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Paxil (Paroxetine)

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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:
Aropax, Casbol, Deroxat, Divarius, Eutimil, Frosinor, Motivan, Parotur, Paroxat, Paroxetina, Paroxetinum, Pexep cr, Pexeva, Sereupin, Seroxat, Tagonis, Xet

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Also known as:  Paroxetine.


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.


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.


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.


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.


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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Depression in late life carries an increased risk of dementia and brittle response to treatment. There is growing evidence to support a key role of the serotonin type 1A (5-HT(1A)) receptor as a regulator of treatment response, particularly the 5-HT(1A) autoreceptor in the dorsal raphe nucleus (DRN). We used [11C]WAY 100635 and positron emission tomography (PET) to test our hypothesis that 5-HT(1A) receptor binding in the DRN and prefrontal cortex is altered in elderly depressives and that these measures relate to treatment responsivity. We studied 17 elderly subjects with untreated (nonpsychotic, nonbipolar) major depression (four men, 13 women; mean age: 71.4+/-5.9) and 17 healthy control subjects (eight men, nine women; mean age: 70.0+/-6.7). Patients were subsequently treated with paroxetine as part of a clinical trial of maintenance therapies in geriatric depression. [11C]WAY 100635 PET imaging was acquired and binding potential (BP) values derived using compartmental modeling. We observed significantly diminished [11C]WAY 100635 binding in the DRN in depressed (BP = 2.31+/-0.90) relative to control (BP = 3.69+/-1.56) subjects (p = 0.0016). Further, the DRN BP was correlated with pretreatment Hamilton Depression Rating Scores (r = 0.60, p = 0.014) in the depressed cohort. A trend level correlation between DRN binding and time to remission (r = 0.52, p = 0.067) was observed in the 14 depressed patients for whom these data were available. Our finding of decreased [11C]WAY 100635 binding in the brainstem region of the DRN in elderly depressed patients supports evidence of altered 5-HT(1A) autoreceptor function in depression. Further, this work indicates that dysfunction in autoreceptor activity may play a central role in the mechanisms underlying treatment response to selective serotonin reuptake inhibitors in late-life depression.

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Extra-pyramidal syndromes in elderly subjects with cognitive impairment are difficult to interpret. The possible causes include interactions between acetylcholinesterase inhibitors, neuroleptics and serotonine reuptake inhibitors and Lewy body dementia.

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Data were pooled from 8 double-blind, randomized, placebo- and active comparator-controlled trials employing patients with MDD that were submitted to the US Food and Drug Administration to support duloxetine's new drug application for treatment of MDD.

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We used hand-held computers to obtain repeated "online" measurements of eating behaviors, moods, and self-concepts in 21 women with bulimic syndromes, and modeled 5-HT system activity with a measure of platelet [3H]paroxetine-binding density.

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The serotonergic system and the orbitofrontal cortex have been consistently implicated in the pathophysiology of obsessive compulsive disorder. Yet, the relations between these two systems and the ways they interact in producing obsessions and compulsions are poorly understood. The present study tested the hypothesis that pathology of the orbitofrontal cortex leads to a dysregulation of the serotonergic system which is manifested in compulsive behavior, using a new rat model of this disorder. In the model, 'compulsive' behavior is induced by attenuating a signal indicating that a lever-press response was effective in producing food. We found that lesion to the rat orbital cortex led to a selective increase in compulsive lever-pressing that was prevented by the serotonin re-uptake inhibitor, paroxetine, and was paralleled by an increase in the density of the striatal serotonin transporter, assessed using high affinity [3H]imipramine binding. These results suggest that the serotonergic system is involved in orbital lesion-induced compulsivity, and provide a possible account for the observed association between obsessions and compulsions and dysfunction of the orbitofrontal cortex and of the serotonergic system in obsessive compulsive disorder.

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The empirical use of methylphenidate added to ineffective or only partially effective SSRI treatment appeared to be a rapid, safe, and efficacious alternative to existing augmentation strategies for the treatment of major depression. Prospective controlled studies are required to confirm or refute these findings.

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Insomnia and depression are widespread diseases causing deterioration of life's quality and increasing morbidity and mortality of cardiovascular diseases. Both of them and certain antidepressants adversely affect physiological structure of sleep, while others restore it. The latter drugs must be preferred in therapy of depression accompanying insomnia, and some of them may be effective in treatment of insomnias without depression. Most antidepressants cause REM-reduction, generally with increased serotonin-function. Selective H1-antagonists readily induce sleep, and also the inhibition of cholinergic neurons in the general arousal networks promotes sleep. Sleep continuity is improved by the rise of synaptic level of serotonin. Among tricyclic antidepressants trimipramine and amitriptyline are the best to improve sleep. However, the former has low antidepressant effect and the latter has many adverse side effects. Selective serotonin reuptake inhibitors, except paroxetine, improve sleep only at the time and to the extent of restoring depression. Paroxetine has beneficial effect on sleep at the beginning of the treatment. Mirtazapine is the first-line sleep promoter among atypical antidepressants, however, its effect on increasing appetite markedly limits its application. Trazodone causes hangover, and mianserin may induce restless legs. Insomnias without depression demand lower dose of antidepressants than depression.

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Antidepressants probably exert tandem neurochemical effects by increasing synaptic monoamine concentrations and by producing phosphoinositides used in 5HT(2) receptor signaling. This combination of actions may constitute the mechanism of at least the acute behavioral effects of the drugs and could implicate aberrant neurolipid signaling in the pathophysiology of depression.

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Paroxetine may be a useful option in the treatment of PPH.

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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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paxil with alcohol 2016-07-27

No baseline differences among Swiss, NMRI, DBA/2 and C57BL/6J Rj strains were observed in our experiments, allowing the comparison of different antidepressants in each strain. Imipramine (16 mg/kg), desipramine, citalopram (4-16 mg/kg) and paroxetine (8 Depakote Er Maximum Dosage and 16 mg/kg) treatment decreased the immobility time in the Swiss strain and the size of the effect reached more than 20% for each of these antidepressants. C57BL/6J Rj was the only strain sensitive to bupropion (2 and 4 mg/kg). In the NMRI strain, only paroxetine treatment decreased the immobility time (16 mg/kg).

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A total of 2687 patients were included in the analyses (escitalopram n = 1345, conventional SSRIs n = 1102, venlafaxine XR n = 240). Escitalopram was superior to all comparators in overall treatment effect, with an estimated difference in treatment effect of Risperdal 4 Mg Kullananlar 1.07 points (95% confidence interval [CI] 0.42-1.73, p < 0.01), and in response (odds ratio [OR] 1.29, 95% CI 1.07-1.56, p < 0.01) and remission (OR 1.21, 95% CI 1.01-1.46, p < 0.05) rates. In analysis by medication class, escitalopram was significantly superior to the SSRIs and comparable to venlafaxine, although the overall results do not necessarily reflect a significant difference between escitalopram and individual SSRIs. These results were similar in the severely depressed population (patients with baseline MADRS > or = 30). The withdrawal rate due to adverse events was 6.7% for escitalopram compared with 9.1% for the comparators (p < 0.05).

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Field potential duration (FPD) in human-induced pluripotent stem cell Stromectol Online Canada -derived cardiomyocytes (hiPS-CMs), which can express QT interval in an electrocardiogram, is reported to be a useful tool to predict K(+) channel and Ca(2+) channel blocker effects on QT interval. However, there is no report showing that this technique can be used to predict multichannel blocker potential for QT prolongation. The aim of this study is to show that FPD from MEA (Multielectrode array) of hiPS-CMs can detect QT prolongation induced by multichannel blockers. hiPS-CMs were seeded onto MEA and FPD was measured for 2min every 10min for 30min after drug exposure for the vehicle and each drug concentration. IKr and IKs blockers concentration-dependently prolonged corrected FPD (FPDc), whereas Ca(2+) channel blockers concentration-dependently shortened FPDc. Also, the multichannel blockers Amiodarone, Paroxetine, Terfenadine and Citalopram prolonged FPDc in a concentration dependent manner. Finally, the IKr blockers, Terfenadine and Citalopram, which are reported to cause Torsade de Pointes (TdP) in clinical practice, produced early afterdepolarization (EAD). hiPS-CMs using MEA system and FPDc can predict the effects of drug candidates on QT interval. This study also shows that this assay can help detect EAD for drugs with TdP potential.

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The alpha(2)-adrenoreceptor antagonist mirtazapine, which is also a 5-HT(2), 5-HT(3) and H(1) receptors antagonist and the selective serotonin (5-HT) reuptake inhibitor paroxetine are effective antidepressant drugs which enhance 5-HT neurotransmission via different mechanisms. The present studies were undertaken to determine whether the mirtazapine-paroxetine combination could induce an earlier and/or a greater effect on the 5-HT system than either drug alone. Using in vivo electrophysiological paradigms, the firing activity of dorsal raphe 5-HT neurons was decreased by 70% in rats treated with paroxetine (10 mg Cheap Botox Los Angeles /kg/day, s.c.) for 2 days and was back to normal after 21 days. In contrast, a 2-day treatment with mirtazapine (5 mg/kg/day, s.c.) did not alter the firing of 5-HT neurons whereas it was increased by 60% after 21 days of treatment. A low dose of mirtazapine (5 mg/kg/day, s.c.x2 days) failed to offset the decremental effect of paroxetine on the 5-HT neuron firing activity, but a higher dose (10 mg/kg/day, s.c.x2 days) did attenuate the decremental effect of paroxetine. In the dorsal hippocampus, neither mirtazapine (5 mg/kg/day, s.c.) nor a paroxetine (10 mg/kg/day, s.c.) treatment altered the responsiveness of 5-HT(1A) receptors to microiontophoretically-applied 5-HT. Both in controls and in rats treated for 2 days with paroxetine alone, the administration of the 5-HT(1A) antagonist WAY 100635 (25-100 microg/kg, i.v.) did not change the firing activity of dorsal hippocampus CA(3) pyramidal neurons. However, WAY 100635 increased significantly the firing activity of these neurons in rats treated with mirtazapine alone but to a greater extent with both mirtazapine and paroxetine for 2 days. After 21 days of treatment, WAY 100635 increased to a greater degree the firing rate of CA(3) pyramidal neurons in rats which received the combination over rats given either drug alone. It is concluded that the mirtazapine-paroxetine combination shortened the delay in enhancing the tonic activation of postsynaptic 5-HT(1A) receptors and produced a greater activation of the postsynaptic 5-HT(1A) receptors than either drug given alone. The present results suggested that mirtazapine may have a faster onset of action than a SSRI, and that the co-administration of mirtazapine and paroxetine may accelerate the antidepressant response and as well as being more effective than either drug alone.

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STEP-BD was conducted from 1998 to 2005, enrolling participants (n = 4361) across 22 clinical sites in the United States. Each individual was followed for up to 2 years in naturalistic practice with blinded research assessments, while subgroups participated in randomized controlled trials (RCTs) for bipolar depression. The naturalistic database Nexium Starting Dose was used to examine the course of BD, comorbidity with other psychiatric disorders, and suicidality. Relevant studies in English, published from January 1, 1994, to May 31, 2009, were identified using computerized searches of electronic databases (PubMed, PsycINFO, and Cochrane Register of Clinical Trials), inspection of bibliographies, and review of other major reports.

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The three treatment groups showed statistically significant improvements. In some measures, combined treatment groups showed greater improvements. The virtual reality Zetia 10 Mg Dosage exposure group showed greater improvement confronting phobic stimuli.

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The 2002 paper "Does 5-HT restrain panic? A tryptophan depletion study in panic disorder patients recovered on paroxetine" by Bell and colleagues - reprinted in this issue of the Journal - reports on a study undertaken in the halcyon days of David Nutt's Psychopharmacology Unit at Ayurslim Capsules Results the University of Bristol, England. In this invited commentary authors of the original work discuss the impact of this paper on the field of acute tryptophan depletion research (especially in the field of clinical anxiety disorders) and the development of disorder-specific anxiogenic provocations over the past decade.

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The increase in resting pupil diameter could be indicative of parasympathetic inhibition and/or sympathetic activation. The shortening of the recovery time of the light reflex response is consistent with sympathetic potentiation resulting from noradrenaline uptake blockade in the iris. The prolongation of the latency and decrease of the amplitude of the light reflex response are indicative of a parasympatholytic effect of venlafaxine. However, as venlafaxine has negligible affinity for muscarinic cholinoceptors, this effect cannot be attributed to the blockade of cholinoceptors in the iris. A possible explanation for this finding is that it reflects a central rather than a peripheral effect of the drug: the blockade of noradrenaline uptake in the brain could lead to the potentiation of the noradrenergic inhibition of central parasympathetic (Edinger- Lasix Generic Name And Classification Westphal) neurones. These results demonstrate the ability of therapeutically relevant single doses of venlafaxine to potentiate noradrenergic responses in man, consistent with the blockade of noradrenaline uptake.

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The efficacy of JG combined Paroxetine for treating Zantac Drug Class RD patients of YDIHS was superior to that of using Paroxetine alone.

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Both paroxetine and imipramine reduced the MADRS and the Clinical Global Impression (CGI) severity-of-illness and global improvement scores at weeks 2, 4, 8 and at endpoint, with no significant differences between treatment groups at any timepoint (MADRS, p > or = 0.368; cgi, p > or = 0.286). There was a statistically significant difference in favour of paroxetine at both the week 4 and week 8 timepoints (analysis of variance, p < or = 0 Myambutol Medicine .049) in the Cornell scale for depression in dementia: at endpoint there was no significant difference between treatments (p = 0.103). Treatment-emergent adverse experiences were reported by 51.5% (51/99) of patients treated with paroxetine and 50.5% (50/99) of patients treated with imipramine. Anticholinergic adverse experiences (paroxetine 6.1%; imipramine 13.1%) and serious non-fatal adverse experiences (paroxetine 4.0%; imipramine 8.1%) were reported by more patients in the imipramine group than in the paroxetine group.

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A dramatic acceleration of the enantioselective copper-catalyzed conjugate reduction of alpha,beta-unsaturated lactones, lactams, and esters is reported Vigrx Capsule Benefits upon addition of alcohol additives. Good to excellent yields and enantioselectivities were realized using a catalyst generated in situ from CuCl(2).H(2)O, t-BuONa, p-tol-BINAP, and PMHS, and this methodology was applied to the synthesis of (-)-Paroxetine.

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Compulsive hoarding is a common and often disabling neuropsychiatric disorder. This article reviews the conceptualization, phenomenology, diagnosis, etiology, neurobiology, and treatment of compulsive hoarding. Compulsive hoarding is part of a discrete clinical syndrome that includes difficulty discarding, urges to save, excessive acquisition, indecisiveness, perfectionism, procrastination, disorganization, and avoidance. It was thought to be part of obsessive-compulsive disorder or obsessive-compulsive personality disorder, but recent evidence indicates that it should be classified as a separate disorder with its own diagnostic criteria. Compulsive hoarding is a genetically discrete, strongly heritable phenotype. Neuroimaging and neuropsychological studies are elucidating its neurobiology, implicating dysfunction of ventral and medial prefrontal cortical areas that mediate decision-making, attention, and emotional regulation. Effective treatments include pharmacotherapy and cognitive-behavioral therapy. More research will be required to determine the prevalence, etiology, and pathophysiology of compulsive hoarding and to develop better treatments.

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Structured searches of PubMed, Medline and Embase conducted in March 2008.