Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous studies have established that there is increased co-morbidity of depressive symptoms among patients with panic disorder with and without agoraphobia, but questions remain as to whether the symptom pattern and clinical course are similar to that of primary depressions. The Cross-National Collaborative Panic Study was initiated to study the effects of alprazolam, a triazolobenzodiazepine, in the treatment of panic disorder. In the first phase, which included more than 500 subjects, alprazolam was compared against placebo. In the second phase, alprazolam was compared with imipramine and placebo in a double-blind, randomized, controlled trial. Results of both the first and second phases will be reviewed as they bear on the issue of drug treatment of secondary depression accompanying panic disorder. The presence of depressive symptoms does not adversely influence anti-panic and anti-phobic response to medication. Equivalent drug-placebo differences occur on multiple measures of anxiety--including the number and intensity of panic attacks, phobias, anticipatory anxiety, and overall anxiety.
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PMID:Depression and panic anxiety: the effect of depressive co-morbidity on response to drug treatment of patients with panic disorder and agoraphobia. 198 Jun 97

Patients who meet DSM-III-R criteria for a diagnosis of panic disorder often show a complex mixture of psychopathological symptoms, including panic attacks (spontaneous and situational), anxiety (anticipatory and generalized), phobias (fear and avoidance), depression/dysphoria, and social and occupational disability. Various theories about the pathogenesis of these symptoms have been advanced that focus on a given symptom (e.g., panic, phobia) being primary in these disorders, with concurrent symptoms seen as epiphenomena or as secondary and reactive to a core symptom. This study, conducted on a large sample of panic disorder patients (N = 1,168), examines the temporal sequential pattern of symptom improvement in these patients, and explores how these relationships relate to various pathogenic theories. Our multiple analyses, when considered together, tend not to support any pathogenic theory that views a given symptom as being central to the overall disorder; our findings have obvious implications for theoreticians and clinicians interested in the study and treatment of panic and anxiety disorders.
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PMID:The sequence of improvement of the symptoms encountered in patients with panic disorder. 177 83

The purpose of the present epidemiological study is to investigate and describe panic disorder and sporadic panic attacks among a cohort of young adults, aged 28 years, from the Canton of Zurich in Switzerland. Both DSM-III panic disorder and sporadic panic are characterized by frequent symptoms of somatic anxiety and tension, as well as by frequent symptoms of depressed mood and low vitality. Sporadic panic is more prevalent than panic disorder and shows a greater excess of females over males. The association with depressions (major depression and recurrent brief depression) is similarly high for both types of panic syndromes, while the association with other anxiety disorders is negligible. Several indicators suggest a marked similarity between sporadic panic and DSM-III panic disorder. More impressive differences were observed between subjects with panic disorder alone and subjects with comorbidity of panic and depression. For the latter group, the SCL-90R scores indicated higher severity. Comparison of the scores of life events, conflicts, self-esteem, and the number of chronic problems in childhood suggests a more specific nosological pattern for subjects with panic and depression as compared with those with panic alone.
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PMID:The Zurich Study. IX. Panic disorder and sporadic panic: symptoms, diagnosis, prevalence, and overlap with depression. 213 46

2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol, hydrochloride (JO 1017) is a novel antidepressant drug. Its biochemical and pharmacological properties were investigated in mice, rats, dogs, rabbits and guinea pigs. In vitro, it selectively inhibited serotonin uptake and had a high affinity for the 3H-paroxetine and 3H-imipramine binding sites. Biochemical studies demonstrated the lack of MAO-A and MAO-B inhibition and the absence of marked affinity for muscarinic, histaminic or other conventional brain receptors. Chronic treatment with JO 1017 induced a decrease in the Bmax values for imipramine sites but did not modify the Bmax for beta-adrenergic and 5-HT2 receptors. The neuropsychopharmacological profile of JO 1017 is characterized by a decrease of the immobility times in behavioural despair tests with mice, a decrease of the escape failures in the rat learned helplessness test, a strong potentiation of L-5-HT P-induced head-twitches in mice and an antagonism of reserpine-induced ptosis in rabbits. It weakly antagonized oxotremorine-induced hypothermia and did not influence the hypothermia induced by apomorphine. In contrast to most other antidepressants, a high dose of JO 1017 induced hypermotility in mice placed in an activity meter without producing stereotyped behaviour and group toxicity. Unlike tricyclic antidepressants, JO 1017 was devoid of severe cardiotoxicity in guinea pigs and had no central anticholinergic nor antihistaminic properties. These results suggest that JO 1017 is a selective serotonin uptake inhibitor with a high safety margin. JO 1017 may have a potential clinical utility both in the treatment of depression and for indications where serotonin transmission is involved, e.g., anxiety, panic attack, obsessive compulsive disorder, obesity and alcohol consumption.
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PMID:Biochemical and pharmacological evaluation of the novel antidepressant and serotonin uptake inhibitor 2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol hydrochloride. 216 3

The arecoline REM induction test, a measurement of central cholinergic sensitivity, was performed in 10 patients with atypical depression. Arecoline induced REM sleep significantly more rapidly than placebo. Atypical depressives without evidence of anxiety, in particular those without panic attacks, had a more rapid REM induction response to arecoline than atypicals with anxiety symptoms. We compared our atypical depressives with normal controls and affectively ill patients studied in other laboratories. The rapid REM induction response observed in atypical depressives without anxiety was comparable to that seen in endogenous depressives and euthymic bipolars. Previous studies have demonstrated the presence of cholinergic supersensitivity in the latter two groups of patients. Our results suggest that atypical depressives may be distinguished in their response to arecoline based on their anxiety history, and that cholinergic supersensitivity is present in atypical depressives without anxiety. Additional studies with larger samples and simultaneously studied control groups are necessary to test these preliminary findings.
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PMID:Cholinergic REM sleep induction in atypical depression. 217 93

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.
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PMID:Clomipramine. An overview of its pharmacological properties and a review of its therapeutic use in obsessive compulsive disorder and panic disorder. 217 9

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosage of clomipramine hydrochloride are described, and clinical studies of the use of clomipramine in treating obsessive-compulsive disorder (OCD), other psychiatric conditions, and chronic pain are reviewed. Clomipramine hydrochloride, a tricyclic antidepressant, is a potent inhibitor of serotonin reuptake and may affect dopaminergic neurotransmission, suppress rapid eye movement sleep, produce changes in electrocardiograms, and elevate plasma prolactin. The drug is well absorbed from the gastrointestinal tract and undergoes extensive first-pass metabolism. Peak plasma concentrations occur three to four hours after a 150-mg oral dose. The mean elimination half-life is 39 hours. Some 66% of a dose is excreted in the urine, the remainder being eliminated in the feces. In clinical trials, clomipramine was significantly more effective than placebo, clorgiline, amitriptyline, imipramine, and doxepin in ameliorating the symptoms of OCD. Initial effects are seen at four weeks; improvement may continue for up to 18 weeks. Clomipramine may also be effective in treating panic attacks, phobias, depression, and chronic pain. The most common adverse effects of clomipramine are anticholinergic; others include nausea, seizures, and sexual difficulties. Interactions between clomipramine and barbiturates, haloperidol, monoamine oxidase inhibitors, and cigarette smoking have been documented. The usual initial adult dosage is 25-50 mg/day, titrated gradually to 250 mg/day if necessary. Clomipramine hydrochloride is a welcome new agent for the treatment of obsessive-compulsive disorder. Although its adverse-effect profile is like that of other tricyclic antidepressants, sexual dysfunction and seizures may be more frequent with this agent and limit its use.
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PMID:Clomipramine: an antiobsessional tricyclic antidepressant. 218 Jun 23

Seventy-nine patients with panic disorder were randomized to an 8-week double-blind treatment with alprazolam, imipramine, or placebo. Patients kept daily records of panic attacks, activity, anxiety, sleep, and medication use. Weekly measures of anxiety, depression, somatic symptoms, fears, avoidance, disability, and improvement were obtained. All patients underwent a symptom-limited exercise treadmill and other cardiovascular measures. By physician and patient global assessment, patients receiving alprazolam or imipramine were significantly better than patients on placebo. The alprazolam effects were apparent by week 1; the imipramine effects by week 4. All groups showed significant reductions in anxiety, depression, somatic measures, and panic attack frequency. At 8 weeks, patients in the alprazolam group reported significantly less fear than patients in the other two groups. Subjects in the imipramine group showed a significant increase in heart rate and blood pressure.
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PMID:Cardiovascular and symptomatic reduction effects of alprazolam and imipramine in patients with panic disorder: results of a double-blind, placebo-controlled trial. 218 12

Little difference was found between the psychiatric symptoms of medical patients and general-population subjects with affective disorder, both groups having been assessed with the same procedure (Present State Examination). Discrimination between medical patients with and without affective disorder was best achieved when patients with depressive and anxiety disorders were considered separately. Depressed mood, morning depression, and hopelessness were the key symptoms in the depressives, and nervous tension, free-floating anxiety, panic attacks, and specific phobias in the patients with anxiety disorders. Symptom profile did not distinguish patients with persistent affective disorders from those whose disorders had resolved at a 4-month follow-up.
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PMID:Significance of psychiatric symptoms in general medical patients with mood disorders. 221 Mar 46

This paper assumes that there are two types of stress-related pathology, the orthodox and the paradoxical, both depending on a positive feedback mechanism controlling the stress-related sympathetic discharge. The paradoxical stress response is speculated to be the common basis for a group of conditions, including depression, panic attacks, obesity, sexual deviations, alcoholism, and drug addiction. Evidence is provided that trazodone inhibits the stress-related sympathetic discharge. This would provide a rationale for its use not only in depression, but also in other conditions depending on an exaggeration of the orthodox or paradoxical stress response.
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PMID:The paradoxical stress response: a possible common basis for depression and other conditions. 221 71


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