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Alexithymia, Fear of Bodily Sensations, and Somatosensory Amplification in Young Outpatients With Panic Disorder

Received January 12, 2006; revised April 3, 2006; accepted April 11, 2006. From the Dept. of Oncology and Neurosciences, Institute of Psychiatry, University "G. d’Annunzio" of Chieti, Italy; the Mental Health Service, Mental Health Dept., Teramo, Italy; the Mental Health Service, ASUR Marche 8, Civitanova Marche (MC), Italy; and the Institute of Psychology, University of Urbino, Italy. Send correspondence and reprint requests to Filippo Maria Ferro, M.D., Dept. of Oncology and Neurosciences, Institute of Psychiatry, University "G. D’Annunzio" of Chieti, Palazzina SE.BI., Scuole di Specializzazione, via dei Vestini, 31-66013 Chieti Italy. e-mail: dodebera{at}aliceposta.it

ABSTRACT

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To elucidate the relationships between alexithymia, fear of bodily sensations, and somatosensory amplification in young patients with panic disorder (PD), authors evaluated 84 patients. Measures were the Panic Attack and Anticipatory Anxiety Scale, the Toronto Alexithymia Scale (TAS–20), the Body Sensations Questionnaire (BSQ), the Somatosensory Amplification Scale, the Agoraphobic Cognitions Questionnaire (ACQ), and the Hamilton Rating Scale for Depression. Alexithymic patients showed higher scores on all rating scales. Higher BSQ and ACQ scores, together with the Difficulty in Identifying Feelings and Difficulty in Describing Feelings subscales of the TAS–20 were predictors of severity of PD. Results of the present study do not support a direct role of somatosensory amplification in PD. Authors discuss study limitations and future research needs.

INTRODUCTION

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It is well documented that the misinterpretation of bodily sensations plays a central role in the development and maintenance of panic disorder (PD). According to Clark,¹ these misinterpretations may occur on a conscious level, but may also be unconscious; in this case, patients may not always be aware of the interpretative process. This latter assumption is necessary to explain why not all panic attacks are preceded by conscious, catastrophic misinterpretations^2,3 and how nocturnal panic attacks may occur without a possible explanation.⁴ PD patients often report cognitions centered around the theme of physical and psychic catastrophes that are directly related to the bodily sensations experienced. Moreover, somatosensory amplification, that is, the tendency to experience normal bodily sensations as intense, noxious, and disturbing, has been implicated as a pathogenic mechanism in hypochondriasis^5,6 and may play a role in PD etiopathogenesis and course.⁷

Alexithymia is characterized by difficulties in recognizing and verbalizing feelings, a paucity of fantasy life, concrete speech, and thought closely tied to external events.^8,9 Alexithymic individuals are prone to both "functional somatic symptoms and symptoms of emotional turmoil."¹⁰ The alexithymia construct, formulated from clinical investigations, is multifaceted and includes four distinct characteristics: 1) difficulty identifying and describing feelings; 2) difficulty distinguishing feelings from bodily sensations; 3) diminution of fantasy; and 4) concrete and minimally introspective thinking.¹¹ An increasing body of studies indicates that alexithymic features exist not only in classic psychosomatic disorders but also in other severe and chronic somatic diseases and psychiatric disorders such as somatoform disorders, major depression, and other Axis I disorders, such as PD.¹²

Strictly concerning alexithymia and PD, the two first studies in the literature using the Toronto Alexithymia Scale (TAS–26) have suggested that alexithymia may constitute one of the psychological characteristics of PD, with a prevalence of 67% and 46.7% for the two studies, respectively.^13,14 Successively, Iancu et al.¹⁵ reported a prevalence for alexithymia of 39% by use of the TAS–26, whereas Cox et al.¹⁶ found a prevalence of 34.0% with the TAS–20. In a recent and well-conducted follow-up study on 52 adult patients with PD, Marchesi et al.¹⁷ reported a prevalence for alexithymia of 44.2%.

Currently, since no studies have investigated the relationships between alexithymia, fear of bodily sensations, and somatosensory amplification in PD subjects, the purposes of our study were 1) to verify whether alexithymic and nonalexithymic PD patients showed different demographic and clinical features; 2) to study the associations between alexithymia, fear of bodily sensations, and somatosensory amplification; and 3) to investigate whether variance in severity of PD might be explained by alexithymia, catastrophic thoughts, fear of bodily sensations, and/or somatosensory amplification.

Moreover, many studies have focused their attention on PD patients with a relatively long history of illness, and this may lead to potential biases because of actual or previous pharmacological treatments that may, on their own, influence several psychological characteristics, such as alexithymia, fear of bodily sensations, and somatosensory amplification. In the present study, we chose to evaluate only young patients with a recent-onset PD and without a history of previous regular, daily treatments in order to avoid potential biases and better elucidate relationships between alexithymia, fear of bodily sensations, and somatosensory amplification.

METHOD

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Patients with PD who applied to the outpatient ambulatory Consultation–Liaison Service of the Psychiatric Clinic of the University of Chieti from January 2002 to December 2004 were considered eligible for the study. Diagnoses were made by psychiatrists with at least 5 years’ clinical experience who were supervised by senior psychiatrists (RMS, FMF), following the Structured Clinical Interview for DSM-IV (SCID). Only patients with an age range of 18 to 31 years and with recent-onset PD at first treatment contact were eligible for the study; patients already under treatment with regular daily therapy with any psychotropic drug and/or psychotherapy were considered not eligible. Recent onset was considered a PD disorder lasting more than 1 month and less than 1 year; a total of 101 patients were considered eligible. Patients were also excluded for serious medical or neurological illness (N=1; 1.0%), for mental illnesses other than panic disorder (N=6; 5.9%), or for substance abuse in the preceding 12 months (N=5; 5.0%).

With five subjects refusing to participate and two providing incomplete data, a total of 84 outpatients with a DSM-IV diagnosis of PD were included, of which 62 (73.8%) had agoraphobia, and 22 (26.2%) did not have agoraphobia. Oral and written informed consent was obtained from all subjects. Participants did not significantly differ from nonparticipants on any studied variables. Mean age of patients was 25.9 years (standard deviation [SD]: 3.6 years); range: 19–31. All the patients had no evidence of underlying medical illnesses, and there were no evident signs of psychiatric comorbidity. In any case, PD diagnosis and psychiatric comorbidity were evaluated through administration of the SCID–I. No patients had received psychotherapy at the time of the assessment.

The Panic Attack and Anticipatory Anxiety Scale (PAAAS),¹⁸ a clinician-rated scale, was used as the instrument of evaluation of PD severity, taking into consideration, specifically, the total number of major and minor panic attacks during the last week and the intensity of the anticipatory anxiety (evaluated on an analog scale without an anchor point, where 0: Absent and 10: Maximum intensity).

Fear of bodily sensations was analyzed with the Body Sensations Questionnaire (BSQ), a 17-item questionnaire that assesses the degree of fear and concern over somatic sensations associated with autonomic arousal (e.g., heart palpitations, dizziness).¹⁹ Items are rated on 5-point scales, ranging from "not frightened or worried by this sensation" to "extremely frightened by this sensation." In the validation study, the scale has demonstrated high internal consistency (Cronbach =0.87) and adequate test–retest reliability (r=0.67).¹⁹

Catastrophic thoughts associated with panic and agoraphobia were evaluated by the Agoraphobic Cognitions Questionnaire (ACQ), a scale made up of 14 items, which investigates catastrophic thoughts often associated with PD.¹⁴ As described by Chambless et al.,¹⁹ the scale is internally consistent (=0.80), and stable (test–retest reliability; r=0.74), and it discriminates between agoraphobic and non-patient controls.

Alexithymia was measured with the 20-item Toronto (Ontario, Canada) Alexithymia Scale (TAS–20), the most widely used measure of alexithymia.^20,21 Each item is rated on a 5-point Likert-type scale, ranging from "strongly disagree" (scored 1) to "strongly agree" (scored 5), with scores ranging from 20 to 100. Cutoff scores for the TAS–20 were provided by Taylor et al.,¹⁰ and a score 61 is considered to be indicative of alexithymia.¹⁰ The TAS–20 has a three-factor structure:²² Factor l (F-1) assesses the capacity to identify feelings and to distinguish between the feelings and the bodily sensations of emotional arousal (Difficulty in Identifying Feelings [DIF]); Factor 2 (F-2) reflects the inability to communicate feelings to other people (Difficulty in Describing Feelings [DDF]); Factor 3 (F-3) assesses Externally-Oriented Thinking (EOT). However, we also performed a Confirmatory Factor Analysis (CFA) on our sample, which showed that the three-factor model met goodness-of-fit criteria (²=515.7, df: 159, p <0.001; Goodness-of-Fit Index=0.87; adjusted Goodness-of-Fit Index=0.85; root mean-square residual=0.0061).

Somatosensory amplification was measured with the Somatosensory Amplification Scale (SSAS).²³ The SSAS evaluates sensitivity to mild bodily sensations that are uncomfortable and unpleasant, but nonpathological; it consists of 10 self-rated statements that are estimated on a 5-point scale, ranging from 1: "Not at all" to 5: "Extremely." Total point score is evaluated as the measure of somatosensory amplification. Barsky et al.^24,25 showed that the SSAS had good internal consistency (Cronbach =0.82), and this suggested that it could be reliably used to measure the intensification of bodily sensations in clinical and non-clinical samples.

Severity of depression was objectively assessed with the 17-item Hamilton Rating Scale for Depression (Ham–D).²⁶

Statistical Analysis
Descriptive statistics (mean and SD, as appropriate) and percentages were computed for the study sample on demographic variables and all psychometric scales. The data were checked for deviations from the Gaussian distribution by use of the Kolmogorov-Smirnov test. The differences between alexithymic and non-alexithymic subjects were tested by using analyses of covariance (ANCOVA), with TAS–20 positivity/negativity as factors, and age, gender, and Ham–D scores as covariates. Chi-square analyses ([²], with the Yates’s correction for 2 x 2 tables) and odds ratios (ORs) were used for categorical variables. Cohen’s index (d-values) were also calculated to obtain a better evaluation of the magnitude of differences on study measures. By convention, d 0.80 denotes a large effect; d 0.50, a medium effect; and d 0.20, a small effect. Pearson’s product-moment correlation coefficient was used to examine the degree of association between alexithymia and other variables. A stepwise linear-regression analysis²⁷ was performed in order to find which variables were associated with severity of PD (with total number of panic attacks as dependent variable). In the first step, gender, age, ACQ, and Ham–D were entered. In the second step, BSQ and SSAS were added to the model, and DIF, DDF, and EOT subscales of the TAS–20 were entered in the last step. The quality of the regression model was also tested, using the Durbin-Watson Laboratories, Inc. statistic (a value between 0 and 4 indicating the amount of auto-correlation within the model, with an optimum level of 2.0). Statistical significance was fixed at a value of <0.05. All statistical tests were two-sided. Statistical analyses were performed with SPSS for Windows, Release 10.0.0 (2000). Quantitative variables were expressed as mean values with SD, and qualitative variables were expressed as absolute values and percentages.

RESULTS

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The total score for the TAS–20 in whole sample was 52.7 (SD: 13.9), and DIF, DDF, and EOT scores were (respectively) 21.9 (SD: 6.4), 15.9 (SD: 5.4), and 14.9 (SD: 4.2). The 38.1% of the 84 patients (N=32) who had a total score 61 on the TAS–20 were categorized as alexithymic. As shown in Table 1, categorical-variable analysis found that alexithymic patients had less education than the non-alexithymic group (p=0.02). The two groups did not differ in terms of gender, marital status, and occupation. Prevalence of agoraphobia was higher in alexithymic patients than non-alexithymic (p=0.01). Alexithymic patients had higher Ham–D scores than non-alexithymic (11.3 [2.8] versus 8.5 [3.0]; F=19.20, df=1; p <0.001; Cohen’s d=0.96). Age did not differ significantly between the two groups, although a tendency toward older age was observed in alexithymic patients (p=0.08).

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TABLE 1. Demographic and Psychometric Data of Alexithymic (Toronto Alexithymia Scale Total Score 61) and Non-Alexithymic (TAS–20 Total Score <61) Patients

The results of the ANCOVA, controlling for age, gender, education, and Ham–D scores (Table 1) showed that alexithymic patients had greater severity of PD (higher number of total, major, and minor panic attacks; respectively, p <0.001, p=0.003, and p=0.03), higher anticipatory anxiety levels (p=0.01), and ACQ scores (p <0.001) than non-alexithymic patients. Moreover, alexithymic patients showed the presence of more prominent fear of bodily sensations as well as higher somatosensory amplification when compared with non-alexithymic patients (for both variables: p <0.001). Effect-size calculation showed that the magnitude of group effect for total and major panic attacks, intensity of anticipatory anxiety, ACQ, BSQ, and SSAS was large, whereas for minor panic attacks, the effect size was medium.

Zero-order Pearson product-moment correlations (r) between study variables (Table 2) showed that TAS–20 total score and subscales DIF, DDF, and EOT were highly intercorrelated. TAS–20 and subscales DIF and DDF significantly correlated with total, major, and minor panic attacks; anticipatory anxiety levels; ACQ; BSQ; SSAS; and Ham–D scores. The EOT subscale of the TAS–20 did not show significant correlations with any other studied variable. BSQ scores were significantly correlated with total and major panic attacks, anticipatory anxiety levels, ACQ, and Ham–D scores. SSAS showed low but significant correlations with total and major panic attacks, anticipatory anxiety levels, BSQ and Ham–D, whereas no correlations were found between SSAS, minor panic attacks, and ACQ.

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TABLE 2. Zero-Order Pearson Product-Moment Correlations (r) Among Study Variables

The results of stepwise linear regression to determine the contributions of the variables for predicting severity of PD (total panic attacks as the dependent variable) in the whole study sample indicated that DIF and DDF subscales of the TAS–20 were significantly associated with higher severity of disorder (Table 3). Higher scores on the ACQ and higher fear of bodily sensations (higher scores on the BSQ) were also significantly associated with a more severe PD. No other variables predicted severity of PD in the linear-regression model. In this analysis, the r² values demonstrated good accuracy of prediction, with the model accounting for 77% of the variance in total panic attacks. Also, the Durbin-Watson Laboratories, Inc. coefficient was 1.86 (near the optimum of 2.0), and the standardized residuals were normally distributed.

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TABLE 3. Stepwise Linear-Regression Analysis, With Total Number of Panic Attacks as Dependent Variable and Potential Predictive Factors as Independent Variables

DISCUSSION

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To our knowledge, this was the first study that evaluated the relationships between alexithymia, fear of bodily sensations, and somatosensory amplification in a sample of young outpatients with recent-onset panic disorder. The prevalence of alexithymia in our sample was 38.1% (N=32). Our prevalence seems globally in accordance with those reported by Iancu et al.¹⁵ and Cox et al.,¹⁶ but not with those of some other studies.^13,14,17 However, in our sample, we restricted the observation only to young patients (age range: 19 to 31 years), and, since it is well known from general-population surveys^25,28 that alexithymia is associated with more advanced age, this may explain the lower prevalence of alexithymia found in the present study. Moreover, our findings seem to confirm an association between alexithymia and lower education level, as has been found previously.^29,30

Consistent with our hypothesis, alexithymic patients reported higher disorder severity than non-alexithymic patients, and this finding is in accordance with previous studies on other DSM-IV disorders, such as major depression and obsessive-compulsive disorder, showing that alexithymic patients generally report higher psychological distress than non-alexithymic patients.^31,32 In our sample, PD patients seem to have difficulty both in identifying and describing feelings and emotions, without a prevalence of externally-oriented thinking. Moreover, from our results, it is possible to argue that alexithymic patients with PD are more often agoraphobic than are non-alexithymic patients. Taken together, these results may support Freyberger’s concept of acute ‘‘secondary alexithymia" as a reaction to stressful situations.³³ Acute secondary alexithymia is described as a transitory state, a state-dependent phenomenon as a consequence of personal distress, which decreases once an acute disease episode has resolved. In such a perspective, alexithymia may be a coping mechanism protecting the self against emotional distress associated with situations of intense vulnerability.³⁴

Moreover, one of the main findings of our study was the association of the Difficulty in Identifying Feelings (DIF) and the Difficulty in Describing Feelings (DDF) dimensions of alexithymia with the degree of fear and concern over somatic sensations associated with autonomic arousal as measured by the Body Sensations Questionnaire (BSQ), which predicted a higher severity of panic disorder (PD) in the linear-regression model. It is reasonable to hypothesize that the presence of DIF and DDF may facilitate the misinterpretation of bodily sensations that often happen in individuals with PD, as postulated by Clark’s cognitive model of PD.³⁵ Specifically, Clark suggested that PD subjects are more likely than non-PD subjects to interpret bodily sensations as precursors to a physical (e.g., heart attack) or psychological (e.g., insanity) catastrophe. As reported above, these misinterpretations are often rapid and automatic, and therefore patients may not always be aware of the misinterpretation involved in these processes.¹ Since alexithymic individuals often have an affective dysregulation and the inability to self-soothe and manage emotions because of a lack of awareness of the emotions, emotional arousal may be perceived only by somatic sensations that, on their own, may be misinterpreted and set off a panic attack. This hypothesis is consistent with that of Parker et al.,²⁹ who demonstrated a relationship between alexithymia and PD and showed that PD patients are unable to relate most panic attacks to any psychological precipitant and tend to focus selectively on one or more somatic sensations of autonomic arousal.²⁹

Moreover, we have also observed that catastrophic thoughts associated with panic and agoraphobia, as measured by the Agoraphobic Cognitions Questionnaire (ACQ), were predictors of PD severity, and alexithymic patients showed higher ACQ scores than non-alexithymic patients. Since it has been suggested that emotionally-negative stimuli produce increased physiological arousal among alexithymic individuals^36,37 and that alexithymia is characterized by a decoupling between subjective and physiological arousal when individuals are exposed to emotionally-negative stimuli,³⁸ it is also possible to deduce that catastrophic thoughts associated with autonomic arousal in PD patients may trigger a panic attack on their own or through the reinforcement of the misinterpretation of bodily sensations. It is also possible to speculate that alexithymic patients may have a higher baseline level of physiological arousal that non-alexithymic patients, as has been demonstrated in some studies^39,40 and that this may predispose these individuals to developing a more severe panic disorder.

Another interesting finding of the present study concerns somatosensory amplification, which seems not to play a direct role in PD psychopathology. In fact, even if alexithymic patients showed higher Somatosensory Amplification Scale (SSAS) scores than non-alexithymic patients, somatosensory amplification was only modestly correlated with clinical variables of PD and fear of bodily sensations, whereas it was highly correlated with TAS–20 total scores and the DIF/DDF subfactors. Moreover, SSAS scores did not predict severity of PD in the linear-regression model. This may suggest that somatosensory amplification is particularly related to the presence of alexithymia, since it is demonstrated that amplification may be associated with the DIF and DDF dimensions of the TAS–20.^41,42 Furthermore, since SSAS scores were significantly correlated with Ham–D scores, this may suggest that amplification may be more closely related to the presence of depressive symptoms, as previously observed.⁴³ On the other hand, if, as according to Clark’s model, panic attacks result from catastrophic misinterpretation of bodily symptoms that are interpreted as signs of an immediate medical catastrophe (as measured by the BSQ, assessing fear of physical sensations that may be misinterpreted as an immediate medical catastrophe), the SSAS assesses bodily sensations, most of which generally do not connote immediate serious disease and are therefore not likely to be misinterpreted as a sign of immediate medical catastrophe. Consequently, this may further explain why Somatosensory Amplification scores were not significantly associated with clinical variables of PD.

One of the findings of the present study is important for the construct of alexithymia, itself. Factor 3 of the TAS–20, that is, Externally-Oriented Thinking (EOT), appears to be a quite independent variable from PD, and this finding resonates with those of previous studies.^44,45 Externally-oriented thinking corresponds closely to "la pensée operatoire," a concept launched by French researchers Marty and de M’Uzan.⁴⁶ The main characteristics of ‘‘la pensée operatoire" are a utilitarian style of thinking and a relative absence of fantasies. However, concerning EOT, in the cross-validation of the factor-structure of the Italian TAS–20, coefficients and mean inter-item correlation coefficients indicated optimal levels of item homogeneity for the DIF and DDF scales, whereas EOT coefficients were considerably lower in magnitude.¹⁷ Also, in other studies, it is reported that the coefficients of the EOT factor were lower than those of the DIF and DDF factors;⁴⁷ so interpretation of EOT results must be viewed with caution.

This study has several limitations that must be considered. These include the use of self-report measures for assessing alexithymia, fear of bodily sensations, and somatosensory amplification. In particular, concerning somatosensory amplification, we may question whether patients themselves can judge whether they amplify sensations or not. An implicit measure or an experimental setting in which sensations are administered and subjective sensations are measured (for instance during inhalation of CO₂ in air) would be useful in future studies. Furthermore, this study used a cross-sectional design, which limits statements regarding causality. A prospective study would also be useful to elucidate whether alexithymia in PD subjects should be considered as a "state" phenomenon or a relatively stable trait. Moreover, prospective longitudinal studies with repeated measures are needed to determine risk factors and especially to evaluate whether alexithymia, fear of bodily sensations, and somatosensory amplification could condition the evolution and outcome of PD after pharmacological treatment. Another area of interest could be the repercussions of alexithymic characteristics and the interrelationships with fear of bodily sensations and somatosensory amplification on psychotherapy for PD. Future work should also include different comparison groups (e.g., normal-controls and/or patients with social phobia or generalized anxiety disorder). Finally, an assessment of disability and the use of more reliable instruments to measure agoraphobia would be useful to better elucidate PD psychopathology.

ACKNOWLEDGMENTS

 
The authors extend their sincere gratitude to Drs. Alessandra Cicconetti, Laura Penna, Salvatore Spinella, Mariella Castrovilli, and Germana Di Loreto, Dept. of Oncology and Neurosciences, Institute of Psychiatry, University of Chieti, for their most helpful advice and review of this manuscript.

This study was not funded by any research grants, and no pharmaceutical companies were informed of or involved in the investigation.

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