Insights from neurophysiological and behavioral studies
Dissertation zur Erlangung des akademischen Grades des Doktors der Naturwissenschaften
an der Universität Konstanz
Eingereicht an der mathematisch-naturwissenschaftlichen Sektion, Fachbereich Psychologie
Vorgelegt von Dipl.-Psych. Britta Balliel
Tag der mündlichen Prüfung: 17.04.08 Referent: Prof. Dr. Thomas Elbert Referentin: Prof. Dr. Johanna Kissler
Abstract... 1
Zusammenfassung... 4
1 General introduction ... 8
2 Core symptoms of PTSD... 12
3 PTSD as memory disorder... 15
3.1 Associative fear structure as central element in PTSD development ... 15
3.2 Are associative fear structures important for PTSD chronification?... 22
3.3 Consequences for PTSD treatment... 26
3.4 From theory to empirical evidence... 28
4 Contributions from previous evidence ... 29
4.1 Why investigate associative fear structures with affective stimuli?... 29
4.2 Cortical responses to affective stimuli ... 32
4.3 Response facilitation and inhibition for affective stimuli ... 47
4.4 Associative learning of affective stimuli ... 60
5 Temporary summary and general aim of the studies ... 71
6 Evaluation of affective words in refugee adolescents ... 73
6.1 Introduction ... 73
6.2 Methods ... 73
6.3 Results ... 76
6.4 Discussion... 77
7.2 Methods ... 85
7.3 Results ... 89
7.4 Discussion... 96
8 Enhanced response inhibition for unpleasant words in PTSD adolescents .. 107
8.1 Introduction ... 107
8.2 Methods A... 115
8.3 Results A ... 119
8.4 Methods B ... 120
8.5 Results B ... 123
8.6 Discussion... 125
9 Altered associative learning in PTSD adolescents: an EEG study ... 135
9.1 Introduction ... 135
9.2 Methods ... 142
9.3 Results ... 147
9.4 Discussion... 157
10 General conclusions... 170
11 References ... 177
12 Appendix ... 198
Danke zu sagen erscheint mir nicht einfach. Denn es gibt viele Menschen, die mich auf sehr unterschiedliche Weise bei Beginn, Fortführung und Beendigung dieses Projekts unterstützt haben. Euch allen gemeinsam ist, dass Ihr mir in grandioser Weise zur Seite steht und Teil des großen Puzzles seid. Ich werde nur einige dieser Puzzleteilchen benennen können, doch wir alle wissen: Das Ganze ist mehr als die Summe seiner Teile!
Dieses Puzzle wird umrahmt von wissenschaftlichen Herausforderungen, bei denen mich Johanna Kissler, Thomas Elbert, Brigitte Rockstroh und Shlomo Bentin sicher geleitet und begleitet haben. Für diesen Weg sowie für die Betreuung und Begutachtung meiner Dissertation danke ich Euch sehr!
Die Basis des Puzzles wird durch alle Teilnehmer gebildet, deren Fleiß und Geduld ich sehr schätze. Dies gilt ebenso für die Helferinnen, die die Datenerhebung möglich machten: Hannelore Kramer, Barbara Missalek und Mrs. Koheela.
Spezieller Dank für Organisation, stetige und bedingungslose Hilfe bei der Datenerhebung sowie das stets offene Ohr gebührt Barbara Awiszus und Heike Riedke.
Über weitere diagnostische und experimentelle Unterstützung (sowie die tolle Bürogenossenschaft) von Dorle Hensel-Dittmann, Martina Ruf, Rosemarie Zimmer, Ursula Lommen, Claudia Catani und Elisabeth Schauer habe ich mich sehr gefreut.
Cornelia Herbert, Anne Hauswald und Susanne Kössler danke ich für das stetige Einspringen im Kampf mit Presentation, Emegs, Matlab und Co. Vor allem danke ich Euch aber dafür, dass Ihr eine zuverlässige Adresse für Spaß zwischendurch seid!
Letzteres gilt ausserdem vielen weiteren Mitarbeitern der Arbeitsgruppe, die mir das tägliche Leben angenehm gestalten.
Den Dank an Dich in Worte zu fassen, liebe Silke, fällt mir schwer. Es ist daher ein Dankeschön „ohne Worte”.
An dieser Stelle möchte ich auch Euch, liebe Barbara und lieber Hugo, danken.
Vielleicht habe ich mich nie explizit für Eure Unterstützung meiner Ausbildung bedankt, weil Ihr mir immer das Gefühl gegeben habt, es sei selbstverständlich. Ich weiß, dass es das bestimmt nicht ist! Ebenso wenig selbstverständlich ist die immerwährende Unterstützung und Aufmunterung von Dir, liebe Anke!
Ich schließe das unvollständige Puzzle mit einem weiteren, sehr liebevollen Dank
„ohne Worte” an Dich, lieber Stephan.
This dissertation aims at empirically demonstrating moderators of the manifestation and chronification of posttraumatic symptoms. The determining factor of PTSD symptom development is commonly assumed to be the mental representation of a traumatic experience (e.g., Ehlers & Clark, 2000; Elbert, Rockstroh, Kolassa, Schauer,
& Neuner, 2006; Foa & Kozak, 1986; Foa, Riggs, & Gershuny, 1995; P. J. Lang, 1979;
Metcalfe & Jacobs, 1996). A pathological representation is characterized by an enlarged associative fear structure with very strong interconnections between the included elements. The connections to autobiographical context information are weak. The size or respective number of included elements increases with every recall and thus enhances the probability for future reactivation. These presumptions are included in several recommended therapeutic approaches (Ehntholt & Yule, 2006; Gotthardt, 2006), but empirical support for the pathological associative (fear) structures is rare.
The pathological associative (fear) structure includes sensory information of all modalities and excessive response components. A general affective (unpleasant) arousal is by definition inherent in any potentially traumatic experience. Hence, affective (unpleasant) arousal should constitute a potent trigger for the associative fear structure.
Behavioral and neurophysiological correlates of the associative fear structure were thus demonstrated by using affective word processing on the basis of the biphasic emotion theory (P. J. Lang, 1979). The current dissertation provides insights in strength and accessibility of the pathologically respresented elements and its interconnections.
Furthermore, indices for a pathologically altered response disposition are investigated.
The current studies addressed these aspects in PTSD refugee adolescents, controls of the same ethnic group, and treated PTSD patients without migration background.
Insights into (altered) affective word processing were provided on different levels of affective word processing. An adapted stimulus selection was performed for the particular refugee sample by subjective stimulus evaluations of 32 healthy refugee adolescents. A nonlinear relationship between the valence and arousal ratings for German nouns confirmed previous reports (e.g. P. J. Lang, Bradley, & Cuthbert, 1997).
Neurophysiological indicators (MEG) for “healthy” affective word processing were demonstrated in an enhanced ventral stream activity and sustained late frontal and parietal activity, particularly for pleasant nouns (N = 18, 9 control and PTSD subjects each; 1 Hz presentation frequency). The results replicate previous literature with respect
in PTSD adolescents was evidenced in a strong early occipital response to emotional (particularly unpleasant) words and a subsequent inhibition of cortical activity. The current experiment thus confirmed previous findings of an enhanced early posterior negativity in response to affective pictures among adult PTSD refugees (Junghofer, Schauer et al., 2003). The literature on affective processing in “healthy” and other clinical samples (e.g. Bernat, Bunce, & Shevrin, 2001; Cuthbert, Schupp, Bradley, Birbaumer, & Lang, 2000; Flor, Knost, & Birbaumer, 1997; Junghofer, Keil, & Peyk, 2003; Öhmann, Dimberg, & Esteves, 1989; Ortigue et al., 2004; Pauli, Amrhein, Muhlberger, Dengler, & Wiedemann, 2005; Schupp, Junghofer, Weike, & Hamm, 2004; Williamson, Harpur, & Hare, 1991) suggests an early activation of the associative fear structure element by the emotional arousal and a subsequent “cortical avoidance”
response.
Affective word processing was further investigated on the level of response biases in evaluative decisions on affective nouns within a priming design (N = 25, n = 15 control, n = 10 PTSD; SOA 400 ms). Results revealed several factors that led to a deceleration of evaluative decisions: Response latencies were generally prolonged for PTSD patients and thus suggested a general pathological impairment. In addition, evaluative decisions were decelerated for unpleasant targets among all participants, but this response inhibition was particularly prominent in PTSD participants. PTSD patients’ response latencies were further decelerated when the target was preceded by a pleasant or neutral prime. Previous literature (e.g. De Houwer, Hermans, Rothermund,
& Wentura, 2002; K.C. Klauer & Musch, 2003; Wentura, 1998, 1999) and the mainly successful replication among PTSD treatment responders and non-responders without migration background suggest a pathologically shifted evaluation of the affective (unpleasant) stimuli: The altered subjective meaning is interpreted as experimental evidence for the extended associative fear structure in PTSD patients. The enhanced associative strength between stimuli with (unpleasant) emotional arousal supports the view of strengthened interconnections within an associative fear structure. The replication trial further revealed that associative fear structures are not influenced by treatment success or treatment type (Narrative exposure therapy vs.
meditation/relaxation).
control and n = 10 PTSD subjects). “Healthy” learning was evidenced in better cued recall performance for pleasant word pairs and repeated list presentation. An early P3 and negative frontal slow wave activity were neurophysiological indicators of “healthy”
associative learning that parallel previous evidence (e.g. Escera, Alho, Schroger, &
Winkler, 2000; Friedman, Cycowicz, & Gaeta, 2001; Knight & Scabini, 1998; Rösler et al., 1997; Rosler, Heil, & Glowalla, 1993; Rosler, Heil, & Roder, 1997). Altered associative learning in PTSD refugee adolescents was characterized by a particular increase in unpleasant false alarms that suggests difficulties in the discrimination of emotionally arousing (unpleasant) stimuli. These pathological difficulties argue for a general PTSD-specific hypersensitivity for unpleasant arousal and may indicate the reactivation of the associative fear structure. The pathological processing of affective word pairs was supported by an inhibited stimulus evaluation process in (left) frontal regions despite task-relevant attention that was indexed by a late P3 component (Cuthbert et al., 2000; Schupp, Ohman et al., 2004). A late positive voltage shift in frontal areas further indicated an inhibition of the underlying cortical areas and thus a continuation of the “cortical avoidance“, described for the mere presentation of affective words.
The generalization of the current findings is limited by the small sample sizes and by some special features of the current dissertation: the investigation of adolescents, mainly with migration background and thus non-natives for German, which are discussed in detail. Nevertheless, the large variety of both methodological approaches and included participants allow for reasoning about a common psychological construct:
the associative (fear) structure.
The current dissertation provides important insights into pathologically altered affective word processing among PTSD patients. The main contribution of the current dissertation thus consists in the empirical basis for several aspects of the associative fear structure that explains the development of posttraumatic symptoms: Although the control subjects mostly experienced life-threatening events, too, systematic group differences were evidenced. The current findings further suggest that these pathological structures are not modified in (successful) PTSD treatment. In conclusion, the current dissertation fills in the discrepancy between the demand for evidence-based therapies and insufficiently investigated presumptions in the therapeutic approaches.
Ziel dieser Dissertation ist es, Moderatoren der Manifestation und Chronifizierung von posttraumatischen Symptomen empirisch zu demonstrieren. Als entscheidender Faktor in der Entwicklung von PTSD-Symptomen wird im Allgemeinen die mentale Repräsentation der traumatischen Erfahrung angenommen (z.B. Ehlers & Clark, 2000;
Elbert, Rockstroh, et al., 2006; Foa & Kozak, 1986; Foa et al., 1995, P. J. Lang, 1979;
Metcalfe & Jacobs, 1996). Eine pathologische Repräsentation ist durch eine vergrößerte assoziative Furchtstruktur mit sehr starken Verbindungen zwischen den eingeschlossenen Elementen charakterisiert. Die Verbindungen zu autobiographischen Kontextinformationen sind schwach. Die Größe bzw. die entsprechende Zahl an eingeschlossenen Elementen nimmt mit jedem Abruf zu und steigert daher die Wahrscheinlichkeit für eine spätere Reaktivierung. Diese Vorannahmen liegen mehreren empfohlenen therapeutischen Ansätzen zugrunde (Ehntholt & Yule, 2006;
Gotthardt, 2006), aber die empirische Untermauerung der pathologischen assoziativen (Furcht-)Strukturen ist gering.
Die pathologische assoziative (Furcht-)Struktur umfasst sensorische Informationen aller Modalitäten sowie exzessive Antwortkomponenten. Eine allgemeine affektive (unangenehme) Erregung ist per Definition in jeder potentiell traumatischen Erfahrung enthalten. Eine affektive (unangenehme) Erregung sollte daher einen potenten Trigger der assoziativen Furchtstruktur darstellen. Verhaltens- und neurophysiologische Korrelate assoziativer Furchtstrukturen wurden daher in der affektiven Wortverarbeitung basierend auf der biphasischen Emotionstheorie (P. J.
Lang, 1979) demonstriert. Die vorliegende Dissertation ermöglicht Einblicke in Stärke und Ansprechbarkeit der pathologisch representierten Elemente und deren Verbindungen. Zudem werden Indikatoren einer pathologisch veränderten Antwortdisposition untersucht.
Die vorliegenden Studien untersuchten diese Aspekte bei jugendlichen Flüchtlingen mit PTSD, Kontrollpersonen der gleichen ethnischen Gruppe und behandelten PTSD-Patienten ohne Migrationshintergrund. Einblicke in (veränderte) affektive Wortverarbeitung wurden auf verschiedenen Ebenen der affektiven Wortverarbeitung ermöglicht. Eine Anpassung der Stimulusauswahl für die besondere Flüchtlingsstichprobe erfolgte durch subjektive Stimulusevaluation von 32 gesunden jugendlichen Flüchtlingen. Ein nichtlinearer Zusammenhang zwischen Valenz- und
Neurophysiologische Indikatoren (MEG) „gesunder“ affektiver Wortverarbeitung wurden in einer gesteigerten Aktivität im ventralen Strom und in einer anhaltenden späten frontalen und parietalen Aktivität gezeigt, insbesondere für angenehme Nomen (N = 18, je n = 9 Kontroll- und PTSD-Probanden; 1 Hz Präsentationszeit). Die Ergebnisse replizieren frühere Literatur in bezug auf den zeitlichen Verlauf, die Lokalisation der Stromquelle und die Präferenz der angenehmen Reize (Kissler et al., 2006, für eine Übersicht). Veränderte affektive Wortverarbeitung bei Jugendlichen mit PTSD wurde in einer starken frühen okzipitalen Antwort auf emotionale (insbesondere unangenehme) Wörter sowie in einer anschließenden Inhibition der kortikalen Aktivität gezeigt. Das vorliegende Experiment bestätigt daher vorherige Befunde einer gesteigerten frühen posterioren Negativierung auf affektive Bilder bei erwachsenen Flüchtlingen mit PTSD (Junghofer, Schauer, et al., 2003). Die Literatur zu affektiver Verarbeitung in „gesunden“ und anderen klinischen Stichproben (z.B. Bernat et al., 2001, Cuthbert et al., 2000; Flor et al., 1997; Junghhofer, Keil, et al., 2003; Öhmann et al., 1989; Ortigue et al., 2004; Pauli et al., 2005, Schupp, Junghofer, et al., 2004;
Williamson et al., 1991) lässt auf eine frühe Aktivierung eines Elements der assoziativen Furchtstruktur durch die emotionale Erregung und auf eine anschließende
„kortikale Vermeidung“ schließen.
Affektive Wortverarbeitung wurde darüber hinaus auf der Ebene von Antworttendenzen in einer evaluativen Entscheidung zu affektiven Nomen innerhalb eines Primingdesigns untersucht (N = 25, n = 15 Kontrollprobanden, n = 10 PTSD- Probanden; SOA 400 ms). Die Ergebnisse offenbarten mehrere Faktoren, die zu einer Verzögerung der evaluativen Entscheidung führten: Die Antwortlatenzen waren grundsätzlich bei PTSD-Probanden verlängert und deuteten daher auf ein allgemein eingeschränktes Funktionsniveau hin. Zudem waren die evaluativen Entscheidungen für unangenehme Targets bei allen Probanden verzögert, allerdings war die Antwortinhibition bei PTSD-Patienten besonders ausgeprägt. Antwortlatenzen von PTSD-Patienten waren darüber hinaus verlängert, wenn das Target auf einen angenehmen oder neutralen Prime erfolgte. Vorhergehende Literatur (z.B. De Houwer, Hermans, et al., 2002; Klauer & Musch, 2003; Wentura, 1998, 1999) und die überwiegend erfolgreiche Replikation unter PTSD-Patienten ohne Migrationshintergrund deuten eine pathologisch veränderte Evaluation der affektiven
Patienten angesehen. Die zugenommene assoziative Stärke zwischen Reizen mit (unangenehmer) emotionaler Erregung unterstützt die Ansicht von verstärkten Verbindungen innerhalb der assoziativen Furchtstruktur. Die Replikationsstudie zeigte darüber hinaus, dass assoziative Furchtstrukturen nicht von Behandlungserfolg oder -art abhängen (Narrative Expositionstherapie vs. Meditation/Entspannung).
Diese Dissertation untersuchte weiterhin affektive Wortverarbeitung höherer Ordnung mittels Paarassoziationslernen und zugehöriger kortikaler langsamer Wellen (EEG; N = 19, n = 9 Kontroll- und n = 10 PTSD-Probanden). „Gesundes“ Lernen zeichnete sich durch eine bessere Leistung im Cued Recall für angenehme Wortpaare sowie für wiederholte Präsentation der Lernliste aus. Eine frühe P3 und negative frontale langsame Wellen waren neurophysiologische Indikatoren “gesunden”
assoziativen Lernens, die mit früherer Evidenz übereinstimmen (z.B. Escera et al., 2000; Friedman et al., 2001; Knight & Scabini, 1998, Rösler et al., 1997; Rosler et al., 1993; Rosler et al., 1997). Verändertes assoziatives Lernen bei jugendlichen Flüchtlingen mit PTSD war durch eine besondere Zunahme an inkorrekten Antworten mit unangenehmer Valenz gekennzeichnet, die auf Schwierigkeiten in der Diskrimination emotional erregender (unangenehmer) Reize hinweist. Diese pathologischen Schwierigkeiten sprechen für eine allgemeine PTSD-spezifische Überempfindlichkeit für unangenehme Erregung und deuten eventuell auf eine Reaktivierung der assoziativen Furchtstruktur hin. Die pathologische Verarbeitung affektiver Wortpaare war begleitet von einem inhibierten Stimulusevaluationsprozess in (links-)frontalen Regionen trotz aufgabenbezogener Aufmerksamkeit, die durch die späte P3-Komponente angezeigt wurde (Cuthbert et al., 2000; Schupp, Ohmann et al., 2004). Eine späte Positivierung in frontalen Bereichen wies darüber hinaus auf eine Inhibition der darunter liegenden kortikalen Areale und daher eine Fortsetzung der
„kortikalen Vermeidung“ hin, wie sie bereits für die einfache Präsentation affektiver Wörter beschrieben wurde.
Die Verallgemeinerung der vorliegenden Befunde wird durch die kleine Stichprobengröße und einige Besonderheiten der vorliegenden Arbeit eingeschränkt:
Die Untersuchungen von Jugendlichen, überwiegend mit Migrationshintergund und damit nicht mit Deutsch als Muttersprache, werden im Detail diskutiert. Dennoch ermöglicht die große Bandbreite sowohl an methodischen Zugängen als auch
Die vorliegende Dissertation bietet wichtige Einblicke in eine pathologisch veränderte affektive Wortverarbeitung bei PTSD-Patienten. Der Hauptbeitrag der vorliegenden Dissertation besteht daher in der empirischen Basis mehrerer Apekte der assoziativen (Furcht-)Struktur, die die Entwicklung posttraumatischer Symptome erklärt: Obwohl die Kontrollprobanden überwiegend auch lebensbedrohliche Erfahrungen gemacht haben, wurden systematische Gruppenunterschiede aufgezeigt.
Die vorliegenden Befunde weisen weiter darauf hin, dass diese pathologischen Strukturen durch (erfolgreiche) Therapie nicht modifiziert werden. Die vorliegende Dissertation füllt daher die Diskrepanz zwischen der Forderung nach evidenzbasierten Therapien und unzureichend untersuchten Annahmen dieser therapeutischen Ansätze aus.
1 General introduction
Every day confrontation with “traumatized” persons takes place. A child that has lost the parents, the death of a loved one, witnessing a car accident or becoming a victim of war, torture or rape are only some examples of traumatic experiences.
Consequently, one might assume an enormous number of humans that have to deal with a „trauma“. However, the number of “traumatized” people is generally overestimated in western cultures. On the one hand, this might be due to the variety in definitions of what constitutes a “trauma”. On the other hand, most of these experiences appear so horrible that it seems unbelievable to not suffer from it once it is over. A recent epidemiologic study actually reports one percent of male and 2.2 percent of female German adolescents (14-24 years) to suffer from a manifest PTSD (Perkonigg, Kessler, Storz, &
Wittchen, 2000).
However, there are populations where PTSD is much more common and the current dissertation addresses one such particular population: refugee adolescents in Germany. In contrast to German civilians, the PTSD prevalence of 40 percent among adult asylum seekers (Gäbel, Ruf, Schauer, Odenwald, & Neuner, 2006) and 20 percent among adolescent refugees (Ruf, in preparation) indicates that this illness is a big issue in the refugee sample. Most of the persons concerned experienced different kinds of organized violence in their country of origin. „Organized violence“ refers to war, torture and other severe human rights violations that wound the psyche and cause mental illness (Neuner, 2003). Neuner (2003) describes three different types of organized violence:
first, the permanent state-sponsored persecution (e.g. torture, extralegal executions, disappearances) that is typically found in dictatorships; second, massive violence that people have to face during interstate or civil wars and third, violence which is committed by terror organizations (such as guerilla rebels, e.g.). The aim of organized violence generally is to raise anxiety and depression among the population and disable parts of the population by causing severe suffering. Hence, mere survival of a life- threatening situation does not mean that the victims have overcome the trauma.
Actually, the victims have to handle a sequence of consequences, which one usually cannot foresee. Some of the consequences are obviously related to the triggering event (e.g. intrusions). Others are more manifest in subtle changes, which often appear with delay and without obvious direct relationship to the past event(s).
Nevertheless, a specific puzzling fact requires further investigation: Despite of low PTSD prevalence rates among German adolescents (Perkonigg et al., 2000), 26 percent of the males and 18 percent of the females reported to have experienced at least one traumatic event in their life. The discrepancy between PTSD prevalence and experienced traumata illustrates that not every survivor of a traumatic experience suffers from pathological impairments later in his life. The current dissertation aims at giving insights into the manifestation and chronification of PTSD symptoms from neurophysiological and behavioral studies.
In the past, research that highlights this puzzle focused e.g. the type and the number of traumatic experiences as well as cognitive processing mechanisms to predict manifestation and chronification of PTSD.
For instance, there has been a lot of research that identified specific traumatic experiences that have a greater „potential“ to cause a pathological processing of the trauma and to provoke the manifestation of PTSD symptoms (Steil & Ehlers, 1998).
The potential of a traumatic experience has been reported in relation to the distance to the aggressor, the power of the stressor, the duration of the trauma, the presence of an advance warning, the weight of the loss, the isolation of the victim and the number of persons concerned, the direct confrontation with the death, the involvement of the victim itself and the amount of moral conflicts.
Besides the type of the traumatic event, Neuner and colleagues (2004) state that the total number of traumatic experiences a single person survived is of particular interest. The authors observed a so-called „dose effect“: In a large field study, every participant suffered from manifest PTSD symptoms as soon as the traumatic load was high enough (28 different traumatic experiences and more). Neuner et al. (2004) suggest that a combination of both approaches applies to predict PTSD manifestation: Beyond a certain (individual) threshold of traumatic experiences, everybody is expected to develop PTSD. Below the threshold, PTSD development depends upon both the character of the traumatic experience and individual premorbid factors.
From a cognitive point of view, Ehlers and Clark (2000) tried to identify predictors for PTSD chronification. Their cognitive model suggest PTSD symptom chronification if the traumatic experience is processed in a way that it is still perceived as ongoing current threat. This perception is assumed to occur on the basis of extremely negative appraisal of the trauma and its consequences on the one hand. On the other hand, characteristic impairments of the autobiographic memory add to the feeling of
current threat: low elaboration and context representations of the traumatic event (see also Metcalfe & Jacobs, 1996), strong associative interconnections between single representations and strong perceptual priming.
The strong associative interconnections and a high number of interconnected elements have been emphasized in the model of an associative fear structure (Foa &
Kozak, 1986; P. J. Lang, 1979), too. The fear structure is hypothesized as a conglomerate of sensory (all modalities), cognitive (e.g. thoughts that came up during the event such as „I can’t do anything“), emotional (e.g. fear, horror, helplessness), and physiological alterations (e.g. sweaty hands, heart beat), which occurred initially during the traumatic event. It is further hypothesized that at each moment in time all nodes forming the propositional network (P. J. Lang, 1979) are at some state of activation and that the activation spreads along connecting links. Whenever activation in a particular part of the network reaches a certain threshold, that part becomes accessible to consciousness. Hence, the structure of the associative connections within the network determines the tendency of one item to “ignite” another one. In line with the original idea of the fear structure and the preceding work of Foa and Kozak (1986), Elbert and colleagues (2006) describe a vicious circle in the manifestation and chronification of PTSD: According to the Hebbian model (1949), the consequences of such a reactivation of the fear network are twofold: The connections between structural elements will be strengthened. In addition, the synchronous activation of elements already included in the fear network and of the retrieval environment facilitates subsequent common activation. Hence, a further enlargement of the associative fear structure is to be expected. An enlargement of a pathological fear network in turn implicates that even more cues are able to activate the whole structure. Again, every reactivation strengthens the connections within the associative structure and so on. In addition, the arousal symptoms of PTSD inhibit a cognitive modification of traumatic representations and foster the maintenance of the PTSD symptoms.
The current dissertation proposes that the core problem of the PTSD development and maintenance circle consists in the above mentioned (pathological) structure of representing the traumatic experiences as described in more detail in section 3. The assumed strongly interconnected associative fear structure (P. J. Lang, 1979) is seen as a special case of an associative network. The associate (fear) structure perspective provides an explanation that even environments that are not trauma-related on the first sight are able to reactivate representations of the terrific experiences. In consequence,
the current dissertation states that the PTSD-specific intrusion symptoms do not really come „out of the blue“ but are the manifestation of large and strongly overlearned associative structures.
The current studies aim at investigating these hypotheses among adolescent refugees suffering from PTSD and matched controls. All experiments were proved by an ethical committee.
Section 2 summarizes the definition of traumatic experiences and the core PTSD symptoms according to DSM-IV (APA, 2000). Comparisons to ICD-10 (WHO, 2000) as well as specifications for children and adolescents will be outlined. Section 3 contains a detailed description of the central idea of this dissertation: the mental representation of a traumatic experience as a central mechanism in manifestation and chronification of PTSD. Section 4 emphasizes the experimental focus of the current approach: Theoretical considerations that support the current experimental procedure are discussed as well as previous evidence in the field. The description of the empirical studies (sections 6 to 9) is preceded by a prestudy that enabled stimulus selection for the particular population. Then, indicators of pathological representational structures in PTSD patients are investigated on different processing levels and with different experimental methods. First, cortical responses during simple presentation of emotional stimuli are studied in an MEG experiment (section 7). Response biases in simple decision tasks are investigated in section 8. Section 9 describes higher level processing in associative learning on both behavioral and EEG measures. The dissertation closes with general conclusions and the consideration of research perspectives in section 10.
2 Core symptoms of PTSD
Posttraumatic stress disorder (PTSD) is a “young” psychological diagnosis.
Symptoms that are part of the trauma spectrum today have been initially described in Vietnam veterans in the 1970s (A. Y. Shalev, 2001). In 1980, Posttraumatic Stress Disorder was specified by the American Psychiatric Association in the Diagnostic and Statistic Manual for Mental Disorders (APA, 1980) for the first time.
The present DSM-IV is non-etiologic but descriptive. In this classification system, the PTSD conceptualization constitutes an exception. It is the only diagnosis that requires a causal event: a potentially traumatic experience. The term refers to a direct personal experience or witnessing of an event, “that involves actual or threatened death or serious injury, or other threat to one’s physical integrity” (APA, 2000, p. 463). In contrast to the ICD-10 (WHO, 2000), even “learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate” is interpreted as potentially traumatic event (APA, 2000, p. 463).
Additionally, the person’s response to a potentially traumatic event “must involve intense fear, helplessness, or horror” (APA, 2000, p. 463).
The core symptoms of PTSD (resulting from the exposure to the potentially traumatic event) can be divided in three clusters (see below). In addition, Shalev (2001) emphasizes that a number of psychobiological, cognitive and biological features are often involved. Some of them are outlined in the following paragraphs.
Intrusions
The PTSD-specific re-experiencing refers to an overwhelming sense of unintended reliving of the traumatic event. While reliving the traumatic experience, the connection to reality might get lost (flashbacks). Such intrusive events can occur during day and night times and disturb psychosocial functioning. The intrusions are accompanied by feelings of fear, panic, or other feelings that emerged also in the original situation and lead to excessive psychological stress. Additionally, corresponding physiologic responses such as tachycardia, sweating, trembling, etc., occur most often.
Avoidance
The re-experiencing cluster is accompanied by persistent avoidance symptoms.
This cluster is often subdivided into active and passive avoidance. Persistent effort not to think and talk about the traumatic experiences is representative for active avoidance, even if the effort is not successful. The avoidance of stimuli, places or activities associated with traumatic experiences are classified as active avoidance as well. In contrast, diminished interests, partial amnesia for the traumatic experience, feelings of detachment and estrangement from others or the sense of having a foreshortened future are summarized as passive avoidance and indicate a general emotional numbing.
Hyperarousal
This cluster comprises symptoms indicating that the body is still in a state of alarm resembling that of the triggering event: Insomnia, outbursts of anger, difficulties concentrating, hypervigilance and an exaggerated startle response are often found in PTSD patients.
The full range of symptoms (1 re-experiencing, 3 avoidance and 2 hyperarousal symptoms) has to persist at least one month and cause significant impairments in psychosocial behavior to allow a diagnosis of PTSD. The diagnosis can be specified as acute (less than 3 months), chronic (more than 3 months) and with delayed onset (symptoms begin at least 6 months after the stressor).
Differences in DSM-IV and ICD-10
With respect to PTSD, some main differences between the two classification systems should be named: While the ICD-10 (WHO, 2000) focuses on objective criteria, the DSM-IV (APA, 2000) emphasizes subjective responses to the traumatic stressor. With regard to symptoms, the ICD-10 puts the main focus on intrusive symptoms, while DSM-IV focuses on avoidance and emotional numbing. Additionally, specific features for children and adolescents are only specified in DSM-IV.
Specific criteria for children/adolescents
In the DSM-IV (APA, 2000), some specific features are added for children. For instance, the person’s response to traumatic stress can be expressed in disorganized or agitated behavior at younger ages. In addition, some particularities are named for the re- experiencing symptoms: repetitive play may occur in which themes or aspects of the
trauma are expressed. Alternatively, there may be nightmares without recognizable content, and trauma-specific re-enactment may occur which is appraised as part of the PTSD symptoms.
Complex PTSD
Herman, van der Kolk, and De Jong (De Jong, Komproe, Spinazzola, van der Kolk, & Van Ommeren, 2005; Herman, 1992; van der Kolk et al., 1996) proposed a particular diagnosis for symptoms that occur after long-lasting and extreme traumatizations such as war experiences, torture, concentration camps, or traumatizations within the family. They argue that in these cases, a particular symptom cluster often comes along with the “normal” PTSD. This cluster is characterized by a more severe affect dysregulation, somatization, dissociation, social withdrawal, and auto-aggressive tendencies.
3 PTSD as memory disorder
The central idea of this dissertation will be outlined in the following paragraphs:
The mental representation of a traumatic experience is suggested to constitute a central mechanism in manifestation and chronification of PTSD.
3.1 Associative fear structure as central element in PTSD development
“Memory is the ability to recall events from the past” (Elbert et al., 2006, p. 8). It has to be noted, however, that a memory is not fixed at the time the episode occurred, but rather modified with every recall. The specific modifications of memories with respect to PTSD are described below.
Elbert, Rockstroh, Kolassa, Schauer and Neuner (2006) claim that the brain is influenced by genetic-biological as well as socio-cultural systems and moderates behavior and societal environment. In turn, new experiences regularly shape the brain and close the interactive circle. However, in cases of traumatic events the influence is so massive that the structure and function of the brain might be changed.
Brain plasticity as basis for associative structures
The brain has an astonishing capacity of plasticity, as shown by various studies with participants with particular skills, e.g. string players (Elbert, Pantev, Wienbruch, Rockstroh, & Taub, 1995) or piano players (Pantev et al., 1998). This phenomenon of pre-existing neuronal connections at the time of birth and later adaptations by highly specialized requirements is often explained by Hebb’s learning model (1949). Hebb (1949) stated that synchronous stimulation of different cell assemblies leads to stronger connections between the two and facilitates future synchronous activity.
These cortical alterations are not only expedient. The system is vulnerable to alterations at the level of neurotransmitters, which are related to specific (psychiatric) disorders, such as psychosis for instance. But external influences may also harm the cortical organization, such as stressful life experiences. Their influence may be even worse during “critical periods” in childhood and adolescence for cognitive and emotional development. Even a single traumatic event can potentially prompt cortical processes that might lead to a greater vulnerability to subsequent stressful experiences and/or psychiatric symptoms as described as e.g. PTSD (Neuner et al., 2004). This is
more prominent for children, who grow up in a violent context being exposed to several stressful life events and perhaps continuing the cruel spiral of violence.
Elbert et al. (2006) state that the symptoms of disorders within the trauma- spectrum result from plastic changes in the neurophysiological architecture after exposure to stressful life events. This assumption follows from previous literature about the pathological memory representation which determines the development of PTSD symptoms (Brewin, 2001; Brewin, Dalgleish, & Joseph, 1996; Ehlers & Clark, 2000;
Metcalfe & Jacobs, 1996; van der Kolk et al., 1996). The following paragraphs outline the suggested influence of stressful life experiences on the neurophysiological architecture and the mental representation of such events. To understand the pathological mechanism, the storage of “normal” (= non-traumatic) life experiences will be focused first.
How are normal life experiences mentally stored?
“Normal” life experiences are stored in autobiographical memory. The knowledge about the context facts in this memory system is called “cold system” (Metcalfe &
Jacobs, 1996) or declarative memory (Squire, 1994). For instance, information about date, place, living conditions, etc. is declared as such. The concept of the cool system is meant to store well-elaborated (complex, informational, emotionally neutral, integrated) autobiographical events. The information is suggested to be stored with respect to their spatio-temporal context and is supposed to be deliberately retrieved. Hippocampal structures are assumed to mediate the storage. In contrast to the “cold facts” about a specific event, sensory-perceptual representations in all modalities (sensory, cognitive, emotional and physiological elements) are referred to as “hot” (Metcalfe & Jacobs, 1996), non-declarative, or implicit memory (Squire, 1994). This “hot system” is assumed to respond to e.g. fear-provoking features of fearful events. The amygdala is expected to be involved in its activation, which is assumed to occur automatically when required. Once the “hot system” is activated, responses are expected to be direct and quick, highly emotional, and inflexible (Metcalfe & Jacobs, 1996).
Metcalfe and Jacobs (1996) conceive of the “hot” and “cool” systems as two subsystems that are involved in human experiences and function parallel, each specialized for a particular area. While hot-system memories are claimed to be stimulus- driven and likely to provoke a feeling of reliving, cool system memories are assumed to have a character of controlled recollection (Metcalfe & Jacobs, 1996). That is, in case of
cool-system memories, the person is well aware that the event occurred in the past, whereas hot-system recollections provoke a here-and-now-quality. For “normal” life experiences, the parallel functioning of the two systems enables the storage of elements of both systems. In addition, both systems are expected to be well interconnected. In consequence, the reciprocal retrieval of elements is possible. For instance, the storage of a first day in school probably contains both context facts (It has been on Tuesday morning in august 19.., the ceremony took place in the school auditorium, parents and siblings have been there, I was wearing a blue dress) as well as sensory-perceptual elements (The stomach felt queasy, the heart was trembling when my name was announced, and so on). When arbitrarily thinking of that day, it is possible to recall both: information about context and sensory-perceptual impressions. It has to be kept in mind that this form of vivid and detailed recollection is hypothesized to occur for all events experienced by an individual. But representations of every-day events that have less impact for the individual are supposed to last only for minutes or hours (Neuner, 2003). A longer lasting stability results from integration with other memory structures and through storage of sensory-perceptual representation in an highly emotional state that indicates individual significance of the episode (Conway & Pleydell-Pearce, 2000).
What characterizes the pathological storage of traumatic experiences?
To summarize, “cold” and “hot” memory components are well connected in case of “normal” life experiences. The same is assumed for traumatic experiences that did not result in a manifest PTSD. In contrast, the storage of traumatic experiences that entail PTSD symptoms is hypothesized to be characterized by disconnected “cold” and
“hot” memory systems (Elbert et al., 2006; Neuner, 2003). By consequence, the sensory and emotional memories can be activated but without autobiographic declarative items, which indicate that these memories stem from a past event. The model provides an explanation for the PTSD-specific here-and-now-quality of flashbacks: In this extreme form of intrusion, any connection between emotional information and context facts got lost. In consequence, the individual is not able to realize that the feelings stem from a past event and that there is no actual threat. A typical feeling of re-occurrence results (Ehlers & Clark, 2000). In the worst case, representations of a traumatic experience lack any connection to the autobiographical memory and cannot be dated by the victim in any way. Hence, if PTSD patients are asked to narrate their traumatic experience, reports are typically disorganized, fragmented and incoherent (van der Kolk, 1995).
Underlying mechanisms for the pathological storage
A possible explanation for the missing link between cold and hot memory systems is assumed in different responses of both systems to increasing stress (Elbert et al., 2006; Metcalfe & Jacobs, 1996). Being confronted with a life threatening danger, a kind of survival response reaction can be observed in living beings: the fight-flight-freeze reaction. From an evolutionary perspective, the initial reaction to fight or flight (if the first answer is not possible) is very adaptive. Even the freezing in front of a stressor might help and can be observed in accident victims, for instance. These automatic responses, which are summarized as “defense cascade” (P. J. Lang et al., 1997) and sometimes culminate in a fainting response, involve excessive physiological processes.
These physiological processes in turn strongly affect the storage of various elements in memory.
The physiological stress response is regulated by three systems: first, the hippocampus and the hypothalamic-pituitary-adrenal (HPA) axis; second the amygdala, locus coeruleus and the adrenal gland, and third an axis which involves vasopressin- oxytocin peptides (Elbert et al., 2006). Clinical disorders are assumed to be associated with dysfunctions in these three systems. For instance, a permanent activation of the HPA axis due to fearful past events is assumed for PTSD. The released stress hormones by this axis influence particularly two brain structures: the hippocampus and the amygdala.
To summarize, Elbert et al. (2006) propose that the relationship between functioning of the cool system and increasing stress levels is non-linear, following the Yerkes-Dodson law. That is, due to enhanced responsivity of mineralcorticoid receptors at low levels of stress, hippocampal function is enhanced. As stress and therefore the glucocorticoid level increases, more and more glucocorticoid receptors become occupied additionally, which leads to a less responsive and therefore less functional hippocampus. For the hot system, the converse is assumed to be true. The responsiveness of the involved structures (e.g. the amygdala) and the stress level are positively correlated: The higher the stress (glucocorticoid) level, the better the hot system functions. As traumatic experiences comprise by definition very high stress levels, the cool system in this case is dysfunctional whereas the hot system is hyper- responsive (Metcalfe & Jacobs, 1996). By consequence, encoded memories under these conditions are predicted to be not spatio-temporally bound, fragmented, and incoherent.
Instead, the fear-evoking features of the respective situation, which are encoded by the
hot system, will be elaborated very well. Thus, the pathological fear structure after a traumatic experience is at least partly due to physiologic maladaptation.
In previous research, the structure and size of the hippocampal structures have been evaluated as indicator for the relationship between the PTSD-specific representation of traumatic experiences and high stress (glucocorticoid) levels (Bremner, 1999; Bremner et al., 1995; Sapolski, 2000). Bremner et al. (1995) initially measured a right hippocampal atrophy in adult male Vietnam combat veterans which has been replicated among Vietnam veterans by Gurvits et al. (1993) for both left and right hippocampi. Investigations among victims of childhood sexual abuse reported a left hippocampal atrophy (Bremner, 1999; Stein, Koverola, Hanna, Torchia, &
McClarty, 1997). Bremner (1999) relates the lateralization of the hippocampal atrophy to the time the traumatic experience occurred: While in victims of childhood traumata a left hemispheric predominance was found, a right dominance is reported for adult victims. But evidence in this field is still sparse and lateralization differences are not very pronounced (Sapolski, 2000). In addition, confounding variables are to be discussed. The role of self-medicating behavior (e.g. consumption of alcohol) and its neurotoxic consequences have to be further investigated, for instance. For PTSD in particular, it remains unclear whether the hippocampal size was already reduced before the traumatic experience and predisposed the development of PTSD or if the hippocampal atrophy is triggered by the high glucocorticoid level during the trauma (Sapolski, 2000). Nevertheless, it should be kept in mind that the hippocampal atrophy might be related to the specific damages in PTSD as the hippocampus is a central element of the limbic system that enables learning and encoding of memory elements.
The role of cortical structures is underestimated in this model. The above explanation seems to implicate that memory contents are stored within the hippocampus or the amygdala themselves. Actually, these two structures have a regulatory role whereas the storage is realized by cortical structures.
The current dissertation emphasizes the mechanisms within the “hot system”. The particular assumptions about e.g. sensory and emotional elements of the trauma that characterize a PTSD-specific storage will be focussed in the following. This aims at enlightening the obvious contradiction between vivid and painful recollections of the trauma but fragmented and incoherent mental representations of the context on the other hand.
The focus of the current dissertation: associative fear structures in PTSD
The hot memory elements have also been referred to as “flashbulb memory”
(Brown & Kulik, 1977), “propositional network” (P. J. Lang, 1979), or “recollective experience” as feature of the episodic memory (Tulving, 2001). Lang (1979) provides a framework that relates the sensory-perceptual representations to emotions. According to him, the memory system or “propositional network” contains also mental representations of emotions. More specifically, such a network is supposed to comprise information about sensory elements (all modalities), cognitive and affective evaluations (e.g. thoughts that came up during a traumatic event such as “I can’t do anything”), emotions (e.g. fear, horror, helplessness), and physiological alterations (e.g. sweaty hands, heart beat) that occurred during the experience, which is supposed to be stored.
Even motor responses or action dispositions may be included. The different elements (nodes) are connected in a way that the activation of single elements enables the activation of other represented elements. Figure 3.1 (next page) illustrates a schematic presentation of a hypothetical associative fear structure with nodes of sensory- perceptual stimulus representations as well as response programs. The activation is triggered by confrontation with external cues that resemble sensory representations in the “hot memory” (e.g. seeing pictures of weapons). Alternatively, an emotional state (e.g. feeling of helplessness) or a physiological reaction (e.g. physiological arousal) that is caused by an actual situation but stimulates the “original” feeling of threat might trigger the network’s activation.
The explicit relation of this network perspective to anxiety disorders and PTSD in particular was presented by Foa and Kozak (1986). The particular sensory-perceptual representation of traumatic experiences was referred to as „fear structure“, a construct that will be of central interest in the current dissertation. The characteristics of such a fear structure are supposed to be the following (Ehlers & Clark, 2000; Foa & Kozak, 1986): Fear structures comprise an unusually large number and variety of single elements (nodes) about a specific experience. In addition, interconnections between the elements are expected to be unusually strong. In consequence, the activation of only a few elements has the potential to activate the whole structure.
Figure 3.1 Schematic presentation of a hypothetical associative fear structure, adapted from Neuner (2003). The boxes below indicate stimuli with the potential to activate representational nodes
According to the above cited Hebbian learning model (1949), the consequences of a reactivation of the fear structure will be at least twofold: On the one hand, the connections between elements within the network will be further strengthened. On the other hand, due to the synchronous activation of elements already included in the fear network and environmental cues present during the reactivation, subsequent common activation will be facilitated. This might lead to further enlargement of the fear network because the new elements are included. An enlargement of a pathological fear network implicates that even more cues are able to activate the whole structure. With every reactivation, the connections within the network are strengthened. Thus, the probability of triggered re-experiencing of traumatic events is enhanced. The Hebbian hypothesis (1949) is fostered by the fact that the triggering stimuli often are not semantically related to the traumatic experience, but have been temporally associated with the event (Ehlers & Clark, 2000).
This fear structure is meant to serve as a program for escape or avoidance behavior which occurs in typical anxiety disorders. For example, Lang (1979) states that
the physiological activity which is often enhanced in PTSD patients is determined by the response structure involved in the underlying fear structure. Thus, measuring physiological activity when a fear structure is activated is a good indicator for the underlying fear structure (Foa & Kozak, 1986).
The crucial difference between structures of normal and pathological fears is that pathological structures comprise excessive response elements on the one hand (avoidance, physiological activity for instance) and, on the other hand, the pathological structure is extremely resistant to modification.
What have we learned from this?
The fear structure perspective explains the apparent contradiction in the PTSD symptoms with fragmented and badly organized recollections, missing details and difficulties to retrieve the exact chronological order on the one hand and the highly frequent involuntary intrusions with re-experience quality on the other hand (Ehlers &
Clark, 2000). A flashback as mentioned above is understood in this perspective as activation of a fear structure. The fear structure perspective further provides an explanation for the PTSD-specific avoidance behavior. As the reactivation of the fear structure is experienced as very painful by the individual, he or she has learned to avoid everything that might provoke it. This results in the effort not to talk and think about it as well as in avoiding specific reminding situations, places, or persons1. Even the avoidance of any emotional arousal is to be observed in these patients as described as passive avoidance behavior in section 2. Furthermore, the arousal symptoms might be seen in light of this perspective: Neuner (2003) proposes them to be the expression of a partially activated fear structure (excluding sensory-perceptual elements) that lead to the action of evaluative cognitions and physiological elements. The resulting feeling of permanent threat is reflected in the pathologically elevated arousal.
3.2 Are associative fear structures important for PTSD chronification?
In addition to the role of associative fear structures in the development of PTSD symptoms after having suffered a trauma, the associative fear structure perspective
1 Additionally, avoidance or flight behavior can be part of the fear structure, too.
provides some assumptions about the chronification process of PTSD. These determinants will be outlined in the following paragraphs.
The vicious circle of triggering – reactivating – enlarging of associative fear structures The described process of enlarged fear structures can occur in “every day life” but is enhanced during traumatic experiences or experiences with a strong emotional component. While the number of (hot) elements in the fear structure increases, the probability of co-activation (and therefore inclusion) of autobiographical (cold) memory decreases: Elbert et al. (2006, p.8) state that typically “only one context in which the fear network was previously activated” can be retrieved at the time. This is true because we know that we cannot be at two places simultaneously or build up a single memory from two different episodes. Consequently, the more different experiences are included in one large (fear) network, the lower the probability that a respective cold memory trace (about when and were) is co-activated and connected with the network. Within this logic, the “end-product” is a large structure of hot memory elements with very strong interconnections. The whole structure is easily triggered by every kind of cue (intern and extern) and without explicit connections to a single episode with clear information about the cold facts. This “free-floating” memory system is able to reactivate within very short time windows a very realistic feeling of life threat and whatever else was included in the traumatic experiences.
The model of the enlarging fear structure due to subsequent traumatic experiences and recollections is encouraged by the evidence of the building block as described by Neuner and colleagues (2004) and Schauer et al. (2003). Neuner et al. (2004) claim that any individual could develop PTSD regardless of other risk factors as long as he/she encounters enough traumatic experiences. This strong statement is based on PTSD prevalence findings in a huge sample of several populations (West Nile regions, refugees from the civil war in southern Sudan, Sudanese nationals and Ugandan residents, Neuner, 2003). Very high individual numbers of traumatic events were reported in this sample. A significant correlation was found for the number of different event types of traumatic experiences and the number of PTSD symptoms. The analysis of different event types considers the fact that it is often too difficult to reliably name the exact number of distinguishable traumatic experiences within war survivors.
Can fear structures of single traumata enlarge, too?
The fear structure perspective also accounts for single traumatic events: As shown in fear conditioning studies, a single traumatic event might lead to a fear network, but it will be relatively connected to contextual information. Only with later reactivation without activation of the context or future traumatic experiences, the network will be more and more separated from the autobiographical information and thus resemble more and more an associative network with the common element of fear, threat and cognitive as well as physiological responses.
In summary, the vicious circle of pathologically encoded traumatic experiences inhibits helpful inclusion and maintenance of context information of the original situation and strengthens the pathological structure. This pathological spiral explains why the easily reactivated associative (fear) structure and the inherent here-and-now- quality easily lead to a PTSD chronification.
As the missing connection between fear structure elements and the autobiographical memory seem to also play a role in the chronification process of PTSD, some explanations for this phenomenon should be given in addition to the hippocampal theory outlined above.
The role of retrieval strategies in the chronification process
Ehlers and Clark (2000) argue that the missing connections to the autobiographic memory and the bad elaboration of the autobiographic memory might be due to retrieval strategies. Two ways of retrieving stored autobiographic episodes are possible: higher- order strategies based on the impact of the episode (e.g. memories of the first day in school) and retrieval on the basis of triggers associated with a special event.
Some authors (e.g. Conway & Pleydell-Pearce, 2000; Ehlers & Clark, 2000) argue that the majority of “normal” processing of autobiographic episodes aims to reduce the unwanted retrieval in order to facilitate every day activities without “intrusions” from past events. The authors suggest that autobiographical events are normally embedded in a memory system which is organized on different levels of specifity: lifetime periods, general events and event-specific knowledge (Conway & Pleydell-Pearce, 2000).
“Lifetime periods” refer to general knowledge of the special period in one’s life, for example of significant others involved, activities, plans or goals, summing up in thematic and temporal knowledge about common features of that period (e.g. “When I was in primary school”). Compared to that, “general events” refer to a more specific
activity, but not necessarily to a single one. The term may either apply for special events like “my driving test” or repeating events like “concerts with my orchestra” as a set of associated events. “Event specific knowledge” stands for the specifying information about a situation or episode on the level of autobiographic memory. Conway and Pleydell-Pearce (2000) point out that the above mentioned information about traumatic experiences comprised in a fear structure are an extreme example of event specific knowledge. This knowledge may or may not (see below) be related later with more abstract general event and lifetime period knowledge.
The organization of the autobiographic memory as proposed by Conway and Pleydell-Pearce (2000) is assumed to facilitate arbitrary retrieval including specific information of a single event as well as general information with respect to living conditions and time period in which the event occurred. On the other hand, this way of organizing the autobiographic memories inhibits involuntary intrusions triggered by a cue associated with past events. Thus, in „normal“ processing of past events, the first retrieval strategy (on the basis of higher-order categories) is fostered and the second (triggered by associated cues) is inhibited.
In case of PTSD, the memory of a traumatic experience is assumed to be badly organized and not sufficiently integrated in temporal and spatial context as well as previous and subsequent events as described above. Thus, the arbitrary retrieval on the basis of higher order categories becomes difficult. Instead, involuntary intrusions without clear temporal or other structuring information but with “here-and-now-quality”
are enhanced due to the large fear network. This re-experiencing of the same event in a variety of contexts leads to a retrospective inclusion of contextual information into the representation of the original event.
Additional remarks from learning theory
Ehlers and Clark (2000) add two aspects with respect to stimulus-stimulus (s-s)- and stimulus-response (s-r)-association learning which explain the frequent persistence of PTSD.
The building of s-s- and s-r-associations (which are all included in the fear structure) is known to enable predictions about what happens next in a specific situation. Furthermore, this mechanism is particularly prominent for stimuli, which already had a high predictive value for the life threatening situation (Foa & Kozak, 1986). Consequently, even stimuli which were present in advance to the life threatening
situation become associated with the life threat and are interpreted as such a predictor in PTSD patients.
As the retrieval of a memory due to s-s- or s-r-associations is not arbitrary or intentional, PTSD sufferer often do not realize that emotional reactions in an everyday situation are part of the traumatic memory. Especially in cases, when the fear structure is partly reactivated including the emotional responses, the sufferers have difficulties in realizing that they are not longer in a dangerous situation. This phenomenon is called
“affect without recollection” (Ehlers & Clark, 2000, p. 324), a common problem in maintaining the pathological associative memory structures.
Additionally, Ehlers and Clark (2000) suggest a very strong perceptual priming for stimuli temporally associated with the trauma, that is a lower perceptual threshold for these associated stimuli. In consequence, trauma-associated stimuli are more easily recognized by PTSD patients. But the representation of the associated stimulus is often very inexact as these implicit retrieval strategies are not well elaborated. Hence, even a small similarity to the associated stimulus is sufficient to appraise the present stimulus as trauma-associated, too. That is, the low perceptual threshold for trauma-associated stimuli is unfortunately endorsed by a low stimulus discrimination (Ehlers & Clark, 2000).
This section pointed out a number of mechanisms within the fear structure perspective that explain the high number of PTSD chronification. The next section will shortly draft conclusions that can be derived for PTSD treatment to prevent a fatalistic view of PTSD. As this is not of central interest for the current dissertation, ideas will be mentioned very briefly.
3.3 Consequences for PTSD treatment
This section aims at pointing out practical consequences from the fear structure perspective for PTSD intervention. In summary, the previous sections showed that the main goals in PTSD treatment should address a linkage between hot and cold memory systems for the traumatic experience and to disrupt the vicious circle in fear structure reactivation and enlargement.
Already in 1986, Foa and Kozak stated that the central element in trauma therapy should consist of exposure. Independently of any therapeutic school and in line with Lang (1979), the authors are convinced that the fear structure can only be modified if the fear structure is reactivated. In addition, Metcalfe and Jacobs (1996) claim that
narrating the fragments of a traumatic memory might enable the inclusion of a cool- system framework and reduce the activated anxiety. Nevertheless, it should be noted that some authors doubt that the original fear structure is modified in therapy. But this point will be addressed later.
Foa and Kozak (1986) expect exposure to reduce anxiety under certain circumstances. On the basis of their statement that “the propositional structure of an evoked memory is assumed to parallel the structure of the material that evokes it” (Foa
& Kozak, 1986, p. 21), the fear structure must be activated in therapy. Information incompatible with its pathological elements should be aggregated. In addition, information that foster fear activation and modifies the fear structure should be identified. According to Foa and Kozak (1986), two conditions are necessary to modify fear structures: Fear-relevant information must be collected so that fear memory will be activated. Then this information must include elements that are incompatible with parts of the fear structure, aiming at building up a new memory. During the therapeutic process, three indicators of emotional processing should be observed: fear responses (indicating that the structure has been accessed), short-term (within sessions) habituation, and long-term (across sessions) habituation.
The suggested way to access the fear structure is the confrontation with the feared situation. This can occur “in vivo”, but also via audio or visual media, verbal descriptions, lifelike enactments, or exposition in sensu.
A therapeutic approach that implements these conclusions in a therapeutic manual is narrative exposure therapy (M. Schauer, Neuner, & Elbert, 2005). The approach aims at actively reconstructing the autobiography in chronological order including the traumatic experiences and to enable a prolonged exposition to the “hot spots”. That is a full activation of the fear structure that enables its modification through a detailed narration and imagination of the trauma. An integration of psychophysiological and somatosensorical reactions is addressed with respect to spatio-contextual information.
Finally, a cognitive reappraisal of behavior patterns is encouraged as well as an orientation to the human rights perspective. The latter is possible through a detailed documentation of each patient’s individual autobiography. The therapeutic approach of NET has been recently recommended amongst others in the meta-analysis of Ehntholdt and Yule (2006). This meta-analysis considers explicitly refugee children and adolescents, thus a comparable population as in the current dissertation. A detailed and
comprehensive overview about therapeutic approaches in PTSD treatment is given by Gotthardt (2006) and Hensel-Dittmann (in preparation).
3.4 From theory to empirical evidence
The associative fear structure perspective offers a good theoretical framework that accounts for the puzzling phenomenon of PTSD symptom manifestation after a traumatic experience. Explanations for symptom chronification as well as consequences for (an effective) PTSD treatment can be concluded from this framework.
However, empirical evidence for the pathologically enlarged fear structures in PTSD patients is sparse. As pointed out in the introduction, the current dissertation aims at filling in this discrepancy between the demand for evidence-based therapies and the lack of empirical foundation. The lack of empirical foundation for pathologically altered associative fear structures in PTSD patients might result from ethical as well as methodological challenges. On the one hand, an experimental manipulation of the traumatic experience is not possible. On the other hand, a provocation of intrusive re- experiencing during the experimental procedure might be feared. From a methodological point of view, the quasi-experimental conditions implicate the lack of comparable traumatic events or living and support conditions across subjects. The variability of traumatic events implicates difficulties in the experimental access to the associative fear network. For instance, a decision between standardized stimuli across subjects and individually trauma-relevant scripts is required. Furthermore, the heterogeneity with respect to the amount of the traumatic load, duration between the traumatic event(s) and start of PTSD symptoms as well as the experimental procedure constricts experimental results and conclusions.
The variety of methodological approaches in the current dissertation addresses several aspects of the hypothesized associative structure. The current studies investigate both strength of the nodes included in the associative fear structure (see Figure 3.1) and its interconnections in between within a mere stimulus presentation and an associative learning experiment. Furthermore, indices for a pathologically altered response disposition are examined in evaluative priming. Thus, the current studies address evidence for both pathologically respresented elements associated to a traumatic event and implications for current action disposition.
