COSTA, 1994). Ao sair da esfera da universalidade e essencialidade, típicas de classificações reducionistas no campo da psiquiatria, para a perspectiva de que existem jogos de linguagem diferentes para se referir ao pânico, percebemos que em vez de o transtorno de pânico existem os pânicos, ou seja, são plurais e diversificadas as diferentes gramáticas para se falar daquilo a que se reduz hoje essa classificação psiquiátrica. / Panic disorder is one of the worrying questions in terms of collective health. We believe that such disorder is a new form of mental illness, a category that has penetrated different social spaces, and its descriptions have been incorporated into the identitary framework of subjects. This study aims to question the cultural origins of the emergence and diffusion of this disorder in the field of subjectivity and identity construction. In post-modernity, on the one hand, we focus on the characteristics of what is called risk society (BECK, 1998), which generates feelings of unpredictability, unrootedness, and disaffiliation; on the other hand, together with the lack of prestige of the interiority ideal, individuals tend to resort to the register of the body and of biology as subjective anchor (COSTA, 2005). With the predominance of a scenario of uncertainty and permanent risk, an atmosphere is created in which predictability and trustworthiness are constantly threatened. That is, the value of trust in the register of ontology refers to existence of an environment that is sufficiently trustworthy and predictable so that the subjects experience a constancy of the surrounding environments of social and material action (WINNICOTT, 1963). We shall verify, within a risk scenario, how panic emerges and is diffused based on deviating origins. The panic disorder, which is supposedly rooted in the brain and determined by genetics, seems to be one of the entities to which people adhere and around which they aggregate. In this sense, we defend that the types of pathology in which the panic disorder is included may also function as belonging networks, forms of sociability that are organized around physical characteristics, both in the sphere of normality and of pathology, among which the anatomo-physiological body emerges as an identitary phenomenon, which some authors call bioidentity (ORTEGA, 2002). Humanizing the concept of panic disorder, therefore, means stating that such symptoms have already known other uses. If one understands the subject as a set of beliefs and desires, whose identity is under permanent reconstruction, these beliefs can be altered, revised, rethought, re-dimensioned (COSTA, 1994). When we leave the sphere of universality and essentiality, typical of reductionist classifications in the field of psychiatry, and embrace the perspective that there are different language games to refer to panic, we perceive that, instead of the panic disorder, there are panics, that is, the different grammars used to talk about that to which this psychiatric classification is reduced today are plural and diversified.