Each is liable to panic, which is exactly, the terror of ignorance surrendered to the imagination.

                                    - Ralph Waldo Emerson (1803-1882)

            The words of this American poet and philosopher describe in poetic form, the power of the imagination to induce fear and panic in the absence of knowledge and rational thought. Primitive man was terrified by events he did not understand and could not explain – imagine the impact of thunder and lightning on earliest hominids that did not yet have even a rudimentary knowledge of physics. Such events and countless others would understandably have been terrifying – the terror of ignorance surrendered to the imagination.

            As modern man has more than ample knowledge of the natural sciences, most individuals do not panic over storms, solar eclipses, or other natural phenomena of which we have the comfort of comprehension. Earthquakes, hurricanes, tornadoes or other “natural disasters” are clearly terrifying for those directly involved, but while terror may be a normal reaction panic is not, for panic is fear of a non-physical imagined threat. The chronic panic attacks that constitute Panic Disorder (PD) are ultimately an acute, irrational fear of the imagined dissolution of the self. The individual who experiences such attacks are not unlike primitive man with an imagination fueled by ignorance. In the case of PD it is not ignorance of the external world of natural science but ignorance of the inner world of cognitions, affects, and somatosensory experiences - the result of arrest at or regression to a primitive level of emotional development. Ignorance in this inner domain fuels imagination, contributes to catastrophic explanations of ambiguous internal events and sensations, and culminates in panic attacks. This lack of internal knowledge and self-awareness constitutes the deficits of alexithymia.

Etiological Theories of PD

            Though an isolated panic attack is experienced by 7% to 34% of the general population (Norton, Harrison, Hauch & Rhodes, 1985; Telch, Lucas & Nelson, 1989), only a small percentage of these individuals develop overwhelming fear of another attack or the fear of fear cycle (Goldstein & Chambless, 1978) that is involved in the recurrent and unexpected panic attacks that define PD. Panic attacks may occur in other anxiety disorders but are situationally bound as in simple or social phobias. Barlow (1988) proposes a model for the etiology of PD based on the similarity between the physiological activation of a panic attack and the fight or flight response. A panic attack is a fight or flight response in the absence of real danger, and as such is a false alarm. Due to the powerful impact of a panic attack, an immediate association develops between the triggering stimuli and the intense physiological sensations activated during the attack, an example of classical conditioning. For individuals who develop PD, whenever a stimulus generates the sensations associated with the first attack, a false alarm of danger is sounded and a panic attack is triggered. When the false alarm becomes associated with the internal cues or sensations of fear, a learned alarm develops. Future panic attacks can then result from the learned alarm of those physiological sensations. Barlow believes that individuals with PD have an inborn susceptibility for somatic preoccupation and over reactivity to physiological cues.          

            PD is but one of several disorders characterized by prominent somatic features which, according to Barsky (1992), are exacerbated by somatosensory amplification or the “tendency to experience somatic and visceral sensation as intense, noxious, and disturbing” (p. 28). He describes amplification as the tendency for hypervigilance of bodily sensations, especially infrequent sensations, and the tendency to interpret them as pathological. All physiological sensations can be amplified including normal reactions such as increases in heart rate; minor dysfunctions such as an eye twitch or autonomic reactions to emotional arousal; or the symptoms of more serious medical diseases. He believes amplification may be a transitional state or an enduring trait acquired in childhood or even “hard wired” in from birth (p. 29). 

            According to Clark (1988), “catastrophic misinterpretation of certain bodily sensations is a necessary condition for the production of a panic attack” (p. 84). By this, he means there is a “cognitive disturbance in panic patients” (1986, p. 469) that causes faulty processing of bodily sensations and the belief that these sensations are more serious than they actually are. This can manifest in mistaking rapid pulse or respiration as an indication of a pending heart attack, or equating breathlessness with suffocation and imminent death. This faulty cognitive process leads to fear of the bodily sensations of fear, or a fear of fear cycle wherein affect becomes dysregulated.

Alexithymia

            Taylor (1992) and Taylor, Bagby and Parker (1997) consider PD as one of several disorders of affect regulation, describing “panic [PD] as a disorder involving deficits in the cognitive processing and regulation of emotion” (1997, p. 142). In the absence of dysfunction on both the cognitive and affective level, PD would not emerge from that first panic attack. Deficiencies in cognitive and affective regulation that predispose an individual to PD are in part a disruption in the internalization of comforting parental introjects due to bonding and attachment failures (Taylor, 1987). The central component of their preeminent theory of affect regulation is the concept of alexithymia, a multifaceted personality construct introduced by Nemiah and Sifneos (1970) that constitutes a deficiency in adequate affective identification, expression and regulation. It was Sifneos (1973) who coined the term from the Greek: a=lack, lexis=word, thymos=emotion. The alexithymia construct contains these features: (a) difficulty identifying feelings and distinguishing between emotions and corresponding bodily sensations, (b) difficulty describing feelings to others, (c) constricted imaginal life and fantasies, (d) externally oriented cognitive style (Nemiah, Freyberger & Sifneos, 1976; Taylor, 1984a, 1994; Taylor, Bagby & Parker, 1991).  Taylor et al. (1997) state that the deficits that constitute alexithymia are the result of disturbances in affect development in early childhood, consistent with the theories of Krystal, Lane and Schwartz, and Bowlby.

Etiological Theories of Alexithymia       

             Krystal’s theory of affect development (1988) describes infantile affects as preverbal, somatized and undifferentiated that progress to become verbalized, unsomatized and differentiated in the absence of childhood psychic trauma. This progression results in affect tolerance as well as the capacity for attenuation of affects and the ability to use affects as signals that assist the evaluation of situations and appropriate responses. Childhood psychic trauma can hinder this development, resulting in the dread of affects that represent a return of trauma. He attributes alexithymia to a developmental arrest following infantile or childhood psychic trauma or a regression in affective-cognitive function resulting from adulthood trauma. Alexithymia represents: “regression from verbalized, desomatized, and differentiated affects toward the resomatized and undifferentiated form [that] represents a predisposition to psychosomatic diseases” (p. 264). Similarly, he describes PD as “a perfect example of regression in affects to their infantile, somatic, undifferentiated form.” (1992, p. 407).

            Lane and Schwartz (1987) propose a cognitive-developmental theory of emotional development that stresses the fundamental role of emotional disturbance in all mental disorders. Their central premise is that emotional awareness is a form of cognitive processing that develops upward through five levels of structural transformation. The emergence of symbolization and language assists in the child’s development of emotional awareness and capacity to regulate affects on both the intrapersonal as well as interpersonal level. With the development of language, the child can verbally represent and think about their emotions with decreasing dependence on the parent. The formation of language and symbolization allow for cognitive-emotional development with the emergence of cognitive schemas of affects that hierarchically elevate the experience of affect. Within their five level epigenetic model of affect development, emotion at the earliest level is experienced as a bodily sensation and a tendency toward action; later it is experienced both on the psychological and somatic level; and at the highest level it is a blend of different and differentiated feelings with an awareness of other’s feelings. Taylor et al. (1997) assert that disorders of affect regulation and alexithymia result from either a disruption in progression within this model or regression to an earlier level.

            Bowlby’s seminal attachment theory (1969, 1973) has influenced the development of models of affect development in that it has much explanatory power for the development of the insecurity involved in the etiology of childhood and adult disorders. His theory challenges the earlier theory of secondary drive as a motivator for attachment behavior. The secondary drive theory states that animal and human desire for proximity to others results from a need for gratification of primary needs such as warmth, shelter, sex, but primarily food. Attachment theory proposes the desire for proximity, or attachment behavior, is driven by a need for protection from predators and the security that protection provides, and that attachment behavior is most highly elicited when threats to personal security cause alarm. When one lacks confidence that protective attachment figures will be available or responsive, the result is what Bowlby termed anxious or insecure attachment. Conversely, confidence in ones attachment figures results in secure attachment. The theory suggests childhood models of attachment persist and individuals with anxious or insecure attachment may therefore be susceptible to manifesting clinging behavior and anxiety symptoms, as “uncertainty about the accessibility and responsiveness of attachment figures is a principal condition for the development of unstable and anxious personality” (1973, p. 322). Bowlby believed that while many factors play a causal role, early life experiences that cause doubt in the availability of attachment figures when most needed contributes to disruption in the formation of secure attachment. In reference to Bowlby’s theory, Taylor (2000) states “alexithymia is associated with insecure attachment” (p. 136).

History of the Alexithymia Construct

            The alexithymia construct was born out of studies by several researchers of patients who suffered from the so-called classical psychosomatic disorders. In the 1950s, Horney (1952) and Kelman (1952) noted poor response to psychoanalytic therapy by patients who evidenced psychosomatic symptoms. These patients were characterized by their limited emotional awareness, minimal inner experiences and concrete thinking styles. Similar traits were noted by Sifneos (1967) and Nemiah and Sifneos (1970) in their work with individuals with psychosomatic disorders, traits such as difficulty describing subjective feelings, limited fantasy life, and a communication style marked by over attention to minute, external detail. In that same time period, Krystal (1968) and Krystal and Raskin (1970) were conducting work with patients with drug addictions and patients with posttraumatic disorder, noting similar cognitive and affective characteristics in these patients that Sifneos and Nemiah were reporting. And in 1984, Nemiah described PD as “the prototypical psychosomatic disorder” (p. 134).

Integrated Theory of Affect Regulation

            The Taylor (1992) and Taylor, Bagby and Parker (1997) theory of affect regulation proffers a comprehensive explanation of the etiology of PD by integrating elements of all these theories and emphasizing the role of alexithymia in the somatic process. Their theory allows for neurobiological involvement in alexithymia with “constitutional-inherited or acquired disturbances in the regulation of neurotransmitter systems that mediate affects” (1997, p.140) or a deficiency in the coordination of function between the two cerebral hemispheres. One study conducted thus far on the heritability of alexithymia has demonstrated a strong genetic involvement (Heiberg & Heiberg, 1977). Within the Taylor et al. model, the panic attacks of PD are “sudden overwhelming floods of undifferentiated affect” (1997, p. 141) the result of catastrophic misinterpretation of bodily sensations consistent with Clark’s model. Although central neurotransmitter systems are involved in regulating the biological reaction to affects such as separation anxiety, threats to security in important relationships can trigger panic attacks. Individuals with insecure attachment patterns (Bowlby’s model) remain excessively dependent on others, not having adequately separated/individuated from mother and integrating her anxiety-regulating capacity. “Alexithymic patients with panic disorder, however, are likely to show incomplete transitional object development . . . and may still rely on sensation objects for self-regulation” (Taylor et al., 1997, p. 147). Their theory considers the somatization of disorders such as PD as regression to or arrest at earlier preverbal and somatized levels of affect development in the Lane and Schwartz (1987) model, consistent with the Krystal model (1988).

Toronto Alexithymia Scale (TAS)

            In 1985 Taylor, Ryan and Bagby developed a self-report instrument to measure for alexithymia, the 26 item Toronto Alexithymia Scale (TAS). This scale drew criticism for its high rate of false positives for alexithymia (Horton, Gewirtz & Kreutter, 1994a, 1994b) and in 1992, Taylor, Bagby and Parker published a revised version. The new Toronto Alexithymia Scale (TAS-20) was shortened to 20 items but demonstrated improved test-retest reliability and internal consistency. It has a three-factor structure theoretically consistent with the alexithymia construct. The three factors are: (a) Factor 1 – difficulty identifying feelings and distinguishing them from bodily sensations of emotion (b) Factor 2 – difficulty describing feelings, and (c) Factor 3 – externally-oriented thinking. This instrument demonstrates superiority of reliability and validity over other available measures such as the MMPI Alexithymia Scale, the Schalling Sifneos Personality Scale, and the Revised Schalling Sifneos Personality Scale, and has been demonstrated to be a psychometrically sound measure of alexithymia (Bagby, Parker & Taylor, 1994; Bagby, Taylor & Parker, 1994).

            Three studies have been conducted using the original 26 item TAS to measure alexithymia in a PD sample compared to a control group. One study reported ‘true’ or ‘probable’ alexithymia in 60% of a PD sample and 12% in a healthy control group (Joukamaa & Lepola, 1994). Another study found alexithymia in 47% of patients with PD compared to 12% of patients with social phobia (Parker, Taylor, Bagby & Acklin, 1993), and a third reported alexithymia levels of 67% for a PD sample and 13% for an obsessive-compulsive disorder (OCD) sample (Zeitlin & McNally, 1993). Three similar studies have been conducted using the revised TAS-20. One measured alexithymia in PD and social phobia samples and found rates of 34% and 28% respectively, a nonsignificant difference (Cox, Swinson, Shulman & Bourdeau, 1995). Another reported alexithymia rates of 54% in a PD sample and 58% in a social phobia sample (a nonsignificant difference) compared to 15% in a healthy sample (Fukunishi, Kikuchi, Wogan & Takubo, 1997). The third reported a PD sample to be significantly associated with a lower total TAS-20 score compared to samples with: somatoform disorder, depression and obsessive-compulsive disorder (Bankier, Aigner & Bach, 2001).  

Statement of the Problem

            This current research explored a correlation between alexithymia and PD in adolescents and adults, and the relationship between PD and the three factors that comprise the TAS-20. Factor one (F1): difficulty identifying feelings and distinguishing them from physical sensations, appears to theoretically overlap both somatization and the amplification construct and would therefore seem to be strongly associated with PD. The covariables of age and gender are considered, as a weak relationship has been demonstrated between TAS-20 scores and age while a significant relationship between TAS-20 scores and gender has been demonstrated (Bagby, Parker & Taylor, 1994). Differences in levels of alexithymia in PD with agoraphobia were compared to levels in PD without agoraphobia. All levels of alexithymia were measured with the TAS-20.

The Hypotheses

            This retrospective research study tested the following hypotheses:

1.  There is a significant relationship between alexithymia and PD.  

2.  There is no significant relationship between alexithymia and other DSM-IV diagnostic groups that have been conceptually associated with the alexithymia construct.

3.  There is no significant difference in alexithymia between PD with Agoraphobia and PD without Agoraphobia.

4.  There is a significant relationship between the TAS-20 Factor 1 and PD.

The Assumptions

1.  The first assumption is that the TAS-20 is a valid and reliable measure of alexithymia.

2.  The second assumption is that subjects will be honest and accurate in their responses to all items on the TAS.

Study Rationale

            This research project was conducted to measure significant differences in the prevalence of alexithymia among disorders that have been associated with alexithymia. This involved a comparison of alexithymia levels in those with PD and those with a disorder characterized by one of the salient symptoms theoretically associated with the construct such as anxiety, depression, phobia, substance abuse, and posttraumatic stress disorder. In conducting this research, I expected to find a significant difference in alexithymia between those with PD and those with other disorders. I did not expect to find significant variance between panic disordered individuals with, and those without, agoraphobia. These expectations are the result of first hand clinical experience with these groups that has strongly suggested high levels of alexithymic characteristics in a PD population, irrespective of agoraphobia, compared to other diagnostic groups. The degree of apparent alexithymia in PD has presented a tremendous therapeutic challenge in assisting these patients to develop the self-awareness necessary to diminish symptoms. Additionally, it was assumed that the TAS -20’s F1: difficulty differentiating between feelings and physical sensations, would be the factor most significantly associated with PD given the predominance of somatization in PD. Confirmation of any of these correlations could provide direction for the development of appropriately focused treatment interventions that target core alexithymic traits in PD as well as alexithymic traits that may present in the general mental health population.