دانلود مقاله ISI انگلیسی شماره 29636
عنوان فارسی مقاله

فعال سازی مغز و ضربان قلب در طول تصویرسازی با هدایت تروماتیک - اسکریپت در اختلال استرس پس از حادثه: یافته های اولیه

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
29636 2012 6 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Brain activation and heart rate during script-driven traumatic imagery in PTSD: Preliminary findings
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Psychiatry Research: Neuroimaging, Volume 204, Issues 2–3, 30 November 2012, Pages 155–160

کلمات کلیدی
تصویربرداری - سیستم عصبی خودکار -
پیش نمایش مقاله
پیش نمایش مقاله فعال سازی مغز و ضربان قلب در طول تصویرسازی با هدایت تروماتیک - اسکریپت در اختلال استرس پس از حادثه: یافته های اولیه

چکیده انگلیسی

Patients with posttraumatic stress disorder (PTSD) experience psychological and physiological distress. However, imaging research has mostly focused on the psychological aspects of the disorder. Considered an expression of distress, heart rate (HR) in PTSD is often elevated. In the current study, we sought to identify brain regions associated with increased HR in PTSD. Nine patients with PTSD and six healthy trauma survivors were scanned while resting, clenching teeth, and listening to neutral and traumatic scripts. Brain function was evaluated using H2O15 positron emission tomography (PET). HR was monitored by electrocardiogram. Data were analyzed using statistical parametric mapping (SPM). Subjects with PTSD exhibited a significant increase in HR upon exposure to traumatic scripts, while trauma survivors did not. Correlations between regional cerebral blood flow and HR were found only in patients with PTSD, in orbitofrontal, precentral and occipital regions. Neither group showed correlation between rCBF and HR in the amygdala or hippocampus. These preliminary results indicate that "top down" central nervous system regulation of autonomic stress response in PTSD may involve associative, sensory and motor areas in addition to regions commonly implicated in fear conditioning.

مقدمه انگلیسی

Posttraumatic stress disorder (PTSD) is a stress-related psychiatric condition, with prevalence rates of 7–12% in the general population (Kessler et al., 2005). It is associated with significant psychiatric comorbidity, functional impairment, compromised health status, and substantial economic costs to society. One in two individuals in the general population will experience a traumatic incident at some point in their lives, and 10–25% of traumatized subjects subsequently develop PTSD. Patients with PTSD suffer from intrusive memories of the trauma, emotional and physiological arousal responses to cues resembling their traumatic experience, and avoidance of such cues. Signs of increased arousal and vigilance, expressed by an exaggerated startle response, elevated blood pressure, sleep disturbance and increased skin conductance accompany the disorder (Pitman et al., 1987). Elevated basal heart rate (HR) and stimulus-triggered HR (Orr et al., 2002) as well as non-extinction of HR elevation on repeated stimuli (Peri et al., 2000, Wessa and Flor, 2007), are perhaps the most common physiological findings in PTSD. HR is regulated by the autonomic nervous system. Increased heart rate in PTSD is considered a measure of increased sympathetic and decreased parasympathetic activity (Orr et al., 2002 and Cohen and Benjamin, 2006). The autonomic nervous system is regulated by a network of cortical and subcortical structures, including the insula, frontoparietal cortex, cerebellum, anterior cingulate, orbitofrontal cortex, amygdala and diverse thalamic and hypothalamic nuclei, referred to in animals as the 'central autonomic network' (Janig and McLachlan, 1992). In humans, changes in blood pressure and heart rate can be elicited by stimulating the insula, medial prefrontal cortex, anterior cingulate gyrus and medial temporal lobe (Fish et al., 1993). Imaging research in PTSD traditionally sought brain correlates of behavioral, emotional and cognitive symptoms. Abnormalities were primarily found in prefrontal cortex (PFC), amygdala and hippocampus (Shin et al., 2006). The amygdala regulates fear conditioning in both animals and humans (Phelps and LeDoux, 2005). Along with visual processing regions, both primary and higher order, the amygdala shows increased response to threat-related stimuli, in subjects without PTSD (van Marle et al., 2009). Increased amygdala response to stressful stimuli has also been found in PTSD (Rauch et al., 2000), in association with decreased response in the medial prefrontal cortex (mPFC) (Shin et al., 2004, Shin et al., 2005 and Etkin and Wager, 2007) and hippocampus (Etkin and Wager, 2007). The amygdala projects to most sensory-related association cortices, and is involved in sensory modulation from the early stages in the cortical hierarchy (Amaral et al., 1992). In particular, a close working relationship has been demonstrated between the amygdale and the occipital cortex (Hendler et al., 2001). Furthermore, it has been repeatedly shown that the occipital lobe, in particular on the right (Daniels et al., 2012), is involved in memory of emotional events. The hippocampus is involved in declarative memory generation as well as in stimuli contextualization, both of which are impaired in PTSD. Hippocampal dysfunction is one of the most consistent findings in functional and anatomical imaging studies in PTSD (Acheson et al., 2012). The mPFC is considered to play a key role in the extinction of fear conditioning, which is thought to be impaired in PTSD. Several functional neuroimaging studies of PTSD have shown decreased or complete lack of mPFC activation during traumatic script driven imagery (e.g. Lanius et al., 2001). Alterations in the insula, orbitofrontal cortex, posterior cingulate and parietal somatosensory regions have also been described (Bremner et al., 2008 and Liberzon and Sripada, 2008). In addition to regionalized brain dysfunction in PTSD, cortical excitability changes in PTSD have been demonstrated by the application of single-pulse transcranial magnetic stimulation (TMS) to the motor cortex of drug naïve patients (Rossi et al., 2009). The authors contend that prolonged illness could be associated with lasting (GABAa related) functional or structural changes even in brain regions such as the motor cortex that are outside, although functionally connected with, regions usually found dysfunctional in PTSD, such as the anterior cingulate cortex, amygdala, limbic and paralimbuc regions. In the current study we set out to determine which brain regions are involved in differential HR response, as an indicator of the exaggerated autonomic response to trauma-related stimuli in PTSD. Central autonomic regulation of cardiovascular response may be similar in PTSD and healthy controls, yet brain regions whose activity correlates with PTSD-specific autonomic activation may be involved in modulation of autonomic response in PTSD. The orbitofrontal cortex, the amygdala, and the hippocampus are involved in processing and integrating stress-related input and in triggering autonomic arousal response to both psychological and physiological stressors (for review, see Ulrich-Lai and Herman, 2009). We assumed that differential autonomic response to repeated trauma-related cues, in PTSD and non-PTSD subjects would be associated with differential activation in these regions. Specifically, we assumed that increased activation would be seen in the hippocampus and amygdala while decreased activation would be seen in the mPFC. We further expected to note differences in regional brain activation in regions functionally related to constituents of the "central autonomic network".

نتیجه گیری انگلیسی

Patients with PTSD scored significantly higher than healthy controls on all symptom severity measures (Table 1). A significant main effect of group (F(1,14.952)=5.75; p=0.03) and a group by condition interaction (F(6,10.171)=7.56; p=0.003) were found for RR interval as dependent variable. Post hoc between-group comparisons revealed significantly lower values of mean RR intervals in PTSD during the four trauma scripts ( Table 2), mostly attributable to an increase in heart rate ( Fig. 1). Table 2. Comparison of mean RR interval values between PTSD patients and controls. Condition Control PTSD P ⁎ Resting 927.469±39.942 848.000±48.489 0.225 Teeth clenching 927.021±36.164 849.500±44.056 0.194 Neutral script 925.333±30.378 858.333±37.205 0.183 Trauma script #1 936.562±30.734 798.148±37.796 0.012 Trauma script #2 962.444±30.828 817.712±38.936 0.011 Trauma script #3 958.222±31.635 835.208±40.852 0.031 Trauma script #4 973.575±30.242 836.122±38.330 0.015 ⁎ Bonferroni-corrected for multiple comparisons. Table options Full-size image (30 K) Fig. 1. Changes in heart rate (1000/RR interval(msec)⁎60) across conditions in PTSD patients and controls. ⁎Depicts statistically significant (p<0.05) group differences. Figure options Significant positive correlations were found between RR interval and rCBF in the left orbitofrontal region (Brodmann area 11), right occipital region (Brodmann area 18) and right high precentral region (primary motor cortex, Brodmann area 4) in patients with PTSD (Table 3 and Fig. 2). No significant positive correlations were found in the non-PTSD group, and no significant negative correlations were found in either group. Neither group showed correlation between rCBF and HR in the amygdala or hippocampus. Table 3. Regions showing correlations⁎ between RR interval and rCBF PTSD patients. Location Cluster size x y z P ⁎⁎ Left orbitofrontal (Brodmann 11) 238 −10 60 −22 0.006 Right precentral gyrus (Brodmann 4) 149 12 −30 76 0.046 Right occipital region (Brodmann 18) 286 18 −82 10 0.002 ⁎ Correlations are all positive. ⁎⁎ Bonferroni cluster corrected. Table options Full-size image (46 K) Fig. 2. Regions showing positive correlations between RR interval and rCBF in PTSD subjects. A: Left orbitofrontal (−10, 60, −22); B: Right precentral gyrus (12, −30, 76); and C: Right occipital region (18, −82, 10). Each region is presented in three planes: sagittal (upper left), coronal (upper right), and transaxial (lower left).

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