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Paxil

Generic Paxil is a medication with highly developed components which is taken in treatment of serious disorders such as panic and social anxiety disorders, female premenstrual dysphoric disorder, post-traumatic stress disorder and depression. Generic Paxil acts as an anti-depression remedy. Generic Paxil operates by giving brains balance and mental stability.

Other names for this medication:

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Paroxetine

 

Also known as:  Paroxetine.

Description

Generic Paxil is found by professionals of medicine to combat mental dangerous disorders (depression, panic and social anxiety disorders, female premenstrual dysphoric disorder, and post-traumatic stress disorder). Target of Generic Paxil is to control and keep brain's balance.

Generic Paxil operates by giving brains balance and mental stability.

Paxil is also known as Paroxetine, Pari, Pexep, Parolin, Seroxat.

Generic Paxil is selective serotonin reuptake inhibitor (SSRI).

Generic name of Generic Paxil is Paroxetine.

Brand names of Generic Paxil are Paxil CR, Pexeva, Paxil.

Dosage

Generic Paxil is available in tablets (10 mg, 20 mg, 30 mg, 40 mg) and oral suspension. You should take it by mouth with meals of without it.

It is better to take Generic Paxil every day at the same time for nearly 4 weeks.

Generic Paxil cannot be given to patients under 18 years.

Take Generic Paxil and remember that its dosage depends on health state of patients.

For depression

Normal starting dose is 25 mg once a day.

For panic and social anxiety disorders

Normal starting dose is 12.5 mg once a day.

For aged people or patients with kidney or liver problems

Normal dose is 12.5 mg once a day.

If you want to achieve most effective results do not stop taking Generic Paxil suddenly.

Overdose

If you overdose Generic Paxil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Paxil overdosage: seizures, confused mental state, coma, tremor, nausea, blurred vision, retching, sweating, decreased urination, aggression, rapid heartbeat.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Paxil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Paxil if you are allergic to Generic Paxil components.

Be careful with Generic Paxil if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Generic Paxil if you take medications as isocarboxazid (Marplan); monoamine oxidase inhibitors as MAOIs (rasagiline (Azilect)); pimozide (Orap); tranylcypromine (Parnate), phenelzine (Nardil), selegiline (Eldepryl, Emsam); thioridazine (Mellaril).

Do not take it if you are under 18.

Be careful with Generic Paxil if you suffer from liver or kidney disease, manic depression, seizures, epilepsy, suicidal thoughts.

Be careful with Generic Paxil if you take medications as blood thinner as warfarin (Coumadin); naproxen (Aleve, Naprosyn); phenothiazine as prochlorperazine (Compazine), chlorpromazine (Thorazine), fluphenazine (Prolixin), mesoridazine (Serentil); St. John's wort, tramadol (Ultram); tryptophan; aspirin; lithium (Lithobid, Eskalith); nabumetone (Relafen); ibuprofen (Advil, Motrin); risperidone (Risperdal); indomethacin; almotriptan (Axert), frovatriptan (Frova), sumatriptan (Imitrex), naratriptan (Amerge), rizatriptan (Maxalt), or zolmitriptan (Zomig); atomoxetine (Strattera); etodolac (Lodine); heart rhythm medication as flecainide (Tambocor) or propafenone (Rhythmol); diclofenac (Voltaren); cimetidine (Tagamet); amitriptyline (Elavil), citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox), imipramine (Tofranil), nortriptyline (Pamelor), or sertraline (Zoloft); piroxicam (Feldene).

Try to be careful with Generic Paxil usage in case ever had drug abuse.

Avoid alcohol.

Try to avoid machine driving.

It can be dangerous to stop Generic Paxil taking suddenly.

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This retrospective study included 179 Japanese patients with major depressive disorder who were being treated with paroxetine. CYP2D6*1, *2, *5, *10, and *41 polymorphisms were observed. A total of 306 steady-state concentrations for paroxetine were collected from the patients. A nonlinear mixed-effects model identified the apparent Michaelis-Menten constant (Km) and the maximum velocity (Vmax) of paroxetine; the covariates included CYP2D6 genotypes, patient age, body weight, sex, and daily paroxetine dose.

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An iodinated cocaine derivative, N-(3'-iodopropen-2'-yl)-2 beta-carbomethoxy-3 beta-(4-chlorophenyl) tropane (IPT), was evaluated as a probe for in vitro and in vivo labeling of dopamine (DA) and serotonin (5-HT) transporters in Sprague-Dawley rat brain. Saturation analysis of [125I]IPT in rat striatal homogenates, in two different buffer solutions, Tris-HCl and phosphate, demonstrated a one-site binding with affinities (Kd) of 0.25 +/- 0.02 and 0.16 +/- 0.02 nM and densities (Bmax) of 939 +/- 161 and 1,982 +/- 137 fmol/mg protein, respectively. Competition by known DA transporter ligands showed a rank order of RTI-55 > IPT > GBR12909 > mazindol > (-)cocaine. Binding to 5-HT transporter sites was evaluated in rat cortical homogenates. Saturation experiment results showed a single site with a Kd value of 1.2 +/- 0.2 nM and a Bmax value of 100 +/- 20 fmol/mg protein. The rank order of potency of several monoamine uptake inhibitors (paroxetine > fluoxetine > mazindol > R-nisoxetine > GBR12909) suggests that [125I] IPT labels 5-HT transporters in rat cortical homogenates. Both ex vivo and in vitro autoradiographic studies revealed high densities of [125I]IPT binding sites in the caudate nucleus, putamen, olfactory tubercle and nucleus accumbens, areas known to be rich in dopaminergic innervation. Moderate accumulation of activity was also observed in the substantia nigra. The dorsal raphe, a region with a high density of 5-HT innervation, was labeled using in vitro autoradiography with [125I]IPT, but the labeling using ex vivo autoradiography was less prominent at 30 min postinjection and not noticeable at 60 min postinjection.(ABSTRACT TRUNCATED AT 250 WORDS)

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Our results confirm that whole-blood 5-HT concentration is a predictor for clinical improvement and indicate that abnormal intracellular mechanisms may be involved in OCD patients, in particular, the overstimulation of the phosphoinositide signaling system.

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Aripiprazole is a new atypical antipsychotic drug with a partial agonist activity at dopamine 2 and serotonin 1A receptors. The metabolism of aripiprazole involves both cytochrome P450 2D6 (CYP2D6) and CYP3A4. This study investigated the pharmacokinetic variability of aripiprazole and the active metabolite dehydroaripiprazole on the basis of 155 drug monitoring samples from psychiatric patients treated with therapeutic doses of aripiprazole (10-30 mg/day). Serum concentrations of drug and metabolite were determined by liquid chromatographic and tandem mass spectrometric detection. Pharmacokinetic variability was expressed as the range in concentration/dose (C/D) ratios, and the effect of sex and occasionally coprescribed CYP2D6 or CYP3A4 inhibitors/inducers was studied. In addition, the dose-concentration relationship and combined interquartile range of concentrations obtained at low dose (10-15 mg/day) and high dose (20-30 mg/day) were described. Individual C/D ratios ranged 37-fold for aripiprazole, 78-fold for dehydroaripiprazole, and 27-fold for the active sum of aripiprazole + dehydroaripiprazole. Median C/D ratios in male and female patients differed by less than 15%, and none of the differences were significant (P > 0.14). Cases of concurrent CYP3A4 inducers/inhibitors were not found, but three patients were coprescribed the potent CYP2D6 inhibitors paroxetine or fluoxetine. No consistent difference in C/D ratio was observed in these three patients compared with the rest of the patients. There was a proportional dose-concentration relationship in the population, and the combined interquartile ranges were 230 to 960 nmol/L for aripiprazole and 330 to 1210 nmol/L for aripiprazole + dehydroaripiprazole. In conclusion, pharmacokinetic variability of aripiprazole is extensive in psychiatric patients but apparently not dependent on dose or sex. The variability of the pharmacologic active sum of aripiprazole + dehydroaripiprazole is 25% to 30% less than aripiprazole, suggesting that variability of aripiprazole is partly determined by metabolism to dehydroaripiprazole.

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The influence of 5-HTTLPR on response to total sleep deprivation is similar to its observed influence on response to serotonergic drug treatments. This finding supports the hypothesis of a major role for serotonin in the mechanism of action of total sleep deprivation in depression.

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A computerized literature search was conducted in MEDLINE, PsycINFO, EMBASE, the Cochrane Library, and ClinicalTrials.gov to locate articles published in any language from the earliest available online year until October 2012, using the following phrase and Boolean logic algorithm: "hepatitis and c and (interferon-alpha OR peginterferon OR (pegylated and interferon)) and (depression OR mood) and (prevention OR prophylactic OR prophylaxis OR antidepressant)."

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Forty-nine patients aged 60+ years with confirmed PD(A) were randomly assigned to 40 mg paroxetine, individual CBT, or to a 14-week waiting list. Outcomes, with avoidance behaviour and agoraphobic cognitions being the primary measures, were assessed at baseline and at weeks 8, 14 (conclusion CBT/waiting list), and at week 26 (treated patients only) and analysed using mixed models.

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Within 1 class of medications, it is possible for a few agents to exhibit the Weber effect, while there is no definite pattern with others. A new observation in adverse event reporting is introduced and suggests that a peak in adverse event reporting occurs 1-2 years after a medication receives approval for a new indication. Future research is necessary to validate this effect and examine the generalizability to other medications.

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Nine-hundred five (905) patients taking sertraline, 492 on paroxetine, and 945 on fluoxetine met inclusion criteria. The groups were similar and representative with respect to gender and age. Mean dose over the 12-month treatment period increased 24%, indicating significant titration in all cohorts. Patients treated with paroxetine had shorter treatment duration (157.0 days) than did patients treated with fluoxetine (192.6 days) or sertraline (166.9 days, P < 0.001). Patients receiving index treatment with paroxetine were most likely to switch to another SSRI (21.3%); those taking sertraline were second most likely to switch (16.1%); and those on fluoxetine were least likely (12.4%, P = 0.001). Mean costs for depression-related outpatient visits and hospitalizations were similar. Mean antidepressant prescription costs differed, being $586, $419, and $446 for fluoxetine, paroxetine and sertraline cohorts, respectively (P < 0.001). In this sample, the fluoxetine cohort did not have lower nonpharmaceutical healthcare costs to offset higher pharmaceutical acquisition costs. Conclusions from median and multivariate analyses were robust to these findings.

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On the Whiteley Index, Helmert contrasts on the intent-to-treat and completer cohorts revealed that pooled CBT and paroxetine were significantly superior to placebo, but did not differ significantly from each other. The responder analysis on the intent-to-treat cohort and completer cohort, respectively, revealed the following percentages of responders per group: CBT group, 45% and 54%; paroxetine group, 30% and 38%; and placebo group, 14% and 12%. In the intent-to-treat analysis, only CBT differed significantly from the placebo. In the completer analysis, both paroxetine and CBT differed significantly from the placebo.

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Independent risk factors for obesity included cancer diagnosed at 5 to 9 years of age (relative risk [RR], 1.12; 95% CI, 1.01 to 1.24; P = .03), abnormal Short Form-36 physical function (RR, 1.19; 95% CI, 1.06 to 1.33; P < .001), hypothalamic/pituitary radiation doses of 20 to 30 Gy (RR, 1.17; 95% CI, 1.05 to 1.30; P = .01), and paroxetine use (RR, 1.29; 95% CI, 1.08 to 1.54; P = .01). Meeting US Centers for Disease Control and Prevention guidelines for vigorous physical activity (RR, 0.90; 95% CI, 0.82 to 0.97; P = .01) and a medium amount of anxiety (RR, 0.86; 95% CI, 0.75 to 0.99; P = .04) reduced the risk of obesity. Results of SEM (N = 8,244; comparative fit index = 0.999; Tucker Lewis index = 0.999; root mean square error of approximation = 0.014; weighted root mean square residual = 0.749) described the hierarchical impact of the direct predictors, moderators, and mediators of obesity.

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The use of antidepressants during pregnancy has undergone considerable scrutiny with respect to safety issues, though limited data with respect to dose management and symptom resolution is available. Previous reports on tricyclic antidepressants (TCAs) have demonstrated the need to adjust maternal dose later in pregnancy to maintain therapeutic serum concentrations. However, there is no data on the dosage of selective serotonin uptake inhibitors (SSRIs) required to maintain symptom resolution in women treated for major depression during pregnancy. The purpose of this study, then, was to assess the medication dosage requirements of SSRIs during this time. In this naturalistic study, pregnant women with a primary diagnosis of major depression were followed prospectively through pregnancy at monthly intervals with symptom assessment. Subjects were included in data analysis if they presented prior to 28 weeks gestation, were treated with SSRI monotherapy, received all psychiatric treatment during the pregnancy at the Emory Pregnancy and Postpartum Mood Disorders Program, and achieved euthymia after initial treatment intervention (CGI = 1 and Beck Depression Inventory (BDI) < 9) during pregnancy or failed to respond after eight weeks of treatment. Medication selection was based on personal treatment history or family treatment history (if any), and the published data on SSRIs in pregnancy. All medication dose adjustments were based on depressive symptoms as measured by the BDI and a psychiatric interview (ZNS). Thirty-four pregnant women were included in final analysis. Two thirds of the subjects (n = 22) required an increase in their daily dose of medication to maintain euthymia. The dose increases occurred at 27.1 +/- 7.1 weeks gestation, with mean BDI scores of 16.4 +/- 9.6, compared to a mean treatment response BDI of 6.9 +/- 5.4. Subject's age, education, past personal and familial psychiatric history were not significantly associated with dose adjustment. These novel data on SSRI daily dose in pregnancy parallels the extant literature with tricyclic antidepressants (TCA). Further work to determine the predictors of dose adjustments will provide guidelines for minimizing fetal exposure to both medication and maternal mental illness.

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Since a long-term administration of antidepressant drugs and mood stabilizers is required in the treatment of mood disorders, the regulation of gene expression by these drugs that is mediated by transcription factors, such as activator protein-1 (AP-1) complex, may play an important role in the therapeutic action. In this study, the authors investigated the influence of lithium, antidepressant drugs and stress on AP-1 binding activity in the rat brain. In addition, we examined pretreatment with these drugs on the expression of AP-1 binding activity in response to stress. A gel shift assay was used to measure the levels of AP-1 binding activity. Our results indicate that neither acute nor chronic treatment with antidepressant drugs affects in AP-1 binding activity in the rat frontal cortex or hippocampus. However, the authors found that acute restraint stress for 90 min upregulated the induction of AP-1 binding activity in the rat frontal cortex. In addition, chronic pretreatment with imipramine, but not lithium or paroxetine, downregulated the induction of AP-1 binding activity in response to acute restraint stress in the frontal cortex. The functional classification of antidepressant drugs based on the downregulation of restraint stress-induced AP-1 binding activity may contribute to the advances in our understanding of the pathogenesis of depression.

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To report a case of palmar-plantar hyperhidrosis (PPH) in which paroxetine was found to be helpful.

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Of 112 cases evaluated, 57 were males and 55 females whose ages ranged from 18 to 65 years. There was a clear and statistically significant efficacy of paroxetine on all the major outcome variables. A total of 88% patients achieved a reduction in the final HAMD-D score at the end of treatment. The total HAM-D score reduced to 10 or less in 73% patients at 6 weeks and by this week 76% and 92% patients achieved a score of 1 or 2 for CGI-S and CGI-I, respectively. The mean Clinical Anxiety Scale score reduced from 12.6 at the baseline to 4.4 at the end of treatment. Safety data was evaluated in all 112 patients and paroxetine was well tolerated. Adverse events were experienced by 10% of patients of whom 4% were dropped from the study. Nausea was the commonest adverse event reported.

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The treatment of geriatric depression is complicated by a variable and delayed response to antidepressant treatment. The present study was undertaken to test the hypothesis that combined total sleep deprivation and paroxetine treatment would produce a persistent reduction in glucose metabolism in the anterior cingulate cortex similar to that reported after long-term antidepressant treatment.

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prospective, randomized, 2-phase crossover.

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A total of 271 therapeutic drug monitoring (TDM) data were retrospectively collected from 127 psychiatric outpatients. A population nonlinear mixed-effects modeling approach was used to describe serum concentrations of paroxetine. For 83 patients with major depressive disorder, the treatment response rate and the incidence of adverse drug reaction (ADR) were characterized by logistic regression using daily dose or area under the concentration-time curve (AUC) estimated from the final model as a potential exposure predictor.

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A total of 116 depressed, type 2 DM patients were recruited for 12 weeks treatment. Patients were randomly assigned to receive either paroxetine or agomelatine. Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were used to assess depression and anxiety, respectively. Hemoglobin A1c, fasting plasma glucose, and body mass index were assessed at baseline and at the end of the trial.

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The aminomethylchroman derivative BAY x 3702 (R-(-)-2-¿4-[(chroman-2-ylmethyl)-amino]-butyl¿-1,1-dioxo-benzo[d] isothiazolone HCl) has recently been characterized as a relatively selective, high affinity 5-HT1A receptor agonist with neuroprotective, anxiolytic- and antidepressant-like effects in animal models. It was the aim of the present study to further confirm its receptor binding profile in an in vivo assay. Rats were trained to discriminate BAY x 3702 (0.1 mg/kg, i.p.) from vehicle in a standard two-lever fixed ratio 10 food-reinforced procedure. All rats learned the discrimination, the median number of sessions to reach criterion being 38 (range: 22-58 sessions). Generalization tests with BAY x 3702 showed dose-dependent and complete generalization after different routes of administration; the ED50 values being: 0.030, 0.007 and 0.36 mg/kg, after i.p., i.v. and p.o. administration, respectively. Assessment of the duration of action after administration of 0.1 mg/kg BAY x 3702, i.p., resulted in a T1/2 of 65 min. Dose-dependent and complete generalization was also obtained with the 5-HT1A receptor agonists 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)-tetralin, ED50 in mg/kg, i.p.: 0.086), flesinoxan (0.30), SR 57746A ((4-(3-trifluoromethylphenyl)-N-(2-(naphth-2-yl)ethyl)-1,2,3,6-tet rahydropyridine HCl, 1.0), the (+)-enantiomer of BAY x 3702 (1.3) and ipsapirone (1.8); the ED50 values being closely correlated with their respective affinities for the 5-HT1A receptor. Pretreatment with the selective 5-HT1A receptor antagonist WAY-100635 ((N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N(2-pyridinyl) cyclohexane carboxamide trihydrochloride) dose-dependently and completely blocked the discriminative effects of 0.1 mg/kg BAY x 3702 (ID50: 0.013 mg/kg, i.p.). WAY-100635, prazosin, idazoxan, raclopride, paroxetine, (-)-BAY k 8644 (methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoro-methyl-phenyl)-p yridine-5-carboxylate), ethanol, and the putative neuroprotectants MK-801 ((+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imin e), CNS 1102 (N-(1-naphthyl)-N'-(3-ethylphenyl)-N'-methyl-guanidine), CGS 19755 (cis-4-(phosphonomethyl) piperidine-2-carboxylic acid) and nimodipine did not induce more than 20% generalization. It is concluded that the BAY x 3702 cue is mediated by its agonistic activity at 5-HT1A receptors.

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Depression is frequently a recurrent and sometimes a chronic illness. Unfortunately, most research on treatment has focused almost exclusively on the short-term. For example, the majority of clinical trials of medications and psychotherapeutic approaches last only 6 to 16 weeks. Relatively little research has been conducted on continuation treatment (usually 3-6 months) to prevent relapses and on maintenance treatment (6-24 months) to prevent recurrences. This paper will review continuation and maintenance phase pharmacotherapeutic trials and will make recommendations for clinical treatment of patients during these periods.

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The ability to revise one's action plans, as reflected in so-called stopping performance, is of fundamental importance to adaptive behavior. Previous studies in children and adults with attention-deficit/hyperactivity disorder (ADHD) have revealed impaired stopping, which improved after the administration of methylphenidate (MPH). Event-related brain potentials revealed that one crucial mechanism in adequate stopping is the link between the cortical areas that process the signal to stop and the motor system (stop N1). This stop N1 was severely compromised in adults with ADHD. The present study investigates whether methylphenidate can restore the stop N1, in addition to improving stopping performance. The acute effect of a serotonergic reuptake inhibition on these parameters was also assessed.

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Two patients (5%) refused CBT after 1 session, and 10 patients (28%) dropped out of the study. Three of the 24 remaining patients completed the trial at 6 months (T1) but did not follow through up to 12 months (T2). The 21 patients completing CBT showed statistically significant improvement (p < .0001) during follow-up on all outcome measures. At T2, 15 (42%) of 36 patients were rated as being "much improved" or "very much improved," as measured by the CGI-I. Symptom reduction was clinically modest but important, with nearly all patients presenting residual symptoms.

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Restraint produced a significant increase in serum corticosterone of stressed rats. The proliferative response to Con A was similar in the controls and stressed animals. Fluoxetine reduced cell proliferation with and without Con A. Restraint diminished the inhibitory effect of fluoxetine on proliferation. Restraint also increased Bmax and Kd, but decreased nH. Treatment of rats with actinomycin D, a transcription inhibitor, reduced Bmax in stressed animals.

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We treated animals with a binge-like regimen of methylone or mephedrone (30 mg/kg, twice daily for 4 days) and, starting 2 weeks later, we performed behavioral tests of memory, anxiety and depression and measured brain levels of dopamine (DA), serotonin (5-HT), their metabolites and norepinephrine (NE). 5-HT and DA transporter (5-HTT and DAT) levels were also measured in rats by [(3)H]paroxetine and [(3)H]mazindol binding.

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The four subscales (core mood, anxiety, insomnia, and somatic) and individual items from the Hamilton Rating Scale for Depression-17 were the focus of this study. These measures were assessed at baseline and Week 8.

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The effects of psychological stress on serotonin (5-HT) release were studied in the basolateral amygdaloid nucleus and the prefrontal cortex in conscious rats with in vivo microdialysis. Psychological stress, wherein emotional factors were predominantly involved, significantly increased extracellular 5-HT levels in these two areas. These findings suggest that activation of serotonergic neurons in these brain regions is involved in the emotional and/or cognitive states in animals.

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paxil depression medication 2015-06-02

Clinicians who treat major depression are faced with a bewildering choice of antidepressants. Given that all have a lag period before they are effective, choice of the right antidepressant can potentially minimize the duration of symptoms, reduce cost and enhance compliance. Unfortunately, there is very little evidence upon which to base such a decision. We developed a treatment algorithm for non-psychotic, unipolar major depression, and applied it in our clinic. It includes progression from a specific serotonin reuptake inhibitor (SSRI), usually fluoxetine, from a dose of 20 mg to a dose of 40 mg in patients who do not respond. Non-responders to this dose receive augmentation with triiodothyronine (T3, 25-50 microg). All interventions are for fixed time periods and guided by overall clinical improvement as defined by the Clinical Global Inventory. Ninety patients commenced open-label treatment with 20 mg SSRI (fluoxetine, n=81; paroxetine, n=9). Seventy-four patients completed 4 wk of treatment and 44 (48.9%) were responders (intent to treat analysis). Raising the SSRI dose to 40 mg for a further 2 wk was effective in only 5 patients (16.6%). Non-responders to SSRI were significantly more depressed at baseline as reflected by their rating scales scores. Addition of T3 was effective in 10 out of 16 women (62.5%) while none of the 9 males responded. Although values were within the normal range, patients who responded to T3 had higher serum thyroid-stimulating hormone levels than those who did not. Our experience with algorithm-based treatment of unipolar, non-psychotic major depression in outpatients suggests that more than 40% of patients will not respond to initial buy paxil treatment with an SSRI even when the dose is increased to 40 mg/d; that severity of depression may be an important predictor of response and that T3 may be useful as an augmenter of response in SSRI non-responders but may be less effective in men than in women. The effect of T3 may be related to thyroid function even within the normal range.

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Depression related cognitive deficits are frequently considered as simple epiphenomena of the disorder. However, whether or not the depression might directly bring about cognitive deficits is still under investigation. This study was to buy paxil investigate the distinct pattern of cognitive deficits in patients with depression by comparing the cognitive function before and after anti-depressive drug therapy.

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A patient with a 30-year history of somnambulism and night terrors is buy paxil described. The use of a home ambulatory sleep electroencephalogram (EEG) recording in clarifying the diagnosis and in monitoring the results of treatment is illustrated and successful treatment using a selective serotonin re-uptake inhibitor is reported.

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Acupuncture appears to have promise for treating male sexual dysfunction, but in view of the small number of studies and their variable quality, doubts remain about buy paxil its effectiveness. Further studies are justified.

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A simple, rapid and sensitive procedure using gas chromatography with electron-capture detection to measure paroxetine levels in human plasma has been developed. The analyte was extracted from plasma with ethyl acetate after basification of the plasma and then derivatized with heptafluorobutyric buy paxil anhydride before gas chromatographic separation. The calibration curves were linear, with typical r2 values >0.99. The assay was highly reproducible and gave peaks with excellent chromatographic properties.

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Our results suggest that the USP46 gene might buy paxil play a role in the pathophysiology of MDD in the Japanese population.

paxil tablets 2016-11-15

Recent evidence has shown that prenatal maternal stress has negative consequences for the mental health of the adult organism. Our aim was to examine the efficacy of using the selective serotonin reuptake inhibitor, paroxetine, to alleviate the symptoms of prenatal maternal stress in Fisher 344 rats. Pregnant rats were subjected to daily restraint stress and concurrent paroxetine treatment (10 mg/kg p.o.) during the last week of gestation. Maternal paroxetine treatment led to a shortened gestational buy paxil length, reduced birth weight and a 10-fold rise in neonatal mortality in both stressed and non-stressed litters. These results reiterate the need for further research on the effects of paroxetine treatment during gestation.

paxil dosage reduction 2017-03-04

The selective 5-hydroxytryptamine (5-HT) uptake inhibitor, [3H]paroxetine, has been used as a specific probe in a series of experiments aimed at characterizing the substrate and 5-HT uptake inhibitor binding domains on the neuronal sodium-ion-coupled 5 buy paxil -HT transporter. In addition, an affinity-chromatographic protocol which provided a greater than 3000-fold purification of this neuronal transporter protein is outlined.

paxil starting dose 2015-08-11

Based on a literature review, a 47-question survey with 1,411 options was developed. Approximately three quarters of the options were scored using a modified version of the RAND 9-point scale for rating appropriateness of medical decisions. For other options, experts were asked to write in answers. The survey was sent to 52 American experts on buy paxil treatment of older adults (38 geriatric psychiatrists, 14 geriatric internists/family physicians), 48 (92%) of whom completed it. In analyzing responses to items rated on the 9-point scale, consensus was defined as a nonrandom distribution of scores by chi-square "goodness-of-fit" test. We assigned a categorical rank (first line/preferred, second line/alternate, third line/usually inappropriate) to each option based on the 95% confidence interval around the mean. Guidelines indicating preferred treatment strategies were then developed for key clinical situations.

paxil good reviews 2015-04-21

This is a randomized, 10-week, controlled, parallel group, pilot study. A total of 75 outpatients with buy paxil panic disorder with or without agoraphobia (DSM-IV and ICD-10) received either (1) exercise plus paroxetine 40 mg/day (n=21), (2) relaxation plus paroxetine (n=17), (3) exercise plus pill placebo (n=20), or (4) relaxation plus pill placebo (n=17). Changes in the Panic and Agoraphobia Scale (P&A), and the Clinical Global Impression Scale (CGI) underwent repeated measure analysis.

paxil recommended dosage 2015-04-20

Randomised, placebo controlled trials involving adult patients with confirmed OSA. We excluded trials if continuous positive airways pressure, mandibular devices or oxygen therapy were used. We excluded studies investigating treatment buy paxil of associated conditions such as excessive sleepiness, hypertension, gastro-oesophageal reflux disease and obesity.

paxil dosage 2016-09-18

Numerous lines of evidence suggest that heterocyclic compounds used as analgesic, anti-inflammatory and anti-migraine agents can be potent regulators of the nitroxidative stress and targeting free nitrogen and oxygen radicals is a very promising strategy for future pain management. Both classical analgesics (nonsteroidal anti-inflammatory drugs, opioid drugs) and many analgesic adjuvants, including desipramine, duloxetine, fluoxetine, paroxetine, escitalopram, phenytoin or carbamazepine and α-lipoic acid can modulate the balance between pro-oxidant and antioxidant processes in the mammalian tissues and these properties of drugs such as indomethacin, meloxicam, tenoxicam, valdecoxib or some metabolites of analgesic drugs formed by the activity of tissue peroxidases may contribute to their buy paxil clinical efficacy and drug-related toxic effects, including gastrointestinal ulcers, hepatic failure, agranulocytosis, aplastic anemia, neutropenia, opiate-induced hyperalgesia and tolerance. The antioxidant capacities of novel heterocyclic compounds, including the compounds acting either by prevention of formation or catalyzed decomposition of peroxynitrite anion (ONOO-), namely the peroxynitrite decomposition catalysts or as superoxide (O2 •-)-scavengers which are the functional mimetics of superoxide dismutase (SOD) enzymes (SODm), as well as the derivatives of 6-nitro-3,4-methylenedioxyphenyl-Nacylhydrazone (LASSBio-881) or γ-butyrolactone (LPP1, BM113, BM113A, BM138 and BM138A) are also discussed as potent and promising future heterocyclic analgesics.

paxil generic cost 2016-04-06

Depression in the elderly is an increasingly prevalent problem affecting some 15% of the elderly population and can be difficult to diagnose and treat. Complicating factors include poor compliance, the high frequency of concomitant disease, and the alterations in drug absorption and metabolism with age. This paper reviews controlled studies of the treatment of depression in elderly patients using paroxetine, a selective serotonin reuptake inhibitor. The studies demonstrate that paroxetine has efficacy in buy paxil these patients which is similar to that of comparative compounds. The side effect profile of paroxetine is favourable, as compared with tricyclics, in terms of cardiovascular effects. The side effects of paroxetine in the elderly are similar to those reported in younger individuals. The improved tolerability profile of paroxetine is particularly welcome for the treatment of the elderly who have an increased sensitivity to adverse effects of drug therapy.

paxil positive reviews 2016-12-26

Paroxetine is a commonly used antidepressant with a safe side-effect profile. A case of paroxetine overdose (560 mg) is reported in an 18-year-old female who attempted suicide and recovered without any sequelae, requiring only supportive treatment. This report highlights a case of pure paroxetine overdose and buy paxil the safety profile of paroxetine in overdose.

paxil reviews 2015-10-21

To compare the safety and antidepressant efficacy of paroxetine, imipramine, and placebo, data from six centres using the same protocol were pooled. A double-blind parallel-group design was used, with therapy lasting six weeks. From week 2 onwards, both the 240 paroxetine-treated and the 237 imipramine-treated patients were significantly different from the 240 placebo-treated patients, but no different from each other. Side-effects with paroxetine were Mysoline Medicine less likely to lead to drop-out than with imipramine. Paroxetine had a possible earlier antidepressant effect than imipramine, and a possible earlier beneficial effect on anxiety symptoms associated with depression.

paxil cr generic 2015-12-12

The patients' scores on a 13-item version of the Hamilton Depression Rating Scale were decreased after total sleep deprivation, after recovery sleep, and after 2 weeks of treatment. The Hamilton depression scores of the comparison subjects were not significantly altered. In the patients, the greatest reductions in normalized, relative glucose metabolism after sleep Medicine Depakote deprivation were observed in the anterior cingulate cortex (Brodmann area 24), and they persisted after recovery sleep and antidepressant treatment. The comparison subjects demonstrated increased metabolism in these areas.

paxil xr generic 2017-09-20

A total of 93 600 prescriptions were issued for fluoxetine, paroxetine and sertraline, in 27 210 treatment episodes. Over the 5-year period, there was a five-fold increase in the number of prescriptions issued, and a four-fold increase in the number of patients treated, reflecting a trend for longer periods of treatment. Patients initiating treatment with fluoxetine were most likely Trileptal Yellow Pill and those initiating treatment with sertraline were least likely to complete 60, 90 and 120 consecutive days of treatment. Differences in dose patterns also emerged and were consistent throughout the study. Fluoxetine-treated patients were most likely to remain on the starting dose of 20mg daily, while large numbers of sertraline-treated patients received doses above the recommended dose of 50mg daily. These differences were not apparent from clinical trials, and this may be an artefact of trial design.

paxil 20 mg 2015-01-27

Besides the improvement of the depressive symptoms (HAMD scores decreased from 22.6 Generic Vantin 100mg to 3.8; and CGI-S scores from 4.7 to 1.3), the scores of work productivity and life satisfaction also significantly decreased (SAS scores from 2.8 to 1.3, SDS scores from 18.2 to 2.8, and LS scores from 14.9 to 7.1, respectively). Following the acute treatment period, work productivity and life satisfaction further continuously improved till the end of the maintenance treatment phase.

paxil cost 2016-10-25

This study was designed to examine neuroendocrine predictors of antidepressant response to the selective serotonin reuptake inhibitor (SSRI) paroxetine. We assessed the prognostic utility of the apomorphine stimulation test by examining the relationship between pretreatment change in growth hormone (GH) Zantac 6 Tablets following apomorphine and acute response to paroxetine treatment. We hypothesized that those subjects with most marked pretreatment dopaminergic supersensitivity, as manifested by greatest change in GH, would be most likely to show an early antidepressant response and would also be more likely to develop manic or hypomanic symptoms on paroxetine. Contrary to our hypothesis, greater dopamine postsynaptic sensitivity was associated with greater resistance to paroxetine treatment. In our sample of 13 subjects with a major depressive episode, pretreatment GH response to apomorphine per unit weight was inversely correlated with change in Hamilton depression rating scale following 6 weeks of paroxetine. Within the group of subjects who showed mood elevation on paroxetine, there was a trend towards greater GH response being associated with slower antidepressant response. With regard to the development of manic or hypomanic symptoms on paroxetine, change in GH per unit weight not did distinguish the two subjects who subsequently developed paroxetine-induced hypomania from other subjects. The seven subjects with previous antidepressant-induced hypomania did not differ from the other subjects in change in GH response per unit weight. The finding that subjects who had low dopamine receptor responsivity pretreatment were more likely to have an antidepressant response with paroxetine is consistent with recent suggestions that the therapeutic effect of SSRIs may be mediated through increased dopamine receptor sensitivity in the mesolimbic system. Further work assessing pretreatment and post-treatment GH response to apomorphine will help to test the hypothesis that low dopamine receptor responsivity predicts antidepressant response to SSRIs.

paxil xr dosage 2015-03-02

We randomised 49 mildly depressed primary care outpatients Pill Cialis Soft with non-optimally controlled diabetes to a 6-month double-blind treatment with either paroxetine 20 mg per day or matching placebo. Primary efficacy measurements were quality of life and glycaemic control. The primary global outcome of the study was defined as a 10 points improvement in the SF-36 quality of life score. The primary metabolic outcome of the study was defined as a 0.8%-units decrease in glycosylated haemoglobin A1c(GHbA1c). Psychiatric symptoms were assessed with the Hospital Anxiety and Depression Scale.

paxil usual dosage 2015-04-01

Included were 14,902 pregnancies for which complete pharmacy records were available from 3 months before pregnancy until delivery. A total of 310 pregnancies were exposed to an SSRI in the year preceding delivery. The exposure rate increased from 12.2 (95% CI 7.0, 19.8) in 1995/1996 to 28.5 (95% CI 23.0, 34.9) in 2003 Claritin Mg Dosage /2004.

paxil generic names 2017-07-13

The effect of light therapy on serotonin uptake capacity in patients suffering from winter Clomid Reviews 2015 depressions (seasonal affective disorders) was examined indirectly by using [3H]paroxetine binding to determine the number of platelet serotonin transporters. In patients who responded to light therapy the number of platelet serotonin transporters decreased significantly following treatment. In contrast, patients who did not respond to light therapy were found to have a relatively low number of serotonin transporters prior to treatment, and the number did not change significantly following treatment.

paxil yellow pill 2015-08-07

In the current analysis due to the mechanism of effect, we evaluated the treatment benefit of duloxetine 40 mg comparing with paroxetine Naprosyn Dosage Maximum 20 mg, based on its effects on personal distress and interpersonal difficulty related to ejaculation, perceived control over ejaculation, and satisfaction with sexual intercourse, as well as the patient-reported global impression of change in premature ejaculation (PE) and the effect on intravaginal ejaculatory latency times (IELT) in men with premature ejaculation.

paxil generic 2015-03-02

A group of 50 subjects took part in the study. The MMPI-2 test and HDRS were used in Singulair 10mg Dosage the study. The HDRS was performed at the therapy onset and reapplied after 8 weeks of its continuation. The MMPI-2 test was applied at the beginning of treatment.

paxil medication 2015-07-20

There have been inconsistent findings from randomised controlled trials (RCTs) and systematic reviews on the efficacies of selective serotonin reuptake inhibitors (SSRIs) as the first-line treatment of major depressive disorder (MDD). Besides inconsistencies among randomised controlled trials (RCTs), their risks of bias and evidence grading have seldom been evaluated in meta-analysis. This study aims to compare the efficacy of SSRIs by conducting a Bayesian network meta-analysis, which will be the most comprehensive evaluation of evidence to resolve the inconsistency among previous studies.