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Atomoxetine is sometimes used in the treatment of cognitive impairment and frontal lobe symptoms due to conditions like traumatic brain injury (TBI). [48] [49] It is used to treat ADHD-like symptoms such as sustained attentional problems, disinhibition, [50] lack of arousal, fatigue, and depression, including symptoms from cognitive disengagement syndrome. [48]
More specifically, it looked at the effect of methylphenidate (brand names Ritalin, Concerta), a stimulant, and atomoxetine (Strattera), a non-stimulant, on the brain.
Atomoxetine reaches C max 1 to 2 hours after administration. The bioavailability of atomoxetine after oral administration is 63-94%, it is dependent on individual differences in the first-pass metabolism. [18] Atomoxetine is widely distributed and is highly (98%) bound to plasma proteins, mainly albumin.
Norepinephrine Epinephrine. A norepinephrine reuptake inhibitor (NRI, NERI) or noradrenaline reuptake inhibitor or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a reuptake inhibitor for the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline) by blocking the action of the norepinephrine transporter (NET).
Attention deficit hyperactivity disorder management options are evidence-based practices with established treatment efficacy for ADHD.Approaches that have been evaluated in the management of ADHD symptoms include FDA-approved pharmacologic treatment and other pharmaceutical agents, psychological or behavioral approaches, combined pharmacological and behavioral approaches, cognitive training ...
Strattera (atomoxetine) – a non-stimulant medication used to treat ADHD Suboxone ( buprenorphine/naloxone ) - a partial opioid agonist used in the treatment of opioid use disorder T
Atomoxetine has been shown to significantly improve academic performance. [293] [294] Meta-analyses and systematic reviews have found that atomoxetine has comparable efficacy, equal tolerability and response rate (75%) to methylphenidate in children and adolescents. In adults, efficacy and discontinuation rates are equivalent.
TCAs do not block dopamine transport directly but might facilitate dopaminergic effects indirectly by inhibiting dopamine transport into noradrenergic terminals of the cerebral cortex. [29] Because they affect so many different receptors, TCAs have adverse effects, poor tolerability, and an increased risk of toxicity.