Monoamine oxidase inhibitors MAOIs

Patients receiving monoamine oxidase inhibitors (MAOI) as antidepressant therapy have been especially subject to the hypertensive effects of vasoactive amines (52). These dietary amines have also been impHcated as causative agents ia migraine. Other aaturaHy occurring alkaloids (qv) have been recognized for centuries as possessing neurological stimulant and depressant properties. 

Monoamine Oxidase Inhibitors. MAOIs inactivate the enzyme MAO, which is responsible for the oxidative deamination of a variety of endogenous and exogenous substances. Among the endogenous substances are the neurotransmitters, norepinephrine, dopamine, and serotonin. The prototype MAOI is iproniazid [54-92-2] (25), originally tested as an antitubercular dmg and a close chemical relative of the effective antitubercular, isoniazid [54-85-3] (26). Tubercular patients exhibited mood elevation, although no reHef of their tuberculosis, following chronic administration of iproniazid. In... 

The term pasaon flower is used to denote many of the approximately 400 species of the herb. F saon flower has been used in medicine to treat pain, anxiety, and insomnia. Some herbalists use the herb to treat symptoms of parkinsonism. F saon flower is often used in combination with other herbs , such a valerian, chamomile, and hops, for promoting relaxation, rest and sleep. Although no adverse reactions have been reported, large doses may cause CNS depression. The use of passion flower is contraindicated in pregnancy and in patientstaking the monoamine oxidase inhibitors (MAOIs). Fission flower contains coumarin, and the risk of bleeding may be increased when used in patientstaking warfarin and pasaon flower. 

The decongestants are contraindicated in patients with known hypersensitivity, hypertension, and severe coronary artery disease These drugs are also contraindicated in patients taking monoamine oxidase inhibitors (MAOIs). Naphazoline is contraindicated in patients with glaucoma. 

Buspirone generally is well tolerated and does not cause sedation. Most common side effects include dizziness, nausea, and headaches. Drugs that inhibit CYP3A4 (e.g., verapamil, diltiazem, itraconazole, fluvoxamine, nefa-zodone, and erythromycin) can increase buspirone levels. Likewise, enzyme inducers such as rifampin can reduce buspirone levels significantly. Bupirone may increase blood pressure when coadministered with an monoamine oxidase inhibitor (MAOI). 

Synergy of unwanted pharmacological effect ginseng and its products will inhibit the central nervous system (CNS) when they are applied with luminal, chloral hydrate, or ephedrine, which can increase the release of dopamine, noradrenaline, and serotonin in the CNS thus inducing a hypertensive crisis if monoamine oxidase inhibitors (MAOIs) are given simultaneously. 

Virtually all types of drug that have been shown to be effective in major depression exert profound effects on the functioning of the serotoninergic or noradrenergic systems, or both. Although some treatments have been shown to decrease the sensitivity of certain postsynaptic 5-HT and NE receptors, it is generally believed that it is an enhancement of neurotransmission in these systems that is responsible for the improvement of the core symptoms of depression. For instance, long-term administration of tricyclic antidepressants (TCAs) or monoamine oxidase inhibitors (MAOIs) decreases the density of (3-adrenoceptors and cortical 5-HT2 receptors (Blier and Abbott 2003). 

A number of medications used in the treatment of anxiety have effects on serotonin neurotransmission (Ch. 13). These medications include tricyclic antidepressant medications, SSRIs, and monoamine oxidase inhibitors (MAOIs). However, because these medications take weeks to exert their full anxiolytic effects, it is unlikely that blocking the reuptake (and thus increasing synaptic levels) of either serotonin or norepinephrine selectively is responsible for their anxiolytic properties — rather it is suspected that the therapeutic effects are due to changes in gene expression, protein levels, and eventually changes in synaptic connections between neurons. 

Buspirone may increase haloperidol levels and elevate blood pressure in patients taking a monoamine oxidase inhibitor (MAOI). 

The monoamine oxidase inhibitors (MAOIs) phenelzine and tranylcypromine increase the concentrations of NE, 5-HT, and DA within the neuronal synapse through inhibition of the monoamine oxidase (MAO) enzyme system. Both drugs are nonselective inhibitors of MAO-A and MAO-B. Selegiline is available as a transdermal patch for treatment of major depression. It inhibits MAO-A and MAO-B in the brain, but has reduced effects on MAO-A in the gut. 

Accordingto the FDA-approved prescribing information for the transdermal selegiline patch, patients receiving the 6 mg/24 hour dose are not required to modify their diet. However, patients receiving the 9 or 12 mg/24 hour dose are still required to follow the dietary restrictions similar to the other monoamine oxidase inhibitors (MAOIs). 

Medication Restrictions for Patients Taking Monoamine Oxidase Inhibitors (MAOIs)... 

Blocking Enzymes. Remember that there are enzymes both in the synapse and in the cytoplasm of the nerve cells that metabolize and thereby inactivate neurotransmitter molecules. One way to promote neurotransmission is to increase the supply of available neurotransmitter. Blocking (or inhibiting) the enzymes that destroy neurotransmitter will do just that. Certain antidepressants known as monoamine oxidase inhibitors (MAOIs) and some medications used to treat Alzheimer s disease act in this manner. 

Listing of antidepressants grouped by principal mechanism of action in the synapse. Abbreviations MAOI—irreversible = irreversible monoamine oxidase inhibitor MAOI—reversible = reversible monoamine oxidase inhibitor NDRl = norepinephrine/ dopamine reuptake inhibitor NRI = norepinephrine reuptake inhibitor NSRl = norepinephrine/serotonin reuptake inhibitor NSSA = norepinephrine/specific serotonin agonist SRI = serotonin reuptake inhibitor SRl/serotonin-2 blocker = serotonin reuptake inhibitor and serotonin-2 receptor antagonist. 

Monoamine Oxidase inhibitors (MAOis). The first antidepressant discovered was iproniazid. This medication was developed in the early 1950s as a treatment for tuberculosis but was unexpectedly found to improve mood in depressed patients. It was later found that its antidepressant effect was due to its action on the MAO enzymes. Unfortunately, iproniazid was subsequently found to cause liver damage and was withdrawn from the market. 

Monoamine Oxidase inhibitors (MAOis). Developed in the 1950s, the MAOIs were the first class of antidepressants. Subsequently, in the 1960s, the MAOis were also found to be effective anxiolytics. Unlike benzodiazepines and barbiturates, the MAOis are not addictive however, their onset of action is delayed not by minutes or hours but by 3 weeks or more. 

Monoamine Oxidase Inhibitors (MAOIs). Shortly after their introduction, MAOIs, snch as phenelzine (Nardil), were found to reduce the frequency of panic attacks. It became a standard treatment for what is now known as panic disorder nntil snpplanted by the benzodiazepines and SSRIs. Although all MAOIs are presumably effective for panic disorder, phenelzine is the best studied and has been shown to be effective at daily doses ranging from 45 to 90 mg. When used to treat panic disorder, phenelzine should be initiated at a dose of 15mg/day and gradually increased in 15 mg increments until reaching a therapeutic dose. 

Monoamine Oxidase Inhibitors (MAOIs). Controlled trials comparing the M AOl phenelzine to clomipramine or fluoxetine have produced mixed results. Given the limited data regarding any efficacy of MAOIs in the treatment of OCD coupled with their potentially dangerous interactions, we cannot recommend MAOIs in the treatment of OCD until other approaches have been tried. 

Monoamine Oxidase inhibitors (MAOis). Many, though not all, antidepressants are effective treatments for social anxiety disorder. Although they do not provide rapid symptom relief and may even transiently worsen anxiety symptoms during the first 1-2 weeks of treatment, antidepressants have the advantage of treating comorbid depression. 

Monoamine Oxidase Inhibitors (MAOIs). Early studies also evaluated the effectiveness of the MAOl phenelzine. Phenelzine, relative to TCAs, provided greater benefit for PTSD however, its usefulness is limited by its potential for drug and food interactions. A recent open label study suggests that the reversible MAOI moclobemide might be helpful for PTSD. It is not available in the United States. 

Monoamine Oxidase inhibitors (MAOis). There are no controlled studies of MAOIs for the treatment of AN. In addition, the dietary restrictions imposed on patients taking this class of antidepressant and their propensity for lowering blood pressure makes their use in AN inadvisable. In the future, the issue of using MAOis may be reopened with the advent of the so-called reversible MAOis such as moclobemide that apparently do not require a tyramine-restricted diet. 

Monoamine Oxidase Inhibitors (MAOIs). MAOI autidepressauts were derived from drugs developed iu the early 1950s to treat tuberculosis. They act by iuterferiug with the MAO euzymes that metabolize aud thus elimiuate dopamiue, uorepiueph-riue, serotouiu, aud other related substauces. The MAO euzyme comes iu two varieties, MAO-A aud MAO-B. It is the MAO-B euzyme that metabolizes dopamiue. 

Monoamine Oxidase Inhibitors (MAOIs). The MAOls work in a unique fashion by blocking the activity of an enzyme that degrades each of three key brain transmitters norepinephrine, dopamine, and serotonin. These widespread effects on several brain transmitter systems make the MAOls a potentially very effective class of medications for a variety of disorders. A few small studies have evaluated the usefulness of the MAOls in the treatment of BPD and found them moderately helpful for the impulsivity associated with this illness. Unfortunately, the requirements for strict dietary restrictions due to a risk of hypertensive crisis severely limit the usefulness of MAOls in the treatment of BPD. These restrictions are a particular concern when treating patients who have problems with impulsivity and are therefore likely to have difficulty maintaining the dietary regimen. For this reason, although they may theoretically be helpful, MAOls should only be used to treat BPD after other more easily tolerated medications have been tried and have failed. In the near future, so-called reversible MAOls that appear to avoid the need for diet restrictions may become available. If so, this will allow us to reconsider their use in the treatment of BPD. For more information regarding the use of MAOls, please refer to Chapter 3. 

Monoamine Oxidase Inhibitors (MAOIs). As mentioned earlier, the MAOIs are excellent treatments for both depression and anxiety. They act by increasing neurotransmission of three neurotransmitter systems serotonin, norepinephrine. 

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