monoamine oxidase inhibitor (MAOI) medication (Parkinson’s disease)

A drug that blocks or interferes with the actions of monoamine oxidase, an enzyme that has a key role in the metabolism of the monoamine neurotransmitters acetylcholine, dopamine, epinephrine, norepinephrine, and serotonin. Scientists have known for decades that MAO activity is involved in functions of the brain related to mood, emotion, and behavior. An imbalance between MAO and neurotransmitters, through either a decrease in MAO production or an increase in neurotransmitter production, is linked to depression.

MAOIs, which became available in the 1950s, were the first drugs available to treat depression and are still used for this purpose today. They work by blocking the action of MAO to extend neurotransmitter presence and action. The earlier formulations of these drugs are nonselective for MAO type; they include phenelzine (Nardil), Isocarbox-azid (Marplan), and Tranylcypromine (Parnate), which block both MAO-A and MAO-B. However, these medications have significant side effects as well as extensive interactions with foods and other medications.

MAOIs to Treat Parkinson’s Disease

Because conventional MAOIs do extend the availability of dopamine, neurologists have tried using them to relieve symptoms of people with Parkinson’s disease. However, this effect also extends the availability of norepinephrine and epinephrine, which can cause rapid heart rate, arrhythmias (irregularities in the heartbeat), and sudden and serious (sometimes fatal) escalations in blood pressure. As well, MAOIs interact with Levodopa, dopamine agonists, and many other anti-parkinson’s MEDICATIONS.


Possible Side Effects

Medication Interactions

Food Interactions

Hypotension, orthostatic hypotension (low blood pressure)

Hypertension (high blood pressure)

Headache, drowsiness

Hallucinations, disorientation, confusion, delirium, delusions, sleep disturbances

Anxiety, psychosis

Levodopa, dopamine agonists

Most antihypertensives (drugs that treat high blood pressure)

Beta-blockers (propanolol, nadolol, metoprolol)

Thiazide diuretics

Tricyclic antidepressants (amitriptyline, nortriptyline)

Fava beans (broad beans, long beans)

Caffeine (coffee, tea, cola)

Chocolate, licorice

Aged cheese (cheddar, brie, camembert, emmenthaler, gruyere, mozzarella, parmesan, romano, bleu, roquefort)

Beer, red wine, sherry

Tremors, myoclonus, ataxia, sensory disturbances, blurred vision

Dry mouth constipation


St.-John’s-wort (hypericum), buspirone

Hard sausage (salami, pepperoni, Lebanon bologna), summer sausage

Smoked meats and fish

Liver damage Edema

Urinary retention, sexual dysfunction

Carbamazepine (Tegretol)

SSRI antidepressants (fluoxetine, paroxetine, citalopram, sertraline)

Other MAOIs including selegiline

Oral antidiabetes medications

Pickled or kippered fish (herring), anchovies, caviar

Avocados, bananas, bean curd, figs, prunes, raisins, raspberries

Liver (including chicken liver), liver pate, liver sausage (braunschweiger)

Decongestants in cold medicines (ephedrine, pseudoephedrine, phenylephrine

Sauerkraut, soy sauce, yeast

Dextromethorphan cough suppressant


Methyldopa (Aldomet)


Sulfonamide antibiotics (oral, topical, ophthalmic)


Phenothiazine antipsychotics




Ginseng, 5-HTP supplement


A new MAO, selegiline (Deprenyl), blocks only MAO-B and extends the availability of dopamine without affecting MAO metabolism of other monoamine neurotransmitters. Doctors sometimes prescribe selegiline as one of the adjunct therapies with Levodopa, to allow a lower levodopa dose. Some people with de novo Parkinson’s (newly diagnosed and not yet treated) are able to forestall levodopa therapy by starting on monotherapy of selegiline. A five-year study conducted from 1987 to 1992, the DATATOP (Deprenyl and Tocopherol Antioxidative Therapy for Parkinson’s Disease) study, found selegiline (as the brand name product Deprenyl) could delay the need for levodopa therapy by one to three years in de novo Parkinson’s. Despite these findings, there remains considerable controversy within the medical community as to whether its use is therapeutically prudent when looking at the entire spectrum of anti-Parkinson’s therapy. Most movement disorders specialists believe that because degeneration continues even with selegiline, symptoms are more severe and accordingly more difficult to control when more potent (levodopa or dopamine agonist) or possibly protective (dopamine agonist) therapy is delayed. Most neurologists believe that dopamine agonists are a better choice than selegiline in delaying the need for levodopa because selegiline is less potent, has similar side effect potential, and, at present, has no stronger (and, in the opinion of most experts, substantially weaker) evidence of a possible neuro-protective effect than dopamine agonists.

MAOIs and Tyramine

As well as blocking the action of MAO to metabolize monoamine neurotransmitters, MAOIs inhibit metabolism of the amino acid tyramine. Tyramine, along with norepinephrine and epi-nephrine, helps to regulate blood pressure. When its levels rise, so does blood pressure. Many foods—especially those that are aged or smoked—contain tyramine. Eating such foods while taking a conventional MAOI causes sudden surges in tyramine levels, as the drug blocks the body’s normal response mechanism (increasing MAO production). This can cause spikes in blood pressure that can result in severe headache as well as brain hemorrhage that causes stroke and death. For this reason, people taking conventional MAOIs have broad dietary restrictions.

The MAOI-B medication selegiline, because it selectively blocks MAO action to metabolize dopamine but not other MAO neurotransmitters, does not have the same effect with tyramine. Although it is prudent to avoid foods that are high in tyramine to minimize fluctuations in blood pressure, dietary restrictions are much less severe for people who use selegiline.


MAOIs, because they block the action of MAO on all brain MAO neurotransmitters, extend the availability of serotonin, a neurotransmitter that often is at lower than normal levels in people who have depression. This is one of the ways in which MAOIs exert an antidepressive effect. However, the newer antidepressants, selective serotonin

REUPTAKE INHIBITOR (SSRI) MEDICATIONS, block the process by which neurons reabsorb serotonin after its release. This action also extends the availability of serotonin. if medications of each type are taken, the result is an excess of serotonin in the brain, which can cause a potentially fatal condition called serotonin syndrome, toxic serotonin syndrome, or serotonin toxicity. Symptoms include euphoria, drowsiness, abnormal movements of the foot, lack of coordination, restlessness, dizziness, sense of intoxication, tremors and twitching, muscle rigidity, elevated body temperature, confusion, diarrhea, and sometimes loss of consciousness and death. Serotonin syndrome requires emergency medical treatment. While much less likely to precipitate a serotonin syndrome than MAO-A inhibitors, taking selegiline or other MAO-B inhibitors with SSRIs is believed to carry some risk of causing this potentially life threatening condition.


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