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Migraine and Food Allergy 
Airborne Causes of Headache
Typical Dietary Advice
Case Histories
Drugs for Migraine
Migraine References

Migraine Rescue

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 Migraine Abstracts from the Medical Literature

 

Neurogenic vascular headaches, food and chemical triggers.

 Authors Trotsky MB .

Institution University of Nebraska College of Medicine, Lincoln.

Source Ear, Nose, & Throat Journal. 73(4):228-30, 235-6, 1994 Apr.

 Abstract: Recent evidence has demonstrated that neurogenic vascular headaches are a combination of neurological primary events and secondary vasomotor changes. The neurological events involve the hypothalamus and sensory cortex with sympathetic hypofunction and noradrenergic abnormalities. A platelet theory has been proposed but has not really been confirmed as a legitimate cause of the neurogenic vascular headaches. Food and chemicals in foods can act as a precipitating factor in the food-sensitive neurogenic vascular headache patient. In these patients evidence is now being demonstrated to confirm this, but larger patient studies are needed. The food-sensitive migraine patient and cluster headache patient must give a good history and food diary to go along with active challenges and provocative testing in order to determine the causative foods. Any concomitant allergies of inhalants or environmentals must also be treated. The treatment modalities of elimination and rotation diets or provocation neutralization may successfully control the headaches without the need for continuous medications.

T cells expressing IL-2 receptor in food induced migraine

Authors Martelletti P .

Institution Centro Cefalee, Universita La Sapienza, Roma, Italia.

Source Acta Neurologica. 13(5):448-56, 1991 Oct.

 Abstract We studied a group of migraine patients for circulating immune complexes, lymphocyte subpopulations, IgG4 and anti-IgG antibodies, before, after 4 hours and after 72 hours a specific challenge test. We found an increased incidence of circulating immune complexes. Total T cells showed a marked increase after challenge test. The most important finding was the presence of T-activated cells. Also K and NK cells showed an early increase after the challenge. In commenting the outcomes of this investigation, it must be stressed that the evidence of an early lymphocyte activation after the challenge test indicates an involvement of interleukin-2 related receptor in food-induced migraine. The results have reinforced the idea of immune mechanism involvement in food-induced migraine, but it seems to be localized at different step from that until now hypothesized, with the involvement of the complex cytokines network. [References: 54]

The role of antihistamine therapy in vascular headaches.

Authors Mansfield LE .

Institution Division of Immunology and Allergy, Texas Tech RHSC, El Paso 79902.

 Source Journal of Allergy & Clinical Immunology. 86(4 Pt 2):673-6, 1990 Oct.

Migraine (vascular) headache is a complex syndrome that involves vascular hyperreactivity. The functions of systemic mediators in migraine are not fully understood. It is unclear which mediators provoke this probably atopic disorder and which represent an attempt to correct an imbalance. However, it has been demonstrated fairly conclusively that increased histamine levels correlate with migraine attacks in susceptible persons. Recent studies showing that histamine seems to have many different receptors and to adopt different conformations for different receptors may serve as a useful guide to future scientific investigation. Further impetus may come from ongoing studies of H3 histamine receptors, which indicate that H3 agonists offer promise as prophylactic agents for people who suffer from vascular headaches.

Migraine is a food-allergic disease.

Author Monro J; Carini C; Brostoff J

Source Lancet, 1984 Sep 29, 2:8405, 719-21

Abstract Foods which provoked migraine in 9 patients with severe migraine refractory to drug therapy were identified. The patients were then given either sodium cromoglycate or placebo orally in a double-blind manner, with foods previously identified as provocants. Sodium cromoglycate exerted a protective effect, thus confirming that it can prevent a hypersensitivity mechanism as well as the symptoms of migraine. Immune complexes were not produced in those patients who were protected by sodium cromoglycate. These observations confirm that a food-allergic reaction is the cause of migraine in this group of patients.

Food allergy in migraine. Study of dietary exclusion and RAST.

Author Monro J; Brostoff J; Carini C; Zilkha K

Source Lancet, 1980 Jul 5, 2:8184, 1-4

Abstract Two-thirds of severe migraineurs were allergic to certain foods, shown by dietary exclusion and subsequent challenge. Radioallergosorbent test confirmed the relevance of these foods. Oral sodium cromoglycate protected these patients from food challenges. The initial specific allergic reaction in the gut may result in increased mucosal permeability which allows food antigens, complexes, or mediators to be absorbed and cause symptoms.

Oligoantigenic diet treatment of children with epilepsy and migraine

Author Egger J; Carter CM; Soothill JF; Wilson J

Address Department of Neurology, Hospital for Sick Children, London.

Source J Pediatr, 1989 Jan, 114:1, 51-8

Abstract We studied the role of oligoantigenic diets in 63 children with epilepsy; 45 children had epilepsy with migraine, hyperkinetic behavior, or both, and 18 had epilepsy alone. Of the 45 children who had epilepsy with recurrent headaches, abdominal symptoms, or hyperkinetic behavior, 25 ceased to have seizures and 11 had fewer seizures during diet therapy. Headaches, abdominal pains, and hyperkinetic behavior ceased in all those whose seizures ceased, and in some of those whose seizures did not cease. Foods provoking symptoms were identified by systematic reintroduction of foods, one by one; symptoms recurred with 42 foods, and seizures recurred with 31; most children reacted to several foods. Of 24 children with generalized epilepsy, 18 recovered or improved (including 4 of 7 with myoclonic seizures and all with petit mal), as did 18 of 21 children with partial epilepsy. In double-blind, placebo-controlled provocation studies, symptoms recurred in 15 of 16 children, including seizures in eight; none recurred when placebo was given. Eighteen other children, who had epilepsy alone, were similarly treated with an oligoantigenic diet; none improved.

Is migraine food allergy? A double-blind controlled trial of oligoantigenic diet treatment.

Author Egger J; Carter CM; Wilson J; Turner MW; Soothill JF

Source Lancet, 1983 Oct 15, 2:8355, 865-9

 Abstract 93% of 88 children with severe frequent migraine recovered on oligoantigenic diets; the causative foods were identified by sequential reintroduction, and the role of the foods provoking migraine was established by a double-blind controlled trial in 40 of the children. Most patients responded to several foods. Many foods were involved, suggesting an allergic rather than an idiosyncratic (metabolic) pathogenesis. Associated symptoms which improved in addition to headache included abdominal pain, behaviour disorder, fits, asthma, and eczema. In most of the patients in whom migraine was provoked by non-specific factors, such as blows to the head, exercise, and flashing lights, this provocation no longer occurred while they were on the diet.

Effect of diet treatment on enuresis in children with migraine or hyperkinetic behavior.

Author Egger J; Carter CH; Soothill JF; Wilson J

Address Hospital for Sick Children, London, England.

Source Clin Pediatr (Phila), 1992 May, 31:5, 302-7

Abstract Twenty-one children with migraine and/or hyperkinetic behavior disorder which was successfully treated with an oligoantigenic (few-foods) diet also suffered from nocturnal and/or diurnal enuresis. On diet, the enuresis stopped in 12 of these children and improved in an additional four. Identification of provoking foods was by sequential reintroduction of the foods that were avoided on the oligoantigenic diet. In eight of the 12 children who recovered on the oligoantigenic diet and in the four who improved, reintroduction of one or more foods provoked a reproducible relapse of the enuresis. Nine children were subjected to a placebo-controlled, double blind reintroduction of provoking foods. Six children relapsed during testing with incriminated foods; none reacted to placebo. Enuresis in food-induced migraine and/or behavior disorder seems to respond, in some patients, to avoidance of provoking foods.

 Food allergy in migraine. Study of dietary exclusion and RAST

Monro J. Brostoff J. Carini C. Zilkha K .

Source Lancet. 2(8184):1-4, 1980 Jul 5.

 Abstract Two-thirds of severe migraineurs were allergic to certain foods, shown by dietary exclusion and subsequent challenge. Radioallergosorbent test confirmed the relevance of these foods. Oral sodium cromoglycate protected these patients from food challenges. The initial specific allergic reaction in the gut may result in increased mucosal permeability which allows food antigens, complexes, or mediators to be absorbed and cause symptoms.

The clinical features of migraine as a manifestation of allergic disease.

Authors Wilson CW. Kirker JG. Warnes H. O'Malley M .

Source Postgraduate Medical Journal. 56(659):617-21, 1980 Sep.

Abstract Patients with a clinical history of migraine were evaluated psychiatrically, and by electroencephalography. They were challenged with food antigens by skin-prick test, and abdominal symptoms were evaluated following oral ingestion of food allergens. A significant correlation was found between challenge with specific food allergens and the development of migraine headaches, the appearance of abdominal symptoms and the occurrence of positive skin reactions. Psychiatric abnormalities and EEG alterations were associated with the occurrence of headaches and allergic clinical features. It is suggested that the clinical features of migraine can be explained as a result of release of chemical mediators following antigen-antibody reactions in the brain and other tissues where specific antibodies are localized. The continuous ingestion of the responsible food allergens would account for the raised tissue concentrations of noradrenaline, histamine and other mediators to which the clinical features of migraine are attributed.

Food allergies and migraine.

Authors Grant EC .

Source Lancet. 1(8123):966-9, 1979 May 5.

Abstract: 60 migraine patients completed elimination diets after a 5-day period of withdrawal from their normal diet. 52 (87%) of these patients had been using oral contraceptive steroids, tobacco, and/or ergotamine for an average of 3 years, 22 years, and 7.4 years respectively. The commonest foods causing reactions were wheat (78%), orange (65%), eggs (45%), tea and coffee (40% each), chocolate and milk (37%) each), beef (35%), and corn, cane sugar, and yeast (33% each). When an average of ten common foods were avoided there was a dramatic fall in the number of headaches per month, 85% of patients becoming headache-free. The 25% of patients with hypertension became normotensive. Chemicals in the home environment can make this testing difficult for outpatients. Both immunological and non-immunological mechanisms may play a part in the pathogenesis of migraine caused by food intolerance.

Title "Food allergy": Fact or Fiction?

Authors Finn R. Cohen HN .

Source Lancet. 1(8061):426-8, 1978 Feb 25.

Abstract Six patients with longstanding physical and mental symptoms who had not been helped by many years of conventional medical investigation and treatment experienced immediate relief of symptoms when they avoided certain foodstuffs. This clinical study supports the view that some foods may cause widespread and disabling symptoms in people who are sensitive to them.

 Allergy of the nervous system: a review

Authors Hall K .

Source Annals of Allergy. 36(1):49-64, 1976 Jan.

Abstract Allergies of the nervous system cause diverse behavioral disturbances, including headaches, convulsions, learning disabilities, schizophrenia and depression. Some of the biological mechanisms have been established by research; others remain to be explored. Effective diagnosis and treatment include the elimination diet, followed by dietary rotation and avoidance of offending substances. [References: 159]

The Bela Schick lecture for 1985. The atopic diseases.

Authors Nelson HS .

Source Annals of Allergy. 55(3):441-7, 1985 Sep.

Abstract Review of the atopic diseases suggests a redefinition of the term "atopy" is indicated to reflect new information that has become available during the 60 years since the term was introduced. Atopy may be viewed as a manifestation of a still undefined defect. It is characterized by certain clinical findings and frequently by derangement of the immune and autonomic nervous systems. The atopic diseases are a group of seemingly unrelated conditions--eczema, asthma, rhinitis, hypertrophic sinusitis, and perhaps vernal conjunctivitis and migraine--which cluster in individuals and families. In the respiratory tract and eye, eosinophils in the tissues and secretions are characteristic and are not dependent on the presence of immediate hypersensitivity. Symptoms suggestive of basophil and mast cell mediator release are common to all the atopic diseases, and there is some evidence that nonimmunologic mediator release is enhanced in atopic patients. In the most clearly defined atopic diseases, eczema and asthma, approximately 80% of patients have an increased IgE response to normal environmental allergens. Accompanying and perhaps underlying these enhanced IgE responses are deficiencies of T cell numbers and function particularly in the suppressor T lymphocytes. Evidence exists that decreased beta-2-adrenergic and increased cholinergic and alpha-adrenergic responsiveness accompany and perhaps underlies the atopic diseases irrespective of the presence or absence of allergy.

Migraine: a diagnostic test for etiology of food sensitivity by a nutritionally supported fast and confirmed by long-term report.

Hughes EC. Gott PS. Weinstein RC. Binggeli R .

Annals of Allergy. 55(1):28-32, 1985 Jul.

Abstract A diagnostic procedure during a nutritionally supported fast week followed by conventional food sensitivity management achieved major improvement for 80% of a migraine panel. This procedure gave a reliable (0.8 correlation coefficient) prognosis on the substantial value of this approach for selection of the treatment of migraine. The study gave two lines of evidence which indicate that migraine has an etiology of food sensitivity.

Mechanisms in adverse reactions to food. The brain.

Authors Anderson JA .

Institution Division of Allergy & Clinical, Henry Ford Hospital, Detroit, Michigan, USA.

Source Allergy. 50(20 Suppl):78-81, 1995.

Abstract Specific chemical mediator release such as histamine and the prostaglandins (PG2a or PGD2) associated with headaches has been found in a few patients who were repeatedly challenged with specific foods, using DBPCFC techniques.

Neurokinin-receptor antagonists: pharmacological tools and therapeutic drugs.

Authors Longmore J. Hill RG. Hargreaves RJ .Institution Merck Sharp and Dohme Research Laboratories, Neuroscience Research Centre,
Harlow, United Kingdom.
Source Canadian Journal of Physiology & Pharmacology. 75(6):612-21, 1997 Jun.

Abstract The mammalian tachykinins (substance P, neurokinin A, and neurokinin B) are widely distributed throughout the central and peripheral nervous systems, where they act as neurotransmitters or neuromodulators. Historically, the tachykinins have been implicated in a wide variety of biological actions such as pain transmission, neurogenic inflammation, smooth muscle contraction, vasodilation, secretion, and activation of the immune system. Their effects are mediated via specific G-protein-coupled receptors (NK1, NK2, and NK3 receptors). The development of nonpeptide receptor antagonists revealed species differences in neurokinin-receptor pharmacology, and the recent cloning of human neurokinin receptors has led to development of compounds with optimized affinity for the human target receptor. The neurokinin-receptor antagonists have been used in preclinical experiments to confirm the physiological roles of the tachykinins. Importantly, it is now recognised that these agents can inhibit the actions of tachykinins released from peripheral nerves, and for the NK1-receptor antagonists (the most widely studied class of neurokinin-receptor antagonists) central sites of action have also been demonstrated. These studies support the development of neurokinin-receptor antagonists as potentially exploitable drug therapies in humans, particularly in the treatment of pain and emesis. [References: 103]

Migraine stroke: a possible complication of both migraine with and without aura

Authors Narbone MC. et al

Institution Istituto di Scienze Neurologiche e Neurochirurgiche, Universita di Messina,
Italy.

Source Headache. 36(8):481-3, 1996 Sep.

Abstract We describe four migraine patients who developed an ischemic stroke during their typical migraine attacks. Cerebral infarction as a possible complication of migraine without aura is discussed. We propose a review of the migraine stroke definition of the International Headache Society. [References: 10]

Migraine-related visual-field loss with prolonged recovery

Authors Sullivan-Mee M. Bowman B .

Institution College of Optometry, State University of New York, York 10010, USA.

Source Journal of the American Optometric Association. 68(6):377-88, 1997 Jun.
Migraine is a complex neurologic syndrome that commonly causes visual disturbances. Although migraine visual disturbances are usually transient in nature, persistent or permanent visual field defects may occur. When persistent visual-field loss is found-even if migraine is suspected-appropriate workup must be performed to rule out other causes of vision loss. CASE REPORTS: Two patients went to the eye clinic for comprehensive examination. One patient with symptomatic visual loss and one patient with asymptomatic visual loss were evaluated by serial ophthalmic examinations, neurologic/medical evaluations, computed tomography of the head, and laboratory results. Each patient reported a history consistent with migraine, and each demonstrated resolution of persistent visual-field defects that had been present longer than 10 days. Since ophthalmic, medical, laboratory, and imaging results did not identify and etiology other than migraine as the cause of the vision loss, it is likely that each case represents a specific form of complicated migraine. CONCLUSIONS: Previous reports suggest that migraine-related visual deficits usually become permanent if persistent for more than 7 days. These reports demonstrate that visual recovery may still occur when field defects are present for 10 days or more.

 

Headache Solution >> Remove the Cause: The Alpha Nutrition Program is a standard method of diet revision that can resolve chronic headaches.  The first phase of the program is an attempt to clear symptoms. This is home science. You start with the hypothesis that your food intake is causing or contributing to your illness and you do an experiment to find out if it is true. When you read Alpha Nutrition Program instructions, you will realize that there are three tracks through the program - fast, medium and slow. You need to decide the best track for you. To help you decide what strategy is best for you, we suggest rating the severity of your existing illness: You can retreat to Phase 1 foods and replace one or two meals per day with Alpha ENF. This is the medium track on Alpha Nutrition- rehearsal mode. If the problem is prolonged headaches, especially a mixed pattern with daily pain punctuated by attacks of migraine, recovery involves a period of reduced food intake or fasting. The most definitive experiment is to take a food holiday. We recommend Alpha ENF to replace food. The best way to begin is to order the Rescue Starter Pack that includes the Program book and a 500 gram jar of Alpha ENF to try.

The book, the Human Brain, provides a comprehensive account of brain disorders in general including the role of brain circulation, high blood pressure, and atherosclerosis in the production of headache and other symptoms of brain dysfunction.

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Human Brain in Health and Disease

 
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