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At least 19 recordsLinked to original sources
PubMed1988

Thyroid hormones in panic disorder, panic disorder with agoraphobia, and generalized anxiety disorder.

Fifty-two patients with generalized anxiety disorder who had symptoms persisting for at least 6 months, 41 patients suffering from either panic disorder (32 patients) or panic disorder with agoraphobia (9 patients), and 14 control subjects were screened for thyroid disease. Total serum thyroxine (TT4), serum-free thyroxine index (FT4I), and triiodothyronine resin uptake (T3RU), were examined for the entire sample, using a one-way analysis of variance (ANOVA). No significant differences were found in TT4 (p = .24), FT4I (p = .24), and T3RU (p = .19). Thyroid-stimulating hormone (TSH) was examined in a subsample of 10 patients with generalized anxiety disorder, 11 with panic disorder or panic disorder with agoraphobia, and 10 controls. One-way ANOVA again showed no significant differences, although there was a trend (p = .07). This is the first report that compares generalized anxiety disorder patients, panic disorder patients, and patients with panic disorder and agoraphobia with controls on measures of thyroid function. It is also the first to report normal values in the thyroid indices of generalized anxiety disorder patients.

Adult↗
PubMed1987

Platelet [3H]imipramine binding in generalized anxiety disorder, panic disorder, and agoraphobia with panic attacks.

The density of platelet [3H]imipramine binding sites is reported to be decreased in unipolar depression and, hence, is a putative biological marker. There is considerable evidence for a phenomenological and biological relationship of panic disorder with affective disorder. We studied platelet [3H]imipramine binding site density in unmedicated subjects with generalized anxiety disorder (GAD; n = 55), panic disorder (PD) with and without agoraphobia (n = 52), and normal controls (n = 26) in order to determine whether or not patients with panic disorder differed from controls in this biological assay. We found no differences in binding site density (Bmax) or affinity (Kd) among the PD, PD with agoraphobia, GAD, and control groups. Nor did we find a relationship between Bmax or Kd and the severity of depressive symptoms or the presence of a family history of affective disorder. In view of two conflicting prior studies, the use of [3H]imipramine binding in panic disorder remains problematic.

Adult↗
PubMedDate not supplied

The relationship between anxiety and depression: a clinical comparison of generalized anxiety disorder, dysthymic disorder, panic disorder, and major depressive disorder.

This study examined the relationship between the chronic disorders, generalized anxiety disorder (GAD) and dysthymic disorder (DD), and the more acute disorders, panic disorder (PD) and major depressive disorder (MDD) in 110 psychiatric outpatients with diagnoses of either PD, MDD, GAD, or DD. Pure, mixed, and early-/late-onset forms of the chronic disorders were compared with each other and then with PD and MDD on clinical measures and psychiatric history. Minimal differences were found between pure GAD and mixed GAD or between pure DD and mixed DD. The chronic disorders, DD and GAD, had distinct clinical symptom profiles when compared with each other and appeared more closely related to their parent disorders than to each other. However, despite these similarities, there were significant differences between DD and MDD in contrast to the minimal differences between GAD and PD, providing less support for GAD as a valid diagnostic category separate from PD. Comparisons of early-/late-onset DD and GAD showed more severe symptoms in late-onset DD, in contrast to more severe symptoms in early-onset GAD. These varying patterns of symptom severity may warrant study for further syndromal delineation.

Adult↗
PubMed1985

The DST in psychiatric outpatients with generalized anxiety disorder, panic disorder, or primary affective disorder.

The authors administered the dexamethasone suppression test (DST) to outpatients, who were free from psychoactive drugs for at least 10 days before the test, with primary affective disorder (N = 60), generalized anxiety disorder (N = 26), panic disorder (N = 22), and agoraphobia with panic attacks (N = 13). With a cortisol value of 5 micrograms/dl considered nonsuppression, there were no significant differences in dexamethasone nonsuppression rates among the diagnostic groups. Scores on the Hamilton Rating Scale for Depression and a melancholia subscale were significantly higher in the depressed group than in the anxiety disorder group. The findings raise questions concerning the specificity of the DST for primary affective disorder in relationship to anxiety disorders.

Adult↗
PubMedDate not supplied

Specificity of lactate response in panic disorder, panic with concurrent depression and major depression.

Lactate infusions with 0.5 molar sodium lactate in a dose of 10 ml/kg within 20 min were given to patients with panic disorder (n = 6), panic attacks with concurrent major depression (n = 7) and major depression without panic (n = 5). Lactate-induced anxiety and symptom attacks without panic were seen more often in the groups with panic attacks, but a full-blown panic attack was provoked in only four subjects, all belonging to the groups with a history of panic attacks. The low incidence of lactate-induced panic attacks can be explained by differences in the procedure that aimed at reducing expectancy biases and baseline anxiety.

Adolescent↗
PubMed1990

A comparative examination of a role for serotonin in obsessive compulsive disorder, panic disorder, and anxiety.

Recent clinical and laboratory studies have suggested that changes in brain serotonin (5-HT) function may contribute to anxiety symptoms and anxiety-type behaviors. Among the anxiety disorders, perhaps the most compelling evidence implicating 5-HT exists for obsessive compulsive disorder (OCD). In controlled trials, patients with OCD were markedly more responsive to treatment with 5-HT-selective uptake inhibitors such as clomipramine, fluvoxamine, or fluoxetine than to norepinephrine-selective or nonselective uptake inhibitors or to other psychoactive drugs. Studies with 5-HT agonists and antagonists also support a role for 5-HT in OCD. In this review, pharmacologic studies involving 5-HT-selective therapeutic and anxiogenic agents and non-5-HT-selective anxiogenic agents in patients with OCD are compared and contrasted with similar studies in patients with anxiety and panic disorder.

Anxiety Disorders↗
PubMed1989

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↗
PubMed1992

The assessment and management of panic disorder.

Panic disorder affects approximately 1.5 percent of the general population in the United States, and individuals with this disorder are seen frequently in primary care settings. Recognition of panic disorder is complicated by the fact that patients tend to focus exclusively on the physical symptoms of the illness. Left untreated, patients with panic disorder suffer considerable impairment in functioning and are at increased risk for substance abuse, depression and suicide. This article provides clinicians with the information necessary to recognize and manage this illness. A detailed description of the disorder, including onset, course, complications, differential diagnosis and management, is presented in this article.

Clinical Protocols↗
PubMed1989

Panic disorder.

Panic disorder affects an estimated 1.4 percent of the general population. Nearly 70 percent of patients with panic disorder may also suffer from a major depressive disorder at some time in their lives. Both disorders respond to tricyclic antidepressants and monoamine oxidase inhibitors. Alprazolam is also an effective antipanic agent. Because avoidance behaviour (agoraphobia) often follows the onset of panic disorder, behavioral interventions are an important adjunct to management.

Antidepressive Agents↗
PubMed1987

A family study of panic disorder.

Panic disorder, as defined by the DSM III diagnostic criteria, was diagnosed in 117 probands for whom age of onset ranged from 10 to 59 years, with a mean of 26.6 years. Diagnosis of parents and siblings was based on interviews with the probands, and only those with "definite" panic disorder by the FISC criteria were considered to be affected. The pattern of concordances for panic across different groups of relatives was estimated concurrently by a log-linear model for binary pedigree data, assuming different values for the cumulative risk. When an adjustment for age was made, based on the age of onset of probands, there was no significant difference between parent-offspring concordance and sibling concordance. There was a negative, but not significant, concordance between spouse pairs. Assuming the lifetime cumulative risk was 1.9% for males and 4.7% for females, values considered appropriate for this population, our model predicted that the presence of an affected parent or sibling incurs an approximately five times increase in the risk of developing panic disorder. Our model assumes in effect that this risk is multiplied for each further affected relative. Although the common concordance across relationship groups is consistent with a genetic hypothesis, it can also be explained by common family environmental factors. There is a need for further pedigree studies, using twins and relatives, for example, and reliable information on the cumulative risk.

Adolescent↗
PubMed1990

Clomipramine. An overview of its pharmacological properties and a review of its therapeutic use in obsessive compulsive disorder and panic disorder.

During the 20 years that have elapsed since clomipramine (chlorimipramine) was first marketed, it has become well established in the treatment of depressive illness, particularly treatment-resistant depression. However, in addition to its role as an antidepressant, attention is being focused on the use of clomipramine in 2 other areas of psychiatry: obsessive compulsive disorder and panic disorder. Short term clinical trials have shown that clomipramine is generally more effective than amitriptyline, imipramine, desipramine, nortriptyline or clorgiline in reducing obsessive compulsive symptoms. Clomipramine appears to produce some short term benefit with exposure therapy in patients with obsessive compulsive disorder. However, the efficacy of the drug after long term follow-up has not been fully investigated. The antiobsessional efficacy of clomipramine appears to be independent of its antidepressant activity. In patients with panic disorder with or without agoraphobia (DSM-IIIR), clomipramine reduces the frequency and severity of panic attacks within 7 to 21 days of beginning treatment and efficacy is maintained for at least 12 months. Clomipramine is more effective than imipramine, the generally accepted standard treatment for patients with panic disorder after 2 weeks' treatment, but after 6 or 10 weeks both drugs are similarly effective. Other double-blind studies have shown that clomipramine is more effective than placebo and at least as effective as fluvoxamine and oxitriptan (5-hydroxytryptophan) in reducing panic attacks and associated anxiety. Adverse effects associated with clomipramine treatment are mild to moderate in nature and are predominantly a result of the drug's anticholinergic activity. The incidence of seizures is dose related, occurring in 0.48% of all patients receiving clomipramine less than or equal to 250 mg/day and 2.1% of patients receiving greater than or equal to 300 mg/day. In conclusion, the available data indicate that clomipramine is a worthwhile addition to the limited treatments available for obsessive compulsive disorder and panic disorder, two psychiatric disorders which have previously been difficult to manage pharmacologically.

Animals↗
PubMedDate not supplied

Management of panic disorders.

Panic disorders are medical conditions requiring an eclectic treatment approach that often combines pharmacotherapeutics with education, cognitive-behavior therapy, and psychodynamic therapy. This article focuses on the management of medication within this framework. The medications that have been found to be effective include tricyclic antidepressants, fluoxetine, monoamine oxidase inhibitors, and higher potency benzodiazepines. Although alprazolam is the most studied medication and acts very rapidly, each type of medication has unique advantages and liabilities. The general treatment strategy with all the medications is to start with a low dose and increase it slowly until side effects develop or panic attacks cease. The treatment approach should be oriented toward a chronic illness that often requires long-term medication.

Humans↗
PubMed1988

Human corticotropin releasing hormone: clinical studies in patients with affective disorders, alcoholism, panic disorder and in normal controls.

1. The 41 amino acid peptide human corticotropin releasing hormone (h-CRH) and its ovine analogue o-CRH are regulators of proopiomelanocortin (POMC) derived neuropeptides and neurosteroids of the limbic-hypothalamic-pituitary-adrenocortical (LHPA) axis such as beta-endorphin, corticotropin (ACTH) and corticosteroids modulating concomitantly hormonal and behavioral systems in animal and man, e.g. adaptation to stress. 2. Challenge tests employing h-CRH stimulation with or without different kinds of pretreatment in affective disorders, alcoholism, and panic disorder demonstrate LHPA alterations that are induced by dysregulations in the limbic area. In depression, the enhanced secretory activity of pituitary corticotrophs or altered feedback regulation is compatible with endogenous CRH hypersecretion followed by enhanced production of proopiomelanocortin whose fragments activate synthesis and release of adrenal corticosteroids. These effects are accompanied by development of a functional hyperplasia of the adrenocortex and/or down-regulation of pituitary CRH-receptors and/or reduced negative feed back capacity of limbic glucocorticoid receptor containing neurones particularly in the hippocampus. Similar disturbances are found in hypercortisolemic patients withdrawn from alcohol and are less pronounced in patients with panic disorder. 3. Repetitive h-CRH administration to normal controls induces sleep-EEG and neuroendocrine effects resembling those in depression. 4. Adrenocortical hormones act back on neurotransmitter/receptor sites of brain systems relevant for neuropharmacoloy (e.g. GABA receptor activity in anxiety disorders and affective disorders). 5. The neuroendocrine approach to the LHPA axis is of value to uncover several aspects of pathology underlying various psychiatric diseases.

Adrenocorticotropic Hormone↗
PubMed1992

Psychopharmacological treatment of panic disorder.

Panic disorder is a serious, often chronic condition that warrants vigorous treatment. The benzodiazepines, particularly the high-potency compounds alprazolam and clonazepam, provide prompt relief, often with few side effects. Tricyclic antidepressants and monoamine oxidase inhibitors are also effective, although patient acceptance may be limited by a slower response and side effects that mimic some symptoms of panic attacks. The author suggests strategies for the most effective use of these agents.

Adult↗
PubMed1986

Pharmacological treatment of panic disorder.

Panic disorder has recently been recognized as a distinct sub-type of anxiety which may occur with or without phobic avoidance. Controlled prospective trials have demonstrated the efficacy of the tricyclic antidepressants and monoamine oxidase inhibitors in the treatment of this disorder. The use of benzodiazepines and beta-blockers has been more controversial. Some preliminary studies assessing other pharmacological agents are available. Methodological problems limit the conclusions which may be drawn from available data.

Anti-Anxiety Agents↗
PubMed1986

Effects of one night's sleep deprivation on mood and behavior in panic disorder. Patients with panic disorder compared with depressed patients and normal controls.

The effects of one night's sleep deprivation on mood and behavior were evaluated in 12 patients with panic disorder, ten depressed patients, and ten controls. In contrast to the improvement in symptoms of anxiety and depression shown by the majority of depressed patients, the response of patients with panic disorder as a group did not differ from that of normal controls, although a subgroup did experience noticeable worsening in their symptoms of anxiety, with 40% experiencing panic attacks on the day following sleep deprivation. Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy.

Adult↗