Methylphenidate Monoamine oxidase inhibitors

Monoamine oxidase inhibitors Paroxetine Protriptyline Sertraline Venlafaxine Stimulants Atomoxetine Dextroamphetamine Methylphenidate Modaflnil Pemoline... 

Patients with marked anxiety, tension, and agitation, because the drug may aggravate these symptoms hypersensitivity to methylphenidate or other components of the product patients with glaucoma, motor tics, or a family history or diagnosis of Tourette s syndrome during treatment with monoamine oxidase inhibitors (MAOIs), and also within a minimum of 14 days following discontinuation of an MAOl (hypertensive crises may result). 

Monoamine oxidase inhibitors Methylphenidate Metoclopramide Niridazole... 

Methylphenidate should not be used with monoamine oxidase inhibitors such as tranylcypromine. Symptoms of overdose may include euphoria, confusion, delirium, coma, toxic psychosis, agitation, headache, vomiting, dry mouth, mydriasis, self-injury, fever, diaphoresis, tremors, hyper-reflexia, muscle twitching, seizures, flushing, hypertension, tachycardia, palpitations, and arrhythmias. 

Amphetamine [XXII) is a central stimulant and many would not classify it with the antidepressant drugs proper. It has, however, been extensively used in the treatment of depression, it produces euphoria and some at least of its actions may be due to inhibition of monoamine oxidase. However, it also inhibits dopamine- S-oxidase, impairs the noradrenaline binding capacity of the brain and has direct sympathomimetic activity. Its classification with the antidepressants seems, therefore, to be justified, but it is not included with the monoamine oxidase inhibitors, since only a small part of its action can be attributed to enzyme inhibition. Amphetamine is a potentially addictive drug and it should be used cautiously and over short periods of time. Other compounds which are used, if at all, only for the treatment of mild depression, include methylphenidate [XXIII), pipradol [Table 5.2) and deanol (XXIV). The last named compound is interesting since it may owe its effectiveness to a stimulant action on acetylcholine synthesis > . ... 

Drug Interactions Barbiturates combine with other CNS depressants to cause severe depression ethanol is the most frequent offender, and interactions with first-generation antihistamines also are common. Isoniazid, methylphenidate, and monoamine oxidase inhibitors also increase the CNS-depressant effects. Other prominent drag interactions occin as a result of the induction of hepatic drug-metabolizing enzymes by barbiturates see above). 

Methylphenidate like cocaine largely acts by blocking reuptake of monoamines into the presynaptic terminal. Methylphenidate administration produces an increase in the steady-state (tonic) levels of monoamines within the synaptic cleft. Thus, DAT inhibitors, such as methylphenidate, increase extracellular levels of monoamines. In contrast, they decrease the concentrations of the monoamine metabolites that depend upon monoamine oxidase (MAO), that is, HVA, but not catecholamine-o-methyltransferase (COMT), because reuptake by the transporter is required for the formation of these metabolites. By stimulating presynaptic autoreceptors, methylphenidate induced increase in dopamine transmission can also reduce monoamine synthesis, inhibit monoamine neuron firing and reduce subsequent phasic dopamine release. 

Inhibitors of monoamine oxidase type B (selegiline, phenelzine) Stimulants (methamphetamine, methylphenidate, pemoline)... 

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