Number Of Panic Attacks Research Articles

Correlations of plasma oxytocin with clinical and hormonal parameters in panic disorder

Aims The potential association between oxytocin (OXT) plasma levels and clinical and hormonal parameters in panic disorder (PD) especially in its acute phase – has not been investigated as yet. This was the aim of this article. Method Twenty-four consecutively-referred, acutely-ill, medication-free PD patients with (PDA, N = 21) or without agoraphobia, moreover without comorbidities, completed the following clinical measures: Hamilton Anxiety Rating Scale (HARS); Agoraphobic Cognitions Questionnaire (ACQ); Mobility Inventory-Alone subscale (MI-alone); and number of panic attacks during last 21 d (PA21d). Plasma levels of OXT, adrenocorticotropic hormone (ACTH) and cortisol were evaluated. Results OXT levels were significantly, negatively associated with the HARS scores (r= −0.59 p=.002) and weakly, negatively correlated with the ACQ scores (r = −0.403 p=.051). No significant correlations were traced between OXT levels and PA21d, MI-alone, ACTH, and cortisol. Conclusion In acutely-ill, medication-free PD patients, OXT plasma levels may be relevant to the severity of their ‘general’ anxiety symptoms, but not to the ‘specific’ panic psychopathology.

THE EFFICACY OF PSYCHOLOGICAL MEASURES RENDERED BY PHYSIOTHERAPISTS SERVING IN COVID WARDS IN ALLEVIATING THE PANIC ATTACKS

Covid-19 can disrupt a person’s circadian rhythm, which can impair his sleep, leading to insomnia and snowball into depression, anxiety and other cognitive changes, not infrequently a panic disorder .Present pandemic also witnessed the shortage of essential medicines including oxygen ,unavailability of intensive care beds ,making the patients and attendants panicky, alike. It has been observed that all the efforts are being put forth to understand the epidemiology, clinical symptoms, transmission patterns and the management of the covid-19 outbreak ,but there has been a little concern put forward over the traumatizing effect on one’s mental health. This pandemic witnessed the utter paucity of qualified medical personnel to serve in wards hence forcing physiotherapy students and interns to compliment their medical counterparts. We understood the need of psychological counselling for these admitted patients and we deputed physiotherapists to render the same. The benefit of counselling was quantified as the fall in the incidence of weekly panic attacks. This study was undertaken to evaluate the efficacy of physiotherapists posted in covid wards in reducing the panic attacks, since physiotherapist do have a basic knowledge of the psychology as a subject and they usually also have ample spare time in the wards, after they have completed their specialized duties. We studied 552 admitted patients of covid-19 in two medical colleges, identified patients with frequent panic attacks, who were then counselled psychologically. The effects of counselling sessions were observed for average 7 days of admission. We found on an average 64% fall in the number of panic attacks in the psychologically disturbed patients. We hence conclude that the physiotherapists posted in the covid wards should also be utilized in rendering psychological counselling to minimize occurrence of the panic attacks.
 Keywords: psychological, physiotherapists & Covid.

MAOA gene hypomethylation in panic disorder-reversibility of an epigenetic risk pattern by psychotherapy.

Epigenetic signatures such as methylation of the monoamine oxidase A (MAOA) gene have been found to be altered in panic disorder (PD). Hypothesizing temporal plasticity of epigenetic processes as a mechanism of successful fear extinction, the present psychotherapy-epigenetic study for we believe the first time investigated MAOA methylation changes during the course of exposure-based cognitive behavioral therapy (CBT) in PD. MAOA methylation was compared between N=28 female Caucasian PD patients (discovery sample) and N=28 age- and sex-matched healthy controls via direct sequencing of sodium bisulfite-treated DNA extracted from blood cells. MAOA methylation was furthermore analyzed at baseline (T0) and after a 6-week CBT (T1) in the discovery sample parallelized by a waiting time in healthy controls, as well as in an independent sample of female PD patients (N=20). Patients exhibited lower MAOA methylation than healthy controls (P<0.001), and baseline PD severity correlated negatively with MAOA methylation (P=0.01). In the discovery sample, MAOA methylation increased up to the level of healthy controls along with CBT response (number of panic attacks; T0–T1: +3.37±2.17%), while non-responders further decreased in methylation (−2.00±1.28% P=0.001). In the replication sample, increases in MAOA methylation correlated with agoraphobic symptom reduction after CBT (P=0.02–0.03). The present results support previous evidence for MAOA hypomethylation as a PD risk marker and suggest reversibility of MAOA hypomethylation as a potential epigenetic correlate of response to CBT. The emerging notion of epigenetic signatures as a mechanism of action of psychotherapeutic interventions may promote epigenetic patterns as biomarkers of lasting extinction effects.

A One-Session Treatment Protocol for Panic Attacks

This article describes in detail a one-session treatment protocol for panic attacks as well as the results of two small studies of its efficacy. The treatment protocol, typically completed in 75 - 120 minutes, uses an innovative approach that combines the identification of bodily sensations and specific thoughts as the precursor or “starter” of the panic attack process. The exact treatment approach is described in detail. The results of two small studies using the protocol are analyzed. The results showed that a single session using the treatment approach produced a statistically significant, immediate decline in the reported number of panic attacks that were sustained over time. These results were achieved in two separate sets of subjects utilizing different facilitators. Descriptive information regarding the sample is also provided.

Dimensional anxiety scales for DSM-5: Sensitivity to clinical severity

PurposePsychometric properties and clinical sensitivity of brief self-rated dimensional scales to supplement categorical diagnoses of anxiety disorders in the DSM-5 were recently demonstrated in a German treatment seeking sample of adults. The present study aims to demonstrate sensitivity of these scales to clinical severity levels. MethodsThe dimensional scales were administered to 102 adults at a university outpatient clinic for psychotherapy. Diagnostic status was assessed using the Munich-Composite International Diagnostic Interview. To establish a wide range of clinical severity, we considered subthreshold (n=83) and threshold anxiety disorders (n=49, including Social Phobia, Specific Phobia, Agoraphobia, Panic Disorder, and Generalized Anxiety Disorder). ResultsIndividuals with either subthreshold or threshold anxiety disorder scored higher on all dimensional scales relative to individuals without anxiety. In addition, individuals with a threshold anxiety disorder scored higher on the dimensional scales than individuals with a subthreshold anxiety disorder (except for specific phobia). Disorder-related impairment ratings, global functioning assessments and number of panic attacks were associated with higher scores on dimensional scales. Findings were largely unaffected by the number of anxiety disorders and comorbid depressive disorders. ConclusionThe self-rated dimensional anxiety scales demonstrated sensitivity to clinical severity, and a cut-off based on additional assessment of impairment and distress may assist in the discrimination between subthreshold and threshold anxiety disorders. Findings suggest further research in various populations to test the utility of the scales for use in DSM-5.

Depression Does Not Affect the Treatment Outcome of CBT for Panic and Agoraphobia: Results from a Multicenter Randomized Trial

Background: Controversy surrounds the questions whether co-occurring depression has negative effects on cognitivebehavioral therapy (CBT) outcomes in patients with panic disorder (PD) and agoraphobia (AG) and whether treatment for PD and AG (PD/AG) also reduces depressive symptomatology. Methods: Post-hoc analyses of randomized clinical trial data of 369 outpatients with primary PD/AG (DSM-IV-TR criteria) treated with a 12-session manualized CBT (n = 301) and a waitlist control group (n = 68). Patients with comorbid depression (DSM-IV-TR major depression, dysthymia, or both: 43.2% CBT, 42.7% controls) were compared to patients without depression regarding anxiety and depression outcomes (Clinical Global Impression Scale [CGI], Hamilton Anxiety Rating Scale [HAM-A], number of panic attacks, Mobility Inventory [MI], Panic and Agoraphobia Scale, Beck Depression Inventory) at post-treatment and follow-up (categorical). Further, the role of severity of depressive symptoms on anxiety/depression outcome measures was examined (dimensional). Results: Comorbid depression did not have a significant overall effect on anxiety outcomes at post-treatment and follow-up, except for slightly diminished post-treatment effect sizes for clinician-rated CGI (p = 0.03) and HAM-A (p = 0.008) when adjusting for baseline anxiety severity. In the dimensional model, higher baseline depression scores were associated with lower effect sizes at post-treatment (except for MI), but not at follow-up (except for HAM-A). Depressive symptoms improved irrespective of the presence of depression. Conclusions: Exposure-based CBT for primary PD/AG effectively reduces anxiety and depressive symptoms, irrespective of comorbid depression or depressive symptomatology.

Psychological treatment for panic disorder with agoraphobia: A randomized controlled trial to examine the role of therapist-guided exposure in situ in CBT.

Cognitive-behavioral therapy (CBT) is a first-line treatment for panic disorder with agoraphobia (PD/AG). Nevertheless, an understanding of its mechanisms and particularly the role of therapist-guided exposure is lacking. This study was aimed to evaluate whether therapist-guided exposure in situ is associated with more pervasive and long-lasting effects than therapist-prescribed exposure in situ. A multicenter randomized controlled trial, in which 369 PD/AG patients were treated and followed up for 6 months. Patients were randomized to 2 manual-based variants of CBT (T+/T-) or a wait-list control group (WL; n = 68) and were treated twice weekly for 12 sessions. CBT variants were identical in content, structure, and length, except for implementation of exposure in situ: In the T+ variant (n = 163), therapists planned and supervised exposure in situ exercises outside the therapy room; in the T- group (n = 138), therapists planned and discussed patients' in situ exposure exercises but did not accompany them. Primary outcome measures were (a) Hamilton Anxiety Scale, (b) Clinical Global Impression, (c) number of panic attacks, and (d) agoraphobic avoidance (Mobility Inventory). For T+ and T- compared with WL, all outcome measures improved significantly with large effect sizes from baseline to post (range = -0.5 to -2.5) and from post to follow-up (range = -0.02 to -1.0). T+ improved more than T- on the Clinical Global Impression and Mobility Inventory at post and follow-up and had greater reduction in panic attacks during the follow-up period. Reduction in agoraphobic avoidance accelerated after exposure was introduced. A dose-response relation was found for Time × Frequency of Exposure and reduction in agoraphobic avoidance. Therapist-guided exposure is more effective for agoraphobic avoidance, overall functioning, and panic attacks in the follow-up period than is CBT without therapist-guided exposure. Therapist-guided exposure promotes additional therapeutic improvement--possibly mediated by increased physical engagement in feared situations--beyond the effects of a CBT treatment in which exposure is simply instructed.

P.2.002 Improvement of resistant depression by combining antidepressive medication with lamotrigine

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population.244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale – Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment.We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

Safety and Efficacy of Levetiracetam for Patients With Panic Disorder

To examine the safety and efficacy of the anticonvulsant levetiracetam in the treatment of patients with panic disorder. In an open-label, fixed-flexible dose study, 18 patients with panic disorder with or without agoraphobia (DSM-IV diagnostic criteria) were treated with levetiracetam for 12 weeks. Outcome was assessed with standard rating instruments (Clinical Global Impressions-Severity of Illness scale [CGI-S], Clinical Global Impressions-Improvement scale [CGI-I], and the 14-item Hamilton Rating Scale for Anxiety [HAM-A]) and by the number of panic attacks during the previous week. The study was conducted in 2 outpatient clinics in New York City from January 2004 through July 2005. Of the 13 patients completing the study, 11 were rated "very much" or "much" improved on the CGI-I. Panic attack frequency, anxiety (HAM-A), and global severity (CGI-S) ratings also demonstrated significant improvement (all p < .00). For most patients, clinical benefits were apparent after only 1 to 2 weeks of treatment. Levetiracetam was well tolerated with minimal side effects. Given its favorable pharmacokinetics, side effect profile, and, if confirmed, early onset of action and efficacy, levetiracetam might represent significant progress in the pharmacologic management of panic disorder.

Tryptophan hydroxylase and serotonin transporter gene polymorphism does not affect the diagnosis, clinical features and treatment outcome of panic disorder in the Korean population

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population. 244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale – Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment. We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

Mirtazapine versus paroxetine in panic disorder: an open study

IntroductionOpen studies suggest that mirtazapine has efficacy in panic disorder treatment. We designed an open study that evaluates changes induced by mirtazapine compared with paroxetine in panic disorder.MethodologyPatients 18–65 years old consecutively referred to a psychiatry liaison service with panic disorder (DSM-IV criteria) were offered either mirtazapine or paroxetine treatment.ResultsThere were statistically significant reductions from baseline to week 3 and from week 3 to 8 for mirtazapine and paroxetine groups for: number of panic attacks, Beck Anxiety or Depression Inventory (BAI, BDI) Clinical Global Impresion (CGI) of panic disorder severity and CGI of panic disorder response (these variables were evaluated by the patient, the clinician or a blind evaluator). Responders at week 3 (BAI decrease of 50%) were 83% for the mirtazapine group and 84% for the paroxetine group. Responders at week 8 (number of panic attacks equal to 0) were 77% for the mirtazapine group and 73% for the paroxetine group Statistically significant differences between mirtazapine and paroxetine were found for number of panic attacks at weeks 3 and 8 and BAI at week 3, suggesting a faster response for mirtazapine. Responders at week 8 maintained a no recurrence figure of 95% at follow-up 6 months later. Panic disorder either with or without comorbid depression improved in both groups of treatment.DiscussionOur study supports the hypothesis that mirtazapine has efficacy in the treatment of panic disorder either with or without comorbid depression.

P.5.033 Apolipoprotein E epsilon 4 is associated with hippocampal volume reduction in females with alcoholism

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population.244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale – Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment.We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

Acute l-5-hydroxytryptophan administration inhibits carbon dioxide-induced panic in panic disorder patients

Previous research showed that lowering the availability of serotonin to the brain by tryptophan depletion increases the vulnerability of panic disorder patients for an experimental 35% CO 2 panic challenge. The results also suggested that increased availability of serotonin inhibits the response to such a challenge. In the present study, this latter possibility is examined. The reaction of 24 panic disorder patients and 24 healthy volunteers to a 35% CO 2 panic challenge was assessed following administration of 200-mg l-5-hydroxytryptophan (the immediate precursor of serotonin) or placebo. l-5-Hydroxytryptophan significantly reduced the reaction to the panic challenge in panic disorder patients, regarding subjective anxiety, panic symptom score and number of panic attacks, as opposed to placebo. No such effect was observed in the healthy volunteers. l-5-Hydroxytryptophan acts to inhibit panic, which supports a modulatory role of serotonin in panic disorder.

Cognitive-Behavioral Treatment of Panic Attacks

Anxiety affects approximately 30 million Americans at some point in their lives. The most common treatment modalities used to treat the continuum are the administration of psychotropic medications and the application of behavioral therapy. The following case details an adult female who suffered from severe panic attacks for a period of 10 years wherein numerous interventions, including psychotropic medications, had failed to ameliorate her suffering. The patient was treated using the Mastery of Your Anxiety and Panic protocol. Prior to treatment, the patient reported that she experienced an average of seven panic attacks per week, her Beck Anxiety Inventory score was 58, and her Beck Depression Inventory was 23. At the completion of treatment, the patient reported that the number of panic attacks was reduced to one per week. At 4-week, 6-week, and 16-week follow-up, the patient had not experienced any panic attacks.

Effektivität psychologischer Therapien von Panik und Agoraphobie: Meta-Analysen auf Störungsebene

Efficacy of Psychological Treatments for Panic and Agoraphobia The present study compared the effectiveness of 7 different psychological treatments for panic and agoraphobia in a meta-analysis of 51 studies that included 99 treatment interventions. Pre-post effect sizes (ES) have been calculated for 7 clinical variables: main symptoms, number of panic attacks, intensity of panic attacks, general anxiety, depression, impairment, and general psychopathology. Long-term outcome has been investigated up to 2 years after the interventions. For panic disorder with agoraphobia exposure yielded the highest mean effect sizes for main symptoms (ES = 1.64). Regarding only the number of panic attacks, exposure and cognitive-behavioral treatments do not differ in their effectiveness (ES = 1.32 and ES = 1.13). Long-term outcome analyses suggest that both interventions were successful in maintaining their treatment gains. For all clinical variables exposure and cognitive-behavioral therapy showed clear and lasting improvements. For panic disorder without agoraphobia cognitive-behavioral therapy and applied relaxation yielded the highest mean effect sizes (ES = 1.32 resp. ES = 1.21) for main symptoms. Both treatments showed also improvements in the reduction of the number of panic attacks (ES = 1.24 resp. ES = 0.97) and the remaining clinical outcome variables. All treatment gains could be maintained up to 2 years after the interventions.

Quality of well being in panic disorder: the assessment of psychiatric and general disability

Background: Panic disorder is a common and debilitating anxiety disorder which significantly disrupts the lives of patients and their family members. Recent epidemiological studies and analyses of data from clinical trials suggest that patients with panic disorder suffer significant work and social dysfunction. The authors hypothesized that this dysfunction could be characterized using both a well-validated, generalized scale of functioning and a specifically designed scale for assessing function in psychiatric patients and that these findings would correlate with symptomatology. Method: Fifty-six patients with panic disorder were characterized using the Sheehan Disability Scale, the Anxiety Sensitivity Index, and the Spielberger State Trait Anxiety Scale. Measures of health related quality of life from the Quality of Well Being Scale were compared with ratings for matched, historical, and population controls. Results: Patients with panic disorder lost 39 quality-adjusted days for each year that they lived with the disorder. This decrease in quality of life is similar to what is observed in patients with non-insulin dependent diabetes. Diminished quality of life is correlated with the number of panic attacks, state anxiety, and depressive symptoms. These patients also demonstrated significant dysfunction in Sheehan total disability and subscale scores, including work-related functioning. Conclusions: This study demonstrates that the specific disabilities inherent in panic disorder can be linked to declines in quality of life as measured by the Quality of Well Being Scale and by measures of work-related dysfunction. Such an association between disease specific measures and a generalized measure of health related quality of life may offer clinicians a new tool to understand panic disorder and to conceptualize it within the broader context of disease and disability.

P.1.135 Neuroendocrine challenge with citalopram in healthy volunteers

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population.244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale – Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment.We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

P.1.144 Citalopram for the treatment of major depression in the elderly: An open naturalistic study

Panic disorder may be associated with defective serotonin (5-HT) neurotransmission. This study was to investigate the association between the tryptophan hydroxylase (TPH) gene and a serotonin transporter gene promoter polymorphism (5-HTTLPR), with panic disorder in a Korean population.244 Korean patients with panic disorder and the 227 controls were genotyped by a polymerase chain reaction-based method. The severity of panic disorders was assessed by number of panic attacks during the previous 1 month, as well as scores for anticipatory anxiety, panic distress, and agoraphobic distress, as determined by a visual analogue scale (VAS). All the subjects completed the assessment measures including Spielberger State-Trait Anxiety Inventory-State (STAI-S), Spielberger State-Trait Anxiety Inventory-Trait (STAI-T), Beck Depression Inventory (BDI), Symptom Checklist-90-Revised (SCL-90-R), Revised Anxiety Sensitivity Index (ASI-R), Clinical Global Impression Scale – Severity of Illness (CGI-S), Panic Disorder Severity Scale (PDSS), and the Hamilton Depression Rating Scale (HAMD). Responder analyses were conducted based on changes in CGI-I scores after 10 weeks of treatment.We found no significant differences in the genotype and allele frequencies in TPH A218C and 5-HTTLPR polymorphisms between the panic patients and the control group. Subgroup analyses in terms of comorbidities, response, and other primary clinical variables, indicated no differences in these polymorphisms. Our findings suggest that the TPH A218C polymorphism and 5-HTTLPR play no significant roles in the pathogenesis and clinical symptomatologies, at least in a Korean population.

Effect of Dose Escalation Pace on Benzodiazepine Clinical Response

Hsu and Laddu (1) have shown that the rate of dose escalation needs to be considered when reviewing adverse event occurrence. The data of a Phase III flexible-dose clinical trial with a titration design were retrospectively examined to assess the effect of dose escalation on benzodiazepine efficacy performance in the treatment of patients with panic disorder. Most of the patients in the low dose group have a slow escalation and therefore, the high dose group was the focus. It was observed that fast dose escalation (an average daily dose increment of more than three tablets) makes benzodiazepine less efficacious. In other words, benzodiazepine-treated patients with fast dose escalation are less likely to respond in a diminishing number of panic attacks. Contrary to patients on benzodiazepine, more patients under placebo with a fast dose escalation pace responded. Similar analysis on medical events, symptoms of disease, or adverse events also showed the same pattern. The logistic regression analysis on the response status and analysis of variance on the medical event improvement scores with dose increment as an additional factor in the model confirmed the effect of dose escalation pace.

Effectiveness of stages of change and adinazolam SR in panic disorder: A neural network analysis

We ascertained the relationship of stages of change (SOC) and adinazolam SR on panic disorder in a randomized double-blind study. Outpatients ( n = 133) with panic disorder and agoraphobia were assessed for readiness to change and then were randomly assigned to adinazolam SR or to placebo in a 4-week double-blind trial. The active drug was significantly more effective than the placebo. After 4 weeks, patients on the drug treatment had significantly lower anxiety on two of the measures. Two neural networks were trained with gender, history of depression, agoraphobia, readiness to change, and five anxiety measures at baseline data as inputs, and the five anxiety measures 4 weeks later as outputs. The five anxiety measures were the Clinical Anxiety Scale, the Hamilton Anxiety Scale, the number of panic attacks, the Clinical Global Impression Scale, and the Phobia Severity Scale. The networks were validated and sensitivity analyses showed that, in agreement with the stages of change model, patients with low predisposition to change (Precontemplators) changed more slowly than those in Contemplation or Action stages of change.