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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In total 28 trials were included in the meta-analysis. Efficacy in reducing ADHD symptoms compared to placebo was small for bupropion (SMD=-0.32, 95% CI; -0.69, 0.05), while modest efficacy was shown for atomoxetine (SMD=-0.68, 95% CI; -0.76, -0.59) and methylphenidate (SMD=-0.75, 95% CI; -0.98, -0.52) and high efficacy was observed for lisdexamfetamine (SMD=-1.28, 95% CI; -1.84, -0.71). Compared to placebo treatment discontinuation was statistically significantly lower for methylphenidate (OR=0.35, 95% CI; 0.24, 0.52), while it was not significantly different for atomoxetine (OR=0.91, 95% CI; 0.66, 1.24), lisdexamfetamine (OR=0.60, 95% CI, 0.22, 1.65), and bupropion (OR=1.64, 95% CI; 0.5, 5.43).
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Even with optimal treatment, based on parents' and teachers' opinions, subtle and not-so-subtle neurocognitive impairments persisted in the ADHD patients. Some ADHD patients may require additional educational assistance, even in the face of successful medication treatment.
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Patients were randomized to treatment with fluoxetine (n = 127) or placebo (n = 46) under double-blind conditions for 8 weeks, with concomitant atomoxetine use the last 5 weeks.
In addition to other reported adverse effects, amphetamines can also cause occlusive intimal hyperplasia of the coronary arteries.
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Two identical 12-week, stratified, randomized, double-blind, placebo-controlled trials were conducted in children who met DSM-IV criteria for ADHD. The primary efficacy outcome measure was the mean change from baseline to endpoint in the Attention-Deficit/Hyperactivity Disorder Rating Scale (ADHD RS) total score. Secondary efficacy measures included the Clinical Global Impressions-ADHD-Severity (CGI-ADHD-S) and the Conners' Parent Rating Scale-Revised: Short Form (CPRS-R:S).
This study aimed to compare the effects of osmotic release oral system-methylphenidate (OROS-MPH) and atomoxetine (ATX) on executive function in children and adolescents with attention deficit hyperactivity disorder (ADHD) by a randomized controlled trial. Subjects who met DSM-IV ADHD criteria were randomized to receive either OROS-MPH or ATX treatment. The doses were titrated to achieve optimal response and then maintained for 4-6 wk. A battery of executive function tests and the Behavior Rating Inventory of Executive Function (BRIEF) were administered to subjects who completed the dose titration (OROS-MPH, n=85; ATX, n=57) at the pre- and post-treatment periods. Forty-six children without ADHD were recruited as controls. Both OROS-MPH and ATX significantly improved scores in the Rey Complex Figure Test (RCFT), digit span, and Stroop color-word task. The scores in RCFT and the reverse digit span were not significantly different from the control group at post-treatment assessment (OROS-MPH=ATX=control, p>0.05), whereas the word interference time of the Stroop test was still more than that of the control group (OROS-MPH=ATX>control, p>0.05). OROS-MPH also significantly improved the total correct response in the verbal fluency test to normal level, and the shifting time in the trail-making test to subnormal level. The current findings suggest both OROS-MPH and ATX improved executive function generally in children and adolescents with ADHD, and could return working memory back to normative performance level.
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ADHD-BD may be associated with more severe symptoms, course, and worst outcome of both conditions. The frequent coexistence with alcohol and substance abuse may further complicate treatment management. Stimulants are the most effective medications for ADHD, but their use may be contraindicated in the presence of a comorbid drug abuse or in patients that simulate or exaggerate ADHD symptoms in order to obtain stimulants for diversion or abuse. ATX may be effective in the treatment of ADHD symptoms in BD patients, with a modestly increased risk of (hypo)manic switches and destabilization of the mood disorder when utilized in association with mood stabilizers. In the majority of the cases, a hierarchical approach is desirable, with mood stabilization preceding the treatment of ADHD symptoms. Although systematic trials on the use of stimulants and ATX in ADHD-BD comorbidity in adulthood are necessary, both treatments should be considered possible options to be carefully evaluated once the patient has been stabilized.
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Atomoxetine was tolerable and effective in improving QoL and executive function as well as ameliorating core ADHD symptoms in adult Asian patients.
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The effects of stimulant medications and atomoxetine on physical growth and on cardiovascular function are reviewed in light of the most recent data, with attention to clinical implications and research needs. Although these medications have a favorable benefit/risk profile and do not induce clinically significant changes in growth or cardiovascular function in the majority of cases, careful patient monitoring is needed to identify individuals at risk for negative outcomes. More research is needed to elucidate the mechanism of growth suppression to estimate better the risk for rare but life-threatening events and test the effectiveness of monitoring procedures.
Clinical experience suggests that some (but not all) patients with attention-deficit/hyperactivity disorder (ADHD) are highly responsive to the nonstimulant atomoxetine. We conducted a retrospective analysis of randomized controlled trials (RCTs) to identify potential baseline (moderator) and on-treatment (mediator) predictors of responses.
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The two treatment groups did not differ in demographics and baseline measures. Compared to the placebo group, the atomoxetine group showed significantly greater reductions in ADHD-related symptoms according to the ratings of investigators, parents, and teachers. The treatment effect size of the primary efficacy measure was 0.70 at the end of study. Adverse events reported significantly more frequently with atomoxetine were decreased appetite (36.1%) and nausea (16.6%). No drug-related serious adverse event was observed.
Adolescent rats show immaturities in executive function and are less able than adult rats to learn reinforcement reversals and shift attentional set. These two forms of executive function rely on the functional integrity of the orbitofrontal and prelimbic cortices respectively. Drugs used to treat attention deficit disorder, such as atomoxetine, that increase cortical catecholamine levels improve executive functions in humans, non-human primates and adult rats with prefrontal lesions. Cortical noradrenergic systems are some of the last to mature in primates and rats. Moreover, norepinephrine transporters (NET) are higher in juvenile rats than adults. The underdeveloped cortical noradrenergic system and higher number of NET are hypothesized to underlie the immaturities in executive function found in adolescents. We assessed executive function in male Long-Evans rats using an intra-dimensional/extradimensional set shifting task. We administered the NET blocker, atomoxetine (0.0, 0.1, 0.9 mg/kg/ml; i.p.), prior to the test of attentional set shift and a reinforcement reversal. The lowest dose of drug facilitated attentional set shifting but had no effect on reversal learning. These data demonstrate that NET blockade allows adolescent rats to more easily perform attentional set shifting.
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There is continuing speculation about the relationship between attention-deficit/hyperactivity disorder (ADHD) and obstructive sleep apnea (OSA) or periodic limb movement disorder (PLMD)/restless legs syndrome. The objective was to determine if a significant portion of children with ADHD diagnosed using DSM-IV criteria have OSA or PLMD.
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We hypothesized that atomoxetine (ATMX) would produce similar brain effects in attention-deficit/hyperactivity disorder (ADHD) as those of methylphenidate (MPH). Eleven ADHD adults performed the Multi-Source Interference Task (MSIT) during functional magnetic resonance imaging (fMRI) at baseline and after 6 weeks of ATMX treatment. ATMX was associated with increased fMRI activation of dorsolateral prefrontal cortex, parietal cortex and cerebellum but not dorsal anterior midcingulate cortex (daMCC). These results suggest that ATMX and MPH have similar but not identical brain effects.
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Skeletal muscle atrophy remains a clinical problem in numerous pathologic conditions. β2-Adrenergic receptor agonists, such as formoterol, can induce mitochondrial biogenesis (MB) to prevent such atrophy. Additionally, atomoxetine, an FDA-approved norepinephrine reuptake inhibitor, was positive in a cellular assay for MB. We used a mouse model of dexamethasone-induced skeletal muscle atrophy to investigate the potential role of atomoxetine and formoterol to prevent muscle mass loss. Mice were administered dexamethasone once daily in the presence or absence of formoterol (0.3 mg/kg), atomoxetine (0.1 mg/kg), or sterile saline. Animals were euthanized at 8, 16, and 24 hours or 8 days later. Gastrocnemius muscle weights, changes in mRNA and protein expression of peroxisome proliferator-activated receptor-γ coactivator-1 α (PGC-1α) isoforms, ATP synthase β, cytochrome c oxidase subunit I, NADH dehydrogenase (ubiquinone) 1 β subcomplex, 8, ND1, insulin-like growth factor 1 (IGF-1), myostatin, muscle Ring-finger protein-1 (muscle atrophy), phosphorylated forkhead box protein O 3a (p-FoxO3a), Akt, mammalian target of rapamycin (mTOR), and ribosomal protein S6 (rp-S6; muscle hypertrophy) in naive and muscle-atrophied mice were measured. Atomoxetine increased p-mTOR 24 hours after treatment in naïve mice, but did not change any other biomarkers. Formoterol robustly activated the PGC-1α-4-IGF1-Akt-mTOR-rp-S6 pathway and increased p-FoxO3a as early as 8 hours and repressed myostatin at 16 hours. In contrast to what was observed with acute treatment, chronic treatment (7 days) with atomoxetine increased p-Akt and p-FoxO3a, and sustained PGC-1α expression and skeletal muscle mass in dexamethasone-treated mice, in a manner comparable to formoterol. In conclusion, chronic treatment with a low dose of atomoxetine prevented dexamethasone-induced skeletal muscle wasting and supports a potential role in preventing muscle atrophy.
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At week 24, mean changes in ADHD-RS-IV Inattention scores were 13.58 points (Cohen's d, -3.08) for OROS-methylphenidate and 12.65 points (Cohen's d, -3.05) for atomoxetine; and mean changes in ADHD-RS-IV Hyperactivity-Impulsivity scores were 10.16 points (Cohen's d, -1.75) for OROS-methylphenidate and 10.68 points (Cohen's d, -1.87) for atomoxetine. In terms of parent-, teacher-, and self-ratings on behavioral symptoms, both of the two treatment groups significantly decreased on the SNAP-IV scores at the end-point, with effect sizes ranging from 0.9 to 0.96 on the Inattention subscale and from 0.61 to 0.8 on the Hyperactivity/Impulsivity subscale for OROS-methylphenidate; and from 0.51 to 0.88 on the Inattention subscale and from 0.29 to 0.57 on the Hyperactivity/Impulsivity subscale for atomoxetine. No statistically significant differences between treatment groups were observed on the outcome measures. Vomiting, somnolence, and dizziness were reported more often for atomoxetine than for OROS-methylphenidate, whereas insomnia was reported more often for OROS-methylphenidate than for atomoxetine.
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Smith, Waschbusch, Willoughby, and Evans (2000) reviewed a small treatment literature on ADHD in adolescents and concluded that methylphenidate stimulant medication was a well-established treatment and behavior therapy (BT) demonstrated preliminary efficacy. This review extends and updates the findings of the prior one based on the previous 15years of research. Studies published since 1999 were identified and coded using standard criteria and effect sizes were calculated where appropriate. Highlights of the last 15years of research include an expansion of pharmacological treatment options and developmentally appropriate psychosocial treatment packages for adolescents with ADHD. Additionally, nonstimulant medications (e.g., atomoxetine) are now approved for the treatment of ADHD in adolescence. The review concludes that medication and BT produce a similar range of therapeutic effects on the symptoms of adolescents with ADHD. However, results suggest that BT may produce greater overall benefits on measures of impairment. There was no evidence that cognitive enhancement trainings, such as working memory training or neurofeedback improved the functioning of adolescents with ADHD. Whether to use medication, BT, or their combination to treat an adolescent with ADHD is complicated and we provide evidence-informed guidelines for treatment selection. The reviewed evidence does not support current American Academy of Pediatrics and American Academy of Child and Adolescent Psychiatry professional guidelines, which state that stimulant medication is the preferred treatment for adolescents with ADHD. Recommendations for assessment, practice guidelines, and future research are discussed.
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This interventional study provides Class II evidence that atomoxetine (target dosage = 80 mg/day) is not efficacious in improving clinically significant depression in PD.
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In a large placebo-controlled, double-blind study, patients ages 6-16 with ADHD, any subtype, were randomly assigned to receive 0.8-1.8 mg/kg per day of atomoxetine (N=222), 18-54 mg/day of osmotically released methylphenidate (N=220), or placebo (N=74) for 6 weeks. The a priori specified primary analysis compared response (at least 40% decrease in ADHD Rating Scale total score) to osmotically released methylphenidate with response to atomoxetine and placebo. After 6 weeks, patients treated with methylphenidate were switched to atomoxetine under double-blind conditions.
Aggression/hostility-related events occurred in less than 2% of patients and were more frequent in pediatric patients treated with atomoxetine versus placebo (risk ratio of 1.33; not statistically significant). The risk of aggression/hostility events was similar in patients treated with atomoxetine or methylphenidate.
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The majority of the 111 patients were male (83.8%, n=93) and mean (SD) age was 11.5 (2.38) years. Mean baseline ADHD-RS total score was 36.0 in the fast and 38.0 in the slow group. Adjusted mean change after 2 weeks was -8.1 (-10.1; -6.1) in the fast and -8.0 (-9.9;-6.0) in the slow group (p=0.927), and after 10 weeks -15.0 (-17.4;-12.6) and -14.3 (-16.7;-12.0), respectively, (p=0.692). GIPD scores did not show differences between groups. Significant differences at week 10 were found in the CHIP-CE achievement domain favoring slow (p=0.036) and the comfort domain favoring fast cross-titration (p=0.030). No significant differences were found for adverse events, and differences for systolic blood pressure (BP) and weight were not considered clinically relevant.
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The comorbidity of attention deficit hyperactivity disorder (ADHD) and schizophrenia poses a considerable diagnostic challenge due to significant symptom overlap, and represents a highly debilitating condition for the patient. This case report aims to present the history of a 19-year-old patient suffering from these two diagnostic entities, and thereby seeks to elucidate diagnostic and therapeutic approaches for this condition.
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To raise awareness, this article provides a commentary on the frequent underdosing of atomoxetine for the treatment of adult attention-deficit/hyperactivity disorder (ADHD) that may be associated with poor patient outcomes. Data suggest an adequate atomoxetine dose for sufficient duration is important for ADHD symptom improvement. Despite the recommended 80 mg/day target dose, real-world data show that an approximately 60 mg/day average adult atomoxetine dose is utilized. This article discusses the factors that may contribute to this suboptimal dosing. Atomoxetine dose titration, setting patient expectations, and the importance of keeping the patient at target dose for an adequate length of time (about 4−6 weeks) prior to judging efficacy are also discussed.
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The results of this study reveal that youths diagnosed with ADHD have a greater risk of developing depressive disorders. Long-term treatment with MPH correlated to the reduced probability of developing a depressive disorder among youths with ADHD.
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The AAQoL was responsive to change in symptoms of ADHD, and it appears to be a useful outcome measure for treatments of ADHD in adults.
It has been proposed that acute hypothalamo-pituitary-adrenal (HPA) axis challenge using noradrenergic drugs may be of utility in assessing the functional integrity of central noradrenaline pathways. Atomoxetine (formerly tomoxetine) is a highly selective noradrenaline reuptake inhibitor, which has recently been licensed for the treatment of attention deficit hyperactivity disorder (ADHD). The aim of this study was to assess the effects of acute atomoxetine on salivary cortisol levels for the first time.A total of 60 healthy male volunteers received 60 mg atomoxetine, 30 mg citalopram, or placebo per os in a double-blind parallel groups design (n = 20 per group). Salivary cortisol, blood pressure and pulse rates were recorded at baseline and at +1.0, +1.5, +2.5 and +3.5 hours after capsule administration.60 mg atomoxetine led to highly significant increases in salivary cortisol and a moderate increase in pulse rate, in the absence of significant effects on blood pressure. 30 mg citalopram had no significant effects on cortisol or cardiovascular parameters. These data support the utility of atomoxetine neuroendocrine challenge for evaluating central noradrenaline pathways, which may be of future use in neuropsychiatric patient studies. Furthermore, the effects of atomoxetine on HPA axis function may have clinical implications given the use of this agent in the treatment of ADHD.
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