whats in the name alexithymia

October 7, 2017 | Author: thebeholder | Category: Self-Improvement, Emotions, Affect (Psychology), Perception, Psychological Trauma
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Neuroscience and Biobehavioral Reviews 68 (2016) 1006–1020

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Neuroscience and Biobehavioral Reviews journal homepage: www.elsevier.com/locate/neubiorev

Commentary

What’s in the name ‘alexithymia’? A commentary on “Affective agnosia: Expansion of the alexithymia construct and a new opportunity to integrate and extend Freud’s legacy.” Graeme J. Taylor a,∗ , R. Michael Bagby b , James D.A. Parker c a

Department of Psychiatry, University of Toronto and Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G1X5, Canada Departments of Psychology and Psychiatry, University of Toronto, 1265 Military Trail, Sy-131, Toronto, Ontario M1C1A4, Canada c Department of Psychology, Trent University, 1600 West Bank Drive, Peterborough, Ontario K9J7B8, Canada b

a r t i c l e

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Article history: Received 6 January 2016 Received in revised form 20 April 2016 Accepted 23 May 2016 Available online 24 May 2016 Keywords: Alexithymia Anomia Agnosia Emotional awareness Mentalization Primal repression Psychotherapy Toronto Alexithymia Scale Trauma

a b s t r a c t The recent proposal of a new type of agnosia termed ‘affective agnosia’ extends Freud’s legacy and captures the concept of not knowing one’s own emotions. This concept links well with the theory of levels of emotional awareness and maps onto a hierarchical model of neural substrates of emotional experience, but does not encompass the pensée opératoire component of the alexithymia construct. Moreover, identifying agnosia and anomia subtypes, which connotes a categorical conceptualization of alexithymia, is inconsistent with the dimensional nature of the construct. We describe a more widely accepted definition of alexithymia, and argue that although aptly descriptive, the concept of affective agnosia does not advance the theory, measurement, and treatment of alexithymia. A review of alexithymia literature indicates that impairment in the mental representation of emotions has been a central aspect of alexithymia theory since the concept was introduced, and guided the development of the Toronto Alexithymia Scale and other measures of the construct. Moreover, techniques to enhance mentalization of emotions have been used by psychotherapists for several decades. © 2016 Elsevier Ltd. All rights reserved.

1. Introduction In a recent article in this journal Lane et al. (2015a) propose a new type of agnosia, which they name ‘affective agnosia’ and describe as “an impairment in the ability to mentally represent or know what one is feeling” (p. 594). They note that affective agnosia is closely related to the alexithymia construct, which was introduced by Nemiah and Sifneos (1970) (Nemiah et al., 1976) in the early 1970s and has since generated a large body of empirical research. Whereas the term affective agnosia captures the concept of not knowing one’s own emotions, Lane et al. point out that the term alexithymia when taken literally (lack of words for emotion) refers to a type of anomia. They propose a continuum between severe forms of alexithymia (the agnosia version) and mild forms of alexithymia (the anomia version), and suggest that the concept of affective agnosia advances the theory, measurement, and treatment of alexithymia. As the developers of three different measures

∗ Corresponding author. E-mail addresses: [email protected] (G.J. Taylor), [email protected] (R.M. Bagby), [email protected] (J.D.A. Parker). http://dx.doi.org/10.1016/j.neubiorev.2016.05.025 0149-7634/© 2016 Elsevier Ltd. All rights reserved.

of alexithymia, and having conducted research on this construct for more than thirty years, we found Lane et al.’s (2015a) ideas interesting and worthy of attention; however, their review of the alexithymia literature was notably selective with several significant omissions and oversights. In addition, we believe that their proposal of subtypes of alexithymia conflicts with their conceptualization of a continuum construct and is more likely to generate confusion rather than advance the field. In this Commentary we offer an alternative perspective on the theory, measurement, and treatment of alexithymia, and attempt to correct some potential misconceptions about the construct. In particular, in Section 6, we address the various issues Lane et al. (2015a) raise in their critical review of the use of the self-report 20-item Toronto Alexithymia Scale (TAS-20) in alexithymia research.

2. Agnosia, anomia, and agnostic aphasia We commend Lane et al. for drawing attention to Freud’s (1891) much neglected treatise On Aphasia and for extending his legacy by integrating his concept of agnosia into the field of alexithymia. In so doing they have added to contributions by other authors

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(e.g., Miller, 1991; Rizzuto, 1989; Stengel, 1954) who extended Freud’s legacy by recognizing that many of the ideas he presented in his treatise anticipated some of his later psychoanalytic concepts; these include his theoretical construct of a ‘speech apparatus’ as an antecedent of the ‘psychic apparatus’, his application of Hughling Jackson’s ideas of neurobehavioral regression to the aphasias and later to mental processes (further on we discuss the application of the concept of regression to alexithymia), and his concept of representation. Whereas Finkelnburg (1870) called disturbances in the recognition of objects asymbolia, Freud proposed the term agnosia because he considered asymbolic a more appropriate designation for the relation between the word (re)presentation and the object (re)presentation rather than for the relation between the object and the object (re)presentation.1 As Lane et al. (2015a) indicate, Freud described asymbolic aphasia (anomia) as a type of aphasia in which the associations between the word (re)presentation and object (re)presentation are disturbed.2 They point out also that a failure of naming necessarily occurs as part of the impaired recognition in individuals with agnosia; however, they fail to mention that Freud gave the name agnostic aphasia to this combination of agnosia and anomia. When applied to emotions, individuals who are unable to adequately represent and recognize the meaning of visceral/somatic emotional reactions (i.e., agnosia) will also manifest difficulty finding words for feelings (i.e., anomia). It is Lane et al.’s (2015a) impression that the distinction between anomia and agnosia has not previously been made or considered in relation to alexithymia or affect. Although other authors may not have made the same distinction, it should be acknowledged that the idea of alexithymia being a form of agnosia has been suggested previously. We draw attention to articles indicating that Sifneos (1967, 1994, 1996) initially contemplated the concept of agnosia, but later suggested that alexithymia may be a type of anomia. In the late 1960s, Sifneos (1967) reported his preliminary clinical observations on randomly selected patients with classic psychosomatic diseases; the most striking characteristic was a marked difficulty many of the patients had in finding appropriate words to describe their feelings, as though they did not understand the meaning of the word ‘feeling’. Although Sifneos (1967) did not refer to Freud’s treatise On Aphasia, he wondered if these patients suffer “from ‘emotional agnosia’ similar to the ‘visual agnosia’ observed by Klüver and Bucy in monkeys” (p. 8). Many years later, influenced by a review article on aphasia by Damasio (1992), Sifneos (1994, 1996) hypothesized that alexithymic individuals, who are unable to link limbic emotions with cognitive activity in the form of images, fantasies, and thoughts, are suffering from a ‘feeling aphasia’. Since Damasio (1992) had defined aphasia as an interruption in the ability “to convert the sequences of nonverbal mental representations that constitute thought into the symbols and grammatical organizations that constitute language” (p. 531), a feeling aphasia suggests a type of anomia even though the deficient cognitive activity referred to by Sifneos involves more than labeling emotions with words. If Sifneos had combined his proposal of a ‘feeling aphasia’ with his earlier proposal of an ‘emo-

1 Freud used the German word Vorstellung, which has been translated variously into English as ‘presentation’, ‘idea’, ‘concept’, and ‘representation’. For example, Strachey (1957) referred to ‘word and object presentations’; Stengel’s translations were ‘word concept’ and ‘idea of the object’. According to the Edinburgh International Encyclopedia of Psychoanalysis (Skelton, 2009), Lacan showed that Freud borrowed the term Vorstellung (translated as representation) from philosophy “to mean, broadly speaking, the elements within the mind from which a world of experience is constructed” (p. 403). 2 Strachey (1957) notes that what Freud called ‘object presentation’ in his treatise On Aphasia he calls ‘thing presentation’ in his paper ‘The Unconscious’; and what he called ‘object presentation’ in ‘The Unconscious’ denotes a complex made up of the combined ‘thing presentation’ and ‘word presentation’, a complex that is not given a name in his treatise.

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tional agnosia’, he might have described alexithymia as an ‘affective agnostic aphasia’. Although Lane et al. cite Prinz’s (2004) book Gut Reactions, they do not credit him for characterizing alexithymia as “an analogue of associative agnosia”. Prinz suggested that rather than alexithymia being a verbal disorder, “it is more likely to be an inability to recognize emotions” (p. 217). They also overlook an article by Primmer (2013), who offers a slightly different perspective. Like Lane et al.’s (2015a) idea of a continuum, Primmer conceptualizes alexithymia as a dimensional construct; but whereas Lane et al.’s conceptualization of severe alexithymia as an affective agnosia seems to include apperceptive agnosia and/or associative agnosia depending on the level of deficit, Primmer considers severe alexithymia analogous only to apperceptive visual agnosia and regards mild alexithymia as analogous to ‘blindsight’ (i.e., an associative visual agnosia).3 Although Primmer employs a bodily theory of emotion, she bases her argument on evidence from some experimental studies that individuals with severe alexithymia are poor at recognizing facial expressions of emotion; she presumes that they respond with low levels of physiological arousal when viewing such expressions and proposes that they are therefore unable to develop accurate percepts of this type of emotional elicitor (for a more detailed discussion see Primmer, 2015). Primmer acknowledges that being poor at identifying other people’s emotions is not one of the salient components of the alexithymia construct, but suggests that as a secondary feature it may help in determining the severity of alexithymia. She is not concerned about the meaning of the term alexithymia, but takes for granted that it refers to a deficit in the processing of emotional information. Since emotional awareness is not a categorical construct, Primmer (2013) argues against the idea of defining subtypes of alexithymia, and says “it is more likely that there exist various degrees of alexithymia” (p. 115), just as “there are various degrees of emotional awareness ranging from mere awareness of bodily sensations to full-blown awareness” (p. 115). If we have followed Lane et al.’s (2015a) reasoning correctly, their understanding of the perceptual deficit in apperceptive affective agnosia is different from Primmer’s view as they are concerned with the perception of one’s own emotions rather than the emotional expressions of others. Consistent with their theoretical model of levels of emotional awareness, and applying Marr’s model of stages in visual perceptual processing to emotion, Lane et al. (2015a) propose that at the lowest level an individual “might have discrete somatic complaints such as stomach pain and muscle tension, but not perceive these complaints as related (i.e., parts of a coherent bodily reaction)” (p.600). At an intermediate level of representation an individual will experience coherent patterns of his or her entire bodily state, and also manifest facial and other bodily expressions of emotion, but may not recognize these experiences as emotional experiences and use their emotional meaning, i.e., an associative agnosia. We agree with both Primmer (2013) and Lane et al. (2015a) for including apperceptive agnosia as well as associative agnosia in their conceptualizations of alexithymia, but we question Primmer’s assumption that severe alexithymia is associated with low physiological arousal when viewing emotional facial expressions since investigations of this relation have yielded inconsistent findings (Grynberg et al., 2012). Although Primmer and Lane et al. share the view that different degrees of alexithymia (i.e., differences in severity) reflect differences in the structure of the cognitive schemata used to process emotional information, Lane et al. (2015a) declare

3 As noted by Lane et al. (1997, 2015a), ‘blindsight’ is the ability of a blind person to perceive visual stimuli, but without conscious awareness of the experience because of lesions in area V1 of the primary visual cortex.

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that “The tendency to jump to the explanation that alexithymia is a continuum obscures a critical issue and prevents the important distinction between anomia and agnosia from being made” (p. 607). Given that findings from taxometric investigations using data from several different samples support a dimensional conceptualization of alexithymia (Mattila et al., 2010a; Parker et al., 2008), we are in agreement with Primmer that it is preferable to conceptualize different degrees of alexithymia, rather than define subtypes.

3. Freud’s concept of primal repression Lane et al. (2015a) raise the question of why Freud did not connect agnosia to affective experience, and suggest that perhaps he did not use it in his psychoanalytic writings because he “focused almost exclusively on mental contents that had been previously mentally represented which were once known but were disguised or barred from consciousness due to defenses such as repression” (p. 606). However, as noted by many psychoanalytic authors (e.g., Cohen and Kinston, 1983; Dorpat, 1985), Freud (1915) described two phases in the operation of repression. The first phase, which he called primal repression, denies entrance of instinctual and affective representatives into consciousness. In the second phase, referred to as repression proper, instinctual, emotional, and other experiences have been mentally represented and gain entry into the conscious mind, but are then excluded from it. Although Freud focused more on instinctual drives than emotions and conceptualized primal repression in different ways at different times, it is clear from his descriptions that the elements under primal repression exist in a form that does not include verbal symbols (see editorial note in A. Freud, 1981). For example, infantile experiences that precede the development of the preconscious system in Freud’s topographical model of the mind are primally repressed and thus are not mentally represented. This primitive defense is not limited to early experiences, but occurs in children and adults when higher level mental capacities are overwhelmed by the impact of trauma (Cohen, 1985; Frank, 1969). Freud (1926) linked primal repression with psychic trauma when he stated that it “is highly probable that the immediate precipitating causes of primal repressions are quantitative factors such as an excessive degree of excitation and the breaking through of the protective shield against stimuli” (p. 94). We elaborate further on the association between trauma and primal repression in Section 9; but here we propose that Freud’s concept of primal repression is analogous to affective agnosia since it encompasses emotions and instinctual states that are not recognized by the individual as they are not linked with verbal symbols and thereby mentally represented. Our proposal is supported by the formulations of several other authors. Basch (1977), for example, anticipating Lane and Schwartz’s (1987) cognitive developmental theory of levels of emotional awareness, employed Piaget’s model of cognitive development and proposed that primal repression “involves sensorimotor schema which have never been given symbolic representation, that is, which have not participated in preoperational transformations” (p. 260). Dorpat (1985) regards primal repression as a primitive form of denial and proposes that it results in an arrest in the cognitive processing and construction of mental representations of perceived stimuli. In contrast to Freud, who based his concept of denial (or disavowal) on the mistaken belief that all perception is conscious, Dorpat emphasizes unconscious perception and argues that primal repression or denial affects the perceptual process after a person has registered a threatening object or situation, but before the person constructs a conscious percept of the object. He notes that the failure to construct a verbal representation of the stimulus object, and thereby provide meanings, is similar to what occurs in individuals with associative visual agnosia where

there is a defect not in the registering of sensory information but in the conceptual stage of perception. Dorpat’s theory could apply to states of arousal whether they arise in response to an external stimulus or internally without any such provocation.

4. What’s in the name ‘alexithymia’? Lane et al. (2015a) suggest that affective agnosia may be a more proper label as the original definition of alexithymia involves a lack of words for emotions. We argue against this suggestion because there is more to the name ‘alexithymia’ than it may seem. Let us briefly review the origins of the term and its use by clinicians and researchers over the past 40 years. Three years after Sifneos (1967) reported his preliminary clinical observations, Nemiah and Sifneos (1970) conducted a more systematic examination of previously tape-recorded interviews of patients with two of the following classic psychosomatic diseases (duodenal ulcer, bronchial asthma, rheumatoid arthritis, ulcerative colitis, atopic dermatitis); in addition to a marked difficulty in describing their feelings, many of these patients showed a thought content consistent with Marty and de M’Uzan’s (1963) concept of pensée opératoire (operative thinking), including a nearly total absence of fantasy or other material related to their inner mental life of thoughts, attitudes and feelings, and a recounting of details of external events. Sifneos (1973) states that for lack of a better term, he proposed the word ‘alexithymia’ (from Greek stems a = lack, lexis = word, and thymos = emotion, mood, or feeling) to denote the specific difficulty in finding appropriate words to describe feelings. A few years later, he told attendees at the 11th European Conference on Psychosomatic Research (ECPR) that “The word was simply used to describe certain clinical observations that were made over very many years. I tried appropriately to use a Greek word or a pseudo-Greek word for descriptive purposes” (Sifneos, 1977; pp. 368–369). Sifneos et al. (1977) had reported the clinical observations in a presentation earlier at the conference; the characteristics they described included more than a difficulty finding appropriate words to describe feelings). In some of his later articles, Sifneos (1994, 1996) made clear that the term alexithymia refers to an “affect deficit” that encompasses all of the characteristics that he and Nemiah had described in 1970, the most salient characteristics being difficulty identifying feelings, differentiating among the range of common affects, and distinguishing between feelings and the bodily sensations of emotional arousal (i.e., not knowing what one is feeling); difficulty finding words to describe feelings to other people; constricted imaginal processes as evidenced by a paucity or absence of fantasies referable to drives and feelings; and a thought content characterised by a preoccupation with the minute details of external events (the last two characteristics correspond to pensée opératoire) (Nemiah et al., 1976). These characteristics comprise what came to be referred to as the alexithymia construct (Lesser, 1981; Taylor et al., 1991). Thus, although the literal meaning of the term alexithymia implies a type of anomia, for Sifneos and Nemiah and for most clinicians and researchers inspired by their contributions, it is the name of a multifaceted construct that involves more than a difficulty finding words for emotional feelings. Lane et al. (2015a) state that “Although alexithymia has often been assumed to be something more than a simple lack of words, it has been challenging to find a more suitable term and conceptual framework to describe and measure it” (p. 595). As we have just shown, the “something more” is not an assumption but is actually included in the definition of the construct. Later in this Commentary, we describe a conceptual framework that has guided clinicians and alexithymia researchers for many years, including psychotherapists and developers of several instruments for measuring alexithymia.

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From time to time the term alexithymia has been challenged or different descriptive labels have been used to denote the cluster of characteristics that comprise the construct. Responding to questions and criticisms of the concept at the 11th ECPR, Sifneos (1977) was adamant that “alexithymia is here to stay, whether we like it or not and it is going to be with us for the rest of our lives” (p. 369). The term alexithymia has not only outlived Sifneos and many of the attendees at that conference, but is widely accepted and has become the lingua franca for clinicians and researchers in countries throughout the world. Although some authors may occasionally overlook the multifaceted nature of the construct and apply the term alexithymia to only one facet, we think that changing the name is ill-advised. The term alexithymia is now deeply entrenched in the scientific literature, and also listed in the Shorter Oxford English Dictionary (Trumble, 2007), and thus available for general public use. The OED defines alexithymia as “An affective disorder characterised by an inability to recognize and express emotions” (p. 50), a definition that clearly encompasses both the agnosia (inability to recognize) and the anomia (inability to express) aspects of the construct.

5. Alexithymia theory 5.1. Early formulations Lane et al. (2015a) propose that the concept of affective agnosia advances the theory of alexithymia. Although affective agnosia is an aptly descriptive label, in our opinion the concept will not advance alexithymia theory because “impairment in the ability to mentally represent or know what one is feeling” is already encompassed in current alexithymia theory. Derived from clinical observations, the alexithymia construct was formulated initially without an underlying theoretical framework. In contrast to how most personality traits are conceptualized, Nemiah et al. (1976) did not postulate a latent variable (viz., alexithymia) that causes and exists apart from the clinically observable features; rather, they formulated what is essentially a mereological construct with the various components assumed to interact with and reinforce one another.4 Nonetheless, from the outset, Nemiah and Sifneos (1970) (Nemiah et al., 1976) suggested some possible explanations for the observable features including not only an arrest in development as proposed much earlier by Ruesch (1948), but also psychodynamic and neurophysiological hypotheses. And within a short time, they placed alexithymia within a theoretical framework that Nemiah (1977) conceptualized for understanding the cognitive processing of emotions. Whereas Lane et al. (2015a) point out that “Emotion has traditionally been equated with the subjective experience of emotional feelings” (p. 608), Nemiah’s theoretical framework reflects a distinction that he and Sifneos made between emotions and feelings. Recognizing that affects have both biological and psychological components, they defined emotions as the neurophysiological and motor-expressive component of affects, and feelings as the subjective, cognitive-experiential component (Nemiah et al., 1976; Sifneos, 1975). This distinction is consistent with Freud’s (1916–1917) description of affects as “highly composite” experiences including “in the first place particular motor innervations or discharges and secondly certain feelings” (p. 395); it is also consistent with a contemporary view expressed by Damasio (2003) that “emotions play out in the theater of the body. Feelings play out in the theater of the mind” (p. 28). Although the distinc-

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Mereology refers to the study of the relations of parts to a whole as well as the relations between the parts within the whole (Stanford Encyclopedia of Philosophy, 2003).

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tion between emotions and feelings is overlooked in parts of Lane et al.’s (2015a) article,5 they acknowledge on page 606 that it is critical and parallels the distinction they make between implicit and explicit processes. Lane et al. (2015a) believe that “The current view that alexithymia may include a deficit in mental representation of emotion, not just in naming it, was ushered in by neuroimaging findings that suggested an impairment in emotional awareness rather than in emotional naming” (p. 608). But this view existed long before neuroimaging studies were conducted; the contribution of such studies was to explore neural correlates of alexithymia and emotional awareness (Lane et al., 1998a; Van der Velde et al., 2013). It is evident in Nemiah’s (1977) theoretical framework for emotional processing that emotions must be mentally represented to be experienced consciously as feelings. In conceptualizing the framework, Nemiah outlined the internal processes that normally occur in individuals in response to an affect-provoking external event. In addition to there being a perception and cognitive appraisal of the elements of the event, he indicated that the somatic components of affect are aroused and undergo a process of ‘psychic elaboration’. In formulating this process, he was probably influenced by Sandler’s (1972) discussion of emotion and the building up of a representational world at a Ciba Foundation Symposium in 1972, which he and Sifneos attended. As we have reviewed elsewhere (Taylor and Bagby, 2013a), Nemiah (1977) described several elements to the process of psychic elaboration, including a refinement and delineation of the raw emotion into a variety of qualitatively different nuances that have the potential for conscious experience as feelings; a linking of the feelings with words to describe them; the production of images and fantasies expressive of the feelings; and the arousal of a network of memories and associations related to the feelings. It was assumed that an awareness of feelings, together with the thoughts, fantasies, and memories they elicit, facilitates regulation of the emotional arousal induced by affect-evoking stimuli. Nemiah suggested that alexithymia could occur as a result of a failure in one or more of the elements of psychic elaboration, such that the activity of the biologic component of affect would be unregulated by cognitive processes and lead to somatic symptoms or be discharged through actions. Formulated a decade after Nemiah’s conceptual framework was published, Lane and Schwartz’s (1987) theory of levels of emotional awareness provides a more detailed and elaborate model for understanding the psychic elaboration of emotions and individual differences in affect awareness. Like Nemiah, Lane and Schwartz first adopt the generally accepted view that emotion is preceded by cognitive appraisal of the environment (Smith and Ellsworth, 1985), and then focus on the structure of emotional experience once an emotional response to a stimulus has been activated. Their central thesis is that “what is experienced as emotion is the consequence of a subsequent cognitive processing of emotional arousal and that the cognitive process itself undergoes a sequence of structural transformations during development which, in turn, determines the structure of subsequent emotional experience” (p. 134). Lane and Schwartz’s theory not only modifies and expands Nemiah’s theoretical framework for the psychic elaboration of emotion, but as we indicated many years ago (Taylor and Bagby, 2000; Taylor et al., 1991, 1997), it also extends earlier contributions of Schur (1955) and Krystal (1974), who conceptualized an epigenetic sequence for affect development involving a progressive desomatization, differentiation, and verbalization of emotions as

5 On pages 595 and 600, for example, Lane et al. (2015a) refer to “an inability to experience emotion”, whereas in a different paragraph on page 595 they refer to “a diminution or absence of the basic human ability to experience feelings”. We comment further on the experiencing of emotions versus feelings in Section 6.3.

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cognitive capacities mature. Along with this process Krystal (1979) described the development of a capacity for affect tolerance, and an increasing ability to use affects as signals to one’s self. It is surprising that Lane et al. (2015a) do not mention Krystal’s contributions even though he reported characteristics similar to those described by Nemiah and Sifneos at around the same time and before becoming aware of their work. Moreover, Krystal (1968) (Krystal and Raskin, 1970) observed these characteristics among patients with severe post-traumatic states and patients with substance use disorders, thereby setting the stage for extending the concept of alexithymia beyond the field of psychosomatic medicine. On the basis of his clinical observations, Krystal (1979, 1982/83, 1997) proposed that alexithymia is a consequence of an arrest in affect development due to psychic trauma in early childhood. And using the concept of regression, he proposed that alexithymia can also result from a regression of affect involving dedifferentiation, deverbalization, and resomatization of affects, which may occur secondary to major trauma in adulthood. As noted earlier, Freud (1891) derived the concept of regression from Hughling Jackson’s doctrine of functional retrogression in the central nervous system, and thereafter used it to describe a reversion to a level of mental functioning that was characteristic of an earlier stage of one’s development. Krystal (1982/83, 1988) noted that the application of the concept of regression to alexithymia permits an understanding of why this construct varies in severity from one person to another and sometimes within the same individual; compared to developmental arrests, regressions are “more spotty, irregular, fluctuating and reversible” (Krystal, 1979; p. 25). Given these ideas, it is possible that patients with alexithymia secondary to psychic trauma in adulthood (e.g., patients with posttraumatic stress disorder) may show changes in their level of emotional awareness as they shift back and forth on the continuum between affective agnosia and anomia proposed by Lane et al. Most importantly, Krystal (1988) observed that patients with severe alexithymia do not understand the meaning of their emotions; because their emotions are undifferentiated and poorly represented mentally, they are experienced predominantly as somatic reactions that “only call attention to themselves rather than to what they signal” (p. 264).

5.2. Interplay of deficit and defense Guided by the above overlapping theories, we proposed that the features comprising the alexithymia construct reflect a deficit in the cognitive processing and regulation of emotions (Taylor, 2000; Taylor et al., 1991, 1997). Sifneos (1994) also referred to alexithymia as “a deficit in the cognitive processing of emotions” (p.194). Similarly, Vanheule (2008) conceptualized alexithymia as “a difficulty in processing and regulating affective arousal by means of mental representations” (p. 332). Some authors (e.g., Knapp, 1983) regard alexithymia as a defense against neurotic conflict rather than an affect deficit. But this is a false dichotomy. As we have outlined elsewhere (Taylor and Bagby, 2013a; Taylor et al., 1997), a deficit/developmental arrest theory of alexithymia does not exclude a role for defenses. Nemiah (1977) included both deficit and defense in his theoretical formulations of alexithymia; Krystal (1982-83) employed the defense mechanism of regression and the idea of developmental arrest in his conceptualizations of alexithymia, but considered alexithymia “a defense in the teleological sense only” (p. 375); McDougall (1982-83) related alexithymia to deficits in the mental representation of emotion, but also conceptualized severe alexithymia as a massive defense against primitive terrors and inexpressive pain. Recognizing primitive denial or primal repression as the first phase in the process of repression, Dorpat (1985) argues that primal repression is associated with or brings

about developmental deficits, and that there is interaction between deficits and defenses in all psychopathology. Along similar lines, we noted that “as with other types of psychic deficit, the presence of alexithymia is likely to both initiate conflict [and defense] and intensify ordinary developmental conflicts” (Taylor et al., 1991; p. 156). As one would predict, several empirical investigations with both clinical and nonclinical samples have demonstrated that severe alexithymia is associated most strongly with immature defenses (such as denial, splitting, somatization), weakly with neurotic defenses (such as reaction formation, idealization), and negatively with mature defenses (such as suppression, sublimation). Moreover, there is evidence that these associations still hold after controlling for anxiety and depression (see Taylor and Bagby, 2013a for a review).

5.3. A multiple code theory More recently, we argued that the conceptualization of a deficit in the cognitive processing of emotion places alexithymia in the broad field of emotion theory and research (Taylor and Bagby, 2013a). We gave as an example Bucci’s (1997a, 2002, 2008) multiple code theory, which was developed in the context of work in cognitive science, emotion theory, and neuroscience. Bucci postulates three modes or systems of representing and processing emotional information; these are the nonverbal subsymbolic, nonverbal symbolic, and verbal symbolic modes. According to the theory, emotion schemas are comprised of components from all three modes, and develop on the basis of repeated interactions with others from the beginning of life. The nonverbal modes develop first and include subsymbolic processes (patterns of sensory, visceral, and kinesthetic sensations and motor activity experienced during states of emotional arousal), and symbolic imagery. The verbal symbolic mode develops later and is organized according to the symbolic format of language. According to Bucci, the verbal and nonverbal components within emotion schemas are connected, to varying degrees, by a referential process; the connections are most distant for subsymbolic representations such as sensory experiences and patterns of autonomic arousal, which may require connections with specific images within the nonverbal domain before they can be connected to language in the verbal domain. As with Lane and Schwartz’s (1987) theory of levels of emotional awareness, the linking does not transform one modality into another, but allows for a transformation of the meanings represented in the nonverbal modes and for translation into logically organized speech. Bucci (1997a) proposes that if the referential process is disrupted (e.g., by conflict or trauma) or fails to develop adequately, the verbal and nonverbal systems within the schemas are dissociated, thereby affecting the organization of the schemas, the regulation of emotional arousal, and the construction of emotional meanings. Applying her multiple code theory to alexithymia, Bucci (1997b) suggests that the dissociation within and between modes when connections are disrupted or fail to develop is “far more complex than being without words for emotions; in some emotional-somatic disorders, the patient is without symbols for somatic states” (p. 165). As Bucci explains, the dissociation between subsymbolic and symbolic components within the emotion schemas may allow physiological activation to occur during emotional arousal without a corresponding cognitive activation. Moreover, “without a symbolic focus and regulation, the activation is likely to be prolonged and repetitive, and the ultimate effects on physiological systems to be more severe” (Bucci, 1997b; p. 165). Depending on the degree of dissociation between somatic and motor patterns of activation and symbolic representations, and also on the interaction with constitutional and other vulnerability factors, a range of somatic

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disorders of varying seriousness may occur, from somatic symptom disorders to medical illnesses and diseases. It has been hypothesized, for example, that the alexithymic deficit in the cognitive processing of emotions leads to a focusing on, and amplification of, the somatic sensations accompanying emotional arousal, and/or to physical action as an immediate response to unpleasant arousal (Barsky and Klerman, 1983; Lane and Schwartz, 1987; Taylor et al., 1997). This is thought to explain the proneness to somatization among high alexithymia individuals (De Gucht and Heiser, 2003; Nakao et al., 2002), as well as their tendency to regulate tension through compulsive behaviors such as binge-eating and abuse of alcohol or drugs (Kauhanen et al., 1992; Pinaquy et al., 2003); such behaviors are risk factors for disease. However, it is primarily the difficulty identifying feelings facet of alexithymia that is associated with somatization (Mattila et al., 2008), whereas the externally oriented thinking facet is associated more with lower attention to internal bodily states (Davydov et al., 2013). When it is simply the primary object of the emotion schema that has been dissociated (e.g., conflict over intense anger toward an abusive spouse), the mind may try to repair the dissociation by using a part of the body to organize the schema, thereby creating a conversion symptom with symbolic meaning. Thus, in the same year that Lane et al. (1997) proposed the ‘blindsight’ model of alexithymia, and focused attention on the vertical axis of the brain to address the physiological dysregulation that may link alexithymia and adverse medical outcomes, Bucci (1997b) proposed that the failure to symbolize emotions at a cognitive level results in physiological dysregulation that might link alexithymia with illness and disease. One of us (Taylor, 1992) had earlier formulated a ‘dysregulation model of disease’ in which prolonged emotion dysregulation as a result of psychological conflict or deficits in the mental representation of emotions may cause perturbations and changes over time in the rhythmic functioning of other biological subsystems; if sustained, such changes might initiate a transition from health to illness or disease. Bucci’s proposal that the connections between words, images, and subsymbolic elements in emotion schema can be disrupted by trauma, and thereby permit prolonged physiological activation, is consistent with Krystal’s hypothesis that alexithymia and increased vulnerability to somatic disorders may result from affect regression induced by psychic trauma.

6. Measurement of alexithymia in empirical research As indicated by Lane et al. (2015a), much of the empirical research on alexithymia has measured the construct with the TAS20, which was developed by us more than two decades ago (Bagby et al., 1994a,b) and is currently the most widely used measure of alexithymia. In Section 3 of their article, however, Lane et al. question whether this scale is a valid measure of alexithymia in individuals who resemble those described by Nemiah and Sifneos. They raise the following issues: First, they doubt that individuals with impaired affect awareness can accurately rate themselves on this lack of awareness on a self-report scale. Second, because the TAS-20 correlates positively with self-reported negative affect, they argue that this “clearly conflicts with the original description of alexithymia as a severe affective deficit including a deficit in the description of affective distress” (p. 596). Third, they declare that most studies using the TAS-20 involve healthy individuals. And fourth, they speculate that “some limitation of the TAS-20 is leading to a failure to detect an association with adverse medical outcome that actually exists” (p. 597). These assertions about measurement of alexithymia with the TAS-20 are quite misleading as some relevant studies have been omitted. We now comment on the four issues, but first make some general comments about the development of the TAS-20.

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6.1. Development of the TAS-20 Lane et al. (2015a) assert that the creation of the TAS-20 was guided by the theory “that alexithymia is a problem in the verbal description (readout or report) of experience (Taylor et al., 1997), analogous to an anomia that reflects a continuum in the population” (p. 597). This is incorrect. To the contrary, when we developed the TAS-20 and its earlier 26-item version, we were guided primarily by Nemiah et al.’s (1976) description of the features they had observed among patients in clinical interviews, which we outlined in Section 4, and were mindful also of the distinction they made between emotions and feelings. It is obvious from an examination of the three factor scales of the TAS-20 that the items were written to assess salient components of the alexithymia construct, and certainly not to assess proneness to experience negative affect. The items on the first factor, Difficulty Identifying Feelings (DIF), assess the level of mental representation of affects (e.g., ‘I am often puzzled by sensations in my body’; ‘I have feelings that I can’t quite identify’). The items on the second factor, Difficulty Describing Feelings (DDF), assess the ability to find words to express feelings to others (e.g., ‘It is difficult for me to find the right words for my feelings’; ‘I am able to describe my feelings easily’ (negatively keyed)). The items on the third factor, Externally Oriented Thinking (EOT), assess operative thinking, including the level of interest in one’s inner emotional life (e.g., ‘I prefer to analyze problems rather than just describe them’ (negatively keyed); ‘I prefer talking to people about their daily activities rather than their feelings’ (negatively keyed)). Although the original 26 item TAS included a factor for assessing the capacity for fantasy and other imaginal activity (Taylor et al., 1985), subsequent evaluation of the scale revealed that the items on this factor, plus some additional items we wrote to assess imaginal processes, showed a social desirability response bias and/or low magnitude corrected item-total correlations and were therefore eliminated in the process of revising the scale. Nonetheless, the EOT factor correlates with other measures of fantasizing (Bagby et al., 1994b; Taylor and Bagby, 2013b; Tibon et al., 2005), which suggests that this factor indirectly assesses the impaired imaginal processes facet of the alexithymia construct. Thus, if we think of the measurement of alexithymia in relation to Lane et al.’s (2015a) proposed concept of affective agnosia, the DIF factor of the TAS20 assesses the agnosia aspect of alexithymia, and the DDF factor assesses the anomia aspect; but in addition, the EOT factor assesses the operative thinking (pensée opératoire) aspect of the construct. 6.2. Self-rating of alexithymia and a multimethod assessment approach It is possible that the self-report TAS-20 alone may not adequately assess capacities that individuals with severe alexithymia may not know they lack. As we have acknowledged elsewhere (Taylor and Bagby, 2004; Taylor et al., 1997, 2000), however, alexithymia research is enhanced by the use of a multi-method approach to measuring the construct.6 Sifneos (1973) developed the observer-rated Beth Israel Hospital Psychosomatic Questionnaire (BIQ) for assessing alexithymia, but this instrument lacked adequate interrater reliability. Following suggestions of Sriram et al. (1988) for enhancing the psychometric properties of the BIQ, we developed a modified version with six items that assess affect awareness (AA) and six items that assess operative thinking (OT) (Taylor et al., 1997). The modified BIQ is administered as a semistructured interview, except by Japanese researchers who use a

6 We also use a multimethod approach for assessing alexithymia in our clinical work, including the TAS-20, a clinical interview, and measures of emotional intelligence and openness to experience.

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structured interview method, and it correlates positively with the TAS-20 (r ranges between 0.26 and 0.53) (Arimura et al., 2002; Bagby et al., 1994b; Lumley et al., 2005; Martínez-Sánchez, 1996; Meganck et al., 2011). We later developed the Toronto Structured Interview for Alexithymia (TSIA; Bagby et al., 2006), which also correlates positively with the TAS-20 in a variety of samples (r ranges between 0.31 and 0.68) (Bagby et al., 2006; Caretti et al., 2011; Grabe et al., 2009; Inslegers et al., 2013). In addition to factor scales for assessing DIF, DDF, and EOT, the TSIA contains a factor scale that assesses fantasizing and other imaginal processes (IMP); the DIF and DDF factors form a higher-order AA factor, and the EOT and IMP factors form a higher-order OT factor. Although a structured interview method proved more reliable than self-report questions for assessing the imaginal processes facet of the alexithymia construct, the items may not adequately capture wish fulfillment fantasies and fantasies referable to instinctual drives and feelings, which was the content emphasized by Krystal (1988) and Nemiah et al. (1976). An alternative method for assessing imaginal capacity is a performance measure, such as the Rorschach Reality-Fantasy Scale (RFS), which assesses the adaptive use, creation, and preservation of the psychoanalytic concept of potential space between reality and fantasy (Tibon et al., 2005). In a sample of 92 patients with inflammatory bowel disease (IBD; which is one of the classic psychosomatic diseases), the mean RFS score correlated positively with the TAS-20 total score (r = 0.60) and with scores on all three factor scales (r ranged between 0.43 and 0.64), which supports the restricted fantasy and concrete reality-oriented cognitive style components of alexithymia. The TAS-20 also correlates positively with the Rorschach Alexithymia Scale (in a combined IBD and psychiatric outpatient sample, r = 0.78), which uses three variables from the Rorschach Comprehensive System that are theoretically consistent with the alexithymia construct (Porcelli and Mihura, 2010). Positive correlations have also been reported between the TAS-20 and the Observer Alexithymia Scale (r ranged between 0.23 and 0.41) (Dorard et al., 2008; Lumley et al., 2005; Meganck et al., 2011). The findings that the TAS-20 correlates positively with structured interview, observer-rated, and performance-based measures of alexithymia, as well as evidence that the total scale and its three factor scales all correlate negatively with measures of closely related constructs (including psychological mindedness, needfor-cognition, affective orientation, emotional intelligence, and openness to experience) (Bagby et al., 1994b; Parker et al., 2001; Taylor and Bagby, 2000), provide strong support that the TAS-20 captures an impairment in experiencing and describing emotions and is a valid measure of the alexithymia construct.

6.3. Relations between alexithymia and negative affect Lane et al. (2015a) refer to a study by Leising et al. (2009), who found that participants with higher TAS-20 scores reported more emotions (particularly negative ones) and more different emotions during interviews than those with lower alexithymia scores. They overlook opposite findings from a later study by Wotschack and Klann-Delius (2013), who conducted interviews that included questions about emotion knowledge for six emotion terms (e.g., What is joy for you? How do your recognize joy in yourself and others?), autobiographical narratives about recent positive and negative events in the person’s life, and oral administration of form B of the Levels of Emotional Awareness Scale (LEAS; Lane et al., 1990). In this study, individuals with high scores on both the TAS20 and the self-report Bermond-Vorst Alexithymia Questionnaire (BVAQ; Vorst and Bermond, 2001) produced fewer negative and positive emotion words, fewer different types of emotion words, fewer synonyms for a target emotion (e.g., joy, fear, anger), and

fewer physiological-expressive terms to describe emotions during the interviews than individuals with low alexithymia scores. Lane et al. (2015a) also refer to a study by Marchesi et al. (2014), who found that differences in TAS-20 scores observed between various psychiatric patient groups and a nonpatient group disappeared after controlling for the effect of anxiety and depression severity. They seem to concur with Marchesi et al.’s conclusion that the TAS20 appears to be a measure of psychological distress. A contrasting view is offered by Lumley (2000), who opines that because of the limited ability of alexithymic individuals to regulate and resolve negative emotions stemming from stressful or conflicting events, “the negative affect remains unmodulated yielding a chronic, yet undifferentiated dysphoria” (p. 52). Lumley notes that although negative affect may contribute to some score elevation, in particular on the DIF and DDF factor scales, the TAS-20 can be differentiated from measures of negative affect, and that this alexithymia scale is not simply a proxy for negative affect. Indeed, Luminet et al. (1999) have shown that alexithymia is not merely equivalent to the construct of neuroticism, but is represented by a cluster of traits across the domains of the five-factor model of personality. Although some researchers report significant positive associations between the TAS-20 and measures of anxiety and depression (e.g., Makino et al., 2013), others have found nonsignificant correlations between the TAS-20 (or original 26-item TAS) and measures of anxiety and/or depression (e.g., Carton et al., 2008; Zunhammer et al., 2015). In several other studies, in which the investigators were mindful of the ostensible association between negative affective states (i.e., depression, anxiety) and alexithymia, measures of negative affect were modelled into the statistical equations in which TAS-20 scores were used to predict a variety of dependent variables, partialling or removing their shared variance with alexithymia from the model. Despite the removal of this variance, positive and statistically significant associations were found between TAS-20 scores and a number of outcomes, including a deficit in remembering emotion words (Luminet et al., 2006), presence of Parkinson disease (Assogna et al., 2012), and dimensions of health-related quality of life (Mattila et al., 2010b). Furthermore, even though TAS-20 scores may be moderately inflated by negative affect and thus lack absolute stability, there is strong evidence of relative stability, which is a true indicator of whether a personality construct is a stable trait and not simply reflective of distress. For example, in an investigation of outpatients with major depression, Luminet et al. (2001) demonstrated a high degree of relative stability of TAS-20 scores by significant correlations between scores at treatment initiation and after 14 weeks of pharmacotherapy, and also by hierarchical regression analyses, which indicated that variance in follow-up TAS-20 scores could be predicted from scores at baseline over the effect contributed by baseline and follow-up depression scores. Similar findings were reported in an investigation of women with breast cancer (Luminet et al., 2007); and also in an investigation of alcoholic inpatients undergoing alcohol withdrawal even though there were large decreases in anxiety and depression (de Timary et al., 2008). In another study, relative stability of TAS-20 scores was demonstrated over a six month treatment period in a group of outpatients with functional gastrointestinal disorders; moreover, the stability of the alexithymia scores could not be accounted for by their associations with anxiety and depression scores (Porcelli et al., 2003). Lane et al. (2015a) also overlook a study in Finland in which Mattila et al. (2008) sought to answer the question of whether alexithymia is an independent determinant of somatization in the general population. With a large nationally representative sample comprising both young and old adults, alexithymia measured with the TAS-20 was associated with somatization independently of anxiety, depression, somatic diseases, and potentially confounding sociodemographic

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variables. The strongest association was between the DIF factor of the TAS-20 and somatization. Based on the findings in the studies by Leising et al. (2009) and Marchesi et al. (2014), Lane et al. (2015b) suggest in another recent article that “the TAS-20 is a measure of distress, not an impairment in the ability to experience and express distress” (p. 399). This is a confusing statement as it ignores the distinction that Nemiah and Sifneos made between emotions and feelings. As Lane et al. would surely agree, individuals with high degrees of alexithymia are impaired in their ability to experience and express distressing and other subjective feelings, but that does not mean that they do not experience emotional distress. The distress may be communicated as somatic sensations or symptoms (Taylor et al., 1992), or expressed through impulsive behaviors such as substance use (Kauhanen et al., 1992) or bingeing on food (Pinaquy et al., 2003), which may serve to downregulate emotional arousal. Indeed, it is evident from Sifneos and Nemiah’s descriptions of patients’ affective experience that the deficit in affect awareness is not an absence of emotions or a total failure to speak of feelings, but an inability or difficulty in elaborating feelings. Sifneos (1967) noted that these patients commonly mention anxiety and complain of depression, and may also talk about nervousness, agitation, restlessness, irritability, and tension (i.e., negative affects). Nemiah et al. (1976) also reported that “Although many individuals may initially speak of being ‘nervous’, or ‘sad’, or ‘angry’, if they are pressed to describe their feelings further and to tell the examiner what being ‘sad’ or ‘nervous’ or ‘angry’ feels like, it rapidly becomes apparent that they are totally unable to do so” (p. 431). Nemiah and Sifneos (1970) (Sifneos, 1967) described patients who, when asked if they were upset or angry, gave responses such as “I have a tight sensation in my throat”; “a dead feeling through my stomach”; and “I could see my muscles twitching”. They observed also that alexithymic patients on occasion have sudden outbursts of rage or crying without any premonitory feeling or fantasy (Nemiah et al., 1976). We have made similar observations to those of Sifneos and Nemiah in our own clinical work, and in earlier contributions we provided some examples of alexithymic patients who spoke of feeling upset, nervous, agitated, lonely, furious, or emotionally distressed, but were unable to elaborate further on their affective experience (Taylor, 1994; Taylor and Bagby, 2013a; Taylor et al., 1997). In our view, alexithymic patients are capable of experiencing emotions and of being distressed by their emotions, but they lack adequate mental representations to experience them as feelings they can easily identify and describe to the examiner. Sifneos (1967) suggested that perhaps as these patients grow older, and have become aware of their difficulties communicating with people, they may try to overcome them by describing physical sensations when they are asked how they feel. Similarly, Krystal (1979) observed that like the color-blind person, many of these patients are aware of their difficulty in recognizing and describing feelings, and use somatic sensations and other clues by which they infer what they cannot discern. It is therefore not surprising that measures of alexithymia would correlate positively with measures of neuroticism or negative affect, which typically include items that ask if the respondent experiences bodily sensations of emotion or unelaborated feelings such as nervousness, restlessness, agitation, tension, jitteriness, a lump in the throat, feeling depressed, upset, or scared. Pandey and Mandal (1996) demonstrated that the strength of the association between the TAS-20 and a measure of neuroticism was significantly reduced after controlling for the contribution of perceived autonomic arousal. 6.4. Variety of samples in alexithymia research Although Lane et al. (2015a) are correct that many studies using the TAS-20 have been conducted with student or healthy adult

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samples, they fail to acknowledge that a large number of studies have also been conducted with medical or psychiatric patient samples in which alexithymia was measured with either the TAS-20 or the original 26-item version of the scale. As reviewed in earlier contributions (Taylor and Bagby, 2012; Taylor et al., 1997), these studies included samples of patients with essential hypertension (Jula et al., 1999), functional gastrointestinal disorders (Porcelli et al., 2003), chronic pain disorders (Cox et al., 1994), eating disorders (Bourke et al., 1992), substance use disorders (Taylor et al., 1990), panic disorder (Galderisi et al., 2008), or posttraumatic stress disorder (Frewen et al., 2008c), a large proportion of whom had high alexithymia scores, just as groups of patients with some of these disorders in later studies cited by Lane et al. (2015a) had lower LEAS scores than some comparison groups. 6.5. Prediction of medical outcomes Contrary to Lane et al.’s (2015a) assertion, several studies have demonstrated that the TAS-20 can predict medical outcomes. For example, in the above mentioned investigation of patients with functional gastrointestinal disorders (Porcelli et al., 2003), baseline depression and TAS-20 scores emerged as significant predictors of treatment outcome; however, alexithymia was the stronger predictor. And in an investigation of patients who underwent laparoscopic cholecystectomy for treatment of gallstones, preoperative TAS20 scores predicted the persistence of gastrointestinal symptoms more strongly than did psychological distress, even after controlling for preoperative gastrointestinal symptoms (Porcelli et al., 2007). In a recent investigation of women who had undergone surgery for breast cancer and were followed for up to 12 months, the TAS-20 predicted the development of persistent postsurgical pain independently of anxiety and depression (Baudic et al., 2016). Lane et al. (2015a) mention a prospective study with 2000 middleaged Finnish men in which the 26-item version of the TAS predicted all-cause mortality over a period of 5.5 years, particularly violent death (Kauhanen et al., 1996). Even though alexithymia theory postulates that emotions that are not represented mentally may be expressed somatically and through actions, Lane et al. (2015a) are critical because “the study does not disentangle whether the TAS captured a problem in ‘actions’ (behavior) or ‘organs’ (pathophysiology)” (p. 597). They seem unaware that the mortality rate of the sample was examined subsequently over an average followup period of 20 years. After adjusting for biological, behavioral, and psychosocial factors, the risk of death from cardiovascular disease increased by 1.2% for every 1-point increase in scores on the TAS (Tolmunen et al., 2010). 7. The levels of emotional awareness construct 7.1. Affect awareness and pensée opératoire As we indicated in Section 3, and have outlined in previous publications (Taylor, 2000; Taylor et al., 1997), we find Lane and Schwartz’s (1987) conceptualization of stages in normal affect development helpful for understanding individual differences in affect awareness. But in our opinion, Lane et al.’s (2015a) emphasis on the levels of emotion awareness construct actually limits the theory, measurement, and treatment of alexithymia. The concept of affective agnosia certainly links well with the developmental model of levels of emotional awareness, which in turn maps onto Lane et al.’s (2015a) hierarchical model of the neural substrates of emotional experience. And their hypothesis that affective agnosia involves a failure to engage areas of the medial prefrontal lobe, in particular the rostral anterior cingulate cortex (rACC), the dorsal ACC, and the dorsomedial prefrontal cortex, is supported partly by findings from some (but not all) studies suggesting that the neural

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correlates of alexithymia include reduced activation in the ACC and the right medial prefrontal cortex when responding to emotioninducing stimuli (e.g, Frewen et al., 2008a; Moriguchi et al., 2006). However, as we outlined above, the alexithymia construct includes a restricted imagination and an externally oriented cognitive style, and is therefore a broader construct than the levels of emotional awareness construct. This difference is emphasized by Lumley et al. (2005) who point out that “Emotional awareness includes attending to, identifying, and correctly labeling emotions in oneself and in others, but it does not include the cognitive components included in the broader construct of alexithymia” (p. 331). Lane et al. (2015a) are well aware that the development of emotional awareness in infancy and early childhood requires the assistance of another person, who is usually the primary caregiver (most often the mother). They consider emotional awareness to be a separate line of development from other domains of cognition. However, they fail to give attention to the child’s capacity for imagination, which develops in tandem with the development of emotional awareness and also plays an important role in affect regulation. And like emotional awareness, the development of the imaginal capacity is dependent on the child’s interactions with affectively engaged primary caregivers. As we outlined almost two decades ago (Taylor et al., 1997), normal affect development requires attunement of the mother to the behavioral emotional expressions of her infant, the mother’s containment and regulation of the infant’s emotional states, and transformation of the infant’s sensations and primitive emotions through her own cognitive processes into meaningful affects and other aspects of experience that can be conveyed back to the infant. With the emergence of symbolization and language during the second year of life, the child’s level of subjective awareness gradually increases as the parents teach words and meanings for their child’s somatic emotional expressions and other bodily experiences. The line of development of an imaginal capacity proceeds from the infant’s formation of images of the mother (which become linked to subsymbolic sensory experiences),7 to the creation of a transitional object (such as a soft toy or blanket, which is a sensation-dominated object before it comes to symbolically represent the mother), to “the 5year-old’s creation of fantasy play that reflects his own subjective world and his understanding of the concepts of mental states and mind” (Mayes and Cohen, 1992; p. 41). Fantasies, dreams, play, and interests involve affects and serve some of the affect regulatory functions initially provided by the primary caregivers; they play an important role in personality development and in the selfregulation of affects throughout life. Imaginative play has been described as one of the most important developmental processes through which children learn to integrate affect, cognition, and action (Izard and Kobak, 1991). Indeed, as the philosopher Susanne Langer argued, the capacity for imagination allows humans to create explicit meanings out of emotions and thereby defer immediate action (Browning, 2006). Children who are unable to engage in imaginative play show degrees of failure in integrating cognitions with emotions, as well as disturbances in the symbolic function of fantasy and an inability to identify with the feelings of others (Galenson, 1984). It is not surprising that arrests in affect development are invariably accompanied by arrests in the development of the imaginative capacity, and that alexithymic individuals manifest both types of deficit. Furthermore, the failure to link feelings with fantasies and to reflect on inner experience pushes the mind toward a preoccupation with the details of external events, which is characteristic of pensée opératoire (Krystal, 1979).

7 Bucci (1998) considers images pivotal in linking words with subsymbolic elements within emotion schemas.

7.2. The levels of emotional awareness scale Although the LEAS (Lane et al., 1990) may adequately assess the levels of emotional awareness construct and the continuum between affective agnosia and anomia, it “was not created as a measure of alexithymia per se” (Lane et al., 1998b, p. 382), and was recently described simply as “a performance measure of the ability to put emotions into words” (Lane et al., 2015b; p. 399). Thus researchers such as Subic-Wrana et al. (2001) are incorrect in referring to the LEAS as “a new alexithymia test” (p. 176). The scoring system of the LEAS evaluates the structure of experience and not its content, and assigns scores based on the use of words that convey the degree of differentiation of emotion. One could infer that the respondent’s imagination is involved in thinking about his or her anticipated feelings and those of another person in each of the 20 scenes in the test, but there is no direct scoring of the respondent’s imaginal capacity or tendency toward an externally oriented style of thinking. Notwithstanding low correlations reported between the TAS20 and the LEAS (around r = −0.20), theoretically alexithymia and emotional awareness are overlapping constructs. Indeed, several studies that have used both the LEAS and the TAS-20 (or TAS-26) have reported similar findings for the two measures. For example, higher alexithymia scores and lower emotional awareness scores have been reported in cigarette smokers seeking help for cessation (Carton et al., 2008), and are associated with reduced accuracy on verbal and nonverbal emotion recognition tasks (Lane et al., 1996). In another study, patients with chronic somatoform pain disorders had significantly lower emotional awareness scores and higher alexithymia scores than a matched healthy control group (Zunhammer et al., 2015), In separate studies, but with the same sample of patients with posttraumatic stress disorder, Frewen et al. (2008b,c) reported higher alexithymia scores and lower emotional awareness scores than in a non-psychiatric control group. However, despite the negative relation between the TAS-20 and the LEAS, both measures correlated negatively with activation in the ventral ACC during trauma-script imagery (Frewen et al., 2008b,c). Divergent findings have also been reported in some other studies that suggest that the TAS-20 and LEAS measure different aspects of emotional functioning. Whereas patients with generalized anxiety disorder (GAD) score higher on the TAS-20 than individuals without GAD (Mennin et al., 2005), contrary to predictions, NovickKline et al. (2005) found that patients with GAD scored significantly higher than controls on the LEAS. And whereas in a sample of pregnant women alexithymia was associated with low relationship satisfaction (Taylor et al., 2014), Croyle and Waltz (2002) found that a higher level of emotional awareness was associated with lower relationship satisfaction in women. Frewen et al. (2008b) and Novick-Kline et al. (2005) offer some possible explanations for these discrepant findings, including method variance, social desirability response bias, the possibility that the LEAS measures being skilled at emotional verbiage rather than at awareness of one’s emotions, and that high levels of emotional awareness may not always be adaptive. These authors also refer to a study by Lundh et al. (2002), who in a sample of undergraduate students observed two subgroups that scored inconsistently on the TAS-20 and LEAS; one group scored low on both measures, and the other group scored high on both measures. While Lane et al. (2015a) focus their attention on the low associations typically found between the LEAS and TAS-20 scores, it is important to note that the LEAS also tends to correlate weakly with other alexithymia measures. Lumley et al. (2005), for example, not only found the TAS-20 to be unrelated to the LEAS, but the LEAS was also not related to the Observer Alexithymia Scale (Haviland et al., 2000) and the Modified BIQ (Bagby et al., 1994b), with correlations that ranged from −0.20 to +0.08 across the var-

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ious alexithymia scales and subscales. A similar pattern of results has also been reported for the related construct of emotional intelligence (EI). Lumley et al. (2005) found low or non-significant correlations between the LEAS and both self-report and performance measures of EI. Ciarrochiet al. (2003), using an earlier version of the same performance measure of EI, found a very low correlation (r = 0.15) between the total LEAS and total EI scores. A more recent study, using youth versions for the LEAS and the performance measure of EI (Veirman et al., 2011), found non-significant to low correlations between the LEAS and the various EI scales and subscales (r = 0.02 to 0.19). For a scale that was developed to assess individual differences in emotional awareness, it is also peculiar, from a construct validity perspective, that the LEAS does not correlate with the dimensional traits located in basic universal models of personality. As we have noted in detail elsewhere (Taylor and Bagby, 2013b), individual differences in identifying and differentiating feelings should be expected to be related to some basic personality dimensions. Although Lane et al. (1990) reported a positive association between the total LEAS and an openness to experience inventory, Ciarrochi et al. (2003), for example, found no significant correlations between total LEAS and any of the dimensions in the five-factor model of personality. Veirman et al. (2011) report similar results, with nonsignificant or low correlations (r =0.01 to 0.17) between the LEAS and the five-factor personality dimensions. Clearly further empirical investigations are needed to illuminate the relation between the alexithymia construct and the levels of emotional awareness construct. It would be important to use multiple measures of alexithymia and to include a measure of imaginal functioning. In a recent study with a university student sample, for example, the LEAS correlated weakly with the TAS-20 (r = −0.20), but more strongly with the TSIA (r = −0.47) (Lichev et al., 2014); future research should also focus on using clinical samples.

8. Alexithymia and the concept of mentalization Lane et al. (2015a) argue that scientific developments since the 1970s, including the concept of ‘theory of mind’ or mentalization, and new knowledge about the brain and emotion, make it not only possible, but even necessary, to expand the alexithymia construct. In their view these advances lead to a formulation that “permits a shift to a perspective that verbal behavior is an indicator of the problem rather than the primary problem itself” (p. 596). Although we fully agree that scientific developments have increased and will continue to advance our understanding of alexithymia, in our opinion the verbal behavior aspect of alexithymia has always been considered an indicator of a problem rather than the primary problem itself; examples of this are Sifneos’s (1967) speculation that difficulty finding appropriate words to describe feelings might reflect an emotional agnosia, and our conceptual idea that alexithymia reflects a deficit in the processing and regulation of emotions by means of mental representations (Taylor et al., 1997). Vanheule et al. (2011) also have emphasized that this conceptualization of the construct “means that alexithymia is a marker of an underlying process, from which it should never be separated” (p. 88). In discussing ‘theory of mind’ or mentalization, Lane et al. (2015a) note that these concepts were introduced six years after the term ‘alexithymia’ was coined. The concept of mentalization was actually introduced in the 1960s by French psychoanalysts in an attempt to understand the role of pensée opératoire in psychosomatic illness (Fain and Marty, 1964; Luquet, 1981; Marty, 1991). Mentalization referred to the linking of somatic affect and drive excitations with mental representations, and is thus a process similar to Bucci’s (1997a) concept of referential activity, provided

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one recognizes that the subsymbolic system in Bucci’s model operates with its own organizing principles and does not have to be transformed to become part of psychic life (Bouchard and Lecours, 1999; Bucci, 1999). In the late 1990s, Lecours and Bouchard (1997) extended the contributions of Marty and other French analysts by proposing a hierarchical conceptual model with levels of mentalization of increasing complexity; this model shows some similarities with Krystal’s (1974) theory of affects and Lane and Schwartz’s (1987) hierarchical model of levels of emotional awareness. It was around that time that Fonagy and Target (1997) (Fonagy et al., 2002) adopted the concept of mentalization and defined it more broadly as the capacity to be aware of and to think about feelings and other mental states (e.g., beliefs, desires, intentions) in oneself and others. Fonagy (2000) indicated that he preferred the term mentalization (or reflective function) to ‘theory of mind’. More recently, Fonagy et al. (2012) described mentalization as a multifaceted construct with cognitive and affective components, and indicated that mentalizing is “not a static and unitary skill”, but a “dynamic capacity that is influenced by stress and arousal, particularly in the context of specific attachment relationships” (p. 19). Fonagy et al. (2012) also described mentalization as a form of social cognition, which they defined as “the imaginative mental activity that enables us to perceive and interpret human behavior in terms of intentional mental states (e.g., needs, desires, feelings, beliefs, goals, purposes, and reasons)” (p. 4). Clearly Fonagy et al.’s (2012) understanding of mentalization, and the way it is applied by Lane et al. (2015a), is very different from how it was conceptualized originally by French psychoanalysts (Fain and Marty, 1964; Luquet, 1981; Marty, 1991). As we outlined in another contribution (Taylor and Bagby, 2013a), alexithymia is a much narrower construct that corresponds most closely with one specific component of mentalization, which involves identifying, processing and communicating affects and is referred to as mentalized affectivity (Fonagy et al., 2002; Jurist, 2005). We emphasized that the alexithymia construct does not encompass the cognitive aspects of the broad mentalization construct, such as ‘thinking about thinking’ and understanding that others have thoughts, feelings, beliefs, and desires that are different from one’s own. Experimental investigations of the role of ‘theory of mind’ in alexithymia, including Lane et al.’s (2015b) recent investigation of patients with somatoform disorders and medical controls, use ‘theory of mind’ tasks that test the ability to detect mental states in others, not in oneself. Lane et al. (2015a) refer to that recent study and note that after controlling for self-reported positive and negative affect, the LEAS correlated positively with several measures of ‘theory of mind’ whereas the TAS-20 did not. Some individuals with a high degree of alexithymia might be impaired in their ability to read the intentions, desires, and emotional states of others, but measures of alexithymia were not designed to assess this ability as it is not included in the definition of the alexithymia construct. Nonetheless, several investigations have found associations between alexithymia and poor empathic abilities (e.g., Grynberg et al., 2010; Moriguchi et al., 2007; Taylor and Bagby, 2000), which is consistent with clinical observations (Krystal, 1979) and suggests that impaired empathy is an important correlate of alexithymia. There is empirical evidence also that alexithymia negatively affects the quality of interpersonal relationships (Foran and O’Leary, 2013; Humphreys et al., 2009; Vanheule et al., 2007).

9. Treatment of alexithymia Lane et al.’s (2015a) proposal that the concept of affective agnosia advances the treatment of alexithymia seems based on a mistaken impression that the usual psychotherapeutic approach has been simply to help patients put emotions into words. They

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assert that “a variety of treatment methods that have been created in recent years that promote mental representation of emotion. . .. . . have not been applied to the alexithymia context to date” (p. 606). They suggest that techniques used in dialectical behavior therapy, mentalization-based therapy, and emotion focused therapy are “potentially applicable to the treatment of alexithymia/affective agnosia” as they “promote the ability to know what one is feeling” (p. 606). They also refer to new approaches used by therapists in Germany to engage implicit emotional processes, such as art therapy, dance therapy, massage and other body-based treatments. In our view, these opinions reflect a failure to review and integrate the existing literature on the treatment of alexithymia. The unsuitability of the classic psychodynamic model of drive and defenses for treating patients with alexithymia was pointed out first by Sifneos (1975) and Nemiah et al. (1976); they therefore recommended supportive psychotherapy. Krystal (1979), however, developed a modified form of psychodynamic psychotherapy, which includes techniques for helping patients to both recognize and verbalize their emotions. We described these techniques and some additional strategies in detail almost two decades ago (Taylor et al., 1997), so there is no need to repeat them in this Commentary. We indicated that “In general, these modifications focus on the form, rather than on the content of the patient’s communications, and they attempt to enhance the patients’ awareness of deficits in the way they process and experience emotions” (Taylor et al., 1997; p. 250). Moreover, consistent with Lane and Schwartz’s (1987) development model of levels of emotional awareness, we emphasized that “The therapeutic approach for alexithymia patients attempts to elevate emotions from the level of perceptually bound experience (a world of sensation and action) to a conceptual representational level (a world of feelings and thoughts) where they can be used as signals of information, thought about, and sometimes communicated to others” (Taylor et al., 1997; p. 252). This approach corresponds to enhancing mentalization in the way this concept was defined by Marty (1991) and other French psychoanalysts (Fain and Marty, 1964; Luquet, 1981). Most clinicians treating alexithymic patients with psychotherapy employ some or all of the techniques described by Krystal (1979), or similar techniques adapted from cognitive-behavioral, mentalization-based, or emotion-focused therapies. There are several single case reports of patients whose alexithymia was reduced using these approaches (e.g., Dimaggio et al., 2011; Kennedy and Franklin, 2002; Taylor, 2012; Vanheule et al., 2011). In addition, there is empirical evidence from some preliminary studies that the level of alexithymia can be reduced by modified group psychotherapy. In one of these studies, which was conducted with post-myocardial infarction patients, the reductions in alexithymia were maintained over a 2-year follow-up period; and during those two years, patients with decreased alexithymia following group therapy experienced fewer cardiac events (re-infarction, sudden cardiac death, or re-hospitalization for rhythm events or severe angina) than patients whose alexithymia remained unchanged (Beresnevaite, 2000). In another study, even after controlling for the influence of changes in depressive symptoms, alexithymia, particularly the DIF facet of the construct, decreased in psychiatric outpatients who participated in a comprehensive group therapy program that was predominantly guided by cognitive-behavioral theory, but included participation in groups with various orientations including psychodynamic and interpersonal therapy that focused on a range of different topics (Ogrodniczuk et al., 2012). As described by the researchers, “The groups [were] co-led by one dedicated group leader (e.g., a psychoanalytically-trained psychiatrist for the psychodynamic group) and one trainee (e.g., a mental health nurse)” (p. 282). The decreased alexithymia in these psychi-

atric patients was associated with improvements in interpersonal problems. Given their proposal that “affective agnosia constitutes a supramodal agnosia consisting of dysfunction in the activation and/or use of high level mental representations of emotional states and their meaning”, Lane et al. (2015a) conclude that clinical intervention should place “special emphasis on using emotional information as opposed to only expressing emotions in words” (p. 608). Clinicians and psychotherapy researchers are well aware that “Alexithymia involves an impaired capacity to construct mental representations of emotions” (Ogrodniczuk et al., 2005; p. 211), and that interventions need to focus not only on developing that capacity but also on increasing patients’ ability to use emotional information to guide thinking and behavior (Krystal, 1979; Taylor et al., 1997). This ability is assessed by a negatively keyed item on the EOT subscale of the TAS-20 (‘I find examination of my feelings useful in solving personal problems.’), and by several items on the EOT subscale of the TSIA (‘Do you find examining your feelings useful when attempting to solve personal problems?’; ‘Do you often rely on your feelings to help guide your actions?’; ‘Do you think about past emotional experiences to help you cope with more recent emotional problems?’; ‘Do you learn much about yourself on the basis of your feelings?’). As Lane et al. (2015a) note, the ability to use emotional information is one of the components of the emotional intelligence construct. In a study with a young adult sample, the TAS-20 correlated negatively with the Using Emotions subscale of a measure of ability emotional intelligence (r = −0.32, p < 0.001, N = 140), whereas the LEAS failed to correlate (r = 0.02, ns, N = 140) (Lumley et al., 2005). Although these results need to be replicated with clinical samples, they suggest that assessing levels of emotional awareness alone may not sufficiently inform therapists about their patients’ capacity to use emotions to guide thinking and behavior. Indeed, in contrast to the TAS-20 and the TSIA, the LEAS does not include scoring for the ability to use emotions. We agree with Lane et al. (2015a) that art therapy and bodybased approaches may be useful in making alexithymic patients more aware of their emotions and for facilitating the conscious experiencing of feelings that can be labeled and described to others. Such approaches are not new, but have been recommended and used by some therapists for several decades. More than thirty years ago, Taylor (1984) suggested several behavioral techniques, such as relaxation training, autogenic training, meditation, guided imagery, and hypnosis, that might help alexithymic patients increase their awareness of relations between the bodily sensations of emotions and environmental triggers; he also referred to the use of biofeedback as an adjunct to psychotherapy with somatizing alexithymic patients. Moreover, as part of group therapy in the above mentioned study with post-myocardial infarction patients, participants were taught Jacobson’s technique of progressive relaxation to help focus their attention on inner experience; participated in role playing and nonverbal communication (e.g., mimicry and eye communication) to improve their ability to identify and communicate subjective feelings; and listened to music while in a relaxed state to enhance imaginal activity (Beresnevaite, 2000). Although Lane et al. (2015a) briefly mention that Ruesch (1948) posited trauma as one potential cause of the impaired mental representation of emotion in psychosomatic patients, their failure to consider Krystal’s (1979,1988) contributions to the field results in a major omission in their discussion of implications of the concept of affective agnosia for treatment. As we indicated in Section 5.1, Krystal attributed alexithymia to early childhood trauma that interrupts the normal development of affects, or to catastrophic adult trauma that triggers a regression of affects to a preconceptual level of organization. Because the mind of the infant or young child is not sufficiently developed to mobilise psychological defenses to moderate the impact of psychic trauma, and the adult’s defenses are

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overwhelmed by the intensity of the traumatic event, traumatic experiences and the associated intense emotions are not represented mentally, but are managed by ‘primal repression’ as opposed to ‘repression proper’ (Freud, 1915). Whereas repression proper is a defensive process that rejects from the conscious mind emotional, instinctual, and other representations, primal repression, as we indicated in Section 3, forecloses traumatic experience from the mind and thus prevents the formation of mental representations of the experience (Cohen and Kinston, 1983; Kinston and Cohen, 1986, 1988). These unmentalized emotional experiences are often associated with alexithymia (Cohen, 1991; Krystal, 1990), and are increasingly seen as having an important role in psychopathology and somatic illness (Busch and Sandberg, 2014; Mitrani, 1995; Taylor, 2010). As several authors point out, trauma-related emotions are encoded on a sensorimotor, enactive level rather than in a semantic and linguistic way, but their presence is manifest through somatic symptoms, physiological reactions, or mindless actions such as compulsive drug abuse and bingeing on food (Cohen and Kinston, 1983; Krystal, 1988; Taylor et al., 1997). Although Freud gave greater attention to conflicts over instinctual drives than to traumatic emotions in psychopathology, as we outlined in Section 3, his concept of primal repression is analogous to affective agnosia since the traumatic emotions are not represented psychically and are therefore inaccessible to consciousness, and their meaning is unknown to the person. It is perhaps because of primal repression that some authors conceptualize alexithymia both as a massive defense against unbearable emotions and as a deficit in the mental representation of emotions (see, Taylor and Bagby, 2013a). As psychotherapy of the alexithymic patient proceeds, there is potential for activation of intense trauma-related emotions, which can be overwhelming for the patient as they emerge from primal repression (Taylor, 2012). If this phase of treatment is reached, it requires a relationship in which the therapist contains and helps the patient tolerate the emotions, and aids the patient in linking them with images and words and understanding their meaning.

10. Conclusion The concept of affective agnosia is a reminder that alexithymia is not simply a difficulty in finding words for feelings, but involves an impairment in the mental representation of emotions, which limits the capacity to regulate emotions through cognitive processes. Deciding whether a patient has the anomia or the agnosia version of alexithymia, however, implies a categorical conceptualization, which is inconsistent with Lane et al.’s (2015a) description of different levels of emotion representation with different degrees of organization and complexity. Nemiah and Sifneos may have regarded alexithymia as a categorical construct, but Krystal (1979) reported that “Most patients are able to experience some feelings some of the time” and declared that alexithymia is not an “all or nothing” phenomenon (p. 24). The results of empirical investigations support a dimensional conceptualization of alexithymia (Mattila et al., 2010a; Parker et al., 2008), and therefore the view that it is preferable to conceptualize different degrees of alexithymia, rather than define subtypes. Following Krystal’s (1988, 1997) ideas about the impact of trauma on affect development and affect regression, the degree of alexithymia in any person is likely to reflect the extent of trauma experienced by the person during childhood or as an adult, and whether or not an attachment figure was available to contain and modulate the person’s distress. Milder degrees of alexithymia likely reflect deficiencies in the parents’ attunement and responsiveness to the child’s affects; severe degrees of alexithymia may reflect more catastrophic traumas such as parental neglect, physical or

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sexual abuse, and exposure to military combat or natural disasters. Janet (1889) believed that it is the ‘vehement emotions’ that accompany extreme experiences that makes them traumatic. Although Freud’s concept of primal repression is seldom used by psychoanalysts, it is an adaptive response that keeps such emotions from being represented, while they continue to exert an indirect effect on the person’s body and mental life. The application of primal repression to alexithymia (Cohen, 1991; Krystal, 1990) is consistent with Bucci’s (1997a, 1997b) conceptualization of trauma-induced dissociation within and among the symbolic and subsymbolic elements of emotion schemas, and directs clinicians to consider patients’ constricted cognitive functioning and somatic or behavioral symptoms as possible manifestations of trauma. Primal repression thus has implications for treatment beyond those of the concept of affective agnosia. It should not reduce attention to the anomia aspect of alexithymia, however, as there is experimental evidence from studies with healthy individuals that putting feelings into words (‘lexithymia’) enhances emotion regulation, partly by reducing amygdala activation in response to emotional stimuli (Burkland et al., 2014; Lieberman et al., 2007).

References Arimura, T., Komaki, G., Murakami, S., Tamagawa, K., Nishikata, H., Kawai, K., Nozaki, T., Takii, M., Kubo, C., 2002. Development of the structured interview by the modified edition of the Beth Israel Hospital Psychosomatic Hospital Questionnaire (SIBIQ) in Japanese edition to evaluate alexithymia. Jpn. J. Psychosom. Med. 42, 259–269. Assogna, F., Palmer, K., Pontieri, F.E., Pierantozzi, M., Stefani, A., Gianni, W., Caltiagirone, C., Spalletta, G., 2012. Alexithymia is a non-motor symptom of Parkinson disease. Am. J. Geriatr. Psychiatry 20, 133–141, http://dx.doi.org/10. 1097/JGP.0b013e318209de07. Bagby, R.M., Parker, J.D.A., Taylor, G.J., 1994a. The Twenty-Item Toronto Alexithymia Scale–I. Item selection and cross-validation of the factor structure. J. Psychosom. Res. 38, 23–32, http://dx.doi.org/10.1016/0022-3999(94)900051. Bagby, R.M., Taylor, G.J., Parker, J.D.A., 1994b. The Twenty-Item Toronto Alexithymia Scale–II: Convergent, discriminant, and concurrent validity. J. Psychosom. Res. 38, 33–40, http://dx.doi.org/10.1016/0022-3999(94)90006-X. Bagby, R.M., Taylor, G.J., Parker, J.D.A., Dickens, S.E., 2006. The development of the Toronto Structured Interview for Alexithymia: item selection, factor structure, reliability and concurrent validity. Psychother. Psychosom. 75, 25–39, http:// dx.doi.org/10.1159/000089224. Barsky, A.J., Klerman, G.L., 1983. Overview: hypochondriasis, bodily complaints, and somatic styles. Am. J. Psychiatry 140, 273–283, http://dx.doi.org/10.1176/ ajp.140.3.273. Basch, M.F., 1977. Developmental psychology and explanatory theory in psychoanalysis. Annu. Psychoanal. 5, 229–263. Baudic, S., Jayr, C., Albi-Feldzer, A., Fermanian, J., Masselin-Dubois, A., Bouhassira, D., Attal, N., 2016. Effect of alexithymia and emotional repression on postsurgical pain in women with breast cancer: a prospective longitudinal 12-month study. J. Pain 17, 90–100, http://dx.doi.org/10.1016/jpain.2015.10. 001. Beresnevaite, M., 2000. Exploring the benefits of group psychotherapy in reducing alexithymia in coronary heart disease patients: a preliminary study. Psychother. Psychosom. 69, 117–122, http://dx.doi.org/10.1159/000012378. Bouchard, M.-A., Lecours, S., 1999. Some comments on Bucci’s multiple code psychoanalytic psychology. Can. J. Psychoanal. 6, 261–270. Bourke, M.P., Taylor, G.J., Parker, J.D.A., Bagby, R.M., 1992. Alexithymia in women with anorexia nervosa. A preliminary investigation. Br. J. Psychiatr. 161, 240–243, http://dx.doi.org/10.1192/bjp.161.2.240. Browning, M.M., 2006. Neuroscience and imagination: the relevance of Susanne Langer’s work to psychoanalytic theory. Psychoanal. Q. 75, 1131–1159, http:// dx.doi.org/10.1002/j.2167-4086.2006.tb00070.x. Bucci, W., 1997a. Psychoanalysis and Cognitive Science: A Multiple Code Theory. Guilford Press, New York. Bucci, W., 1997b. Symptoms and symbols: a multiple code theory of somatization. Psychoanal. Inq. 17, 151–172, http://dx.doi.org/10.1080/07351699709534117. Bucci, W., 1998. Transformations of meanings in the analytic discourse: a strategy for research. Can. J. Psychoanal. 6, 233–260. Bucci, W., 1999. Response to the comments of Bouchard and Lecours. Can. J. Psychoanal. 7, 23–29. Bucci, W., 2002. From subsymbolic to symbolic −and back: therapeutic impact of the referential process. In: Lasky, R. (Ed.), Symbolization and Desymbolization. Essays in Honor of Norbert Freedman. Karnac, London, pp. 50–74. Bucci, W., 2008. The role of bodily experience in emotional organization. New perspectives on the multiple code theory. In: Anderson, F.S. (Ed.), Bodies in Treatment. Analytic Press, New York, pp. 51–76.

1018

G.J. Taylor et al. / Neuroscience and Biobehavioral Reviews 68 (2016) 1006–1020

Burkland, L.J., Cresell, J.D., Irwin, M.R., Lieberman, M.D., 2014. The common and distinct neural bases of affect labeling and reappraisal in healthy adults. Front. Psychol. 5, 221, http://dx.doi.org/10.3389/fpsyg.2014.00221. Busch, F.N., Sandberg, L.S., 2014. Unmentalized aspects of panic and anxiety disorders. Psychodyn. Psychiatry 42, 175–196, http://dx.doi.org/10.1521/pdps. 2014.42.2.175. Caretti, V., Porcelli, P., Solano, L., Schimmenti, A., Taylor, G.J., Bagby, R.M., 2011. Reliability and validity of the Toronto Structured Interview for Alexithymia in a mixed clinical and nonclinical sample from Italy. Psychiatry Res. 187, 432–436, http://dx.doi.org/10.1016/j.psychres.2011.02.015. Carton, S., Bayard, S., Jouanne, C., Lagrue, G., 2008. Emotional awareness and alexithymia in smokers seeking help for cessation: a clinical analysis. J. Smok. Cessat. 3, 81–91, http://dx.doi.org/10.1375/jsc.3.2.81. Ciarrochi, J., Caputi, P., Mayer, J.D., 2003. The distinctiveness and utility of a measure of trait emotional awareness. Personal. Individ. Differ. 34, 1477–1490, http://dx.doi.org/10.1016/SO191-8869(02)00129-0. Cohen, J., Kinston, W., 1983. Repression theory: a new look at the cornerstone. Int. J. Psychoanal. 65, 411–422. Cohen, J., 1985. Trauma and repression. Psychoanal. Inq. 5, 163–189, http://dx.doi. org/10.1080/07351698509533580. Cohen, J., 1991. Papers on primal repression. II: Alexithymia as a manifestation of primal repression. (Unpublished manuscript). Cox, B.J., Kuch, K., Parker, J.D.A., Shulman, I.D., Evans, R.J., 1994. Alexithymia in somatoform pain disorder patients with chronic pain. J. Psychosom. Res. 38, 523–527, http://dx.doi.org/10.1016/0022-3999(94)90049-3. Croyle, K.L., Waltz, J., 2002. Emotional awareness and couples’ relationship satisfaction. J. Marital Fam. Ther. 28, 435–444. Damasio, A.R., 1992. Aphasia. N. Engl. J. Med. 326, 531–539, http://dx.doi.org/10. 1056/NEJM199202203260806. Damasio, A., 2003. Looking for Spinoza. Joy, Sorrow, and the Feeling Brain. Harcourt, Orlando. Davydov, D.M., Luminet, O., Zech, E., 2013. An externally oriented style of thinking as a moderator of responses to affective films in women. Int. J. Psychophysiol. 87, 152–164, http://dx.doi.org/10.1016/j.ijpsycho.2012.12.003. De Gucht, V., Heiser, W., 2003. Alexithymia and somatisation. A quantitative review of the literature. J. Psychosom. Res. 54, 425–434, http://dx.doi.org/10. 1016/S0022-3999(02)00467-1. de Timary, P., Luts, A., Hers, D., Luminet, O., 2008. Absolute and relative stability of alexithymia in alcoholic inpatients undergoing alcohol withdrawal: relationship to depression and anxiety. Psychiatry Res. 157, 105–113, http:// dx.doi.org/10.1016/j.psychres.2006.12.008. Dimaggio, G., Carcione, A., Salatore, G., Nicolò, G., Sisto, A., Semerari, A., 2011. Progressively promoting metacognition in a case of obsessive-compulsive disorder treated with metacognitive interpersonal therapy. Psychol. Psychother. Theor. Res. Pract. 84, 70–83, http://dx.doi.org/10.1348/ 147608310X527240. Dorard, G., Berthoz, S., Haviland, M.G., Phan, O., Corcos, M., Bungener, C., 2008. Multimethod alexithymia assessment in adolescents and young adults with a cannabis use disorder. Compr. Psychiatry 49, 585–592, http://dx.doi.org/10. 1016/j.comppsych.2008.05.001. Dorpat, T.L., 1985. Denial and Defense in the Therapeutic Situation. Aronson, Northvale, NJ. Fain, M., Marty, P., 1964. Perspective psychosomatique sur la fonction des fantasmes. Rev. Franc¸. Psychoanal. 28, 609–622. Finkelnburg, R., 1870. Vortrag in der Nierdernheim Gessellschaft der Aertz. Klinische Wochenschrifte, 7, 449. Fonagy, P., 2000. Attachment and borderline personality disorder. J. Am. Psychoanal. Assoc. 48, 1129–1146, http://dx.doi.org/10.1177/ 00030651000480040701. Fonagy, P., Target, M., 1997. Attachment and reflective function: their role in self-organization. Dev. Psychopathol. 9, 679–700. Fonagy, P., Gergely, G., Jurist, E.L., Target, M., 2002. Affect Regulation, Mentalization, and the Development of the Self. Other Press, New York. Fonagy, P., Bateman, A.W., Luyten, P., 2012. Introduction and overview. In: Bateman, A.W., Fonagy, P. (Eds.), Handbook of Mentalization in Mental Health Practice. American Psychiatric Publishing, Washington, DC, pp. 3–42. Foran, H.M., O’Leary, K.D., 2013. The role of relationships in understanding the alexithymia-depression link. Eur. J. Personal. 27, 470–480, http://dx.doi.org/10. 1002/per.1887. Frank, A., 1969. The unremarkable and unforgettable: passive primal repression. Psychoanal. Stud. Child 24, 48–77. Freud, S., 1891. On Aphasia: A Critical Study. International Universities Press, New York, Translation by E. Stengel., 1953. Freud, S., 1915. Repression. Standard Edition 14, 141-158. Hogarth Press, London, 1957. Freud, S., 1916–1917. Introductory lectures on psychoanalysis (Parts I and II). Standard Edition, 15, 243–463. Hogarth Press, London, 1963. Freud, S., 1926. Inhibitions, symptoms, and anxiety. Standard Edition 20, 77–172. Hogarth Press, London, 1959. Freud, A., 1981. Anna Freud answers students’ questions. Bull. Anna Freud Centre 4, 31–36. Frewen, P.A., Dozois, D.J.A., Neufeld, R.W.J., Lanius, R.A., 2008a. Meta-analysis of alexithymia in posttraumatic stress disorder. J. Trauma. Stress 21, 243–246, http://dx.doi.org/10.1002/jts.20320. Frewen, P., Lane, R.D., Neufeld, R.W.J., Densmore, M., Stevens, T., Lanius, R., 2008b. Neural correlates of levels of emotional awareness during trauma

script-imagery in posttraumatic stress disorder. Psychosom. Med. 70, 27–31, http://dx.doi.org/10.1097/PSY.0b013e31815f66d4. Frewen, P.A., Lanius, R.A., Dozius, D.J.A., Neufeld, R.W.J., Pain, C., Hopper, J.W., Densmore, M., Stevens, T.K., 2008c. Clinical and neural correlates of alexithymia in posttraumatic stress disorder. J. Abnorm. Psychol. 117, 171–181, http://dx.doi.org/10.1037/0021-843X.117.1.171. Galderisi, S., Mancuso, F., Mucci, A., Garramone, S., Zamboli, R., Maj, M., 2008. Alexithymia and cognitive dysfunction in patients with panic disorder. Psychother. Psychosom. 77, 182–188, http://dx.doi.org/10.1159/000119738. Galenson, E., 1984. Influences on the development of the symbolic function. In: Call, J.D., Galenson, E., Tyson, R.L. (Eds.), Frontiers of Infant Psychiatry, vol. 2. Basic Books, New York, pp. 30–37. Grabe, H.J., Löbel, S., Dittrich, D., Bagby, R.M., Taylor, G.J., Quilty, L.C., Spitzer, C., Barnow, S., Mathier, F., Jenewein, J., Freyberger, H.J., Rufer, M., 2009. The German version of the Toronto Structured Interview for Alexithymia: factor structure, reliability, and concurrent validity in a psychiatric patient sample. Compr. Psychiatry 50, 424–430, http://dx.doi.org/10.1016/j.comppsych.2008. 11.008. Grynberg, D., Luminet, O., Corneilli, O., Grèzes, J., Berthoz, S., 2010. Alexithymia in the interpersonal domain: a general deficit in empathy? Personal. Individ. Differ. 49, 845–850, http://dx.doi.org/10.1016/j.paid.2010.07.013. Grynberg, D., Chang, B., Corneille, O., Maurage, P., Vermeulen, N., Berthoz, S., Luminet, O., 2012. Alexithymia and the processing of emotional facial expressions (EFEs): Systematic review, unanswered questions and further perspectives. PLoS One 7 (8), e42429, http://dx.doi.org/10.1371/journal.pone. 0042429. Haviland, M.G., Warren, W.L., Riggs, M.L., 2000. An observer scale to measure alexithymia. Psychosomatics 41, 385–392, http://dx.doi.org/10.1176/appi.psy. 41.5.385. Humphreys, T.P., Wood, L.M., Parker, J.D.A., 2009. Alexithymia and satisfaction in intimate relationships. Personal. Individ. Differ. 46, 43–47, http://dx.doi.org/ 10.1016/j.paid.2008.09.002. Inslegers, R., Meganck, R., Ooms, E., Vanheule, S., Taylor, G.J., Bagby, R., De Fruyt, F., Desmet, M., 2013. The Dutch language version of the Toronto Structured Interview for Alexithymia: reliability, factor structure and concurrent validity. Psychol. Belg. 53, 93–116, http://dx.doi.org/10.5934/pb-53-1-93. Izard, C.E., Kobak, R.R., 1991. Emotions system functioning and emotion regulation. In: Garber, J., Dodge, K.A. (Eds.), The Development of Emotion Regulation and Dysregulation. Cambridge University Press, Cambridge, pp. 303–321. Janet, P., 1889. L’automatisme Psychologique. Alcam, Paris. Jula, A., Salminen, J.K., Saarijärvi, S., 1999. Alexithymia: a facet of essential hypertension. Hypertension 33, 1057–1061, http://dx.doi.org/10.1161/01.HYP. 33.4.1057. Jurist, E., 2005. Mentalized affectivity. Psychoanal. Psychol. 22, 426–444, http://dx. doi.org/10.1037/0736-9735.22.3.426. Kauhanen, J., Julkunen, J., Salonen, J.T., 1992. Coping with inner feelings and stress: heavy alcohol use in the context of alexithymia. Behav. Med. 18, 121–126, http://dx.doi.org/10.1080/089642.89.1992.9936962. Kauhanen, J., Kaplan, G.A., Cohen, R.D., Julkunen, J., Salonen, J.T., 1996. Alexithymia and risk of death in middle-aged men. J. Psychosom. Res. 41, 541–549, http:// dx.doi.org/10.1016/S0022-3999(96)00226-7. Kennedy, M., Franklin, J., 2002. Skills-based treatment for alexithymia: an exploratory case series. Behav. Change 19, 158–171, http://dx.doi.org/10.1375/ bech.19.3.158. Kinston, W., Cohen, J., 1986. Primal repression: clinical and theoretical aspects. Int. J. Psychoanal. 67, 337–355. Kinston, W., Cohen, J., 1988. Primal repression and other states of mind. Scand. Psychoanal. Rev. 11, 81–105. Knapp, P., 1983. Emotions and bodily changes: a reassessment. In: Temoshok, L., Van Dyke, C., Zegans, L.S. (Eds.), Emotions in Health and Illness: Theoretical and Research Foundations. Grune and Stratton, New York, pp. 15–27. Krystal, H., Raskin, H., 1970. Drug Dependence. Wayne State University Press, Detroit. Krystal, H., 1968. Massive Psychic Trauma. International Universities Press, New York. Krystal, H., 1974. The genetic development of affects and affect regression. Annu. Psychoanal. 2, 98–126. Krystal, H., 1979. Alexithymia and psychotherapy. Am. J. Psychother. 33, 17–31. Krystal, H., 1982/83. Alexithymia and the effectiveness of psychoanalytic treatment. Int. J. Psychoanal. Psychother. 9, 354–378. Krystal, H., 1988. Integration and Self-healing: Affect, Trauma, and Alexithymia. Analytic Press, Hillsdale, NJ. Krystal, H., 1997. Desomatization and the consequences of infantile psychic trauma. Psychoanal Inq. 17, 121–150, http://dx.doi.org/10.1080/ 07351699709534116. Krystal, H., 1990. An information processing view of object-relations. Psychoanal. Inq. 10, 221–251, http://dx.doi.org/10.1080/07351699009533808. Lane, R.D., Schwartz, G.E., 1987. Levels of emotional awareness: a cognitive developmental theory and its application to psychopathology. Am. J. Psychiatry 144, 133–143, http://dx.doi.org/10.1176/ajp.144.2.133. Lane, R.D., Quinlan, D.M., Schwartz, G.E., Walker, P.A., Zeitlin, S.B., 1990. The Levels of Emotional Awareness Scale: A cognitive-developmental measure of emotion. J. Personal. Assess. 55, 124–134, http://dx.doi.org/10.1080/00223891. 1990.9674052.

G.J. Taylor et al. / Neuroscience and Biobehavioral Reviews 68 (2016) 1006–1020 Lane, R.D., Sechrest, L., Riedel, R., Weldon, V., Kasniak, A., Schwartz, G.E., 1996. Impaired verbal and nonverbal emotion recognition in alexithymia. Psychosom. Med. 58, 203–210. Lane, R.D., Ahern, G.L., Schwartz, G.E., Kaszniak, A.W., 1997. Is alexithymia the emotional equivalent of blindsight? Biol. Psychiatry 42, 834–844, http://dx.doi. org/10.1016/S0006-3223(97)00050-4. Lane, R.D., Reiman, E.M., Axelrod, B., Yun, L.-S., Holmes, A., Schwartz, G.E., 1998a. Neural correlates of levels of emotional awareness: evidence of an interaction between emotion and attention in the anterior cingulate cortex. J. Cogn. Neurosci. 10, 525–535, http://dx.doi.org/10.1162/089892998562924. Lane, R.D., Sechrest, L., Riedel, R., 1998b. Sociodemographic correlates of alexithymia. Compr. Psychiatry 39, 377–385, http://dx.doi.org/10.1016/S0010440x(98)90051-7. Lane, R.D., Weihs, K.L., Herring, A., Hishaw, A., Smith, R., 2015a. Affective agnosia: expansion of the alexithymia construct and a new opportunity to integrate and extend Freud’s legacy. Neurosci. Biobehav. Rev. 55, 594–611, http://dx.doi.org/ 10.1016/j.neubiorev.2015.06.007. Lane, R.D., Hsu, C.-H., Locke, D.E.C., Ritenbaugh, C., Stonnington, C.M., 2015b. Role of theory of mind in emotional awareness and alexithymia: implications for conceptualization and measurement. Conscious. Cogn. 33, 398–405, http://dx. doi.org/10.1016/j.concog.2015.02.004. Lecours, S., Bouchard, M.-A., 1997. Dimensions of mentalization: outlining levels of psychic transformation. Int. J. Psychoanal. 78, 855–875. Leising, D., Grande, T., Faber, R., 2009. The Toronto Alexithymia Scale (TAS-20): A measure of general psychological distress. J. Res. Personal. 43, 707–710, http:// dx.doi.org/10.1016/jrp.2009.03.009. Lesser, I.M., 1981. A review of the alexithymia concept. Psychosom. Med. 43, 531–543. Lichev, V., Rufer, M., Rosenberg, N., Ihme, K., Grabe, H.-J., Kugel, H., Donges, U.-S., Kersting, A., Suslow, T., 2014. Assessing alexithymia and emotional awareness: relations between measures in a German non-clinical sample. Compr. Psychiatry 55, 952–959, http://dx.doi.org/10.1016/j.comppsych.2013.12.013. Lieberman, M.D., Eisenberger, N.I., Crockett, M.J., Tom, S.M., Pfeifer, J.H., Way, B.M., 2007. Putting feelings into words. Affect labeling disrupts amygdala activity in response to affective stimuli. Psychol. Sci. 18, 421–428, http://dx.doi.org/10. 1111/j.1467-9280.2007.01916.x. Luminet, O., Bagby, R.M., Wagner, H., Taylor, G.J., Parker, J.D.A., 1999. Relation between alexithymia and the five-factor model of personality: a facet-level analysis. J. Personal. Assess. 73, 345–358, http://dx.doi.org/10.1207/ S15327752JPA7303 4. Luminet, O., Bagby, R.M., Taylor, G.J., 2001. An evaluation of the absolute and relative stability of alexithymia in patients with major depression. Psychother. Psychosom. 70, 254–260, http://dx.doi.org/10.1159/000056263. Luminet, O., Vermeulen, N., Demaret, C., Taylor, G.J., Bagby, R.M., 2006. Alexithymia and levels of processing: evidence for an overall deficit in remembering emotion words. J. Res. Personal. 40, 713–733, http://dx.doi.org/10.1016/jrp. 2005.09.001. Luminet, O., Rokbani, L., Ogez, D., Jadoulle, V., 2007. An evaluation of the absolute and relative stability of alexithymia in women with breast cancer. J. Psychosom. Res. 62, 641–648, http://dx.doi.org/10.1016/j.jpsychores.2007.01. 003. Lumley, M.A., Gustavson, R., Partridge, T., Labouvie-Vief, 2005. Assessing alexithymia and related emotional ability constructs using multiple methods: interrelationships among measures. Emotion 5, 329–342, http://dx.doi.org/10. 1037/1528-3542.5.3.329. Lumley, M.A., 2000. Alexithymia and negative emotional conditions. J. Psychosom. Res. 49, 51–54, http://dx.doi.org/10.1016/S0022-3999(00)00161-6. Lundh, L.-G., Johnsson, A., Sundqvist, K., Olsson, H., 2002. Alexithymia, memory of emotion, emotional awareness, and perfectionism. Emotion 2, 361–379, http:// dx.doi.org/10.1037//1528-3542.2.4.361. Luquet, P., 1981. Le changement dans la mentalization. Rev. Franc¸. Psychoanal. 45, 1023–1028. Makino, S., Jensen, M.P., Arimura, T., Obata, T., Anno, K., Iwaki, R., Kubo, C., Sudo, N., Hosoi, M., 2013. Alexithymia and chronic pain. The role of negative affectivity. Clin. J. Pain 29, 354–361, http://dx.doi.org/10.1097/AJP.0b013e7182579c63. Marchesi, C., Ossola, P., Tonna, M., De Panfils, C., 2014. The TAS-20 more likely measures negative affects rather than alexithymia itself in patients with major depression, panic disorder, eating disorders and substance use disorders. Compr. Psychiatry 55, 972–978, http://dx.doi.org/10.1016/j.comppsych.2013. 12.008. Martínez-Sánchez, F., 1996. The Spanish version of the Toronto Alexithymia Scale (TAS-20). Clinica y Salud 7, 19–32. Marty, P., de M’Uzan, M., 1963. La ‘pensée opératoire’. Rev. Franc¸. Psychanal. 27 (Suppl), 1345–1356. Marty, P., 1991. Mentalisation et Psychosomatique. Laboratoire Delagrange, Paris. Mattila, A.K., Kronholm, E., Jula, A., Salminen, J.K., Koivisto, A.-M., Mielonen, R.-L., Joukamaa, M., 2008. Alexithymia and somatization in general population. Psychosom. Med. 70, 716–722, http://dx.doi.org/10.1097/PSY. 0b013e31816ffc39. Mattila, A., Keefer, K.V., Taylor, G.J., Joukaama, M., Jula, A., Parker, J.D.A., Bagby, R.M., 2010a. Taxometric analysis of alexithymia in a general population sample from Finland. Personal. Individ. Differ. 49, 216–221, http://dx.doi.org/10.1016/ j.paid.2010.03.038. Mattila, A.K., Saarni, S.I., Alanen, E., Salminen, J.K., Kronholm, E., Jula, A., Sintonen, H., Joukamaa, M., 2010b. Health-related quality-of-life profiles in nonalexithymic and alexithymic subjects from general population. J.

1019

Psychosom. Res. 68, 279–283, http://dx.doi.org/10.1016/jpsychores.2009.09. 010. Mayes, L.C., Cohen, D.J., 1992. The development of a capacity for imagination in early childhood. Psychoanal. Stud. Child 47, 23–47. McDougall, J., 1982–83. Alexithymia, psychosomatosis, and psychosis. Int. J Psychoanal. Psychother. 9, 379–388. Meganck, R., Inslegers, R., Vanheule, S., Desmet, M., 2011. The convergence of alexithymia measures. Psychol. Belg. 51, 237–250. Mennin, D.S., Heimberg, R.G., Turk, C.L., Fresco, D.M., 2005. Preliminary evidence for an emotion dysregulation model of generalized anxiety disorder. Behav. Res. Ther. 43, 1281–1310, http://dx.doi.org/10.1016/j.brat.2004.08.008. Miller, L., 1991. On Aphasia at 100: the neuropsychodynamic legacy of Sigmund Freud. Psychoanal. Rev. 78, 365–378. Mitrani, J.L., 1995. Toward an understanding of unmentalized experience. Psychoanal. Q. 64, 68–110. Moriguchi, Y., Ohnishi, T., Lane, R.D., Maeda, M., Mori, T., Nemoto, K., Matsuda, H., Komaki, G., 2006. Impaired self-awareness and theory of mind: an fMRI study of mentalizing in alexithymia. Neuroimage 32, 1472–1482, http://dx.doi.org/ 10.1016/j.neuroimage.2006.04.186. Moriguchi, Y., Decety, J., Ohnishi, T., Maeda, M., Mori, T., Nemoto, K., Matsuda, H., Komaki, G., 2007. Empathy and judging other’s pain: an fMRI study of alexithymia. Cereb. Cortex 17, 2223–2234, http://dx.doi.org/10.1093/cercor/ bhl130. Nakao, M., Barsky, A.J., Kumano, H., Kuboki, T., 2002. Relationship between somatosensory amplification and alexithymia in a Japanese psychosomatic clinic. Psychosomatics 43, 55–60, http://dx.doi.org/10.1176/appi.psy.43.1.55. Nemiah, J.C., 1977. Alexithymia. theoretical considerations. Psychother. Psychosom. 28, 199–206, http://dx.doi.org/10.1159/000287064. Nemiah, J.C., Sifneos, P.E., 1970. Affect and fantasy in patients with psychosomatic disorders. In: Hill, O.W. (Ed.), Modern Trends in Psychosomatic Medicine, vol. 2. Butterworths, London, pp. 26–34. Nemiah, J.C., Freyberger, H., Sifneos, P.E., 1976. Alexithymia: a view of the psychosomatic process. In: Hill, O.W. (Ed.), Modern Trends in Psychosomatic Medicine, vol. 3. Butterworths, London, pp. 430–439. Novick-Kline, P., Turk, C.L., Mennin, D.S., Hoyt, E.A., Gallagher, C.L., 2005. Level of emotional awareness as a differentiating variable between individuals with and without generalized anxiety disorder. J. Anx. Dis. 19, 557–572, http://dx. doi.org/10.1016/j.janxdis.2004.06.001. Ogrodniczuk, J.S., Piper, W.E., Joyce, A.S., 2005. The negative effect of alexithymia on the outcome of group therapy for complicated grief: what role might the therapist play? Compr. Psychiatry 46, 206–213, http://dx.doi.org/10.1016/j. comppsych.2004.08.005. Ogrodniczuk, J.S., Sochting, I., Piper, W.E., Joyce, A.S., 2012. A naturalistic study of alexithymia among psychiatric outpatients treated in an integrated group therepy program. Psychol. Psychother. Theor. Res. Pract. 85, 278–291, http:// dx.doi.org/10.1111/j.2044-8341.2011.02032.x. Pandey, R., Mandal, M.K., 1996. Eysenckian personality dimensions and alexithymia: examining the overlap in terms of perceived autonomic arousal. Personal. Individ. Differ. 20, 499–504, http://dx.doi.org/10.1016/01918869(95)00214-6. Parker, J.D.A., Taylor, G.J., Bagby, R.M., 2001. The relationship between emotional intelligence and alexithymia. Personal. Individ. Differ. 30, 107–115, http://dx. doi.org/10.1016/S0191-8869(00)00014-3. Parker, J.D.A., Keefer, K.V., Taylor, G.J., Bagby, R.M., 2008. Latent structure of the alexithymia construct: a taxometric investigation. Psychol. Assess. 20, 385–396, http://dx.doi.org/10.1037/a0014262. Pinaquy, S., Chabrol, H., Simon, C., Louvet, J.-P., Barbe, P., 2003. Emotional eating, alexithymia, and binge-eating disorder in obese women. Obes. Res. 11, 196–201. Porcelli, P., Mihura, J.L., 2010. Assessment of alexithymia with the Rorschach Comprehensive System: The Rorschach Alexithymia Scale (RAS). J. Personal. Assess. 92, 128–136, http://dx.doi.org/10.1080/00223890903508146. Porcelli, P., Bagby, R.M., Taylor, G.J., De Carne, M., Leandro, G., Todarello, O., 2003. Alexithymia as predictor of treatment outcome in patients with functional gastrointestinal disorders. Psychosom. Med. 65, 911–918. Porcelli, P., Lorusso, D., Taylor, G.J., Bagby, R.M., 2007. The influence of alexithymia on persistence of symptoms of dyspepsia after laparoscopic cholecystectomy. Int. J. Psychiatry Med. 37, 173–184. Primmer, J.W., 2013. Understanding the dimensional nature of alexithymia. J. Conscious Stud. 20 (9–10), 111–131. Primmer, J.W., 2015. A Somatic-perceptual Theory of the Emotions, Unpublished Doctoral Dissertation. McMaster University, Hamilton, Ontario. Prinz, J., 2004. Gut Reactions: A Perceptual Theory of Emotion. Oxford University Press, New York. Rizzuto, A.M., 1989. A hypothesis about Freud’s motive for writing the monograph ‘On Aphasia’. Int. Rev. Psychoanal. 16, 111–117. Ruesch, J., 1948. The infantile personality. Psychosom. Med. 10, 134–144. Sandler, J., 1972. The role of affects in psychoanalytic theory. In: Physiology, Emotion and Psychosomatic Illness. Ciba Foundation Symposium 8. Elsevier, London, pp. 32–46. Schur, M., 1955. Comments on the metapsychology of somatization. Psychoanal. Stud. Child 10, 110–164. Sifneos, P.E., Apfel-Savitz, R., Frankel, F.H., 1977. The phenomenon of ‘alexithymia’. Observations in neurotic and psychosomatic patients. Psychother. Psychosom. 28, 47–57, http://dx.doi.org/10.1159/000287043.

1020

G.J. Taylor et al. / Neuroscience and Biobehavioral Reviews 68 (2016) 1006–1020

Sifneos, P.E., 1967. Clinical observations on some patients suffering from a variety of psychosomatic diseases. Acta Med. Psychosom. 7, 3–10. Sifneos, P.E., 1973. The prevalence of ‘alexithymic’ characteristics in psychosomatic patients. Psychother. Psychosom. 22, 255–262, http://dx.doi. org/10.1159/000286529. Sifneos, P.E., 1975. Problems of psychotherapy of patients with alexithymic characteristics and physical disease. Psychother. Psychosom. 26, 65–70, http:// dx.doi.org/10.1159/000286912. Sifneos, P.E., 1977. Comments in panel- and plenum discussion: psychotherapeutic problems with psychosomatic patients. In: Brautigam, W., von Rad, M. (Eds.), Toward a Theory of Psychosomatic Disorders. Alexithymia, Pensée Opératoire, Psychosomatisches Phänomen. Karger, Basel, pp. 361–375, Proceedings of the 11th European conference on psychosomatic research. Sifneos, P.E., 1994. Affect deficit and alexithymia. New Trends Exp. Clin. Psychiatry 10, 193–195. Sifneos, P.E., 1996. Alexithymia: past and present. Am. J. Psychiatry 153, 137–142, http://dx.doi.org/10.1176/ajp.153.7.137. Skelton, R.M. (Ed.), 2009. The Edinburgh International Encyclopedia of Psychoanalysis. Edinburgh University Press, Edinburgh. Smith, C.A., Ellsworth, P.C., 1985. Patterns of cognitive appraisal in emotion. J. Personal. Soc. Psychol. 48, 813–838, http://dx.doi.org/10.1037/0022-3514.48.4. 813. Sriram, T.G., Pratap, L., Shanmugam, V., 1988. Towards enhancing the utility of the Beth Israel Hospital Psychosomatic Questionnaire. Psychother. Psychosom. 49, 205–211, http://dx.doi.org/10.1159/000288085. Stanford Encyclopedia of Philosophy, 2003. http://plato.stanford.edu/entries/ mereology. Stengel, E., 1954. On re-evaluation of Freud’s book On Aphasia: its significance for psychoanalysis. Int. J. Psychoanal. 35, 85–89. Strachey, J., 1957. Editor’s note to The Unconscious. In: Freud, S, The Unconscious. Appendix C: Words and things. Standard Edition 14, 209 (1914–1916). Hogarth Press; London, 1957. Subic-Wrana, C., Thomas, W., Huber, M., Köhle, K., 2001. Levels of Emotional Awareness Scale (LEAS): The German version of a new alexithymia test. Psychotherapeut 46, 176–181. Taylor, G.J., 1984. Alexithymia: concept, measurement, and implications for treatment. Am. J. Psychiatry 141, 725–732, http://dx.doi.org/10.1176/ajp.141.6. 725. Taylor, G.J., 1992. Psychosomatics and self-regulation. In: Barron, J.W., Eagle, M.N., Wolitsky, D.L. (Eds.), Interface of Psychoanalysis and Psychology. American Psychological Association, Washington, DC. Taylor, G.J., 1994. The alexithymia construct: conceptualization, validation, and relationship with basic dimensions of personality. New Trends Exp. Clin. Psychiatry 10, 61–74. Taylor, G.J., 2000. Recent developments in alexithymia theory and research. Can. J. Psychiatry 45, 134–142. Taylor, G.J., 2010. Symbolism, symbolization, and trauma in psychosomatic theory. In: Aisenstein, M., Rappoport de Aisemberg, E. (Eds.), Psychosomatics Today. A Psychoanalytic Perspective. Karnac, London, pp. 181–199. Taylor, G.J., 2012. Loneliness in the disaffected (alexithymic) patient. In: Willock, B., Bohm, L.C., Coleman Curtis, R. (Eds.), Loneliness and Longing. Routledge, London, pp. 147–158. Taylor, G.J., Bagby, R.M., 2000. An overview of the alexithymia construct. In: Bar-On, R., Parker, J.D.A. (Eds.), The Handbook of Emotional Intelligence. Jossey-Bass, San Francisco, pp. 40–67. Taylor, G.J., Bagby, R.M., 2004. New trends in alexithymia research. Psychother. Psychosom. 73, 68–77, http://dx.doi.org/10.1159/000075537. Taylor, G.J., Bagby, R.M., 2012. The alexithymia personality dimension. In: Widiger, T.A. (Ed.), The Oxford Handbook of Personality Disorders. Oxford University Press, New York, pp. 648–673. Taylor, G.J., Bagby, R.M., 2013a. Psychoanalysis and empirical research: the example of alexithymia. J. Am. Psychoanal. Assoc. 61, 99–133, http://dx.doi. org/10.1177/0003065112474066.

Taylor, G.J., Bagby, R.M., 2013b. Alexithymia and the five-factor model of personality. In: Widiger, T.A., Costa, P.T. (Eds.), Personality Disorders and the Five Factor Model of Personality. , third edition. American Psychological Association, Washington, DC, pp. 1193–1207. Taylor, G.J., Ryan, D., Bagby, R.M., 1985. Toward the development of a new self-report alexithymia scale. Psychother. Psychosom. 44, 191–199, http://dx. doi.org/10.1159/000287912. Taylor, G.J., Parker, J.D.A., Bagby, R.M., 1990. A preliminary investigation of alexithymia in men with psychoactive dependence. Am. J. Psychiatry 147, 1228–1230, http://dx.doi.org/10.1176/ajp.147.9.1228. Taylor, G.J., Bagby, R.M., Parker, J.D.A., 1991. The alexithymia construct: a potential paradigm for psychosomatic medicine. Psychosomatics 32, 153–164. Taylor, G.J., Parker, J.D.A., Bagby, R.M., Acklin, M.W., 1992. Alexithymia and somatic complaints in psychiatric outpatients. J. Psychosom. Res. 36, 417–424, http:// dx.doi.org/10.1016/0022-3999(92)90002-J. Taylor, G.J., Bagby, R.M., Parker, J.D.A., 1997. Disorders of Affect Regulation. Alexithymia in Medical and Psychiatric Illness. Cambridge University Press, Cambridge, UK. Taylor, G.J., Bagby, R.M., Luminet, O., 2000. Assessment of alexithymia. Self-report and observer-rated measures. In: Bar-On, R., Parker, J.D.A. (Eds.), The Handbook of Emotional Intelligence. Jossey-Bass, San Francisco, pp. 301–319. Taylor, G.J., Bagby, R.M., Kushner, S.C., Benoit, D., Atkinson, L., 2014. Alexithymia and adult attachment representations: associations with the five-factor model of personality and perceived relationship adjustment. Compr. Psychiatry 55, 1258–1268, http://dx.doi.org/10.1016/j.comppsch.2014.03.015. Tibon, S., Weinberger, Y., Handelzalts, J.E., Porcelli, P., 2005. Construct validation of the Rorschach reality-fantasy scale in alexithymia. Psychoanal. Psychol. 22, 508–523, http://dx.doi.org/10.1037/07369735.22.4.508. Tolmunen, T., Lehto, S.M., Heliste, M., Kuri, S., Kauhanen, J., 2010. Alexithymia is associated with increased cardiovascular mortality in middle-aged Finnish men. Psychosom. Med. 72, 187–191, http://dx.doi.org/10.1097/PSY. 0b013e3181c65d00. Trumble, W.R. (Ed.), 2007. Shorter Oxford English Dictionary, vol. 1. Clarendon Press, Oxford. Van der Velde, J., Servaas, M.N., Goerlich, K.S., Bruggerman, R., Horton, P., Costafreda, S.G., Aleman, A., 2013. Neural correlates of alexithymia: a meta-analysis of emotion processing studies. Neurosci. Biobehav. Rev. 37, 1774–1785, http://dx.doi.org/10.1016/j.neubiorev.2013.07.008. Vanheule, S., 2008. Challenges for alexithymia research: a commentary on the construct of alexithymia: associations with defense mechanisms. J. Clin. Psychol. 64, 332–337, http://dx.doi.org/10.1002/jclp.20467. Vanheule, S., Desmet, M., Meganck, R., Bogaerts, S., 2007. Alexithymia and interpersonal problems. J. Clin. Psychol. 63, 109–117, http://dx.doi.org/10. 1002/jclp.20324. Vanheule, S., Verhaeghe, P., Desmet, M., 2011. In search of a framework for the treatment of alexithymia. Psychol. Psychother. Theory Res. Pract. 84, 84–97, http://dx.doi.org/10.1348/147608310X520139. Veirman, E., Brouwers, S.A., Fontaine, J.R.J., 2011. The assessment of emotional awareness in children: Validation of the Levels of Emotional Awareness Scale for children. Eur. J. Psychol. Assess. 27, 265–273, http://dx.doi.org/10.1027/ 1015-5759/a000073. Vorst, H.C.M., Bermond, B., 2001. Validity and reliability of the Bermond-Vorst Alexithymia Questionnaire. Pers. Indivd. Differ. 30, 413–434, http://dx.doi.org/ 10.1016/S0191-8869(00)00033-7. Wotschack, C., Klann-Delius, G., 2013. Alexithymia and the conceptualization of emotions: a study of language and use of semantic knowledge. J. Res. Personal. 47, 514–523, http://dx.doi.org/10.1016/jrp.2013.01.011. Zunhammer, M., Halski, A., Eichhammer, P., Busch, V., 2015. Theory of mind and emotional awareness in chronic somatoform pain patients. PLoS One 10 (10), e0140016, http://dx.doi.org/10.1371/journal.pone.0140016.

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