DISORDER AFFECT MODULATION IN HEMISPHERIC DYSFUNCTION

描述（改编自申请人摘要）：神经病学 文献众所周知，中枢神经系统损伤可产生 精神病理学的形式（例如，抑郁症，“否认”疾病，获得性 精神病），这实际上是无法区分他们的“功能” 精神病学同行 我们研究的总体重点是使用 消融范例，以了解更多关于皮质部位在 行为的情感调节 最近的人类证据表明 在消极情感状态下， 在积极的影响中减少。 尽管动物研究已经针对 杏仁核作为恐惧中的关键结构增强惊吓和焦虑状态， 在某些将信息传递给杏仁核的皮质部位出现病变， 减轻啮齿类动物的恐惧增强惊吓， 他们跟着别人。 目前没有关于以下方面的人类数据： 皮质部位可能有助于影响惊吓的调制，或者是否 可能存在半球不对称。 这是一个很大的问题。 研究者目前的研究。 在拟定的研究中，研究者希望延长其正在进行的研究 在杏仁核受损的人类中进行的资助研究， 个体与皮质病变，相互作用显着， 杏仁核 她假设这些皮层系统的破坏（例如， 与杏仁核联系最紧密的脑区， 改变惊吓和其他情绪行为方面的效价调节。 为了解决这一假设，患者的离散病变， 眶额、背外侧额或颞后部位 将评估右半球或左半球。 眨眼惊吓反应将 当受试者同时进行情感诱发任务时， （休克引起的预期焦虑，观看情绪化的场景，听 情感的声音）。 在这些任务中，多种情绪测量 将获得反应性，包括口头报告和心理生理 对唤醒敏感的测量（皮肤电导），效价（惊吓眨眼， 面部EMG）和处理需求。 按照设计，她希望学习 是否：a）这些情绪反应之间存在差异解耦 系统由于特定皮质部位的完整性; B）是否效价 惊吓反应的调节受损伤的影响不同 涉及额或后颞部位; c）是否获得模式 的研究结果更符合神经心理学中的一个 情绪处理的偏侧模型（二价，右半球等）。 希望所获得的数据将提供有关情绪的有用信息， 在特定功能障碍后发生的疾病和精神病理学 大脑中的神经系统。

DESCRIPTION (Adapted from applicant's abstract): In the neurology literature it is widely known that central nervous system damage can produce forms of psychopathology (e.g., depression, "denial" of illness, acquired psychopathy) that are virtually indistinguishable from their "functional" psychiatric counterparts. The overall focus of our research is to use an ablative paradigm in order to learn more about the role of cortical sites in the affective modulation of behavior. Recent evidence from humans suggests that startle eyeblinks are enhanced during negative affective states and reduced during positive affect. Although animal studies have targeted the amygdala as a key structure in fear potentiated startle and anxiety states, lesions at some cortical sites that relay information to the amygdala appear to attenuate fear potentiated startle in rodents of completely eliminate them following others. No human data currently exist concerning which cortical sites might contribute to affect modulation of startle, or whether hemispheric asymmetries might exist. This is the focus of the investigator's present research. In the proposed studies, the investigator wishes to extend her ongoing funded research in humans with amygdala damage to more broadly encompass individuals with cortical lesions that interact prominently with the amygdala. She hypothesizes that disruption of those cortical systems (e.g., orbitofrontal) that are most closely linked with amygdala will dramatically alter valence modulation of startle and other aspects of emotional behavior. To address this hypothesis, patients with discrete lesions involving orbitofrontal, dorsolateral frontal, or posterior temporal sites within the right or left hemisphere will be evaluated. Eyeblink startle responses will be elicited while subjects concurrently engage in affect eliciting tasks (shock induced anticipatory anxiety, viewing emotional scenes, listening to affective sounds). During these tasks, multiple measures of emotional reactivity will be obtained including verbal report and psychophysiologic measures sensitive to arousal (skin conductance), valence (startle eyeblink, facial EMG), and processing demands. As designed, she hopes to learn whether: a) there is differential decoupling among these emotion response systems due to integrity of particular cortical sites; b) whether valence modulation of the startle response is differently affected by lesions involving frontal or posterior temporal sites; c) whether obtained patterns of findings are more consistent with one of several neuropsychological laterality models of emotion processing (bivalent, right hemisphere, etc.). Hopefully, the obtained data will provide useful information about emotional disorders and psychopathology that occur following dysfunction of specific neural systems within the brain.