![]() ![]() Patients must not use methylphenidate if they are currently on monoamine oxidase inhibitors (MAOIs). ĭrug Interactions: Methylphenidate can inhibit the metabolism of warfarin, phenytoin, tricyclic antidepressants, or SSRIs and can increase plasma concentration. Due to the risk of such fatal side effects, it is advisable to avoid methylphenidate in patients with a structural cardiac abnormality, cardiomyopathy, or arrhythmias. Stroke and myocardial infarction also have been observed in adults. It is important to note that there have been reported cases of sudden death in both children and adults with a pre-existing structural cardiac abnormality. While many common side effects can be relieved by adjusting the dosage or avoiding an afternoon or evening dose, some require treatment emergently to prevent complications. ![]() Patients are more prone to become easily agitated, irritable, or depressed and go through mood swings/lability. Some patients may even develop blurry vision or decreased libido. While it rarely occurs, priapism is a medical emergency that requires immediate attention. Other frequent side effects mainly involve the CNS (dizziness, headache, tics, restlessness/akathisia), gastrointestinal (nausea/vomiting, dry mouth, decreased appetite, weight loss, abdominal pain), and cardiovascular systems (tachycardia, and palpitations).ĭermatologically, patients can complain of excessive sweating and ulceration of their digits. Growth retardation (decreased height, weight, and bone marrow density) is observed when taken long-term in children. Insomnia and nervousness are the most commonly reported adverse effects in patients using methylphenidate. This accumulation of deltaFosB in the nucleus accumbens activates a series of signaling cascades that further triggers the addiction. However, excessively higher dosages taken by those who intentionally abuse the drug lead to an overexpression of deltaFosB, a transcriptional activator, in specific neurons within the striatum. The therapeutic dosages for ADHD or narcolepsy that physicians prescribe are not harmful enough to activate the reward system within the CNS, known as the nucleus accumbens. The combined interactions methylphenidate has on both of these transporters reduce the amount of dopamine that accumulates within the cytoplasm in patients with these conditions, thereby preventing the formation of reactive oxygen species that would otherwise be dangerously toxic to the brain. This effect occurs not only through its direct inhibition of the dopamine transporter but also via indirect regulation of the vesicular monoamine transporter 2. With the increase in dopamine levels, methylphenidate can provide neuroprotection in certain conditions like Parkinson disease, which involves loss of dopaminergic neurons and methamphetamine abuse. It is also a weak agonist at the 5HT1A receptor, which is an additional mechanism that contributes to the increased levels of dopamine. Compared to other medications (i.e., amphetamines) that are phenethylamine derivatives, methylphenidate appears to increase the firing rate of neurons. It undergoes metabolism by the liver to ritalinic acid through a process called de-esterification via carboxylesterase CES1A1. It chemically derives from phenethylamine and benzylpiperazine. This creates its classic stimulant effect within the central nervous system (CNS), mainly in the prefrontal cortex. More specifically, it inhibits the transporters of these neurotransmitters, increasing the concentration of dopamine and NE in the synaptic cleft. Methylphenidate blocks the reuptake of two neurotransmitters, norepinephrine (NE) and dopamine, in presynaptic neurons. Most of these relatively newer uses are still being studied and implemented into clinical practice. The efficacy of methylphenidate for its off-label uses varies from limited to moderate. Since it can be abused as a cognitive enhancer, it is a federally controlled Schedule II substance. Off-label uses of methylphenidate include treatment for fatigue in patients with cancer, refractory depression in the geriatric population, apathy in Alzheimer disease, and enhancing cognitive performance (e.g., memory). The treatment of both ADHD and narcolepsy have significantly better outcomes when used concurrently with nonpharmacologic therapies (i.e., social skills training in ADHD or sleep hygiene measures in narcolepsy). Ĭhildren diagnosed with ADHD should be at least six years of age or older before being started on this medication. Methylphenidate is FDA-approved for treating attention deficit hyperactivity disorder (ADHD) in children and adults and as a second-line treatment for narcolepsy in adults. ![]()
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