Prolonged exposure therapy

The emotional processing theory (EPT), formulated by Foa and Kozak (Reference Foa and Kozak1986), underpins prolonged exposure (PE), a frontline trauma-focused therapy for PTSD. This theory draws on Lang’s bio-informational theory of fear (Lang, Reference Lang1977; Lang, Reference Lang1979), positing that fear is represented in memory networks consisting of interconnected stimulus, response and meaning components that collectively function to signal and avoid danger. For instance, a fear memory network might link a specific stimulus like a gun to various behavioural and physiological responses (e.g. increased heart rate, urges to flee or hide) and meanings (‘I am in danger’). When an environmental cue triggers one or more elements of this fear network, activation spreads throughout the connected elements. Extending the EPT theory to PTSD, Foa and Rothbaum (Reference Foa and Rothbaum1998) suggested that the fear memory in PTSD patients is marked by exaggerated stimuli and responses coupled with distorted meanings. For example, a person who has suffered an assault might irrationally perceive walking alone at night or encountering bald men (if the assailant was bald) as threatening, despite these being generally harmless. They might also hold unhelpful beliefs, like self-blame (‘I should have defended myself’). In PTSD, such fear structures often include maladaptive cognitions that can instigate and perpetuate PTSD symptoms, such as a pervasive belief in the world’s inherent danger or doubts about one’s competence. Therefore, according to Foa and Kozak, effective psychological interventions for PTSD focus on emotionally processing these fear memories to alter their maladaptive aspects, facilitating healthier cognitive and emotional responses.

Two pre-requisites are essential for the emotional processing and alteration of a fear structure. Initially, the fear structure needs to be triggered or activated. Subsequently, information incongruent with the elements of the fear structure must be introduced and assimilated into the fear structure, aiming to substitute pathological elements with realistic ones. Data from clinical studies have shown a set of responses in patients who improve with PE treatment and are therefore taken as signs of emotional processing. The initial response is characterised by an increased physiological reactivity to imagery associated with fear or when exposed to stimuli related to trauma (as noted by Jaycox et al. in Reference Jaycox, Foa and Morral1998, Pitman et al. in Reference Pitman, Orr, Altman, Longpre, Poiré, Macklin, Michaels and Steketee1996, and Wangelin and Tuerk in Reference Wangelin and Tuerk2015), suggesting the activation of fear memories. Furthermore, there is a gradual reduction (habituation) in the distress experienced in response to these activated fear structures across therapy sessions (highlighted in studies by Foa and Kozak in 1986 and Foa and Rothbaum in 1998). The first is characterised by an increased physiological reactivity to imagery associated with fear when exposed to stimuli related to trauma (Jaycox et al., Reference Jaycox, Foa and Morral1998; Pitman et al., Reference Pitman, Orr, Altman, Longpre, Poiré, Macklin, Michaels and Steketee1996; Wangelin and Tuerk, Reference Wangelin and Tuerk2015), suggesting the activation of fear memories. Habituation is assessed throughout treatment using subjective units of distress (SUDS) and observed autonomic physiological reactions within and between exposure trials.

Although PE has been validated as an efficacious treatment for PTSD, approximately 50% of those who undertake PE will fail to demonstrate a treatment response indicative of disorder remission (for a review, see Schottenbauer et al., Reference Schottenbauer, Glass, Arnkoff, Tendick and Gray2008; Steenkamp et al., Reference Steenkamp, Litz, Hoge and Marmar2015). Furthermore, a number of controversies are associated with PE in clinical practice. The primary one is the relatively high drop-out, which is reported to be an average of 28% (Hembree et al., Reference Hembree, Foa, Dorfan, Street, Kowalski and Tu2003; Najavits, Reference Najavits2015). However, drop-out rates as high as 62% have also been reported (Belleau et al., Reference Belleau, Chin, Wanklyn, Zambrano-Vazquez, Schumacher and Coffey2017).

Trauma-focused cognitive behavioural therapy

Trauma-focused cognitive behavioural therapy (TF-CBT), an alternative trauma-focused evidence-based treatment for PTSD, is also partially informed by the EPT (Cohen and Mannarino, Reference Cohen and Mannarino2019). Extending the EPT, Ehlers and Clark’s (Reference Ehlers and Clark2000) cognitive model offers insights into both the onset and persistence of PTSD, detailing interconnected elements such as re-experiencing symptoms, fear extinction learning, avoidance behaviours, and physiological dysregulation. This model posits that PTSD is linked to evaluations of trauma and its aftermath, creating a sense of ongoing threat, which may also arise from inadequately integrated trauma memories within autobiographical memories (van der Kolk and Fisler, Reference van der Kolk and Fisler1995). The perpetuation of maladaptive trauma memory structures is attributed to maladaptive behaviour (e.g. avoidance of trauma-related stimuli) and cognitive processing styles (e.g. rumination, distraction, thought suppression).

In applying TF-CBT to each patient, a formulation of the Ehlers and Clark (Reference Ehlers and Clark2000) model is constructed. This conceptualisation involves finding the pertinent appraisals, memory characteristics, triggers, and behavioural and cognitive strategies that contribute to the individual’s PTSD maintenance. The initial objective is to amend maladaptive appraisals of the trauma, identified through targeted questioning, particularly focusing on the significance of ‘hot spots’ or moments of distress in the trauma memory (Kleim et al., Reference Kleim, Grey, Wild, Nussbeck, Stott, Hackmann, Clark and Ehlers2013). Once an alternative, convincing appraisal is determined, it is actively integrated into the trauma memory (Ehlers and Wild, Reference Ehlers, Wild, Schnyder and Cloitre2015). Modifying excessively negative appraisals of trauma consequences involves information dissemination, Socratic questioning, and behavioural experiments. The second aim is to diminish intrusive symptomology by processing traumatic memories and discerning triggers (Ehlers, 2010). The therapist and patient construct a narrative, starting at pre-trauma to a point of relative safety post-trauma. This examination of autobiographical memory facilitates the identification and modification of excessively negative appraisals and inhibits re-experiencing symptoms in the presence of trauma-related stimuli. The third goal is to eradicate dysfunctional behaviours and cognitive strategies, such as avoidance (Ehlers and Wild, Reference Ehlers, Wild, Schnyder and Cloitre2015). Common in PTSD, these strategies aim to diminish the current sense of threat but inadvertently sustain the disorder in the long term by impeding trauma memory elaboration, preventing reappraisal, or directly intensifying PTSD symptoms.

TF-CBT stands apart from PE by emphasising, identifying and modifying problematic appraisals. While there are shared treatment techniques, significant distinctions arise. Firstly, TF-CBT employs imaginal reliving not for emotional habituation but to pinpoint ‘hot spots’ for subsequent cognitive restructuring and narrative elaboration within the trauma context. Unlike PE, where imaginal exposure and cognitive processing are separate, TF-CBT intricately intertwines these techniques. Secondly, TF-CBT’s in vivo exercises aim to test predictions about danger overgeneralisation and reduce immediacy triggered by activated trauma memories, departing from PE’s focus on emotional habituation. Thirdly, TF-CBT introduces innovative techniques, including stimulus discrimination, modification of the trauma memory with new information emerging throughout treatment, behavioural experiments illustrating various maintaining processes, and imagery transformation methods (Ehlers, 2013).

Nonetheless, a commonality between the two treatments is the foundational role of emotional engagement and emotional clarity. Emotional engagement is pivotal for the effective processing of traumatic memories, particularly when targeting various trauma responses such as cognitions, emotions, behaviours, and physiological reactions (Foa and Kozak, Reference Foa and Kozak1986). Furthermore, TF-CBT’s success lies in its multi-modal approach, examining helpful and unhelpful trauma responses as predictors of client outcomes, transcending isolated variables (Alpert et al., Reference Alpert, Hayes and Foa2023). The therapy facilitates the recognition of connections among thoughts, feelings, and behaviours, replacing maladaptive cognitions with adaptive ones (Ehlers, 2013). This process allows patients to develop a more adaptive appraisal(s) of the traumatic experience, identifying and correcting previously assumed rigid beliefs. Without emotional clarity, the challenging task of identifying and correcting these maladaptive cognitions, critical for reducing trauma-related fear and enhancing treatment outcomes, would be compromised (Butler et al., Reference Butler, Boden, Olino, Morrison, Goldin, Gross and Heimberg2018).

Like PE, treatment non-response rates for TF-CBT range between 25 and 50% (Brady et al., Reference Brady, Warnock-Parkes, Barker and Ehlers2015). Several factors have been identified that may influence the response to TF-CBT in adults. These responses include perseveration of responses observed in early therapy sessions and the strength of the therapeutic alliance (Brady et al., Reference Brady, Warnock-Parkes, Barker and Ehlers2015). For instance, greater patient perseveration (repetition of a particular response), less articulation of thoughts and feelings, and weaker therapeutic alliance have been inversely associated with treatment outcomes (Brady et al., Reference Brady, Warnock-Parkes, Barker and Ehlers2015).

A potential explanation for the elevated occurrence of non-response to trauma-focused treatments may lie in the challenges some patients encounter when attempting to connect with emotions and stimuli related to trauma (Wangelin and Tuerk, Reference Wangelin and Tuerk2015). Wangelin and Tuerk (Reference Wangelin and Tuerk2015) observed that heightened arousal to trauma stimuli at the outset of treatment correlated with the process of habituation to the trauma memory throughout prolonged exposure (PE) treatment. Evaluations were conducted at pre-treatment, session 4, and post-treatment, during which participants were exposed to personalised trauma scripts based on their respective index trauma. Those who successfully completed PE exhibited significantly diminished heart rate and skin conductance reactivity to trauma imagery throughout therapy. Individuals exhibiting higher trama-specific heart rate reactivity at pre-treatment demonstrated more substantial reductions in subjectively reported PTSD symptoms at post-treatment. Conversely, patients who discontinued therapy were more likely to exhibit hypo-arousal, underscoring the critical role of activating the fear memory network and fostering emotional engagement, as indicated by physiological arousal. Wangelin and Tuerk’s (Reference Wangelin and Tuerk2015) research highlights the crucial link between physiological responses to trauma stimuli and the effectiveness of PE in treating PTSD, suggesting that the ability to activate and engage with fear memories is key to successful treatment outcomes.

Advances in affective science

Over the past 20 years, there has been an exponential advance in affective sciences from theories of emotion generation (constructed emotion; Barrett, Reference Barrett2006; predictive coding accounts of emotion; Seth, Reference Seth2013), which define emotions as complex interplays of sensed and anticipated top-down and bottom-up processes. This interplay contrasts with traditional theories of emotion, which lie across a dichotomy of top-down and bottom-up processes (Cannon, Reference Cannon1927; Damasio, Reference Damasio1994; James, Reference James1894; Lange, Reference Lange, Dunlap and Haupt1922). However, these new accounts of affective experience are not well integrated into the PTSD literature. The importance of affective processing in PTSD treatment response suggests that the field may benefit from integrating advances in affective science with predominant models of associative learning, i.e. using fear extinction learning to explain treatment response better and guide more precision treatments.

Research has demonstrated a link between the concordance or intra-person correlation of various emotion components (such as physiological arousal, expressed feelings, and behaviour) and improved emotional processing and well-being (Brown et al., Reference Brown, Van Doren, Ford, Mauss, Sze and Levenson2019; Sommerfeldt et al., Reference Sommerfeldt, Schaefer, Brauer, Ryff and Davidson2019). This concordance among cognitive, emotional, and physiological factors is underscored by studies highlighting the role of the interaction between cortisol and noradrenaline in the basolateral amygdala in the formation of emotional memories (McGaugh, Reference McGaugh2004). In the realm of emotional memory processing, both the initial learning phase (consolidation) and the advanced phase (reconsolidation) are adversely affected when physiological cues are diminished, for instance, through the use of beta-blockers (Lonergan et al., Reference Lonergan, Olivera-Figueroa, Pitman and Brunet2013). While certain medications, such as those used in the management of acute emotional arousal discordance stemming from traumatic memories, have shown some effectiveness (Giustino et al., Reference Giustino, Fitzgerald and Maren2016), a continuous misalignment of emotional and cognitive signals can hinder therapeutic intervention and prolong the underlying issues. In acute scenarios, drugs like propranolol, which disrupt physiological and emotional indicators, can facilitate unlearning processes (Elsey et al., Reference Elsey, Filmer, Galvin, Kurath, Vossoughi, Thomander, Zavodnik and Kindt2020), especially when stress levels are high and norepinephrine concentrations are beyond the ideal learning range (Fitzgerald et al., Reference Fitzgerald, Giustino, Seemann and Maren2015).

In contrast, benzodiazepines, which broadly inhibit neural activity across the brain (Guina et al., Reference Guina, Rossetter, DeRhodes, Nahhas and Welton2015), can impede the cognitive engagement with fear needed for effective exposure (Rosen et al., Reference Rosen, Ortiz and Nemeroff2020). Benzodiazepine use has been linked to reduced effectiveness in trauma-focused treatment approaches (Guina et al., Reference Guina, Rossetter, DeRhodes, Nahhas and Welton2015). Consequently, a limited correlation between emotional facets might limit optimal engagement with feared emotional states, key for safety learning. Recognising individual variations in emotional engagement and concordance in emotional responses is important.

Alexithymia

Alexithymia, originating from Greek (a = lack, lexis = word, thymos = emotions), was first used clinically to describe the psychological characteristics of patients with psychosomatic illness (Sifneos, Reference Sifneos1973). The construct includes difficulties articulating feelings, limited imaginative ability, and excessive pre-occupation with physical symptoms and external events (Nemiah and Sifneos, Reference Nemiah and Sifneos1970). Individuals with alexithymia also demonstrate general difficulties with emotion regulation, including deficits in cognitive reappraisal ability (Swart et al., Reference Swart, Kortekaas and Aleman2009). Recent research on alexithymia, showing an estimated correlation of r = .43 between alexithymia and PTSD across various trauma-exposed populations, has attracted significant attention (Edwards, Reference Edwards2019; Frewen et al., Reference Frewen, Dozois, Neufeld and Lanius2008; Putica et al., Reference Putica, Van Dam, Steward, Agathos, Felmingham and O’Donnell2021). Trauma-exposed adults high in alexithymia demonstrate a disconcordant emotion response style in anticipation of fear-related stimuli (Putica et al., Reference Putica, O’Donnell, Felmingham and Van Dam2022b), which suggests that alexithymia’s impact on emotion and memory processing is multi-faceted in that it does not just impact one component of emotionality, but rather the interaction between emotional components. The findings above are in line with previous work which has shown that those with alexithymia show hypo-arousal (Peasley-Miklus et al., Reference Peasley-Miklus, Panayiotou and Vrana2016) attenuated habituation (Panayiotou and Constantinou, Reference Panayiotou and Constantinou2017), and emotion response disconcordance (Eastabrook et al., Reference Eastabrook, Lanteigne and Hollenstein2013; Kleiman et al., Reference Kleiman, Kramer, Wegener, Koch, Geiser, Imbierowicz, Zur and Conrad2016) to emotional stimuli, which becomes more pronounced as the stimuli become more personal and high-stakes for the individual (Kleiman et al., Reference Kleiman, Kramer, Wegener, Koch, Geiser, Imbierowicz, Zur and Conrad2016). The emotion response disconcordance, due to its disconnection of emotional components, interferes with one’s ability to fully assess the context and specific emotional states to be regulated, thus impacting their ability to engage in adaptive emotion regulation (Levenson, Reference Levenson2014; Luhmann et al., Reference Luhmann, Hofmann, Eid and Lucas2012).

Alexithymia and PTSD treatment response

Considering the deficits in emotional processing in those high in alexithymia, it is not surprising that alexithymia has been implicated in PTSD treatment resistance (Kosten et al., Reference Kosten, Krystal, Giller and Dan1992; Putica et al., Reference Putica, Van Dam, Felmingham and O’Donnell2023; Zorzella et al., Reference Zorzella, Muller, Cribbie, Bambrah and Classen2020). Putica et al. (Reference Putica, Van Dam, Felmingham and O’Donnell2023) examined the impact of alexithymia on PE outcomes. Most notably, they found that impairment in emotional clarity was a significant predictor of treatment drop-out. They also found that participants with high alexithymia were more likely to maintain a full PTSD diagnosis immediately post-treatment and at a 6-month follow-up. Alexithymia was also associated with delayed treatment effects on avoidance, with a significant reduction in symptomology observed from pre- to follow-up but not from pre- to post-treatment. The study concluded that while PE is effective, those with alexithymia show a delayed treatment response and may be at greater risk of pathology after treatment.

Furthermore, Kosten and colleagues (Reference Kosten, Krystal, Giller and Dan1992) examined the effect of alexithymia on PTSD treatment response among a sample of 57 Vietnam veterans. The veterans engaged in 8-week randomised, controlled, double-blind trials and were randomised to one of the following conditions: (1) imipramine and brief psychodynamic psychotherapy; (2) phenelzine and brief psychodynamic psychotherapy; and (3) brief psychodynamic psychotherapy only. Each participant concurrently received individual psychotherapy grounded in a brief psychodynamic framework. In the psychotherapy group, alexithymia was inversely associated with a reduction in avoidance outcomes, irrespective of the severity of trauma. No impact was observed on intrusion symptomology or among subjects in the psychopharmacology group. Given that all three treatment cohorts received both psychotherapy and the pharmacological agent, the study findings imply that psychotherapy in isolation might not be efficacious in mitigating avoidance symptoms in individuals with alexithymia and PTSD.

Thirdly, Zorzella et al. (Reference Zorzella, Muller, Cribbie, Bambrah and Classen2020) explored the role of alexithymia in treatment outcomes for women with childhood abuse histories participating in a specialised trauma-focused group therapy. Their research involved 167 participants in the Women Recovering from Abuse Program (WRAP), an 8-week comprehensive intervention incorporating aspects of affect regulation, self-care, stabilisation, and cognitive-behavioural therapy skills. The therapy, both group and individual, was specifically designed for women with significant childhood trauma. They found that high alexithymia levels at baseline were linked to greater severity of PTSD, increased dissociation, and more severe interpersonal problems before treatment. Notably, reductions in alexithymia during treatment were closely correlated with improved outcomes in PTSD symptoms, dissociation, and interpersonal challenges. While these findings contribute to understanding the impact of alexithymia on the manifestation and treatment of PTSD, they stop short of examining the influence of alexithymia and related emotional deficits on primary trauma-focused treatments for PTSD.

Clinical implications

In the context of TF-CBT, the diverse therapeutic approaches and the patient–therapist collaborative discovery method may inherently offer greater efficacy for individuals concurrently experiencing PTSD and alexithymia. Specifically, the amalgamation of appraisal and imaginal work appears particularly advantageous for those with alexithymia, given their challenges in identifying emotional triggers and targets for reappraisal. Engaging in these processes collaboratively with the therapist throughout treatment could facilitate a mutual learning experience concerning trauma cues and reminders, with each being systematically addressed during sessions. Moreover, the incorporation of thought suppression experiments and other demonstrative techniques elucidating the detrimental consequences of maladaptive trauma coping mechanisms proves beneficial in addressing avoidance and suppression tendencies through an educational and experiential approach. However, it is important to highlight that alexithymia-related difficulties, particularly challenges in mentalisation (the cognitive capacity to understand and interpret one’s own and others’ thoughts, feelings, intentions, and beliefs; Lüdemann et al., Reference Lüdemann, Rabung and Andreas2021), may compromise aspects of TF-CBT treatment protocols related to mental inference and integration.

Several treatment considerations could be implemented across both TF-CBT and PE to enhance treatment response for those with alexithymia and PTSD. Firstly, given that alexithymia is distinct from but highly associated with PTSD severity across trauma-exposed populations, this construct should be considered in clinical assessment. Assessment can be facilitated by a brief screening tool such as the Toronto Alexithymia Scale (TAS-20; Bagby et al., Reference Bagby, Parker and Taylor1994) or the license-free Perth Alexithymia Questionnaire (PAQ; Preece et al., Reference Preece, Becerra, Robinson, Dandy and Allan2018). If high levels of alexithymia are endorsed or evident, therapists should emphasise psychoeducation on emotional literacy, helping individuals develop a vocabulary for their emotional experiences. Additionally, interventions can be adapted to focus on concrete, observable behaviours and physical sensations associated with emotions rather than relying solely on verbal expression. Furthermore, therapy sessions can be structured to gradually build emotional awareness and expression skills, fostering a safe and supportive environment for individuals to explore and articulate their emotional states.

Screening for alexithymia may help identify those with difficulties with therapeutic engagement (Nunes da Silva, Reference Nunes da Silva2021) and may help with individual differences in interpersonal style and rapport building. Those who present with severe PTSD can be challenging for clinicians. However, those who also present with a cold, detached, emotionally incongruent interpersonal style (alexithymia) may elicit confusion and frustration from their treater(s) (Ogrodniczuk et al., Reference Ogrodniczuk, Piper and Joyce2011). This alexithymia-related interpersonal style is inversely associated with the therapist-rated therapeutic alliance (Ogrodniczuk et al., Reference Ogrodniczuk, Piper and Joyce2011; Quilty et al., Reference Quilty, Taylor, McBride and Bagby2017) and treatment outcomes across treatment modalities (Ogrodniczuk et al., Reference Ogrodniczuk, Piper and Joyce2011; Quilty et al., Reference Quilty, Taylor, McBride and Bagby2017). Screening for alexithymia and incorporating such presentations into clinical formulations may foster clinician understanding and empathy rather than frustration or misattribution of patient motivation (for example, ‘the patient is not motivated or taking treatment seriously’). Screening and formulating for alexithymia have been suggested by Nunes da Silva (Reference Nunes da Silva2021), who presents intervention guidelines for fostering emotional skills and therapeutic alliance for patients with alexithymia. Specifically, Nunes da Silva (Reference Nunes da Silva2021) posits that alexithymic functioning is particularly relevant in conceptualising emotional processing and emotional aspects of the therapeutic relationship (guideline 2.3; Nunes da Silva, Reference Nunes da Silva2021).

Beyond being a generalised interpersonal style, it may be that alexithymia, as measured by the TAS-20, is a sophisticated measure of avoidance or screener for trauma-focused treatment under-engagement. For example, as a means of avoiding acute distress following trauma exposure or in the case of severe pathology, some patients may avoid tending to unwanted or distressing emotional states. One of the most challenging emotional experiences that a survivor of trauma may encounter is the confrontation of the traumatic memory(ies). It is not, therefore, surprising that individuals with this emotion-response style would modulate their emotional engagement during trauma memory exposures as a means of attenuating their experienced distress, resulting in under-engagement. Therefore, if alexithymia is identified, the clinician may incorporate emotion exposures and emotion regulation skill-building as part of, or as an adjunct to, trauma-focused treatments (Cameron et al., Reference Cameron, Ogrodniczuk and Hadjipavlou2014). For example, emotion exposures may be incorporated as part of in vivo exposures or as preparatory work prior to trauma-focused intervention. Incorporating targeted adjunct treatment modules is affirmed by Nunes da Silva (Reference Nunes da Silva2021), who posits that experiential interventions may help increase awareness, while experiential interventions could enhance emotional awareness (guideline 3.4; Nunes da Silva, Reference Nunes da Silva2021). Therefore, if alexithymia presents an initial barrier to trauma-focused treatments or is a residual clinical concern after treatment, clinicians are encouraged to directly address alexithymia-related difficulties to promote treatment engagement or the retention of treatment gains (Cameron et al., Reference Cameron, Ogrodniczuk and Hadjipavlou2014).

Moreover, individuals with elevated alexithymia may perceive ordinary bodily changes as alarming or disengage through anticipatory anxiety, characterised by atypical interoception (Brewer et al., Reference Brewer, Cook and Bird2016). Therapeutic approaches could be refined to incorporate elements specifically designed to address these inclinations. Interoceptive exposures (Boettcher et al., Reference Boettcher, Brake and Barlow2016) or instruction in additional strategies for recognising, expressing, and managing emotions more adeptly could be integrated. This adaptation aims to help patients comprehend that affective information is not inherently uncontrollable or perilous. Techniques like emotion labelling, emotion differentiation, and the implementation of emotion-focused coping strategies may contribute to this comprehensive therapeutic approach.

Furthermore, given that those with alexithymia demonstrate a disconcordant emotional response style that is hypothesised to stem from difficulties in present-focused, non-judgemental emotional awareness, mindfulness-based interventions should also be considered (for example, see Putica et al., Reference Putica, Felmingham, Garrido, O’Donnell and Van Dam2022a; Watford and Stafford, Reference Watford and Stafford2015). The intricate interplay between physiological arousal and cognitive processing underscores the complexity of trauma-related emotional experiences, emphasising the need for nuanced approaches in therapeutic interventions to bridge the gap between physiological reactions and conscious awareness of the cognitive appraisal processes associated with traumatic events. In essence, tailoring PTSD treatments for those high in alexithymia involves a nuanced and patient-centred approach that recognises the unique emotional processing challenges of this population. For a summary of the potential impacts of alexithymia on individual treatment components and potential treatment augmentations, see Table 1 below.

Table 1. Impact of alexithymia on treatment components with recommended augmentations

Limitations and considerations

It is important to note the heterogeneity of PTSD when considering treatments. The distinction between reactive and dissociative PTSD subtypes, as highlighted by Lanius et al. (Reference Lanius, Brand, Vermetten, Frewen and Spiegel2012), underscores the complexity of PTSD’s impact on individuals. Research indicates that alexithymia may affect treatment outcomes differently across these subtypes, suggesting a nuanced interaction that warrants further investigation. Reactive PTSD is characterised by symptoms primarily as responses to stressors, including hyperarousal, intrusive memories, and avoidance behaviours. In contrast, the dissociative subtype includes symptoms of dissociation alongside other PTSD symptoms. This distinction is crucial for treatment; for instance, treatments for reactive PTSD might focus more on managing arousal and anxiety, processing traumatic memories, and reducing avoidance behaviours. Conversely, treatments for the dissociative subtype may include strategies specifically aimed at addressing dissociative symptoms, such as grounding techniques, integrating dissociated parts of the self, and processing trauma without causing further dissociation.

It is also of note that interventions specifically designed for alexithymia show encouraging outcomes and may also be considered as adjuncts to trauma-focused treatments. Levant and colleagues (Reference Levant, Hall, Williams and Hasan2009) observed a marked decrease in alexithymia levels among individuals participating in a psychoeducational group focused on correcting dysfunctional beliefs about emotions, enriching emotional vocabulary, enhancing the ability to interpret others’ emotions, recognising emotions or physical sensations, and engaging in exercises for emotional experience. Furthermore, Melin and associates (Reference Melin, Thulesius and Persson2010) reported a significant reduction in alexithymia, particularly with challenges in recognising and articulating emotions, following an 8-week psychological program aimed at identifying, distinguishing, and expressing emotions and their physical manifestations verbally. Additionally, preliminary evidence suggests the potential of dialectical behaviour therapy in addressing alexithymia-specific issues (refer to Salles et al., Reference Salles, Maturana de Souza, Dos Santos and Mograbi2023, for a review).

Finally, alexithymia has been identified as a dimensional and multi-faceted construct (Kooiman et al., Reference Kooiman, Spinhoven and Trijsburg2002; Zimmermann et al., Reference Zimmermann, Rossier, Meyer de Stadelhofen and Gaillard2005), consisting of various primary challenges for individuals. For instance, difficulty in identifying feelings may hinder engagement with core practices of CBT, such as cognitive restructuring, whereas an external focus could impede mindfulness efforts. Assessing the subscales of alexithymia allows for a more customised therapeutic approach, enabling interventions to directly target the specific traits of alexithymia affecting therapy.

Summary and conclusion

Primary interventions for PTSD, such as prolonged exposure therapy (PE) and trauma-focused cognitive behavioural therapy (TF-CBT), have made significant strides in addressing the intricate and multi-faceted nature of trauma-related experiences. While both therapies have demonstrated efficacy, many individuals still do not respond adequately to these frontline treatments. The emphasis on emotional engagement and clarity in PE and TF-CBT underscores the critical role of individual differences in emotional processing. Moreover, the integration of advances in affective science into PTSD treatment models can provide a more nuanced understanding of treatment response and guide more precise interventions.

Despite the successes of PE and TF-CBT, challenges persist, particularly in the context of treatment non-response and high drop-out rates. Notably, the role of alexithymia, characterised by difficulties in articulating and understanding emotions, emerges as a factor influencing PTSD treatment response. Understanding and addressing alexithymia-related challenges, including emotional disconcordance and difficulties in mentalisation, are crucial for enhancing therapeutic engagement and treatment outcomes.

Clinical implications highlight the need for tailored approaches that consider individual variations in emotional processing, with specific attention to alexithymia. Screening for alexithymia can inform treatment strategies, including psychoeducation on emotional literacy, therapy session adaptations, and mindfulness-based interventions. Additionally, recognising alexithymia-related difficulties in interpersonal style can guide clinicians in building effective therapeutic alliances. Overall, the integration of these considerations into PTSD treatment protocols offers a more comprehensive and personalised approach to address the diverse needs of individuals with PTSD, ultimately optimising treatment response and fostering long-term recovery.