12
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Event-related potential studies of post-traumatic stress disorder: a critical review and synthesis

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Despite the sparseness of the currently available data, there is accumulating evidence of information processing impairment in post-traumatic stress disorder (PTSD). Studies of event-related potentials (ERPs) are the main tool in real time examination of information processing. In this paper, we sought to critically review the ERP evidence of information processing abnormalities in patients with PTSD. We also examined the evidence supporting the existence of a relationship between ERP abnormalities and symptom profiles or severity in PTSD patients. An extensive Medline search was performed. Keywords included PTSD or post-traumatic stress disorder, electrophysiology or EEG, electrophysiology, P50, P100, N100, P2, P200, P3, P300, sensory gating, CNV (contingent negative variation) and MMN (mismatch negativity). We limited the review to ERP adult human studies with control groups which were reported in the English language. After applying our inclusion-exclusion review criteria, 36 studies were included. Subjects exposed to wide ranges of military and civilian traumas were studied in these reports. Presented stimuli were both auditory and visual. The most widely studied components included P300, P50 gating, N100 and P200. Most of the studies reported increased P300 response to trauma-related stimuli in PTSD patients. A smaller group of studies reported dampening of responses or no change in responses to trauma-related and/or unrelated stimuli. P50 studies were strongly suggestive of impaired gating in patients with PTSD. In conclusion, the majority of reports support evidence of information processing abnormalities in patients with PTSD diagnosis. The predominance of evidence suggests presence of mid-latency and late ERP components differences in PTSD patients in comparison to healthy controls. Heterogeneity of assessment methods used contributes to difficulties in reaching firm conclusions regarding the nature of these differences. We suggest that future ERP-PTSD studies utilize standardized assessment scales that provide detailed information regarding the symptom clusters and the degree of symptom severity. This would allow assessment of electrophysiological indices-clinical symptoms relationships. Based on the available data, we suggest that ERP abnormalities in PTSD are possibly affected by the level of illness severity. If supported by future research, ERP studies may be used for both initial assessment and treatment follow-up.

          Related collections

          Most cited references53

          • Record: found
          • Abstract: found
          • Article: not found

          The development of a Clinician-Administered PTSD Scale.

          Several interviews are available for assessing PTSD. These interviews vary in merit when compared on stringent psychometric and utility standards. Of all the interviews, the Clinician-Administered PTSD Scale (CAPS-1) appears to satisfy these standards most uniformly. The CAPS-1 is a structured interview for assessing core and associated symptoms of PTSD. It assesses the frequency and intensity of each symptom using standard prompt questions and explicit, behaviorally-anchored rating scales. The CAPS-1 yields both continuous and dichotomous scores for current and lifetime PTSD symptoms. Intended for use by experienced clinicians, it also can be administered by appropriately trained paraprofessionals. Data from a large scale psychometric study of the CAPS-1 have provided impressive evidence of its reliability and validity as a PTSD interview.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Failure of extinction of fear responses in posttraumatic stress disorder: evidence from second-order conditioning.

            Posttraumatic stress disorder (PTSD) is characterized by the re-experiencing of a traumatic event, although the trauma itself occurred in the past. The extinction of the traumatic response might be impeded if trauma reminders maintain fear responses by their association with the original trauma through second-order conditioning. A differential conditioning paradigm with a trauma-specific picture, used as an acquired unconditioned stimulus, and graphic representations, used as conditioned stimuli, were employed in 14 PTSD patients, 15 trauma-exposed subjects without PTSD, and 15 healthy comparison subjects. The authors used event-related potentials of electroencephalogram (EEG), self-report measures, skin conductance responses, heart rate, and startle modulation to assess the differential conditioned response among subjects. Trauma-exposed subjects with and without PTSD but not healthy comparison subjects showed successful differential conditioning to the trauma-relevant cue indicative of second-order conditioning. Only PTSD patients exhibited enhanced conditioned responses to the trauma reminder during acquisition and impaired extinction as evident in more negative evaluations of the conditioned stimuli associated with a trauma reminder as well as enhanced peripheral and brain responses. These findings suggest that PTSD may be maintained by second-order conditioning where trauma-relevant cues come to serve as unconditioned stimuli, thus generalizing enhanced emotional responses to many previously neutral cues and impeding extinction. The extinction deficit in PTSD patients observed in this study underlines the need for therapies focusing on the extinction of learned responses, such as behavioral treatment, with or without the addition of pharmacological substances that enhance the extinction of a learned response.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Neurophysiological evidence for a defect in neuronal mechanisms involved in sensory gating in schizophrenia.

              The action of CNS inhibitory neuronal mechanisms was tested in acutely psychotic unmedicated schizophrenic patients and in normal controls. An early positive component of the auditory average evoked response recorded at the vertex 50 msec after a click stimulus was studied. Stimuli were delivered at 10-sec intervals to establish a base-line response. Inhibitory mechanisms were then tested using a conditioning-testing paradigm by assessing the change in response to a second stimulus following the first at either 0.5, 1.0, or 2.0-sec intervals. At the 0.5-sec interval, normal controls had over a 90% mean decrement in response, whereas schizophrenics showed less than a 15% mean decrement. At 2-sec intervals, responses from normals were still 30 to 50% diminished, but those from schizophrenics showed an increased response to the stimulus compared to base line. The data suggest that normally present inhibitory mechanisms are markedly reduced in schizophrenics. Failure of these inhibitory mechanisms may be responsible for the defects in sensory gating which are thought to be an important part of the pathophysiology of schizophrenia.
                Bookmark

                Author and article information

                Journal
                Biol Mood Anxiety Disord
                Biol Mood Anxiety Disord
                Biology of Mood & Anxiety Disorders
                BioMed Central
                2045-5380
                2011
                12 October 2011
                : 1
                : 5
                Affiliations
                [1 ]Department of Psychiatry, University of Michigan, Ann Arbor, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA
                [2 ]Department of Psychiatry and Behavioral Neurosciences, Wayne State University, 540 E Canfield, Detroit, MI 48201-1998, USA
                Article
                2045-5380-1-5
                10.1186/2045-5380-1-5
                3377169
                22738160
                5d7a3576-e942-4e0b-aaf0-6b90c7fbd93e
                Copyright ©2011 Javanbakht et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 April 2011
                : 12 October 2011
                Categories
                Review

                Neurology
                Neurology

                Comments

                Comment on this article