[Anxiety disorders, panic disorder].
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Anxiety Disorders↗
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Psychosocial treatment prescriptions for generalized anxiety disorder, panic disorder, and social phobia, 1991-1996.
OBJECTIVE: Pharmacologic prescriptions for anxiety disorders have changed significantly in the last decade. This article investigates whether psychosocial treatments, as reported by 362 subjects in the Harvard/Brown Anxiety Disorders Research Program from 1991 to 1996, changed as well. METHOD: Subjects were interviewed in 1991 and 1995-1996 to determine which psychosocial treatments (behavioral, cognitive, dynamic, or relaxation or meditation) they had received. RESULTS: The percentage of subjects who received each type of psychosocial treatment either declined or remained the same from 1991 to 1995-1996. Dynamic psychotherapy remained the most frequently used method of these four. The percentage of subjects receiving any such method declined. CONCLUSIONS: Behavioral and cognitive treatment, two empirically validated forms of psychotherapy, were less frequently used than dynamic psychotherapy, which lacks such validation. All use of verbal treatment methods declined from 1991 to 1995-1996.
Adolescent↗
Information from your family doctor. Panic disorder: panic attacks and agoraphobia.
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Agoraphobia↗
Non-fearful panic disorder: panic attacks without fear.
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Adult↗
[Separation anxiety and anxiety attack disorders ("panic disorder"). A comparative study].
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Adult↗
Clinical differentiation between major depression only, major depression with panic disorder and panic disorder only. Childhood, personality and personality disorder.
A consecutive sample of 298 nonpsychotic psychiatric outpatients was classified according to DSM-III and divided into 4 diagnostic groups: pure major depression, mixed major depression/panic disorder, pure panic disorder and a remaining group of other disorders. The patients' report of childhood relationship to parents and siblings, family atmosphere, their own personality characteristics as children and precipitating events were compared in the various groups. In addition, differences in personality and frequencies of personality disorders were investigated by means of various instruments. Our results show that the type of relationship to parents in childhood differed in the various groups. The mother seems to be the most crucial person for the development of depression, the father for the development of panic disorder. Patients with major depression are more obsessive and patients with panic disorder more infantile and avoidant with less control of their personality. Finally, patients with mixed conditions are more in accordance with the DSM-III anxious personality disorder cluster.
Adult↗
Differential performance on tasks of affective processing and decision-making in patients with Panic Disorder and Panic Disorder with comorbid Major Depressive Disorder.
BACKGROUND: Neuropsychological studies have provided evidence for deficits in psychiatric disorders, such as schizophrenia and mood disorders. However, neuropsychological function in Panic Disorder (PD) or PD with a comorbid diagnosis of Major Depressive Disorder (MDD) has not been comprehensively studied. The present study investigated neuropsychological functioning in patients with PD and PD + MDD by focusing on tasks that assess attention, psychomotor speed, executive function, decision-making, and affective processing. METHODS: Twenty-two unmedicated patients with PD, eleven of whom had a secondary diagnosis of MDD, were compared to twenty-two healthy controls, matched for gender, age, and intelligence on tasks of attention, memory, psychomotor speed, executive function, decision-making, and affective processing from the Cambridge Neuropsychological Test Automated Battery (CANTAB), Cambridge Gamble Task, and Affective Go/No-go Task. RESULTS: Relative to matched healthy controls, patients with PD + MDD displayed an attentional bias toward negatively-valenced verbal stimuli (Affective Go/No-go Task) and longer decision-making latencies (Cambridge Gamble Task). Furthermore, the PD + MDD group committed more errors on a task of memory and visual discrimination compared to their controls. In contrast, no group differences were found for PD patients relative to matched control subjects. LIMITATIONS: The sample size was limited, however, all patients were drug-free at the time of testing. CONCLUSIONS: The PD + MDD patients demonstrated deficits on a task involving visual discrimination and working memory, and an attentional bias towards negatively-valenced stimuli. In addition, patients with comorbid depression provided qualitatively different responses in the areas of affective and decision-making processes.
Adult↗
Panic disorder versus panic disorder with major depression; defining and understanding differences in psychiatric morbidity.
The present study examined the impact of comorbid major depressive disorder (MDD) on psychiatric morbidity, panic symptomatology and frequency of other comorbid psychiatric conditions in subjects with panic disorder (PD). Four hundred thirty-seven patients with PD were evaluated at intake as part of a multicenter longitudinal study of anxiety disorders; 113 of these patients were also in an episode of MDD. Patients were diagnosed by DSM-III-R criteria utilizing structured clinical interviews. The 113 PD/MDD patients were compared with the 324 remaining PD subjects regarding panic symptoms at intake, sociodemographic, quality of life and psychiatric morbidity variables. Differences in frequency of other comorbid Axis I psychiatric disorders were assessed at intake; personality disorders were evaluated twelve months after intake. The results revealed the PD/MDD patients exhibit increased morbidity and decreased psychosocial functioning as compared to PD patients. Personality disorders were more prevalent in the PD/MDD group at six month follow-up assessment; the PD/MDD group also had an increased frequency of posttraumatic stress disorder (PTSD) and more comorbid Axis I anxiety disorders as compared to the PD group. The total number and frequency of panic symptoms was highly consistent between the two patient groups.
Adolescent↗
Moclobemide and fluoxetine for panic disorder. International Panic Disorder Study Group.
An international, multicentre, double blind parallel group study compared the tolerability and efficacy of moclobemide with the selective serotonin reuptake inhibitor (SSRI) fluoxetine for panic disorder. SSRIs have been shown effective for panic. The target dose of moclobemide was 450 mg and of fluoxetine was 20 mg. There were two consecutive studies. An eight week study of acute adverse events, tolerability and efficacy was followed by a long-term extension study to 1 year. The efficacy data showed no significant difference between moclobemide and fluoxetine. Both had acute efficacy, with 63% moclobemide and 70% fluoxetine patients (ns) panic free at 8 weeks. Both agents were well tolerated to 8 weeks, but moclobemide had fewer severe adverse events (5) than fluoxetine (9). There were no severe adverse events in the extension phase with either drug, and almost all patients completing 1 year extension treatment (moclobemide 61 patients, fluoxetine 65) were much or very much improved. These data suggest moclobemide and fluoxetine are tolerated and effective for both acute panic treatment and maintenance therapy.
Adult↗
The novel brain-specific tryptophan hydroxylase-2 gene in panic disorder.
Panic disorder is a common psychiatric disorder characterized by recurrent anxiety attacks and anticipatory anxiety. Due to the severity of the symptoms of the panic attacks and the frequent additional occurrence of agoraphobia, panic disorder is an often debilitating disease. Elevation of central serotonin levels by drugs such as clomipramine represents one of the most effective treatment options for panic disorder. This points to an important role of dysregulation of the serotonergic system in the genetic etiology of panic disorder. The novel brain-specific 5-HT synthesizing enzyme, tryptophan hydroxylase-2 (TPH2), which represents the rate-limiting enzyme of 5-HT production in the brain, may therefore be of particular importance in panic disorder. We focused on the putative transcriptional control region of TPH2 and identified two novel common single nucleotide polymorphisms (SNPs) of TPH2 in and close to this region. Moreover, a recently described loss-of-function mutation of TPH2 which results in an 80% reduction of serotonin production, was assessed. In an analysis of the putative transcriptional control region SNPs in a sample of panic disorder patients and controls no association of the disorder with the TPH2 SNPs or haplotypes was found. Moreover, the loss-of-function R441H mutation of TPH2 was not present in the panic disorder patients. The results of this first study of TPH2 in panic disorder argue against an importance of allelic variation of TPH2 in the pathogenesis of panic disorder with or without agoraphobia.
Adult↗
Treatment of panic disorder.
Panic disorder with or without agoraphobia occurs commonly in patients in primary care settings. This article assesses multiple evidence-based reviews of effective treatments for panic disorder. Antidepressant medications successfully reduce the severity of panic symptoms and eliminate panic attacks. Selective serotonin reuptake inhibitors and tricyclic antidepressants are equally effective in the treatment of panic disorder. The choice of medication is based on side effect profiles and patient preferences. Strong evidence supports the effectiveness of cognitive behavior therapy in treating panic disorder. Family physicians who are not trained in cognitive behavior therapy may refer patients with panic disorder to therapists with such training. Cognitive behavior therapy can be used alone or in combination with antidepressants to treat patients with panic disorder. Benzodiazepines are effective in treating panic disorder symptoms, but they are less effective than antidepressants and cognitive behavior therapy.
Antidepressive Agents↗
Potential effectiveness and safety of olanzapine in refractory panic disorder.
Panic disorder is a common and disabling psychiatric disorder. Despite treatment advances, refractory panic disorder requires novel interventions. One such pharmacologic intervention with theoretical and case study support includes olanzapine, a thienobenzodiazepine medication currently approved for schizophrenia in the United States. Ten people with refractory DSM-IV diagnosed panic disorder completed an 8-week, open-label, flexible-dose clinical trial. Baseline, in-treatment, and end-of-treatment data for panic attacks, anticipatory anxiety, phobic avoidance, and impairment were collected. Data were analyzed using SPSS software. Refractory panic disorder patients required a wide dose range averaging 12.3 mg/day of olanzapine to significantly improve or ablate panic attacks. On the average, number of attacks decreased from 6.1/week at baseline to 1.1/week at the end of treatment, and anticipatory anxiety from 32% of the day to 8% of the day. At treatment end, 5 of 10 participants (50%) were panic free, 4 (40%) had one attack in the previous week, 1 (10%) had seven attacks in the previous week, and 6 of 10 participants (60%) were anticipatory anxiety free. There were also statistically and clinically significant improvements in impairment over the course of the trial. There were no significant changes in vital signs, emergent side effects, or average weight, although 6 of 10 people did gain weight. Olanzapine is potentially effective and safe in panic disorder. Due to study limitations, further clinical trials are needed to demonstrate effectiveness.
Adult↗
Current concepts in the treatment of panic disorder.
Panic disorder is a prevalent psychiatric condition that often is chronic and rarely resolves without medical intervention. Many patients with panic disorder initially present with a variety of somatic symptoms, including chest pain, nausea, or dizziness, and patients frequently seek care in ambulatory care settings. Although panic disorder is classified as a single entity, it can have many dimensions and may be associated with significant morbidity. During the past 2 decades, there have been significant advances in the treatment of panic disorder, and a range of therapeutic choices is now available. Four classes of medications, including the selective serotonin reuptake inhibitors (SSRIs), high-potency benzodiazepines, tricyclic antidepressants, and monoamine oxidase inhibitors, may be considered for the management of patients with panic disorder. Emerging clinical data favor the SSRIs as first-line treatment for patients with panic disorder, and paroxetine and sertraline have been approved by the U.S. Food and Drug Administration for use in panic disorder. This article reviews the efficacy and safety of these treatments, as well as their relative merits and disadvantages, and assists the practicing clinician in choosing among the various pharmacotherapies to tailor therapy to each patient's individual needs.
Antidepressive Agents, Tricyclic↗
Human nuclear transcription factor gene CREM: genomic organization, mutation screening, and association analysis in panic disorder.
Panic disorder is an anxiety disorder with an estimated heritability of 48%. Variation in the gene of the nuclear transcription factor "cAMP-responsive element modulator" (CREM) might contribute to its pathogenesis. CREM knock-out mice exhibit significantly less anxiety behavior than wild-type mice and the alternative CREM gene product "inducible cAMP early repressor" (ICER) plays a pivotal role in the hypothalamo-pituitary-adrenal (HPA) axis, which is disturbed in panic disorder. We characterized the genomic organization of the human CREM gene and performed a systematic mutation screening by means of single stranded conformational analysis (SSCA) in a sample of 40 German patients with panic disorder (DSM-III-R). Four novel single nucleotide polymorphisms in CREM promoters P 1 and P 4, one trinucleotide (ATT)-repeat polymorphism in CREM promoter P 2-generating the ICER isoform-and a rare amino acid substitution in CREM exon glut 2 were identified. Association analysis in an extended sample of German patients (n = 88) revealed a significant excess of the shorter CREM P 2 promoter eight-repeat trinucleotide allele and of genotypes containing the eight-repeat trinucleotide allele in panic disorder (P = 0.02), in particular in panic disorder without agoraphobia (P = 0.001). A replication study in independent Italian (n = 76) and Spanish (n = 62) samples, however, failed to confirm this observation. This suggests that the CREM P 2 promoter trinucleotide polymorphism is not a major susceptibility factor in the pathogenesis of panic disorder. Functional analysis of the observed CREM P 2 promoter polymorphism as well as studies in independent panic disorder samples are necessary.
Agoraphobia↗
[Diagnosis and treatment of panic disorder].
Panic disorder is defined as, recurrent, unexpected panic attacks. Panic attack means a period of intensive fear or discomfort, accompanied by a range of physical or psychological symptoms. Subsequently, anticipatory anxiety and avoidance behavior often develop. Panic disorder may or may not be accompanied by agoraphobia. Panic disorder can be treated both by psychotherapeutic and pharmacological measures. An ideal approach is combination therapy in the sense of a multimodal concept; with regard to cognitive behavioral therapy in particular, its effectiveness in the treatment of panic disorder is well documented. For pharmacotherapy, antidepressive agents, in particular selective serotonin reuptake inhibitors, are the drugs of first choice. Benzodiazepines should be given for only a few weeks until the antipanic effect of the antidepressants kicks in. With appropriate treatment, the prognosis is favorable.
Anti-Anxiety Agents↗
Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder.
Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
Biogenic Monoamines↗
Toward an integrated neurobiology of panic disorder.
Panic disorder is a common psychiatric illness that causes considerable short- and long-term morbidity. Although drug treatment and cognitive behavior therapy are beneficial, the etiology of panic disorder and the mechanisms of effective treatment remain unclear. Developments in the preclinical neuroanatomy and neurophysiology of neuronal structures relevant to fear and anxiety promise to provide fresh insights into the neurobiology of panic. In this article, we propose a functional neuroanatomic model of fear and anxiety and review brain imaging studies of panic disorder with this model in mind. In addition, we discuss the implications of integrating functional neuroanatomy and the clinical neurochemistry of panic disorder. An integrated neurobiology of panic disorder will provide a broader conceptual framework with which to tackle the complex questions about the pathophysiology and treatment of this condition.
Amygdala↗
Nonpsychiatric medical comorbidity, health perceptions, and treatment outcome in patients with panic disorder.
Panic disorder is frequently complicated by high rates of co-occurring nonpsychiatric medical conditions. The present study examined the relationship between medical morbidity, perceived physical health, and treatment outcome in panic disorder. Patients meeting the American Psychiatric Association's Diagnostic and Statistical Manual of mental disorders (1994) criteria for panic disorder (N = 71) completed 12 sessions of cognitive-behavioral treatment and were assessed at posttreatment and 6-month follow-up. Medical comorbidity and perceived health were both found to be related to end-state functioning. Medical comorbidity did not uniquely predict outcome beyond its shared variance with perceived health. At posttreatment, 71% of patients who perceived their physical health as good met recovery criteria compared with only 35% of those who perceived their health as poor. At follow-up, 67% of those who perceived their physical health as good met composite recovery criteria compared with only 33% of those with perceived poor health. These findings offer preliminary support for the impact of physical health, both actual and perceived, on treatment outcome of patients with panic disorder.
Adult↗