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PubMed2003

Trazodone hydrochloride attenuates thermal hyperalgesia in a chronic constriction injury rat model.

BACKGROUND AND OBJECTIVE: Trazodone hydrochloride is used in the treatment of neuropathic pain. However, the analgesic effects of trazodone on neuropathic pain are controversial. The study was undertaken to determine the analgesic effect of trazodone on a chronic constriction injury model. METHODS: We tested the effect of trazodone on thermal hyperalgesia due to a chronic constriction injury of the sciatic nerve in rats and examined the effects of lesions in the descending and ascending serotonergic system induced by 5,7-dihydroxytriptamine (5,7-DHT). RESULTS: The analgesic effects of trazodone showed a clear dose dependency. Furthermore, the analgesic effect of trazodone was observed in rats injected with 5,7-DHT into the dorsal raphe nucleus and medial raphe nucleus. CONCLUSIONS: The results suggest that a mainly serotonergic descending pain control pathway mediates the analgesic effects of trazodone.

Animals↗
PubMed2001

Survey on the usefulness of trazodone in patients with PTSD with insomnia or nightmares.

BACKGROUND: Trazodone is commonly used in the treatment of insonmia and nightmares in patients with PTSD. There is little evidence in the literature for this practice. METHOD: Seventy-four patients from the Palo Alto Veterans Affairs Health Care System in California who were admitted to a specialized 8 week inpatient treatment program for PTSD were surveyed regarding their use of trazodone in the treatment of insomnia or nightmares. Patients were asked to complete a questionnaire regarding trazodone's effectiveness, side effects, and optimal doses. RESULTS: Of 74 patients surveyed, 60 patients were able to maintain an effective dose of trazodone. The other 14 patients were unable to tolerate the medication. Seventy-two percent of the 60 patients assessed found trazodone helpful in decreasing nightmares, from an average of 3.3 to 1.3 nights per week (p<.005). Ninety-two percent found it helped with sleep onset, and 78% reported improvement with sleep maintenance. There was a significant correlation between the effectiveness in decreasing nightmares and improving sleep (r= .57, p < .005). The effective dose range of trazodone for 70% of patients was 50 to 200 mg nightly. Of the 74 patients surveyed, 9 (12%) reported priapism. CONCLUSION: Trazodone appears effective for the treatment of insomnia and nightmares associated with chronic PTSD. However, controlled trials are needed before any definite conclusions can be drawn. The higher than expected occurrence of priapism warrants clinicians asking directly about this side effect.

Adult↗
PubMed1994

The acute effects of nefazodone, trazodone and buspirone on sleep and sleep-related penile tumescence in normal subjects.

This study examined the effects of nefazodone, trazodone and buspirone on sleep and sleep-related penile tumescence. Trazodone is a sedating antidepressant without anticholinergic properties. Nefazodone is a new antidepressant that is a structural analogue of trazodone but is less sedating. Buspirone is a nonsedating, nonbenzodiazepine anxiolytic with antidepressant properties. Nefazodone was compared to trazodone and buspirone in a double-blind, placebo-controlled crossover study in 12 normal healthy males. Nefazodone increased rapid eye movement (REM) sleep, whereas trazodone and buspirone suppressed REM sleep. The drugs only minimally affected other sleep stages. Trazodone increased total tumescence time by delaying the onset of detumescence; nefazodone increased total tumescence time only insofar as it increased REM sleep; buspirone did not change total tumescence time when compared to placebo. The results support a growing body of data indicating that not all antidepressants suppress REM sleep. The results also are consistent with the interpretation of an earlier study showing that trazodone prolongs penile tumescence during sleep as a result of its alpha-adrenergic blocking properties that suppress detumescence. Nefazodone, with less alpha-adrenergic blocking activity, did not abnormally penile tumescence beyond REM sleep.

Adult↗
PubMed2002

Relationship between plasma concentrations of trazodone and its active metabolite, m-chlorophenylpiperazine, and its clinical effect in depressed patients.

Relationships between plasma concentrations of trazodone and m-chlorophenylpiperazine (m-CPP) and the clinical effects were studied in 26 patients (12 males and 14 females) with major depression during three weeks' treatment of 150 mg/d trazodone using an open-study design. Depressive symptoms were evaluated by Montgomery Asberg Depression Rating Scale (MADRS), and subjective side effects were assessed by UKU side effects rating scale (UKU) before treatment and at weekly intervals. Plasma concentrations of trazodone and m-CPP were measured by HPLC. There were significant linear relationships between the steady-state plasma concentration (Css) of trazodone and both the final MADRS score (rs = -0.529, P < 0.01) and the percent improvement at 3 weeks (r = 0.442, P < 0.05). Moreover, the proportion of responders (a final MADRS score of 10 or less) was significantly higher in the group with a trazodone concentration greater than 714 ng/mL (6/8 vs 3/18, P = 0.008). No significant correlation was found between UKU score and the Css for either compound nor between the UKU score and the ratio of m-CPP/trazodone. The current study suggests that a therapeutic response is dependent on the plasma concentration of trazodone but not m-CPP and that a plasma trazodone concentration of about 700 ng/mL may be a threshold for a good therapeutic response.

Adult↗
PubMed1984

Comparative bioavailability of trazodone formulations using stable isotope methodology.

The bioavailability of trazodone, a new antidepressant, from 50 mg dividose (A) or film-sealed (B) tablets relative to an oral solution was determined in six healthy male subjects using 50 mg of D4-trazodone as a stable isotope labelled standard. Concentrations of trazodone and D4-trazodone were measured by GCMS. The pharmacokinetics of trazodone and D4-trazodone were identical indicating no isotope effect. For formulation A, B and solution, the relative (trazodone/D4-trazodone) Cmax values were 0.84 +/- 0.09, 0.90 +/- 0.05 and 1.05 +/- 0.04. The relative bioequivalence of the dosage formed with a power of 85% (power by conventional ANOVA was 54%). Among subjects % relative standard deviations (RSD) for the D4-trazodone AUC values, a measure of intra-subject variability, were 6 to 38% while the % RSDs by period, a measure of inter-subject variability, were 26 to 55%.

Adult↗
PubMed1995

High-performance liquid chromatographic determination of trazodone and 1-m-chlorophenylpiperazine with ultraviolet and electrochemical detector.

A high-performance liquid chromatographic (HPLC) assay was developed for the determination of trazodone and its metabolite, 1-m-chlorophenylpiperazine (m-CPP), in plasma. The high level of trazodone in plasma was detected by ultraviolet absorbance at 254 nm and the low level of m-CPP in plasma was detected by coulometric electrochemical detection at 840 mV on the series arrangement of two detectors. Pilsicainide as an internal standard for both compounds was monitored by both detectors. Trazodone and m-CPP in plasma were extracted by a rapid and simple procedure based on CN bonded-phase extraction, and C8 reversed-phase HPLC separation. Determination was possible for trazodone in the concentration range 100-2000 ng mL-1 and for m-CPP in the concentration range 5-100 ng mL-1. The recoveries of trazodone and m-CPP added to plasma were 81.0-84.2 and 68.0-73.2%, respectively, with coefficients of variation of less than 7.3 and 8.2%, respectively. The method is applicable to high level monitoring of trazodone and low level monitoring of m-CPP in plasma of healthy volunteers and patients treated with trazodone.

Chromatography, High Pressure Liquid↗
PubMed1984

Trazodone and mianserin in general practice.

In a double-blind, noncrossover study, general practice patients suffering from depression were treated with either trazodone (100-200 mg, nocte ) or mianserin (60-120 mg, nocte ) for 6 weeks. For entry into the study, a minimum score of 14 on the 17-point Hamilton Depression Rating Scale ( HDRS ) was necessary. By random allocation, 125 patients (61 on trazodone and 64 on mianserin) entered the study. Altogether there were 43 withdrawals, of whom 31 (72%) had received mianserin. At least one of the reasons for 22 withdrawals from the mianserin group was an unacceptable side effect, frequently being daytime drowsiness. In contrast, only 5 of the trazodone group withdrew because of side effects. These differences in the withdrawal rates for those patients entering the study were statistically significant (p less than 0.001). A total of 82 patients completed treatment and entered the analysis for efficacy; 49 on trazodone and 33 on mianserin. Results show that both treatments were equally effective in reducing symptoms of depression and anxiety. Thus, the mean HDRS score was 21.3 and 21.5 for trazodone and mianserin, respectively, at the start of treatment which decreased to 6.2 and 5.9, respectively, at the end of 6 weeks. The mean Zung self-rating anxiety scores for trazodone and mianserin were 45.6 and 44.4 at the start of treatment and 33.6 and 31.1 at the end of the study. The results suggest that, on the basis of fewer significant side effects, trazodone is more acceptable to mianserin in treating depression, with or without anxiety, in general practice patients.

Adult↗
PubMed1984

Acute trazodone poisoning: clinical signs and plasma concentrations.

A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3-4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.

Adolescent↗
PubMed1987

Trazodone: a 5-year review of antidepressant efficacy.

Results from double-blind studies reported since 1981 were reviewed to evaluate trazodone's relative antidepressant efficacy and its safety profile. Trazodone's therapeutic efficacy compared favorably with that of the tricyclic antidepressant (TCA) agents in both endogenous and nonendogenous patients. Data also suggested that trazodone had a more pronounced, earlier anxiolytic action than the TCA agents. Trazodone may be more effective at lower than maximal doses; some studies that used high dosages--starting at 200 mg/day and rapidly titrated doses to as high as 600 mg/day--reported poorer therapeutic responses than did those that employed more conservative dosages. Trazodone therapy generally produced less pronounced anticholinergic effects than did the comparison TCA agent and it is often as sedating as amitriptyline but more sedating than imipramine. Untoward side effects may be reduced by taking trazodone after meals, and by using bedtime dosing. Issues of possible cardiotoxicity and priapism are reviewed briefly. Overall, studies in the past 5 years point to trazodone as being an effective antidepressant agent with a relatively favorable safety profile.

Depressive Disorder↗
PubMed1994

Trazodone for antidepressant-associated insomnia.

OBJECTIVE: The authors investigated trazodone as a hypnotic for depressed patients who had persistent, exacerbated, or new insomnia while taking either fluoxetine or bupropion. METHOD: Seventeen depressed patients who had insomnia while taking fluoxetine or bupropion were given either trazodone or placebo in a double-blind crossover trial. Sleep was assessed by self-report with the Pittsburgh Sleep Quality Index and the sleep items of the Yale-New Haven Hospital Depressive Symptom Inventory. RESULTS: Improvement with trazodone, but not with placebo, was shown by the total Pittsburgh index scores and Yale-New Haven inventory total sleep scores and by the Pittsburgh index measures of sleep duration and Yale-New Haven inventory measures of early morning awakening, and there was a trend toward improvement in the Yale-New Haven inventory item regarding middle of the night awakenings. Subjective sleep quality and sleep latency also showed a trend toward improvement, but the Pittsburgh index measures of sleep efficiency and disturbances and the Yale-New Haven inventory item regarding difficulty falling asleep were unaffected by trazodone. One patient dropped out because of excessive daytime sedation with trazodone, and another dropped out because of nonresponse to placebo. Of the completers, 67% experienced overall improvement in sleep with trazodone according to a priori criteria, whereas only 13% experienced improvement with placebo. CONCLUSIONS: Trazodone is an effective hypnotic for patients with antidepressant-associated insomnia.

Adult↗
PubMed2003

Short-term exposure to low-dose ritonavir impairs clearance and enhances adverse effects of trazodone.

Antiretroviral agents may participate in drug interactions that influence the efficacy and toxicity of other antiretrovirals, as well as pharmacologic treatments of coincident or complicating diseases. The viral protease inhibitor, ritonavir, may cause drug interactions by inhibiting the activity of cytochrome P450-3A (CYP3A) isoforms. In a single-dose, blinded, four-way crossover study, 10 healthy volunteer subjects received 50 mg of trazodone hydrochloride or matching placebo concurrent with low-dose ritonavir (four doses of 200 mg each) or with placebo. Compared to the control condition, ritonavir significantly reduced apparent oral clearance of trazodone (155 +/- 23 vs. 75 +/- 12 ml/min, p < 0.001), prolonged elimination half-life (6.7 +/- 0.7 vs. 14.9 +/- 3.9 h, p < 0.05), and increased peak plasma concentrations (842 +/- 64 vs. 1125 +/- 111 ng/ml, p < 0.05) (mean +/- SE). Coadministration of trazodone with ritonavir increased sedation, fatigue, and performance impairment compared to trazodone plus placebo; differences reached significance only for the digitsymbol substitution test. Three subjects experienced nausea, dizziness, or hypotension when trazodone was given with ritonavir; 1 of these subjects also experienced syncope. Thus short-term low-dose administration of ritonavir impairs oral clearance of trazodone and increases the occurrence of adverse reactions. The findings are consistent with impairment of CYP3A-mediated trazodone metabolism by ritonavir.

Administration, Oral↗
PubMed2005

A comparative, randomised, double-blind study of trazodone prolonged-release and paroxetine in the treatment of patients with major depressive disorder.

OBJECTIVES: To evaluate the efficacy and safety of trazodone prolonged release compared with paroxetine in the treatment of patients with major depression. RESEARCH DESIGN AND METHODS: A total of 108 patients aged 20-68 years were enrolled in this multicentre, double-blind, double-dummy, randomised, paroxetine-controlled study. Each patient received 3 days single-blind placebo treatment followed by 6 weeks double-blind treatment with either trazodone prolonged release 150-450 mg/day (n = 55) or paroxetine 20-40 mg/day (n = 53). OUTCOME MEASURES: Efficacy was evaluated by the rate of patients responding to each treatment and considered to be in remission, and by mean changes from baseline in the Hamilton Depression Rating scale scores (HAM-D), Montgomery Asberg Depression Rating Scale scores (MADRS), and Clinical Global Impression (CGI)--Severity and Global Improvement scores. Time to onset of efficacy and safety were assessed. RESULTS: Trazodone and paroxetine were equally effective at reducing symptoms of depression and promoting remission. Onset of efficacy was slightly faster for patients treated with paroxetine. Overall, there were no significant differences between the groups at endpoint in efficacy measures, and in percentage of responders (> 85%) or patients in remission (> 65%). Sleep disorders (HAM-D subset) were significantly less evident for patients in the trazodone group at the end of the study (p < 0.05). Adverse drug reactions were reported by 35% of trazodone-treated patients (mainly of the nervous system) and 26% of paroxetine-treated patients (mainly gastrointestinal), although none was considered to be serious. CONCLUSIONS: This study showed that after a 6-week period trazodone and paroxetine are not different in reducing the symptoms of depression and, in many patients, in producing the remission of the illness. The known divergence in tolerability profile of the two medications, related to their differing pharmacological properties, was also confirmed. Trazodone may be of advantage in depressed patients with sleep difficulties.

Adult↗
PubMed1981

Trazodone: a review of its pharmacological properties and therapeutic use in depression and anxiety.

Trazodone is a triazolopyridine derivative with antidepressant activity, that is chemically unrelated to other currently available antidepressants. Its pharmacological properties differ from those of most other antidepressants. Trazodone exhibits antiserotonin activity in animal studies, but its mechanism of action in depressive illness in humans is not clear. It has an overall therapeutic efficacy comparable with imipramine and amitriptyline in depressive illness but, at dosages which have achieved a similar overall clinical improvement, trazodone causes fewer anticholinergic side effects than the tricyclic antidepressants. Trazodone appears also to have activity against the concomitant anxiety in depressed patients and in limited studies was comparable with diazepam and chlordiazepoxide in anxiety neurosis. Trazodone has been reported to be of value in tremors and chronic alcoholism. Studies in animals, limited human studies and the low incidence of cardiovascular side effects in controlled therapeutic trials, suggest that trazodone is less likely than imipramine to cause cardiotoxicity at therapeutic doses, but the effects of overdosage are not known at present. Trazodone appears to be well tolerated by the elderly, seldom aggravates psychotic symptoms and does not produce neurological side effects.

Aged↗
PubMed2004

The use of trazodone as a hypnotic: a critical review.

BACKGROUND: The last few years have seen a remarkable rise in the off-label use of trazodone for inducing sleep in nondepressed patients, to a degree that it is prescribed for this purpose as commonly as the leading hypnotic. In view of this widespread popularity, it seems prudent to review what is known of the safety and efficacy of trazodone when used in this context. DATA SOURCES AND SELECTION: A MEDLINE search of the literature published in English between 1975 and 2003 that included the keywords sleep, trazodone, Desyrel, depression, sleeping pill, and sedative-hypnotics was conducted. DATA SYNTHESIS: From this review, it is concluded that there are very few data to suggest that trazodone improves sleep in patients without mood disorder, though it does increase total sleep in patients with major depressive disorder. There are virtually no dose-response data for trazodone vis-à-vis sleep and, similarly, no available data on tolerance to its possible hypnotic effects. Areas of concern with its use include reports of significant dropout rates and induction of arrhythmias, primarily in patients with histories of cardiac disease, as well as the development of priapism. CONCLUSION: In summary, there are few data to support the use of trazodone in nondepressed subjects. When the risk-benefit ratio of trazodone is assessed, its side effect profile, which is much more significant than that of conventional hypnotics, should be considered.

Aged↗
PubMed1999

Oral trazodone is not effective therapy for erectile dysfunction: a double-blind, placebo controlled trial.

PURPOSE: The unusual side effect of priapism associated with the antidepressant trazodone has led researchers to evaluate its use for the treatment of erectile dysfunction. Previous studies have shown nearly 70% efficacy in patients. Unfortunately, these studies have been anecdotal, retrospective or of combination therapy with yohimbine. A placebo controlled, fixed dose, double-blind crossover study was performed to evaluate the safety and efficacy of oral trazodone for the treatment of erectile dysfunction. MATERIALS AND METHODS: A total of 51 patients with at least 3 months of complete erectile dysfunction were randomized in a double-blind fashion to receive 50 mg. trazodone or placebo at bedtime. Evaluation consisted of a history, physical examination and laboratory studies, including hormonal evaluation, nocturnal penile tumescence evaluation, penile Doppler ultrasound and the Index of Sexual Satisfaction. Patients were followed at monthly intervals with an in clinic interview. After a 3-month treatment interval patients were reevaluated with index scores and crossed over after a 3-week washout period. Study end points included patient diary evaluations and index scores at the beginning of the study interval and the end of the first treatment period. RESULTS: Of the 51 patients who enrolled in the study 48 completed both phases. Mean patient age was 65 years (range 31 to 80). After the first 3-month treatment interval 19% of patients receiving trazodone had improved erections compared to 24% receiving placebo (p < 0.50). Of the trazodone group 35% had improvement in sex drive compared to 20% of the placebo group (p < 0.36). Mean Index of Sexual Satisfaction scores changed after treatment from 31.7 to 27.5 for the trazodone group (p < 0.50) and from 28.5 to 30.8 for the placebo group (p < 0.49). Side effects included drowsiness in 31% of the patients, dry mouth in 1% and fatigue in 19%. CONCLUSIONS: Trazodone is no more effective than placebo in improving erections and sexual function in patients with severe physiological erectile dysfunction.

Administration, Oral↗
PubMed1992

A double-blind, placebo controlled study of trazodone in patients with obsessive-compulsive disorder.

Patients with obsessive-compulsive disorder (OCD) have been shown to be preferentially responsive to serotonin (5-HT) uptake-inhibiting antidepressants including clomipramine, fluoxetine, fluvoxamine, and sertraline. The nontricyclic antidepressant, trazodone, also possesses serotonin reuptake inhibiting properties and has been reported to be efficacious in OCD in several case reports and open trials. In order to investigate trazodone's potential antiobsessive efficacy in a controlled fashion, 21 patients with OCD were entered into a double-blind, parallel design comparison of trazodone and placebo. There were no significant differences in baseline rating scores of OCD or depressive symptoms between those who entered the trazodone phase (N = 13) versus those who entered the placebo phase (N = 8). As measured by standardized OCD and depression rating scales, there was no significant difference in OCD or depressive symptoms in the 17 patients who completed 10 weeks of trazodone (N = 11, mean daily dose, 235 +/- 10 mg) versus 10 weeks of placebo (N = 6) administration. In comparison to clomipramine and fluoxetine treatment which we have found to be associated with greater than 95% reduction in platelet 5-HT concentration, there was only a 26% mean reduction in platelet 5-HT concentration after 10 weeks of trazodone administration. These results indicate that trazodone lacks substantial antiobsessive effects and is associated with only modest reductions in platelet 5-HT concentrations.

Adolescent↗
PubMed1994

The role of trazodone in the treatment of erectile dysfunction.

The effects of trazodone on the nocturnal penile erection were demonstrated in 14 impotent patients by Rigiscan recordings. Trazodone significantly increased the total erectile time, per cent of sleep with erection and maximum rigidity, while it had no effect on increment of tumescence size. Trazodone (150 mg to 200 mg) was administered to 35 clearly organic impotent patients in a 5-week single-blind design. Patients were evaluated by questionnaire. The study showed an improvement in 68.6 per cent of the patients receiving trazodone versus 11.4 per cent receiving placebo. In vitro, trazodone could relax rabbit corporeal smooth muscle contractions induced by exogenous norepinephrine and inhibit contractions elicited by transmural electrical stimulation of adrenergic nerve endings. The effects of trazodone on penile erection may be due to a peripheral alpha adrenoceptor antagonism and central unknown mechanism. We conclude that trazodone may prove an effective treatment for impotent patients.

Adult↗
PubMed1993

Trazodone in benzodiazepine dependence.

BACKGROUND: The authors set forth to test the usefulness of trazodone as an alternative anxiolytic in benzodiazepine-dependent patients. METHOD: Ten benzodiazepine-dependent patients according to DSM-III-R were hospitalized during a 2-4 week period and treated with trazodone (100 mg t.i.d.) while their benzodiazepine intake was progressively tapered; they left the hospital on a regimen of only a 300-mg daily dose of trazodone and were followed as outpatients at monthly intervals. The dose of trazodone was individually adapted according to condition. RESULTS: Very limited withdrawal phenomena occurred during the benzodiazepine taper period; during the 1-year follow-up, all patients remained off benzodiazepines and showed no evidence of abuse of trazodone. The dose of trazodone was significantly reduced to 185 mg (p = .003); the ratings of anxiety and depressive symptoms also significantly improved during follow-up: from 12.3 to 5.4 on the Hamilton Rating Scale for Anxiety (p = .002) and from 11.6 to 4.8 on the Hamilton Rating Scale for Depression (p = .002). CONCLUSION: These findings suggest the usefulness of trazodone as an alternative anxiolytic in patients at risk for benzodiazepine abuse.

Adult↗