Chapter V





            The data derived from this study provide evidence of a significant relationship between alexithymia and Panic Disorder, and support for the theory that the component of alexithymia most significantly associated with alexithymia is the difficulty in identifying feelings and differentiating between emotions and concomitant physiological sensations (F1 on the TAS-20). The purpose of this discussion is to provide interpretation of the study results, evaluate their implications and theoretical consequences, as well as address limitations of the study.


The Hypotheses

            Hypothesis 1.

            There is a significant relationship between alexithymia and PD.


            The data support the first hypothesis that there is a significant group difference in alexithymia levels between the experimental (PD) group and the control group. While there is no significant main effect of the group variable of men vs. women in total alexithymia scores with respective mean scores of 58.4 and 53.1, there is a very significant group by gender interaction effect. This is demonstrated by the significant elevation of alexithymia in the PD group women compared to control group women, but non-significant increase in alexithymia in the PD group men compared to control group men. This indicates that the significant PD group vs. control group difference in alexithymia is strictly the result of the very significant difference in alexithymia scores between the PD group women and control group women.

            The TAS-20 alexithymia cut-off score of 61 is reached by the PD Group with a mean score of 61.6. Of the 30 individuals in the PD group, 16 (53.3%) score in the alexithymic range, 8 (26.7%) are in the possibly alexithymic range of 52 to 60, and 6 (20%) are in the non-alexithymic range. Of the 16 participants in the PD group who reach the alexithymia cutoff score, 8 (50%) are women and 8 (50%) are men. But the 18 men in the PD group comprise 60% of the PD sample while the 12 women comprise 40%.

            Over half of the PD group evidences alexithymia and another quarter of the group is in the possibly alexithymic range. Only one-fifth of the PD group is non-alexithymic.


            Hypothesis 2.  

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


             The data support the null hypothesis that there is no relationship between alexithymia and other diagnostic categories that are associated with the alexithymia construct. The control group fails to achieve the TAS-20 cutoff score of 61 with a mean score of 50.47, below the non-alexithymia cutoff score of 51. Of the 30 control group participants, 8 (26.7%) score in the alexithymic range, 3 (10%) are in the possibly alexithymic range, and 19 (63.3%) are in the non-alexithymic range. Of the 8 in the alexithymic range, 6 (75%) are men, and 2 (25%) are women. The control group is comprised of 15 (50%) men and 15 (50%) women.

            The control group as a whole evidences a lack of alexithymia with two-thirds of its individual participants scoring in the non-alexithymic range. Only one-quarter of the control group evidences alexithymia.


            Hypothesis 3.

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


            The data support the hypothesis that there is no significant group difference in alexithymia levels between PD with Agoraphobia, and PD without Agoraphobia. Participants with agoraphobia (N=14) have a mean total alexithymia score of 63.5 and participants without agoraphobia (N=16) have a mean total alexithymia score of 59.9, a non-significant difference. Of the 14 with agoraphobia, 7 (50%) reached the TAS-20 cutoff score of 61. Of the 16 without agoraphobia, 9 (56%) reached the cutoff score of 61. Theoretical consideration for these results will be discussed later in this section under the topic of avoidant type “Safety Behaviors”.


            Hypothesis 4.

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


            The data also support the hypothesis of a significant group effect for F1 with means of 24.3 for the PD group and 17.3 for the control group, a significant difference, and it is the only TAS-20 subscale with significant between group difference. It is also the only subscale without significant gender variance, with mean scores of 25.5 and 23.4 respectively for the PD group women and PD group men, and 17.0 and 17.6 respectively for the control group women and control group men.


Gender as a Covariable

            The significant effect by gender is consistent with the literature on the design and validation of the TAS-20 (Bagby, Parker & Taylor, 1994). It is noted that the derivation sample demonstrated a “small but statistically significant difference between the mean TAS-20 score for men . . . and the mean score for women” (p. 27). Another study by members of this group stated “a significant main effect was found for gender … with men scoring higher than women” (Parker, Bagby, Taylor, Endler & Schmitz, 1993,

p. 227). That study also found no gender effect for the TAS-20 subscale F1, but found significant gender effect for F2 and F3, with men scoring higher than women.

            This current research study found gender to have a considerable effect on total TAS-20 alexithymia scores, and on the F2 and F3 subscale scores. The only component of the TAS-20 that was not influenced by gender was subscale F1.


Implications of Gender Differences

            While this study finds a significant group difference in alexithymia prevalence between a PD sample and a control sample, that overall difference is attributable to the women in the study. The women in the control group are non-alexithymic with a TAS-20 mean score of 45.5 (51 or less = non- alexithymia), while the men in the control group fall into the possibly alexithymic range with an overall mean score of 55.5 (52 to 60 = possible alexithymia). Both the men and women in the PD group are alexithymic with mean scores of 60.9 and 62.7 respectively (61 or greater = alexithymia). Only the difference between the control group women and PD group women is significant, with mean scores of 45.5 and 62.7 respectively. The non-significant difference between the men is 55.5 and 60.9 for the control and PD groups respectively.

            The gender differences demonstrated by this study are consistent with the common perception that women tend to be more emotionally attuned than men, and are consistent with the findings of earlier studies. While the control women were non-alexithymic, the control men were possibly alexithymic. The gender effect in this study may facilitate identification of the most prominent alexithymic trait in the etiology of PD. It may also serve to differentiate the relative involvement of each alexithymic trait in PD.

The only dimension in which there were no significant gender differences - no gender interaction effect - is on the TAS-20 F1 subscale. This is the only portion of the TAS-20 that reflected a common effect of PD on both men and women.

            These results would seem to suggest that the alexithymic trait most significant in the etiology of PD involves difficulty with affect identification and differentiation of affects from their attendant physiological sensations. The TAS-20 F1 subscale of difficulty in identifying emotions and differentiating between an emotion and its physiological sequelae is clearly associated with somatization, resonating with Nemiah’s original formulation of PD as “the prototypical psychosomatic disorder” (1984, p. 134).



Gender Effect in Earlier Studies

            Of the six earlier cited studies that measured alexithymia in PD samples compared to control samples, three found no effect by gender on TAS-20 overall scores while the other three did not test for gender effect. One study (Zeitlin & McNally, 1993) noted that while “men are often more alexithymic than women” (p. 659) their results did not show a gender effect on TAS-20 scores. That study did not conduct a subfactorial analysis to separate results on the three TAS-20 subscales.


TAS-20 Subscale Results in Earlier Studies

            Conducting subfactorial analysis facilitates differentiation of the relative involvement of each factor in the etiology or manifestation of PD. Of the six previous studies of alexithymia in PD compared to a sample, three measured the multidimensionality of the alexithymia construct by separate evaluation of the three TAS-20 subscales. The other three only considered overall TAS-20 alexithymia scores. One study (Bankier, Aigner & Bach, 2001) reported no gender effect on overall TAS-20 scores but found that female gender was significantly associated with Factor 1 and male gender was significantly associated with Factor 3 of externally oriented thinking. A 1995 study (Cox, Swinson, Shulman & Bourdeau) found a highly significant association between Factor 1 and a PD group (n=100), but also found a similar association between F1 and a social phobia control group (n=46). This same study did not measure for a gender effect.



Age Effect

            A two-way ANOVA on age found a significant negative correlation between age and alexithymia scores. As age increases, alexithymia scores tend to decrease. Older individuals demonstrate lower alexithymia levels, possibly reflecting a positive correlation between increased self-awareness and advanced age.


Age Effect in Earlier Studies

            Of the six previously cited studies, one found an age effect while two did not and the other three did not test for age effect. The one study that found an age effect described a highly significant positive correlation between advanced age and alexithymia scores in individuals with both alexithymia and a “psychiatric disturbance” as determined by the General Health Questionnaire (GHQ-36) (Joukamaa & Lepola, 1994). The additional covariate of another psychiatric diagnosis might confound the evidence for an independent age effect.


Evidence of Alexithymic Traits in the Early Treatment of PD

            The significant presence of alexithymia in individuals with PD is supported by my clinical experience in treating these individuals. From the inception of treatment to the point of termination, a primary focus of treatment is reducing alexithymic features by increasing affect awareness and affect regulation. The cognitive and affective deficits that constitute alexithymia are prominent in the process that facilitates entry into treatment and become a focal point in the early phase of treatment.

            Many of these individuals do not self-identify an emotional difficulty and seek relief by contacting a psychotherapist. Instead, a sizeable percent have a history of identifying somatic concerns and seeking out medical solutions. Often this includes extensive use of medical facilities including their own primary care physician (PCP) and emergency medical services such as hospital emergency rooms. According to a 1984 study (Katon), 6% to 10% of patients in primary medical care actually have PD, with somatic complaints that tend to be neurological, cardiological and/or gastrointestinal. Other diagnostic categories such as substance abuse are also strongly associated with a circuitous route to treatment, often through legal channels or through exasperated family members.

            Individuals with PD often come to psychotherapy after extensive use of medical services in the vain attempt to find symptom relief. They seek psychotherapeutic interventions out of their own frustration with the limited relief obtained from medical services, or by referral from the medical provider. Even before the first appointment in a therapist’s office, there is often a lengthy history of frustrated efforts to find medical solutions that is usually not present with individuals seeking therapy for other diagnoses. This type of faulty self-appraisal and related behavior would seem to be closely associated with the TAS-20 F1 subscale: difficulty identifying feelings and differentiating between emotional sensations and physical sensations. The tendency for somatization predisposes the panic disordered individual to overuse of medical services. The data from this study is consistent with this observation in the elevation on F1 for both panic disordered males and females. This finding is also consistent with Clark’s hypothesis (1986) that panic attacks are the consequence of the catastrophic misinterpretation of strange or uncomfortable physical sensations.

            When panic disordered individuals present for treatment, the initial symptoms they present focus on their intense anxiety as well as on the somatic components of their symptoms, and there may be a degree of disorganization in the presentation. Alexithymic traits are evident in their confusion between emotional and physiological symptoms, and frequent uncertainty as to whether they are experiencing a medical or psychological crisis. While they are generally certain that they are extremely anxious, they are often uncertain as to whether the anxiety is the central problem or is a symptom of another more insidious physical disorder. Their affective awareness is generally limited to intense anxiety over another panic attack and/or the strong fear of the possible catastrophic implications of another panic attack. They may or may not be aware of the considerable depression that is often comorbid to PD. There is often limited awareness of the precipitants of their initial attacks; with an over focus on the external circumstances that surround initial and subsequent attacks, similar to the TAS-20 F3 subscale of externally oriented thinking.

            While their recollection of their first panic attack is usually quite vivid, it is not uncommon that recollection of even earlier panic attacks emerges later in treatment.  Difficulty identifying emotional issues and affect laden events that preceded the onset of their first panic attacks appears to be directly related to the traits that define the alexithymia construct. Quite often the onset of panic attacks is related to separation fears or significant life events: death, illness, geographical move, relationship breakup, pregnancy/childbirth, injury, accident, or threat of any of these. It is an early marker for the presence of alexithymia when a client, during the initial evaluation period, struggles to identify any such issue or related affect as a precipitant to the onset of panic, only to have it surface later in therapy - a frequent occurrence in my work with these individuals.

            Often several sessions are necessary before the individual begins to develop insight into the underlying psychosocial dynamics that contributed to their initial attack(s). This insight only develops with consistent psychotherapeutic probing which underscores the patient’s limited capacity for achieving these insights without assistance, consistent with the cognitive deficits of alexithymia. Insight into the underlying issues responsible for the individual’s first panic attack is vital to the treatment of PD as this insight challenges their previously unproductive formulation that their anxiety is appropriate dread of a physiological catastrophe. This insight can facilitate identification of the alexithymic traits that precipitate and perpetuate panic attacks especially the tendency toward external thinking, somatic preoccupation, and difficulty identifying and verbalizing feelings and their causes. After a period of insight-oriented therapy, the individual often seems to develop a better capacity to elucidate the precipitating events of panic attacks, as well as their emotional sequelae. This could be an argument for the mutability of alexithymia – that it can be mitigated with insight-oriented, psychodynamic or cognitive psychotherapy.

            Insight seems to develop in tandem with decreasing anxiety, reflecting a circular relationship. As anxiety decreases, the capacity for higher level cognitive functioning is enhanced; and the development of cognitive mastery contributes to reduced anxiety. Individuals with PD who seek treatment tend to minimize the extent and significance of anxiety disorders or symptoms in family of origin members. Often at least one parent has or had panic attacks or is a chronic anxious worrier, typically involving health or safety issues. The PD individual may have limited awareness of the impact of this role-modeling, or possible genetic loading, on their own anxious tendencies. It is common for PD individuals to evidence limited separation and emancipation from a parent, often the mother, and often the similarly anxious parent.  This tends to manifest in frequency of contact, by telephone or in person, not uncommonly daily or even multiple daily contacts. This symbiosis represents the lack of internalized affect regulating capacity consistent with the cognitive and affective deficits of alexithymia. The lack of an internalized comforting maternal object contributes to perpetual reliance on the original object as a comforting source. The characteristic reliance on a safe person by individuals with PD has its roots in this lack of internalized comforting and affect regulation, reflecting Bowlby’s (1973) formulation of proximity-maintaining behavior in insecure or anxious attachment patterns.


The Role of Alexithymia in the Perpetuation of PD

            The cognitive and affective deficits of alexithymia involved in the etiology of PD are also involved in the maintenance of the disorder. A vital dilemma exists as to the chronicity of PD: how is it that even hundreds of trials of an unreinforced catastrophic fear can resist extinction? Seligman (1988) wondered why individuals would continue to misinterpret panic attacks as heart attacks after multiple experiences to the contrary. In response, Salkovskis (1988) theorized that these individuals continue to catastrophically misinterpret sensations because they believe they avert catastrophe with protective maneuvers. He suggests these individuals engage in subtle avoidance or safety behaviors that undermine the test of the catastrophic hypothesis. Clark (1988) recognized the impact these preventative measures have on sustaining irrational fears: if someone has the erroneous thought that they may faint and therefore quickly sit down to avoid falling, they miss an opportunity to disprove their false belief.

            Another explanation is that individuals refuse to reject a catastrophic hypothesis for reasons described by the philosopher Hume (1748, 1977) who suggested that a generalization cannot be proven by a finite number of positive occurrences. Because someone has not driven off a bridge during a dizzy spell one hundred times, does not mean they could not drive off it during the next dizzy spell. While panic disordered individuals may begin to accept the lack of probability that their catastrophic fear will materialize, it is ultimately an act of faith when they do so (McNally, 1994).

            It is my proposition that the deficits of alexithymia are central to the perpetuation of PD as they support reliance on the use of safety behaviors to avert catastrophic outcomes. The safety behaviors in turn support these cognitive and affective deficits and inhibit the testing of catastrophic hypotheses. In other words, I believe there exists a circular relationship between alexithymia and safety behaviors, each sustaining the other and thereby PD. This relationship appears to be closely related to the fear of fear cycle which Goldstein and Chambless termed “the most central phobic element” (1978, p. 51).

            Limited awareness of faulty, irrational cognitions and resultant catastrophic fears perpetuates reliance on safety behaviors to avoid catastrophe. Many of these maneuvers are conscious efforts to avoid catastrophe, but many seem to have developed without conscious participation. A part of the uncovering process of insight and cognitive therapy is the revealing of these behaviors, their intent, and their positive and negative consequences. It is of significance that these behaviors often have a magical thinking or superstitious quality to them, suggesting their primitive nature. It appears to me that alexithymic deficits are prominent in interfering with the conscious awareness and evaluation of these behaviors and thereby perpetuate them. The catastrophic hypothesis these behaviors seemingly prevent remains untested and the fear of fear cycle continues.


The Role of Safety Behavior

            Psychotherapeutic success with individuals with PD involves identification of irrational cognitions, fears, and safety behaviors, so as to facilitate conscious testing of underlying catastrophic hypotheses. This becomes possible when alexithymic traits are adequately mitigated to facilitate this conscious process. In the event that underlying cognitive and affective processes do not become conscious, hundreds of further unreinforced trials may continue without significant increase in the likelihood of spontaneous extinction. In my clinical experience with panic disordered individuals, it appears that remission of panic attacks proceeds from amelioration of the cognitive and affective deficits of alexithymia.


Examples of Safety Behaviors

            The degree to which safety behaviors contribute to the perpetuation of panic level anxiety is considerable and widely recognized. They are similar to the avoidance behaviors of simple phobia or agoraphobia and can be explained by operant or classical conditioning models. An operant model suggests that safety behaviors can best be understood as freely emitted behaviors that increase or decrease relative to their consequence or value. If any behavior reduces anxiety and seems to prevent a panic attack, heart attack or other catastrophe, it is reinforced and likely to be repeated. A classical conditioning model suggests that anxiety has become associated with certain stimuli and the avoidance of these stimuli is reinforced by the termination of the anxiety state.

             In simple phobias or agoraphobia, avoidance behavior reinforces fear of the avoided object or situation by precluding desensitization via exposure to the feared stimuli. Similarly, safety behaviors reinforce fear of external or interoceptive cues by avoiding a test of the catastrophic hypothesis associated with those cues. Safety behaviors are reinforced by their capacity to terminate aversive anxiety states but contribute to the continuation of an anxiety disorder. This study found no significant difference in alexithymia prevalence between the PD with agoraphobia individuals, and the PD without agoraphobia individuals. I suggest this is the result of their difference without a difference. That is, both these groups employ avoidance behaviors with identical function and consequence but with apparently insignificant surface distinctions.


            One type of safety behavior is avoidance. This includes the set of behaviors that constitute agoraphobia, but also include more subtle avoidance behaviors manifested by individuals with PD either with or without agoraphobia. Often the difference in the avoidant behaviors demonstrated by individuals within these two different diagnostic categories is the degree of subtlety, or symbolization, of the behavior. It is not accurate to consider only the individual with PD and agoraphobia as a phobic avoider, and one with PD without agoraphobia as a non-avoider. Each group generally manifests some degree or variant of avoidant safety behaviors, blurring the clear distinction between the two diagnostic categories.

             Panic disordered individuals with agoraphobia manifest classic symptoms and behaviors that constitute agoraphobia. Anxiety over situations and places of limited escape, or unavailability of assistance in the event of panic, cause them to avoid going far from home or leaving home altogether. Their anxiety can prompt them to avoid crowds, certain modes of transportation, or standing in line. These and similar situations are avoided or are endured with marked anxiety (American Psychiatric Association, 1994).

            But there are other avoidance behaviors that do not qualify as classic agoraphobic manifestations as they constitute subtler forms of avoidance. They are more subtle as they are selective, discriminating forms of avoidance as compared to the more generalized agoraphobic forms of avoidance. Specific aspects of anxiogenic situations may be avoided such as avoiding one particular stretch of road as opposed to avoiding all driving situations. Specific bridges, tunnels, roads, or driving conditions may be avoided, while others are not. Anxiogenic physiological sensations such as dizziness, breathlessness, or accelerated heart rate may be avoided by avoiding substances or activities that produce them. These may include avoidance of: caffeine; sugar; amusement park or playground rides; physiological exertion such as sports activities or exercise; or even the witnessing of others participating in these behaviors.

            A significant variant of avoidant-type safety behavior employed in the presence or absence of agoraphobia, is the avoidance of being alone via the use of a safe person. The safe person is an external comforting source, typically a spouse or first degree relative such as a parent. The overt reliance on a comforting individual suggests delay in the development of internalized, comforting parental introjects and the continuation of proximity-maintaining behavior (Bowlby, 1973). The dependence on a safe person also represents significant lack of “differentiation of the self” - what Bowen (1978) considered the highest level of maturational development.

            The agoraphobic individual may be obvious about their resistance or refusal to leave home without a safe person. The non-agoraphobic individual may manifest this behavior in symbolized form involving the use of an object representation or transitional object. Instead of requiring the presence of a safe person, there may be reliance on a cell phone that represents immediate connection with a comforting source. A transitional object can be any object imbued with comforting value – a picture, a ‘good luck charm’, or any object with representational or talisman value. This transitional object can be similar to a child’s but tends to have more symbolic meaning as opposed to comforting sensory properties like a child’s security blanket or stuffed animal.

            Closely related to the safe person is the concept of a safe place. The agoraphobic is unwilling to leave their only true safe place – their home, but may do so with a safe person or alone but with considerable anxiety. For non-agoraphobics, a safe place is a place with representational value - places away from home wherein the person is in proximity to a source of perceived safety or assistance. Examples are a hospital, a restroom or freeway rest area, or a friend or relative’s home.


            Another form of safety behavior is distraction. An individual experiencing an internal or external anxiety cue while driving a car may turn up the radio, open a window, sing aloud, or force conversation with anyone else in the car in an attempt to distract their attention from the cue and incipient catastrophic cognitions. Physiological maneuvers such as shifting in one’s seat, muscle clenching, or moving about can be attempts to distract one’s attention from incipient cues for panic.


            Another type of safety behavior is the use of escape, or taking flight from an anxiogenic situation. These behaviors constitute fleeing from a store or mall, leaving the line at a cash register, or pulling off a road or freeway. Often the flight is from a situation that represents suffocation or restriction of breathing, to one that represents a capacity for unrestricted breathing. Examples are: leaving an enclosed or crowded room, escaping a traffic jam or backup, going to an open door or window or going outside for fresh air.


            Another set of safety behaviors involve the use of relaxation techniques to avoid a panic attack. These responses include deep breathing, progressive relaxation techniques, and meditation. While there is a very legitimate use of these methods during the early phase of treatment of PD, they become potentially counterproductive measures when they become the solution to panic.

            Most of these safety behaviors have preliminary value for the panic disordered individual in their attempts to find ways to abort the fear of fear cycle. Behaviors that constitute mastery of relaxation techniques have an inherent generalized value that can contribute to a legitimate sense of self-control and affect regulation. But relaxation techniques, like other safety behaviors, become counterproductive and self-limiting if they interfere with identification and resolution of the underlying process of panic. These behaviors can interfere with the identification of internal and external anxiogenic cues, and the amplification and catastrophic misinterpretation that follow. These safety behaviors not only support the alexithymic deficits that impede the awareness of and challenge of false catastrophic hypotheses, they also promote the alexithymic tendency to consider a problem as physiological that can be ameliorated with palliative physiological interventions.


Case Illustration of Safety Behavior and Alexithymia

            A case illustration that revealed to me the powerful role of safety behavior and its relationship to alexithymia, involved a woman in her mid-thirties diagnosed with PD without agoraphobia. Panic attacks that she had experienced on a frequent basis for several years were in remission for several months after approximately one year of insight and cognitive therapy, with me as her therapist. Despite the absence of panic attacks, she revealed in a session that she still experienced significant anticipatory anxiety each morning when first leaving her home. She complained of not understanding why she still remained so anxious on a daily basis when her panic attacks had been absent for many months.

            In my attempt to help reveal the chain of negative cognitions that precede the anxiety she experiences each morning when she leaves her home, she could only identify that her head “feels foggy.”  Not only could she not identify specific cognitions, she could not identify specific affects and was only able to identify a vague somatic sensation. In pursuing identification of more specific cognitions or affects, she said “I feel afraid of how I feel.” With further exploration, she identified a fear that her “anxiety could escalate . . . could overwhelm me . . . be out of control . . . go crazy”. She was surprised to realize that everyday she had the identical sequence of thoughts and feelings and yet never recognized them on her own. It was evident that despite these fears, she had developed adequate coping strategies to preclude catastrophizing these thoughts to the point of panic. She asked me an important question that essentially asked why she continues to experience the same thoughts and feelings each morning when nothing bad ever happens.

            Her question prompted me to explore for the existence of safety behaviors that may have been preventing further panic attacks, but were interfering with identification and modification of negative cognitions. She was able to reveal that each morning she employs the use of deep breathing and muscle clenching while driving her car, and her strong feeling that these techniques were preventing further panic attacks. After we established more rational cognitions that challenged her irrational ones, I wrote down her chain of negative cognitions on a 3” x 5” index card along with the positive, rational alternate cognitions. She was given the homework assignment: to review this chain of irrational thoughts and the rational alternate cognitions, each morning before she left her home. And she was to refrain from using her safety behaviors. At her next appointment two weeks later, she stated her index card was dog-eared as she takes it with her wherever she goes, though only read it a few times as she remembers vividly what it says. She reported a dramatic decrease in her anxiety to the point it had been negligible for that entire two week period. She said, “just being aware of it [the card and what it said] stops it in its tracks [her anxiety] . . . keeps it from building . . . keeps it logical . . . stops it from mounting.” She also said that she felt comforted by carrying around that index card, “I know its there.” She stated the main benefit of recounting her chain of negative thoughts, and the positive alternate thoughts, each morning came from “identifying it [her anxiogenic thoughts] versus pushing it away which doesn’t help”.

            What occurred?

            This woman evidences the alexithymic trait congruent with the TAS-20 F1 subscale when she identifies a physiological feeling in lieu of an emotional feeling in her description of her emotions as a “foggy” head sensation. She had difficulty congruent with the TAS-20 F2 subscale of difficulty verbalizing emotions, evident in her limited vocabulary for affects. Her paucity of affects was also evidenced during these sessions by her wooden affect and frequent blank look and stare while discussing these powerful emotional experiences. She also demonstrated considerable lack of affective and cognitive awareness as she had previously been unaware of the underlying, catastrophic cognition of her fear of going crazy. While her safety behaviors facilitated a decrease in panic attacks, they were also counter productive to the extent they kept her irrational thoughts out of her consciousness, and therefore unavailable to evaluation, challenge and potential extinction.

            What helped?

            It appeared that the identification of her core catastrophic cognition was most instrumental in the remission of her anxiety. Identifying this facilitated the cognitive evaluation and challenge of her catastrophic hypothesis, and conscious daily test of it without reliance on safety behaviors that could render these thoughts unconscious.



            What are other possible explanations?

            While the presence of alexithymic traits and safety behavior is evident in this case illustration, there are other possible explanations for the decrease in anxiety that resulted from my interventions. She may have found comfort in the transitional object value of the index card, having been hand-written by me and representing my omnipresence during her trips away from home. This possibility would imply employment of another safety behavior, albeit one with more symbolic value and suggestive of hierarchical advancement in affect regulation (Taylor, 1987). Also, given her alexithymic traits, she may have been sustaining herself without panics by reliance on other, as of yet unidentified, safety behaviors. Lastly, a placebo effect may be responsible for progress, derived from a sense of safety or nurturance resulting from my involvement, or our expectation that a homework assignment was to be effective.


My Formulation of the Role of Alexithymia in the Etiology of Panic Disorder

            My formulation of panic disorder and the role of alexithymia in its etiology constitute a biopsychosocial model.

            Biological components.

             Biological deficits may be significant to the alexithymic difficulties experienced by those with psychosomatic disorders, which I believe includes PD, in identifying and verbalizing affects. These deficits contribute to the tendency to discharge affects somatically instead of cognitively (MacLean, 1949; Nemiah, 1984). There is also considerable support for the theory of disruption in communication between the emotional right hemisphere and verbal left hemisphere (Hoppe, 1981). The biological alarm triggered by a sense of suffocation seems to be frequently involved in PD. Many panic attacks involve the fight or flight response, manifested by the attempt to escape from a sense of enclosure and restricted breathing, such as crowds, stores or traffic jams (Barlow, 1988; Klein 1993). I give much consideration to Barlow’s conceptualization of a biological vulnerability for panic attacks in the face of the multi-generational presence of PD in families.

            Psychosocial components.

            Alexithymia seems to result from biological deficits and deficits in personality development, rather than stemming from unconscious conflicts - consistent with a deficit model rather than a defense model. Bowlby’s attachment theory (1969, 1973) accurately describes the impact of early life attachment patterns in the clinging behavior manifested by adults with PD, exemplified by the manifestation of a safe person. I see evidence of his proposition that anxiety is activated attachment behavior in the many safety behaviors of PD that seek to avoid separation and maintain proximity. Bowlby’s model provides explanation for the high rate of occurrence of PD in multiple generations. An anxiously attached parent seems to be high risk for replicating a faulty attachment pattern with their child, and/or model anxiety for their child.

            My formulation of affect development is predicated upon Krystal’s (1988) infantile precursor states of contentment or distress, and the development of adult affective states via differentiation, verbalization and desomatization. I believe Krystal is precise in his conceptualization of alexithymia as arrest at or regression to an earlier undifferentiated and somatized affective level. This formulation has considerable heuristic value for conceptualizing psychosomatic disorders such as PD.

            Also of considerable theoretical value is the Lane and Schwartz (1987) epigenetic model of cognitive and affective development that explains development of affects proceeding from increasing verbalization and differentiation. I find value in their hierarchical model especially for its capacity to explain the somatic traits of PD as they represent arrest at, or regression to, an early somatized affective level.

            It appears to me that somatosensory amplification is generally involved in the panic process (Barlow, 1988; Barsky, 1992). The amplification theory provides considerable explanation for the dread of normal physiological sensations by individuals with PD, and why normal sensations are often experienced as noxious sensations by these individuals. The amplification concept suggests reasons for the overwhelming power of sensations and why individuals with PD feel they may be overwhelmed by their physiological experiences and lose control of themselves. The amplification concept provides insight into the somatization process as it explains how somatic sensations can become the primary or even exclusive focus of attention. The significant elevation on the TAS-20 F1 subscale (difficulty identifying emotions and differentiating them from physiological sensations) by the PD men and women in this study appear to be evidence of the involvement of somatosensory amplification in individuals with PD.

            In my judgment, the dynamic of greatest prominence in the etiology of PD is that of the catastrophic misinterpretation (Clark, 1986). It seems to me that the catastrophic hypothesis is the spark that ignites the ingredients of biological factors, cognitive and affective deficits of alexithymia, life events and somatic sensations into the explosion of the panic reaction or panic attack. But I believe the term attack is a misnomer, suggesting as it does a spontaneous event, for a panic attack is more accurately a reaction to multiple factors and events with the catastrophic misinterpretation or hypothesis being the flashpoint. The cognitive and affective deficits of alexithymia and the principles of classical and operant learning theories become prominent in the chronicity of panic attacks as they support the “fear of fear cycle”.


Limitations of this Study

            Limitations to this present research seem to fall into three categories: (a) sample characteristics, (b) instrumentation, and (c) theoretical limitations. Limitations of the sample selection include small sample size. Inferences drawn from small samples make it questionable to generalize these results to a larger population. The significant effect of gender might make it beneficial to conduct similar research with more homogeneous populations to reduce gender by group interaction and develop better understanding of the reasons for such significant gender differences in alexithymia, in both PD groups as well as control samples. The age range of this study’s participants is another limitation. As this study found a decrease in alexithymia with advanced age, future studies with more homogeneous by age samples could provide clearer data as to alexithymia prevalence between groups without the confounding effect of age.

            This current research may have limitations due to instrumentation. The TAS-20 is a self-report measure designed for this type of research and is currently the most accepted instrument for these purposes. It was therefore deemed the most appropriate psychometric tool for this research project. But it is well-known that self-report measures may not provide an accurate portrayal of reality and may unintentionally reflect bias on the part of the participant. Another limitation is the absence of data from a second instrument or other measure of alexithymia. While at this time there are no other self-report instruments with adequate construct validity, standardized observer-ratings of alexithymia could provide cross comparison of data.

            Other limitations of this research are a function of the topic of research itself. There are inherent limitations to research on abstract concepts such as alexithymia. A tester must rely on accuracy and honesty in the participant’s self-report of traits such as affective awareness and verbalization, and tendencies for somatization. It is uncertain if a participant with limitations in the area of objective self-awareness can therefore be expected to produce an accurate self-portrayal.


Treatment Implications

            This current research yielded results that lend themselves to important treatment implications. The positive correlation between PD and somatic traits inferred by the TAS-20 F1 subscale, in both men and women, has implications of value. That these are the only consistent alexithymic traits distinguishing both genders with PD from controls, it can be implied that these traits require specific treatment interventions. The alexithymic deficits of PD suggest a primitive affective level of functioning wherein the individual operates from an early non-verbal, somatized level of affective development. Treatment interventions need to facilitate functioning at higher developmental levels via affective identification and verbalization to effect the desomatization of affects.




DISSERTATION:  "Alexithymia: A Pathogenic Factor in the Etiology of Panic Disorder"

Chapter I

Chapter II

Chapter III

Chapter IV

Chapter V

Chapter VI



Click here for more information on:
"Anxiety to Serenity"
an anxiety recovery self-help program --

plus shipping & handlingCD_PROGRAM.html