ویژگی کاهشی حافظه شرح حالد بدنبال القای احساس منفی
|کد مقاله||سال انتشار||تعداد صفحات مقاله انگلیسی||ترجمه فارسی|
|37981||2006||10 صفحه PDF||سفارش دهید|
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Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Behaviour Research and Therapy, Volume 44, Issue 10, October 2006, Pages 1481–1490
Reduced autobiographical memory specificity (AMS) to emotional and neutral cue words appears to be a stable cognitive marker of clinical depression. For example, reduced AMS is present in remitted/recovered depressed patients and shows no reliable relationship with current levels of depressed mood in correlational studies. The present study examined whether reduced AMS could be induced in healthy volunteers with no history of depression, using a negative mood manipulation and whether levels of AMS and induced mood were positively correlated. Results showed a reduction in AMS following negative mood induction, compared to a neutral induction, whereas positive mood induction had no effects on AMS. Furthermore, lower happiness following the induction phase correlated positively with reduced AMS, and the extent of happiness reduction from pre- to post-induction correlated positively with reduction in AMS. These results suggest that AMS is, at least in part, a function of current emotion state. The implications for the literature on AMS as a stable marker of clinical depression are discussed.
When prompted to generate detailed and specific (in time and place) autobiographical memories in response to cue words (the autobiographical memory test (AMT); Williams & Broadbent, 1986), people sometimes find it difficult to produce suitably specific responses, instead generating overly general summaries of their past. So, for example, the cue “summer” might prompt the generic recollection “I enjoyed every summer when I was a child”, instead of the more specific “I remember the summer's day that we went to Disneyland”. Williams and Broadbent (1986) discovered that reduced autobiographical memory specificity (AMS) was more common in depressed parasuicide patients than in matched controls. Since this initial finding, reduced AMS has been found to be a characteristic of performance on the AMT in individuals suffering from clinical depression (e.g. Brittlebank, Scott, Williams, & Ferrier, 1993; Dalgleish, Spinks, Yiend, & Kuyken, 2001; Kuyken & Dalgleish, 1995; Wessel, Meeren, Peeters, Arntz, & Merckelbach, 2001), posttraumatic stress disorder (PTSD; e.g. McNally, Lasko, Macklin, & Pitman, 1995), acute stress disorder ( Harvey, Bryant, & Dang, 1998), and eating disorders ( Dalgleish et al., 2003), though not, for example, generalized anxiety disorder ( Burke & Mathews, 1992). Mackinger, Pachinger, Leibetseder, and Fartacek (2000) also showed that recovered clinically depressed patients exhibited reduced AMS, relative to never-depressed controls, matched on level of depressive symptoms over the previous week. Related to this, a number of studies have shown no reliable relationship between past-week levels of depression symptoms (on self-report questionnaires) and AMS (e.g. Dalgleish et al., 2001; Wessel et al., 2001). These data have been taken as evidence that reduced AMS is a stable marker for a vulnerability to clinical depression (and potentially other disorders also), rather than simply a function of current mood state ( Mackinger et al., 2000). Stable markers of depression are particularly important as they may potentially reveal ways in which asymptomatic depression-vulnerable individuals represent or process emotional information differently from their never-depressed peers. These differences might therefore provide a window into why depression-vulnerable people relapse into depression (or indeed develop the disorder in the first place). Consequently, targeting such differences therapeutically represents a promising relapse-prevention strategy (e.g. Teasdale et al., 2001). However, data from the three published studies that have examined the effects of induced mood on the AMS paint a slightly different picture regarding AMS as a strictly stable marker of depression (Maccallum, McConkey, Bryant, & Barnier, 2000; McBride & Cappeliez, 2004, Expt. One; Svaldi & Mackinger, 2003). Maccallum et al. (2000) showed that hypnotically induced negative mood led to reduced AMS relative to induced neutral or positive mood. Svaldi and Mackinger (2003) reported similar findings in response to a musical mood induction allied to remembering and reflecting on a negative autobiographical event. However, McBride and Cappeliez (2004) found no effects on AMS of elated or depressed mood inductions, using a Velten procedure. These studies would therefore seem to indicate that the data are equivocal as to whether AMS can be simply a function of current mood state. There seem to be 4 possible explanations of these data and the literature on AMS as a stable marker. One possible explanation is that the AMS effect is multifaceted, with one or more facets that are mood-state dependent (independent of any history of clinical depression), and one or more facets that are a stable function of a history of clinical depression. This would mean that any mood-induced AMS effects could sometimes be detectable but could also be ‘washed out’ as a function of differential levels of depression history across groups, leading to the mixed findings reviewed above. A second possibility is that there are no pure effects of induced mood on AMS and that the existing positive results using mood induction procedures (Maccallum et al., 2000; Svaldi & Mackinger, 2003) were a function of depression history. This could have manifested itself in two ways. First, by chance, there could have been more individuals with a history of depression in the negative mood induction groups in these studies. Secondly, and more likely, proportions of recovered-depressed participants could have been broadly comparable across mood-induction conditions, but the induction of negative mood could have differentially elicited reduced AMS in the recovered-depressed individuals in the negative-mood induction, due to a process of differential activation (Lau, Segal, & Williams, 2004). A third possibility is that the AMS effects in the mood-induction studies are related to neither depression history nor to induced mood. Instead, they could be due to differential priming across conditions whereby a negative induction procedure semantically primes generic negative representations thus leading to reduced AMS, independently of mood (e.g. negative mood primes concepts such as failure, helplessness, that are then given as generic responses to negative cue words on the AMT). This is particularly plausible in the Svaldi and Mackinger (2003) study where the negative mood induction led to decreased AMS only in response to negative cue words. Finally, a more radical possibility is that AMS is not a stable marker for clinical depression at all but is always a function of mood state. This account would argue that the key studies cited in support of the stable marker hypothesis (e.g. Mackinger et al., 2000) have not detected the state-dependency of the AMS phenomenon for various methodological reasons. For example, although studies such as that by Mackinger et al. (2000) were careful to control for current levels of self-reported depression over the past week (using the Beck Depression Inventory (BDI); Beck, Ward, Mendelson, Mock, & Erbaugh, 1961), they did not actually measure mood state per se at the time of experimental testing. It may therefore be the case that the experimental protocol involving the AMT, with its emphasis on emotive autobiographical material, induced a relatively more negative mood in the recovered depressed participants (compared to the never-depressed controls), thus leading to reduced AMS in the depression-vulnerable group. This final account would need to propose that the null findings of McBride and Cappeliez (2004) using a mood induction procedure were anomalous, perhaps due to a low level of induced mood, or insufficient statistical power. These different theoretical accounts are all rendered possible for several reasons. First, none of the existing 3 studies of mood induction and AMS (Maccallum et al., 2000; McBride & Cappeliez, 2004; Svaldi & Mackinger, 2003) endeavoured to control for history of depression in its samples. Furthermore, none of the studies examined the relationship between current depression levels and AMS in its participants, although in all three studies participants were group-matched on baseline levels of depression symptoms. Finally, none of these studies examined whether levels of AMS following the mood inductions were related to the participants’ actual current emotional state. It therefore remains possible that some other aspect of the induction procedure, such as semantic priming of memory categories, is driving the key effects, independent of mood (the third explanation above). There are other methodological problems with these studies also. For example, the induction effects on AMS in the Maccallum et al. (2000) study were only present in highly hypnotizable individuals and the Svaldi and Mackinger (2003) study protocol did not screen out participants who were currently depressed. The primary aim of the present study was therefore to address the question of whether a negative mood-induction could bring about a relative reduction in AMS in healthy participants, even when levels of current and past depression were controlled for. A second aim of the study was to examine whether levels of AMS are significantly related to current emotional state, irrespective of their relationship to past-week levels of depression symptomatology. If this was the case, this would be clear evidence that reduced AMS could be a function of mood/emotion state per se. Resolving such issues concerning the potential mood-state dependency of AMS is particularly important because, as well as its proclaimed status as a stable marker of clinical depression, reduced AMS seems to have an independent causal relationship in the maintenance of the disorder. For example, Brittlebank et al. (1993) found that reduced AMS predicted clinical recovery in major depressive disorder (MDD) over and above initial levels of depressive symptoms. This finding has been replicated, for instance in Seasonal Affective Disorder ( Dalgleish et al., 2001). Reduced AMS is therefore not simply a cognitive curiosity associated with clinical depression but a signature of some more fundamental underlying process implicated in maintenance and possibly onset. The present study involved testing 3 groups of healthy participants on the AMT both before and after a mood manipulation. One group received a sad mood manipulation, one a happy manipulation, and the control group a neutral mood manipulation. We included the happy mood manipulation to investigate whether any effects of induced mood were valence-specific. Based on the possibility that reduced AMS is a function of acute negative mood states (Maccallum et al., 2000; Svaldi & Mackinger, 2003), our first experimental hypothesis was that the sad mood induction group would show reduced AMS (as indexed by a reduction in the proportion of specific memories following the mood manipulation, compared to the neutral comparison group (even after covarying for any differential effects of current depression levels [baseline BDI scores]. In contrast, we predicted that there would be no effects of the happy mood manipulation on AMS. In order to verify that the relationship between mood induction and AMS was due to change in mood, rather than some other aspect of the induction procedure (e.g. semantic priming), our second hypothesis was that change in AMS from pre-post mood induction (across the sample) would correlate with change in mood state, again even after covarying baseline BDI scores. Finally, to examine the possibility that reduced AMS may be a correlate of current negative mood/emotion state, irrespective of any relationship to depression symptoms over the previous week, our third experimental hypothesis was that levels of AMS, following the mood induction, would correlate with current mood state across the whole sample (again, even after covarying for baseline BDI scores), but may or may not show a significant simple association with baseline BDI scores themselves (cf. Wessel et al., 2001).