Desyrel is a high-quality medication which is taken in treatment of depression. This remedy is acting by increasing the amount of serotonin. It is serotonin modulator.
Other names for this medication:
Desyrel is a high-quality medication which is taken in treatment of depression. This remedy is acting by increasing the amount of serotonin. It is serotonin modulator.
Other names for this medication:
Also known as: Trazodone.
Desyrel is a perfect remedy in struggle against depression.
This remedy is acting by increasing the amount of serotonin.
Desyrel is also known as Trazodone, Molipaxin, Deprax, Trittico, Thombran, Trialodine, Trazorel.
It is serotonin modulator.
Generic name of Desyrel is Trazodone.
Brand names of Desyrel are Desyrel, Desyrel Dividose.
Take Desyrel tablets orally with food.
Do not crush or chew it.
Take Desyrel at the same time every day with water.
Desyrel can be used by 18 year-old patients or over.
If you want to achieve most effective results do not stop taking Desyrel suddenly.
If you overdose Desyrel and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Desyrel overdosage: abnormal heartbeats, difficulty breathing, painful erection that does not go away, vomiting, feeling drowsy, convulsions.
Store at room temperature between 15 and 30 degrees C (59 to 86 degrees F) away from moisture and heat. Protect from light. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Desyrel are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Desyrel if you are allergic to its components.
Do not take Desyrel if you are pregnant, planning to become pregnant, or are breast-feeding.
Do not take it if you are under 18.
Be careful with Desyrel if you suffer from schizophrenia, other psychiatric illness, suicidal thoughts, heart attack, bipolar disorder (manic depression), drug abuse.
Try to avoid machine driving.
Be careful! Taking Desyrel you can become suicidal.
If you are going to have a surgery, be careful with Desyrel.
It can be dangerous to stop Desyrel taking suddenly.
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Of antidepressants studied, only mirtazapine had a statistically significantly greater SD/VA risk versus paroxetine. However, baseline differences between these users suggest that this finding may be attributable to residual confounding. Eleven other antidepressants had SD/VA risks no greater than that of paroxetine, thereby providing reassurance regarding the comparative cardiovascular safety of antidepressants.
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The present paper reports about a spontaneous rib fracture in a female patient (age 52) taking neuroleptics (mainly risperidone), antidepressants (mainly sertraline), and anxiolytics (mainly lorazepam). At the time of the fracture a severe osteoporosis and a strongly enhanced plasma prolactin level (117 ng/ml; normal values: 3-24 ng/ml) were detected. The latter one normalized 2 months after abandoning sertraline and risperidone. After this normalization, the patient did not report further accidents up to now.
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Possible intranasal quetiapine misuse was detected in a patient with schizoaffective disorder and a history of substance abuse. While antipsychotic medications are not typically thought of as drugs with an abuse potential, reports of the use and diversion of intranasal quetiapine among prison inmates, i.v. quetiapine abuse, and this case report indicate otherwise.
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Chest pain is a common and frightening symptom. Once cardiac disease has been excluded, an esophageal source is most likely. Pathophysiologically, gastroesophageal reflux disease, esophageal dysmotility, esophageal hypersensitivity, and anxiety disorders have been implicated. However, treatment remains a challenge. Here we examined the efficacy and safety of various commonly used modalities for treatment of esophageal (noncardiac) chest pain (ECP) and provided evidence-based recommendations.
All patients perceived significant subjective sleep improvements. Sleep latency significantly shortened (p=0.03), sleep efficiency increased (p=0.004) and the total sleep time was significantly prolonged (p=0.006) after the CBT treatment in both groups. Sleep architecture showed that the combined approach (CBT + trazodone) resulted in a significant increase in slow wave sleep duration compared to treatment by CBT only (p=0.04).
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Rats were treated with trazodone (2.5 or 10 mg kg-1) twice a day (at light and dark onset) for 11 days, after chronic injection of physiological saline. The sleep-wake activity was recorded for 24 h on the baseline day (saline), on trazodone days 1, 5 and 11, and also on day 12, when physiological saline was injected again (withdrawal day). Trazodone administration increased non-REM sleep. The enhancement of non-REM sleep was dose-related and more pronounced during the dark cycle. The promotion of non-REM sleep was enhanced during the chronic treatment. There were no consistent changes in REM sleep. Spectral analysis of the EEG revealed an increase in slow-wave activity after administration of the high dose (10 mg kg-1) of the drug. It is concluded that trazodone, a clinically effective antidepressant, has a non-REM sleep-promoting effect. It is speculated that the promotion of sleep by trazodone may be mediated by serotonergic mechanisms.
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Assessment of seizure risk in individuals involves consideration of predisposing factors, the antidepressant selected, and the bioavailability of the drug. Future studies of seizure risk would benefit from the use of specified criteria for determination of probable seizure events, a priori definition of predisposing exclusions, samples sufficiently large to provide adequate power, blood level monitoring, and inclusion of duration of drug treatment in the calculation of risk.
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Patients exhibited a significantly lower variance and HF, but a higher LF/HF compared to the control group across all age categories. The changes in variance and HF were severity dependent. In addition, all the HRV parameters of the patients with a satisfactory response after treatment have significantly improved.
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In fully adjusted models, antidepressant use was associated with a small increase in all-cause mortality.
(1). Trazodone turned out to be an efficacious medicine in the therapy of adjustment disorders. On the 56th day of the study the illness of 65.4% of patients was in remission, 26.9% of them responded to treatment, and 7.7% of them didn't. (2). Trazodone on the 7th day of therapy diminishes considerably the anxiety intensity and sleep disorder, and on the 14th day of the therapy it has an antidepressive effect. (3). As result of treating patients with trazodone the level of self-acceptance measured by ACL test has increased.
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Trazodone improves sleep quality and daytime functioning independently from prior history of hypnotics use.
Single photon emission computed tomography (SPECT) and positron emission tomography (PET) are examination procedures that have shown that repetitive transcranial magnetic stimulation (rTMS) is biologically active. The aim of the present study was to investigate the patterns of regional cerebral 18F-fluorodeoxyglucose (18F-FDG) uptake and regional 99mTc-hexamethylpropyleneamine oxime (99mTc-HMPAO) uptake simultaneously during a series of therapeutic rTMS at low frequency. Four drug-resistant depressed patients underwent 10 rTMS as an add-on measure over 14 days. One day before and one day after TMS, simultaneous measurements of 18F-FDG, representing regional cerebral metabolic rate (rCMR), and 99mTc-HMPAO, representing regional cerebral blood flow (rCBF), were carried out. A conventional double head SPECT camera with 511 keV collimators was used. Statistically significant simultaneous overall changes of rCBF and rCMR were found in the upper prefrontal regions bilaterally in terms of increased uptake rates and in the left gyrus frontalis inferior in terms of decreased uptake rates of both isotopes compared to controls. Although this method improves our understanding of rTMS mechanism, there are limitations due to the lower resolution provided. Therapeutic rTMS seems to influence distinct, cortical regions affecting rCBF and rCMR.
The chronic effects of five 2-substituted 4-phenylquinoline derivatives on the sensitivity of the noradrenergic cyclic AMP-generating system in the rat brain cortex have been determined, and compared with those of the typical and atypical antidepressants imipramine and trazodone, respectively. Acute treatment (single i.p. dose of 20 mg kg-1) and sub-chronic treatment (20 mg kg-1 daily for 10 days) induced no significant desensitization of the beta-adrenoceptors. However, chronic treatment (20 mg kg-1 daily for 3 weeks) significantly decreased the isoprenaline-induced increase in cyclic AMP, suggesting desensitization. This effect, coupled with previous findings, points to a potential role of these compounds as antidepressants.
In this microiontophoretical study trazodone (TR) was applied on rat brainstem neurones to verify its effects on spontaneous firing and neuronal responses to administrations of 5-hydroxytryptamine (5HT), noradrenaline (norepinephrine, NA) and acetylcholine (Ach). TR was able to modify the spontaneous firing likely by an indirect action, potentiated the excitatory responses to 5HT and reduced the inhibitory ones, was ineffective on the inhibitory responses to NA, while tended to antagonize the excitatory ones. Moreover TR did not show anticholinergic properties.
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During a first one year period a random treatment for climacteric symptoms with "Estriol vaginal cream" vs "Trazodone and Estriol vaginal cream" and, after it and only in patients not complaining of dyspareunia, with "Trazodone" vs "Veralipride" has been conducted. After the first year all women complaining of dyspareunia were treated with Estriol vaginal cream. Eighty women were enrolled in the five treatment groups. After three months of treatment, a good remission of symptoms was shown, with differences in relations to treatment schedules. Dyspareunia subsided for more than 70% in women treated with Estriol vaginal cream (either by itself or in association), and Estriol vaginal cream achieved the best response from the highest number of the considered symptoms, besides being the only active treatment in insomnia. A good answer on hot flushes and "irritability, anxiety, depression" was obtained by Trazodone, while Veralipride showed to be more active on all neurovegetative symptoms (hot flushes, sweatings, tinglings, palpitations, astenia).
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1. The objective was to assess long-term efficacy of antidepressant medications in dysthymia. 2. In a naturalistic study, patients with DSMIII-R dysthymia who had participated in previous antidepressant trials with fluoxetine and trazodone were evaluated at a mean of 40.0 weeks of follow-up to assess whether medication response persisted over time. A multivariate analysis was performed for patients on vs. off medication. Relapse rates (with relapse defined as HDRS score > 13) were also compared for these two groups. 3. Of 40 patients, the 24 still on medication showed significantly lower scores on most rating scales (HDRS, Cornell Dysthymia Rating Scale, and CGI, but not on the SCL-58) than the heterogeneous group of 16 patients not taking medication. Relapse was low (17.4%) among patients remaining on medication. 4. These preliminary findings suggest that dysthymia patients who remain on medication maintain improvement over time.
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We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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Trazodone is an atypical antidepressant with additional anxiolytic effects. Recent European experience with trazodone is reviewed with respect to antidepressant efficacy, side effects (particularly anticholinergic), anxiolytic actions, cardiotoxicity, overdosage, and use in the elderly. From the data presented in this paper it is concluded that trazodone is effective both as an antidepressant and as an anxiolytic agent, with few side effects and low cardiotoxicity. It is safer than tricyclic antidepressant agents in overdosage and better tolerated in the elderly patient.
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Anecdotal reports of increased libido and sexual function in patients taking trazodone have led to its empirical use in patients with erectile dysfunction. A retrospective review of patient-reported responses to trazodone was performed to outline the efficacy and side-effect profile of this agent.
Fear of possible cardiovascular side effects has prevented many physicians from treating older patients with antidepressants. However, we believe that it is the rare patient who cannot or should not be treated with some agent. Start with a low dose of desipramine, doxepin, or trazodone, depending upon the tolerance for sedation and anticholinergic side effects. Barring specific contraindications, the choice of drugs is usually based on the side-effect profile, rather than any differences in efficacy.
A fatal suicidal ingestion of drugs, together with activated charcoal, is reported. The death occurred 31 hours after the self-administration. The autopsy revealed a large amount of gastric content that appeared to be a compact mass of black color. Toxicologic analyses showed the presence of toxic levels of desalkylflurazepam and trazodone; metamizole and pridinol were also detected. The obtained results supported the hypothesis of a death due to acute intoxication delayed by the self-administration of activated charcoal, which elimination was probably hindered by the action of pridinol.
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Results of this study indicated oral administration of trazodone resulted in acceptable absolute bioavailability, with substantial variability in time to maximum plasma concentration. Individualized approaches in dosing intervals may be necessary for dogs receiving oral trazodone. An orally administered dose of 8 mg/kg was well tolerated in dogs; IV administration of a dose of 8 mg/kg caused substantial adverse effects, including tachycardia and behavior disinhibition.
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The number one indication for the use of an antidepressant was depression. Within this indication, mostly the recommended SSRIs were used, in dosages equal to or higher than the MED. Furthermore, we noticed that there was substantial use of sedative antidepressants for insomnia and that the physicians preferred to prescribe benzodiazepines over the recommended SSRIs to treat anxiety chronically.
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Drugs acting within the central nervous system (CNS) that reduce the sympathetic antierectile flow and enhance the parasympathetic proerectile flow to the penis may restore penile erection in cases of erectile dysfunction of both psychogenic and organic origin. The best characterized of such drugs is the dopaminergic agonist apomorphine, which acts on the hypothalamus and, perhaps, the autonomic nuclei in the spinal cord. Other drugs that target the CNS and have been registered and tested are the a(2)-adrenoceptor antagonists yohimbine and delequamine, the alpha-melanocyte-stimulating hormone agonist melanotan II, and the serotonin reuptake inhibitor trazodone. Androgens also may influence sexual behavior by acting within the CNS, notably by modifying the neurotransmitter system targeted by these drugs. Our knowledge of the mode of action of CNS drugs comes mainly from experiments on rodents. Consequently, explanations regarding the way they work in humans are only speculative.
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Using microdialysis, extracellular concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined in the striatum of rats. In rats given trazodone, m-chlorophenylpiperazine dihydrochloride, or imipramine, the concentrations of 5-HT were unchanged. 5-HIAA in trazodone- or imipramine-treated rats, however, was respectively, decreased to 80 or 65% of preinjections levels. When the potassium concentration (K(+)) was increased up to 150 mmol/l in the perfusate, the concentrations of 5-HT increased to about ten times the basal levels in the rats given saline. In rats treated with trazodone, K(+)-evoked elevations of 5-HT were less than five times the basal level. Multiple trazodone administrations prolonged the duration of inhibition of 5-HT release. In rats treated with other drugs, the K(+)-evoked 5-HT release was not affected. These observations suggest that trazodone itself might reduce 5-HT neural transmission.
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An open pilot trial of combined trazodone and tryptophan for 11 patients with Obsessive-Compulsive Disorder was conducted to test the hypothesis that increasing serotonin activity is therapeutic for this condition. Results were not encouraging; several patients tolerated the combination poorly, but even among patients completing 2 weeks' treatment benefit was marginal.
Serotonin can induce analgesia when injected directly into the brain, but analgesia after peripheral administration has been more difficult to show. The pentobarbital anesthetized mouse (PAM) model, developed to alleviate some of the problems involved in the measurement of tail flick latency, was used to assess the action of peripherally administered serotonin. Mice were anesthetized with about 65 mg/kg of sodium pentobarbital IP and their tail flick latencies measured while they were in stage III anesthesia. In these anesthetized mice, IP serotonin induced a significant analgesia that was much more robust than that found in awake mice. The analgesic effect was dose-dependent from 0.25 mg/kg to 10 mg/kg but was not blocked by the antiopiate naltrexone. Of several psychotropic agents tested, only amitriptyline, mianserin, and trazodone had significant effects on analgesia in the PAM model. The analgesic effect of serotonin was reproduced by the 5HT2 agonist DOI and totally blocked by the 5HT2 antagonist NPP. These results show the utility of the PAM model in studying nonopiate analgesia and suggest that the analgesic action of serotonin is mediated primarily through the 5HT2 receptor.
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Membrane potential changes induced by 5-hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA) and 1,1-dimethyl-4-phenyl piperazinium (DMPP) were recorded from nodose ganglia (NG) by the sucrose-gap method. An amount of 0.002-0.5 mumol of the depolarizing agent was injected into the superfusion stream to the ganglion. Responses to 5-HT were also evoked from superior cervical (SCG) and dorsal root ganglia (DRG). 5-Hydroxytryptamine elicited depolarizations of graded amplitude. Maximal responses were 4.5 +/- 0.4 mV in nodose ganglia compared to 2.2 +/- 0.2 mV in superior cervical and 0.6 +/- 0.1 mV in dorsal root ganglia (means +/- SEM). In nodose ganglia, GABA induced smaller maximal depolarizations than did 5-HT, similar to those evoked by DMPP; dopamine was a weak depolarizing agent while substance P was apparently inactive. The dose-response curve for 5-HT in nodose ganglia was parallel to that for 5-HT in superior cervical ganglia and significantly to the left (ED50 values 0.029 and 0.098 mumol). Curves for 5-HT and GABA in nodose ganglia were superimposable. The high sensitivity of nodose ganglia cells to 5-HT is briefly discussed. Analogues of 5-HT lacking a hydroxyl group at position 5 on the nucleus were relatively inactive as depolarizing agents. Picrotoxin (10(-6)-10(-5) M) reduced or suppressed responses in nodose ganglia to GABA, whereas responses to 5-HT and DMPP were not much affected or, in the case of 5-HT, sometimes somewhat reduced. Quipazine (10(-6) M) was a selective antagonist of 5-HT responses in nodose ganglia; those to GABA and DMPP were not significantly altered. Neither trazodone nor LSD displayed antagonist properties at 5-HT receptors in nodose ganglia.
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Sexual dysfunctions appear to be frequently occurring adverse events in treatment with antidepressants. Due to methodological reasons, a reliable estimation of the frequency of such events is currently not yet possible. There is evidence, that antidepressants could be differentiated with respect to their potency and specificity for disturbances of certain sexual subfunctions according to their pharmacological profile. With SSRIs in particular impaired functions of orgasm and ejaculation can be observed. No deteriorations are reported for buproprion and an improvement of sexual dysfunctions within the course of treatment for moclobemide. Viloxazine and trazodone appear to possess marked stimulating effects on libido and erectile functions. Generally the incidence of sexual adverse events is underestimated, although there is a pronounced impact on patient compliance. Taking into account this well documented side effect, sexual impairments should be monitored carefully within antidepressive treatment.
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We examined seven major journals in psychiatry from 1980 through 1990, inclusive, and selected those investigations of imipramine, trazodone, bupropion, and fluoxetine that met our minimal criteria for interpretability. These criteria included: (1) the presence of a placebo control, (2) double-blind status, (3) the use of the Hamilton Rating Scale for Depression as a dependent variable measure, (4) the use of nongeriatric adults with a diagnosis of major depression by DSM or RDC standards, and (5) the presence of reported means and standard deviations in the investigation, or sufficient data that allowed such to be computed. Each study of four antidepressants was analyzed for an effect size of the drug investigated. The effect size allows for a determination of the efficacy of a particular drug as compared with placebo, measured in standard deviation units.
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