سهم کنترل درک شده از حوادث استرسزا و سرکوب افکار به علائم اختلال وسواس در هر دو نمونه غیر بالینی و بالینی

The two studies presented in this paper investigated the impact of controllable versus uncontrollable stressful life events (SLE) and low versus high thought suppression upon symptoms of obsessive–compulsive disorder (OCD) in both a non-clinical sample (Study 1) and a clinical sample (Study 2). The sample for Study 1 consisted of 269 undergraduate university students and the sample for Study 2 consisted of 91 participants obtained from the Obsessive Compulsive and Anxiety Disorders Foundation of Victoria, Australia. Participants in both studies were given identical questionnaires measuring anxiety, depression, thought suppression, OCD, and, the control, magnitude and number of SLEs suffered during the previous 18 months. In both studies, analysis of covariance (ANCOVA) followed by post hoc tests indicated that high OCD scores were associated with high thought suppression and low perceived control over high magnitude stressful life events relative to controls. The results suggest that high thought suppression coupled with low control over stressful life events may interact with other predisposing factors, such as genetic vulnerability to produce OCD symptoms.

Obsessive–compulsive disorder (OCD) is one of the most debilitating and prevalent anxiety disorders, with a cross-cultural lifetime prevalence of about 2.5% (Karno, Golding, Sorenson, & Burnam, 1988; Nelson & Rice, 1997; Stein, Forde, Anderson, & Walker, 1997; Trivedi, 1996 and Weissman et al., 1994). Sufferers typically spend large amounts of time obsessing about intrusive phenomena and feel compelled to carry out extensive rituals that are both distressing and time consuming (Abramowitz, 1997). A number of laboratory studies have demonstrated that subjects who display a strong tendency to suppress their thoughts experience an increased frequency of the suppressed thoughts in what has become known as the “rebound effect” (Clark, Ball, & Pape, 1991; Lavy & van den Hout, 1990; Wenzlaff, Wegner, & Klein, 1991). In addition, some researchers have found that people with OCD tend to suppress their thoughts more than non-OCD subjects (Muris, Merckelbach, & Horselenberg, 1996; Salkovskis, 1985). In line with this, the “rebound” phenomenon has been postulated to be an important factor in the maintenance of OCD symptomatology, particularly the obsessional component of the disorder (Salkovskis & Campbell, 1994). However, the relationship between thought suppression and psychopathology remains unclear, since a number of researchers have failed to identify thought suppression as a predictor variable for increased intrusive phenomena (Kelly & Kahn, 1994, Roemer & Borkovec, 1994 and Salkovskis & Campbell, 1994). While considerable evidence is now available indicating that there is a major genetic contribution to the emergence of the disorder (e.g., Pauls & Alsobrook, 1999 and Pollock & Carter, 1999) and to its co-morbidity with Tourette’s syndrome (Pauls et al., 1987), less interest has focused upon the environmental factors that might govern the initial onset of OCD. There are good reasons for connecting onset of OCD with certain types of SLE. In a comprehensive review of the literature, Paykel and Dowlatshahi (1988) found that SLE were implicated in a number of psychological disorders including anxiety and depression. Similarly, Angst and Vollrath (1991) found that anxiety disorders are likely to be triggered by SLE. Other studies have found that SLE often precipitate depressive episodes (Brown & Bifulco, 1985; Overholser, Norman, & Miller, 1990). One study which attempted to differentiate between the types of events involved in particular patterns of symptomatology found that events involving loss were more likely to lead to depressive symptoms, whereas events involving danger were more likely to lead to anxiety symptoms (Finally-Jones & Brown, 1981). On the other hand, other studies have found that recent SLE often play an important role in mixed forms of depression–anxiety, whereas they appear to only play a minor role in “pure” forms of depression and anxiety, where childhood and genetic factors are noted to be of greater importance (Alnaes & Torgersen, 1988 and Torgersen, 1985). Although a number of theorists (see Warren & Zgourides, 1991) have proposed that SLE might be implicated in the onset of OCD, to date there appears to have been an absence of empirical work specifically addressing this issue. One related study did, however, find that patients reported that SLE usually led to a worsening of OCD symptoms (Rasmussen & Eisen, 1991). SLE can be argued to involve different degrees of controllability, some where change is quite controllable and others where there is little or no perceived capacity to control events. Recent research has linked OCD with the notion of control, and in particular, with a lack of perceived mental control (Clark & Purdon, 1995, Edwards & Dickinson, 1987 and Freestone et al., 1994). Controlled studies employing human subjects have found that uncontrollable stress leads to higher levels of anxiety than controllable stress (Netter, Croes, Merz, & Muller, 1991; Sanderson, Rapee, & Barlow, 1989). Huether’s extensive review of this literature (Huether, 1998) observed that long-lasting uncontrollable stress that activated sustained levels of glucocorticoid release was associated with the destabilization and reorganization of neuronal networks in the cortical and limbic brain structures of young children. Taken together, the above studies suggest a relationship between SLE and the psychological states observed in anxiety and depression. Lack of perceived mental control has been identified by a number of researchers as a possible factor in OCD. Some controlled studies indicate that the extent of perceived control over stressful events could be an important factor in determining responses to stress, and, hence psychopathological outcome. It seems likely that uncontrollable SLE could lead to heightened levels of fear and anxiety, and a heightened sense of subjective threat relative to controllable life events. If such an uncontrollable life event were combined with a tendency towards thought suppression then OCD could be a predictable outcome. Thus, in the current studies it was hypothesized that experiencing at least one high magnitude uncontrollable stressful life event combined with high scores for thought suppression would lead to high scores of OCD-type symptomatology. In addition, it was predicted that experiencing at least one high magnitude, but controllable stressful life event without a tendency towards thought suppression, would result in fewer symptoms of psychological distress.

In both studies, preliminary analyses indicated high internal consistency (alpha>.9) for each of the instruments measuring anxiety, depression, thought suppression and OCD. In Study 1, 54% of the student sample had experienced a SLE of high magnitude in the past 18 months. In contrast, in Study 2, 84% of the clinical sample reported having experienced a SLE of high severity in the previous 18 months. The mean number of high magnitude SLE within the student sample (Study 1) was only .76 events per person, compared to 1.3 events per person in the clinical sample (Study 2). In Study 1, tests of between-subjects effects revealed a significant main effect for thought suppression (F(1,268)=30.837, P=.001) and a significant main effect for control over stressful life events (F(2,267)=8.036, P=.001). There was a significant interaction effect between thought suppression and the control of stressful life events (F(2,267)=6.012, P=.003). Tukey post hoc simple comparisons revealed a significant difference in OCD total scores for high thought suppressers dependent upon the extent of perceived control during a SLE. High thought suppressers who reported low control of a recent SLE reported significantly more OCD symptoms than high thought suppressers who reported high levels of perceived control over a recent SLE (F(2,119)=6.496, P=.002). Similarly, low thought suppressers who reported low control over a recent SLE scored significantly more OCD symptoms than other low thought suppressers who reported high control over a recent SLE (F(2,144)=10.568, P=.005). There was no difference found between the OCD scores of high thought suppressers who had no recent SLE and high thought suppressers who reported low perceived control over a recent SLE (F(2,84)=.408, P=.820). On the other hand, low thought suppressers who reported low perceived control over a recent SLE endorsed significantly more OCD symptoms than either low thought suppressers who reported high control of a recent SLE or low thought suppressers who reported no recent SLE. Post hoc t-tests for simple main effects revealed significantly lower OCD scores for low thought suppressers who reported low perceived control of an SLE compared with high thought suppressers who also reported low control of an SLE (t(2,75)=−1.989, P=.05). It was found that participants who reported that they had not undergone a recent stressful life event reported more OCD symptoms when they were high thought suppressers compared to if they were low thought suppressers (t(2,120=−10.426, P=.005). OCD scores for participants who reported high control over recent SLE did not differ significantly in relation to the extent of thought suppression measured (t(2,62)=−1.534, P=.130). For the control participants, an ANCOVA indicated that high psychopathology scores for OCD, depression, and anxiety were correlated with the extent of thought suppression (F(1,268)=94.030, P=.005) and the level of perceived control over a recent stressful life event (F(2,267)=4.345, P=.014). There was a significant interaction effect between thought suppression and the perceived level of control of stressful life events (F(2,267)=6.429, P=.002). In addition, post hoc tests revealed that the symptoms of OCD, depression, and anxiety were specifically correlated with high thought suppression scores (F(2,119)=3.755, P=.026) and with low control of recent stressful life events (t(16,66)=−2.745, P=.015). In comparison, the control group (normal) were found to have low psychopathology scores which were correlated with low thought suppression (F(2,146)=12.850, P=.005) and either no recent SLE or a controlled SLE (F(2,144)=25.271, P=.005). With the clinical sample (see Table 2) tests of between-subjects effects produced a significant main effect for thought suppression (F(1,90)=8.650, P=.004) and a significant main effect for control of SLE (F(2,89)=3.850, P=.025). There was no significant interaction effect between thought suppression and the control of SLE (F(2,89)=.664, P=.517).