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Simor P.1, Pajkossy P.1, Bódizs R.2,3 PROCEEDINGS OF THE 15TH WORLD CONGRESS OF PSYCHOPHYSIOLOGY of the International Organization of Psychophysiology (I.O.P.) Budapest, Hungary September 1-4, 2010 1.Budapest Univ. Techn. Economics, Department of Cognitive Sciences, Budapest, Hungary Introduction: Different lines of research suggest that REM sleep and dreaming involve the intense functioning of an emotional frontolimbic network facilitating off-line emotional information processing (Walker, 2009). Moreover, this emotional processing may facilitate the regulation of affective states by restructuring emotional memories into broader cortical networks. Dysphoric dreaming and frequent nightmares may reflect the impairment of such emotional integration and reorganization. Recently, Levin and Nielsen (2007) traced a neurocognitive model of dreaming that integrates the advances of the neuroscience of sleep, clinical sleep research, and the neuroscientific literature on affective regulation. One of the model’s main assumptions is that nightmare sufferers may be characterized by impaired prefrontal inhibitory functions causing amygdalar over-reactivity, and thus, malfunctioning affective regulation during the intense emotional state of dreaming. In order to test this hypothesis, we aimed to characterize the frontally localized inhibitory functions of nightmare sufferers. Methods: Thirty two nightmare sufferers and matched controls were selected from a large pool of university students after completing different sleep and dream-related questionnaires. A neuropsychological test battery (emotional go/no-go, fluency, and Porteus maze tasks) and the STAI questionnaire were used to assess the participants’ frontal inhibitory functions and levels of anxiety. Results: Nightmare sufferers were characterized by significantly higher rates of perseveration errors in the Fluency tasks and dream disturbances were associated with impaired frontal inhibitory functions. These results remained significant after controlling for sleep quality and levels of anxiety. Conclusion: Our results provide partial support for the neurocognitive model of dreaming (Levin and Nielsen, 2007) and suggest that the neuropsychological and psychophysiological characterization of nightmare sufferers would shed more light on the cortical mechanism of affective regulation in sleep. We consider that the neuropsychological and psychophysiological investigations of different parasomnias are an intriguing way to integrate clinical and experimental sleep research.
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