In their target article Lane et al. attempt to provide a general model for “therapeutic change.” The authors argue that any psychotherapeutic intervention at its core acts on reactivated memories via the process of reconsolidation, leading to modified memory traces. From our perspective, this ambitious approach is flawed by two major concerns: (1) the authors ignore that therapeutic change is processed by a multiplicity of diverse mechanisms, whereof change of dysfunctional emotional memory processing is only one of many; (2) given that guided adaption of dysfunctional memory traces is an important component of psychotherapeutic mechanisms, it remains unclear whether the mechanisms of memory consolidation as studied under experimental conditions can be transferred to therapeutic practice.
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(1) Psychotherapy is an iterative process aiming to adapt client's dysfunctional experience and behaviors to a normative social environment. Based on many years of our own work in psychotherapy research and development, we can state that in modern psychotherapeutic treatments the selected targets are based on individualized functional analyses including cognitive, emotional, behavioral, neurobiological, and social aspects. Therapeutic interventions and techniques are selected according to predefined treatment algorithms or by the intuitive wisdom of the therapist. The variety of evidence-based therapeutic mechanisms can be structured in (1) more general interventions – for example, psycho-education, relaxation-training, metacognitive awareness, cognitive restructuring, contingency management, skills acquisition, and problem solving, and (2) disorder-specific interventions – for example, training in impulse-control in ADHD, coping with illusions and coping with family interventions in schizophrenia, emotion regulation in borderline personality disorder, anti-craving skills in substance dependence, shifting of attention in social phobia, physical activation in chronic fatigue, imagery rehearsal therapy for nightmares, and sexual therapy for sexual dysfunctions. These interventions are not, or are only in part, processed by changes of the emotional memory system. Thus, the idea to propose changes of emotional memories not only at the core, but as “the essential ingredient” (target article, sect. 4, para. 7) of therapeutic change might be a bit simplistic.
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(2) Disrupting reconsolidation processes is a tricky act of balance. In fact our own experience from many years of research on reconsolidation, as well as a very careful analysis of the limited number of original investigations in laboratory animals (Tronson & Taylor Reference Tronson and Taylor2007) and humans regarding this phenomenon, tells us that it is extremely difficult to generate a reliable experimental condition that allows interference of reconsolidation processes, and, if successful, the interference is usually of a transient nature.
From a molecular perspective, memory reconsolidation requires new protein synthesis. More than 50 studies in rodents have examined the effects of protein synthesis inhibitors after reactivation of a previously consolidated memory. Protein synthesis inhibitors were given either intracerebroventricularly or brain site–specifically (e.g., to the hippocampus, amygdala, or other site), and disruption of reconsolidation was usually tested 24 hours later. In approximately 20 studies, protein synthesis inhibition did not disrupt reconsolidation, despite this being an essential prerequisite for the reconsolidation theory. There are also many conflicting findings on the existence of reconsolidation per se. The problem is that the existing literature shows only the tip of the iceberg in terms of negative findings of reconsolidation effects. As so often happens in science, many laboratories have tried to study the phenomenon of reconsolidation without success – and have not reported their findings, as scientific journals are not keen on reporting negative results. Another complicating factor is that each nonreinforced reactivation session designed to induce memory retrieval and reconsolidation also involves extinction mechanisms to a certain degree, which makes the interpretation of results difficult.
These complications by no means imply that memory reconsolidation phenomena do not exist, but they certainly suggest that these phenomena do not translate to all memories, and likely occur under very specific experimental conditions that make good reproducibility very difficult to achieve. Hence, the current state of knowledge does not allow us to clearly define determining factors and experimental conditions that can be transferred to a psychotherapeutic setting. We do know that the age of a memory, memory strength, and in particular the length of the reactivation session is of importance for determination of the reconsolidation process; however, brain scientists do not know about the causality of these factors and cannot provide guidance for psychotherapy. It is obvious that, for example, memories strengthened during 20 years of cigarette smoking, which likely involves millions of repetitions of inhalation plus smoking cue associations, cohere into an extremely strong, habitual memory that is very difficult, if not impossible, to disrupt or modify – an assumption that is underlined by the fact that relapse can occur even after decades of abstinence. On the other end of the spectrum, a person who suffers from one clearly described traumatic experience is perhaps more likely to be responsive to disruption of that particular memory. It is thus not surprising that positive results in the human literature have primarily been obtained with disruption of reconsolidation of human fear and episodic memories (Schwabe et al. Reference Schwabe, Nader and Pruessner2014). But most patients who seek psychotherapy are suffering from highly distinct and complex emotional and motivational disturbances, which make it less likely to define any general rules and guidelines for reactivation of a distinct memory that is amenable to disruption of reconsolidation.
Finally, little is known about the lasting nature of treatment success, as only a handful of papers have described memory disruption more than 24 hours following reactivation manipulations. To date there are no reports that demonstrate permanent alterations in memory; at best these disruptions have been demonstrated to last up to a few weeks.
In conclusion, changing emotional memories is an important mechanism in psychotherapy, but it is one among many. It fits into some models (e.g., trauma-memory processing). However, more complex issues that are fundamental to psychotherapy, such as changing human habits, learning social skills, developing compassion, modifying human values, reappraising social issues under different social conditions, and so forth, are beyond the scope of the reconsolidation phenomenon.
In their target article Lane et al. attempt to provide a general model for “therapeutic change.” The authors argue that any psychotherapeutic intervention at its core acts on reactivated memories via the process of reconsolidation, leading to modified memory traces. From our perspective, this ambitious approach is flawed by two major concerns: (1) the authors ignore that therapeutic change is processed by a multiplicity of diverse mechanisms, whereof change of dysfunctional emotional memory processing is only one of many; (2) given that guided adaption of dysfunctional memory traces is an important component of psychotherapeutic mechanisms, it remains unclear whether the mechanisms of memory consolidation as studied under experimental conditions can be transferred to therapeutic practice.
(1) Psychotherapy is an iterative process aiming to adapt client's dysfunctional experience and behaviors to a normative social environment. Based on many years of our own work in psychotherapy research and development, we can state that in modern psychotherapeutic treatments the selected targets are based on individualized functional analyses including cognitive, emotional, behavioral, neurobiological, and social aspects. Therapeutic interventions and techniques are selected according to predefined treatment algorithms or by the intuitive wisdom of the therapist. The variety of evidence-based therapeutic mechanisms can be structured in (1) more general interventions – for example, psycho-education, relaxation-training, metacognitive awareness, cognitive restructuring, contingency management, skills acquisition, and problem solving, and (2) disorder-specific interventions – for example, training in impulse-control in ADHD, coping with illusions and coping with family interventions in schizophrenia, emotion regulation in borderline personality disorder, anti-craving skills in substance dependence, shifting of attention in social phobia, physical activation in chronic fatigue, imagery rehearsal therapy for nightmares, and sexual therapy for sexual dysfunctions. These interventions are not, or are only in part, processed by changes of the emotional memory system. Thus, the idea to propose changes of emotional memories not only at the core, but as “the essential ingredient” (target article, sect. 4, para. 7) of therapeutic change might be a bit simplistic.
(2) Disrupting reconsolidation processes is a tricky act of balance. In fact our own experience from many years of research on reconsolidation, as well as a very careful analysis of the limited number of original investigations in laboratory animals (Tronson & Taylor Reference Tronson and Taylor2007) and humans regarding this phenomenon, tells us that it is extremely difficult to generate a reliable experimental condition that allows interference of reconsolidation processes, and, if successful, the interference is usually of a transient nature.
From a molecular perspective, memory reconsolidation requires new protein synthesis. More than 50 studies in rodents have examined the effects of protein synthesis inhibitors after reactivation of a previously consolidated memory. Protein synthesis inhibitors were given either intracerebroventricularly or brain site–specifically (e.g., to the hippocampus, amygdala, or other site), and disruption of reconsolidation was usually tested 24 hours later. In approximately 20 studies, protein synthesis inhibition did not disrupt reconsolidation, despite this being an essential prerequisite for the reconsolidation theory. There are also many conflicting findings on the existence of reconsolidation per se. The problem is that the existing literature shows only the tip of the iceberg in terms of negative findings of reconsolidation effects. As so often happens in science, many laboratories have tried to study the phenomenon of reconsolidation without success – and have not reported their findings, as scientific journals are not keen on reporting negative results. Another complicating factor is that each nonreinforced reactivation session designed to induce memory retrieval and reconsolidation also involves extinction mechanisms to a certain degree, which makes the interpretation of results difficult.
These complications by no means imply that memory reconsolidation phenomena do not exist, but they certainly suggest that these phenomena do not translate to all memories, and likely occur under very specific experimental conditions that make good reproducibility very difficult to achieve. Hence, the current state of knowledge does not allow us to clearly define determining factors and experimental conditions that can be transferred to a psychotherapeutic setting. We do know that the age of a memory, memory strength, and in particular the length of the reactivation session is of importance for determination of the reconsolidation process; however, brain scientists do not know about the causality of these factors and cannot provide guidance for psychotherapy. It is obvious that, for example, memories strengthened during 20 years of cigarette smoking, which likely involves millions of repetitions of inhalation plus smoking cue associations, cohere into an extremely strong, habitual memory that is very difficult, if not impossible, to disrupt or modify – an assumption that is underlined by the fact that relapse can occur even after decades of abstinence. On the other end of the spectrum, a person who suffers from one clearly described traumatic experience is perhaps more likely to be responsive to disruption of that particular memory. It is thus not surprising that positive results in the human literature have primarily been obtained with disruption of reconsolidation of human fear and episodic memories (Schwabe et al. Reference Schwabe, Nader and Pruessner2014). But most patients who seek psychotherapy are suffering from highly distinct and complex emotional and motivational disturbances, which make it less likely to define any general rules and guidelines for reactivation of a distinct memory that is amenable to disruption of reconsolidation.
Finally, little is known about the lasting nature of treatment success, as only a handful of papers have described memory disruption more than 24 hours following reactivation manipulations. To date there are no reports that demonstrate permanent alterations in memory; at best these disruptions have been demonstrated to last up to a few weeks.
In conclusion, changing emotional memories is an important mechanism in psychotherapy, but it is one among many. It fits into some models (e.g., trauma-memory processing). However, more complex issues that are fundamental to psychotherapy, such as changing human habits, learning social skills, developing compassion, modifying human values, reappraising social issues under different social conditions, and so forth, are beyond the scope of the reconsolidation phenomenon.