[Activity of toloxatone, antidepressive agents and various other reserpine antagonists on three behavior tests, in the mouse treated with nialamide].
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A successful application of an Apple II microcomputer in determining pharmacokinetic parameters from on-line data is described.
Somatic complaints are core symptoms of depressive illness. Although none can be said to be specific, some combinations appear typical of depression. In the field of somatic complaints, depression constitutes a factor of good prognosis because of a positive response to antidepressants. On the other hand, in the field of depression, somatic complaints constitute a factor of poor prognosis and of resistance to treatment. Peripherally to depression, the clinical picture of anxiety, somatoform disorders and hypochondriasis contains somatic complaints. Anxiety is less refractory to treatment than somatoform disorders and somatoform disorders less than hypochondriasis. Antidepressants are a major treatment in those cases. No study could identify a mechanism of action but dopaminergic antidepressants could be particularly interesting. Ohayon and Caulet reported the efficacy of amoxapine in a population of 134 patients with somatic complaints and diagnoses of depression, anxiety or somatoform disorders.
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Effective 5-HT concentration eliciting the half-maximal rate of platelet deformation (aggregation) in drug-free bipolar or unipolar depressed women was significantly (p less than 0.001) lower as compared with matched controls (0.13 +/- 0.04 microM and 0.532 +/- 0.1 microM, respectively). After 1-3 months of antidepressant treatment this value increased to 0.47 +/- 0.16 microM and was no longer different from control. Possible mechanisms controlling the activity of serotonin2 platelet receptors are discussed.
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In an open study 17 patients with depressive disorders, 5 patients with unipolar affec. Only 9 patients completed the trial. The frequency of side-effects, especially nausea and vomiting was high, which will probably limit the clinical use of the drug. Of the sion NUD, were treated with a new potential antidepressant, ICI 58.834 (Vivalan). tive psychosis, 9 patients with reactio-neurotico-depressiva and 3 patients with deprespatients who completed the trial 1 was recovered and 4 were improved. Thus the antidepressive effect is dubious and must be tested in controlled studies.
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Brugada syndrome is an arrhythmogenetic disease characterized by electrocardiographic ST segment elevation in right precordial leads, which is called "coved type", and an increased risk of sudden death as the result of ventricular fibrillation. We presented a case of Brugada syndrome with a convulsive seizure, during administration of a tricyclic antidepressant for the treatment of a depressive state. A 43-year-old man with bipolar II disorder and obsessive-compulsive disorder was admitted to our hospital for the treatment of a depressive state. There was no medical history of heart failure. Nortriptyline was effective for his depressive as well as for obsessive symptoms. During the treatment, however, he presented a convulsive syncope. Electrocardiography (ECG) showed "coved type" ST segment elevation, and the patient consulted a cardiologist. Electrophysiological study revealed Brugada syndrome, and an implantable cardioverter defibrillator was placed. An overdose of antidepressants has been reported to produce a Brugada-type ECG because of its Na channel antagonism. However, in the present case, the abnormal ECG findings occurred following a usual dosage of nortriptyline. Thus, it is suggested that Brugada syndrome is related to a susceptibility to antidepressants in the present case. Every psychiatrist managing antidepressant therapy should be aware of Brugada syndrome and this ECG pattern, which may be a marker of sudden death.
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