Psychiatry Research 187 (2011) 382–386
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Psychiatry Research j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p s yc h r e s
Defense style in panic disorder before and after pharmacological treatment Carlo Marchesi ⁎, Paola Parenti, Sonia Aprile, Chiara Cabrino, Chiara De Panfilis Psychiatric Section, Department of Neuroscience, University of Parma, Parma, Italy
a r t i c l e
i n f o
Article history: Received 11 August 2009 Received in revised form 2 July 2010 Accepted 3 July 2010 Keywords: Defense style Panic disorder Symptom severity Comorbidity Treatment Remission
a b s t r a c t Whether or not the use of maladaptive defense style is a trait, as opposed to a state dependent phenomenon, in panic disorder (PD) is a topic still very much up for debate. The aim of the study was to verify whether PD patients, both before and after treatment, used different defense style than the control group. Sixty-one PD patients (recruited from an original sample of 90 patients) and 64 healthy controls were evaluated against the Structured Clinical Interview for DSM-IV disorders, the Symptoms Check List-90, the Hamilton Rating Scales for Anxiety and for Depression and finally the Defense Style Questionnaire-40 (DSQ). The patients were treated with paroxetine or citalopram and were evaluated monthly for one year to assess the remission. The DSQ was re-administered to the patients at the end of the study. Before treatment, PD patients used more neurotic and immature forms of defense than controls. After treatment, those in remission used the same defense styles as the control group, whereas non-remitters still used more immature defenses. However, all the aforementioned difference disappeared, after excluding the effect of symptom severity. Our data supports the hypothesis that the use of maladaptive defenses might be the consequence of PD: when subjects fall ill, their capacity to use mature adaptive defenses may diminish, but when they recover their defensive style returns to a greater maturity. The present results are however limited by the dropout rate (one third of patients did not complete the study) and the use of just one questionnaire to evaluate the complexity of defense styles. © 2010 Elsevier Ireland Ltd. All rights reserved.
1. Introduction According to psychodynamic theory, subjects with a particular difficulty in acknowledging feelings of anger, which they find to be a threat to important attachments to persons they feel dependent on, are considered to be psychologically vulnerable to panic disorder (PD)(De Masi, 2004; Shear et al., 1993). It is postulated that defense mechanisms are involved in controlling anxiety and other intense negative emotions in an effort to protect a needed relationship (De Masi, 2004; Perry and Cooper, 1989). As such, the use of maladaptive defenses might be involved in the onset, persistence and recurrence of anxious symptoms (Busch et al., 1995). Nevertheless, the study of defense mechanisms in PD patients gives contradictory results. A greater use of neurotic and immature defenses were found not only in PD patients (Bogren et al., 2002; Busch et al., 1995; Kipper et al., 2004, 2005; Pollock and Andrews, 1989; Spinhoven and Kooiman, 1997) but also in patients affected by other mental disorders such as obsessive–compulsive disorder, social phobia and major depression (Akkerman et al., 1999;
⁎ Corresponding author. Università di Parma, Dipartimento di Neuroscienze, Sezione di Psichiatria Strada del Quartiere 2, 43100 Parma, Italy. Tel.: + 39 0521 303774x792; fax: + 39 0521 230611. E-mail address:
[email protected] (C. Marchesi). 0165-1781/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2010.07.001
Andrews et al., 1989; Kneepkens and Oakley, 1996; Mullen et al., 1999; Pollock and Andrews, 1989), which confirms that defense mechanisms are not specific for any one mental disorder (Bond, 2004; Bond et al., 1983; Bond and Vaillant, 1986). Moreover, the use of less mature defenses was found to be associated with the severity of symptoms, and the clinical improvement was accompanied by a shift toward the use of more mature defenses (Bond, 2004). This finding leaves the question regarding the causal relationship between the defense style and symptoms severity unresolved. This means that the hypothesis that the use of maladaptive defenses is a state-dependent phenomenon cannot be rejected yet (Bond, 2004; Bond and Perry, 2004; Holi et al., 1999; Sammallahti et al., 1994). Finally, it has been postulated that persons with an immature defense style will respond less effectively to both pharmacological (Kipper et al., 2005, 2007) and psychological (Bond and Perry, 2004; Drapeau et al., 2003; Heldt et al., 2003, 2007) treatment. However, most of these studies did not control the effect of variables known to negatively influence the outcome of treatment. Therefore, in the present study the defense style was assessed in PD patients to verify whether: 1) they used less adaptive defense mechanisms compared to healthy controls; 2) a successful treatment might change the defense style; 3) the response to treatment might be predicted by the pre-treatment defense style, controlling for the effect of confounding variables.
C. Marchesi et al. / Psychiatry Research 187 (2011) 382–386 2. Methods 2.1. Sample Subjects were recruited in the study after giving their informed consent (the study protocol was approved by the Local Ethics Committee). They were all out-patients who consecutively sought treatment for panic disorder (PD) at the Centre for Mood and Anxiety Disorder of the Psychiatric Clinic of the University of Parma—Italy since January 2001. PD was the first mental disorder diagnosed in all patients. Patients with severe suicidal risks, schizophrenia or other psychotic disorders, organic mental disorders, substance abuse or dependence, history of neurological or medical illnesses (i.e. cardiovascular, haematological, liver, respiratory, endocrinological diseases) were excluded from the study. The control group, selected from the relatives of university employees, was chosen to match the age and sex of the test subjects, but precluded those with lifetime mental disorders and chronic medical illness (see assessment). All participants gave their informed consent. 2.2. Assessment During the first visit, all subjects received the Structured Clinical Interview for Diagnostic and Statistical Manual for Mental Disorders-IV edition (SCID-IV) (Mazzi et al., 2000), the Symptoms Checklist-90 (SCL-90) (Derogatis, 1977), the Hamilton Rating Scale for Anxiety (Hamilton, 1959)(Ham-A) and for Depression (Hamilton, 1960)(Ham-D), the Defence Style Questionnaire-40 items (DSQ-40) (Andrews et al., 1993) and a semi-structured interview performed ad-hoc to collect clinical and anamnestic information. Furthermore, patients received a diary, where they registered the daily frequency and severity of panic attacks and anticipatory anxiety (American Psychiatric Association, 1998; Shear et al., 1998). All patients were followed over 12 months. During the follow-up period, they were evaluated monthly; during each visit the SCL-90, Ham-A and Ham-D were administered and the panic diaries were evaluated to assess the resolution of symptoms. Moreover at the end of the follow-up period the DSQ-40 was readministered. Controls were evaluated with SCID-IV (to detect and exclude the presence of mental disorders), a semi-structured interview to collect socio-demographic and anamnestic information (to exclude the presence of mental disorders in family members), SCL-90, Ham-A, Ham-D and DSQ-40 (this questionnaire was administered once). Two psychiatrists (CDP and SA) were specifically trained to administer the SCID-IV. The training consisted of the administration of the SCID-IV to 10 patients affected by Panic Disorder, Major Depression, Dysthymia, and Generalized Anxiety Disorder. Regarding the PD diagnosis, a good reliability was obtained during both the training phase (κ = 0.85) and the screening phase of the study (κ = 0.89). The psychiatric diagnoses of patients included in the study were also discussed with a senior psychiatrist (CM). Using DSQ-40, the mature, neurotic and immature defenses and the overall defensive functioning (ODF) scores were all calculated. The ODF was obtained according to the method used by Trijsburg et al. (2000). 2.3. Treatment All patients were treated with paroxetine or citalopram at an initial dose of 10 mg, which was maintained for 1 week and then increased by 10 mg up to the dose at which symptoms disappeared or side-effects became intolerable. However, the maximum daily dose was limited to 60 mg. From the study outset, lorazepam (LRZ) was allowed be added, when necessary, to control anticipatory anxiety and insomnia, as well to reduce anxiety, insomnia, tremulousness and tachycardia induced by the selective serotonin re-uptake inhibitor. LRZ treatment started with a minimum dose of 1 mg/day (0.5 mg, twice/day), which was increased up to a maximal dose of 3 mg (1 mg, three times/day). After 2 months of treatment, LRZ was slowly tapered (1 mg/week). 2.4. Remission criteria Patients were defined as being in remission (Ballenger et al., 1998) if, for a period of 3 months, they reported: 1) no panic attacks and anticipatory anxiety in their daily diary; 2) a score of lower than 1 according to the phobic anxiety subscale of SCL-90 for phobic avoidance (SCL-90-pa) (den Boer, 1998); 3) a total score, in the Ham-A, of lower than 10 for global severity of anxious symptoms (Ballenger, 1999, 2001; Doyle and Pollack, 2003); 4) and a total Ham-D score lower than 7 for depressive symptoms (Ballenger, 1999, 2001; Doyle and Pollack, 2003). 2.5. Statistical analysis Comparisons between-groups were made with the χ2 test for categorical variables, and with the student's t-test (two tailed) or one-way analysis of variance (ANOVA) with the Bonferroni post-hoc analysis for numerical variables. The analysis of covariance (ANCOVA) was used for testing the hypothesis that the use of maladaptive defenses is involved in the onset, persistence and recurrence of anxious
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symptoms (Busch et al., 1995). If the differences of symptom severity between the diagnostic groups disappeared after controlling for the effect of defense style, the hypothesis would be confirmed. Therefore, in the analysis the symptom severity scores (Ham-A, Ham-D and SCL-90-pa) were entered as dependent variables, the diagnostic groups as independent variables and defense scores as covariates (with mature, neurotic and immature defenses in one analysis and ODF in another one). Nevertheless, to account for the possibility that the use of maladaptive defenses might be the consequence of the PD, an ANCOVA analysis was used to verify whether the differences on defense scores between diagnostic groups disappeared after controlling for the effect of symptom severity. Therefore, in the analysis the defense scores were entered as dependent variables, the diagnostic groups as independent variables and the symptom severity scores as covariates. Finally, two logistic regressions were used to evaluate whether the pre-treatment DSQ-40 scores predicted the outcome of treatment. In the analysis, the outcome of treatment (remitted vs non-remitted patients) was entered as a dependent variable and DSQ-40 scores (mature, neurotic and immature defenses in one analysis and ODF in the other one) as independent variables, together with all the following confounding variables known to influence the outcome of treatment: gender, age at onset and duration of PD, symptoms severity and anxious and depressive comorbidity. All data analyses were performed using the statistical software package SSPS 17.0.
3. Results 3.1. Sample Out of the original sample (90 patients), 61 patients completed the study, whereas 29 patients dropped-out ( six due to side-effects, six due to inefficacy, seven due to improvement, and ten were lost during follow-up). Socio-demographic and clinical features were similar in patients who completed the study and in those who dropped-out (Table 1). The study was completed by 43 women (70.5%) and 18 men (29.5%) from the PD group, and 45 women (70.3%) and 19 men (29.7%) from the healthy controls. The socio-demographic characteristics of patients and controls were shown in Table 1. 3.2. Pre-treatment assessment 3.2.1. Axis I comorbidity Agoraphobia was found in 47 patients (77%) and at least one other anxiety disorder was diagnosed in 22 patients (36.0%, consisting of social phobia in 13, generalized anxiety disorder in 11, obsessive– compulsive disorder in 8). Major depression was diagnosed in 23 patients (37.7%). 3.2.2. Symptoms severity PD patients showed higher Ham-A, Ham-D and SCL-90-pa scores than controls (Table 1). Symptom severity was higher in non-remitting (NR) patients than in remitting (R) patients (Table 2). After controlling for defenses (mature, neurotic and immature) or ODF, the differences between PD patients and healthy subjects when comparing anxious (ANCOVA, defense style: F = 43.4; df = 2,125; P b 0.001; ODF: F = 55.0; df = 2,125; P b 0.001), phobic (ANCOVA, defense style: F = 29.7; df = 2,125; P b 0.001; ODF: F = 54.4; df = 2,125; P b 0.001) and depressive (ANCOVA, defense style: F = 42.1; df = 2,125; P b 0.001; ODF: F = 38.9; df = 2,125; P b 0.001) symptoms remained. 3.2.3. Defense style PD patients used more neurotic and immature defenses than controls, whereas the two groups did not show any difference in the use of mature defenses (Table 1). Moreover, the ODF was lower in PD patients than in controls (Table 1). Among PD patients, the use of neurotic and immature defenses was higher in NR patients than in R patients (Table 2). Similarly, the ODF score was lower in NR patients than in R patients (Table 2). After controlling for the effect of symptom severity, the differences in neurotic and immature defenses or in the ODF between PD patients
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Table 1 Socio-demographics and clinical features of both patients with panic disorder, who completed the one-year follow-up (completers) and who dropped-out (drop-out), and healthy controls. Panic disorder
Controls
Completers n=61 Female gender Age years Education years Marital status Never married Married Separated/divorced Widowed Occupation Unemployed Student Housewife Employed
Drop-outs n=29
n=64
43 35.7 ± 10.9 10.3 ± 4.1
70.5%
18 36.1 ± 10.6 10.1 ± 4.5
62.0%
45 34.6 ± 11.0 9.8 ± 4.7
70.3%
24 30 6 1
39.3% 49.1% 9.8% 1.6%
11 15 2 1
37.9% 51.7% 6.8% 3.4%
25 32 6 1
39.0% 50.0% 9.3% 1.5%
2 10 7 42
3.2% 16.3% 11.4% 68.8%
1 5 4 19
3.4% 17.2 13.7% 65.5%
3 8 8 45
4.6% 12.5% 12.5% 70.3%
χ2 = 0.03; df = 2; P = 0.96 t = 0.72; df = 2,151; P = 0.49 t = 0.45; df = 2,151; P = 0.76 χ2 = 0.09; df = 3; P = 0.88
χ2 = 0.2; df = 3; P = 0.69
Symptom severity Ham-A Ham-D SCL-90-pa
17.2 ± 8.7 14.2 ± 7.4 1.62 ± 1.3
16.8 ± 8.6 12.5 ± 6.5 1.60 ± 1.1
3.8 ± 2.7 3.5 ± 2.3 0.14 ± 0.1
t = 11.3; df = 1,151; P b 0.001 t = 12.4; df = 1,151; P b 0.001 t = 9.6; df = 1,151; P b 0.001
Defense mechanisms Mature Neurotic Immature ODF
4.5 ± 1.3 4.1 ± 1.5 4.1 ± 1.2 3.7 ± 0.3
4.6 ± 1.2 4.0 ± 1.6 4.1 ± 1.3 3.7 ± 0.4
4.7 ± 1.2 3.4 ± 1.2 3.1 ± 0.8 3.9 ± 0.2
t = 1.9; t = 3.1; t = 4.8; t = 3.8;
df = 1,151; df = 1,151; df = 1,151; df = 1,151;
P = 0.41 P = 0.01 P b 0.001 P b 0.001
and healthy subjects disappeared (ANCOVA: neurotic defenses F = 0.63; df = 2,125; P = 0.53; immature defenses: F = 0.94; df = 2,125; P = 0.39; ODF: F = 2.22; df = 2,125; P = 0.14).
df = 2,119; P b 0.001) and depressive (ANCOVA, defense style: F = 22.8; df = 2,119; P b 0.001; ODF: F = 43.7; df = 2,119; P b 0.001) symptoms remained between PD patients and healthy subjects.
3.3. Treatment
3.4.3. Defense style The use of neurotic and immature defenses decreased in PD patients: R patients used the same defense style as controls, whereas NR patients still used more immature defenses than either of the former groups (Table 2). Moreover, the ODF scores increased in both R and NR patients. Nevertheless, NR patients showed lower ODF scores than R and controls, whereas the same ODF scores were found in R patients and controls. After excluding the effect of symptom severity, the differences in immature defenses or in the overall defense functioning between NR patients and R patients together with controls disappeared (ANCOVA: immature defenses F = 0.16; df = 2,119; P = 0.84; ODF: F = 0.64; df = 2,119; P = 0.52).
Paroxetine was administered in 32 patients (52.4%) at the mean daily dose of 32.4 ± 12.6 mg, whereas 29 patients (47.5%) were treated with citalopram at a mean daily dose of 33.1 ± 13.8 mg. LRZ co-treatment was administered in 10 patients (31.2%) in the paroxetine group at the mean daily dose of 2.0 ± 1.1 mg and in 8 patients (27.5%) from the citalopram group at the mean daily dose of 1.8 ± 0.5 mg. 3.4. Post-treatment assessment 3.4.1. Remission rate Complete remission was achieved by 28 (45.9%) patients, whereas some anxious and depressive symptoms were still present in the remaining 33 patients at the end-point. The rate of remission was similar in patients treated with paroxetine (n. 14; 43.7%) and in those who received citalopram (n. 14; 48.2%) (χ2 =0.7; df = 1; P = 0.49). The outcome of treatment was not predicted by the pre-treatment defense style of PD patients, after controlling for the effect of confounding variables (Neurotic defenses: OR = 1.16; CI 95% =0.63– 2.11; P = 0.71; Immature defenses: OR = 0.75; CI 95% = 0.36–1.58; P = 0.45; ODF: OR = 1.95; CI 95% = 0.39–9.61; P = 0.41). 3.4.2. Symptoms severity The severity of symptoms decreased in both R and in NR patients after treatment, however whereas the Ham-A, Ham-D and SCL-90-pa scores were similar in R patients and in controls, they were higher in NR patients (Table 2). After controlling for the effect of defense style or ODF, the differences in anxious (ANCOVA, defense style: F = 21.9; df = 2,119; P b 0.001; ODF: F = 24.9; df = 2,119; P b 0.001), phobic (ANCOVA, defense style: F = 38.0; df = 2,119; P b 0.001; ODF: F = 26.1;
4. Discussion In this naturalistic prospective study, the defense style was compared in PD patients, before and after treatment, as well as in healthy subjects. Before treatment, PD patients demonstrated the use of less mature defensive functioning which was indicated by higher scores of neurotic and immature defenses and a lower ODF score, thus confirming the previous observation that a less adaptive defense style was used in PD patients when they experienced acute symptoms (Busch et al., 1995; Kipper et al., 2004, 2005; Pollock and Andrews, 1989; Spinhoven and Kooiman, 1997). Nevertheless, the following difference was found among PD patients: patients who did not achieve remission after treatment showed a less mature defensive functioning (scoring higher for neurotic and immature defenses and lower for ODF score) than remitters, confirming the results of a previous study (Kipper et al., 2005). Moreover, in non-remitters the use of less adaptive defenses was associated with more severe anxious and depressive symptoms.
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Table 2 Defense mechanisms and severity of symptoms in remitted (R) and in non-remitted (NR) patients affected by panic disorder, before (t0) and after treatment (t12), and in healthy controls. Panic disorder
Controls
Remitted (R) n=28 t0
Non-remitted (NR) n=33 t12
t0
R vs. NR vs. C, one-way ANOVA, df = 2,122
(C) n=64 t12
t0
t12
F
P
Defenses Mature Neurotic Immature ODF
4.6 ± 1.2 3.8 ± 1.5 3.7 ± 1.2 3.7 ± 0.3
4.4 ± 1.3 3.1 ± 1.3 3.3 ± 1.0 3.9 ± 0.3
4.4 ± 1.3 4.3 ± 1.5 4.3 ± 1.1 3.6 ± 0.2
4.5 ± 1.2 4.0 ± 1.2 3.8 ± 0.9 3.7 ± 0.2
4.7 ± 1.2 3.4 ± 1.2 3.1 ± 0.8 3.9 ± 0.2
0.55 4.66 15.6 11.9
0.57 0.01a b0.001b b0.001e
Symptoms Ham-A Scl-90-pa Ham-D
16.7 ± 9.2 1.2 ± 1.2 12.0 ± 7.3
5.5 ± 4.6 0.4 ± 0.5 3.5 ± 2.3
17.6 ± 8.3 1.9 ± 1.3 16.0 ± 7.0
12.6 ± 7.9 1.1 ± 0.8 10.5 ± 6.8
3.8 ± 2.7 0.1 ± 0.1 3.5 ± 2.3
67.9 48.4 67.8
b0.001c b0.001b b0.001b
F
P 0.53 2.31 4.65 4.13
33.8 48.6 36.2
0.58 0.10 0.01a 0.01e
b0.001d b0.001d b0.001d
One-way ANOVA with Bonferroni post-hoc analysis: aNR N C; bNR N R N C; cNR, R N C; dNR N R, C; eNR b R b C.
After one year of treatment, the defenses changed with a shift toward the use of more adaptive styles. Patients in remission showed the same defense style as healthy subjects, whereas non-remitters, who achieved only a reduction of pre-treatment symptom severity (without remission), showed a decrease in the use of immature defenses (without a normalization), a normal use of neurotic defenses and an increase of the ODF score. These findings confirm that the improvement in symptom severity is associated with greater use of mature defenses (Akkerman et al., 1999; Bond, 2004; Bond and Perry, 2004; Drapeau et al., 2003; Heldt et al., 2007; Kipper et al., 2005). As a whole, our findings suggest that the onset of PD induces the use of less mature defenses and that when the disorder remits, defense styles return to a more normalized function. In our study, the following data support this hypothesis: 1) first of all, the normalization of the defense style for those achieving 3 months of remission; 2) second, the improvement of symptoms severity in non-remitters, which was associated with a lower use of less mature defenses at the end of treatment. This was demonstrated by evidence that the use of neurotic defenses normalized and that the use of immature defenses decreased, as further indicated by an improvement in more adaptive defensive functioning; 3) third, the use of less mature defenses in non-remitters was associated with higher symptom severity both at baseline and one year after treatment; 4) and finally, the differences in defense style between PD patients and healthy controls disappeared when the effect of symptom severity was controlled, whereas the difference in symptom severity did not disappear after controlling for the defense mechanisms. Therefore, our data support the hypothesis that the use of less mature defensive functioning may be, ipso facto, the consequence of PD: when subjects fall ill, their capacity to use mature defenses may diminish, and, as the anxious, phobic and depressive symptoms remitted, their defensive style returned to a greater level of maturity. Thus, our data seem to suggest that the use of less mature defensive functioning may be a state dependent phenomenon. However, another hypothesis might explain our data. The DSQ-40 does not measure patient defenses per se (which are intrapsychic phenomena that may be out of a subject's awareness) but their rather conscious derivates (behaviours) (Bond, 2004). Therefore, it is plausible that an overlap might exist between some defensive behavioural derivatives and behaviours induced by anxious symptoms. Also the DSQ-40 items might measure merely “anxious” behaviours, rather than those specifically “belonging” to defense mechanisms. For example, the DSQ-40 items “Doctors never really understand what is wrong with me” and “No matter how much I complain, I never get a satisfactory response,” may inquire at a broader angle than fit for this study. Such exploration of certain
aspects of immature defenses could also measure the common experience of PD patients when they seek medical assistance. It is well known that PD patients are higher users of the medical setting (Ballenger, 1997; Marchesi et al., 2001) and in this setting they may receive the correct diagnosis and treatment only after many consultations. Therefore, the feeling of not being understood or not receiving a satisfactory response by the doctors is common in PD patients. In this regard, the relationship between maladaptive defenses and PD may represent an artefact of the measure used in the assessment of behaviour derivatives of defenses. Therefore, it's possible that PD patients might score high on some DSQ-40 items only because they are anxious. This hypothesis may partially explain the positive correlation between anxiety and immature defenses observed in previous studies (Holi et al., 1999; Kipper et al., 2004; Sammallahti et al., 1994; Spinhoven and Kooiman, 1997). Finally, in our study the pre-treatment defense style did not predict the outcome of treatment. This finding contradicts our observation that at baseline non-remitters showed a less adaptive defensive functioning ( higher use of neurotic and immature defenses and a lower ODF score) than remitters. It also challenges the results of previous studies (Bond and Perry, 2004; Heldt et al., 2003; Kipper et al., 2005, 2007) which found that the pre-treatment use of immature defenses predicted a poor outcome of treatment. Nevertheless, when the effect of confounding variables (such as gender, age at onset and duration of PD, anxious and depressive comorbidity, pre-treatment symptom severity, known to negatively influence the response to treatment) was controlled, the outcome of treatment was not predicted by the use of neurotic and immature defenses or by the ODF score. Only one previous study (Kipper et al., 2007) controlled the effect of some of the aforementioned confounding variables. In that study, immature defenses predicted clinical remission in PD. The different results of our study may be explained by the following observations. Kipper et al. (2007) identified remission as disappearance of panic attacks, whereas our study used the following more restrictive remission criteria: disappearance of panic attacks, anticipatory anxiety, phobic avoidance and depression for at least 3 months. A previous study (Marchesi et al., 2006) demonstrated that the identification of predictable response factors depended on the remission criteria used. Kipper et al. (2007) evaluated remission after short-term treatment (16 weeks), whereas a long-term treatment (52 weeks) was considered in our study. It is well known that the predictors of the treatment outcome are different depending on the duration of treatment (Slaap and den Boer, 2001). Kipper et al. (2007) did not control for the effect of anxious comorbidity and severity of phobic avoidance, which negatively influenced the
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achievement of remission (Marchesi et al., 2006). Therefore, when remission was defined using more restrictive criteria and evaluated over a longer term, with the effects of all confounding variables controlled, our study seems to suggest that the outcome of pharmacological treatment on PD patients could not be predicted by pretreatment defense style. Some methodological limitations reduced the strength of our findings. Firstly, given the small sample size of PD patients, firm conclusions should be drawn from our results with caution and the present data need to be verified by using larger sample groups with longer follow-up period. Secondly, the dropout rate of about one third of patients, who did not complete the study, reduces the reliability of the conclusions drawn from our results. Thirdly, we used just one specific questionnaire (DSQ-40) to evaluate the complexity of defense style. Particularly the identification of three styles has received weak empirical support and considering that Andrew et al. (1993) found that the individual items loaded from 0.47–0.59 on the mature style, 0.33–0.55 on the neurotic style, and 0.32–0.60 on the immature style. Even though the use of ODF confirms that DP patients used a less adaptive defense style, our results need to be confirmed with a more complete assessment of the defense mechanisms. Finally, our sample is more representative of patients treated in a psychiatric setting and therefore our data need to be confirmed in patients seeking assistance at a primary care level. References Akkerman, K., Lewin, T., Carr, V., 1999. Long-term changes indefense style among patients recovering from major depression. Journal of Nervous and Mental Disease 187, 80–87. American Psychiatric Association, 1998. Practice Guideline for the Treatment of Patients With Panic Disorder. American Journal of Psychiatry 155 (5, suppl), 1–34. Andrews, G., Pollock, C., Stewart, G., 1989. The determination of defense style by questionnaire. Archives of General Psychiatry 46, 455–460. Andrews, G., Singh, M., Bond, M., 1993. The Defense Style Questionnaire. Journal of Nervous and Mental Disease 181, 246–256. Ballenger, J.C., 1997. Panic disorder in the medical setting. Journal of Clinical Psychiatry 58 (Suppl 2), 13–17. Ballenger, J.C., 1999. Clinical guidelines for establishing remission in patients with depression and anxiety. Journal of Clinical Psychiatry 60 (Suppl 22), 29–34. Ballenger, J.C., 2001. Treatment of anxiety disorders to remission. Journal of Clinical Psychiatry 62 (Suppl 12), 5–9. Ballenger, J.C., Davidson, J.R.T., Lecrubier, Y., Nutt, D.J., Baldwin, D.S., den Boer, J.A., 1998. Consensus statement on panic disorder from the international consensus group on depression and anxiety. Journal of Clinical Psychiatry 59 (Suppl 8), 47–54. Bogren, L., Bogren, I., Ohrt, T., Sjödin, I., 2002. Panic disorder and the Defense Mechanism Test. Nordisk Journal of Psychiatry 56, 195–199. Bond, M., 2004. Empirical studies of defense style: relationships with psychopathology and change. Harvard Review of Psychiatry 12, 263–278. Bond, M., Gardner, S.T., Christian, J., Sigal, J.J., 1983. Empirical study of self-related defense styles. Archives of General Psychiatry 40, 333–338. Bond, M., Perry, J., 2004. Long-term changes in defense styles with psychodynamic psychotherapy for depressive, anxiety and personality disorders. American Journal of Psychiatry 161, 1665–1671. Bond, M.P., Vaillant, J.S., 1986. An empirical study of the relationship betweendiagnosis and defense style. Archives of General Psychiatry 43, 285–288. Busch, F.N., Shear, M.K., Cooper, A.M., Shapiro, T., Leon, A.C., 1995. An empirical study of defense mechanism in panic disorder. Journal of Nervous and Mental Disease 183, 299–303.
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