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Previous reports document visual illusions resembling hallucinogen persisting perception disorder (HPPD) after risperidone treatment in patients with histories of previous LSD exposure.
Depressive and schizophrenic patients frequently suffer from sexual dysfunctions. Antidepressants and antipsychotics can aggravate them leading to discontinuation of the treatment. The strategy to decrease these dysfunctions is the following: 1) reducing the dose of medication; 2) changing antidepressant: replace SSRI by moclobemid, trazodone, bupropion, mirtazpine, which do not delay ejaculation; switching to another antipsychotic: quietiapine, olanzapine, aripripazol, which do not increase serum prolactin; 3) taking a drug holiday for two or three days and 4) adding another drug such as sildenafil if impotence, or a dopaminergic agonist (aripripazol, a partial agonist) or cabergoline, in case of hyperprolactinaemia.
A theory of excessive transmission of serotonin (5-HT) in depression has been previously proposed. The purpose of the present study was to test this theory further by using the model of depression in rats induced by L-5-hydroxytryptophan (5-HTP), the precursor of 5-HT. The drug effects on 5-HTP (25 mg/kg) induced behavioral depression were tested by chronic administration using methysergide which is a postsynaptic blocker of 5-HT, or by comparable clinical doses of antidepressant drugs. Methysergide (2 mg/kg) blocked 5-HTP induced depression on days 8 and 22 after initiation of medication by 70% and 83%, respectively. Among antidepressants, mianserin (2 mg/kg) was the first to produce an effect, displaying a 38% effect as early as 1 day after the start of medication and having blocking effects of 52% and 72% on days 8 and 22. Desipramine (5 mg/kg), doxepine (5 mg/kg), imipramine (5 mg/kg) and trazodone (10 mg/kg) showed no significant effect on days 1 and 8, and on day 22, 64, 36, 33 and 32% blocking, respectively. Amitriptyline had an initial effect of 41% at a dose of 10 mg/kg. Clomipramine (5 mg/kg), zimelidine (6 mg/kg) and chlorpromazine (2.5 mg/kg), which is a neuroleptic, showed no effect. Considering these results in light of recent data reported on the 5-HT synapse, it was suggested that 5-HTP induced depression may be induced by excessive transmission of 5-HT and that some antidepressant drugs may produce their effect by blocking this postsynaptic transmission. Based on these results, the mechanisms of human depression were discussed.
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Benzodiazepine medications have well-documented side effects, and their prescription rates in older adults have been declining. Trazodone and quetiapine are medications with sedative properties when used at low doses and are commonly used off-label for sleep or behavioral symptoms in older adults.
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A 59-year-old male was admitted to the Intensive Care Unit from the Emergency Department approximately 12 hr after the ingestion of 30 to 40 mg of colchicine, TYLENOL with codeine, IMODIUM, DESYREL and ethanol. He suffered severe systemic manifestations and succumbed approximately 36 hr post-ingestion. Although this is a case of a mixed ingestion, the complications seen suggest that colchicine was responsible for the fatality.
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During the 6-year period, it was determined that 3829 inpatients had received tricyclic antidepressants (TCAs), 2981 fluoxetine, 2603 trazodone, 809 bupropion, 743 monoamine oxidase inhibitors (MAOIs), 592 stimulants, 588 sertraline, 48 paroxetine, and 894 ECT. There were significant increases over time in prescriptions of MAOIs compared with fluoxetine (chi 2 = 14.36, p = .006), and bupropion compared with TCAs (chi 2 = 6.45, p = .04). There was a trend for bupropion to be prescribed more over time compared with fluoxetine (chi 2 = 5.09, p = .08). There were no significant changes in the prescribing of other antidepressants or in the use of ECT.
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To determine the potential procholinergic nature of some of the commonly used drugs by examining their cholinesterase inhibiting properties.
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A 6-week placebo-controlled trial evaluated the efficacy of trazodone hydrochloride for the relief of chronic low back pain. Forty-two subjects (22 trazodone, 20 placebo) with a 20.3-year average history of back pain were titrated to an average dose of trazodone 201 mg or placebo 238 mg and evaluated daily on a Visual Analogue Scale of pain intensity, at 2-week intervals on an observer rating of pain behavior while walking, and before and after the trial on the Beck Depression Inventory, the Sickness Impact Profile, and a solid state microcomputer (Vitalog) that measured physical activity. Trazodone blood levels and urine toxicology screens were also obtained. There were no significant differences between groups in treatment effect. The results of this study require confirmation by longer trials with larger, less chronic, more homogeneous samples at higher doses with follow-up assessments.
To compare the relative central nervous system and cardiac toxicity of amoxapine, maprotiline, and trazodone with the older tricyclic antidepressants, a three-year (1981 through 1983) retrospective review was performed on 1,313 cases involving cyclic antidepressant exposures reported to the Maryland Poison Center. Seizures were more common in the amoxapine (24.5%) and maprotiline (12.2%) groups, compared with either the tricyclic antidepressants (3.0%) or trazodone (0%) (P less than .01). A higher incidence of seizures also was observed in desipramine ingestors (17.9%) compared with other tricyclic antidepressants. No significant differences in the incidence of central nervous system depression or cardiotoxicity was found between the groups. These findings support reports of an increased incidence of seizures in overdoses of amoxapine and maprotiline, but do not substantiate claims of less cardiotoxicity.
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Among all the symptoms of major depressive disorder, trazodone proved to be more effective in controlling insomnia.
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Five neuroleptic-free patients exhibited syndromes that were indistinguishable from idiopathic or neuroleptic-induced akathisia in association with antidepressant administration. While antidepressant-related akathisia may be produced by any of a variety of antidepressants, the susceptibility of each individual patient to the development of this disorder may be limited to only one or a few of these agents. A considerably rarer syndrome than neuroleptic-induced akathisia, antidepressant-related akathisia appears to respond to established pharmacologic treatments for neuroleptic-induced akathisia.
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The aim of this study was to investigate the efficacy of trazodone administration in the management of SSRI-induced sexual dysfunction.
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Although the improvement was not statistically significant, treatment with testosterone and trazodone could be used as an adjuvant therapy in nonorganic male sexual dysfunction. The only treatment superior to placebo seemed to be hypnosis. A more effective treatment may be obtained by combining these therapeutic modalities, but this needs further study.