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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.