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Stimulants dextroamphetamine

Indications Attention-deficit hyperactivity disorder (ADHD) Category CNS stimulant Dextroamphetamine prodrug Half-life I Hour... [Pg.341]

The prototype, amphetamine (52), is obtained by reductive amination of phenylacetone by means of ammonia and hydrogen. Isolation of the (+) isomer by resolution gives dextroamphetamine, a somewhat more potent stimulant than the racemate. [Pg.70]

The amphetamines, such as amphetamine, dextroamphetamine (Dexedrine), and metliainphetainine (Desoxyn), are sympatiiomimetic (ie, adrenergic) dru that stimulate the CNS (see Chap. 22). Their drug action results in an elevation of blood pressure, wakefulness, and an increase or decrease in pulse rate The ability of these drugs to act as anorexiants and suppress the appetite is thought to be due to their action on the appetite center in the hypothalamus. [Pg.247]

When a CNS stimulant such as dextroamphetamine is administered to treat a child with ADD, the drug regimen will be periodically interrupted to determine if the child still exhibits the symptoms of ADD. [Pg.250]

Arnold, L.E. Kirilcuk, V. Corson, S.A. and Corson, E.O. Levoampheta-mine and dextroamphetamine Differential effect on aggression and hyperkinesis in children and dogs. Am J Psychiatry 130 165-170, 1973. Bain, G.T., and Kometsky, C. Naloxone attenuation of the effect of cocaine on rewarding brain stimulation. Life Sci 40 1119-1125, 1987. [Pg.90]

The proposed mechanism of ADHD pharmacotherapy is to modulate neurotransmitters in order to improve academic and social functioning. Pharmacologic therapy can be divided into two categories stimulants and non-stimulants. Stimulant medications include methylphenidate, dexmethylphenidate, amphetamine salts, and dextroamphetamine, whereas non-stimulant medications include atomoxetine, tricyclic antidepressants (e.g., imipramine), clonidine, guanfacine, and bupropion. [Pg.636]

Psychostimulants (e.g., methylphenidate and dextroamphetamine with or without amphetamine) are the most effective agents in treating ADHD. Once the diagnosis of ADHD has been made, a stimulant medication should be used first line in treating ADHD (Fig. 39-1). Stimulants are safe and effective, with a response rate of 70% to 90% in patients with ADHD.3,13,14 Generally, a trial of at least 3 months on a stimulant is appropriate, and this includes dose titration to response... [Pg.636]

Initial response to short-acting stimulant formulations (e.g., methylphenidate and dextroamphetamine) is seen within 30 minutes and can last for 4 to 6 hours.13,14 This short duration of effect frequently requires that short-acting stimulant formulations be dosed at least twice daily, thus increasing the chance of missed doses and non-compliance. Further, patients using any stimulant formulation but especially shortacting formulations can experience a rebound effect of ADHD symptoms as the stimulant wears off.14... [Pg.637]

Dextroamphetamine (Dexedrine). Dextroamphetamine is the second most widely used stimulant and the most commonly used amphetamine in the United States. It is about twice as potent as methylphenidate and should be initiated in the treatment of ADHD at 2.5 mg taken twice daily with breakfast and lunch. Like other stimulants, the benefits of dextroamphetamine can be seen almost immediately. With weekly visits while starting treatment, the dose can be increased in 2.5-5 mg increments until the effective dose is found. Because dextroamphetamine is also slightly longer acting than methylphenidate, patients may be less likely to need an evening dose. If an after-school dose is used, then like methylphenidate it should be 25-50% of the daytime dose. [Pg.241]

The side effects of dextroamphetamine are comparable to other stimulants. Patients may experience insomnia, poor appetite, weight loss, and occasional nausea and diarrhea. Taking the medication just before meals helps to minimize the nausea and diarrhea. To avoid insomnia, dextroamphetamine should rarely be taken any later than 6 PM. [Pg.241]

Close to 70% of children with ADHD will respond to a stimulant. When the child is not helped by the first stimulant that is prescribed, there is still a good chance of responding to a different one. If an initial trial of methylphenidate isn t successful, then switching to dextroamphetamine or Adderall is a reasonable strategy. If dextroamphetamine or Adderall was used first and did not work well, then we recommend switching to methylphenidate. Because dextroamphetamine and Adderall are more similar, it makes less sense to switch between these two. We do not recommend pemoline as a first-line treatment. [Pg.250]

Starting Treatment in Adults with ADHD. Beginning treatment of an adult is not significantly different from doing so in a child. The stimulants and atomoxetine remain the most effective medications. Methylphenidate, dextroamphetamine, and Adderall appear to be equally effective in group trials, but individuals may respond preferentially to one medication or the other. [Pg.250]

Monoamine oxidase inhibitors Paroxetine Protriptyline Sertraline Venlafaxine Stimulants Atomoxetine Dextroamphetamine Methylphenidate Modaflnil Pemoline... [Pg.265]

Methylphenidate (Ritalin, Concerta, Focalin). Methylphenidate was introduced in the late 1950s and is now the most widely used prescription stimulant. It was first used to treat ADHD in children but is also effective for narcolepsy. Like dextroamphetamine, methylphenidate should be started at 5 mg per dose given two to three times each day with meals. The average effective dose is 20-30 mg/day, but some patients require as much as 60 mg/day. The benefit of methylphenidate should also be apparent on the first day or so, and the dose can be increased every 5-7 days as needed. Focalin dosing is approximately half that of methylphenidate. [Pg.278]

Pemoline is a less potent stimulant than methylphenidate or dextroamphetamine. It should be initiated at 18.75 mg taken each morning with breakfast and can be increased in increments of 18.75mg every week or so. Typical dosing for pemoline ranges from 60 to 200mg/day in treating narcolepsy. Because pemoline is less potent than other stimulants, it is more likely to be ineffective, even at its higher doses. When pemoline does not relieve daytime sleepiness or sleep attacks, then the patient should be switched to a different stimulant. [Pg.279]

Stimulants. Methylphenidate (Ritalin) and dextroamphetamine (Dexedrine) are the most widely used and perhaps the most effective medications when treating post-TBI apathy. They act by enhancing the activity of dopaminergic, noradrenergic and, to a certain extent, serotonergic brain systems. Stimulants act quickly to relieve the core symptoms of apathy, and they may also improve the impairments in attention and short-term memory that often follow TBl. Please refer to Chapter 8 for more information about the stimulants. [Pg.344]

Stimulants. A handful of case reports hint that treatment with stimulants (meth-ylphenidate or dextroamphetamine) can help manage behavioral agitation in patients who have suffered a TBI. Certainly, stimulant therapy helps control the impulsivity and hyperactivity of children with attention deficit-hyperactivity disorder. Despite these encouraging signs, we have to discourage any routine use of stimulants when attempting to manage behavioral lability in TBI patients. Because stimulants have the potential to exacerbate behavioral lability, we recommend that they only be considered when other medication alternatives have been exhausted. [Pg.352]

Dopamine activity can be enhanced in one of four main ways. Medications can stimulate dopaminergic nerve cells to release dopamine into the synapse. This is the way that stimulants such as methylphenidate (Ritalin), dextroamphetamine (Dexe-drine), and dextroamphetamine/amphetamine (Adderall) work. In addition, certain drugs of abuse, notably cocaine and methamphetamine, act in part in this way. Providing more of the raw material that nerve cells use to manufacture dopamine can also increase dopamine activity. This is the approach that neurologists use when they prescribe L-DOPA (Sinemet) to patients with Parkinson s disease. Nerve cells convert L-DOPA into dopamine. L-DOPA otherwise has little place in the treatment of psychiatric disorders. Dopamine activity can also be increased by medications that directly stimulate dopamine receptors. Bromocriptine, another medication used to... [Pg.363]

There are four classes of antidepressants tricyclic antidepressants (imipramine, trimipramine, amitriptyline, doxepin, desipramine, protriptyline, nortriptyline, amoxapine, maprotiline) monoaminooxidase (MAO) inhibitors (phenelzine, isocarboxazid, tranylcypromine) second-generation antidepressants or atypical antidepressants, which are a chemically dissimilar group of recently proposed drugs (bupropion, trazodone, fluoxetine) and amphetamines and other stimulators of the CNS (dextroamphetamine, methylphenidate). [Pg.103]

Amphetamines are synthetic sympthetomimetic amines that are powerful CNS stimulators, of few of which, in particular dextroamphetamine (8.1.2.2) and methylphenidate (8.1.2.6), are sometimes used for treating depressive conditions. They elevate mood, stimulate motor activity, vigilance, and allow one to concentrate better. However, depending on the dosage and personality of the patient, it may cause various degrees of euphoria, which frequently leads to dependence and addiction. [Pg.114]

CNS stimulants can be classified as Psychomotor stimulants compounds that display a stimulatory effect primarily on brain functions and which activate mental and physical activity of the organism. They are made up of methylxanthines (caffeine, theophylline, pentoxifyllin), amphetamines (dextroamphetamine, methamphetamine), and also methylphenidate and pemoline. Respiratory stimulants or analeptics compounds, which cause certain activations of mental and physical activity of the organism, and primarily excite the vasomotor and respiratory centers of the medulla (doxapram, almitrine).Drwgi that suppress appetite or anorectics drags that activate mental and physical activity of the organism, but primarily accentuate the excitatory center of satiation in the hypothalamus (phentermine, diethylpropion).In order to increase mental capability, nootropics — drugs that increase the functional state of the brain — are sometimes used, the effect of which is associated with blood flow and metabolism of the brain. [Pg.117]

Dextroamphetamine is a powerful stimulant of the nervous system that manifests its effects by releasing dopamine and norepinephrine from presynaptic nerve endings, thus stimulating central dopaminergic and noradrenergic receptors. In certain doses it strengthens the excitatory process in the CNS, reduces fatigue, elevates mood and the capacity to work, reduces the need for sleep, and decreases appetite. [Pg.120]

The therapeutic uses of amphetamine are based on its ability to stimulate the CNS. The o-isomer (dextroamphetamine) is three to four times as potent as the L-isomer in producing CNS effects. It has been used in the treatment of obesity because of its anorexic effect, although tolerance to this effect develops rapidly. It prevents or overcomes fatigue and has been used as a CNS stimulant. Amphetamine is no longer recommended for these uses because of its potential for abuse. Amphetamine is useful in certain cases of narcolepsy or minimal brain dysfunction. [Pg.106]

The acute effects of psychomotor stimulant overdoses are related to their CNS stimulant properties and may include euphoria, dizziness, tremor, irritability, and insomnia. At higher doses, convulsions and coma may ensue. These drugs are cardiac stimulants and may cause headache, palpitation, cardiac arrhythmias, anginal pain, and either hypotension or hypertension. Dextroamphetamine produces somewhat less cardiac stimulation. Chronic intoxication, in addition to these symptoms, commonly results in weight loss and a psychotic reaction that is often diagnosed as schizophrenia. [Pg.351]

Mechanism of Action A sympathomimetic amine structurally similar to dextroamphetamine and is most likely mediated via norepinephrine and dopamine metabolism. Causes stimulation of the hypothalamus. Therapeutic Effect Decreased appetite. [Pg.976]

Stimulant treatment of ADHD has generated the largest body of treatment literature of any childhood psychiatric disorder. Between 1962 and 1993, over 250 reviews and over 3000 articles were published on stimulant effects (Swanson, 1993). By 1996, 161 randomized controlled trials (RCTs) had been published, encompassing 5 preschool, 150 school-age, 7 adolescent, and 9 adult studies. Improvement occurred in 65 %-75% of the children randomized to stimulants (meth-ylphenidate) [MPH] n = 133 trials dextroamphetamine [DEX] n = 22 trials pemoline [PEM] n = 6 trials) compared to 5%-30% of those assigned to pla-... [Pg.255]

Pelham, W., Greenslade, K., Vodde-Hamilton, M., Murphy, D., Greenstein, J., Gnagy, E., Guthrie, K., Hoover, M., and Dahl, R. (1990) Relative efficacy of long-acting stimulants on children with attention deficit-hyperactivity disorder a comparison of standard methylphenidate, sustained-release methylphenidate, sustained-release dextroamphetamine, and pemoline. Pediatrics 86 226-237. [Pg.463]

The risk of tachycardia, hypertension, and cardiotoxicity is increased with coadministration of dronabinol (an antiemetic) and dextroamphetamine. In addition, administration of dextroamphetamine with MAOIs may increase the risk of hypertensive crisis. Al-kalinizing agents can speed absorption (e.g., antacids) or delay urinary excretion (e.g., acetazolamide, thiazide diuretics) of dextroamphetamine, thus potentiating its effects. Gastric or urinary acidifying agents (e.g., ascorbic acid, ammonium chloride) can decrease the effects of dextroamphetamine. Propoxyphene overdose can potentiate amphetamine central nervous system stimulation, potentially resulting in fatal convulsions. [Pg.187]


See other pages where Stimulants dextroamphetamine is mentioned: [Pg.116]    [Pg.63]    [Pg.116]    [Pg.63]    [Pg.464]    [Pg.637]    [Pg.892]    [Pg.104]    [Pg.147]    [Pg.242]    [Pg.242]    [Pg.279]    [Pg.280]    [Pg.342]    [Pg.349]    [Pg.208]    [Pg.354]    [Pg.270]    [Pg.588]    [Pg.619]    [Pg.659]    [Pg.171]   
See also in sourсe #XX -- [ Pg.186 ]




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Dextroamphetamine

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