Having spent a lot of time on this blog talking about embodied cognition, I went and wrote my 3rd year psychology dissertation firmly within a traditional neurocognitive paradigm - sorry Andrew and Sabrina! Nevertheless it gives a reasonably detailed overview of overgeneral autobiographical memory, its association with psychopathology and potential underlying mechanisms. It got a decent first so I thought I'd whack it on the blog anyway as it's been a while.
Autobiographical Memory (AM) refers to the recollection of personal events or experiences from an individual’s past. Broadly, AM consists of a knowledge base of episodic memories and semantic information about the conceptual self (Griffith et al 2011, Conway 2005). Autobiographical memory is intimately linked with our experience of a continuous sense of self and identity (Conway and Playdell-Pearce 2000), providing a key role in problem solving and future goal setting, in light of past experience (Williams 2006).
It has been well established over the last 20 years, that when cued to retrieve a specific autobiographical memory of less than a day's duration, using the Autobiographical Memory Task (AMT), some participants consistently form less specific, overgeneral autobiographical memories (OGM) (e.g. Williams et al 2007, Dalgleish et al 2007). For example, in response to the cue word `party', participants may respond with the more general `I used to go to a lot of parties' as opposed to retrieving Event Specific Knowledge (ESK) such as `I remember my brother's 18th…'. Briefly, the AMT consists of a number of cue words (both positive and negative in affect) presented to participants who have to produce a unique specific memory within a given time frame (e.g. 45 seconds). Their responses are then rated as specific or overgeneral, with the number or proportion of OGM’s providing the final score.
OGM has consistently been shown to be associated with a variety of emotional disorders, most prominently Depression and trauma, such as PTSD (Williams et al 2007). The phenomenon was first discovered by Williams and Broadbent 1986, when they found that OGM was more widespread in their parasuicidal sample compared with two matched control groups. All three control groups performed equally well on a task measuring semantic memory, indicating that the reduced AM specificity could not be explained by other more general cognitive deficits across the samples (Williams et al 2007).
Since then, OGM has been shown to be associated with a variety of clinical disorders including Depression (e.g. Williams et al 2007 see table 1 for review), PTSD (e.g. McNally 94), Acute Stress Disorder (e.g. Harvey 1998) and Borderline Personality Disorder (e.g. Startup 2001) as well as preliminary evidence for an association in Bipolar Disorder (Mansell & Lam 2004). More recently, Raes et al 2010 extended research on adults and adolescents (e.g. Kuyken et al 2006) to confirm the presence of OGM in children with depressed mood.
Interestingly, OGM has not been found to be present in a variety of anxiety disorders, such as Generalised Anxiety Disorder (Burke 1992), Social Phobia (Wessel 2002) or in a mixed group of anxiety patients (Wessel 2001). As such, Williams et al 2007 argue OGM is not simply a marker for any psychopathology in general, but seems to be present only in those disorders involving Depression and/or trauma. That said, a lack of OGM in anxiety disorders may be due to the choice of cue words insufficiently addressing current concerns (Harvey et al 2004).
There is less certainty with regards to the role of OGM in more severe disorders such as psychosis and Schizophrenia. Although there is evidence that episodic memory deficits (e.g. Bilder et al (2000), Heinrichs & Zakzanis, 1998;) and autobiographical memory deficits (e.g. Riutort et al 2003) are present in Schizophrenia patients, to date there has been only one study that we are aware of addressing OGM specifically, in patients suffering with psychosis (Kaney et al 1999). Their findings showed that deluded participants recalled significantly more OGMs than the control group, thus providing preliminary evidence that OGM may extend beyond emotional psychopathology.
Not only has the OGM phenomenon been found to be associated with certain clinical disorders, it has also been shown to have direct clinical implications, predicting onset, maintenance and recovery in Depression and/or PTSD, acting as a potential stable marker for patients in remission and being associated with impaired problem solving and impaired ability to imagine (and plan for) future events. A variety of studies have shown OGM to predict both the onset of (Kleim & Ehlers 2008) and recovery from (Brittlebank et al 1993, Peeters et al 1992, Dalgleish et al 2001, Harvey et al 1998) affective disorders. In a recent meta-analysis, Sumner et al 2010 confirmed the findings of Kleim & Ehlers 2008, that OGM predicts subsequent PTSD and Depression over and above what would be predicted from the initial diagnoses and severity of symptoms, thus highlighting OGM as a possible therapeutic target.
It is important to note however, that whilst findings do indicate there may be some potential in developing psychological interventions aimed at increasing autobiographical memory specificity, the effect size for the relationship between OGM and course of Depression is rather modest (r = -.10). As such, the efficacy of any such intervention remains to be confirmed. That said, Raes et al 2009’s MEmory Specificity Training (MEST), provides a promising start, with reduced OGM being associated with increased problem solving abilities and a reduction in ruminative thinking.
A further replicated finding is that OGM remains present in those with a history of affective disorder, even when not currently experiencing an episode (Brittlebank et al 1993 Mackinger, Pachinger et al 2000, Mackinger, Loschin & Leibetseder 2000, Williams & Dritschel 1988). This is significant in that it indicates OGM may be used as a stable marker in remitted or recovered clinical samples and suggests that reduced autobiographical specificity is not merely a result of a patient’s current symptoms. Lastly, OGM is associated with impaired problem solving (Goddard et al 1996, Scott et al 2000, Raes et al 2005), difficulties with imagining future events/goals (Williams et al 1996) and feelings of increased hopelessness (Evans et al 1992). This has obvious implications for social cognition, functional outcome and ultimately quality of life.
In light of the important clinical implications relating to OGM, there has been a flourish in current research to examine the possible mechanisms underlying reduced autobiographical specificity. The most prominent and robust attempt is the CaR-FA-X model proposed by Williams et al 2007. The model postulates three possible mechanisms that influence OGM; Capture & Rumination, Functional Avoidance and impaired eXecutive control.
Capture & rumination refers to the disruption or dysfacilitation of the retrieval process by the activation of conceptual self-related semantic knowledge, which then prevents a more refined search for relevant specific episodic memory, leading to what is known as a ‘capture error’. Functional avoidance - essentially analogous to the ‘Affect-Regulation Hypothesis’ (Williams et al 2007) – refers to the use of a nonspecific or overgeneral retrieval style in order to passively avoid any potentially negative experiences or visual imagery associated with a specific episodic memory. The third mechanism, and the focus of this study, is impaired executive control, occurring when deficits in executive resources lead to an inability to complete a successful retrieval from the autobiographical memory knowledge base. The various processes by which this may occur and the implications of the way in which words are cued will be addressed below.
All three mechanisms share one common process, namely the disruption of the retrieval process, leading to a truncated search that ultimately fails to access event specific knowledge. Conceptually, this maps directly onto Conway and & Pleydell-Pearce’s 2000 model of autobiographical memory - the Self Memory System. The Self Memory System is composed of a hierarchy of autobiographical memories. Descending down the hierarchy, representations are arranged from a) general thematic experiences from our personal narrative (e.g. jobs or relationships) to b) lifetime periods (e.g. when I was at school) to c) general events, which may be repeated events (e.g. playing Sunday morning football) or single events (e.g. my trip round Europe) to d) event specific knowledge (e.g. the party celebrating the Millennium).
ESK is accessed by one of two potential processes; direct or generative retrieval. The former involves the direct and passive retrieval of ESK based on activation from environmental cues. In contrast, the latter requires an intentional search down the hierarchy via the delineation of a retrieval model with the specific memory in mind and the inhibition of irrelevant competing information. It is this search down the hierarchy which becomes truncated as a result of one of the three proposed mechanisms or perhaps more likely, a combination of them all.
The role of impaired executive function has been researched extensively by Dalgleish et al. Dalgleish et al 2007 showed that executive control mediates the relationship between depressed mood and OGM. Interestingly, Dalgleish’s research suggests that this relationship is not merely due to the effects of depressed mood, with the association remaining even when levels of depressive symptoms have been controlled for. This has since been supported by Rutherford 2010 who demonstrated that AMT scores did not differ as a result of the valance of the mood induced. For further evidence of the role of executive control in autobiographical memory see Williams et al 2007.
Whilst the relationship between OGM and impaired executive control has been well established, it remains unclear which specific process(es) best explain the results. It is widely acknowledged (e.g. Williams et al 2007, Dalgleish 2007, Sumner 2012) that there are several potential stages at which a deficit in executive control may impair the retrieval process. These include a) the generation and holding in working memory of a retrieval model b) the inhibition of unwanted or irrelevant autobiographical knowledge (e.g. capture errors) or other information during the search and c) the updating and holding in working memory of a final search result.
Although any one or combination of these processes may explain the means by which executive control deficits contribute to OGM, particular attention has been focused on its role in the inhibition of competing information when attempting to retrieve a specific autobiographical memory. This emphasis on inhibitory control stems from Dalgleish et al 2007 (studies 2 & 3) who reported that OGM only correlated significantly with executive control measures that included error scores, with non significant correlations between those that corrected for errors, such as verbal fluency. Dalgleish et al argued that the error scores are indicative of one particular aspect of executive function, namely inhibitory control, in that they reflect an individual’s (in)ability to inhibit unwanted information. As such, inhibitory control is a main contender in understanding the specific mechanism by which executive control could generate OGMs. Further, the association of inhibitory control and OGM has since been replicated by Raes et al 2010, who demonstrated that inhibitory control mediates the relationship between OGM and depressed mood in children.
It is argued then, that executive control error scores reflect a sub-process of executive functioning, namely the inhibition of unwanted, irrelevant information specifically, as opposed to a measure of executive capacity in general, found in measures that correct for error. High error scores, therefore, indicate an increased impairment in the ability to suppress competing information during a cognitive task. Since error scores were the only measures to correlate significantly with OGM, it is argued that these measures are tapping into the specific process (inhibitory control) that links executive control with OGM.
The promising association between OGM, Depression and inhibitory control, also has the advantage of parsimony. Raes et al 2010 point out that not only is this finding consistent with current literature on Depression and executive capacity (e.g. see Ellis and Ashbrook’s 1988 Resource allocation model of cognitive processing in Depression and Hertel & Hardin’s 1990 cognitive-initiative account) but it is also consistent with the Capture and Rumination model of autobiographical memory, with impairment in inhibitory control potentially causally linked to capture errors and rumination. As such, the role of executive control (specifically inhibition) and OGM in affective disorder remains a relevant and rich research area.
It is important to note that, although the current literature provides convincing evidence in favour of both the relationship between OGM and affective disorders and the CaR-FA-X model, it is not without its limitations, providing potential requirement of further research to fill the gaps. Of particular interest and the subject of improvement for this study, are the following:-
a) Dalgleish et al 2007 report the need for further research on reduced autobiographical memory specificity (AMS) in a wider range of clinical samples, with the majority of their studies focusing on sub-clinical groups. This will allow for a better established understanding of how current research on OGM and executive control generalise to the clinical community.
b) Williams et al 2007 and Griffith et al 2011 have highlighted potential issues with the AMT and the way in which autobiographical memory is cued; The majority of studies using the AMT, although often differing slightly in terms of methodology, have tended to use the same cue words. This means that any potential idiosyncrasies associated with these cue words are repeated across the literature, with studies replicating any anomalous results.
c) Further, AMTs have predominantly used emotional cue words both positive and negative in valence, with relatively few incorporating neutral cues (Griffith et al 2011). As such there is an incomplete understanding of how emotion in general relates to OGM. This is particularly relevant in light of the focus on inhibitory control, which, unlike the other two models, would predict an association between OGM and neutral cues that don’t directly address current concerns. This is because its proposed mechanism does not rely on the avoidance of or rumination on affective content necessarily, but rather the inhibition of task-irrelevant information.
d) Lastly, the current AMT may not sufficiently allow for distinguishing between the possible mechanisms of executive control. One such problem is that any correlation between executive control and OGM may be confounded by the participant’s inability to maintain the task instructions in working memory. In other words, OGM would appear to correlate with executive function simply because participants are unable to keep in mind the task instructions – this is termed ‘secondary goal neglect’ (Dalgleish 2004). Secondary goal neglect has been investigated by Yanes et al 2008 who found that OGM was related to poor memory for the task’s instructions and found an instruction set reminder for AMT improved AMS. Whilst this provides evidence for the secondary goal neglect hypothesis, it remains unclear to what extent it accounts for associations between OGM and to what extent inhibitory control plays a role. As such, and based on the suggestion by Williams et al 2007, there is a need for an adapted AMT which will eliminate the role of secondary goal neglect, for example, simply through repeating task instructions before each cue word.
In summary there is a need for replicated findings in clinical samples and “…[a]need to diversify in the methodology used to assess overgenerality” (Williams et al 2007) in order to better understand the role of executive capacity, inhibitory control and OGM in affective disorder.
In addition, are two further limitations not addressed by the current study but worthy of note: Many studies assessing OGM do not control for IQ or other more general memory domains and thus are unable to eliminate these variables as confounders (Williams et al 2007). Williams reports, however, that in those studies that do control for IQ, the association remains, and whilst other memory domain deficits may explain some of the variance, a significant proportion is left, explained by OGM.
Secondly, as mentioned previously, there has been relatively little attention on the role of OGM in more severe disorders, such as Bipolar Disorder (though see Mansell and Lamm 2004) and Schizophrenia (though see Kaney et al 1999) with essentially no mention from leading scholars such as Williams and Dalgleish. Presumably (and in fact explicitly stated by Williams et al 2007), it is viewed that OGM is very much an emotionally-linked phenomenon, yet there has been little research to establish this fact beyond simply its presence in various affective disorders. This is far from trivial, as the wider implications for OGM in other disorders include its role as a potential transdiagnostic marker of psychopathology in general (see Harvey et al 2004), thus making its confirmation or disconfirmation in other disorders a significant finding.
Aims and Hypotheses
The following study, aims to address the discussed limitations of and provide additional evidence for the role of executive control (particularly inhibition) as a potential mechanism for OGM in depressed patients. The primary aim of the pilot, is to test the practicality and reliability of an adapted AMT (AMT-a) and to see if scores correlate with a) Scores on the Autobiographical Memory Interview, b) executive function total scores and c) scores on executive function errors (indicative of inhibitory control).
Based on previously discussed evidence from Dalgleish et al 2007 and Raes 2010, we predict a stronger correlation between OGM and inhibitory control scores (indicated by error scores) than with OGM and executive capacity generally, as measured by the executive control total. The reasoning is that if inhibitory control is the main mechanism by which executive control impairments cause OGM, then any additional measures i.e. that of other aspects of executive functioning aside from inhibition, will create ‘noise’ in the data, thus weakening the correlation between executive errors and AMT-a.
In addition, we aim to give some indication of the reliability of the AMT-a by correlating scores with a simplified version of the AMI-a, with the prediction that scores should correlate positively. (The AMI is not entirely ideal, in that it gives a measure of autobiographical memory as a whole, incorporating semantic and episodic knowledge, rather than giving a score specifically for reduced AMS. Due to the nature and limitations of a student project, however, we were unable to obtain the AMT in time, which would have served as the appropriate gold standard to measure our AMT-a against.)
As such the hypotheses are as follows:-
Hypothesis 1 – AMT-a scores will correlate negatively with Executive Control Error Scores.
Hypothesis 2 – AMT-a scores will not significantly correlate or will correlate less strongly with executive control total scores compared with executive control Error scores.
Hypothesis 3 – AMI-a scores will correlate positively with AMT-a scores.
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