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Abstracts
  • Ambach, W., Stark, R., Peper, M., & Vaitl, D. (2008). An interfering Go/No-go task does not affect accuracy in a Concealed Information Test. International Journal of Psychophysiology : Official Journal of the International Organization of Psychophysiology, 68(1), 6–16. https://doi.org/10.1016/j.ijpsycho.2007.11.004

    Following the idea that response inhibition processes play a central role in concealing information, the present study investigated the influence of a Go/No-go task as an interfering mental activity, performed parallel to the Concealed Information Test (CIT), on the detectability of concealed information. 40 undergraduate students participated in a mock-crime experiment and simultaneously performed a CIT and a Go/No-go task. Electrodermal activity (EDA), respiration line length (RLL), heart rate (HR) and finger pulse waveform length (FPWL) were registered. Reaction times were recorded as behavioral measures in the Go/No-go task as well as in the CIT. As a within-subject control condition, the CIT was also applied without an additional task. The parallel task did not influence the mean differences of the physiological measures of the mock-crime-related probe and the irrelevant items. This finding might possibly be due to the fact that the applied parallel task induced a tonic rather than a phasic mental activity, which did not influence differential responding to CIT items. No physiological evidence for an interaction between the parallel task and sub-processes of deception (e.g. inhibition) was found. Subjects' performance in the Go/No-go parallel task did not contribute to the detection of concealed information. Generalizability needs further investigations of different variations of the parallel task.

  • Zimmermann, M., Stark, R., Kern, G., Laiacker, M., Kirsch, P., & Vaitl, D. (2006). Positive and negative spatial priming in schizophrenia. Journal of Clinical and Experimental Neuropsychology, 28(5), 706–720. https://doi.org/10.1080/13803390590954290

    Priming tasks are used for investigating the deficits of selective attention in schizophrenia, which are thought to be related to the psychotic symptoms. Priming was assessed in acutely psychotic unmedicated (n = 22) and medicated (n = 36) schizophrenia patients and in control subjects (n = 42). The subjects had to indicate the location of a target stimulus in two consecutive stimulus displays (prime and probe). Each stimulus appeared together with a distractor on a screen. Negative Priming is characterized by an increase in reaction time, whenever a probe target is presented at a prime distractor location. Positive Priming is characterized by a decrease in reaction time, when the probe target is presented at the prime target location. Schizophrenia patients altogether showed no abnormalities in priming effects, neither in the acute phase of illness (medicated and unmedicated) nor in partial remission (one month later, medicated). In unmedicated patients however Negative Priming was inversely correlated with the severity of positive symptoms. This indicates a priming deficit in a small subgroup of severely ill patients. The data support the notion that automatic (implicit) mechanisms of learning are unimpaired in schizophrenia patients unless symptoms exceed a certain critical level.

  • Schweckendiek, J., Klucken, T., Merz, C. J., Tabbert, K., Walter, B., Ambach, W., Vaitl, D., & Stark, R. (2011). Weaving the (neuronal) web: fear learning in spider phobia. NeuroImage, 54(1), 681–688. https://doi.org/10.1016/j.neuroimage.2010.07.049

    Theories of specific phobias consider classical conditioning as a central mechanism in the pathogenesis and maintenance of the disorder. Although the neuronal network underlying human fear conditioning is understood in considerable detail, no study to date has examined the neuronal correlates of fear conditioning directly in patients with specific phobias. Using functional magnet resonance imaging (fMRI) we investigated conditioned responses using phobia-relevant and non-phobia-relevant unconditioned stimuli in patients with specific phobias (n=15) and healthy controls (n=14) by means of a differential picture-picture conditioning paradigm: three neutral geometric figures (conditioned stimuli) were followed by either pictures of spiders, highly aversive scenes or household items (unconditioned stimuli), respectively. Enhanced activations within the fear network (medial prefrontal cortex, anterior cingulate cortex, amygdala, insula and thalamus) were observed in response to the phobia-related conditioned stimulus. Further, spider phobic subjects displayed higher amygdala activation in response to the phobia-related conditioned stimulus than to the non-phobia-related conditioned stimulus. Moreover, no differences between patients and healthy controls emerged regarding the non-phobia-related conditioned stimulus. The results imply that learned phobic fear is based on exaggerated responses in structures belonging to the fear network and emphasize the importance of the amygdala in the processing of phobic fear. Further, altered responding of the fear network in patients was only observed in response to the phobia-related conditioned stimulus but not to the non-phobia-related conditioned stimulus indicating no differences in general conditionability between patients with specific phobias and healthy controls.

  • Alexander, N., Klucken, T., Koppe, G., Osinsky, R., Walter, B., Vaitl, D., Sammer, G., Stark, R., & Hennig, J. (2012). Interaction of the serotonin transporter-linked polymorphic region and environmental adversity: increased amygdala-hypothalamus connectivity as a  potential mechanism linking neural and endocrine hyperreactivity. Biological Psychiatry, 72(1), 49–56. https://doi.org/10.1016/j.biopsych.2012.01.030

    BACKGROUND: Gene by environment (G×E) interaction between genetic variation in the promoter region of the serotonin transporter gene (serotonin transporter-linked polymorphic region [5-HTTLPR]) and stressful life events (SLEs) has been extensively studied in the context of depression. Recent findings suggest increased neural and endocrine stress sensitivity as a possible mechanism conveying elevated vulnerability to psychopathology. Furthermore, these G×E mediated alterations very likely reflect interrelated biological processes. METHODS: In the present functional magnetic resonance imaging study, amygdala reactivity to fearful stimuli was assessed in healthy male adults (n = 44), who were previously found to differ with regard to endocrine stress reactivity as a function of 5-HTTLPR × SLEs. Furthermore, functional connectivity between the amygdala and the hypothalamus was measured as a potential mechanism linking elevated neural and endocrine responses during stressful/threatening situations. The study sample was carefully preselected regarding 5-HTTLPR genotype and SLEs. RESULTS: We report significant G×E interaction on neural response patterns and functional amygdala-hypothalamus connectivity. Specifically, homozygous carriers of the 5-HTTLPR S' allele with a history of SLEs (S'S'/high SLEs group) displayed elevated bilateral amygdala activation in response to fearful faces. Within the same sample, a comparable G×E interaction effect has previously been demonstrated regarding increased cortisol reactivity, indicating a cross-validation of heightened biological stress sensitivity. Furthermore, S'S'/high SLEs subjects were characterized by an increased functional coupling between the right amygdala and the hypothalamus, thus indicating a potential link between neural and endocrine hyperreactivity. CONCLUSIONS: The present findings contribute to the ongoing debate on 5-HTTLPR × SLEs interaction and are discussed with respect to clinical implications.

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