Links to a list of papers on the trauma-memory argument.
Proponents of the trauma-memory argument and recovered-memory therapy often argue that traumatic memories have special properties that render the usual rules of memory processing inapplicable. In 1997, Katherine Krause Shobe and I questioned whether traumatic memories are special, and concluded that the major theories of traumatic memory were either incoherent or inadequately supported by empirical evidence ("Is Traumatic Memory Special?").
Approximately one year later, Lynn Nadel and W. Jake Jacobs published another paper in Current Directions, entitled "Traumatic Memory is Special". As their title suggests, their paper was evidently written in response to ours. Neither Shobe nor I was given the opportunity to review the Nadel & Jacobs paper before its acceptance, though we were sent a courtesy copy of the final version prior to to its actual publication. Moreover, the editorial policies of Current Directions preclude the "reply and rejoinder" format common in many scientific journals. This situation is unfortunate, because -- although the Editor of Current Directions indicated, in his letter of transmission to me, that he felt the Nadel & Jacobs paper "broadens the issues" (emphasis original), contains substantial errors of fact and interpretation that, if uncorrected, may be taken as supporting the trauma-memory argument and recovered-memory therapy.
Nadel & Jacobs's argument proceeds as follows:
In support of the first proposition, Nadel & Jacobs cite a number of animal studies showing that "various aspects of an episode memory are represented and stored in dispersed neocortical modules" (p. 155), collected into a "hippocampal ensemble" (p. 155). As far as it goes, this view of the neural substrates of memory is unobjectionable. The distributed nature of memory processing -- in which, for example, emotional valence is contributed by the amygdala, recognition mediated by the rhinal cortex, spatial context by the parahippocampal gyrus, and the whole trace bound together by the hippocampal formation -- is widely accepted within cognitive neuropsychology and cognitive neuroscience.
In principle, the fact that different aspects of a memory are processed by different brain structures could provide the foundation for the fragmentary nature of emotional memory noted by vdK&F, among other proponents of the trauma-memory argument and recovered-memory therapy. If one module were impaired (for example, by the biological consequences of traumatic stress), the information processed by that module might well be missing from the resulting memory.
However, this proposition must be considered purely speculative, because Nadel & Jacobs offer no evidence in support of the second proposition, that the functioning of these cortical subsystems, or the representational components generated by them, are differentially impaired by traumatic stress. On the contrary, there are good reasons to think that the amygdala is activated by stress, resulting in robust memory for emotional events, as demonstrated convincingly by Cahill, Prins, Weber, & McGaugh, (1994; see also Cahill & McGaugh, 1996) in a widely-known study that Nadel & Jacobs fail to cite. The trauma-memory argument seeks to explain why people forget trauma; it cannot be supported by evidence that the involvement of the amygdala makes events more memorable.
Nadel & Jacobs do cite a number of animal studies showing that increased stress impairs hippocampal functioning, and thus memory. But the stress in question is chronic stress (e.g., 21 days of restraint), and the memory task in question is unrelated to the stressful event (e.g., maze learning). It is highly plausible, as Sapolsky (1998) has suggested, that exposure to chronic stress releases neurotoxins which damage the hippocampus and consequently impair memory. But this memory impairment would be general in nature, not specific to the trauma. It would be anterograde in nature, not including the initial trauma itself (the retrograde effects of hippocampal damage remain highly controversial). It would be general, including memories unrelated to the trauma. And it would be progressive, producing denser amnesic lacunae as the stress continued. There is no evidence from controlled research on either humans or animals that stress specifically impairs memory for the central details of the stressful event itself -- which is what the claim of "repressed" or "dissociated" traumatic memories is all about. Holocaust survivors do not forget the Holocaust.
Moreover, Nadel & Jacobs' third proposition, that traumatic memory is fragmentary, is the outcome to be explained by the first two propositions. If the second of these propositions is invalid, what is there to be said about the third? In fact, Nadel & Jacobs seem to base their third proposition entirely on the work of van der Kolk & Fisler (1995):
Within a certain range, stress could enhance all forms of explicit memory, but high levels of stress could enhance some aspects of explicit memory while impairing others. And here is the critical point: When stress is high enough to impair the function of the hippocampus, resulting memories will be different from those formed under more ordinary circumstances. These empirical data may be available as isolated fragments rather than as coherently bound episodes (e.g., van der Kolk & Fisler, 1995). This hypothesis contrasts with the position espoused by Shobe and Kihlstrom (1997), who did not take into account the differential effects of stress on the various memory modules (p. 156).
Note, first, that the material quoted is presented only as a "hypothesis", and it is qualified with hedge words -- "could" and "may". In fact, nowhere in their paper do Nadel & Jacobs offer any evidence that stress has the predicted effect on memory; it is not clear why they should criticize Shobe & Kihlstrom (1997) for failing to take into account evidence that did not exist at the time, and apparently still does not exist.
It is ironic that, in bolstering their "hypothesis" concerning the fragmentary nature of traumatic memories, Nadel & Jacobs rely heavily on van der Kolk & Fisler (1995), because -- as Shobe and I discussed in some detail -- the van der Kolk & Fisler study is badly confounded, and no conclusions about the qualities of traumatic memory should be drawn from it. For example, as we wrote, "the poor narrative quality of the traumatic memories, and even the periods of amnesia, may have been due to normal processes associated with infantile and childhood amnesia, rather than any special qualities of traumatic memory (Shobe & Kihlstrom, 1997, p. 72). Yet Nadel & Jacobs accept van der Kolk & Fisler's evidence uncritically.
Nadel & Jacobs attempt to bolster their position further by citing a paper by Jacobs, Laurence, Thomas, Luzcak, & Nadel (1996) as supporting the notion that "even in the presence of extensive autobiographical amnesia, intrusive emotions or images associated with the trauma (and related events) may appear" (p. 156). Unfortunately, the paper in question (which is misreferenced in the Nadel & Jacobs paper) presents no empirical data to support this or any other notion about traumatic memory. Instead, Jacobs et al. (1996) offer another hypothesis about "the conditions under which a memory for a traumatic event has a high, medium, or low probability of accurately reflecting the target event", as well as a series of fictional (sic) cases illustrating the basic points of the proposed model. The model was not tested in the Jacobs et al. (1996), paper, and as such remains highly speculative. Nevertheless, Nadel & Jacobs conclude their discussion as if the model had been supported by empirical data: "What distinguishes these intrusive memory states is the absence of the time-and-place contextual information that typically characterizes autobiographical episode memory" (p. 156).
In further support of their arguments, Nadel & Jacobs cite a paper by Metcalfe and Jacobs (1998; see also Metcalfe & Jacobs, 1996), which proposes that there are separate "cool" and "hot" memory systems which are affected differently by stress. M&J propose that "As stress increases, the cool-memory system at first becomes increasingly responsive but then, as the level continues to grow, becomes less responsive until, at traumatic levels, of stress, it becomes dysfunctional.... In contrast, the hot system becomes increasingly responsive to increasing levels of stress in a monotonic manner up to and including very extreme levels, breaking down only at extremely high levels" (pp. 205-206). Note, again, that this assertion takes the form of a hypothesis. In fact, Metcalfe and Jacobs (1998) review available evidence that low levels of stress can enhance processing of both the "cool" (hippocampus-based) and "hot" (amygdala-based) memory systems, as well as available evidence that moderate levels of stress can enhance "hot" memory while impairing "cool" memory to some degree. However, they offer no evidence for the critical prediction that traumatic stress can produce profound amnesia for the spatio-temporal components of memory processed by the "cool" system. Aside from two anecdotal case reports of unknown representativeness, Metcalfe and Jacobs (1998) rely entirely on the study by van der Kolk & Fisler (1995) -- a study that Shobe & Kihlstrom (1997) criticized in considerable detail.
In summary, Nadel and Jacobs offer no empirical support for their prediction that individuals subjected to traumatic levels of stress can retain strong memories for their emotional state while forgetting the spatio-temporal context in which this emotion was aroused. Although they refer to the papers by Jacobs et al. (1996) and Metcalfe & Jacobs (1998) as if they presented such evidence, these papers both rely solely on the highly questionable study by van der Kolk & Fisler (1995). As such, their hypothesis remains just that -- a hypothesis that has no grounding in actual empirical data.
A hypothesis (Nadel & Jacobs, 1998) cannot be supported merely by repetitions of the same hypothesis in other publications (Jacobs et al., 1996; Metcalfe & Jacobs, 1998). Is there any evidence, beyond the van der Kolk & Fisler (1995) study, that trauma causes amnesia for the traumatic event? While this idea has been part of the folklore of psychiatry and clinical psychology since the 19th century (Janet and Freud both made it a central part of their theories of neurosis and psychotherapy), the best that can be said is that after more than 100 years evidence favoring the existence of traumatic memory is highly debatable (e.g., Brown, Scheflin, & Whitfield, 1999; Piper, Pope, & Borowiecki, 2000). In one review of 63 studies encompassing thousands of trauma victims, not a single victim was reported a developing amnesia for the traumatic event (Pope, Hudson, Bodkin, & Oliva, 1998; see also Pope, Oliva, & Hudson, 1999). In any event, Nadel & Jacobs (1998) do not analyze any of this evidence, or even cite it. So far as published work is concerned, they rely almost exclusively on the study by van der Kolk & Fisler (1995).
Despite the lack of pertinent evidence, Nadel and Jacobs (1998) concluded that "Traumatic stress can cause amnesia for the autobiographical context of stressful events, but stronger than normal recall for the emotional memories produced by them" (p. 156). But then they go even further, concluding that despite the allegedly fragmentary nature of traumatic memories, "an autobiographical memory eventually emerges" by a process of "'inferential narrative smoothing' whereby disembodied fragments are knit together into a plausible autobiographical episode.... The present analysis suggests that at least some memories 'recovered' during therapy should be taken seriously" (p. 156).
The evidence provided that memory fragments can be knitted into autobiographical narratives is, once again, the study by van der Kolk and Fisler (1995). Unfortunately, van der Kolk & Fisler did not attempt to corroborate their subjects' narratives against independent records of the traumatic events in question. Accordingly, we have no idea how much of their subjects' narratives were accurate accounts of the traumatic events in question -- or, frankly even that the events occurred at all. In fact, Nadel & Jacobs concede that "The narratives associated with [recovered traumatic] memories are less likely to be veridical in their entirety" (p. 156). Given that, according to their own hypothesis, the contextual information underlying these narratives was not properly encoded at the time the events ostensibly occurred, this would seem to be an understatement.
In the final analysis, Nadel & Jacobs attempt to support their proposition that traumatic memory is special by offering little more than an unproven "hypothesis" about why this should be so. Although the theoretical basis for their prediction is clear, empirical evidence that trauma actually causes amnesia is lacking in their paper, and indeed in the wider body of evidence on emotion and memory. Nor does even their own hypothesis give us any reason to have any confidence in traumatic narratives "recovered" through psychotherapy. Far from "broadening the issues" (in the words of the editor who justified their publication in a personal communication), Nadel & Jacobs muddy the waters by substituting conjecture for evidence, and in so doing feed the excesses of the industry that surrounds the trauma-memory argument and recovered-memory therapy.
It may well be that traumatic memory is special in the ways asserted by Nadel & Jacobs, but for the present we have only their word for it. All the evidence appears to be to the contrary.
Brown, D., Scheflin, A.W., & Whitfield, C.L. (1999). Recovered memories: The current weight of the evidence in science and in the courts. Journal of Psychiatry & Law, 27, 5-156.
Cahill, L., & McGaugh, J.L. (1996). Modulation of memory storage. Current Opinion in Neurobiology, 6, 237-242.
Cahill, L., Prins, B., Weber, M., & McGaugh, J.L. (1994). B-Adrenergic activation and memory for emotional events. Nature, 371, 702-704.
Jacobs, W.J., Laurance, H.E., Thomas, K.G.F., Luzcak, S.E., & Nadel, L. (1996). On the veracity and variability of recovered traumatic memory. Traumatology, 2(2) [On-line]. Available: http://rdz.stjohns.edu/trauma/traumaj.html.
Metcalfe, J., & Jacobs, W.J. (1996). A "hot-system/cool-system" view of memory under stress. PTSD Research Quarterly, 7(2) 1-3.
Mecalfe, J., & Jacobs, W.J. (1998). Emotional memory: The effects of stress on 'cool' and 'hot' memory systems. In D.L. Medin (Ed.), The psychology of learning and motivation: Advances in research and theory, Vol. 38 (pp. 187-222). San Diego: Academic Press.
Nadel, L., & Jacobs, W.J. (1998). Traumatic memory is special. Current Directions in Psychological Science, 7, 154-156.
Piper, A., Pope, H.G., & Borowiecki, J.J. (2000). Custer's last stand: Brown, Scheflin, and Whitfield's latest attempt to salvage "dissociative amnesia". Journal of Psychiatry & Law, 28, 149-213.
Pope, H.G., Hudson, J.I., Bodkin, J.A., & Oliva, P. (1998). Questionable validity of "dissociative amnesia" in trauma victims. British Journal of Psychiatry, 172, 210-215.
Pope, H.G., Pliva, P.S., & Hudson, J.I. (1999). The scientific status of research on repressed memories. In D.L. Faigman, D.H. Kaye, M.J. Saks, & J. Sanders (Eds.), Modern scientific evidence: The law and science of expert testimony (pp. 115-155). St. Paul, Mn,: West Group.
Shobe, K.K., & Kihlstrom, J.F. (1997). Is traumatic memory special? Current Directions in Psychological Science, 7, 154-156.
van der Kolk, B., & Fisler, R. (1995). Dissociation and the fragmentary nature of traumatic memories: Overview and exploratory study. Journal of Traumatic Stress, 8, 505-525.
This article last updated 01/26/12 11:31:02 AM.