Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Other names for this medication:
Also known as: Atomoxetine.
Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Generic Strattera is a selective norepinephrine reuptake inhibitor. Exactly how Generic Strattera works to treat ADHD is not known. Generic Strattera increases certain chemicals (e.g., norepinephrine) in the brain. This may affect attention span and behavior.
Strattera is also known as Atomoxetine, Attentrol, Tomoxetin, Attentin, Axepta.
Generic name of Generic Strattera is Atomoxetine.
Brand name of Generic Strattera is Strattera.
Take Generic Strattera by mouth with or without food. If stomach upset occurs, take with food to reduce stomach irritation.
Swallow Generic Strattera whole. Do not open or take the capsules apart.
Taking Generic Strattera at the same time each day will help you remember to take it.
If you want to achieve most effective results do not stop taking Generic Strattera suddenly.
If you overdose Generic Strattera and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medication after the expiration date. Keep out of the reach of children.
The most common side effects associated with Strattera are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Strattera if you are allergic to Generic Strattera components.
Do not take Generic Strattera if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not Generic Strattera if you are taking or have taken a monoamine oxidase inhibitor (MAOI) (e.g., phenelzine) within the last 14 days.
Do not Generic Strattera if you have certain heart problems (e.g., heart defect, heart failure), certain types of irregular heartbeat, severe blood vessel problems, or narrow-angle glaucoma.
Children and teenagers who take Generic Strattera may be at increased risk for suicidal thoughts or actions. Adults may also be affected. The risk may be greater in patients who have had suicidal thoughts or actions in the past. The risk may also be greater in patients who have had bipolar (manic-depressive) illness, or if their family members have had it. Watch patients who take Generic Strattera closely!
Do not try to open the capsules or take them apart. Wash your hands immediately after using Generic Strattera. Do not get Generic Strattera in your eye. It may irritate your eye if you do. If you get Generic Strattera in your eyes or nose, rinse at once with cool water.
Lab tests, including heart rate, blood pressure, and liver function, may be performed while you use Generic Strattera.
Use Generic Strattera with caution in the elderly. They may be more sensitive to its effects, especially dizziness.
Corticosteroids may affect growth rate in children and teenagers in some cases. They may need regular growth checks while they take Generic Strattera.
Generic Strattera should be used with extreme caution in children younger than 6 years old. Safety and effectiveness in these children have not been confirmed.
Sit up or stand slowly, especially in the morning.
Avoid driving machine.
Do not stop taking Generic Strattera suddenly.
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An economic model with Markov processes was developed to estimate the costs and benefits of atomoxetine versus either MPH or 'no medication'. The incremental cost per quality-adjusted life-year (QALY) was calculated for atomoxetine relative to the comparators. The Markov process incorporated 14 health states, representing a range of outcomes associated with treatment options. Utility values were obtained from the utility valuation survey of 83 parents of children with ADHD. The clinical data were based on a thorough review of controlled clinical trials and other clinical literature, and validated by international experts. Costs and outcomes were estimated using Monte Carlo simulation over a 1-year duration, with costs estimated from the perspective of the National Health Service in Spain.
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Spontaneously hypertensive rats (SHRs) are used as a model for attention-deficit/hyperactivity disorder (ADHD), since SHRs are hyperactive and show defective sustained attention in behavioral tasks. The psychostimulants amphetamine and methylphenidate and the selective norepinephrine reuptake inhibitor atomoxetine are used as ADHD medications. The effects of high K(+) stimulation or psychostimulants on brain norepinephrine or dopamine release in SHRs have been previously studied both in vitro and in vivo, but the effects of atomoxetine on these neurotransmitters have not. The present study examined the effects of administration of atomoxetine on extracellular norepinephrine, dopamine, and serotonin levels in the prefrontal cortex of juvenile SHRs and Wistar-Kyoto (WKY) rats. Baseline levels of prefrontal norepinephrine, dopamine, and serotonin were similar in SHRs and WKY rats. Systemic administration of atomoxetine (3 mg/kg) induced similar increases in prefrontal norepinephrine and dopamine, but not serotonin, levels in both strains. Furthermore, there was no difference in high K(+)-induced increases in extracellular norepinephrine, dopamine, and serotonin levels in the prefrontal cortex between SHRs and WKY rats. These findings indicate that monoamine systems in the prefrontal cortex are similar between SHRs and WKY rats.
To determine the effects of long-term atomoxetine treatment on sexual development in children and adolescents with attention-deficit/hyperactivity disorder (ADHD) as compared with placebo and with a national US survey in non-Hispanic white children and adolescents.
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Mean on-treatment costs in the atomoxetine group (SEK [Swedish Krona] 4,558) were significantly lower compared with placebo (SEK 7,684) after adjusting for baseline costs and site (p = .007). All 99 patients entered an open atomoxetine extension phase. Both groups had numerical reductions in direct and indirect costs while on atomoxetine treatment during the extension phase. The atomoxetine medication costs were offset by the reductions in direct nonmedical and indirect costs.
There were no treatment group differences on the primary study outcome measure (overall mean z-score: Wilcoxon chi(2) = 0.21, df = 1, p = .64); nor was there significant evidence of variation in treatment effects on z-score changes across the individual neuropsychological tests (chi(2) = 8.22, df = 8, p = .41). No between-group differences were noted in symptom changes. Atomoxetine was well tolerated and was associated with a trend for improvement in extrapyramidal side effects relative to placebo (p = .063).
ADHD is the most frequent diagnosis seen by Australian pediatricians, with some patients being seen into early adult life. Comorbidities appear to be inconsistently identified, with some possibly underdiagnosed. Older children are more likely to be prescribed medication.
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Tobacco dependence remains a global epidemic and the largest preventable cause of morbidity and mortality around the world. Smoking cessation has benefits at all ages but remains challenging for several reasons, among which are the complexities of nicotine addiction and limitations of available pharmacotherapies.
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Study subjects were 7 to 17 years old, met Diagnostic and Statistical Manual of Mental Disorders-IV criteria for ADHD, and had concurrent Tourette syndrome or chronic motor tic disorder. Patients were randomly assigned to double-blind treatment with placebo (n = 72) or atomoxetine (0.5 to 1.5 mg/kg/day, n = 76) for up to 18 weeks.
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Once-daily administration of atomoxetine is an effective treatment for children and adolescents with ADHD.
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A total of 1350 and 753 participants (aged 6-18 years, mean age 10.7 ± 2.8) were treated with methylphenidate and atomoxetine, respectively, from 2007 to 2012. Ninety participants (7 %) were switched from methylphenidate to atomoxetine, and 138 (18 %) from atomoxetine to methylphenidate. Thirty-seven children treated with atomoxetine and 12 with methylphenidate had their medication withdrawn. Overall, 645 patients (26.8 %) experienced at least one mild AE (including decreased appetite and irritability, for both drugs) and 95 patients (3.9 %) experienced at least one severe AE (including severe gastrointestinal events). IR100PY were significantly higher in the atomoxetine-treated group compared with the methylphenidate-treated group for a number of mild and severe AEs and for any severe or mild AEs. After controlling for comorbidities, IRR was still significantly higher in the atomoxetine group compared with the methylphenidate group for a number of mild (decreased appetite, weight loss, abdominal pain, dyspepsia, stomach ache, irritability, mood disorder and dizziness) and severe (gastrointestinal, neuropsychiatric, and cardiovascular) AEs.
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The primary efficacy endpoint was the change in the Attention Deficit Hyperactivity Disorder Rating Scale, Version IV (ADHD-RS-IV) total score from baseline (day 1) to the end of the treatment phase (day 42), and included all randomized participants who received one or more doses of study drug and had baseline and one or more post-baseline assessments (intent-to-treat [ITT] population). Safety assessments included treatment-emergent adverse events (TEAEs), laboratory tests and ECG readings.
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Compare observed and forecasted efficacy of mixed amphetamine salts extended release (MAS-XR; Adderall) with atomoxetine (Strattera) in ADHD children.
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Our meta-analysis included nine studies involving 477 subjects. We assessed the efficacy of six medications-dextroamphetamine, methylphenidate, alpha-2 agonists (clonidine and guanfacine), desipramine, atomoxetine, and deprenyl. Methylphenidate, alpha-2 agonists, desipramine, and atomoxetine demonstrated efficacy in improving ADHD symptoms in children with comorbid tics. Alpha-2 agonists and atomoxetine significantly improved comorbid tic symptoms. Although there was evidence that supratherapeutic doses of dextroamphetamine worsens tics, there was no evidence that methylphenidate worsened tic severity in the short term.
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Pertaining to the technology assessment report, potential problems were identified relating to an unnecessarily narrow scope, data search and selection strategy, the distinction between efficacy and effectiveness, data synthesis across studies and clinical effect measures, and limitations of the economic model. The appraisal process moderated the asserted 'clear conclusions' of the assessment but could not compensate for some of its gaps.
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A comprehensive in vivo evaluation of brain penetrability and central nervous system (CNS) pharmacokinetics of atomoxetine in rats was conducted using brain microdialysis. We sought to determine the nature and extent of transport at the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCB) and to characterize brain extracellular and cellular disposition. The steady-state extracellular fluid (ECF) to plasma unbound (uP) concentration ratio (C(ECF)/C(uP)=0.7) and the cerebrospinal fluid (CSF) to plasma unbound concentration ratio (C(CSF)/C(uP)=1.7) were both near unity, indicating that atomoxetine transport across the BBB and BCB is primarily passive. On the basis of the ratios of whole brain concentration to C(ECF) (C(B)/C(ECF)=170), brain cell (BC) concentration to C(ECF) (C(BC)/C(ECF)=219), and unbound brain cell concentration to C(ECF) (C(uBC)/C(ECF)=2.9), we conclude that whole brain concentration does not represent the concentration in the biophase and atomoxetine primarily partitions into brain cells. The distributional clearance at the BBB (Q(BBB)=0.00110 l/h) was estimated to be 12 times more rapid than that at the BCB (Q(BCB)=0.0000909 l/h) and similar to the clearances across brain parenchyma (CL(ECF-BC)=0.00216 l/h; CL(BC-ECF)=0.000934 l/h). In summary, the first detailed examination using a quantitative microdialysis technique to understand the brain disposition of atomoxetine was conducted. We determined that atomoxetine brain penetration is high, movements across the BBB and BCB occur predominantly by a passive mechanism, and rapid equilibration of ECF and CSF with plasma occurs.
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Of the 12,412 adult patients with ADHD newly initiated on atomoxetine, 4548 (36.6%) were suboptimally dosed, whereas 3323 (26.7%) were treated at recommended dose. Overall, study patients were treated at a mean (standard deviation [SD]) dose of 68.5 (44.9) mg/day. The suboptimal dosing cohort included significantly more females (54% vs. 44%, P < 0.001) and had fewer patients with pre-index use of other ADHD medications (17% vs. 20%, P < 0.001) compared with the recommended dosing cohort.
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Atomoxetine was approved in the United States in November 2002 for the treatment of ADHD in children, adolescents, and adults. The present study uses data from a clinical trial of atomoxetine in adult patients with ADHD that incorporated a measure of health-related quality of life (the Medical Outcomes Study 36-item short-form health survey [SF-36]) as part of the overall assessment of the success of this relatively new treatment. The primary outcome measure for ADHD symptoms was the Conners Adult ADHD Rating Scale-Investigator Rated: Screening Version (CAARS) ADHD total symptom score.
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To evaluate the effect of atomoxetine hydrochloride versus placebo on attention-deficit/hyperactivity disorder (ADHD) and substance use disorder (SUD) in adolescents receiving motivational interviewing/cognitive behavioral therapy (MI/CBT) for SUD.
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The results of this double-blind placebo-controlled study showed that ATX facilitated corticospinal and intracortical excitability in motor cortex. 10 Hertz rTMS applied during a motor task was able to further increase intracortical excitability only in combination with ATX. In addition, only the combination of 10 Hz rTMS and ATX was capable of enhancing the total number of correct responses and reaction time significantly, indicating an interaction effect between rTMS and ATX without signs of homeostatic metaplasticity.
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Amphetamines have been reported to cause myocardial infarct, cerebral hemorrhage, aortic dissection, hypertension, vasculitis, aneurysms, and, occasionally, death from direct toxicity. To date, there have been no reports of coronary intimal hyperplasia in an amphetamine user.
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Recent studies suggest that the severity and drug response of depression and anxiety are correlated with childhood abuse. However, whether a history of child abuse can predict the severity and/or drug response of attention-deficit/hyperactivity disorder (ADHD) is unclear. Therefore, we conducted a retrospective study to assess the efficacy of atomoxetine in children with a history of child abuse.
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Stimulants are a highly efficacious and safe treatment for attention-deficit/hyperactivity disorder (ADHD), with 75% to 90% of patients responding well if two different stimulants (amphetamine and methylphenidate) are used. Nonetheless, a subset of ADHD patients will either fail to respond to stimulants or have side effects that preclude their use (tics, severe loss of appetite, marked insomnia). For such patients, there are a number of non-stimulant agents that serve as second-line treatments. Tricyclic antidepressants (TCAs) are the most studied of these drugs. They are superior to placebo in the treatment of ADHD and may reduce abnormal movements in patients with ADHD/tic disorder. TCAs often produce side effects of sedation, dry mouth, and constipation. Bupropion is superior to placebo in the treatment of ADHD and has a more favorable side-effect profile than the TCAs. A new selective norepinephrine reuptake inhibitor, atomoxetine, has been shown to be efficacious in the treatment of ADHD and has recently received an approvable letter from the Food and Drug Administration. The a-agonists clonidine and guanfacine have also been used as alternative agents in ADHD, though the controlled data are more limited. A recent controlled clinical trial suggests a combination of methylphenidate and clonidine has advantages in the treatment of comorbid ADHD and tics over either medication alone. Clinical guidelines for each of these agents, as well as their use in combination with stimulants in comorbid conditions, will be discussed.
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Parallel group design with an ATX and a waiting list group. At baseline and endpoint patients were evaluated with a standardized on-road driving test (SDBO), a driving-related neuropsychological test battery (Act and React Test System [ART2020]), and subjective measures of driving performance (one-week driving diary, Driver Coping Questionnaire).
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Psychostimulants and non stimulants are effective in the treatment of ADHD. Efficacy of both methylphenidate and atomoxetine has been established in placebo controlled trials. Direct comparison of efficacy is now possible due to availability of results from several head-to-head trials of these two medications.
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How the brain monitors ongoing behavior for performance errors is a central question of cognitive neuroscience. Diminished awareness of performance errors limits the extent to which humans engage in corrective behavior and has been linked to loss of insight in a number of psychiatric syndromes (e.g., attention deficit hyperactivity disorder, drug addiction). These conditions share alterations in monoamine signaling that may influence the neural mechanisms underlying error processing, but our understanding of the neurochemical drivers of these processes is limited. We conducted a randomized, double-blind, placebo-controlled, cross-over design of the influence of methylphenidate, atomoxetine, and citalopram on error awareness in 27 healthy participants. The error awareness task, a go/no-go response inhibition paradigm, was administered to assess the influence of monoaminergic agents on performance errors during fMRI data acquisition. A single dose of methylphenidate, but not atomoxetine or citalopram, significantly improved the ability of healthy volunteers to consciously detect performance errors. Furthermore, this behavioral effect was associated with a strengthening of activation differences in the dorsal anterior cingulate cortex and inferior parietal lobe during the methylphenidate condition for errors made with versus without awareness. Our results have implications for the understanding of the neurochemical underpinnings of performance monitoring and for the pharmacological treatment of a range of disparate clinical conditions that are marked by poor awareness of errors.
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Although both stimulant and nonstimulant medications are effective for treating ADHD in adults, stimulant medications show greater efficacy for the short durations of treatment characteristic of placebo-controlled studies. We found no significant differences between short- and long-acting stimulant medications. Study design features vary widely among studies and can confound indirect comparisons unless addressed statistically as we have done in this study.
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