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Related Terms
  • Acquired immune deficiency syndrome, acquired immunodeficiency syndrome, acrodermatitis enteropathica, AIDS, AIDS-defining illness, antifungal, aphthous stomatitis, aphthous ulcers, Candida albicans, canker sores, celiac disease, celiac sprue, chemotherapy, cold sores, fever blisters, fungal infection, fungal spores, fungi, fungus, gastroesophageal reflux disease, GERD, hairy leukoplakia, herpes simplex, herpes simplex virus, herpes virus, HIV, human immunodeficiency virus, immune, immune defense system, immune system, immunocompromised, immunodeficiency, infection, inflammation, leukoplakia, mucositis, opportunistic infection, oral candidiasis, oral herpes, oral mucositis, oral thrush, radiation mucositis, radiation-induced mucositis, throat culture, thrush, zinc, zinc deficiency.

  • Mouth ulcers are open lesions or sores in the mouth that can be caused by many different disorders or conditions, such as viral or fungal infections, immune deficiency, or cancer. Types of mouth ulcers include acrodermatitis enteropathica, canker sores, cold sores, oral leukoplakia, oral candidiasis (oral thrush), and oral mucositis.
  • Acrodermatitis enteropathica is a medical condition in which the body is unable to absorb zinc.
  • Canker sores are common but mostly harmless, and they appear inside the mouth as white or gray ulcers, which are eroded areas of the oral cavity that are marked by tissue disintegration, with a red border. A small percentage of patients may develop severe canker sores (complex aphthosis), which are persistent and painful sores. In infants, painful sores may interfere with eating and may require a visit to the pediatrician. In patients with a weakened immune system (for example, patients who are HIV positive or receiving chemotherapy), the fungus may spread throughout the body, causing infection in the esophagus (esophagitis), brain (meningitis), heart (endocarditis), joints (arthritis), or eyes (endophthalmitis).
  • Cold sores, or herpes labialis, is a condition that involves sores on the lips and inflammation of the gums and mouth. It is caused by the herpes simplex virus type 1 (HSV-1).
  • Oral leukoplakia is a condition in which thickened, white patches form on the gums, on the inside of the cheeks, and sometimes on the tongue. The cause of leukoplakia is unknown, but it is considered to result from chronic irritation. A subtype of leukoplakia is oral hairy leukoplakia (OHL). Hairy leukoplakia of the mouth is an unusual form of leukoplakia that is seen only in people who are infected with the human immunodeficiency virus (HIV) or have acquired immunodeficiency syndrome (AIDS) or AIDS-related complex.
  • Oral thrush is a fungal or yeast infection in the mouth caused by an overgrowth of the fungus Candida albicans.
  • Oral mucositis is an inflammation of mucous membranes of the mouth, and it has been reported in many patients receiving radiation therapy.
  • Symptoms of mouth ulcers include pain and redness at the site of the lesion. Diagnosis is usually performed by examination of the appearance of the lesion or further tests, such as a blood test or biopsy. Treatment involves oral hygiene, topical preparations, and avoidance of irritating substances on or near the lesion.

Risk factors and causes
  • Central nervous system disorder: The precise cause of a migraine attack is not completely understood. There appears to be general agreement, however, that a key element is changes in the blood flow within the brain due to a variety of triggers. The most widely accepted theory suggests that a migraine attack is precipitated when pain-sensing nerve cells in the brain (called nociceptors) release chemicals called neuropeptides (nerve proteins) in response to stimulation of the trigeminal nerve system. At least one of the neurotransmitters (chemicals that transmit impulses to the brain), substance P, increases the pain sensitivity of other nearby nociceptors. Other neuropeptides act on the smooth muscle surrounding cranial (skull) blood vessels, causing inflammation. This smooth muscle regulates blood flow in the brain by causing vasodilation (relaxation of blood vessels) or vasoconstriction (contracting the blood vessel). At the onset of a migraine headache, neuropeptides are thought to cause muscle relaxation, allowing vessel dilation and increased blood flow. Other neuropeptides increase the permeability of cranial (skull) blood vessels, allowing fluid containing inflammatory chemicals to leak and promote inflammation and tissue swelling. The pain of migraine is though to result from this combination of increased pain sensitivity, tissue, and vessel swelling, and inflammation.
  • Heredity: Susceptibility to migraine may be inherited. A child of a migraine sufferer has as much as a 50% chance of developing a migraine attack in their lifetime. If both parents are affected, the chance rises to 70%. However, the gene or genes responsible have not been identified. Genetics also increase the chances of having migraine attacks that are chronic (or long-term).
  • Neurotransmitters: Neurotransmitters are chemical messengers in the brain. Two important ones, serotonin and dopamine, appear to be critical in the processes leading to a migraine attack. Serotonin (also called 5-hydroxytryptamine or 5-HT) is involved in regulation of pain perception and mood, among other important functions. A number of studies have suggested that serotonin can stop the migraine process. To support this observation, higher-than-normal levels of a serotonin compound are excreted in urine and levels of serotonin in the blood drop during a migraine attack. Also, drugs that target receptors in the brain for serotonin are generally effective in stopping a migraine. The receptors for serotonin implicated in a migraine attack are found on the trigeminal nerve endings. Serotonin appears to block the peptides (including substance P) involved in over-stimulating nerves and producing inflammation.
  • Dopamine, another important neurotransmitter, may act as a stimulant or accelerator of the migraine process. Some evidence suggests that certain genetic factors make people over-sensitive to the effects of dopamine, which include nerve cell excitation. Such nerve-cell over-activity could trigger the events in the brain leading to migraine. The prodromal symptoms (including mood changes, yawning, or drowsiness), for example, have been associated with increased dopamine activity. Dopamine receptors are also involved in regulation of blood flow in the brain, which may be of importance when dealing with vasoconstriction and vasodilation.
  • Calcium-channels: Some migraines may be due to abnormalities in the channels within cells that transport the electrical ions calcium, magnesium, sodium, and potassium. Calcium-channels regulate the release of serotonin, an important neurotransmitter in the migraine process. Magnesium interacts with calcium-channels and magnesium deficiencies have been detected in the brains of migraine patients. Calcium-channels also play a major role in cortical spreading depression (CSD), a brain event that includes a "wave" of nerve impulses (firing) that spreads across the surface of the brain, moving from the back (occipital region) of the cerebral cortex toward the front at about one-eighth to three-sixteenth inches (three to five millimeters) per minute. After the nerve excitation, a depression in nerve cell function occurs that can last for minutes. CSD is thought to be one of the causes of a migraine attack. Some individuals with migraine may inherit one or more factors that impair calcium-channels, making them susceptible to headaches. For example, mutations in a gene that encodes calcium channels appears to be responsible for familial hemiplegic migraine.
  • Gender and Age: A migraine attack is three times more common in women than in men. Although the exact relationship between hormones and headaches is not clear, fluctuations in estrogen and progesterone seem to trigger headaches in many women with migraine headaches, including those with premenstrual syndrome (PMS) and menopause. It seems to be hormonal fluctuations, or changes, that trigger migraine attacks, not the presence of the hormone. Prepubescent females, or females prior to reproductive maturity, can also suffer from migraines. Women with a history of migraines often have reported headaches immediately before or during their periods. Others report more migraines during pregnancy or menopause. Hormonal medications, such as oral contraceptives (birth control pills) and hormone replacement therapy (HRT, including estrogen and progesterone therapy), may also worsen migraines. In children younger than 10 years, boys appear to have migraines more often than girls. After puberty starts, migraine headaches are much more common in females (female-to-male ratio, 3:1), most likely due to hormonal changes.
  • In general, the rate of migraine occurrence in males drops to a low by age 28-29 years, with one case per 1,000 people in this age group.
  • Migraine occurrence among females increases sharply up to age 40 years and then declines gradually.
  • The age when migraine headache with aura begins appears to peak at or before age 4-5 years (6.6 cases per 1000 people in that age group), while the highest rate for migraine without aura occurs at age 10-11 years (10.1 cases per 1000 people in that age group).
  • The severity and frequency of attacks tend to lessen with age. Data suggests that migraine attacks are a chronic (long-term) condition, although long remissions (illness-free periods) are common. One study showed that 62% of young adults were free of migraine headaches for more than two years, but only 40% continued to be free of them after 30 years.
  • Diet: Certain foods and beverages appear to trigger headaches in sensitive individuals. Common dietary triggers include alcohol (especially beer and red wine), aged cheeses, chocolate, fermented, pickled, or marinated foods (tofu, kim chee, miso), aspartame (an artificial sweetener), caffeine, monosodium glutamate (MSG, a key flavor enhancer in some Asian foods), and many canned and processed foods. Skipping meals or fasting also can trigger migraines. Eating proper food is very important in migraine prevention because a continuous supply of proper nutrients is essential to keeping chemical balance in the brain. Brain chemistry can be changed significantly by a single meal and, in turn, some changes in food composition can rapidly affect brain function. While all foods eaten modify brain function, some specifically alter mood or energy, such as caffeine or refined sugars. Eating unhealthy foods that do not supply adequate nutrients for proper brain function, or foods that alter brain function can cause migraine attacks in susceptible individuals
  • Magnesium deficiency: Because levels of magnesium (a mineral involved in nerve cell function) also drop right before or during a migraine headache, it is possible that low amounts of magnesium may cause nerve cells in the brain to misfire. About 20% of the population consumes less than two-thirds of the RDA (recommended dietary allowance) for magnesium.
  • Stress: A period of hard work followed by relaxation may lead to a "weekend migraine" headache. Acute (immediate) or chronic (long-term) stress at work or home also can set off a migraine.
  • Sensory stimulus: Bright lights, sun glare, and unusual smells, including pleasant scents (such as perfume or flowers), and unpleasant odors (such as paint thinner and secondhand smoke) can trigger a migraine attack.
  • Physical factors: Intense physical exertion, including sexual activity, may provoke migraines. Changes in sleep patterns, including too much or too little sleep, also can initiate a migraine headache. Sleep changes are usually seen in both adults and children with migraines. Healthcare professionals recommend eight hours of uninterrupted sleep nightly for adults. Sleep helps regulate certain neurochemicals (brain chemicals), including serotonin. Decreases in serotonin may cause a migraine attack.
  • Environmental changes: A change of weather, season, altitude level, barometric pressure, or time zone can prompt a migraine headache. Environmental changes such as moving to a new area where the plants and pollens are different may also trigger a migraine attack.
  • Medications: Taking certain medications can aggravate migraines, including oral contraceptives (birth control pills), estrogen replacement therapy, nitrates (nitroglycerin), theophylline (Slobid®), reserpine (Serpasil®), nifedipine (Procardia® or Adalat®), indomethicin (Indocin®), cimetidine (Tagamet®), decongestant overuse (such as pseudoephedrine or Sudafed®), and anti-anxiety drug withdrawal, including alprazolam (Xanax®) and diazepam (Valium®). Caffeine withdrawal and the discontinuation of pain medications can trigger a migraine.

Signs and symptoms
  • Most individuals with mitral valve prolapse (MVP) have no symptoms, and do not require treatment or close monitoring. MVP is often not diagnosed until after complications (such as infectious endocarditis, sudden cardiac death, heart attack, stroke, or severe mitral regurgitation) arise. Echocardiography may be used to identify patients at higher risk of complications.
  • In some patients, the mitral valve leaflets make a clicking sound when they close. A doctor may hear this when listening to the heart with a stethoscope. Individuals with MVP may also have a heart murmur, which is the sound caused by the leaking blood.
  • Individuals with MVP may also experience dizziness or light-headedness, anxiety, exhaustion, breathlessness (especially when playing or exercising), heart palpitations, chest pain, or fainting episodes. Symptoms of MVP in children may go away as they age.

  • Because mitral valve prolapse (MVP) often presents with no symptoms, diagnosis is usually made during echocardiography performed for other purposes. MVP may also be diagnosed based on heart sounds in routine physical examinations, and confirmed with echocardiography. MVP is often not diagnosed until after complications arise, such as infectious endocarditis, sudden cardiac death, heart attack, stroke, or severe mitral regurgitation. Echocardiography is a non-invasive test that may also be used to diagnose and assess MVP.
  • MVP is most accurately diagnosed using three-dimensional echocardiography. True MVP is diagnosed if mitral leaflet prolapse is at least 2 millimeters in the long-axis view of the mitral valve. Prolapse of at least 5 millimeters, accompanied by leaflet thickening, is defined as classic MVP. If there is little to no thickening of the mitral leaflets, non-classic MVP is diagnosed. Because non-classic MVP and prolapse of less than 2 millimeters are not significantly associated with the complications of classic MVP, they are thought to be normal variants of mitral valve structure.
  • Transesophageal echocardiography is often used to determine the location of the prolapse (anterior, posterior, or which leaflet is prolapsed) and the severity of the prolapse (symmetric vs. asymmetric or flail vs. non-flail).

  • Mitral valve prolapse (MVP) is most often an inherited disorder with no symptoms. However, in rare cases, serious complications may occur. Complications associated with MVP include infectious endocarditis, sudden cardiac death, heart attack, stroke, or severe mitral regurgitation. in a subset of patients with MVP
  • Patients with classic MVP (defined as prolapse of at least 5 millimeters accompanied by leaflet thickening) are at a higher risk for complications than those with non-classic MVP (defined as prolapse with little or no mitral valve thickening). Leaflet thickening of at least 5 millimeters increases the risk of complications 14-fold. Other risk factors for complications include mitral regurgitation during exercise (but not at rest).
  • The rate of complications may be predicted by a patient's symptoms and the number of major and minor risk factors. Major risk factors include mitral regurgitation (mild to moderate) and left ventricular ejection fraction of less than 50%. Minor risk factors include mild mitral regurgitation, floppy leaflets, atrial fibrillation, increased age (>50 years), and enlargement of the left atrium. In MVP patients with no symptoms and only minor risk factors, the 10-year risk of complications is very low (2-15% for 0-2 risk factors). For MVP patients with major risk factors, the rate of complications is much higher (78% for one or more major risk factors).
  • Infective endocarditis: MVP increases the risk of infective endocarditis, a microbial infection of the heart, by about 800%. However, the annual risk of developing infective endocarditis in MVP patients is low (about 0.02). In MVP patients with a systolic murmur, the risk is higher (about 0.05%). Prophylactic (preventive) antibiotics may be used in high-risk MVP patients, especially those undergoing dental procedures (which increase the risk of developing infective endocarditis), those over age 50, and those with left ventricular dilatation, left atrial enlargement, or leaflet thickening.
  • Sudden cardiac death: Sudden cardiac death (SCD) is a rare complication of MVP, occurring in about one of every 250 cases of MVP annually (about twice the rate of the normal population). It is unclear what causes SCD in MVP patients, though arrhythmias, particularly ventricular tachyarrhythmias (abnormal heart rhythms that are rapid, with or without other abnormalities) appear to increase the risk of SCD in MVP.
  • Cerebrovascular ischemic events: Patients with MVP also have a 0.7% risk of cerebrovascular ischemic events, such as heart attack and stroke, which represents a slight increase (about 2-fold) over the rest of the population. The increased risk of cerebrovascular events may be caused by increased coagulation associated with mitral regurgitation.
  • Severe mitral regurgitation: Mitral regurgitation may progressively worsen in MVP patients, requiring corrective surgery. Severe mitral regurgitation risk increases with body weight, which may explain why MVP-related complications are generally more common in men than in women.

  • Most individuals with mitral valve prolapse (MVP) have no symptoms, and do not require treatment or close monitoring. However, for symptomatic MVP, surgical repair is the treatment of choice. Experienced surgeons may also perform valve repair surgery for asymptomatic MVP if there is increased risk of complications (such as a flail asymmetric leaflet).
  • Surgical procedures in mitral valve repair include leaflet resection (removal). Annuloplasty (plastic repair of the heart valve) rings (rigid or flexible) may be inserted to repair the structure of the annula.
  • Mitral valve repair has a 10-year success rate of 93% and a 20-year success rate of 80%. Risks from the surgery include bleeding, infection, and anesthesia-associated complications. Less than one percent of patients undergoing mitral valve repair die during surgery.
  • Guidelines for managing patients with heart valve diseases, including MVP, are set forth by the American College of Cardiology/American Heart Association (ACC/AHA) Task Force. Interventions are categorized as ACC/AHA Classes I-III based on evidence or consensus opinion on effectiveness.
  • ACC/AHA Class I: For Class I recommendations, there is either evidence or consensus opinion that the interventions are useful and effective. Valve surgery is recommended for severe or acute mitral regurgitation when the valve is repairable, in symptomatic mitral regurgitation with normal left ventricular (LV) function and dimensions, and in mild-to-moderate LV abnormalities, such as enlargement, or in reduced systolic function.
  • ACC/AHA Class II: In Class II recommendations, there is either conflicting evidence or a disagreement about the usefulness or efficacy of an intervention.
  • Class IIa recommendations have evidence or opinion in favor of the intervention. Therapies in this class include surgery for severe mitral regurgitation accompanied by atrial fibrillation or pulmonary hypertension, in asymptomatic patients with atrial fibrillation and normal LV, and in patients with pulmonary hypertension.
  • In Class IIb recommendations, the usefulness or effectiveness of the intervention is less established by evidence or opinion. These include surgery for MVP patients in whom repair is possible, and those with refractory ventricular arrhythmias.
  • ACC/AHA Class III: Class III recommendations have evidence and/or consensus opinion that an intervention is not beneficial, and may, in fact, be harmful. Treatments in this class include surgery for patients in whom repair is unlikely and patients with normal LV function and no symptoms. For these patients, close monitoring is recommended instead of surgery.

Integrative therapies
  • Unclear or conflicting scientific evidence:
  • Coenzyme Q10: Coenzyme Q10 (CoQ10) is produced by the human body and is necessary for the basic functioning of cells. Promising preliminary evidence suggests that CoQ10 supplements may help reduce the risk of cardiovascular disease, including heart attack and high blood pressure. There is also early data to support the use of CoQ10 in children with mitral valve prolapse. Well-designed clinical trials are needed before a recommendation can be made.
  • Magnesium: Magnesium supplementation has been reported to improve most mitral valve prolapse (MVP) symptoms. Several studies indicate patients with MVP are low in magnesium. Additional study is needed to reach a conclusion.
  • Historical or theoretical uses that lack sufficient evidence:
  • Pycnogenol: Pycnogenol® is the registered trade name for a patented water extract of the bark of the French maritime pine (Pinus pinaster ssp. atlantica), which grows in coastal southwestern France. Pycnogenol® contains oligomeric proanthocyanidins (OPCs), as well as several other bioflavonoids: catechin, epicatechin, phenolic acids (such as ferulic acid and caffeic acid), and taxifolin. Procyanidins are oligomeric catechins found at high concentrations in red wine, grapes, cocoa, cranberries, and apples. Procyanidins are often incorporated into supplements, such as Pycnogenol®, for their antioxidative properties. Pycnogenol® is thought to be beneficial for MVP, but there is a lack of research on its effectiveness.

  • Mitral valve prolapse (MVP) is most often an inherited disorder with no symptoms. Therefore, prevention is not usually a consideration. However, because there is an increased risk of serious complications (such as infectious endocarditis, sudden cardiac death, heart attack, stroke, or severe mitral regurgitation) in a subset of patients with MVP, echocardiography may be used to identify patients at higher risk of complications. The appropriate treatment and preventative measures for these complications (including mitral valve surgery) then may be performed.
  • Prophylactic (preventative) antibiotics may be used in high-risk MVP patients, especially those with systolic murmur or those undergoing dental procedures that increase the risk of developing infective endocarditis.
  • Risk of cardiovascular events (such as sudden cardiac death, heart failure, heart attack, and stroke) and associated mortality may be reduced through weight loss (through diet and exercise), reducing alcohol and sodium consumption, and quitting smoking.

Author information
  • This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (

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Copyright © 2011 Natural Standard (

The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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