Author(s): Markus Burgmer 2, Maimu Alissa Rehbein 1, Marco Wrenger 2, Judith Kandil 3, Gereon Heuft 2, Christian Steinberg 1, Bettina Pfleiderer 4, Markus Junghöfer 1,*
Introduction
Post-traumatic stress disorder (PTSD) is a severe mental disorder that can occur after the experience of a highly stressful or traumatic event. Its core characteristics are hyperarousal, behavioral avoidance and/or emotional numbing, and frequent intrusions of traumatic material into consciousness [1], [2]. Among others [3], one theoretical approach explains the pathology of PTSD by drawing on the nature of the traumatic event itself and its storage in a fear structure [4], [5]. All aspects of the trauma, including cognitions, emotions, sensory, and physiological responses, are stored as 'nodes' in a fear network, which provides information templates for quickly activating a fear response. Due to spreading activation between nodes, excitement of a single element is sufficient to activate the whole network and to initiate a fear reaction. With repeated exposure to stressful experiences, elements are added and connections between different nodes are established or strengthened by ways of Hebbian learning, so that the activation threshold of the fear structure is lowered [6], [7]. As a result, fear-related stimuli may readily excite the fear network, which, in turn, can trigger a fear response and interrupt on-going cognitive mechanisms [8].
Several functional brain imaging studies revealed relevant brain areas involved in the trauma network by investigating brain responses to emotional stimuli in PTSD patients. For example, amygdala activation was enhanced towards trauma-related [9], [10] and not trauma-related, emotional information [11], [12]. Furthermore, disturbed prefrontal cortex (PFC) function was recorded during the processing of emotional information. More specifically, both hypoactivation [12], [13] and hyperactivation [14] within the medial prefrontal cortex, including orbitofrontal areas and the anterior cingulate cortex, were reported [15].
Due to their excellent temporal resolution, event-related potential or magnetic field (ERP, ERF) studies can reveal the temporal dynamics of disturbed information processing in PTSD and, thus, complement the view of hemodynamic functional imaging studies. Indeed, ERP studies using auditory stimuli found alterations in stimulus processing already at 50 ms after stimulus onset pointing towards impaired sensory gating processes in PTSD [16]-[18]. In vision, altered processing of trauma-related and not trauma-related emotional material was reported as early as 100 ms post-stimulus [19]-[21] and also later processing stages, such as the P200 [22], [23] and P300 [19], [24], seem to be affected. However, results about altered ERP-amplitudes in vision appear rather inconsistent, since both augmented and attenuated amplitudes have been reported [25], [26].
Recent whole-head ERF-studies using distributed source models may provide a solid explanation to these mixed results. Indeed, both decreased and increased steady-state responses towards negative pictures were recorded in PTSD, but the first stemmed from occipital areas and the latter from superior parietal areas [27]. This biphasic pattern was confirmed by findings showing a decrease in affective modulation of parieto-occipital areas during 206-256 ms, preceded by enhanced PFC activation towards negative pictures [28]. It was concluded that such heightened PFC responsiveness displays a rapid...