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Contents A. Case study B. More information C. Editors' comments D. References E. CEU questions

Index

A. Case study
A 17-year-old girl presented with episodes of moderate to severe migraines. She had experienced these episodes for over a year, about once every 2 months, but when they started occurring more frequently (about once a week), her mother suggested that she go to the doctor. After a consultation, the doctor was unwilling to prescribe medication before determining whether any foods or other entities might be precipitators, so he referred her to a dietitian. He thought that if there were precipitators that could be eliminated, medication would not be necessary.

The dietitian confirmed that the doctor had considered the possible organic causes, e.g., sinus headaches, tumours) before embarking on her assessment.

TYPES OF PRECIPITATORS TO BE CONSIDERED
a. Non-dietary: stress, fatigue, exertion, sleep deprivation, sleeping too long or deeply, bright lights, head trauma, weather changes, high altitude, and hormonal changes (menstruation and oral contraceptives)
b. Dietary: Foods and related substances such as tyramine, chocolate, caffeine, aspartame, nitrites, MSG, alcohol, and fatty foods; food allergy; fasting and hypoglycemia

HOW COULD THE PRECIPITATING FACTOR(S) BE DETERMINED?
a. Conduct a clinical and diet history.
b. Ask the patient to keep a diary including all possible precipitators.
c. Conduct tests.
d. Put the patient on an elimination diet and follow it with challenges.

DISCUSSION:
a. This could be very helpful.
b. This could also be very helpful, but should be undertaken only if the history is not enough to determine the cause.
c. There are very few tests that can be done to assist in the diagnosis of precipitating factors to migraine.
d. This can be helpful if the results from the history and diary do not reveal the precipitating factors.

A thorough clinical and dietary history was taken, and the following was found:
a. Non-dietary: Stress, fatigue, sleep deprivation: these were isolated as possible factors, as the patient was busy with exams, which she found very stressful, and she could not sleep well.
Exertion, exercise, sleeping too long or deeply, bright lights, head trauma, weather changes, high altitude, and hormonal changes (menstruation and oral contraceptives): these were not applicable to her.

b. Dietary:
Tyramine: this was ruled out as a possibility, as she had eaten foods with high levels of tyramine before without experiencing a headache.
Chocolate: she did not eat chocolate on a regular basis.
Caffeine: she did not drink coffee or caffeine-containing tea; she consumed around 1 liter of cola per day on weekdays, but nothing on weekends.
Aspartame: there was no known regular intake.
Nitrites: there was no association between intake and headaches.
MSG: there was no association between intake and headaches.
Alcohol: she did not drink any alcoholic beverages.
Fatty foods: although she did eat fatty foods on occasion, it was not a regular occurrence at home.
Food allergy: this was ruled out as a possibility.
Fasting & hypoglycemia: she always ate regular meals, and careful evaluation did not indicate that hypoglycaemic episodes were occurring.

DISCUSSION:
The possible causes were therefore stressful events and sleep deprivation (e.g., during exam time), as well as caffeine withdrawal on weekends following consumption of large amounts of caffeine-containing beverages during the week.

HOW IS THIS TREATED?
Stress and sleep deprivation: relaxation techniques and possible referral to a psychologist.
Caffeine: Although there was no clear association between her caffeine intake and her headaches, intake of intermittent large quantities may result in caffeine withdrawal headaches. If caffeine is confirmed as a cause, then gradual withdrawal can be achieved without a headache.

A report was written to the referring doctor stating the findings. It was recommended that medication be considered during periods of stress if the cessation of large amounts of cola was not a sufficient treatment.

TIP for Allergy Advisor users: To investigate whether cola can cause adverse reactions, type in cola on the main menu under “items, substances and allergens”. This will bring up an option where you can read up on adverse reactions to cola that have been recorded. Under the “possible additional constituents”, one will see that “tyramine” and “caffeine” carry the highest risk of being the culprit constituent in cola to cause adverse reactions. When one clicks on either, more details on each will appear.

B. More information:
Migraine is a chronic headache disorder with episodes lasting 4-72 hours. The headache is characteristically unilateral, pulsating, of moderate or severe intensity, aggravated by routine physical activity, and associated with nausea, photophobia (visual intolerance of light) and phonophobia (sensitivity to sound). Migraine aura is a complex of neurological symptoms that occur just before or at the onset of migraine headache.^1,2,3,4 Auras are focal neurologic (usually visual) symptoms that are present in approximately 20% of cases.⁴

About 20% of migraine sufferers experience prodromal changes before the actual aura or pain commences; these can be food cravings, thirst, or altered emotional states.¹

Migraine attacks may occur frequently and for extended periods. Many attacks are disabling and lead to withdrawal from usual activities. In the long term, this may impair school and work performance and adversely affect family and social life.^4,5,6

1. What is the prevalence of migraine?
Migraine headache is a common condition, occurring in 5%-30% of the general population, with a familial predisposition in 60%-80% of cases.⁷ In the USA and Europe the condition affects about 12% of the population;^{3, 6, 8} and in Australia up to 10%.⁸ Migraine has been estimated to affect 1.5% of people in Hong Kong, 2.6% in Saudi Arabia and 3% in Ethiopia. Prevalence rates in Japan and Malaysia are nearer to those found in Western countries, with rates of 8.4 and 9.0%, respectively.⁴

The prevalence of migraine is age- and gender-dependent. Migraine develops most commonly during adolescence and young adulthood. The age of onset is earlier in boys than in girls. Migraine is 2-3 times more common in women than in men, with peak prevalence occurring during mid-life (35-45 years).4,7,9 The prevalence appears to be higher in Caucasians than in Africans or Asians 4,10,11 and is also higher in individuals from lower-income households.12 It was extrapolated that moderate to severe disability from migraine affects 8.7 million women and 2.6 million men of the US population.7,9

Migraine is the most common cause of severe recurrent headache in children. Around 1 in 10 schoolchildren in the UK has the condition and, on average, misses almost 4 days of school a year because of it.^5,13 Children may experience abdominal migraine, which manifests as recurrent paroxysmal abdominal pain. This is headache-free migraine.¹⁴

2. Pathophysiology of migraine and migraine triggers
The etiology of migraine is thought to involve inherited characteristics and/or other specific factors, including stress, hormonal influences, and the ingestion of foodstuffs and additives. Genetics are involved more often in migraine with aura, as compared with migraine without aura. Migraine has been reported to be associated with depression, anxiety, panic disorder, epilepsy, asthma, menstrual disorders, and chest pain (see figure below).⁴ This review will focus on the possible role of dietary factors.

An understanding of the aura and headache components of migraine provides a paradigm for the mechanisms of dietary triggers. Millichap and Yee⁶ give the following account: “The primary event is neuronal, with depolarization of cortical neurons and sensitization of trigeminal nerve ganglia. A secondary phase of vasoconstriction, vasodilatation, and sterile vascular inflammation is mediated by chemical neurotransmitters, especially serotonin receptors. The close anatomic relation between the trigeminal innervation of cerebral vessels, dura, and scalp explains the forehead location of referred migraine pain.”

“Dietary migraine triggers may influence the pathophysiology of migraine at one or more phases of the migraine attack. They could affect the cerebral cortex, trigeminal nerve, brainstem trigeminal nuclei, thalamus, and brain-stem or limbic pathways. The potential mechanisms of action and chemical mediators of these triggers include release of norepinephrine mediated by tyramine and phenylethylamine, release of nitric oxide by nitrates and nitrites, and effects on histamine and glutamate receptors by histamine and MSG. The chemical trigger may stimulate neuroreceptors, cause release of neurotransmitters, or have a direct effect on neurons within the trigemmovascular migraine pathways.”⁶ The mechanisms are further described below.

3. Migraine triggers
In addition to certain foods and beverages, factors known to precipitate headaches in migraine sufferers include stress, fatigue, exercise, exertion, sleep deprivation, sleeping too long or deeply, fasting, bright lights, head trauma, weather changes, high altitude, infection, hormonal changes (menstruation and oral contraceptives) and chemical additives such as specific drugs.^4,6 Children, like adults, often associate headache with stress; adolescents, especially females, are particularly susceptible. Stress and anxiety can influence the severity and threshold to the occurrence and frequency of headaches.⁶

Dietary Triggers
Diet can play an important role in the precipitation of headaches. Between 7% and 44% of migraine patients report a particular food or drink as a precipitant. The diet factor is frequently neglected in favor of preventive drug therapy.⁶

A wide variety of foods and beverages has been implicated as migraine precipitants, the most common being chocolate, cheese, citrus fruit, and alcoholic drinks. In a study of 500 food-sensitive migraine sufferers, 75% implicated chocolate as a precipitant, 48% cheese, 30% citrus fruit and 25% alcoholic drinks. In children, cheese, chocolate and citrus fruit were the principal dietary triggers.¹⁵ Similar results were found in other studies.^16,17

The table below shows a list of food items that have been reported to trigger migraine headaches, and the chemical constituent thought to be specifically involved.⁶

* “Ice cream headache” is probably a cold-induced vasoconstrictor reflex response.⁶

a. Tyramine
Tyramine is a biogenic amine and is found in various foods and beverages, including aged cheese, wine, beer, broad beans and sauerkraut. Tyramine is normally metabolized by monoamine oxidase in the gastrointestinal tract and liver and conjugated by enzymes, bypassing the systemic circulation. It is suggested that migraine patients affected by tyramine have a deficiency in monoamine oxidase and conjugating enzymes, resulting in tyramine being absorbed into the circulation. The result is a vasoconstrictor effect caused by the release of norepinephrine from sympathetic nerve endings.⁶

However, Jansen et al.¹⁸ evaluated 13 oral challenge studies of purported intolerance to dietary biogenic amines. They concluded that the current scientific literature shows no relation between the oral ingestion of biogenic amines and food intolerance reactions.

b. Chocolate
The ingredients in chocolate implicated in chocolate-triggered migraine include phenylethylamine, theobromine, caffeine and catechin. Phenylethylamine is a biogenic amine metabolized by monoamine oxidase enzymes. Theobromine and caffeine are methylxanthines, and catechin is a phenolic compound. These chemicals initiate a headache by altering cerebral blood flow and the release of norepinephrine from sympathetic nerve cells.^6,7

c. Caffeine
Caffeine consumed regularly in large amounts and the abrupt withdrawal of it may lead to headaches and the exacerbation of migraine. Headaches begin within 24-48 hours after discontinuing caffeine ingestion and last for 1-6 days. Cerebral vasoconstriction during caffeine intake is followed by a rebound vasodilatation and increased arterial blood flow when caffeine is discontinued. Children who regularly consume 200 mg of caffeine or more daily are at risk of withdrawal headaches, especially if they are migraine sufferers. Analgesics (containing 30-50 mg of caffeine) may be taken to control the pain, but they can lead to caffeine addiction.⁶ Gradual withdrawal can be achieved without withdrawal headache, and with complete disappearance of the headache.¹⁹ Hospitalization is sometimes necessary to manage serious caffeine dependency.⁶

d. Aspartame
Although aspartame is cleared for general consumption (except for phenylketonuric children), many scientists express caution concerning its use by patients with migraine, epilepsy, and neuropsychiatric problems. It has been shown that aspartame may exacerbate headaches in migraine patients, especially when the exposure is prolonged. The effect of aspartame in pediatric migraine needs to be confirmed with more research, but patients and parents should be warned about its potential adverse effect.⁶

e. Nitrites
Most disorders associated with the consumption of nitrates result from the conversion of nitrates to nitrites in the saliva and intestine.⁶ High concentrations of nitrites are found in hot dogs, bacon, ham, luncheon meats, smoked fish and some cheeses. It is not uncommon to find levels much higher than the FDA-recommended limits of 200 ppm.⁷ Nitrites that are converted from nitrates account for 75% of the average daily intake. Cured meats contain 3.5-20% of the average daily nitrite intake, and 2% comes from vegetables. The headache associated with nitrite consumption has been termed “hot-dog headache”.⁶

Henderson and Raskin20 reported on an adult who had headaches within 30 minutes after eating frankfurters, bacon, salami or ham. In a blinded controlled challenge, he developed headaches after 8 of 13 nitrite doses, compared with none of the placebo. This is the only confirmed report of nitrites causing headaches, although there are numerous reports of headache after nitro-vasodilators, such as nitroglycerine. The postulated mechanism is the release of nitric oxide, acting on the vascular endothelium to produce vasodilatation.6

f. Monosodium Glutamate
Monosodium glutamate is added to many foods as a flavour enhancer, particularly to Asian dishes. It is found in frozen foods, canned soups, salad dressings, processed meats, sauces and snack foods. The term “Chinese restaurant syndrome” was coined after a report by Kwok²¹ that associated Chinese food with headache and a group of other symptoms, including flushing, paresthesias, sweating, palpitations and facial swelling.^6,7 When the symptoms were later attributed to MSG, the name was changed to MSG symptom complex. MSG is a potent vasoconstrictor, and a vascular basis for the symptoms appears most likely. Symptoms generally appear within 15-60 minutes after ingesting relatively large amounts of MSG on an empty stomach.⁶ Thresholds vary from 1.5 to 12 g, but are commonly below 3 g (the amount found in a portion of wonton soup).⁷

However, many studies have failed to show a relationship between this syndrome and MSG intake. Therefore, many clinicians do not believe in MSG causing adverse reactions. Other clinicians have estimated that the prevalence may be as high as 1.8% of the adult population.⁷ The term MSG symptom complex is considered more appropriate than Chinese restaurant syndrome, as Chinese food would not be the only culprit.⁶

g. Alcoholic Beverages
Alcoholic beverages such as wine, especially red wine, have been implicated as potential migraine triggers in adults. Alcohol may seem an unlikely cause of headaches in children, but a recent report entitled "Teen Tipplers" found that 12- to 17-year-olds accounted for 25% of alcohol con¬sumption in the United States, and that their beverages included wine in addition to beer and liquor. When ingested in large quantities, alcohol will often lead to an ordinary hangover headache, but wine, even in moderate amounts, can trigger a migraine headache in sensitive individuals. The substances that can be involved in the headache mechanism are tyramine, histamine, phenolic flavonoids and sulfites. Red wine has higher levels of histamine and phenolic flavonoids than white wine. These chemicals induce headache by various mechanisms: tyramine by releasing norepinephrine, histamine by releasing nitric oxide from the vascular endothelium, and flavonoids by releasing serotonin from platelets.^6,7,22 Alcohol is also a histamine-liberator; i.e., it can enhance the effect of histamine in sensitive individuals.²³

h. Fatty Foods
Fatty acids, primarily linoleic and oleic acids, may be involved in precipitating migraine headaches. During a migraine attack, a significant rise in the blood levels of free fatty acids and blood lipids occurs simultaneously with enhanced platelet aggregability, decrease of serotonin, and heightened prostaglandin levels. Free fatty acids may cause the release of serotonin from platelets, with variable effects on cerebral blood vessels, but with vasodilation usually a prominent one. A decrease in dietary fat to a maximum of 20g/day has been associated with a significant decrease in headache frequency, intensity, and duration.^6,24

i. Ice Cream
Ice cream and other frozen foods may cause headache in migraine sufferers; this headache is usually located over the forehead or behind the eyes. The proposed mechanism is that the application of a cold stimulus to the mouth or throat causes a reflex constriction of blood vessels around the head, resulting in a headache. Ice cream headache is, however, not specific for migraine sufferers; others may also experience this.⁶

j. Food Allergy
Migraine is only rarely immune-mediated. Skin tests for food allergy are therefore generally unhelpful for migraine management.^6,7 A psychological bias has been demonstrated by studies in which double-blind testing confirmed a headache response in only 4 of 23 patients who considered themselves allergic to foods.²⁵ One study showed that in 40% of cases migraine was associated with allergy.²⁶ Another study showed that migraine attacks have been produced most frequently by cow’s milk (in 10 out of 17 patients), cabbage, flour and eggs (in 5 patients), preservatives, cottage and Swiss cheese, and porcine meat (in 4 patients), colorants and chocolate (in 3 patients), beef, strawberries, lemons and butter (in 2 patients). Migraine and other symptoms have diminished after an individual elimination diet. IgE was involved in 3 patients.²⁷

k. Fasting and Hypoglycemia
A computerised behavioural assessment done on children with headaches found that headache was associated with a missed meal in 20-25% of children evaluated.²⁸ In patient-based and subspecialty clinic-based studies, fasting was reported to precipitate headaches in 56% and 45% of migraine patients, respectively.^29,30 Headaches after fasting are more common in individuals with a history of chronic migraine than those without.⁶

Proposed mechanisms for fasting-induced headaches include altered levels of serotonin and norepinephrine, release of stress hormones, hypoglycemia and withdrawal of caffeine beverages. The role of hypoglycemia is questioned because migraine attacks are rarely associated with insulin-induced hypoglycemia in diabetics.⁶

l. Celiac Disease
There have been reports that suggest a causative association between Celiac Disease (CD) and migraine. One study suggests that a significant proportion of patients with migraine may have CD, and that a gluten-free diet may lead to an improvement in migraine in these patients.³¹ In another study, treatment of CD coincided with the total disappearance of severe migraine attacks.³²

4. How is migraine diagnosed?
No definitive laboratory tests exist to confirm the diagnosis of migraine. The diagnosis of migraine is based primarily on history.⁷ The International Headache Society has established diagnostic criteria for migraine.¹ To establish precipitating dietary factors, a diary of headaches and eating habits can be kept for a period of time (usually the time that it takes to experience 2 or more migraine episodes). A selective elimination diet can be implemented, followed by reintroduction of each food to determine the precipitator. The prevention of debilitating headaches by focussing on precipitating factors may be preferable to long-term prophylactic drug treatment with its possible adverse reactions.⁶

Other medical conditions that may mimic migraine should be excluded in the diagnostic process: aneurysm, temporal arteritis, carcinoid tumor, pheochromocytoma, brain tumor, arteriovenous malformation, glaucoma, mastocytosis, and carotid or vertebrobasilar vascular insufficiency.⁷

5. How is it treated?

Migraine is an inherited biological condition that is not curable.1 Restoring a patient's ability to function normally is now recognised as the primary treatment goal - not merely relieving pain.33 There is a wide variety of pharmacological treatments for the acute and preventative management of migraine. The choices depend on the individual’s headache pattern, including frequency, intensity, disability and pain tolerance.34 However, the documentation and avoidance of factors that act as migraine triggers could provide a more effective approach to the management of management of migraine.6 Daily preventive drug therapies are
warranted in about 20% to 30% of young migraine sufferers.35

After diagnosis, the next step should be identifying lifestyle contributors; then there should be appropriate modification of sleep, activity, stress, diet and other provocative influences (often through behavioral therapies).³⁴ Non-pharmacological management of migraine consists largely of lifestyle advice to help sufferers avoid situations in which attacks will be triggered.^1,10

The use of a common migraine diet which purports to simultaneously eliminate all known dietary triggers is not generally recommended, for safety and nutritional reasons. A well-balanced diet is important, and skipping of meals or fasting should be avoided. Long-term prophylactic drug therapy is appropriate only after exclusion of headache-precipitating trigger factors, including dietary factors.⁶

C. Comments by our editor

Dr. Harris Steinman M.B.Ch.B. This review points out a number of very important aspects of migraine: that it may have a number of causes, that a number of factors interplay and play a role, and the significance food. In some instances, making the diagnosis may be simple. But finding "hidden" causes that precipitate, effect the severity or frequency of the migraine, may need some detective work. If a precipitating or aggravating cause can be found and removed from the environment of these patients, the result may have a dramatic influence on that individual's quality of life. Although food may not always play a role in migraine, it is imperative that health professionals at least consider this - even if no foods are implicated following a thorough interrogation. After all, this is a very debilitating illness that may be ameliorated with no more than identifying and removing a precipitating food or substance.

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D. References
1. Joubert J. Migraine--diagnosis and treatment. Aust Fam Physician. 2005 Aug;34(8):627-32.
2. Arulmozhi DK, Veeranjaneyulu A, Bodhankar SL. Migraine: current concepts and emerging therapies. Vascul Pharmacol. 2005 Sep;43(3):176-87.
3. Gobel H. Botulinum toxin in migraine prophylaxis. J Neurol. 2004 Feb;251 Suppl 1:I8-11.
4. Breslau N, Rasmussen BK. The impact of migraine: Epidemiology, risk factors, and co-morbidities. Neurology. 2001;56(6 Suppl 1):S4-12.
5. Kabbouche MA, Linder SL. Management of migraine in children and adolescents in the emergency department and inpatient setting. Curr Pain Headache Rep. 2005 Oct;9(5):363-7.
6. Millichap JG, Yee MM. The diet factor in pediatric and adolescent migraine. Pediatr Neurol. 2003 Jan;28(1):9-15.
7. Metcalfe DD, Sampson HA, Simon RA. Food Allergy: Adverse Reactions to Foods and Food Additives. Third Edition. Blackwell Publishing, 2003
8. Woolhouse M. Migraine and tension headache - a complementary and alternative medicine approach. Aust Fam Physician. 2005 Aug;34(8):647-51.
9. Lipton RB, Stewart WF, von Korff M. Burden of migraine: societal costs and therapeutic opportunities. Neurology. 1997 Mar;48(3 Suppl 3):S4-9.
10. Goadsby PJ. Migraine: diagnosis and management. Intern Med J. 2003 Sep-Oct;33(9-10):436-42.
11. Leira R, Rodriguez R. [Diet and migraine] Rev Neurol. 1996 May;24(129):534-8.
12. Lipton RB, Bigal ME. The epidemiology of migraine. Am J Med. 2005 Mar;118 Suppl 1:3S-10S.
13. [No authors listed] Managing migraine in children. Drug Ther Bull. 2004 Apr;42(4):25-8.
14. Kwiecien J, Piasecki L, Kasner J, Karczewska K. [Abdominal migraine as a cause of chronic recurrent abdominal pain in a 9-years-old girl--case report] Pol Merkuriusz Lek. 2005 Aug;19(110):191-2.
15. Dalton K, Dalton M. Food intake before migraine attacks in children. J Roy Coll Gen Prectitioners 1979;29:662-5.
16. Peatfield RC. Relationships between food, wine, and beer-precipitated migrainous headaches. Headache. 1995 Jun;35(6):355-7.
17. Berg MM, Braham J. Response to dietary restrictions in migraine: a comparison of results in children and adults. Postgrad Med J. 1994 Dec;70(830):937-8.
18. Jansen SC, van Dusseldorp M, Bottema KC, Dubois AE. Intolerance to dietary biogenic amines: a review. Ann Allergy Asthma Immunol 2003;91(3):233-40.
19. Hering-Hanit R, Gadoth N. Caffeine-induced headache in children and adolescents. Cephalalgia. 2003 Jun;23(5):332-5.
20. Henderson WR, Raskin NH. “Hot dog” headache: Individual susceptibility to nitrite. Lancet 1972;2:1162-3.
21. Kwok R. Chinese restaurant syndrome [Letter]. N Engl J Med 1868 ;278 :796.
22 . Frieri M, Kettelhut B. Food Hypersensitivity and Adverse Reactions. A Practical Guide for Diagnosis and Management. Marcel Dekker Inc., 1999.
23. Serghini-Idrissi N, Ravier I, Aucouturier H, Ait Tahar H, Sonneville A. Food allergy in the chronic alcoholic and alcohol in food allergy: apropos of 38 cases. [French] Allerg Immunol (Paris) 2001;33(10):378-82.
24. Bic Z, Blix GG, Hopp HP, Leslie FM, Schell MJ. The influence of a low-fat diet on incidence and severity of migraine headaches. J Womens Health Gend Based Med. 1999 Jun;8(5):623-30.
25. Person DJ, Rix KJB, Bentley SJ. Food allergy: How much is in the mind? A clinical and psychiatric study of suspected food hypersensitivity. Lancet 1983;1:1259-61.
26. Wendorff J, Kamer B, Zielinska W, Hofman O. [Allergy effect on migraine course in older children and adolescents] Neurol Neurochir Pol. 1999;33 Suppl 5:55-65.
27. Mylek D. [Migraine as one of the symptoms of food allergy] Pol Tyg Lek. 1992 Jan 20-27;47(3-4):89-91.
28. Levton A, Slack WV, Masek B, Bana D, Graham JR. A computerized behavioral assessment for children with headaches. Headache 1984;24:182-5.
29. Martin VT, Behbehani MM. Headache. Toward a rational understanding of migraine trigger factors. Med Clin N Am 2001;85:1-20.
30. Robbins L. Precipitating factors in migraine: A retrospective review of 494 patients. Headache 1994;34:214-6.
31. Gabrielli M, Cremonini F, Fiore G, Addolorato G, Padalino C, Candelli M, De Leo ME, Santarelli L, Giacovazzo M, Gasbarrini A, Pola P, Gasbarrini A. Association between migraine and Celiac disease: results from a preliminary case-control and therapeutic study. Am J Gastroenterol. 2003 Mar;98(3):625-9.
32. Serratrice J, Disdier P, de Roux C, Christides C, Weiller PJ. Migraine and coeliac disease. Headache. 1998 Sep;38(8):627-8.
33. Wenzel R, Dortch M, Cady R, Lofland JH, Diamond S. Migraine headache misconceptions: barriers to effective care. Pharmacotherapy. 2004 May;24(5):638-48.
34 . Lewis DW. Migraine headaches in the adolescent. Adolesc Med. 2002 Oct;13(3):413-32.
35. Lewis DW, Yonker M, Winner P, Sowell M. The treatment of pediatric migraine. Pediatr Ann. 2005 Jun;34(6):448-60.

E. CEU Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CEU hours related to this resource can be included in your APD log.)

PLEASE ANSWER ALL THE QUESTIONS
(There is only one correct answer per question.)

1. Which of the following is NOT a characteristic of migraine headaches?
a. unilateral
b. dull constant pain
c. moderate or severe intensity
d. associated with nausea, photophobia and phonophobia.

2. In which of the following countries is migraine most common?
a. USA
b. Australia
c. China
d. Saudi Arabia
e. Ethiopia

3. Which of the following is not a known migraine trigger?
a. stress
b. lack of exercise
c. bright lights
d. hormonal changes

4. What percentage of migraine sufferers report a particular food or drink as a precipitant to their migraine?
a. 1-3%
b. 7-44%
c. 54-56%
d. 100%

5. Which ingredient in chocolate is implicated in chocolate-triggered migraine?
a. phenylethylamine
b. theobromine
c. caffeine
d. all of the above

6. Which ingredient is responsible for “hot-dog headache”?
a. Nitrate
b. Nitrite
c. Sulphur dioxide
d. Pork

7. True or False: Food allergy is a common cause of migraine.
a. True
b. False

8. True or False: The use of a universal migraine diet which simultaneously eliminates all known dietary triggers is recommended as a treatment of migraine.
a. True
b. False

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Migraine
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