استعداد ابتلا به حافظه کاذب در بیماران مبتلا به آنوریسم ACoA
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32911||2010||12 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neuropsychologia, Volume 48, Issue 10, August 2010, Pages 2811–2823
We examined ACoA patients regarding their susceptibility to a range of false memory phenomena. We targeted provoked confabulation, false recall and false recognition in the Deese–Roediger–McDermott-paradigm (DRM-paradigm) as well as false recognition in a mirror reading task. ACoA patients produced more provoked confabulations and more false recognition in mirror reading than comparison subjects. Conversely, false recall/false recognition in the DRM-paradigm were similar in patients and controls. Whereas the former two indices of false memories were correlated, no relationship was revealed with the DRM-paradigm. Our results suggest that rupture of ACoA aneurysm leads to an increased susceptibility to a subset of false memories types.
Rupture of aneurysms of the anterior communicating artery (ACoA) may lead to the so-called ACoA syndrome. The ‘full blown’ ACoA syndrome is characterized by amnesia, personality changes, executive dysfunctions, and confabulations (for a review see DeLuca & Diamond, 1995). However, the concomitant occurrence of all symptoms is rather rare due to significant improvements in neurosurgery and medical care (DeLuca and Locker, 1996, Eslinger and Damasio, 1984, Hütter and Gilsbach, 1992 and Teissier du Cros and Lhermitte, 1984). Brain damage after ruptured ACoA aneurysm primarily affects the basal forebrain and the frontal lobes (DeLuca, 1993, DeLuca and Diamond, 1995, Parkin et al., 1994 and Van der Linden et al., 1993). Impairment of anterograde memory, especially a reduced delayed recall, is the most robust and consistent finding in patients with ruptured ACoA aneurysm (Damasio et al., 1985, DeLuca, 1993 and DeLuca and Diamond, 1995). Its anatomical substrate is generally ascribed to lesions within the basal forebrain (Alexander and Freedman, 1984, Babinsky et al., 1997, Böttger et al., 1998 and Damasio et al., 1985). Meanwhile, executive dysfunctions and personality changes following rupture of aneurysm of the ACoA are generally associated with lesions in frontal lobe regions (Böttger et al., 1998, Damasio et al., 1985, Fujii et al., 2005 and Stenhouse et al., 1991). The anatomical basis of confabulations that can be found in a subset of ACoA patients is less clear. Some authors assume that damage either to the (pre)frontal cortex or the basal forebrain is alone sufficient to produce confabulations (Gilboa et al., 2006, Hashimoto et al., 2000, Schnider et al., 1996 and Stuss et al., 1978). Others found that only patients with combined damage of the basal forebrain and the frontal lobes will show confabulations (DeLuca, 1993 and DeLuca and Cicerone, 1991). Confabulations together with intrusions and false recognition are generally subsumed under the topic of false memory phenomena. Intrusions refer to the production of non-studied information in memory experiments (Dodson and Schacter, 2002 and Schacter et al., 1998a). False recognition describes the effect that subjects falsely recognize a novel item, object or event as familiar even though it was not presented during studying (Dodson and Schacter, 2002 and Schacter et al., 1998a). In the laboratory, intrusions and false recognition can be reliable elicited with the so-called Deese–Roediger–McDermott-paradigm (DRM-paradigm). In this paradigm, individuals study word lists of semantic associates that are all converging on a non-studied critical word (‘critical lure’) representing the gist of the list. In a subsequent test phase, subjects disproportionately often falsely recall or recognize the critical lure (e.g. Blair et al., 2002, Ciaramelli et al., 2006, Coane and McBride, 2006, Melo et al., 1999 and Roediger and McDermott, 1995). While characteristics of intrusions and false recognition are more clear-cut, a unique definition of confabulation does not exist. In a very broad sense, confabulations can be defined ‘as statements or actions that involve distortions of memory’ (Metcalf, Langdon, & Coltheart, 2007). Often they concern retrograde aspects of autobiographical/episodic memory (Benson et al., 1996, Dalla Barba et al., 1990 and Gilboa and Moscovitch, 2002), but they may also affect current reality or personal future (Dalla Barba et al., 1997b and Dalla Barba et al., 1999). Occasionally, confabulations even affect semantic memory (Dalla Barba, 1993b, Kopelman et al., 1997 and Moscovitch and Melo, 1997). Confabulations may occur ‘spontaneously’ in a patient's everyday life without any external trigger or they may arise ‘provoked’ by questions probing memory. Whether these two subtypes of confabulation are the same or distinct entities with similar or different anatomical correlates is controversial. While some authors consider only patients to be confabulators who display spontaneous confabulation in everyday life (Kopelman, 1987, Kopelman, 1999 and Schnider, 2003), others consider also experimentally induced false narratives as confabulations (Dalla Barba et al., 1997a, Fotopoulou et al., 2007b, Nedjam et al., 2004 and Turner et al., 2008). Partly due to this conceptual ambiguity in the definition of confabulation, it is difficult to compare studies of ACoA patients’ confabulation and those of ACoA patients’ false memory tendencies. Comparability between studies is further complicated by the fact that the vast majority of studies describe single cases of ACoA confabulators (e.g. Dalla Barba et al., 1997b, Fotopoulou et al., 2007a and Schnider et al., 2005), whereas others examine groups of confabulating patients per se, but with different aetiologies and different onset times after surgery or in the course of diseases (e.g. Moscovitch and Melo, 1997, Schnider et al., 1996 and Stuss et al., 1978). Moreover, most of the studies investigating false memories in ACoA patients concentrate only on one form of manifestation, i.e. provoked confabulation (e.g. Ciaramelli et al., 2009, Dalla Barba et al., 1997b and Fotopoulou et al., 2007a) or susceptibility to intrusions or false recognitions (e.g. Hanley et al., 2001, Parkin et al., 1999 and Schnider, 1999). Likewise, although some have postulated that (provoked) confabulation and false recall/recognition are dissociated phenomena of false memories (for a review see Schnider, 2001 and Schnider, 2008), experimental studies examining the relationship between these different types of false memories are rare (for exceptions see Fischer et al., 1995, Gilboa et al., 2006 and Van Damme and d’Ydewalle, in press). For that reason, in our study we examined a larger group of ACoA patients regarding their susceptibility to different types of false memory phenomena, i.e. provoked confabulations, intrusions and false recognitions. Further, we investigated whether these different forms do have a relationship or whether they are independent from each other and hence can be regarded as distinct false memory phenomena. To elicit provoked confabulations we selected the Confabulation Interview (Borsutzky, Fujiwara, & Markowitsch, 2006), the German adaptation of Dalla Barba's Confabulation Battery (Dalla Barba, 1993a, Dalla Barba, 1993b and Dalla Barba et al., 1997b). With this test, confabulation tendencies in different memory domains, such as personal semantic memory, episodic/autobiographical memory, general semantic memory, personal future and orientation, can reliably be assessed. To provoke intrusions and false recognition we used the DRM-paradigm, well-known for its reliability of inducing false memories: Whereas healthy subjects produce false recognition to critical lures in the DRM-paradigm (Blair et al., 2002 and Roediger and McDermott, 1995), amnesic patients show reduced rates of false recognition to critical lures, possibly due to a lack of gist memory (Melo et al., 1999 and Schacter and Slotnick, 2004). In contrast, confabulating patients again tend to be more susceptible to false recognition of unrelated lures in the DRM, as several studies suggest (Ciaramelli et al., 2009, Ciaramelli et al., 2006 and Van Damme and d’Ydewalle, in press). Therefore, if our ACoA patients should represent a group of noticeable confabulators, they may also produce higher rates of false recognitions of unrelated lures in the DRM. Moreover, we were interested in whether false memories may also occur in non-declarative memory, i.e. procedural memory. To our knowledge studies investigating false memories in the procedural memory domain do not yet exist. Procedural memory skills are usually preserved after ACoA rupture (Bondi et al., 1993, Stefanova et al., 2000 and Thomas-Anterion et al., 1996). However, procedural memory performance may also depend on explicit memory strategies, so that interference or other problems affecting explicit memory processes in pathological conditions may also impact implicit memory tasks (Bayley, Frascino, & Squire, 2005) Thus, it may be possible to observe ACoA patients’ faulty memory production also within procedural memory. A new version of the mirror reading task was created for this purpose, suitable to elicit reading errors reflecting false recognitions that in turn affected procedural memory.