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.
