Review of the Literature

 

            The following literature review explores the relationship between alexithymia and PD. This includes the history of the identification of the alexithymia construct (Nemiah & Sifneos, 1970; Sifneos, 1973) as well as various theories of affect development that contribute explanatory theory to the construct (Bowlby, 1969, 1973; Krystal, 1988; Lane & Schwartz, 1987). This review particularly focuses on the comprehensive theory of affect regulation proffered by Taylor (1992) and Taylor, Bagby and Parker (1997) as well as the prominent tool for measuring alexithymia, the TAS-20 (Taylor, Ryan & Bagby, 1985; Taylor, Bagby & Parker, 1992). Also covered are the prominent theories of PD (Barlow, 1988; Clark, 1986, 1988; Klein, 1993; Krystal, 1988) and the amplification and somatization process involved in PD (Barsky, 1992).  Finally this review summarizes the research studies that have measured and compared levels of alexithymia in subjects with PD as compared to control samples using the original TAS (Joukamaa & Lepola, 1994; Parker, Taylor, Bagby & Acklin, 1993; Zeitlin & McNally, 1993) and the revised TAS-20 (Bankier, Aigner & Bach, 2001; Cox, Swinson, Shulman & Bourdeau, 1995; Fukunishi, Kikuchi, Wogan & Takubo, 1997).

           

 

 

Genesis of the Alexithymia Construct

            The earliest description of alexithymic characteristics was reported by MacLean (1949) when he noted psychosomatic patient’s inability to verbalize their feelings. Ruesch (1948) noted similar limitations in symbolism and verbalization in post traumatic and psychosomatic patients, and considered them to have an ‘immature’ or ‘infantile personality’. Horney (1952) and Kelman (1952) observed similar characteristics in psychosomatic psychiatric patients who demonstrated very poor response to psychoanalytic treatment due to concrete thinking and limited emotional awareness. Around the same time, Krystal (1962, 1968) was describing a similar lack of differentiation of affects in drug addicts and in patients with severe post traumatic states. In the 1960s and 1970s, Sifneos (1967) and Nemiah and Sifneos (1970) were conducting studies into similar cognitive and affective traits. In the absence of a better term, Sifneos (1973) coined the term alexithymia to describe the deficits in affective identification and awareness that were evidenced by patients with psychosomatic disorders he interviewed from 1954 to 1968 while the director of the Psychiatric Clinic at Massachusetts General Hospital.

 

Characteristics of Alexithymia

            The traits Sifneos (1973) noted in some, though not all, of these psychosomatic patients included: difficulty finding words to describe emotions, a tendency to act out to express emotion and avoid conflict, poverty of fantasy life, an “overall appearance of being dull . . . and a relative constriction in emotional functioning” (p.256). He also noted the presence of externally-oriented or operative thinking termed “pensee operatoire” (Marty & de M’Uzan, 1963) and he speculated that these deficits may result from developmental or biological factors.

            Alexithymia is considered a dimensional trait that has a normal distribution in the general population, as opposed to a categorical trait that is either present or absent. It also does not appear to be related to intelligence, socioeconomic status, educational level or culture (Taylor, Bagby & Parker, 1997). Alexithymic individuals are prone to states of undifferentiated negative affects and limited positive affects. Krystal (1988) and Sifneos (1987) have described this limited capacity for positive emotional states like happiness and love as constituting anhedonia. Alexithymic individuals have a propensity to develop overly dependent relationships, or conversely, may prefer to be alone and avoid formation of relationships, an apparent adult manifestation of an insecure attachment style (Taylor et al., 1997).

            Additional characteristics associated with the alexithymia construct include a tendency toward action to express emotions, avoidance of conflict, poor dream recollection, social conformity, and wooden posture with few facial expressions (Taylor et al., 1997). Sifneos (1967) noted frequent complaints of anxiety and depression with very limited ability to describe those emotions. Taylor (1984b) noted of individuals with alexithymia: “speech is lacking in nuance, meager in the use of metaphor and devoid of affect” (p. 218). As affects are not adequately verbalized, it is very difficult for alexithymic individuals to elicit support and comfort from others. They have difficulty imagining themselves in another’s situation which limits their empathy and support for others. A 1993 study (Schaffer) demonstrated that while non-alexithymic individuals tend to employ interpersonal contact or soothing fantasy activity to regulate affects, alexithymic individuals tend to rely on oral or somatic modes of affect regulation such as overeating or somatization. (Taylor et al., 1997).

 

Alexithymia: State or Trait

            There is considerable debate whether alexithymia is an enduring trait or a state reaction to some external event, or both. Freyberger (1977) refers to constriction of emotions in medically ill patients or those in a life-threatening state as secondary alexithymia. In these situations, emotional numbing appears to be the result of the defense mechanism of denial. Sifneos (1988) differentiated primary alexithymia: the result of neurobiological deficits, from secondary alexithymia: the consequence of early or late psychological trauma or developmental arrest. Taylor et al. “distinguish between alexithymia as a stable personality trait that is independent of etiology and alexithymia that is state-dependent and disappears after the evoking stressful situation has changed.

 . . . Strong empirical support for alexithymia being a stable personality trait, rather than just a consequence of psychological distress, has been provided by several prospective studies” (1997, p. 37). 

            Krystal (1988) states that alexithymia and anhedonia are separate but concomitant consequences of significant trauma, but the presence of anhedonia with alexithymia is a key indicator that the alexithymia is the result of trauma – a state reaction. “Posttraumatic alexithymics have such guilt about any pleasure and gratification that they conceal even minimal gratification” (p. 253).  Sifneos (1967, 1975) viewed the alexithymia phenomenon as a state of biological or developmental origin, proposing a possible inborn predisposition for alexithymia. He believed it should not be treated with anxiety-provoking therapy such as psychoanalysis which may only increase the psychosomatic symptoms that result from anxiety.

            A 1997 study (Fukunishi, Kikuchi, Wogan & Takubo) in Tokyo conducted pre and post treatment measures of alexithymia among two sample groups. Using the TAS-20, they found pretreatment elevation in alexithymia levels among 26 patients with PD (54%) and 24 patients with social phobia (58%). After treatment, they conducted a 6-month follow-up study and found the prevalence rate of alexithymia was 30.8% for the PD group and 33.3% for the social phobia group, a significant decrease for both patient groups. Overall, there was a decrease in TAS-20 scores for 88.5% and 83.3% of the patients in the PD group and social phobia group, respectively. Based on these findings, the authors conclude that the change in alexithymia that results from psychotherapeutic interventions and reduced anxiety suggests that alexithymia is a state reaction to anxiety.

 

First Comparative Research Study of Alexithymic Traits

            Sifneos (1972/1973) conducted a study to compare the rate of these alexithymic traits in a group of 25 psychosomatic patients with a control group of 25. The so-called psychosomatic group consisted of 9 patients with ulcerative colitis, 9 with asthma, 5 with peptic ulcer, and 2 with rheumatoid arthritis. The control group involved patients with diagnoses such as: borderline personality, depression, alcoholism and what was termed hysterical personality. Using the 17 item Psychosomatic Questionnaire of the Beth Israel Hospital Psychiatric Service, the experimental group endorsed twice as many positive responses to the key alexithymic questions as did the control group. His work convinced Sifneos that while these characteristics are evident in psychosomatic type disorders, there is an even wider distribution of some alexithymic traits in the general population than he had originally anticipated. In particular he noted alexithymic characteristics among drug addicts, alcoholics, paranoid and borderline personalities.

 

Theories of the Etiology of Alexithymia

            Biological model.         

            MacLean (1949) proposed that psychosomatic individuals have difficulty verbalizing feelings because of a lack of connections between the limbic system and the neocortex. He speculated that their emotions cannot be adequately processed by the neocortex to find expression in the symbolic use of words, but instead are immediately discharged through autonomic pathways of physiological arousal and expression. Nemiah (1975) and Nemiah, Freyberger and Sifneos (1976) also posit a neurological theory of a deficiency in the flow of information between the ‘visceral brain’ or the hypothalamus, and the language centers of the cerebral cortex. Nemiah posits the efficacy of antidepressant medication in the treatment of PD as support of a biological model of panic.

            The ‘split brain’ studies by Hoppe and Bogen (1977) who researched 12 cases of commisurotomized or surgically divided hemispheres, provided solid anatomical evidence of severe resultant alexithymia. Their data reported the “left hemisphere is linguistic, analytic, logical, sequential, and constructive, whereas the right hemisphere is specialized in visual-spacial [sic], synthetic, and Gestalt perception. Without the right hemisphere we are not able to sing in a melodic way and we have difficulty in perceiving the whole Gestalt. The right hemisphere senses the forest, so to speak, while the left one cannot see the forest for the trees (Hoppe, 1981, p. 6)” (Krystal, 1988, p. 257).  

 

            Deficit model vs. defense model.

            Nemiah, Freyberger and Sifneos (1976) propose a deficit model, similar to that of Marty and de M’Uzan (1963), suggesting alexithymic traits result from deficits in personality organization as opposed to a defense model of alexithymia as a product of defense mechanisms. Nemiah (1984) suggested that psychosomatic symptoms, whether panic or physiological, result when a deficit in higher order processing leads to a “short-circuiting of arousal into autonomic channels” (p. 134).  Nemiah (1997) elaborated on the processes that occur in response to affect provoking events, describing two sets of reactions: perceptual-cognitive and affective. First there is a conscious perception and cognitive evaluation of the event and a secondary somatic/emotional arousal response. This secondary response undergoes a process of psychic evaluation of several components. This evaluation process involves: redefining the raw emotion into identifiable feelings such as anger, sadness, joy or fear; identifying descriptive words for the feeling; producing fantasies expressive of the feelings; and associating these feelings to related memories. Nemiah suggests alexithymia as a disturbance somewhere along this chain of processes in the affective response, due to either psychological defenses or deficits, or due to physiological disturbances in the neuronal structures and pathways that underlie psychological processing.     

             Treatment with psychosomatic individuals indicates they do not respond to a conflict model of treatment, as psychological exploration does not reveal the presence of unconscious feelings or fantasies that would constitute internal conflict and generate symptom formation. Instead, it appears that the psychosomatic process is a manifestation of “ego deficits in the capacity for fantasy production and for experiencing and differentiating affects … the result of disturbances in early growth and development or of regression from more mature forms of psychological functioning” (Nemiah, 1984,

p. 133). Therefore a deficit model is essential for understanding the development of psychosomatic disorders. Nemiah notes the similarity of a deficit model to Freud’s early conceptualization of anxiety as the somatic manifestation of internal arousal without higher level cerebral processing.     

 

            Psychoanalytic perspective.

            Joyce McDougall, (1974) one of the most prominent psychoanalytic contributors to the body of theoretical knowledge of affective disturbances, postulates the problems of alexithymic and psychosomatic individuals are rooted in early preverbal mothering difficulties. The child perceives the mother’s ambivalence over the loss of the child via differentiation, separation and individuation, thereby diminishing the child’s comfort over becoming a separate individual. Denial of the child’s own identity results, eroding the connection between self-representations and love-object representations, and a lack of identification with a soothing, caretaking mother. This contributes to limited spontaneous fantasy and a robot like consequence: adapting well to reality but without a world of imagination or feeling. McDougall (1984) additionally states that: “Sexual perversions are probably the most alexithymic form of libidinal expression that exist!” (p. 392).             

 

First Connection of Alexithymia to PD

            Nemiah (1984) is credited for the first elucidation of a relationship between alexithymia and PD. In an article describing the differences between the symptoms of neurotic patients and those with psychosomatic disorders, he noted these traits of the psychosomatic population. “They could not associate like neurotic patients, they were unable to talk about feelings or fantasies, and they maintained a stubborn, unchanging inability to recognize internal psychological conflicts or problems despite the attempts of skilled therapists to uncover emotional factors” (p. 132). He further described their limited involvement in therapy, and premature termination with minimal degree of therapeutic progress. Nemiah cited the earlier emergence of the alexithymic construct whose salient features correlate with the psychosomatic process and symptomatology. He noted the presence of prominent alexithymic characteristics in his psychosomatic patients, such as difficulty describing and differentiating between feelings, limited production of fantasy and preoccupation with external events. Within this context, he states that one could consider “panic anxiety … as the prototypical psychosomatic disorder” (p. 134), putting forward the association between PD and alexithymia.

            Krystal (1992) later supported the association of alexithymia and PD when he described panic as “an attack of mixed physiological elements of dysphoric affects …. a perfect example of regression in affects to their infantile, somatic, undifferentiated form” (p. 407) and described alexithymia as “regression from verbalized, desomatized, and differentiated affects toward the resomatized and undifferentiated form” (1988, p. 264). Taylor, Bagby and Parker (1997) consider panic to be a disorder of affect regulation in which alexithymia is central to its etiological cognitive and affective deficits.          

 

Theories of Affect Development

            John Bowlby.

            Bowlby’s attachment theory (1969, 1973) provides elucidation of the impact of early bonding disruptions on affect development and affect regulation – concepts central to the alexithymia construct. Bowlby purports attachment behavior manifests in most human infants within the first four to seven months of life, with many infants of four months of age already capable of distinguishing between mother and others as evidenced by different responses to each. Proximity-maintaining behavior is demonstrated by the infant’s cries when mother leaves the room with attempts to follow her as soon as they are able to crawl, and attachment behaviors intensify when the child is alarmed by environmental stimuli such as mother’s departure or the approach of a stranger. During the second and much of the third year, the child’s increasing awareness of the impending departure of the mother triggers attachment behaviors: crying, protesting, or attempting to cling and follow.

             Bowlby notes a sudden development when the child approaches their third birthday – an increased capacity for temporary separations from the mother and the ability to feel secure in a strange place. This security is conditional upon: the presence of a familiar subordinate caregiver, the absence of any sense of alarm or illness, awareness of the mother’s whereabouts with knowledge of reunion within a short timeframe. Attachment behavior is demonstrated with less frequency and intensity after age three, decreasing further throughout adolescence as attachment to parents grows weaker while attachment and attraction to others increase. Throughout adulthood it remains a normal response, in illness or times of stress, for attachment behavior to manifest in seeking proximity to known or trusted individuals. Attachment behavior is accompanied by the most powerful of human affects: threat of loss causes anxiety, actual loss causes sorrow, and proximity to an attachment-figure creates a sense of security.

            Bowlby’s theory challenges the earlier theory of secondary drive as an explanation for proximity-seeking behavior. Secondary drive theory, evolved from assumptions versus direct observations, suggests the attachment to caregivers derives from primary drives: food, liquid, warmth and sex. This theory was seriously challenged by the early work on imprinting by Lorenz (1935/1957). His work and that of subsequent researchers (Cairns, 1966; Cairns & Johnson, 1965; Scott, 1963; Shipley, 1963) demonstrated attachment behavior developing not out of primary drive gratification, but rather out of the need for contact comfort. Harlow’s groundbreaking work with rhesus monkeys in the early 1960’s corroborated the primacy of contact comfort over food. His experiments demonstrated monkeys consistently favoring a soft, cloth non-feeding surrogate mother figure over a wire model that included a feeding bottle. While some time was spent feeding on the wire model, most time was spent on the cloth model. Some of these infant monkeys would even cling to the soft figure while leaning over to suck from the feeding model. These monkeys would increase their attachment to the cloth model when alarmed, finding no reassurance from the wire model, and intensifying their clinging behavior when their sense of alarm increased (Harlow, 1961).

            Harlow’s experiments provided explanation for the paradoxical clinging response to an abuser, be it parent or partner. The increased alarm and sense of threat posed by abuse triggers a proximity-seeking response to an attachment figure, even when the attachment figure is the source of the abuse. Bowlby elucidates the ultimate function of attachment behavior is survival of the species. Not only does attachment behavior provide protection from predators, but allows the infant to learn basic survival skills from the mother or primary caregiver.

            Bowlby suggested that individuals, who demonstrate behaviors that can be described as dependent or over-dependent, are exhibiting attachment behavior more frequently and urgently than their age or circumstances warrant. He termed this condition anxious or insecure attachment, due to the lack of confidence that attachment figures will be accessible and/or adequately responsive to one’s needs. Bowlby believed the cause of this condition to be experiences that gave an individual reason to question the availability of their attachment figures – either the result of actual separations or threats of abandonment. He defined anxiety as the feeling precipitated when “attachment behavior is activated” (p. 405). This includes the feeling triggered by the unsuccessful seeking of an attachment figure or the uncertainty over the availability of an attachment figure. “When an insecure individual, uncertain whether his attachment figures are going to be accessible and responsive, or even alive, is faced with a potentially fear-arousing situation, he is more likely to respond to it with fear, and also more likely to respond with intense fear, than is an individual who feels secure and confident in his attachment figures” (p. 313). Adult anxiety disorders, including agoraphobia and panic attacks, may be adult sequelae of insecure attachment patterns laid down in childhood (1973).

            Conversely, Bowlby cites confidence in ones attachment figures as the foundation for the stable and self-reliant personality he terms secure attachment. “Uncertainty about the accessibility and responsiveness of attachment figures is a principal condition for the development of unstable and anxious personality so is there [sic] a strong case for believing that an unthinking confidence in the unfailing accessibility and support of attachment figures is the bedrock on which stable and self-reliant personality is built”

(p. 322). Elements that contribute to this secure personality include a balance of parental support with appropriately timed encouragement toward autonomy, and healthy communication patterns. Children identify with their parents and adopt their parenting pattern, “Thus the inheritance of mental health and of mental ill health through the medium of family microculture is certainly no less important, and may well be far more important, than is their inheritance through the medium of genes” (p. 323). He believed that early life models of attachment figures persist throughout life, secure or insecure.

 

            Henry Krystal. 

            Krystal’s epigenetic model of affect development (1988) offers insight into the developmental arrest or regression that contributes to the traits that constitute alexithymia.  Krystal assumes infantile affective precursors comprised of states of contentment or distress, out of which develop the adult affects. Contentment is the precursor to the pleasurable affects, and distress the precursor to painful affects. “In the course of maturation, affects evolve from two affect precursors into specific emotions” (p. 41). Affect development occurs along two lines: affect differentiation, and affect verbalization with concomitant desomatization. This affect development process is directly affected by the infant’s subjective experiences. As “described by Ramzy and Wallerstein (1958): The neonate has internal tensions (homeostatic disequilibria) which are ‘perceived’ (referring to a precursor of perception) not as mental status, but as diffuse tensions on an undifferentiated biopsychological level. It is only later in development that such a tension state, as for example, hunger, can be separately viewed both on the psychological level (the feeling of hunger) and on the physiological level (concomitant discernible somatic processes) [p. 175]” (p. 43).

            Out of direct infant observation, Greenspan (1981) concluded that homeostasis, the regulation of excitation by the calming response, is the most crucial achievement in the first three months of life. This develops by the comforting response of the mother and gradually evolves into the child’s self-comforting ability. A considerable degree of affect differentiation occurs before affects are specific enough to be verbalized. By the age of two the child can identify affects differentiated out of contentment: delight, joy, affection; and out of distress: fear and anger. The presence of massive psychic trauma in infancy or toddler age may hinder the development of affects, and the extent to which affects remain undifferentiated and somatized is the extent to which they will lack meaning as a signal.

            In adolescence the child develops the capacity to grieve loss, especially of infantile attachment to parents as well as infantile omnipotence. Affect tolerance develops parallel with the development of the affects, reflecting developing self-awareness as well as comfort with and ease in handling affects. The adolescent also confronts the need to develop tolerance for boredom, discomfort and pain; necessitating their giving themselves credit for accomplishments as would an appreciative parent. Temporary devices that assist the adolescent until they develop adult level affect tolerance include a sense of counter phobic narcissistic invulnerability and exhibitionistic tendencies. Prominent among adolescent challenges is the process of separation-individuation and establishment of ego identity. (Erikson, 1956).

           

 

            Krystal on alexithymia.

            Consistent with his affect theory, Krystal (1988) conceives alexithymia as “a regression or an arrest in affective and cognitive development, with severe distortions resulting from infantile or catastrophic adult trauma” (p. 328) and that this is an arrest or regression from “verbalized, desomatized, and differentiated affects toward the resomatized and undifferentiated form [which] represents a predisposition to psychosomatic diseases” (p. 264). He states individuals with alexithymia have difficulty utilizing emotions as signals due to the form of their emotional responses. That is, their affects are basically somatic with minimal verbalization. Though they may function very well in their work and appear to be of superior intellectual function, he notes “a sterility and monotony of ideas and a severe impoverishment of the imagination” (p. 247) and describes them as “dull, colorless, and boring” (Krystal, 1979, p. 19) with expressionless faces and rigid posture.

             Due to inadequate capacity for fantasy-making and symbolization they are left with the physiological aspects of their affects and therefore are prone to psychosomatic disorders. They may attempt to medicate these responses with drugs or alcohol which leaves them susceptible to drug addiction or alcoholism. Krystal also suggests that these individuals can only signal their distress, leaving all the functions of verbalizing such as soothing and care giving to the mother. They cannot adequately organize their thoughts into logical, coherent communication and feel they must not take over the maternal role of making sense of their distress or engage in any independent thinking, so they merely signal their distress with a lot of trivial material in chronological order. Their affective responses therefore tend to be physical and may involve various bodily systems.

 

            Lane & Schwartz.

            In 1987 Lane and Schwartz proffered their epigenetic model of the cognitive development of affects, a “seminal contribution” as per Krystal (1988, p. 311). They emphasize that emotional disturbance may well be inherent in every mental health diagnostic category from mood disorders, schizophrenia and psychosomatic disorders, to the personality disorders. Emotion is a complex phenomenon of three domains: physiological (or biological); psychological (or experiential); and expressive (or social). Most mental health patients seek treatment for distress in the psychological/ experiential domain as they are in a state of emotional pain (Lane & Schwartz, 1987). They concur with Lazarus (1984) that emotion is preceded by cognition; that cognitive appraisal of the environment activates the affective response. Their theory proposes that the cognitive process undergoes transformation throughout the individual’s development, and thereby affects subsequent emotional experiences. “Our primary thesis is that emotional awareness is a type of cognitive processing which undergoes five levels of structural transformation along a cognitive-developmental sequence derived from an integration of the theories of Piaget and Werner” (p. 134). Their theory is influenced by Werner’s (1957) principle that wherever development occurs, it proceeds from a global state devoid of differentiation to a state of increasing differentiation, verbalization and hierarchic integration. The development of symbolization and language facilitates not only articulation of affect but a cognitive structure for affect. Lane and Schwartz build their developmental model upon Piaget’s hierarchical model of four stages of cognitive development – sensorimotor, preoperational, concrete operational, and formal operational periods. Their model encompasses the following five levels of structural transformation of awareness:

            1. Sensorimotor reflexive – At this first level of emotional awareness the involuntary motor responses that accompany emotional arousal become activated. These include autonomic changes and facial expression, with global arousal consisting of bodily sensation only. The individual cannot report anything though an observer can identify the quality of the emotion being experienced. There is minimal to nonexistent awareness of the separate existence of others.

            2. Sensorimotor enactive – In the second level emotion is experienced as a bodily sensation and an action tendency though conscious awareness of emotion has not yet developed. Affective states are global states of pleasure or displeasure, and action is aimed to maximize pleasure or minimize distress. The awareness of another as a separate individual is minimal.

            3. Preoperational – The representation and awareness of emotion is possible for the first time at the third level of development. Emotions are becoming a psychological as well as somatic experience and are singular – happy or sad without nuances. They are also limited in range along with their verbal descriptions. Others are recognized as separate from the self but without awareness of the other’s emotional experiences. 

            4. Concrete operational – Awareness of a blend of feelings including concurrent opposing feelings and a wider range of emotions becomes manifest at this level. Emotions have become differentiated from one another both qualitatively and quantitatively. There is a capacity to modulate emotional extremes, to maintain hope in the face of challenges, and maintain different feelings for another despite current circumstances. There is a capacity to articulate complex and differentiated affects and an ability to anticipate the responses of others. Although others are recognized as separate and different based on internal as well as external attributes, the perception of another’s emotional experience is relatively undifferentiated from the perception of one’s own experience.  

            5. Formal operational – The major advance at this level is greater differentiation and integration in ones appreciation of the emotional experience of others compared to ones own. There is a greater capacity for a blend of feelings of varying qualities or intensities with greater differentiation among them. The ability to describe emotions and their nuances in novel ways or with metaphors is evident. It is possible to perceive the differentiated experience of others unbiased by ones own feelings and see ones self and another’s situation through the eyes of another. The capacity to anticipate emotional consequences of personal or professional decisions increases the likelihood of making wiser decisions. By being able to anticipate the needs and reactions of ones self and others, one is able to make more satisfying and appropriate decisions or take more effective courses of action. The self has reached peak differentiation from others with recognition of the uniqueness as well as similarities between both.

 

            Lane & Schwartz on alexithymia.

            The authors identify (1987) the clinical entity perhaps most directly addressed by their theory is alexithymia. They state that alexithymic individuals may self-perpetuate their undifferentiated emotions by avoiding “reflecting on and generating symbolic representations of experience. Our model suggests that an important reason for this avoidance is that unpleasant emotional arousal is experienced as overwhelming somatic distress when it is attended to” (p. 140). They suggest that individuals with high levels of cognitive complexity experience less emotional distress than those individuals with lower levels of cognitive complexity.

 

Theory of Affect Regulation 

            The most comprehensive theory of affect development is the theory of affect regulation by Taylor (1992) and Taylor, Bagby and Parker (1997). They recognize a biological basis of emotions as established by Darwin who believed emotions are an adaptation that organizes survival behavior. Emotions are a biologically based readiness toward action, but the actions taken to control how these impulses are experienced and expressed constitutes the concept of affect regulation.  They also concur with Lazarus (1991) and Zajonc (1984) who promote a cognitive theory of emotion, noting that both phylogenetically and ontogenetically, affect precedes the development of cognition but “cognition becomes linked inseparably with affects early in development . . . . cognitive processes play a vital role in the regulation of affects” (Taylor et al., p. 13). They also “regard affect regulation as a process involving reciprocal interactions between the neurophysiological, motor-expressive, and cognitive-experiential domains of emotion response systems” (p. 14). All three domains are involved in the regulation of affects, with activation in one influencing the others. Additionally, ones interaction within social relationships provides interpersonal regulation that may be either soothing or distressing. “Affects themselves may also regulate other affects . . . the positive affect of interest may attenuate fear and sadness” (p. 14).

 

            Affect development.     

            Taylor et al. (1997) state that undifferentiated precursor states of contentment and distress, consistent with Krystal’s theory (1988), are evident in newborn children and appear to be similar in all cultures, manifesting both physiologically and behaviorally. As maturation proceeds, these affect states undergo progressive differentiation and desomatization, while language development facilitates the articulation of symbolic representations of emotions. The authors concur with the cognitive development of affects model posited by Lane and Schwartz (1987) of structural transformation in a hierarchical developmental sequence. They credit this model for its conceptualization of affect development and the explanation it provides for the range of differences between individuals in the capacity to experience and express affects, as well as capacity for empathy.

            The development of affect and the corresponding cognitive skills for regulating affect are clearly influenced by the child’s relationship with primary caregivers. Affect development in the infant will be negatively impacted by failure on the parent’s part to read the infant’s emotional cues and respond properly to externally regulate the infant’s emotional state (Bion, 1962, 1965). The development of symbolization and language facilitates growth of the child’s subjective emotional awareness during their second year. This is facilitated by the parents providing words and meaning for the child’s somatic emotional experience (Edgcumbe, 1984; Emde, 1984; Furman, 1992). But it is the child’s acquisition of language that has considerable effect upon the development of affect regulation by facilitating their verbalization of affects, receiving of feedback from others, and hearing and thinking about their feelings and how to manage them (Kopp, 1989). “The verbalization of affects leads to new experiences and a growing awareness of more complex and differentiated emotional states (Stern, 1985). This will occur only if the child is reared in a family environment where feelings are verbally labeled and validated” (Taylor et al., 1997, p. 18). Teaching children to label emotions and express them in words not only transforms behavioral expression into verbal expression but encourages cognitive appraisal of emotions (Katan, 1961). Affect tolerance, the capacity to “contain and tolerate the tensions generated by feelings and needs without always having to rely on parents” (Taylor et al., p. 19) increases with the verbalization and cognitive awareness of affects. The child also develops the capacity to use feelings of sadness, anxiety, and other emotions as signals that can be evaluated to provide guidance for reducing or managing stressors (Krystal, 1975). The ability to represent awareness of affect as well as awareness of another’s affect is generally achieved in the third year of life (Fonagy, 1991; Hobson, 1994).

 

            Attachment development.

            A significant determinant of a child’s ability to regulate distressing affects and relate to others is the degree of sensitivity and responsiveness to their emotional states by their caregivers in infancy and childhood (Bretherton, 1985; Goldberg, MacKay-Soroka, & Rochester, 1994). Children can achieve secure attachment when they have experienced consistent and supportive responsiveness from caregivers. They seek comfort from their parents when they are emotionally distressed and display more positive affect, have higher levels of symbolic play than insecurely attached children and demonstrate more competence and adaptability in their relationships (Malatesta, 1990; Slade & Aber, 1992).

            Insecure attachment impedes the development of affect tolerance and regulation. Insecurely attached children experienced a caregiver who was insensitive to the child’s emotional cues or rejected the child’s proximity-seeking behavior. Insecure attachment patterns can manifest in avoidance of frustrated comfort-seeking behavior and suppression of affect display; or escalating, disorganized affect displays that attempt to elicit a comforting parental response. Numerous variables on behalf of the infant or mother can contribute to disruption in the formation of secure attachment.

            Early attachment experiences influence the development of an internal model of the self and others that impacts both affect regulation as well as future relationships. The attachment style developed in childhood appears to endure for a lifetime and may influence future generations. Securely attached adults seem to experience more positive affect and develop relationships that provide support in times of emotional distress. Adults with insecure attachment styles experience higher levels of negative affects such as anxiety and depression and develop relationships that provide limited emotional support.

 

            Affect regulation development.

            While infant precursor emotional states are largely regulated by parents, independent affect regulating behaviors such as thumb or finger sucking quickly evolve. These precede the later emergence of a transitional object, such as a blanket or soft toy, for self-comforting in periods of distress such as separations from the mother. While these behaviors manifest even in children who later develop secure attachment, the use of a transitional object is even more critical for infants who are weaned early or have experienced early separation from the mother (Taylor, 1987). Discouragement by the mother of the child’s creation of transitional objects inhibits the development of fantasy, imaginal activities and play. These children are left with auto sensual behaviors such as hair twirling, thumb sucking or masturbation, which are primitive modes of affect regulation. Adolescent and adult equivalents may be sensation seeking behaviors such as cigarette smoking, alcohol use or overeating.

            The development of pleasant self-comforting dreams, fantasies and play are largely influenced by the extent of relatedness between the infant and a nurturing mother. Imagination and creative ability play an important role in the development of personality and affect regulation. Early childhood play is an important developmental process that allows a child to manage negative affects and increase positive affects of interest and joy. Imaginal activity in play also manifests through the formation of symbolization evident in wish-fulfilling dreams and creative stories. The ability to symbolize facilitates the organization and modulation of affective experiences. As transitional objects are discarded, the acquisition of new interests and activities help provide self-soothing functions. Interests provide positive affects and enhance social relationships which in turn facilitate affect regulation.

            Affect development and regulation are complex developmental processes influenced by temperamental, neurobiological and social factors. For example, an infant with a neurological defect may not be capable of adequately responding to an emotionally responsive mother. Or a depressed and emotionally unavailable or insensitive mother may be impaired in her ability to properly respond to her infant’s emotional states. Cultural factors may impact the development of affect and its regulation as they influence the degree of maternal responsiveness to an infant’s emotional cues based on sociocultural norms regarding affect significance and expression. A comprehensive theory of affect development and regulation considers the complex relationship between affect, cognition and attachment behavior as a major influence on the organization of the personality. “Crittenden (1994), for example, relates successful affect development and regulation to the experience of secure attachment; it provides predictable positive outcomes to affective communications, and thereby facilitates a satisfactory integration of affective information with cognition information. Consequently, the child is able to ‘use cognition to moderate affect and affect to inform cognition’ ” (Taylor et al., 1997, p. 24-25).

 

            Taylor, Bagby and Parker on alexithymia.

            Early life failures in developing the capacity to cognitively experience and regulate affects can result in affect dysregulation and psychopathology or physical ailments. The authors consider these failures the result of arrest at or regression to lower levels of affect development as proposed by the Lane and Schwartz (1987) model. They consider functioning at these lower developmental levels to be the personality trait of alexithymia. Furthermore, though alexithymia has been associated with primitive defenses, it is not a defense mechanism itself. (Taylor et al., 1997).

 

           

Recognition of Panic Disorder as a Distinct Disorder

            Klein significantly influenced the recognition of PD as a distinct diagnostic category in the 1980 American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III), while Barlow influenced the 1994 DSM-IV definition of PD. The DSM-IV conceptualization of PD considers the significant role played by the persistent anxiety over physical sensations, termed fear of fear (Goldstein & Chambless, 1978) or anxiety sensitivity (Reiss & McNally, 1985). The DSM-IV also distinguishes between unexpected (or uncued) attacks; situationally bound (or cued) attacks; and situationally predisposed attacks. See Appendix C for complete DSM-IV definition.

            The DSM-IV definition of PD was also influenced by Klein’s model (1993) which restricts panic triggering cues to external stimuli and does not include internal cues. Barlow (1988) believes triggers can be external events as well as internal,  interoceptive stimuli, and Craske (1991) believes that panic attacks in PD result from internal cues including stressful life events, whereas panic by phobics is triggered by external cues. The Clark (1986) and Barsky (1992) models are predicated upon a presumption of panic that stems from interoceptive cues.

 

Prominent Etiological Theories of PD

            Barlow - false alarm theory.

            Barlow (1988) proffers a biopsychosocial model that postulates panic as the misfiring of a biological system designed to serve as an alarm of pending danger. It is well established that fear is a natural reaction to environmental threats, serving to trigger a survival response to the threat. Ancestral threats such as an animal attack, to more modern threats such as armed robbery, trigger a true alarm. This alarm mobilizes a physical and cognitive fight or flight response of innate and significant evolutionary value, to either fight off the attack or take flight. But this same set of biological and psychological reactions, triggered in the absence of a life-threatening stimulus, learned or unlearned, constitutes a false alarm or a panic attack. Barlow states the causes of false alarms include biological predisposition, a history of childhood separation anxiety, and stress generated by life events.

            While Barlow says “It would certainly seem logical that a biological dysregulation underlies false alarms” he goes on to explain that “at the present time there is no evidence for any specific biological marker; nor, for that matter, is there evidence for any important neurobiological differences between patients with panic disorder and nonpanickers” (1988, p. 211). He does suggest that a biological marker for panic may be chronic hyperarousal. Though it is an attribute of all with an anxiety disorder, it may interact with other variables to precipitate a false alarm.

            Barlow cites a Russian study (Razran, 1961) that demonstrates fear can become conditioned to internal physiological stimuli. An association developed between a negative external event and internal sensations can be extremely resistant to extinction, even persisting indefinitely. If an association between internal cues and false alarms develops, the internal cues can signal the possibility of another false alarm. “The association of false alarms with internal or external cues results in the phenomenon of learned alarms” (Barlow, 1988, p. 229). Fear can be learned to numerous somatic cues – cardiovascular or respiratory. If a sense of threat by driving over a bridge triggers a false alarm and a racing heart which then generates fear of a heart attack, future false alarms could be triggered by the learned alarm of heart palpitations. “The association of false alarms with interoceptive or somatic cues is particularly crucial in the development of panic disorder” (p. 366). Considerable evidence indicates that people with PD have learned to fear interoceptive cues, and that therapeutic desensitization to those cues is very effective in the treatment of PD.

            Barlow’s model begins with biological vulnerability: the tendency toward neurobiologically based over reactivity to stressful events that forms a platform for an initial “hard-wired alarm reaction” (p. 366). He believes the tendency to over react to stressors with exaggerated neurobiological arousal is genetically based and that “panic disorder patients are biologically predisposed to react to negative life events with neurobiological lability” (p. 368). The second component in his model is the stress trigger, which precipitates the first false alarm/panic attack. By association with interoceptive cues, the first false alarm becomes a learned alarm. That association leads to psychological vulnerability, the anxious apprehension that focuses on future alarms. This then leads to autonomic and cognitive symptoms of anxiety and further somatic cues that trigger more learned alarms. Finally, this process may lead to development of agoraphobic avoidance.

            Barlow believes that panic attacks, especially in conjunction with agoraphobia, may be an adult analogue of separation anxiety experienced by children confronted with separation from their mother. However, he does note the conflicting evidence regarding a positive correlation between adult PD and childhood separation anxiety. The role of stress as a precipitant of panic attacks is well documented, and various studies have demonstrated that up to 96% of individuals with PD can identify a significant life stressor as a precursor of their first panic attack. Certain individuals may be more susceptible to the impact of stressful events based on the extent of social support, constitutional factors and a combination of cognitive and psychological traits. They would then be disposed to react to a negative life event as if it were a life threatening danger analogous to an animal attack. Barlow’s theoretical contributions to the body of knowledge regarding PD influenced the classification and description of PD in the DSM-IV.

 

            Clark - catastrophic misinterpretation theory.

            Individuals with a history of panic attacks can develop panic in response to physiological agents such as inhalation of carbon dioxide, infusions of lactate or yohimbine, excessive caffeine or voluntary hyperventilation. Though these substances produce the same physiological sensations associated with panic in all individuals, those without a history of panic attacks will not experience panic in response. This fact led some theorists to suggest the difference to be the result of a biochemical disorder present only in those who react with panic. Clark (1986) suggested the difference to be the result of different interpretations as to the significance of the physiological sensations:

 

It is proposed that panic attacks result from the catastrophic misinterpretation of certain bodily sensations. The sensations which are misinterpreted are mainly those which are involved in normal anxiety responses (e.g. palpitations, breathlessness, dizziness etc.) but also include some other bodily sensations. The catastrophic misinterpretation involves perceiving these sensations as much more dangerous than they really are. Examples of catastrophic misinterpretations would be a healthy individual perceiving palpitations as evidence of impending heart attack; perceiving a slight feeling of breathlessness as evidence of impending cessation of breathing and consequent death; or perceiving a shaky feeling as evidence of impending loss of control and insanity (p. 462).

 

 

            Clark further described the vicious cycle that develops in those who panic. An external stimulus (such as driving on a freeway) or an internal stimulus (a physical sensation, thought or image) may be perceived as a threat which generates apprehension. Physiological sensations develop or intensify from the apprehension of this inaccurately perceived threat. If these sensations are interpreted as signals of pending catastrophe, further intensification of sensations result and intensify the sense of threat. This vicious cycle can escalate and trigger a panic attack. This model can explain panic attacks that appear to ‘come out of the blue’ and those that result from heightened anxiety. Panic attacks that manifest from heightened anxiety are one of two types: a panic attack resulting from heightened anxiety about having an attack, or a panic attack triggered by the physical sensations of anxious arousal. Panic attacks ‘out of the blue’ often result from catastrophic misinterpretation of the sensations of benign physiological arousal. Normal emotions such as anger or excitement can cause increased heart rate, increased respiration or flushing. Exercise can cause increased heart rate, palpitations, or breathlessness. And actions such as bending over or quickly standing up can cause dizziness. These physical sensations can be misinterpreted as a catastrophic cue and result in panic. Individuals who misinterpret these benign sensations are often unaware of doing so and therefore the panic attack appears to come ‘out of the blue’.

            The individual’s general beliefs also affect attacks. If an individual believes there is something wrong with his heart, or has ever had heart problems, there will be greater likelihood that palpitations may be interpreted as an indicator of a heart attack. Sensations related to mental functioning can also be misinterpreted such as sudden forgetfulness, confusion or depersonalization. The fear of losing one’s mind may then be triggered which may culminate in a panic attack. Clark further notes that perceiving a sensation as unpleasant is as significant as interpreting it in a catastrophic manner. Some individuals experience voluntary hyperventilation as positive and therefore do not become frightened. Those who perceive it as unpleasant will be likely to interpret it catastrophically.

            Clark accepts a biological component to panic attacks in addition to his cognitive model. He believes biology can influence panic attacks in one of three ways. First, some individuals may be more physiologically sensitive and reactive to certain sensations such as breathlessness.  Second, biology may influence the degree of physiological responses to a sense of threat. Third, biology may affect the psychological processes that are involved in the catastrophic misinterpretation process.

 

            Klein – suffocation alarm theory.

            Klein (1993) proposes a biological model of panic attacks in his suffocation false-alarm theory, claiming many spontaneous panic attacks are related to carbon dioxide (CO₂) hypersensitivity. The central nervous system is extremely sensitive to any cues of partial suffocation. The brain, comprising only 2% of body weight but consuming 24% of used oxygen, quickly senses any rise in CO₂ as a signal that suffocation is eminent. Elevated levels of CO₂ can result either from extreme enclosure and resultant increased levels of inhaled CO₂, or from hypoventilation. Either circumstance signals a lack of useful air and triggers a suffocation alarm system. The sense of suffocation is intense and universal, and appropriate in circumstances of actual threat of suffocation, triggering panic and the urge to flee. But in individuals with PD, “a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. . . . followed swiftly by a brief hyperventilation, panic, and the urge to flee” (Klein, 1993, p. 306).

            Though an actual rise in CO₂ can be a panic stimulus, numerous psychosocial indicators can simulate suffocation and falsely trigger this suffocation alarm, resulting in distressing breathlessness, panic and the urgent need to escape to an open space to breathe. Dyspnea – difficulty in breathing or breathlessness – is practically a universal feature of PD and a frequent trigger of panic. Psychosocial stimuli such as: a sense of entrapment, immobilizing crowds, uncomfortable heat, humidity or stale air can also create a sense of limited exit and restricted capacity to breathe. Klein suggests respiratory disorders may result in PD and that PD occurs frequently with pulmonary disease. His theory holds that cues for panic attacks are external stimuli only, those situational cues arising from the environment. Sensory cues arising from within the body are not considered. Therefore the sight of an imminent uncomfortable situation is considered a cue, while the interoceptive cue of the resultant skip in heartbeat is not.

            The role of suffocation anxiety in PD is illustrated by the differences between non-clinical individuals who have experienced an isolated panic attack, and those with PD. In the Norton, Harrison, Hauch & Rhodes study (1985) of young adults who had experienced one or more panic attacks within the preceding year, the most severe symptoms were trembling, sweating and pounding heart, but not difficulty with breathing. Dyspnea is a common symptom in most individuals with PD, but is absent in most with generalized anxiety disorder (Klein, 1993). In his considerable research on the biological etiology of panic, he found that bicarbonate, 5% CO₂, lactate and isoproterenol can be panicogenics for those with PD but not in individuals without PD. Following up on Klein’s work with CO₂, one study demonstrated that inhalation of 35% CO₂/ 65%O₂ precipitates symptoms of panic in individuals with PD as well as in those without PD (van den Hout, 1988). Another study reported a challenge of 35% CO₂ precipitated panic in 72% of panic patients but only 4% of control subjects. McNally (1994) concludes that “the data are mixed concerning the validity of the hypersensitive carbon dioxide chemoreceptor hypothesis” (p. 57) as an explanation of PD. Although Klein’s model is biological, stating “genetic derangement may be necessary for many spontaneous panics” (1993, p. 314), it does not rule out the possibility that psychosocial factors such as separation anxiety, loss or grief may lower the suffocation alarm threshold.

            Klein believes there is a qualitative difference between generalized anxiety or fear, and panic. “Spontaneous panic is not fear, although it is often confused with it”

(p. 308). He considers agoraphobia the result of frequent traumatic suffocation panic attacks. His research with the antidepressant imipramine demonstrated efficacy with spontaneous panics but not with chronic anxiety, contributing to his contention that panic does not exist on the same continuum as anxiety but is an independent phenomenon. “Acute anxiety derives from fear as a recently evolved anticipation of danger. Chronic anxiety may be a primitive response to repeated traumatic sensitization. Panic seems an even more primitive response to an endogenously detected danger, specifically suffocation” (p. 308).

 

 

            Taylor, Bagby and Parker – integrative theory.

            In addition to their comprehensive theory of affect regulation, the authors offer an integrated biological and psychological model of the etiology of PD. They consider panic to be a disorder resulting from “deficits in the cognitive processing and regulation of emotion” (Taylor, Bagby & Parker, 1997, p. 142), consistent with the alexithymia construct.  They consider panic a flood of dysregulated affect resulting from catastrophic misinterpretations of either internal physical or mental cues, or from external cues. A panic attack is considered a failure in the signal function of anxiety - instead of being perceived as a warning sign it is experienced as a flood of undifferentiated emotion - what Krystal considers “a perfect example of regression in affects to their infantile, somatic, undifferentiated form” (1992, p. 407).

            They credit Bowlby’s (1969, 1973) theories of attachment and separation for explaining the process of separation and individuation from the mother and the internalization of her anxiety-regulating functions by the formation of transitional objects. These transitional objects are sensation objects in that they provide olfactory or tactile stimulation and comfort. They later acquire symbolic meaning and encourage development of imaginative ability and interests that increase the child’s capacity for self-regulation of emotions. Alexithymic individuals experience incomplete transitional object formation due to limitations in their capacity for symbolizing, and are therefore prone to continued reliance on sensation objects for soothing. Taylor et al. suggest overeating and substance abuse are adult analogues of this dependence on early sensation objects.

            Consistent with Bowlby’s concept of insecure attachment, many adults with PD are very dependent on others as safe people, someone who can help regulate their anxiety and provide a sense of safety. The authors consider this reliance to be compensation for failure in the development of adequate self-regulation:

 

In summary, our integrated model of panic disorder includes a role for disturbances in early object relationships, which might influence certain biological mechanisms involved in affect regulation, and also influence the internal representations (Bowlby’s working model) of early experience that function as modulators of affect at a cognitive level. In addition, the model places importance on a predisposed person’s current relationships, which might trigger dysregulation of brain stem loci through separations, or function as external regulators that help stabilize hypersensitive loci (Taylor et al.,

 p. 148).

 

 

Barsky – Theory of Amplification

            The involvement of somatic cues, symptoms, and preoccupation is readily evident in the classification and description of PD as well as its etiological models. Barlow (1988) states “patients with panic disorder seem sensitized to somatic symptoms and overreport and exaggerate these events” (p. 110). Clark’s model is based on the faulty interpretation and consequential dread of somatic cues, and Klein’s theory is predicated upon over reactivity to physiological stimuli that are consistent with suffocation cues. Barsky’s (1992) amplification theory offers insight into the somatic process inherent to PD as well as other somatoform disorders. Somatosensory amplification, or what he simply terms amplification, is the “tendency to experience bodily sensation as intense, noxious, and disturbing. It includes an individual’s disposition to focus on unpleasant sensations and to consider them as pathological rather than normal” (p. 28). He proposes that amplification may play a pathogenic role in PD, as well as in hypochondriasis and major depression. He further states, “Amplification may play a role in the process of somatizing in general” (p. 31). Individuals who are more sensitive and have a low threshold to pain are amplifiers. Those less sensitive and with a higher pain tolerance are termed minimizers.

            The amplification process involves three elements. First is hypervigilance to physical sensations and the tendency to focus on those that are unpleasant. Second is over focus on unusual or infrequent sensations. And third is interpretation of sensations as pathological or dangerous as opposed to benign and normal. The full range of physiological sensations can be amplified, from normal bodily functions, to minor and transient abnormalities such as an eye twitch. Or physiological symptoms of affect and symptoms of serious diseases may be amplified.

            Amplification shows trait and state characteristics. Some individuals have a lifelong history of sensitivity to bodily sensations which may be learned in childhood or may be a constitutionally inherited trait. Evidence of state-like qualities manifests in the variability of one individual to amplify differently across various circumstances. Four factors can influence this variability. First is cognition, the thoughts one has about a symptom. It is normal to amplify a symptom more when it is attributed to a serious disease rather than a benign cause. Second is the context of the symptoms. If an individual recently had close contact with somebody with tuberculosis, they might react more negatively to their own sudden cough than if they had recently been exposed to someone with a cold. Third is attention to a symptom. “Attention to a symptom amplifies it, whereas distractions diminish it” (p. 29). And fourth is mood. Negative affects tend to increase an individual’s tendency to negatively assess health and symptoms. Depression tends to turn one’s focus inward and cause an individual to think they are defective and damaged. And anxiety causes individuals to catastrophize sensations as well as lower tolerance for unpleasant symptoms. Barsky reports that individuals, who report high levels of negative affects on self-report scales, also tend to report high levels of somatic symptoms (1992).

 

Construct Validation

            Empirical validation of a new psychological construct is critical in confirming the validity of the construct and affirming that it is not a previously identified concept with a new name. “Indeed, Cronback and Meehl (1955) have argued that the validity of a construct cannot be evaluated independently of the tests that purport to measure that construct” (Taylor et al., 1997, p. 46). Toward that goal, several psychometric instruments have been devised to attempt the measure and validation of the alexithymia construct.

            An interviewer-completed questionnaire, the Beth Israel Hospital Psychosomatic Questionnaire (BIQ) was developed by Sifneos in 1973 as a tool for the assessment of alexithymia. It has good face validity but several studies suggest inadequate inter-rater and test-retest reliability. Bagby, Taylor and Parker (1994) developed a modified version of the BIQ which enhanced its psychometric properties and correlation with scores on the self-report TAS-20. In the attempt to develop a standardized interview to measure for alexithymia, Krystal, Giller and Cicchetti in 1986 devised the Alexithymia Provoked Response Questionnaire (APRQ). It has high concurrent validity with the BIQ, from which it was developed, but low correlation with the TAS-20. One of the most commonly used self-report instruments for assessing alexithymia has been the MMPI Alexithymia scale (MMPI-A). The empirical criterion method of its scale construction has several flaws and several studies have demonstrated low levels of internal reliability. Both the APRQ and MMPI-A scales provide “no support for the validity of the alexithymia construct and cannot be recommended for clinical or research purposes” (Taylor et al., 1997, p. 51). Other instruments to assess the alexithymia construct, including projective techniques such as the Rorschach alexithymia indices, all lack sufficient validity and internal reliability.

 

Development of the TAS-20

            In the absence of valid and reliable instruments to measure the alexithymia construct, Taylor, Ryan and Bagby (1985) devised the original self-report Toronto Alexithymia Scale (TAS). They used both empirical and rational methods in scale construction, initially defining five domains of alexithymia: (a) difficulty describing feelings, (b) difficulty distinguishing between feelings and accompanying bodily sensations, (c) lack of introspection, (d) social conformity, and (e) impoverished fantasy life and poor dream recall (Taylor et al., 1997). Responses were rated with a 5-point Likert scale ranging from ‘strongly disagree’ to ‘strongly agree’. After factor and item analysis, the 41 item questionnaire was pared to 26 items and four domains that were more theoretically consistent with the alexithymia construct. These four domains, or factors, were: Factor 1 (F1) difficulty identifying and distinguishing between feelings and bodily sensations, Factor 2 (F2) difficulty describing feelings, Factor 3 (F3) reduced daydreaming, and Factor 4 (F4) externally oriented thinking.

            While studies demonstrated support for the discriminant and convergent validity of the TAS, and the psychometric properties of the TAS were a considerable improvement over other available instruments, the construction of the TAS prompted refinement of the alexithymia construct and its essential facets. Daydreaming, for example, was determined to negatively correlate with the first factor (Taylor et al., 1997). In 1992 the attempt at scale reconstruction led to the development of a revised, 23 item self-report scale, the TAS-R. Continuing shortcomings with the scale prompted further examination of its compositional structure. There was high correlation between factors 1 and 2, and several items cross-loaded on each factor. Further revision resulted in the TAS-20 (Bagby, Parker &Taylor, 1994; Bagby, Taylor & Parker, 1994), a 20-item self-report scale consisting of 3 factors: Factor 1 (F1) difficulty identifying feelings, Factor 2 (F2) difficulty describing feelings, and Factor 3 (F3) externally-oriented thinking. These three factors represent essential intercorrelated traits that are theoretically congruent with the alexithymia construct. The TAS-20 eliminates the theoretical overlap of the three factors and the cross-loading of items that was a liability in earlier versions, and demonstrates good internal consistency and test-retest reliability. “The psychometric properties of the TAS provide considerable empirical support for the validity of the alexithymia construct” (Taylor et al., p. 49).

 

 

 

Research Studies Using the Original TAS

            Zeitlin and McNally.

            These researchers conducted a study (1993) to assess for alexithymia in patients with PD and patients with obsessive-compulsive disorder (OCD). Referencing Nemiah’s postulation (1984) that alexithymia may be prevalent in those with PD, they noted an absence of any studies to test that hypothesis. Referring to the high incidence of anxiety sensitivity among those with PD, or the fear of anxiety symptoms resulting from a belief they could have harmful consequences, the authors noted Barlow’s proposal (1988) that those with PD may try to avoid experiencing frightening physical sensations by a generalized constriction of emotional experience. They surmised that if a function of alexithymia is a constriction of emotion, individuals with PD should be more alexithymic than those with an anxiety disorder of less anxiety sensitivity such as OCD.

            The PD group consisted of 27 new referrals to an anxiety disorders clinic that had been referred by their MD, meeting DSM-III-R criteria for PD. The group comprised 6 men and 21 women with a mean age of 34.4 years (SD=8.6) and age range of 23 to 57. The control group consisted of 31 new referrals to the same clinic that met DSM-III-R criteria for OCD, having been referred by an MD. This group comprised 20 men and 11 women with a mean age of 32.9 years (SD=11.8) and age range of 18 to 64.

            All participants completed the original TAS and Anxiety Sensitivity Index (ASI), a 16 item self-report scale that measures fear of anxiety symptoms. Using a 4 point Likert scale, scores can range from 0 (no anxiety sensitivity) to 64 (high anxiety sensitivity), with a normative mean score of 17.8 (SD=8.8). The authors describe reliability and validity data for the ASI as favorable (1993).

            The mean TAS score for the PD group was 76.48 (SD=12.36), above the cutoff score of 74 indicative of alexithymia. The mean TAS score for the OCD group was 61.16 (SD=9.82), below the cutoff score of 62 indicative of no alexithymia. The PD group scored higher on the ASI with a mean score of 37.00 (SD=10.20) compared to the OCD group mean score of 27.94 (SD=11.67). The PD group was more alexithymic than the OCD group even when the anxiety sensitivity effect was controlled through ANCOVA (F=16.21, df=1, 55, p<0.001). To measure for group gender effect, TAS and ASI scores were compared by gender for both diagnostic groups by t tests. There was no significant group gender effect demonstrated. Eighteen (67%) of the 27 in the PD group scored at or above the TAS cutoff score of 74, four (13%) of the 31 in the OCD group scored at or above the cutoff of 74.

            The study concludes that PD has more association with alexithymia and anxiety sensitivity than does OCD. The authors speculate that higher levels of alexithymia stem from constriction of emotion to minimize related physiological sensation due to high anxiety sensitivity. It remains unclear as to whether alexithymia is primary and precedes PD or is a secondary consequence of PD, and whether the somatic preoccupation which is characteristic of alexithymia may predispose the individual for anxiety sensitivity and subsequent panic attacks.

 

            Parker, Taylor, Bagby and Acklin.

            In 1993 these researchers published a study that evaluated the hypothesized association between alexithymia and PD, compared to alexithymia in simple phobia. Their rationale for comparing these two disorders is the association of alexithymia with PD but not with simple phobia. They expected a high incidence of alexithymia in individuals with PD due to their somatic preoccupation, difficulty identifying psychological precipitants to panic, and propensity to negatively interpret somatic symptoms of autonomic arousal consistent with the alexithymia construct. They theorized a low incidence of alexithymia in simple phobia as it is a neurotic disorder with greater capacity for regulating anxiety through complex psychological defenses.  

            The PD group consisted of 30 consecutive referrals to an outpatient hospital based psychiatric clinic in Honolulu, Hawaii who met DSM-III-R criteria for PD. The group comprised eight men and 22 women with a mean age of 35.6 years (SD=5.9) and age range of 25 to 53 years. Twenty (66.7%) of the patients with PD also had agoraphobia. The control group consisted of 32 consecutive referrals to the same clinic who met DSM-III-R criteria for simple phobia. This group comprised 13 men and 19 women with a mean age of 43.6 years (SD=10.4) and age range of 26 to 66 years. The PD group was significantly younger than the control group (t=3.71, df=60, p<0.001). The mean scores on Hollingshead’s educational scale were not significantly different and were within the range that corresponds to middle-class populations with some university education.

            All participants completed the TAS and MMPI. The groups were compared on the TAS and selected MMPI scales by two-tailed t tests with a significance level of p<0.007. The PD group scored significantly higher on the TAS and on MMPI scales assessing dependency, anxiety, and somatic complaints. The two groups did not differ significantly on the repression or hysteria MMPI scales. A score of 74 or higher on the original TAS indicates a significant presence of alexithymic traits. Of the PD group, fourteen (46.7%) scored 74 or higher on the TAS, compared to four (12.5%) of the simple phobia group. A score of 62 or lower on the TAS indicates an absence of alexithymic traits. Of the PD group, six (20.0%) scored at or below 62, compared to 21 (65.6%) with simple phobia. There was no measure for group effect by age or gender.

            The authors state that the results confirm the hypothesized prediction of higher rates of alexithymia in those with PD compared to those with simple phobia. They state that the 46.7% rate of alexithymia in the PD sample   is higher than the rate of 37% in a general psychiatric outpatient sample that was found in one unpublished study. The 12.5% rate found in the simple phobia sample compares to the rate found in another study of normal college students and adults (Taylor, Bagby & Parker, 1993). The authors were unable to determine whether alexithymia was an antecedent of panic or secondary to the effect of anxiety on these individuals. Given the rate of alexithymia found in the PD group, the authors concur with Nemiah (1984) that every individual seeking treatment for panics should be assessed for the presence of alexithymia as it has significant implications for treatment.

 

            Joukamaa and Lepola.

            This Finnish pair of researchers conducted a study (1994) to test for alexithymia in individuals with PD, compared to alexithymia in a normal control group. Their purpose was to “ascertain how alexithymia and panic disorder are interrelated” (p. 33). Noting the strong association between alexithymia and somatic disorders,   psychosomatic disorders and chronic pain, they comment on the scarcity of studies of the association between alexithymia and psychiatric disorders like PD.

            The PD group consisted of 50 consecutive referrals to a private outpatient clinic in Finland that were diagnosed with PD by one of the researchers. The group comprised 12 men and 38 women with a mean age of 41.7 years (SD=7.3). The control group consisted of 50 healthy students at a nursing college without noteworthy somatic or psychiatric disturbances. The group comprised 5 men and 45 women with a mean age of 28.7 years (SD=6.8). No age range data was provided on either group. The difference in mean age of each group was statistically highly significant. And the difference in social status and education levels between the groups was also considered statistically significant.

            All participants completed the TAS and the General Health Questionnaire (GHQ), a 36 item self-report scale used as a measure of neurotic type psychopathology. In the PD sample, 12 (24%) were considered “true alexithymics” due to a score at or above the cutoff of 74, 20 (40%) were considered not alexithymic due to scores at or below the bottom cutoff of 62, and 18 (36%) were “probable alexithymics” due to a score between the cutoffs. The control group had no true alexithymia, and 6 (12%) were “probable”, a highly significant difference. Of the PD group, 34 (68%, p<0.001) were assessed as “psychiatric cases” on the GHQ, compared to 11 (22%) of the control group. Both alexithymia and psychiatric disorder had highly significant association with age and socioeconomic stratum, specifically oldest age and lowest socioeconomic level.

            The authors conclude that alexithymia and psychic disturbance had a highly significant association in the PD sample. They consider 60% to be alexithymic (true and probable), 68% to be psychiatric, and 48% to be both, with no alexithymia within the control sample. Using both multidimensional ANOVA and logistic regression analysis, “panic disorder was highly significantly associated with alexithymia but not with psychic disturbance” (p. 35). They identify a limitation of the study in the small sample size.

           

Research Studies Using the TAS-20 

            Cox, Swinson, Shulman and Bourdeau.

            Citing the studies of Zeitlin and McNally (1993) and Parker, Taylor, Bagby & Acklin (1993) that found elevated levels of alexithymia in PD, these researchers conducted a study (1995) to test the hypothesis that only one dimension of the alexithymia construct may be responsible for this elevation. Cox et al. cited the need to investigate a “conceptual and measurement issue” (p. 195) and posited an alternate hypothesis to the reputed link between alexithymia and PD. They identified overlap between Clark’s (1986) catastrophic misinterpretation model, the anxiety sensitivity construct (Reiss, Peterson, Gursky & McNally, 1986), and the alexithymic dimension of difficulty identifying and differentiating emotions from physical sensations. These researchers hypothesized that a PD sample would score high only on the TAS factor (F-1) related to difficulty identifying emotions and differentiating them from physical sensations. They did not believe there would be significant correlation with the other TAS factors: difficulty describing emotions (F2) and externally oriented thinking (F3). They chose to use another anxiety disorder as a control group, social phobia. Their rationale was two-fold. Individuals with social phobia and PD experience anxiety in various circumstances as compared to simple phobia. And while both groups experience very intense anxiety, PD involves “endogenous” anxiety attacks, whereas social phobia involves “exogenous” attacks precipitated by external circumstances.

            The PD group consisted of 100 outpatients at an anxiety disorders clinic that were diagnosed by a psychiatrist or clinical psychology doctoral student and met DSM-III-R criteria for PD. Levels of assessed agoraphobia among this group were: 14% without agoraphobia, 34% mild agoraphobia, 41% moderate agoraphobia, and 11% severe agoraphobia. The group comprised 33 men and 67 women with a mean age of 34.28 years (SD=9.82). The control group consisted of 46 outpatients at the same clinic that met DSM-III-R criteria for a diagnosis of social phobia. The group comprised 23 men and 23 women with a mean age of 32.46 years (SD=8.01). No age range data was provided on either group.

            All participants completed the TAS-20, ASI, Panic Attack Questionnaire, Beck Anxiety Inventory, and Symptom Checklist 90 – Somatization Subscale. The mean TAS-20 results revealed no significant between group differences on any of the three TAS-20 factors. The TAS-20 cutoff scores are: 61 or greater - alexithymia; 51 or less - not alexithymia; 52 to 60 - probable alexithymia. Based on this scoring, 34.0% of the PD group was alexithymic, 28.3% of the social phobia group was alexithymic, a non- significant difference. However in both groups the identifying emotions factor, F1, was significantly higher than F2 or F3. And in both groups difficulty describing emotions, F2, was higher than externally oriented thinking, F3. The researchers also correlated the PD group’s TAS-20 results with the other anxiety assessment scales and found highly significant correlation between them and the TAS-20’s F1 and weak correlation with F2 and F3.

            Cox et al. (1995) state that alexithymia levels of 34.0% in the PD group and 28.3% in the social phobia group are not only a non-significant difference, but approximate the prevalence figures of alexithymia in the general outpatient psychiatric population. They suggest that the tendency for those with PD to score high on the F1 trait can lead to many false positives on the TAS. They further speculate that the social phobia level of alexithymia may be relatively high and close to the PD level as both groups experience panic attacks that may be reflective of the F1 trait of difficulty identifying emotions.

 

            Fukunishi, Kikuchi, Wogan and Takubo.

            Noting the preceding three cross-sectional studies of alexithymia prevalence in PD samples, these researchers published a longitudinal follow-up study (1997) of alexithymia in PD and social phobia samples. In a 6 month follow-up study they examined three factors: the prevalence of alexithymia in these two groups, the effect of psychiatric treatment on alexithymic traits, and what psychiatric factors are associated with a decrease in alexithymia.

            The PD group consisted of 26 patients admitted to the psychiatric inpatient unit or outpatient unit at a Tokyo hospital, who met DSM-IV criteria for PD. The group comprised 12 men and 14 women with a mean age of 31.7 years, and age range of 22 to 49 years. The mean education was 13.5 years with a range of 10 to 16 years. The social phobia group consisted of 24 patients at the same inpatient and outpatient facility, who met DSM-IV criteria for social phobia without panic attacks. The group comprised 9 men and 15 women with a mean age of 33.7 years, and age range of 18 to 47 years. The mean education was 12.9 years with a range of 8 to 16 years. For a healthy control group, they recruited 25 individuals living in the Tokyo metropolitan area. The group comprised 10 men and 15 women with a mean age of 33.0 years, and age range of 20 to 48 years. The mean education was 13.4 years with a range of 11 to 16 years. Using ANOVA, chi-square and student two-tailed t tests, the demographic variables of age, educational level and gender were demonstrated to have non-significant variances.

            All participants completed the TAS-20, the Hamilton Depression Scale (HDS) and Hamilton Anxiety Scale (HAS). Six months after initiation of treatment, participants again completed the TAS-20. Before initiation of treatment, 14 (53.8%) of the 26 individuals in the PD group, and 14 (58.3%) of the 24 in the social phobia group were alexithymic based on meeting or exceeding the TAS-20 cutoff score for alexithymia. The difference between these two groups was considered a non-significant difference. After treatment, the alexithymia prevalence rates were: 8 (30.8%) in the PD sample and 8 (33.3%) in the social phobia sample, again a non-significant difference. Treatment reduced the TAS-20 scores in 23 (88.5%) of the 26 in the PD group, and in 20 (83.3%) of the 24 in the social phobia group. The alexithymia prevalence rate in the healthy control group of 25 was 4 (16%) with a TAS-20 score of 52 or greater, a significant difference from the two patient groups. After psychiatric treatment there were no significant differences between the three groups.

            The total TAS-20 scores were positively and significantly correlated with the HDS and HAS scores for all three groups. After treatment, there were no significant differences on the TAS-20, HDS, or HAS scores for either patient group. Also after treatment, patients who were still alexithymic (n=16) showed significantly higher HAS scores than those who were not alexithymic (n=44). The results were considered not significantly influenced by gender, age or educational level.

            Noting that 23 of the 26 (88.5%) patients with PD, and that 20 of the 24 (83.3%) with social phobia showed a decrease in TAS-20 scores, the authors suggest that alexithymic traits can be reduced by psychiatric treatment for anxiety. They also found that scores on both F1 and F2, though not for F3, were reduced with treatment. They suggest that these alexithymia components are related to anxiety, whereas F3 (external thinking) may not be. The significant level of alexithymia in both patient groups (before treatment) compared to the control group, suggests alexithymia exists in many with PD and social phobia.

            Fukunishi et al. (1997) reference the state or trait question about the nature of alexithymia. Freyberger (1977) suggests two types of alexithymia: primary which is a personality trait, and secondary which is a state reaction. They state that in contrast to Salminen, Saarijarvi, Aarela & Tamminen (1994) who found alexithymia to be a trait instead of a state, their study found an overall decrease in alexithymia by psychiatric treatment suggests alexithymia to be a reversible state reaction.

 

            Bankier, Aigner and Bach.

            In 2001 these researchers published a comparative assessment of alexithymia levels in several psychiatric disorders: somatoform, panic, obsessive-compulsive, and in depression. They note inconsistent evidence of a correlation between alexithymia, PD, and psychosomatic symptoms, and reference a study (Bach, Bach & deZwaan, 1996) that suggests alexithymia and somatization to be separate but simultaneously occurring constructs. Similarly conflicting evidence is cited regarding a correlation between alexithymia and depression, including some evidence suggesting each exists independent of the other.

            The sample groups consisted of 234 patients admitted over a four year period to the Behavior Therapy Ward at the Department of Psychiatry, University of Vienna, Austria. All diagnoses were made by use of the Structured Clinical Interview for DSM-IV. The PD group of 123 individuals consisted of 48 men and 75 women with a mean age of 36 years (SD=11.3). The somatoform disorder (SOM) group of 24 individuals consisted of 3 men and 21 women with a mean age of 38 years (SD=8.6). The obsessive-compulsive disorder (OCD) group of 59 individuals consisted of 34 men and 25 women with a mean age of 32 years (SD=9). The depression group of 28 individuals consisted of 10 men and 18 women with a mean age of 38 years (SD=11). The mean age for all participants was 35.3 years (SD=10.7) with an age range of 18 to 71 years. Of all 234 participants, 139 (59%) were women, and 95 (41%) were men.

            The mean TAS-20 total score of 49 (SD=11.4) for the PD group was lower than the SOM group score of 54.9 (SD=12.4), the OCD group score of 51.9 (SD=8.7), and the depression group score of 56.6 (SD=13.6). Of the TAS-20 subfactors, F1 was significantly associated with SOM and depression; F2 with depression; F3 with OCD; while PD had a significant negative correlation with F3. Age was a non significant variable with total TAS-20 scores or any of the three subfactors. Female gender was significantly associated with F1 (difficulty identifying feelings and distinguishing them from bodily sensations) and male gender was significantly associated with F3 (externally-oriented thinking). There was significant correlation between lower educational level and TAS-20 total score and F3.

            The authors note the contrast between this study and that of Zeitlin and McNally  (1993) who found significantly higher prevalence of alexithymia in a PD sample compared to an OCD sample. This study found the reverse, possibly the result of a larger sample size. The earlier study also did not investigate the multidimensionality of the alexithymia construct with a multi-factorial analysis. These researchers reference the debate as to the diagnostic value of total TAS-20 alexithymia scores, and note greater diagnostic specificity in a multifactorial application of the TAS-20. They state that the three TAS-20 subfactors can provide valuable diagnostic information about cognitive and affective aspects of various psychiatric disorders.

 

Conclusions and Intent of this Research Study

            The alexithymia construct involves complexities of cognitive and affective processing deficits and possesses heuristic value for conceptualizing those deficits. Bowlby’s model (1969, 1973) of insecure attachment provides clarification of the etiology of limited internalized affect regulating capacity evident in the alexithymia construct. The alexithymia construct is analogous to Krystal’s (1988) model of affective regression to a somatized and undifferentiated state and is consistent with the Lane and Schwartz (1987) model of affective delay at or regression to an earlier epigenetic level of development. These developmental arrests appear to coincide with the somatization involved in the F1, and the affective verbalization deficits involved in F2, of the TAS-20.

            The alexithymia construct also appears to be consistent with the salient features of PD. The somatic preoccupation, intense autonomic arousal, and affective dysregulation involved in Barlow’s false alarm (1988) and Klein’s suffocation alarm (1993) models are conceptually congruent with the somatic preoccupation of alexithymia. Clark’s (1986) catastrophic misinterpretation theory and Barsky’s (1992) amplification theory are consistent with the cognitive and affective deficits contained in the alexithymic model and appear to correlate with the TAS-20 F1 deficits in differentiating emotions from corresponding physiological sensations. By that misinterpretation and confusion between the psyche and soma, Barlow’s (1988) ‘deranged’ false alarm is triggered.

            While alexithymia has been associated with several psychiatric disorders including somatoform, PTSD, OCD, depression, eating disorders and substance abuse, it would seem that alexithymia might have an even higher correlation with PD. The degree and velocity of the regression that is a panic attack is unique and extreme, while the extent of personality disorganization and affect intensity is acute. Alexithymia has been described as having a “cognitive analogue in the thought disorders of schizophrenics” (Taylor et al., 1997, p. xiii), a comparison that could also be drawn with panic attacks and the inherent, though transient, disconnection from reality that they comprise.

            The data from the six research studies on the correlation between alexithymia and PD has been inconsistent. It was suggested by Bankier, Aigner and Bach (2001) that some of the inconsistency results from comparisons between studies which rely on a TAS-20 total alexithymia score only, and studies that use the total score in addition to scores from the three TAS-20 subfactors. As alexithymia is a multidimensional construct, a multifactorial analysis provides greater specificity as to the gradational involvement of each factor in a disorder.

            It is therefore the purpose of this study to measure and compare TAS-20 total alexithymia scores and subfactor scores of a PD sample compared to a sample comprised of a cross-section of outpatient psychiatric diagnoses. The multiple diagnoses group was selected for a cross-section of disorders that have been associated with the alexithymia construct. The rationale is to investigate the prevalence of alexithymia in PD compared to a wide spectrum of disorders that may have variable degrees of association with the construct. Analysis of the TAS-20 subfactor scores is considered crucial in evaluating the contribution of each factor to the overall alexithymia score. It is also considered essential to measure for significant group effect by age or gender.