1
initiated antidepressant use, subjects who stopped antidepressant use, and persistent antidepressant users during follow-up. Results: As compared to healthy controls, subjects who developed, remitted from, or persistently had a MDD or anxiety diagnosis showed similar 2-year changes in RSA and heart rate. However, compared to continuous non-users, subjects who started using a tricyclic antidepressant or a serotonergic and noradrenergic working antidepressant showed significantly greater 2-year increase in heart rate and decrease of RSA. Subjects who started selective serotonin reuptake inhibitors use also showed greater RSA decrease, but no heart rate increase. Stopping antidepressant use systematically caused opposite effects with RSA levels almost returning to the levels in non-users. Conclusions: These 2-year longitudinal results do not support the idea that depression and anxiety disorders cause diminished vagal control, but instead indicate that all antidepressants cause a decrease in cardiac vagal control. After stopping the use of antidepressants autonomic function nearly completely recovers, suggesting that unfavorable effects are reversible. References [1] Licht, C.M.M., de Geus, J.C.N., Zitman, F.G., Hoogendijk, W.J., van Dyck, R., Penninx, B.W.J.H., 2008]. Association between major depressive disorder and heart rate variability in the Netherlands Study of Depression and Anxiety (NESDA). Arch Gen Psychiatry 65 (12), 13581367. [2] Licht, C.M.M., de Geus, J.C.N., van Dyck, R., Penninx, B.W.J.H., 2009]. Association between anxiety disorders and heart rate variability in The Netherlands Study of Depression and Anxiety (NESDA). Psychosom Med 71 (5), 508518. doi:10.1016/j.ijpsycho.2010.06.021 The ruminatorendophenotype: Autonomic dysregulation and risk for health Cristina Ottaviani a , David Shapiro b a Department of Psychology, University of Bologna, Italy b Department of Psychiatry, University of California, Los Angeles, USA After stressful events, people may think perseveratively about the causes and consequences of these episodes without being actively engaged in problem-solving thinking. Ruminative thoughts can be especially disturbing during a particularly stressful period and may result in depression and anxiety. In fact, rumination appears to have a unique relationship to depression, even after statistically controlling for other negative cognitive styles (e.g., Flett et al., 2002), and longitudinal prospective studies have found that people prone to rumination also have higher levels of general anxiety and posttrau- matic stress symptoms (e.g., Kocovski et al., 2005). We hypothesized that the negative effects of rumination on health can be attributed to the autonomic dysregulation that characterizes this mental process. We studied the effects of rumination induced in the laboratory and subsequent changes over 24h. Impedance cardiography-derived measures, ECG, and beat-to-beat blood pres- sure (BP) were monitored continuously in 60 participants (27 men and 33 women; mean age= 33.4 (±9.5)) during baseline, an Anger Recall Interview, a reading task, and two recovery periods. Rumina- tion was experimentally manipulated by the use of a distracter. Plasma concentrations of inflammatory biomarkers (CRP, sICAM-1) were obtained at baseline and at the end of the session. The laboratory session was followed by a 24-h ambulatory heart rate (HR) and BP recording and by self reports of mood and rumination. Rumination induced in the lab was associated with a series of well known risk factors for cardiovascular diseases, all of which cause mortality, such as reduced overall autonomic regulatory capacity (i.e., CAR; t=-3.15; p<.0001), diminished contribution of the para- sympathetic branch (i.e., CAB; t= -3.61; p<.0001), reduced baroreceptor sensitivity, and a shift towards a more vascular system compared to the relatively more efficient regulation of BP via cardiac mechanisms (t = 3.32, p < .0001). Moreover, after controlling for age and body mass index, rumination outside the lab proved to be a strong predictor of daily moods and ambulatory HR and BP. The specific pattern of autonomic dysregulation that characterized rumination appeared to be more pathogenic in subjects with higher levels of depression, anxiety, and anger, and was associated with the activation of the inflammatory biomarkers. Preliminary data collected on a clinical sample of personality borderline disorder patients suggest that the negative effects of ruminative thoughts on health are greater in psychopathological conditions. Therapeutic approaches are needed to address this specific symptomatology. doi:10.1016/j.ijpsycho.2010.06.022 Autonomic responsivity in neurodevelopmental disorders (ADHD, TS, and ASD) N.A. Harrison a , F. Beacher a , M. Gray a , Y. Nagai a,b , H. Critchley a a Psychiatry, Brighton and Sussex Medical School, University of Sussex, Brighton, UK b Department of Psychology, University of Essex, Colchester, UK Background: Autism Spectrum Disorders (ASD), Attention Deficit Hyperactivity Disorder (ADHD) and Tourette Syndrome (TS) are neurodevelopmental disorders with strikingly different clinical manifestations and presentations. However, despite such disparate clinical presentations, they frequently show co-morbidity suggesting potentially similar etiological mechanisms. Autonomic dysregulation has been reported independently in each of these conditions, though comparisons of the nature of this dysregulation across disorders are rare. Methods: In this talk, I shall comprehensively review the em- pirical evidence for autonomic dysregulation in each of these disorders, highlighting similarities and differences, and present new empirical data highlighting how a knowledge of autonomic dysfunc- tion and its link to the neural systems governing motivational, social, and emotional behaviour, may enhance our understanding of these complex disorders and potentially offer novel treatment pathways. Results: In two recent studies we show that individuals with ASD show qualitative and quantitative differences in autonomic responses to emotionally arousing stimuli. For example, in a task investigating effects of contextual frame on decision making processes, not only did individuals with ASD show diminished behavioral susceptibility to framing effects, but they also did not mount a differential skin conductance response (unlike healthy controls), suggesting that they fail to incorporate emotional context into decision-making processes. In the second study investigating effects of gender on autonomic responses to emotionally arousing stimuli, individuals with ASD showed the opposite relationship between parasympathetic modula- tions of heart rate (high frequency power) than that observed in neurotypical individuals. Conclusions: Autonomic dysregulation is frequently reported across neurodevelopmental disorders; a greater understanding of the nature of these differences in autonomic responsivity across these disorders may enhance our understanding of their neurobiological bases. doi:10.1016/j.ijpsycho.2010.06.287 212 Abstracts / International Journal of Psychophysiology 77 (2010) 206238

Autonomic responsivity in neurodevelopmental disorders (ADHD, TS, and ASD)

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initiated antidepressant use, subjects who stopped antidepressantuse, and persistent antidepressant users during follow-up.

Results: As compared to healthy controls, subjects who developed,remitted from, or persistently had a MDD or anxiety diagnosisshowed similar 2-year changes in RSA and heart rate. However,compared to continuous non-users, subjects who started using atricyclic antidepressant or a serotonergic and noradrenergic workingantidepressant showed significantly greater 2-year increase in heartrate and decrease of RSA. Subjects who started selective serotoninreuptake inhibitors use also showed greater RSA decrease, but noheart rate increase. Stopping antidepressant use systematicallycaused opposite effects with RSA levels almost returning to thelevels in non-users.

Conclusions: These 2-year longitudinal results do not support theidea that depression and anxiety disorders cause diminished vagalcontrol, but instead indicate that all antidepressants cause a decreasein cardiac vagal control. After stopping the use of antidepressantsautonomic function nearly completely recovers, suggesting thatunfavorable effects are reversible.

References[1] Licht, C.M.M., de Geus, J.C.N., Zitman, F.G., Hoogendijk, W.J., van Dyck, R., Penninx,

B.W.J.H., 2008]. Association between major depressive disorder and heart ratevariability in the Netherlands Study of Depression and Anxiety (NESDA). Arch GenPsychiatry 65 (12), 1358–1367.

[2] Licht, C.M.M., de Geus, J.C.N., van Dyck, R., Penninx, B.W.J.H., 2009]. Associationbetween anxiety disorders and heart rate variability in The Netherlands Study ofDepression and Anxiety (NESDA). Psychosom Med 71 (5), 508–518.

doi:10.1016/j.ijpsycho.2010.06.021

The “ruminator” endophenotype: Autonomic dysregulation andrisk for health

Cristina Ottaviania, David Shapiroba Department of Psychology, University of Bologna, Italyb Department of Psychiatry, University of California, Los Angeles, USA

After stressful events, people may think perseveratively about thecauses and consequences of these episodes without being activelyengaged in problem-solving thinking. Ruminative thoughts can beespecially disturbing during a particularly stressful period and mayresult in depression and anxiety. In fact, rumination appears to have aunique relationship to depression, even after statistically controllingfor other negative cognitive styles (e.g., Flett et al., 2002), andlongitudinal prospective studies have found that people prone torumination also have higher levels of general anxiety and posttrau-matic stress symptoms (e.g., Kocovski et al., 2005).

We hypothesized that the negative effects of rumination on healthcan be attributed to the autonomic dysregulation that characterizesthis mental process. We studied the effects of rumination induced inthe laboratory and subsequent changes over 24h. Impedancecardiography-derived measures, ECG, and beat-to-beat blood pres-sure (BP) were monitored continuously in 60 participants (27 menand 33 women; mean age=33.4 (±9.5)) during baseline, an AngerRecall Interview, a reading task, and two recovery periods. Rumina-tion was experimentally manipulated by the use of a distracter.Plasma concentrations of inflammatory biomarkers (CRP, sICAM-1)were obtained at baseline and at the end of the session. Thelaboratory sessionwas followed by a 24-h ambulatory heart rate (HR)and BP recording and by self reports of mood and rumination.Rumination induced in the lab was associated with a series of wellknown risk factors for cardiovascular diseases, all of which causemortality, such as reduced overall autonomic regulatory capacity (i.e.,CAR; t=−3.15; p<.0001), diminished contribution of the para-

sympathetic branch (i.e., CAB; t=−3.61; p< .0001), reducedbaroreceptor sensitivity, and a shift towards a more vascular systemcompared to the relatively more efficient regulation of BP via cardiacmechanisms (t=3.32, p<.0001). Moreover, after controlling for ageand body mass index, rumination outside the lab proved to be astrong predictor of daily moods and ambulatory HR and BP. Thespecific pattern of autonomic dysregulation that characterizedrumination appeared to be more pathogenic in subjects with higherlevels of depression, anxiety, and anger, and was associated with theactivation of the inflammatory biomarkers. Preliminary data collectedon a clinical sample of personality borderline disorder patientssuggest that the negative effects of ruminative thoughts on health aregreater in psychopathological conditions.

Therapeutic approaches are needed to address this specificsymptomatology.

doi:10.1016/j.ijpsycho.2010.06.022

Autonomic responsivity in neurodevelopmental disorders(ADHD, TS, and ASD)

N.A. Harrisona, F. Beachera, M. Graya, Y. Nagaia,b, H. Critchleyaa Psychiatry, Brighton and Sussex Medical School, University of Sussex,Brighton, UKb Department of Psychology, University of Essex, Colchester, UK

Background: Autism Spectrum Disorders (ASD), Attention DeficitHyperactivity Disorder (ADHD) and Tourette Syndrome (TS) areneurodevelopmental disorders with strikingly different clinicalmanifestations and presentations. However, despite such disparateclinical presentations, they frequently show co-morbidity suggestingpotentially similar etiological mechanisms. Autonomic dysregulationhas been reported independently in each of these conditions, thoughcomparisons of the nature of this dysregulation across disorders arerare.

Methods: In this talk, I shall comprehensively review the em-pirical evidence for autonomic dysregulation in each of thesedisorders, highlighting similarities and differences, and present newempirical data highlighting how a knowledge of autonomic dysfunc-tion and its link to the neural systems governing motivational, social,and emotional behaviour, may enhance our understanding of thesecomplex disorders and potentially offer novel treatment pathways.

Results: In two recent studies we show that individuals with ASDshow qualitative and quantitative differences in autonomic responsesto emotionally arousing stimuli. For example, in a task investigatingeffects of contextual frame on decision making processes, not onlydid individuals with ASD show diminished behavioral susceptibilityto framing effects, but they also did not mount a differential skinconductance response (unlike healthy controls), suggesting that theyfail to incorporate emotional context into decision-making processes.

In the second study investigating effects of gender on autonomicresponses to emotionally arousing stimuli, individuals with ASDshowed the opposite relationship between parasympathetic modula-tions of heart rate (high frequency power) than that observed inneurotypical individuals.

Conclusions: Autonomic dysregulation is frequently reportedacross neurodevelopmental disorders; a greater understanding ofthe nature of these differences in autonomic responsivity across thesedisorders may enhance our understanding of their neurobiologicalbases.

doi:10.1016/j.ijpsycho.2010.06.287

212 Abstracts / International Journal of Psychophysiology 77 (2010) 206–238