I am not at all in disagreement with you, not at all inclined to leave the psychology hanging in the air without an organic basis. But apart from this I do not know how to go on.;>–Freud letters to Fliess in September of 1898 (Masson Reference Masson1985)
Are we better equipped today to anchor psychological processes in a biological foundation than Freud was in 1898? The manuscript of Lane et al. speaks to the core of these questions: Do advances in neuroscience offer us tools and knowledge to explore the biology of psychological concepts, and how does “psychotherapy ultimately use biological mechanisms to treat mental illness” (Ledoux Reference LeDoux2002, p. 299)? In their target article, Lane et al. propose a heuristic, integrated model with an overarching conceptual structure in which effects of seemingly distinct and presumably irreconcilable therapies can be understood and reconciled within their proposed framework, without over- or undervaluing any particular approach. Based on the suggested model, both episodic and semantic memories and the associated implicit and explicit emotional experiences are seen as components of a single integrated memory network that is stable but also plastic under certain conditions. Activation of a node in this network (accessed via different therapeutic approaches) triggers all other nodes, making the system malleable to therapeutic change. Thus, the pathological memory “system” can be accessed and modified through its different features.
One important and unique aspect of the proposed model is the anchoring of the psychotherapeutic process in the current understanding of cognitive and affective neuroscience (see Freud's lamentation above). The manuscript places recent work on memory reconsolidation as a central, key process in psychotherapeutic change. Memory reconsolidation has indeed been both a promising and controversial concept in the context of psychotherapy. Although it offers a plausible candidate mechanism for the process of therapeutic “change” in old memories and percepts, it was described primarily in animal models and in relationship to relatively simple memory traces of fear conditioning. More complex memory systems in humans might work differently. Does memory plasticity and reconsolidation extend to complex traumatic memories with emotional and autobiographical elements that are repeatedly reinforced through time? Also, animal lesion studies suggest that overtrained or highly aversive memories survive hippocampal inactivation (Garin-Aguilar et al. Reference Garín-Aguilar, Medina, Quirarte, McGaugh and Prado-Alcalá2014; Markowitsch et al. Reference Markowitsch, Kessler and Streicher1985), demonstrating resistance to modification and independence from the hippocampal memory system, a key system in proposed reconsolidation. Are repeatedly reinforced, traumatic memories in humans more like overtrained rodent memories, and therefore not subject to reconsolidation?
Alternatively, is it possible to explain effects of therapy by a process of contextualization rather than reconsolidation of memory (Liberzon & Sripada Reference Liberzon and Sripada2008; Maren et al. Reference Maren, Phan and Liberzon2013)? Contextualization is conceptualized here as a process that updates old memories by adding novel contextual elements to them, and it does not require bringing the old memory into a state of instability that allows it to be altered before being reconsolidated. Another question that arises about extension of reconsolidation research to psychopathology is that reconsolidation is performed days to weeks after learning. Human “pathological” memories can be present or even repeated similarly, and consolidated over many years. The question here is: How long is too long a lapse between the event and the reconsolidation for reconsolidation to happen? Addressing these questions and better defining the real boundaries of reconsolidation processes in the context of psychotherapy will further enhance the utility of the proposed model.
Are there clinical implications for Lane et al.'s conceptualization? Is it at all fundamentally different from stating that every therapy could be effective? True understanding of the mechanisms involved in therapeutic change should be able to help in developing more effective interventions, as well as predicting what will not be effective, or what could even potentially be harmful. From this perspective, the proposed model indeed suggests that combining therapeutic techniques from different modalities might be more effective than adhering to a single orthodoxy. Similarly, it predicts that some approaches might not be useful or could even be counterproductive if they recapture but do not modify traumatic or negative experiences. For example, it emphasizes the importance of an empathic and supportive therapist in helping patients modify and update trauma or fear memories, as opposed to a “blank screen” approach that might recapitulate prior experience of an unempathic caregiver. Similarly, it suggests that in trauma-processing groups, repeated retelling of trauma memories, without correction of cognitive distortions or reflection on authentic emotions, might lead to further consolidation of fear memories rather than their modification through reconsolidation. Finally, in behavioral therapy, in vivo exposure conducted without establishment of a safe environment and perceptions of self-efficacy might lead to a higher than optimal level of arousal, preventing reconsolidation and reinforcing avoidance.
Lane et al.'s model raises additional questions in the clinical context. It suggests, for example, that the integrated memory structure can be approached through each of its nodes. If that is indeed the case, how does it explain the differential efficacy of therapeutic approaches? For instance, cognitive and interpersonal therapies have been particularly effective in treatment of depression, whereas behavioral (exposure) therapy is most effective for treatment of phobias or anxiety. Psychodynamic principles are used in treatments of personality disorders but there is no evidence for their effectiveness in treatment of obsessive-compulsive disorder. It is also argued that there is an optimal level or “window” of emotional arousal for psychotherapy to work. However this observation is based on correlational and not causal data. It is plausible for example that patients who respond better to treatment may be able to better tolerate their emotions and higher arousal. Empirical research that manipulates arousal level during memory reconsolidation will have to address the question of optimal arousal level. If indeed excessive arousal can impair treatment efficacy, the establishment of “optimal arousal” levels could guide more sophisticated use of combined psychotherapy and pharmacotherapy. Here, excessive levels of arousal can be reduced to “optimal” levels with the judicious use of anxiolytics. The same medications may impair reconsolidation of memories, however, further underscoring the urgent need to advance accurate understanding of the specific mechanisms involved in therapeutic change. The target article offers an important conceptual step indeed in the ongoing process of discovery.
I am not at all in disagreement with you, not at all inclined to leave the psychology hanging in the air without an organic basis. But apart from this I do not know how to go on.;>–Freud letters to Fliess in September of 1898 (Masson Reference Masson1985)
Are we better equipped today to anchor psychological processes in a biological foundation than Freud was in 1898? The manuscript of Lane et al. speaks to the core of these questions: Do advances in neuroscience offer us tools and knowledge to explore the biology of psychological concepts, and how does “psychotherapy ultimately use biological mechanisms to treat mental illness” (Ledoux Reference LeDoux2002, p. 299)? In their target article, Lane et al. propose a heuristic, integrated model with an overarching conceptual structure in which effects of seemingly distinct and presumably irreconcilable therapies can be understood and reconciled within their proposed framework, without over- or undervaluing any particular approach. Based on the suggested model, both episodic and semantic memories and the associated implicit and explicit emotional experiences are seen as components of a single integrated memory network that is stable but also plastic under certain conditions. Activation of a node in this network (accessed via different therapeutic approaches) triggers all other nodes, making the system malleable to therapeutic change. Thus, the pathological memory “system” can be accessed and modified through its different features.
One important and unique aspect of the proposed model is the anchoring of the psychotherapeutic process in the current understanding of cognitive and affective neuroscience (see Freud's lamentation above). The manuscript places recent work on memory reconsolidation as a central, key process in psychotherapeutic change. Memory reconsolidation has indeed been both a promising and controversial concept in the context of psychotherapy. Although it offers a plausible candidate mechanism for the process of therapeutic “change” in old memories and percepts, it was described primarily in animal models and in relationship to relatively simple memory traces of fear conditioning. More complex memory systems in humans might work differently. Does memory plasticity and reconsolidation extend to complex traumatic memories with emotional and autobiographical elements that are repeatedly reinforced through time? Also, animal lesion studies suggest that overtrained or highly aversive memories survive hippocampal inactivation (Garin-Aguilar et al. Reference Garín-Aguilar, Medina, Quirarte, McGaugh and Prado-Alcalá2014; Markowitsch et al. Reference Markowitsch, Kessler and Streicher1985), demonstrating resistance to modification and independence from the hippocampal memory system, a key system in proposed reconsolidation. Are repeatedly reinforced, traumatic memories in humans more like overtrained rodent memories, and therefore not subject to reconsolidation?
Alternatively, is it possible to explain effects of therapy by a process of contextualization rather than reconsolidation of memory (Liberzon & Sripada Reference Liberzon and Sripada2008; Maren et al. Reference Maren, Phan and Liberzon2013)? Contextualization is conceptualized here as a process that updates old memories by adding novel contextual elements to them, and it does not require bringing the old memory into a state of instability that allows it to be altered before being reconsolidated. Another question that arises about extension of reconsolidation research to psychopathology is that reconsolidation is performed days to weeks after learning. Human “pathological” memories can be present or even repeated similarly, and consolidated over many years. The question here is: How long is too long a lapse between the event and the reconsolidation for reconsolidation to happen? Addressing these questions and better defining the real boundaries of reconsolidation processes in the context of psychotherapy will further enhance the utility of the proposed model.
Are there clinical implications for Lane et al.'s conceptualization? Is it at all fundamentally different from stating that every therapy could be effective? True understanding of the mechanisms involved in therapeutic change should be able to help in developing more effective interventions, as well as predicting what will not be effective, or what could even potentially be harmful. From this perspective, the proposed model indeed suggests that combining therapeutic techniques from different modalities might be more effective than adhering to a single orthodoxy. Similarly, it predicts that some approaches might not be useful or could even be counterproductive if they recapture but do not modify traumatic or negative experiences. For example, it emphasizes the importance of an empathic and supportive therapist in helping patients modify and update trauma or fear memories, as opposed to a “blank screen” approach that might recapitulate prior experience of an unempathic caregiver. Similarly, it suggests that in trauma-processing groups, repeated retelling of trauma memories, without correction of cognitive distortions or reflection on authentic emotions, might lead to further consolidation of fear memories rather than their modification through reconsolidation. Finally, in behavioral therapy, in vivo exposure conducted without establishment of a safe environment and perceptions of self-efficacy might lead to a higher than optimal level of arousal, preventing reconsolidation and reinforcing avoidance.
Lane et al.'s model raises additional questions in the clinical context. It suggests, for example, that the integrated memory structure can be approached through each of its nodes. If that is indeed the case, how does it explain the differential efficacy of therapeutic approaches? For instance, cognitive and interpersonal therapies have been particularly effective in treatment of depression, whereas behavioral (exposure) therapy is most effective for treatment of phobias or anxiety. Psychodynamic principles are used in treatments of personality disorders but there is no evidence for their effectiveness in treatment of obsessive-compulsive disorder. It is also argued that there is an optimal level or “window” of emotional arousal for psychotherapy to work. However this observation is based on correlational and not causal data. It is plausible for example that patients who respond better to treatment may be able to better tolerate their emotions and higher arousal. Empirical research that manipulates arousal level during memory reconsolidation will have to address the question of optimal arousal level. If indeed excessive arousal can impair treatment efficacy, the establishment of “optimal arousal” levels could guide more sophisticated use of combined psychotherapy and pharmacotherapy. Here, excessive levels of arousal can be reduced to “optimal” levels with the judicious use of anxiolytics. The same medications may impair reconsolidation of memories, however, further underscoring the urgent need to advance accurate understanding of the specific mechanisms involved in therapeutic change. The target article offers an important conceptual step indeed in the ongoing process of discovery.