ΨΥΧΙΑΤΡΟΣ Δασκαλόπουλος, ΨΥΧΙΑΤΡΙΚΗ, ΑΓΧΟΣ, ΠΑΝΙΚΟΣ, ΚΑΤΑΘΛΙΨΗ, αντικαταθλιπτικά φάρμακα, DNA, υπνωτικά, ύπνος, Venfax, Remeron, σοκολάτα, ύπνωση
Μύθοι και Αλήθειες: ΨΥΧΙΑΤΡΟΣ, Ψυχιατρική, Ψυχοθεραπεία, φάρμακα στην Ψυχιατρική, ΥΠΝΟΣ, αϋπνία, υπνωτικά, ΑΓΧΟΣ, ΚΑΤΑΘΛΙΨΗ, αντικαταθλιπτικά, DNA, ΣΟΚΟΛΑΤΑ, placebo, ΥΠΝΩΣΗ και άλλα μυστήρια.

Ο Δείκτης Ευαισθησίας Άγχους
και η συσχέτιση με την Διαταραχή Πανικού

«Αυτό που φοβάμαι περισσότερο είναι ο φόβος»

Michel de Montaigne, φιλόσοφος, 16ος αιώνας

Η «Ευαισθησία στο Άγχος» (Anxiety Sensitivity - AS), είναι ένας δείκτης φόβου των ανθρώπινων βιολογικών συμπτωμάτων που χαρακτηρίζουν την αυτόνομη διέγερση του νευρικού συστήματος. Περιγράφεται από τη δεκαετία του 1980 και από τότε χρησιμοποιείται ολοένα και περισσότερο στην επεξήγηση και τη θεραπεία πολλών ψυχιατρικών διαταραχών. Η «Ευαισθησία στο άγχος» είναι το μέτρο της τάσης να παρερμηνεύονται τα συμπτώματα που συνοδεύουν το άγχος (ακανόνιστο αναπνοή, αίσθημα παλμών της καρδιάς , τρόμος, έξαψη, εφίδρωση, πόνος και σφίξιμο του στομάχου) :

weber, ΑΓΧΟΣ, ΦΟΒΟΣ, ΠΑΝΙΚΟΣ

Η παρερμηνεία μπορεί να έχει διάφορους τύπους:

  • 1. Επικείμενης επέλασης φυσικού κινδύνου («έχω ένα κακό προαίσθημα» - «κάτι κακό θα συμβεί») ή

  • 2. Σοβαρής ασθένειας ( «πάω να πάθω καρδιακή προσβολή» - «θα λιποθυμήσω»), ή

  • 3. Απώλειας του ελέγχου ( «δεν μπορώ να συγκεντρωθώ» – «χάνω το μυαλό μου» - «τρελαίνομαι!»), ή

  • 4. Ταπεινωτικής κοινωνικής απόρριψης («όλοι θα καταλάβουν ότι τρέμω»).

Έχουν αναπτυχθεί τυποποιημένα ερωτηματολόγια για τη μέτρηση του φαινομένου. Η πιο διαδεδομένη μέτρηση είναι (Anxiety Sensitivity Index 16), που ζητά από τους ανθρώπους να επιβεβαιώσουν ή να διαψεύσουν 16 δηλώσεις όπως «Με τρομάζουν οι όποιες ασυνήθιστες αισθήσεις στο σώμα μου».

Μετρήστε την Ευαισθησία στο ΑΓΧΟΣ - Πρόγνωση κινδύνου Κρίσεων Πανικού.

Ένα άτομο με υψηλό σκορ στον Δείκτη Ευαισθησίας Άγχους μπορεί να έχει χαμηλό σκορ στην κλίμακα μέτρησης της Αγχώδους Διαταραχής, και αντιστρόφως. Αλλά ένα υψηλό σκορ στον Δείκτη Ευαισθησίας Άγχους, ευνοεί την ανάπτυξη όλων των αγχωδών διαταραχών, των υποχονδριακών φόβων και της κατάθλιψης. Μάλιστα ειδικά η συσχέτιση με την Διαταραχή Πανικού είναι ιδιαίτερα μεγάλη (Olatunji and Wolitzky-Taylor 2009). Πιθανολογούμε πλέον όσον αφορά τη διαταραχή πανικού, ότι προκαλείται λόγω της υψηλής ευαισθησίας στο άγχος. Πρέπει να ξεκαθαρίσουμε ότι η Διαταραχή Πανικού, είναι μία πάθηση που γεννιέται πάνω στο έδαφος της Αγχώδους Διαταραχής. Οι ασθενείς με διαταραχή Πανικού σκοράρουν υψηλά νούμερα (τυπικά άνω του 25) στον Δείκτη Ευαισθησίας Άγχους.

Ας πούμε ότι οδηγείτε στην Αττική Οδό ή στην Κατεχάκη και το μποτιλιάρισμα έχει ακινητοποιήσει το αυτοκίνητό σας, κάπως μακριά από την επόμενη έξοδο. Κοιτώντας τις ατελείωτες σειρές από αυτοκίνητα, ξαφνικά σκέφτεστε: «Τι θα συμβεί αν τώρα λιποθυμήσω ή πάθω ένα καρδιακό επεισόδιο; Το ασθενοφόρο δεν θα μπορέσει να έρθει και να με μεταφέρει γρήγορα στο κοντινότερο νοσοκομείο!» Καταλήγετε στην απειλητική σκέψη ότι η ζωή σας μπορεί πράγματι να κινδυνεύει. Αρχίζετε να τρέμετε, αισθάνεστε πίεση στο στήθος σας, η καρδιά σας αρχίζει να χτυπά γρήγορα, και αν ο Δείκτης Ευαισθησίας Άγχους σας είναι υψηλός, νομίζετε (ουσιαστικά πλέον φοβόσαστε) ότι μπορεί να πάθετε ή να έχετε ήδη υποστεί καρδιακή προσβολή. Τα σωματικά συμπτώματα και η προαίσθηση του κινδύνου, αλληλο-ενισχύονται. Μπορεί να γίνετε ακόμη περισσότερο ανήσυχοι, η καρδιά σας χτυπάει τρελά, οι τρεμούλες δυναμώνουν, φοβόσαστε ότι θα λιποθυμήσετε και ο πανικός πλέον αρχίζει να μεγαλώνει. Αν όμως ο Δείκτης Ευαισθησίας Άγχους σας είναι χαμηλός, πιθανότατα να μην είχατε το κύμα σωματικών συμπτωμάτων, να είχε γρήγορα φύγει η όποια ενοχλητική σκέψη από το νου σας και η κρίση πανικού δεν θα είχε δημιουργηθεί.

Όπως και το χρόνιο άγχος, ο Δείκτης Ευαισθησίας Άγχους φαίνεται να εμφανίζεται περισσότερο σε μερικές οικογένειες, ενδεχομένως για λόγους γενετικούς (κληρονομικότητα) και ενδεχομένως, επειδή οι γονείς χρησιμεύουν ως πρότυπο για τα παιδιά τους. Μελέτες με διδύμους έχουν πλέον αποδείξει την ισχυρή αυτή οικογενειακή συσχέτιση (Jang, Stein et al. 1999; Stein, Jang et al. 1999; Tambs, Czajkowsky et al. 2009). Η δυσλειτουργία του συστήματος της σεροτονίνης στον εγκέφαλο, είναι η κεντρική αιτιολογική υπόθεση της Διαταραχής Πανικού και μάλιστα θεωρούμε ως πιθανή βλάβη τον πολυμορφισμό των γονιδίων που κατασκευάζουν τους υποδοχείς 5-ΗΤ2A της σεροτονίνης (Stein, Schork et al. 2008; Yoon, Yang et al. 2008). Η φαρμακευτική θεραπεία εδράζεται σε αυτό ακριβώς το σημείο με τη χρήση φαρμάκων SSRI και SNRI.

Τα αποτελέσματα της έρευνας δείχνουν ότι ο Δείκτης Ευαισθησίας Άγχους, έχει σημαντική προγνωστική αξία για μελλοντικά συμπτώματα κρίσεων πανικού, τόσο για τα σωματικά όσο και τα γνωσιακά συμπτώματα της κρίσης πανικού αλλά και για την μεταβλητότητα αυτών. Τα ευρήματα αυτά υπογραμμίζουν τη σημασία και το μοναδικό ρόλο του Δείκτη Ευαισθησίας Άγχους στην πρόγνωση του κινδύνου για την εμφάνιση της Διαταραχής Πανικού (Olatunji, Feldner et al. 2008; Schmidt, Keough et al. 2008; Benitez, Shea et al. 2009; Chavira, Stein et al. 2009; Hinton, Lewis-Fernandez et al. 2009; Kutz, Marshall et al. 2009).

Είναι σημαντικό να τονίσουμε ότι ο Δείκτης Ευαισθησίας Άγχους, μετράει το φόβο του φόβου και όχι την ίδια την ύπαρξη ή τη βαρύτητα της Αγχώδους Διαταραχής ή της Διαταραχής Πανικού.

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Μετρήστε την Ευαισθησία στο ΑΓΧΟΣ - Πρόγνωση κινδύνου Κρίσεων Πανικού.

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Βιβλιογραφικές Αναφορές για τον Δείκτη Ευαισθησίας Άγχους

Benitez, C. I., M. T. Shea, et al. (2009). "Anxiety sensitivity as a predictor of the clinical course of panic disorder: a 1-year follow-up study." Depress Anxiety 26(4): 335-342. BACKGROUND: There is evidence that negative affect (NA) and anxiety sensitivity (AS) predict the development of anxiety disorders, particularly panic disorder (PD). The main purpose of this study was to examine whether NA and AS will also predict the clinical course of PD. METHODS: Participants were 136 individuals with a DSM-III-R diagnosis of PD (with or without agoraphobia) enrolled in a naturalistic and longitudinal study of anxiety disorders, the Harvard/Brown Anxiety Research Project (HARP). Participants were administered the Anxiety Sensitivity Index and the Negative Affect Scales of the Positive and Negative Affect Schedule-Expanded Form (PANAS-X-NA) and their percentage of time in PD episode was followed for 1 year after the administration of the measures. RESULTS: Multiple regression analyses indicated that AS, but not NA, was a significant predictor of percentage of time in PD episode after controlling for previous time in PD episodes, comorbid depression, other anxiety disorders, and exposure to psychopharmacological and behavioral treatments. As expected, the Physical Concerns subscale of the Anxiety Sensitivity Index had a significant independent contribution in predicting the course of the disorder. CONCLUSIONS: Overall, these findings suggest that AS, as a unique construct, may be predictive of the amount of time patients are in episode of PD.

Chavira, D. A., M. B. Stein, et al. (2009). "Predictors of clinical improvement in a randomized effectiveness trial for primary care patients with panic disorder." J Nerv Ment Dis 197(10): 715-721. This study's aim was to prospectively examine and identify a model of demographic, clinical, and attitudinal variables that impact improvement among patients with panic disorder. Subjects were 232 primary care patients meeting criteria for DSM-IV panic disorder. Eligible patients were randomly assigned to a collaborative care intervention or to treatment as usual. Assessments occurred at 3-month intervals during the course of 1 year. In final multivariate logistic regression models, patients with higher anxiety sensitivity and higher neuroticism scores at baseline were less likely to show clinical improvement (using a criterion of 20 or less on the Anxiety Sensitivity Index) at 3 months. Those who were non-white, had higher anxiety sensitivity, and higher overall phobic avoidance at baseline were less likely to show clinical improvement at 12 months. A greater understanding of these predictors may help clinicians identify who is at greatest risk for persistent panic-related symptoms and to plan the intensity of interventions accordingly.

Hinton, D. E., R. Lewis-Fernandez, et al. (2009). "A model of the generation of ataque de nervios: the role of fear of negative affect and fear of arousal symptoms." CNS Neurosci Ther 15(3): 264-275. This article examines a model of the generation of ataque de nervios, according to which both fear of negative affectivity and fear of arousal symptoms are associated with the emergence of ataques. We examine the relationship of fear of negative affectivity and fear of arousal to the severity of ataque de nervios during the last month and the last 6 months among Caribbean Latinos residing in the United States. The measures include a Fear of Anger Scale and the Anxiety Sensitivity Index (ASI), the ASI augmented with two items that assess fear of arousal symptoms common in ataques: chest tightness and a sense of inner heat. In keeping with the model of ataque generation, one-way analysis of variances (ANOVAs) and discriminant function analyses illustrated that items assessing "fear of negative affect" and "fear of somatic and psychological symptoms of arousal" both differentiated well among the levels of ataque severity. In addition, key ataque symptoms-mental incapacitation fears, shakiness, chest tightness, palpitations, and a sense of inner heat-were the best discriminators among levels of ataque severity. In patients with severe ataques, the scores of "fear of negative affect" and "fear of ataque-de-nervios-type somatic and psychological symptoms" were extremely elevated. This further suggests that both these types of fears are associated with this idiom of distress and that the specific content of the fears is linked to the symptom picture of the idiom. This suggests specific therapeutic targets for the treatment of ataque, namely, the reduction of anxiety sensitivity (and more generally negative-emotion and arousal sensitivity) using cognitive behavioral therapy (CBT), relaxation, and mindfulness techniques.

Jang, K. L., M. B. Stein, et al. (1999). "Gender differences in the etiology of anxiety sensitivity: a twin study." J Gend Specif Med 2(2): 39-44. OBJECTIVE: To estimate the magnitude of genetic and environmental factors on anxiety sensitivity by gender. DESIGN: Classic twins reared-together study design. PATIENTS: A community sample of 337 twin pairs, including 179 monozygotic (45 brother and 134 sister pairs) and 158 dizygotic (28 brother, 94 sister, and 36 brother-sister pairs). METHOD: Twin pairs completed the Anxiety Sensitivity Index (ASI) using a postal survey design. The ASI is composed of three factors: (1) fear of anxiety-related somatic sensations; (2) fear of cognitive dyscontrol due to beliefs that sensations like depersonalization are signs of mental illness (e.g., fear of concentration problems); and (3) fear of publicly observable anxiety reactions (e.g., fear of trembling). Biometrical modeling techniques were used to estimate heritability of the ASI dimensions by gender. RESULTS: ASI factors are heritable only in women, accounting for 37% to 48% of the total variance (median, 44.5%). Environmental factors accounted for all the variability in men. CONCLUSIONS: These findings have implications for understanding the etiology of panic disorder. Previous research suggests that anxiety sensitivity is a risk factor or diathesis for this disorder, and that panic disorder is more prevalent in women than men. Our findings suggest the hypothesis that the increased prevalence in women may occur because anxiety sensitivity is heritable in women.

Kutz, A., E. Marshall, et al. (2009). "Evaluating emotional sensitivity and tolerance factors in the prediction of panic-relevant responding to a biological challenge." J Anxiety Disord. The current study investigated anxiety sensitivity, distress tolerance (Simons & Gaher, 2005), and discomfort intolerance (Schmidt, Richey, Cromer, & Buckner, 2007) in relation to panic-relevant responding (i.e., panic attack symptoms and panic-relevant cognitions) to a 10% carbon dioxide enriched air challenge. Participants were 216 adults (52.6% female; M(age)=22.4, SD=9.0). A series of hierarchical multiple regressions was conducted with covariates of negative affectivity and past year panic attack history in step one of the model, and anxiety sensitivity, discomfort intolerance, and distress tolerance entered simultaneously into step two. Results indicated that anxiety sensitivity, but not distress tolerance or discomfort intolerance, was significantly incrementally predictive of physical panic attack symptoms and cognitive panic attack symptoms. Additionally, anxiety sensitivity was significantly predictive of variance in panic attack status during the challenge. These findings emphasize the important, unique role of anxiety sensitivity in predicting risk for panic psychopathology, even when considered in the context of other theoretically relevant emotion vulnerability variables.

Olatunji, B. O., M. T. Feldner, et al. (2008). "A comparative evaluation of panicogenic processes and quality of life in a sample of non-clinical panickers and age and sex matched non-panicking controls." J Anxiety Disord 22(2): 175-186. Contemporary models of panic attacks suggest that panic problems exist on a continuum and highlight the need to understand what differentiates persons who have never had a panic attack versus persons who have had panic attacks but have not yet developed panic disorder (i.e., non-clinical panickers). Accordingly, the present study evaluated several theoretically-relevant factors that were expected to distinguish a sample of (conservatively defined) non-clinical panickers (n=72) from an age and sex-matched comparison sample of non-panicking controls (n=72). As expected, panickers were characterized by higher levels of anxiety sensitivity, perceived uncontrollability, and state and trait anxiety relative to their non-panic counterparts. Moreover, higher levels of trait anxiety emerged as a predictor of poorer quality of life among panickers. Results are considered within the context of biopsychosocial continuum models of panic attacks and panic disorder and future directions for research are suggested.

Olatunji, B. O. and K. B. Wolitzky-Taylor (2009). "Anxiety sensitivity and the anxiety disorders: A meta-analytic review and synthesis." Psychol Bull 135(6): 974-999. There has been significant interest in the role of anxiety sensitivity (AS) in the anxiety disorders. In this meta-analysis, we empirically evaluate differences in AS between anxiety disorders, mood disorders, and nonclinical controls. A total of 38 published studies (N = 20,146) were included in the analysis. The results yielded a large effect size indicating greater AS among anxiety disorder patients versus nonclinical controls (d = 1.61). However, this effect was maintained only for panic disorder patients compared to mood disorder patients (d = 0.85). Panic disorder was also associated with greater AS compared to other anxiety disorders except for posttraumatic stress disorder (d = 0.04). Otherwise the anxiety disorders generally did not differ from each other in AS. Although these findings suggest that AS is central to the phenomenology of panic disorder and posttraumatic stress disorder, causal inferences regarding the role of AS in these anxiety disorders cannot be made. Moderator analyses showed that a greater proportion of female participants was associated with larger differences in AS between anxiety and nonclinical control groups. However, more female participants were associated with a smaller AS difference between anxiety and mood disorder groups. This finding suggests that AS is less robust in distinguishing anxiety from mood disorders among women. Age also moderated some observed effects such that AS was more strongly associated with anxiety disorders in adults compared to children. Type of AS measure used also moderated some effects. Implications of these findings for the conceptualization of AS in anxiety-related disorders are discussed. (PsycINFO Database Record (c) 2009 APA, all rights reserved).

Schmidt, N. B., M. E. Keough, et al. (2008). "Anxiety sensitivity profile: predictive and incremental validity." J Anxiety Disord 22(7): 1180-1189. Anxiety sensitivity (AS) is a well-researched risk factor for the development of anxiety psychopathology. AS is typically measured using the anxiety sensitivity index (ASI) but limitations have led to the creation of second generation measures of AS including the anxiety sensitivity profile (ASP). The ASP has not been used very extensively, however, and we believe this may be due to two important issues: (1) the ASP is lengthy, and (2) the predictive validity of the ASP is unexplored in relation to critical outcomes such as anxiety psychopathology. The purpose of the present report was to address these two issues. We evaluated whether an abbreviated form of the ASP was viable and also conducted tests of the scale's predictive validity. Findings suggest that a 22-item version of the ASP (i.e., ASP-22) is comparable to the original 60-item ASP. Moreover, the ASP-22 was predictive of anxious responding to a CO(2) challenge. In fact, the ASP-22 outperformed the ASI as a predictor of CO(2) reactivity. Also, the ASP-22 was a significant longitudinal predictor of incidence of Axis I diagnoses. In regard to predictive validity, the ASP-22 was comparable to the original ASP. In summary, the ASP-22 appears to represent a viable measure of AS that may complement the ASI.

Stein, M. B., K. L. Jang, et al. (1999). "Heritability of anxiety sensitivity: a twin study." Am J Psychiatry 156(2): 246-251. OBJECTIVE: In attempting to explain the familial predisposition to panic disorder, most studies have focused on the heritability of physiologic characteristics (e.g., CO2 sensitivity). A heretofore unexplored possibility is that a psychological characteristic that predisposes to panic-anxiety sensitivity-might be inherited. In this study, the authors examined the heritability of anxiety sensitivity through use of a twin group. METHOD: Scores on the Anxiety Sensitivity Index were examined in a group of 179 monozygotic and 158 dizygotic twin pairs. Biometrical model fitting was conducted through use of standard statistical methods. RESULTS: Broad heritability estimate of the Anxiety Sensitivity Index as a unifactorial construct was 45%. Additive genetic effects and unique environmental effects emerged as the primary influences on anxiety sensitivity. There was no evidence of genetic discontinuity between normal and extreme scores on the Anxiety Sensitivity Index. CONCLUSIONS: This study suggests that one psychological risk factor for the development of panic disorder-anxiety sensitivity-may have a heritable component. As such, anxiety sensitivity should be considered in future research on the heritability of panic disorder.

Stein, M. B., N. J. Schork, et al. (2008). "Gene-by-environment (serotonin transporter and childhood maltreatment) interaction for anxiety sensitivity, an intermediate phenotype for anxiety disorders." Neuropsychopharmacology 33(2): 312-319. Anxiety sensitivity (AS) is a dispositional characteristic that predisposes to the development of anxiety disorders (eg, panic and post-traumatic stress disorder) and major depression. AS is subject to genetic and environmental influences, the former as yet unidentified and the latter known to include childhood maltreatment. The serotonin transporter gene (SLC6A4) promoter polymorphism (5-HTTLPR) has been associated with depression, but most consistently in the context of environmental stress. We tested the hypothesis that 5-HTTLPR genotype and childhood maltreatment would interact to increase susceptibility to AS in young adults. Subjects were European-American college undergraduates (N=150, median age 18 years) characterized on a measures of AS (Anxiety Sensitivity Index) and retrospective childhood maltreatment (Childhood Trauma Questionnaire [CTQ]). 5-HTTLPR genotypes were obtained from blood-derived DNA. Linear regression was used to model relationships between 5-HTTLPR, childhood emotional abuse, and AS; covariates such as sex, neuroticism, and ancestral proportion scores were incorporated into some models in a larger, ethnically heterogenous sample (N=247) to evaluate robustness of the findings to model assumptions. A statistically signficant interaction was observed between levels of childhood emotional (or physical) maltreatment and 5-HTTLPR genotype. Specifically, S/S individuals with higher levels of maltreatment had significantly higher levels of AS than subjects in other groups. No such relationship was found for neuroticism, attesting to the possible specificity of the findings for AS. Findings were consistently robust to the inclusion of covariates, and were not confounded by population stratification. In conclusion, these results provide evidence of a specific genetic influence on anxiety sensitivity-an intermediate phenotype for anxiety (and depressive) disorders; this effect is modified by severity of childhood maltreatment. These findings are consistent with the notion that 5-HTTLPR operates broadly to moderate emotional responsivity to stress.

Tambs, K., N. Czajkowsky, et al. (2009). "Structure of genetic and environmental risk factors for dimensional representations of DSM-IV anxiety disorders." Br J Psychiatry 195(4): 301-307. BACKGROUND: Twin data permit decomposition of comorbidity into genetically and environmentally derived correlations. No previous twin study includes all major forms of anxiety disorder. AIMS: To estimate the degree to which genetic and environmental risk factors are shared rather than unique to dimensionally scored panic disorder, generalised anxiety disorder, phobias, obsessive-compulsive disorder and post-traumatic stress disorder. METHOD: Data obtained from 2801 young-adult Norwegian twins by means of the Composite International Diagnostic Interview were analysed with the Mx program. RESULTS: A multivariate common factor model fitted best. The latent liability to all anxiety disorders was substantially more heritable (54%) than the individual disorders (23% to 40%). Most of the genetic effect was common to the disorders. Genes contributed just over 50% to the covariance between liabilities. CONCLUSIONS: The five anxiety disorders all share genetic and environmental risk factors. This has implications for the revision of the anxiety disorder section in DSM-V.

Yoon, H. K., J. C. Yang, et al. (2008). "The association between serotonin-related gene polymorphisms and panic disorder." J Anxiety Disord 22(8): 1529-1534. Dysfunction of the serotonergic system has been hypothesized to play an important role in panic disorder. We investigated the 5-HT2A receptor (5HTR2A) and tryptophan hydroxylase (TPH) genes for an association with panic disorder (PD). Patients with PD (n=107) and control subjects (n=161) were genotyped for 5HTR2A 1438A/G, 5HTR2A 102T/C, and TPH218 A/C. The severity of their symptoms was measured using the Spielberger State-Trait Anxiety Inventory (STAI), Panic Disorder Severity Scale (PDSS), Anxiety Sensitivity Index (ASI), Acute Panic Inventory (API), and Hamilton's Rating Scale for Depression (HAMD). There were no significant differences in the genotype distributions or allelic frequencies in the three serotonergic polymorphisms between PD patients and normal controls. However, we found a significant difference in symptom severity among the genotypes of both the 5HTR2A 1438A/G and 102T/C polymorphisms. Although there were no significant differences in the genotype and allele distributions, we found a significant association between panic symptom severity and the serotonin 2A receptor gene. This result suggests that 5HTR2A 1438A/G and 102T/C polymorphic regions can be associated with the phenotype or the pathogenesis of panic disorder.

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