Psychotherapy: Theory, Research, Practice, Training 2006, Vol. 43, No. 2, 201–215
Copyright 2006 by the American Psychological Association 0033-3204/06/$12.00 DOI: 10.1037/0033-3184.108.40.206
CAUSAL ATTRIBUTIONS IN POSTTRAUMATIC STRESS DISORDER: IMPLICATIONS FOR CLINICAL RESEARCH AND PRACTICE PHILLIP M. MASSAD
TIMOTHY L. HULSEY
Idaho State University
Virginia Commonwealth University
In this paper we seek to illuminate connections among basic research findings in cognition and causal inference, clinical research on the treatment of Posttraumatic Stress Disorder (PTSD), and the practices of clinicians who work with trauma survivors. We examine one particular (and, we believe, important) aspect of PTSD: The creation and maintenance of causal attributions about trauma. We suggest that elements of two principal theories of causal induction (the connectionist model and the ⬙Power PC⬙ causal power model) clarify the role of causal attributions in creating and sustaining the symptoms of PTSD. By exploring the role of causal attributions in creating and sustaining posttraumatic symptoms, we hope to understand better the subjective experience of trauma and its sequelae. We then suggest new directions for clinical research on cognitive restructuring in PTSD patients as well as ideas for optimizing attribution-based therapies for trauma survivors. Keywords: causal induction, attribution theory, attribution retraining, Posttraumatic Stress Disorder, trauma Phillip M. Massad, Institute of Rural Health, Idaho State University, Pocatello, Idaho, and Timothy L. Hulsey, Department of Psychology, Virginia Commonwealth University, Richmond, VA. Correspondence regarding this article should be addressed to Timothy L. Hulsey, Institute of Rural Health, Box 8174, Idaho State University, Pocatello, ID 83209. E-mail:[email protected]
Posttraumatic Stress Disorder (PTSD) is defined by “the development of characteristic symptoms following exposure to an extreme traumatic stressor. . .” (American Psychiatric Association, 2000, p. 463). The principal symptoms of PTSD include reexperiencing phenomena, avoidance of stimuli associated with the trauma and autonomic hyperarousal (American Psychiatric Association, 2000). PTSD is among the most common psychiatric diagnoses with approximately 8% of the U.S. adult population meeting diagnostic criteria for PTSD at some point in life (Green & Kaltman, 2003). Studies of lifetime prevalence rates among U.S. ethnic groups have produced equivocal results with some studies finding that rates among groups do not differ and others suggesting that they do (Perilla, Norris, & Lavizzo, 2002). PTSD is typified by both automatic, involuntary symptoms (e.g., flashbacks, intrusive thoughts, autonomic hyperarousal) and consciously mediated attempts to make meaning of the trauma experience(s). The automatic and involuntary symptoms appear to represent conditioned responding to environmental triggers associated with the trauma (Brewin, Dalgleish, & Joseph, 1996; Brewin & Holmes, 2003; Ehlers & Clark, 2000; Massad & Hulsey, in press). However, much less is known about the origins and consequences of victims’ efforts to understand their trauma(s) or about how best to treat the symptoms associated with personal beliefs about trauma (Brewin et al., 1996; Fleming & Robinson, 2001; Foa & Rothbaum, 2001; Joseph, 1999; McCann & Pearlman, 1990; Meichenbaum, 1994; Neimeyer, 2003; Neimeyer & Mahoney, 1995). Although there is a growing consensus that exploring the personal meaning of trauma is important for understanding and treating posttraumatic symptoms (Herman, 1992; Janoff-Bulman & McPherson Frantz, 1997; Janoff-Bulman & Yopyk, 2004), specific approaches to examining
Massad and Hulsey trauma meaning and treating its sequelae are only beginning to emerge. The most comprehensive and widely cited guidelines for treating PTSD, the Expert Consensus Guideline Series (ECGS) on the Treatment of PTSD (Foa, Davidson, & Frances, 1999) and the International Society for Traumatic Stress Studies (ISTSS) Task Force on PTSD Treatment Guidelines (Foa, Keane, & Friedman, 2000), both recommend variants of cognitive therapy (including attribution retraining and cognitive restructuring) among their treatments of choice for PTSD. Although there are different approaches to cognitive restructuring (e.g., Courtois & Bloom, 2000; Foa & Kozak, 1986; Lang, 1977; Resick & Schnicke, 1993), the basic mechanisms for modifying or replacing maladaptive cognitions include corrective feedback, new information, and counterargument.1 The basic assumption of cognitive restructuring is that changing attributions of responsibility (i.e., retraining attributions) produces concomitant changes in negative emotional symptoms (Alford & Beck, 1997; Dalbert, 1998; Dalgleish, 2004; Hazzard, 1993; Kubany et al. 1996; Spaccarelli & Fuchs, 1997; Stratton, 2003; Tennen & Affleck, 1990). Attribution retraining, for example, appears to be particularly effective at modifying the feelings of shame, guilt, and self-blame which typify PTSD (Boeschen, Koss, Figueredo, & Coan, 2001; Resick, Nishith, & Weaver, 2002; Smucker, Grunert, & Weis, 2003; Ulman, 1997). This suggests that, at least in those posttrauma patients who exhibit intense shame or guilt, attribution retraining is clinically indicated. At present, the causal mechanisms that underlie cognitive change are not clearly understood. We suggest that the cognitive processes that create causal attributions follow the laws of causal induction. Accordingly, we review the two principal theories of causal induction, the connectionist and causal power models, and integrate the principal tenets of these models with those of attribution theory. By exploring the role of causal attributions in creating and sustaining posttraumatic symptoms, we hope to understand better the subjective experience of trauma and its sequelae and how to optimize attribution-based therapies for trauma survivors. We also seek to address therapists’ interests by offering examples that bridge theory and clinical practice. We begin with an overview of causal attribution theory to underscore its role in self-blame and trauma meaning.
Deconstructing Trauma Meaning: The Role of Causal Attributions It seems reasonable to suggest that at least one element of trauma meaning resides in victims’ attempts to make causal attributions and assign responsibility or blame for their trauma. Attribution of causation involves a number of dimensions including: 1. Locus (Internal/External): Causes for events are assigned either to personal agency or to factors in the environment; 2. Stability (Persistent/Transient): Causes for events are thought to be either fixed and predictable or unpredictable and subject to fluctuation; 3. Controllability (Controllable/Uncontrollable): Causes for events are viewed as either contingent or beyond one’s control; and 4. Generalizability (Global/Specific): Causes are viewed as either global and generalizable to many facets of life or specific and relating only to a particular aspect of life (Gray, Pumphrey, & Lombardo, 2003; Weiner, 1992). A review of the attribution literature reveals a consensus that internal (causation attributed to self), stable (persistent across time), and global (extending to many situations) attributions are most associated with mental health problems (Gray et al., 2003; Gray & Lombardo, 2004; Seligman et al., 1988). Table 1 provides an overview of the results of several studies of attribution style and trauma, categorized by type of trauma.2 As this literature reveals, child sexual-abuse survivors, rape victims, and crime victims tend to make internal, stable, and global attributions (i.e., self-blame) about their traumas, all of which are associated with the development of severe psychological distress (Briere & Runtz, 1989; Dalbert, 1998; Falsetti & Resick, 1995; Feiring, Taska, & Chen, 2002; Frazier, 1990; Joseph, Wil1 As a related aside, we note that cognitive behavior theory has never successfully countered criticisms that it fails to explain the genesis of irrational and “distorted” thoughts (Brewin, 1989; Beidel & Turner, 1986; Eschenroeder, 1982; Holt & Lee, 1989; Martell, Addis, & Dimidjian, 2004; Tversky and Kahneman, 1981). 2 We conducted a search of PsycINFO using “attribution,” “PTSD” and “trauma” as keywords. Table 1 contains all articles that specifically examined the relationship between attribution style and trauma.
Causal Attributions and PTSD TABLE 1. Self-Blame by Predominant Attribution Type of trauma Child abuse Combat
Crime victims Accidents
Natural disasters Catastrophic illness Rape
Attribution style(s) associated with poorer posttrauma outcome
Study Wenninger & Ehlers, 1998 Casella & Motta, 1990 Ginzburg, Solomon, Dekel, & Neria, 2003 Hyer, Boudewyns, & O’Leary, 1987 Mikulincer & Solomon, 1988 McCormick, Taber, & Kruedelbach, 1989 Orr, Claiborn, Altman, Forgue, de Jong, Pitman, et al., 1990 Solomon, Mikulincer & Avitzur, 1988 Falsetti & Resick, 1995 Kusherner, Riggs, Foa, & Miller, 1992 Hickling, Blanchard, Buckley, & Taylor, 1999 Delahanty, Herbman, Craig, Hayward, Fullerton, & Ursano, 1997 Joseph, Brewin, Yule, and Williams, 1991 Solomon, Regier, & Burke, 1989 Malcarne, Compas, Epping-Jordan, & Howell, 1995 Arata & Burkhart, 1996 Coffey, Leitenberg, Henning, Turner, & Bennett, 1996 Feinhauer & Stuart, 1996 Frazier, 1990 Frazier & Schauben, 1994 Hill & Zautra, 1989 Meyer & Taylor, 1986 Regehr, Cadell, & Jansen, 1999
liams & Yule, 1992; Resick & Schnicke, 1993; Spaccarelli, 1994; Wenninger & Ehlers, 1998; Wolfe, Sas, & Wekerle, 1994; Xavier, Law, Tobias, & Hawton, 1998). As Hall, French and Marteau (2003) observed, it appears that internal, global, and stable attributions are problematic specifically because they are persistent and selfblaming. Indeed, self-blaming attributions have been associated with a wide variety of psychological symptoms (Barker-Collo, 2001; McMillan & Zuravin, 1997; Steel, Sanna, Hammond, Whipple, & Cross, 2004; Wyatt, Newcomb, & Notgrass, 1991). Given that self-blaming attributions contribute to the creation and exacerbation of PTSD symptoms, treatments aimed at changing causal attributions about trauma would seem essential to the treatment of trauma-related symptoms (Brewin & Antaki, 1982; Courtois, 2004). Changing Self-Blame Unfortunately, examination of the attribution retraining literature reveals little about how to identify the elementary processes that create the problematic attributions that lead to self-blame or how best to modify them. Most research on at-
Internal, stable, global External Internal, unstable, uncontrollable External External, stable, uncontrollable Internal, stable, global External External Internal, stable, uncontrollable Uncontrollable External Internal Internal Internal Internal Internal Internal Internal Internal, stable, global Internal Internal Internal Internal
tribution retraining per se (i.e., not related specifically to the treatment of trauma-related symptoms) involves laboratory studies on reversing learned helplessness and failure attributions (e.g., Abramson, Seligman, & Teasdale, 1978) and applied work on changing students’ sense of helplessness and negative internal attributions when they encounter failure (e.g., Ruthig, Perry, Hall, & Hladkyj, 2004; Yasutake, Bryan, & Dohrn, 1996). This literature is not particularly instructive for clinical researchers and therapists seeking an empirical basis upon which to model attribution retraining programs for PTSD sufferers. The attribution retraining literature that does specifically examine the treatment of trauma has focused predominantly on childhood sexual abuse victims. Most of these approaches have emphasized shifting attributions from internal to external, stable to unstable, and global to specific dimensions. Internal to external shifts have been induced through techniques that deconstruct the motives of story characters (e.g., “What had made Jay think that sort of touching was okay?”), visual techniques (e.g., the “Responsibility Ruler” which measures relative responsibility of various
Massad and Hulsey individuals in the abuse event), and musical techniques (e.g., inclusion of lyrics such as “bad things happen to good people”; see Celano, Hazzard, Campbell, & Lang, 2002, for a review). These interventions also frequently attempt to alter ideas that the perpetrator picked the child because of personal characteristics by emphasizing alternative explanations such as the victim being proximal to the perpetrator (thereby accentuating specific rather than global attributions; Hazzard, 1995). The few existing outcome studies of these treatment approaches suggest that older children and adults may be more likely to benefit from increasing unstable attributions regarding the trauma that emphasize a change in the perception of the individual or the situation (e.g., “You went with him because you were naively trusting. Now, you are different and will be more cautious”; see Celano et al., 2002). Given the lack of research on attribution retraining and trauma per se, we turn to a related area of research to elucidate more clearly how to change misattributions and self-blame. This research focuses on the nature of self-blaming attributions, specifically on a phenomenon known as “counterfactual thinking” (Roese, 1997). Counterfactual thinking refers to the cognitive process undertaken when persons imagine different courses of action that lead to alternative outcomes (Williams, Lees-Haley, & Brown, 1993). “Upward” counterfactual thinking is an attempt to undo harm by imagining a better outcome than the one that actually occurred (e.g., “If only I had unloaded the gun, he wouldn’t have shot himself.”). Imagining a scenario worse than the actual outcome (e.g., “He would have killed me if I had struggled.”) defines “downward” counterfactual thinking. In a study of rape victims who engaged in upward counterfactual thinking, 14% imagined drinking less on the night of the rape, 47% reflected on ways they could have reduced assault opportunities (e.g., “I should not have been alone.”), and 29% indicated that they should have resisted the attacker (Branscombe, Wohl, Owen, Allision, & N⬘gbala, 2003). Branscombe and colleagues (2003) infer from these findings that people tend to focus on aspects of the event that are controllable (i.e., they focus on their own behavior because they believe the rapist’s actions were uncontrollable; N’gbala & Branscombe, 1995; Roese & Olson, 1995a; 1995b; Wrightsman,
1991). Consequently, individuals who engage in upward counterfactual thinking are more likely to engage in self-blame since their focus has been on what they might have done differently to avoid being raped (Branscombe et al., 2003). Research on counterfactual thinking suggests that self-blame can be reduced by considering how the outcome might have been worse if the victim had acted differently, thereby shifting the attribution from an internal locus (the self) to an external one (the perpetrator; Branscombe, Owen, Garstak, & Coleman, 1996). But this research has found that the benefit of a shift from internal to external attributions occurs only if self-blame decreases concomitantly (Branscombe et al., 2003). In fact, related research has shown that blaming others (especially if it takes the form of cathartic anger) is associated with “a wide range of behavioral and emotional problems” in child victims (Chaffin, Wherry, & Dykman, 1997, p. 227). Making Sense of Trauma: How Attributions Are Formed What is missing from the attribution retraining literature is a detailed discussion of the elementary processes by which causal attributions are acquired and how they may be changed (Algom & Bizman, 1983). In fact, there is no generally accepted theory of how attributions are formed following traumatic events (Hall et al., 2003). Building a comprehensive theory of causal attribution (and attributional change) requires careful delineation of the cognitive processes involved in the creation of causal attributions. To approach this task we begin with a review of 2 principal models of causal induction: The connectionist and causal power models. Although it is not our claim that these models of causal induction are the only mechanisms through which to explore attribution theory, we do believe that they provide a useful heuristic for understanding how attributions are formed and how to change them. Theories of Causal Induction Hume’s (1739/1987) assertion that humans perceive covariation as causation has had a profound effect on our understanding of cause and effect relationships (Kelley, 1967; 1971). The 2 most prominent contemporary models of causal
Causal Attributions and PTSD induction (the connectionist and causal power models) both rely on Hume’s principle. Specifically, they describe the cognitive processes used in making the cause-and-effect judgments that form the bases of causal attributions. A fundamental assumption of both models is that learning occurs across trials. This assumption may not seem applicable to trauma attributions, especially traumas that involve a single incident. However, the repetitive thoughts about the trauma that are a hallmark of PTSD are similar to learning trials. Thus, self-blaming attributions may arise from repetitive thoughts about the trauma. Furthermore, traumas do not befall an empty vessel. Individuals susceptible to selfblame after a trauma may have had prior learning experiences that were magnified by 1 significant learning trial—the trauma.3 Furthermore, some traumas, such as abuse, can be extended, which increases the likelihood of internalized blame (Arata, 2000; Quas, Goodman, & Jones, 2003; Steel et al., 2004). The connectionist model. The connectionist model of causal induction and causal attributions arise from classical conditioning (Rescorla & Wagner, 1972; Lober & Shanks, 2000). Weights (i.e., emphases of importance) are assigned to causes as a result of co-occurrences between proximate events (Van Overwalle & Van Rooy, 2001). Thus, a cause may be thought of as a conditioned stimulus (CS) that is paired with an unconditioned stimulus (US) or effect. For example, a woman who dresses “seductively” (CS) might, through association (e.g., societal biases) be thought to “cause” a rape (US). Thus, the CS (seductive attire) comes to be associated with the assault via temporal contiguity and gains explanatory significance to the victim and/or perceiver.4 In addition, the explanatory pairing of potential causes and effects is affected by the saliency of both variables— events that stand out require a more immediate causal explanation than less important ones (Algom & Bizman, 1983).5 To fully understand this theoretical calculus, it is necessary to make the underlying mathematical assumptions clear. This is particularly important if we wish to explain the ways in which this model predicts counterintuitive outcomes. Since a central thesis of this paper is the importance of explicating elementary processes in clinical research, we include details of the equations associated with each assumption in
footnotes. We hope that this additional information will serve to advance the understanding of causal judgments in particular and cognitive restructuring in general. As mentioned above, the connectionist model allows for explanation of certain counterintuitive results (Cramer et al., 2002). For example, increments in the perceived importance of a specific cause will occur as long as the total causative significance of all possible causes paired with the outcome is less than the total associative strength supportable by this outcome.6 To illustrate, suppose 2 “causes” (A ⫽ “seductive” attire and B ⫽ excessive drinking) are paired with an outcome variable (sexual assault) to the point that each reaches a plateau in perceived explanatory value. When presented together, the connectionist model predicts a decline, rather than increase by
3 “. . .[A] connectionist model. . . can also address how people make a quick causal judgment in situations where they do not receive a stream of new causal information. In such cases, contextual cues about the appropriate place, time, and content spread their activation automatically to a host of potential causal candidates in memory. The cause that is most strongly connected with the outcome (because of strong weights built up during prior learning) will then be selected as the most likely cause” (Van Overwalle & Van Rooy, 2001, p. 1622). 4 The causal relationship for a single stimulus “A” is represented as ⌬VA ⫽ ␣A ␤ (-VT) where (V) is the associative strength between stimulus and outcome. The amount of associative strength (⌬V) is determined by the difference between the theoretical asymptote strength supportable by the outcome () and the total associative strength (VT) of all social and nonsocial stimuli in the context of conditioning. Associative strength is also affected by the saliency of the potential cause (␣) and outcome (␤). 5 When 2 stimuli or causes are considered together, the learning relationship can be represented as ⌬VA ⫽ ␣A ␤ (-VAX) and ⌬VX ⫽ ␣X ␤ (-VAX), where VA and VX are the strengths associated with the two causes. The ␣ coefficient is the a priori salience of each cause, suggesting that potential causes may acquire causal strength at different rates. The ␤ coefficient represents the rate at which different causal attributions are associated with the effect. 6 Increments in the associative strength of a specific stimulus (VA) will occur as long as the total associative strength of all stimuli paired with the outcome (VT) is less than the asymptote of associative strength supportable by the US analogue (). Thus, when VT ⬎ 1, the model predicts losses in CR strength.
Massad and Hulsey summation in their combined explanatory value.7 This is an important point because it exemplifies the need for clear explication of basic processes of causal induction to facilitate research and clinical practice into the role and treatment of causal attributions. This reduction in responding is similar to the discounting effect in social psychology. The discounting effect recognizes that the role of a given cause may be deemphasized in the presence of other plausible causes (Kelley, 1972). Unfortunately, an underlying mechanism for the discounting effect has not been articulated. By viewing this phenomenon in light of the elementary processes of the connectionist model, we gain new insight into this previously unexplained phenomenon (Cramer et al., 2002). When the connectionist model is applied to attribution retraining, the critical issue is how to replace a faulty causal attribution with one that is more adaptive. The connectionist model conceptualizes this as a problem of “overshadowing” (Kamin, 1969; Mackintosh, 1976). Overshadowing is a learning phenomenon in which the simultaneous presence of a stimulus that is easy to condition creates interference with conditioning of another, less salient stimulus (Domjan, 2003). That is, a person has assigned greater causal importance to his or her own agency than to external causes. The result is the creation of selfblaming attributions regarding the trauma. In cases involving self with no clear external person cause (e.g., natural disaster, enemies in combat without a distinct personal identity, etc.) it may be that in the face of serious unexpected negative events, internal attributions are likely to supplant external ones (Green, Lightfoot, Bandy, & Buchanan, 1985). Consistent with the predictions of the connectionist model, evidence suggests that the tendency to attribute causal primacy to persons rather than environmental factors is learned (Alloy & Tabachnick, 1984; Cramer et al., 2002; Miller, 1984; Morris & Peng, 1994). As a result, explanations based on external attributions are overshadowed by the historical saliency of the person-stimulus (Gilbert & Malone, 1995; Jones & Harris, 1967). From this perspective, historical reinforcement contingencies lead to the overuse of personattributions. This, in turn overshadows external causal attributions (those involving nonsocial stimuli; Green et al., 1985). The result is a tendency to view people, rather than external stimuli
as causal (Gilbert & Malone, 1995; Jones & Harris, 1967). As we shall see, this tendency toward person-causes and away from external causes represents an important consideration in the creation of attribution retraining treatment regimens. The causal power model. The other principal model of causal induction, the causal power model (often called the Power PC theory, short for “causal-power theory of the probabilistic contrast model”) is based on the idea that people make attributions and form causal judgments by estimating and comparing probabilities.8 The causal power model asserts that stimuli have causal importance because they either generate or prevent an outcome (Buehner, Cheng, & Clifford, 2003; Cheng, 1997; Novick & Cheng, 2004). For example, a person might be asked to determine whether excessive drinking by an assault victim “caused” a sexual assault. The Power PC model would portray the victim’s thinking in terms of contingent and noncontingent relationships between drinking and rape. The victim (or perceiver) might assign high causal importance to excessive drinking when it is always/never associated with rape (i.e., it has generative or preventive significance). The matrix of possible events is presented in Table 2. In attribution retraining, a therapist would likely concentrate on Conditions P(E兩C) ⫽ 0 and P(E 兩⬃ C) ⫽ 1. That is, in order to counter the person’s probabilistic bias (P(E兩C) ⫽ 1), 7 For example, when 2 CSs (e.g., A-light; X-buzzer) are paired with an outcome until the CR strength of each CS reaches asymptote then, contrary to intuitive reasoning, the CR of each CS declines when both are presented in tandem with the outcome (i.e., VA ⫽ Vx and VA ⫹ Vx ⫽ VT ⬎ l; Domjan, 2003). 8 The central difference between the connectionist and causal power models pertains to assumptions about base rate occurrences of a candidate cause (i.e., the occurrence of the effect in absence of the candidate cause [P(E兩-i]). The causal power of candidate cause i is represented as [Pi ⫽ ⌬ Pi/ 1P(E兩-i)]. Other differences between the connectionist model and the causal power model are esoteric and beyond the scope of the present work. Suffice it to say that connectionist models, strictly speaking, operate on the temporal contiguity between a candidate cause and an effect and not on their covariation. So situations in which covariation cannot be calculated do not pose a problem for the connectionist model (cf., Lober & Shanks, 2000; Novick & Cheng, 2004; ValleeTourangeau, Murphy, Drew, & Baker, 1998 for a detailed discussion).
Causal Attributions and PTSD TABLE 2. Matrix of possible events Effect Cause
Excessive drinking No drinking
P(E 兩 C) ⫽ 1 P(E 兩 ~ C) ⫽ 1
P(E 兩 C) ⫽ 0 P(E 兩 ~ C) ⫽ 0
Note. P ⫽ probability; E ⫽ effect; C ⫽ candidate cause.
the therapist would likely ask whether the victim drank excessively in the past, what the context of the drinking was and what the outcome was in those instances. Similarly, the therapist might underscore that many rapes occur in contexts similar to the victim’s in which there was no excessive drinking P(E兩⬃ C) ⫽ 1). Note that the therapist should not accentuate the cell P(E兩⬃ C) ⫽ 0 (i.e., “You weren’t raped when you weren’t drinking) so as not to inflame the patient’s sense of guilt. This strategy has much in common with traditional attribution theory concepts of consensus, distinctiveness, and consistency (Kelley, 1967). That is, the fact that a lot of others may drink excessively (i.e., there is consensus) counters the idea that the behavior is abnormal and deviant (i.e., if others do it, excessive drinking loses its distinctiveness as a causal agent). And the fact that rape rarely occurs as a consequence of drinking (i.e., drinking is not consistently associated with rape) underscores the faulty nature of the self-blaming attribution (Roese & Olson, 1995a; 1995b). However, unlike traditional attribution theory, the causal power model provides a detailed model of probabilistic manipulation that may explain the formation of causal attributions. For further explication of this model, the reader is referred to Novick and Cheng (2004). Implications of Causal Induction Theories for Clinical Research and Practice: Procedural Priming Investigations regarding the accuracy of causal attributions have found significant discrepancies between patient self-ratings of attribution style and those of independent, objective scorers (Schulman, Castellon, & Seligman, 1989). Gray and colleagues (2003, 2004), for example, have suggested that people may not understand how they make attributions and that the success of attribution retraining may hinge on persons’
awareness of how they assign causal importance. These researchers suggest that participants may have to be taught the attributional process directly. Consequently, priming tasks that teach basic assumptions of causal induction may have particular therapeutic value (Higgins, 1989). Procedural priming occurs when prior use of a cognitive procedure increases the likelihood of subsequent use of the same procedure (Hong, Morris, Chiu, & Benet-Martinez, 2000; Kirmani, Lee, & Yoon, 2004; Smith & Branscombe, 1987). In this vein, knowledge of the base-rate occurrences of various incidents (e.g., motor vehicle accidents, child-abuse, rape, etc.) might prove valuable in helping patients consider alternative or additional causal factors they have previously ignored. This might in turn help uncouple personal responsibility from causal attributions about the trauma. Studies have demonstrated the effectiveness of using priming procedures to induce changes in causal attributions. Shifts in the loci of attributions (external to internal) have been accomplished by explicitly specifying various contrasts (Fenigstein & Levine, 1984; Hilton, 1990; McGill, 1989, 1990; Slugoski, Lalljee, Lamb, & Ginsburg, 1993). In clinical research studies, priming tasks have been used with children to explore the locus of responsibility for events. Cohen and Mannarino (1993) presented children with descriptions of positive and negative situations unrelated to the treatment issue of sexual abuse (e.g., you leave your bike in the driveway and your father hits it with his car). The child then was asked who is responsible for the different events. This was followed by a series of prompts that explored various aspects of causation (e.g., “Did anything else contribute to it?”). Finally, a similar procedure was followed to explore the child’s causal attributions regarding his or her own abuse. With adults, strategies for decreasing feelings of self-blame have included asking patients to list people and factors external to themselves that may have contributed to the trauma— even assigning percentages of outcome responsibility to each of these factors (Fleming & Robinson, 2001; Kubany, 1998). The similarity to the assumptions of the causal power model is obvious. To illustrate how a priming task might be used to explore the predictive value of the connectionist and causal power models, we borrow an example from the research on perceptions of rape.
Massad and Hulsey This literature suggests that raters ascribe blame to rape victims as a function of previous sexual activity (L’Armand & Pepitone, 1982) and degree of intoxication at the time of the rape (Richardson & Campbell, 1982), among other variables (Anderson, Beattie, & Spencer, 2001). To address the degree to which rape victims internalize such beliefs, these variables could be included in a series of judgment tasks that would serve as the priming exercise for investigating self-blaming attributions and causal inferences about the rape event(s). Let us suppose that a participant is asked to consider two candidate causes for a rape, namely alcohol intake (A: which would be a constant variable) and number of previous sexual encounters (X), the number of which would vary across trials (i.e., zero or more). Base rates of rape occurrences would also be offered but varied in frequency. The victim’s task would be to rate the importance of both causes to the frequency of rapes. The causal power model, unlike the connectionist model, predicts that the emphasis placed on drinking history will be greater as the base rate of rape incidents increases.9 This test, examining as it does the differential predictions of how elementary processes affect causal attributions, would allow for a test of the relative accuracy of these two approaches. Clinically, the importance of knowledge about the base rates of traumas may affect patients’ attributions of responsibility. The impact of base rates aside, the critical point of a priming task for the connectionist model would be to manipulate changes in the salience and associative strength of possible explanatory causes. Unlike the causal power model, the causal candidate in the connectionist model accrues greater associative strength via contiguity (i.e., occurring together in space and time) rather than purely through covariation (i.e., how often the effect occurs in the presence or absence of the candidate cause). Thus, according to the connectionist model, noncontingent base rate occurrences of an outcome (e.g., assault) with a candidate cause (e.g., drinking) should not effect judgments of causal explanations (Chapman & Robbins, 1990; Vallee-Tourangeau, Murphy, Drew, & Baker, 1998). Similarly, with the causal power model the goal is to change the perceived generative power of causal attributions. In either
model, the question is whether priming for heretofore ignored probabilities, outcomes and events will change causal judgments and thereby reduce exaggerated self-blame. Conceptual and Methodological Issues in the Attribution Retraining Research We would be remiss if we did not point out various methodological and conceptual issues that limit the application of research on attribution to trauma treatments. Existing research on PTSD and attribution have examined both trauma-specific attributions and more general dispositional attribution styles. So-called “dispositional” studies typically ask respondents to complete an attribution style questionnaire that measures general attribution tendencies. These tendencies are not tied to particular traumatic events (cf. Ginzburg, Solomon, Dekel, & Neria, 2003). Trauma-specific studies, on the other hand, ask survivors about attributions that are tied directly to their traumas. In a study by Joseph, Brewin, Yule, and Williams (1991), for example, survivors of a ferryboat sinking were asked to make attributions about the cause(s) of their subsequent reactions. Those who blamed themselves for not holding onto rescue ropes were more likely to report depressive symptoms and intrusive thoughts than those who did hold on. Studies of trauma-specific attributions typically add self-report measures to the attribution style questionnaire (Greening, Stoppelbein, & Docter, 2002; Hickling, Blanchard, Buckley, & Taylor, 1999). Still others have used a combination of questionnaires and independent judges’ assessments of trauma attributions based on subjects’ narratives (Gray et al., 2003; Gray & Lombardo, 2004). The disparate findings of these bodies of research suggest that the interpretation of results must consider whether dispositional or trauma-specific attributions are being examined. 9 In the case of a variable cause (A) in tandem with a constant cause (X), the PC model predicts that explanatory judgment for the variable candidate cause X will increase in line with a higher base rate as long as the variable cause has a nonzero (i.e., contingent) relationship with the effect. This relationship is explained by the fact that higher base rates will produce smaller denominators in the equation above and is depicted as follows (recall that the base rate is exemplified as: P(E兩-i) or, in this case, P(E兩- A-X): Px ⫽ ⌬ Px/1-P(E-A-X) ⫽ P(E兩- AX) - P(E兩- A-X)/1 – P(E兩- A-X) ⫽ P(E兩- A-X).
Causal Attributions and PTSD Further muddying the waters is the fact that most studies aggregate several types of trauma into a single “trauma” variable (i.e., combat, physical assault, natural disasters, etc.). Failing to differentiate participants by trauma type can obscure links between causal attributions and trauma-specific reactions following trauma. For instance, rape victims who make internal attributions have worse PTSD sequelae than do those who make external attributions (e.g., Falsetti & Resick, 1995; Regehr, Cadell, & Jansen, 1999) while PTSD severity is greater among combat veterans who make external (i.e., other responsible) attributions (Delahanty et al., 1997; Hickling et al., 1999). However, even when researchers focus on a specific type of trauma, connections between posttraumatic functioning and causal attributions are not always clear. For example, some investigators have reported that Vietnam combat veterans with PTSD attribute both positive and negative events to external causes (Mikulincer & Solomon, 1988; Orr et al., 1990). Other studies with combat veterans have found correlations between an internal attribution style and subsequent development of PTSD (Falsetti & Resick, 1995; McCormick, Taber, & Kruedelbach, 1989). To add yet another wrinkle, while locus of attribution varies among PTSD sufferers, combat veterans tend to have “uncontrollable” attributions (i.e., attributing trauma to unstable factors outside their control; Falsetti & Resick, 1995; McCormick et al., 1989; Mikulincer & Solomon, 1988). Oversimplifying the causal attribution-post traumatic outcome relationship is also problematic. Many researchers have attempted to identify and examine single attributions (or attribution types) in relation to posttraumatic functioning. However, the investigation of single attributions in isolation (e.g., only focusing on internal attributions) may lead to a false picture of causal induction since attributions are typically complex, involving several aspects of the attribution process (Stratton, 2003). Gray and colleagues (2003, 2004) offer what may be the most methodologically advanced work on attribution and PTSD. Specifically, they point out that subjects’ attribution ratings may be misleading since they have not been trained to comprehend the construct of attribution beforehand. Consequently, in their research they provide an independent assessment (by judges) of the subjects’ trauma narratives. Their current re-
search examines the possibility that internal attributions may induce blame with trauma involving interpersonal violence, whereas, external attributions may engender guilt with accidents and disasters (M.J. Gray, personal communication, April 26, 2005). It is also difficult to determine whether the negative attributions that typify PTSD sufferers are the precursor to or the byproduct of trauma (Fo¨rsterling & Bu¨hner, 2003). Greening and colleagues (2002) have observed that a pretrauma depressogenic attribution style (i.e., self-blaming that predates the trauma) may place individuals at risk for depressive symptoms following trauma. Accordingly, the adverse effects of internal, stable, and global self-blaming attributions are more pronounced when traumatized individuals are characterologically predisposed to make internal, stable, and global attributions for negative life events (Gray et al., 2003). It is important to remember that some findings are based on relative group comparisons rather than absolute scores. For example, Ginzburg and colleagues (2003) noted that Israeli combat veterans with PTSD were less inclined to have internal attributions than were decorated veterans and combat vets without PTSD. One might conclude incorrectly that the PTSD subjects were, therefore “externalizers.” In fact, they were not. They scored closer to the internal than external extreme on the attribution measure. As always, qualitative descriptions of results must be made within a relative frame of reference. We must also note that the effects of culture, ethnicity, and gender on causal judgments are not well understood. Earlier, we alluded to the possibility that individuals may learn the idea that they possess control over outcomes and that this perceived control may impede the acquisition of situation-outcome associations. This seems to be less true in “collectivist” cultures in which the idea that personal power is weak holds sway. Indeed, there is some data that demonstrates the interference in learning person-outcome associations in such cultures (Matsumoto, Weissman, Preston, & Kupperbusch, 1997; Miller, 1984; Morris, Menon, & Ames, 2001; Morris & Peng, 1994). Additionally, some cultures appear to promote situational rather than dispositional attributions in causal judgments (Ji, Nisbett, & Su, 2001). The literature on the effects of ethnicity and gender on causal induction per se is notably
Massad and Hulsey thin. There are some studies that suggest race and gender may mediate judgments of attributional dimensions (e.g., Gerber, Cronin, & Steigman, 2004; Moghaddam, Taylor, Lambert, & Schmidt, 1995; Morgan, Griffin, & Heyward, 1996). However, there is little beyond this knowledge to indicate the role(s) that gender and ethnicity may play in the actual acquisition of causal attributions. Conclusions We have attempted to deconstruct the subjective meaning of trauma by focusing on the role of causal attributions in creating and sustaining certain PTSD symptoms. Central to our argument is the contention that causal attributions constitute an essential element of the meaning-making process that follows traumatic experiences. We maintain that causal attributions are formed according to the principles of causal induction theories and that understanding the nature of causal induction is fundamental to understanding the relation between attributions and post trauma functioning. Though the connectionist and causal power models may not be able to explain all the complexities of causal judgments, it is our contention that the explication of the elementary processes that underlie attributions of responsibility may be valuable both experimentally and clinically (Brewin, 1989; Beidel & Turner, 1986; Eschenroeder, 1982; Fonagy, 1989; Holt & Lee, 1989; Martell, Addis, & Dimidjian, 2004). Of course, the question may arise as to whether an excursion into elementary processes invites a reductio ad infinitum, with identification of one set of principles giving rise to a new set of potential underlying causes. However, building analogues from an area with a basic, empirical foundation to phenomena that are not as clearly understood is a basic form of theory construction (Campbell, 1920; Oppenheimer, 1956). Moreover, molecular and molar theoretical explanations of the same behavior are not necessarily contradictory, and the value of illuminating basic processes that may underlie global theories can advance both approaches (Turner, 1965). We have argued that the fundamentals of attributional change are not well understood. This remains a matter for future research. In the meantime, we can ask how awareness of the fundamentals of causal induction might guide clinical
work. As noted earlier, the crux of attributional retraining is to encourage the patient to consider causalities in ways that he or she previously had not. The idea of “priming” is an attempt to induce patients to adopt new cognitive paradigms when thinking about cause-effect relationships. As Gray and colleagues (2003, 2004) have noted, people may not explicitly consider attributional dimensions until they are directly apprised to do so. It may be helpful to describe the use of such an approach in a brief clinical vignette. Suppose that Larry is very depressed and blames himself for the breakup of his marriage. He tells himself that he could have tried harder. He worries that he could have dealt with spousal conflict more maturely. His divorce has triggered an internal dialogue dominated by self-criticism, resulting in marked decompensation. Before engaging in a clinical examination of the patient’s view of causal responsibilities in his former relationship, a clinician might consider a preliminary exercise. Namely, the therapist could ask the patient about his parent’s marital conflicts. By assaying the patient’s understanding of each parent’s individual contributions to the conflicts evident in their marriage, the patient is forced to adopt a cause-effect framework that recognizes multiple constituents. If need be, the patient’s own description of his parents’ troubles can be referenced when analyzing his breakup so that he is reminded of the numerous contributors to any significant conflict. Such clinical maneuvers represent a systematic intent to alter attributional schemas by addressing directly the faulty causal inferences thought to underlie symptoms. To this, we would add only the obvious reminder that cognitive change in therapy is rarely linear. That is, although patients may benefit from straightforward cognitive challenges, many instances of self-blame are irrational and fused with longstanding and primitive notions about the self. These types of causal attribution may require the uncovering of 2nd- and even 3rd-order causal links in a complex web of associative generalization gradients (Massad & Hulsey, in press). Many constituents of the causal attribution/ posttraumatic functioning link remain to be explored. Foa and Rothbaum (2001), for example assert that individuals with rigidly polarized beliefs about the self (i.e., as extremely competent/ incompetent) and the world (i.e., as extremely safe/dangerous) have a greater likelihood of developing PTSD symptoms following trauma than
Causal Attributions and PTSD do people with a more flexible cognitive style. Self-efficacy may also play an important role in explaining how a person interprets the meaning of trauma (cf., Ginzburg et al., 2003). A greater sense of self-efficacy and an internal locus of control may help immunize a person from trauma sequelae and explain why some trauma victims do not develop self-blaming attributions (Greening et al., 2002). Another important component of trauma meaning is the violation of strongly held worldviews (Everly & Lating, 2003). Social– cognitive theories of trauma response (cf. Horowitz, Wilner, Kaltreider, & Alvarez, 1980; Janoff-Bulman, 1992, 1989) focus on the dissonance created when trauma violates preexisting notions about the world. For example, upon the senseless and tragic death of a loved one, a person may experience anxiety not only because of the loss but because the event has challenged a preexisting belief that life is fair. Coupled with causal attributions, self-efficacy and worldviews provide additional lenses through which we might deconstruct further the concept of trauma meaning. We must emphasize that the use of causal inference theories in creating therapeutic interventions for PTSD is but 1 aspect of a complex approach to understanding and treating the symptoms of trauma. Ideally, we would have a series of longitudinal studies integrating treatment of both the primary and secondary symptoms of PTSD to give researchers and practitioners a framework to guide their work. However, by refocusing the discussion around efforts to understand the elementary processes involved in the creating of trauma meaning, we hope to decrease the gap between those concerned primarily with treating PTSD sufferers and those concerned with evaluating the effectiveness of PTSD treatments. References ABRAMSON, L. Y., SELIGMAN, M. E. P., & TEASDALE, J. D. (1978). Learned helplessness in humans: Critique and reformulation. Journal of Abnormal Psychology, 87, 49 –74. ALFORD, B., & BECK, A. T. (1997). The integrative power of cognitive therapy. New York: Guilford Press. ALGOM, D., & BIZMAN, A. (1983). Attribution theory: A conditioning interpretation. Perceptual and Motor Skills, 56, 767–774. ALLOY, L. B., & TABACHNICK, N. (1984). Assessment of covariation by humans and animals: The joint influence of prior expectations and current situational information. Psychological Review, 91, 112–149.
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