Migranes Essay, Research Paper
migraine In America approximately 45 million people each year consult physicians for relief of chronic headache pain (1). Chronic headache pain is second only to the common cold in loss of work and wages due to ailment (8). In the past decade advancements in the understanding and treatment of vascular headache syndromes have increased drastically. The activity in this field is plagued and sometimes hindered with competing theories about migraine pathogenesis. The many symptoms that have broadened clinical recognition of the migraine have caused investigators to propose new headache syndromes. Even with the increased research and technology, a breakthrough is not yet within reach. Complete understanding and treatment of migraines and related headaches continues to be unclear. As a result, research is branching in all possible directions not favoring any one avenue. In this paper I will attempt to shed light on new information brought about from recent studies. I will divide it into four categories: epidemiology, clinical description and diagnosis, pathophysiology, and treatment.EpidemiologyMigraine is one of twelve headache types with more than 60 sub-types (5). Migraine headaches affect 16-18 million Americans two-thirds of whom are woman. Migraine sufferers are described as individuals who have at least two attacks with aura or five attacks without aura a year (6). Migraines are thought to be passed through familial generations, although this has not been proven, patterns of the prevalence in families tend to give support to this theory. Any one person can have a migraine at some point; it is not the attack but the recurrence of the attack that labels one as a migraineur. Approximately 10% (6% male, 15% female) of the general population are active migraineurs (4). Both sex and age are primary factors when looking at the prevalence of migraines in populations. Between the ages 10 and 19 there is a sharp rise in the prevalence of attacks with a peak around age 14-16 (4). From age 16, migraines are 2-3 times more frequent in females than in males. Females around age 40 have the highest prevalence that of 24% (4). Peak incidence is at age 10-12 for males and at age 14-16 for females. Migraineurs often seem to be at increased risk for other health problems, particularly psychological diseases. Bouts with depression or anxiety are common among migraineurs. The use of anti-depressant medication with success in past studies has added strength to such theories. Even between headaches, migraine patients report more somatic and affective symptoms, including emotional distress and sleep disturbances (2). Yet other studies show that migraines, especially those accompanied with aura, might predispose patients toward panic and other anxiety disorders (3). More common headaches such as tension headaches seem associated with a history of depression. This, gives rise to an entire theory that depression, anxiety and headache may be linked in some way. Economist, have proven that migraines consume a considerable sum in health care costs and time lost from work. Recent economic data from an Ontario Health Survey estimated the prevalence of people suffering migraines was 1.4% of the Ontario, Canada population. An in depth look of these individuals showed increased use of pain medication and hospital services at times of onset. 9.3% of these individuals experienced an average of 2.4 days of restricted activity over a 2-week period (8). When estimated, costs ran to $2 million for hospitalizations alone, and an additional $31 million in productivity costs (8). Clinical description and diagnosis The domineering stimulus causing the onset of migraine headaches is vascular in nature like that of vasodilation and/or constriction. There are two migraine sub-types: migraine with aura (classic migraine), and migraine with out aura (common migraine). Migraines with auras the classic type generally have three stages: the aura, the headache, and post headache stage. Researchers believe that auras are brought about due to intense vasoconstriction to a particular region of the brain thus limiting the oxygen reaching such areas. These same vessels reacting to the brain s lack of oxygen dilate releasing pain causing chemicals called prostaglandins as well as other chemicals that increase sensitivity to pain. The aura is an episode of focal neurologic symptoms lasting between 15-30 minutes. This preceding event is a premonition of the upcoming attack. The aura rarely continues after the onset of the migraine. Aura symptoms consist of visual disturbances such as flashing lights, zigzagging lines, vertigo and sometimes temporary loss of vision (5). Other symptoms occurring may be pins and needles on one side of the face followed by numbness. The next stage, the headache, is when the real pain starts. Most patients describe it as a period of intense throbbing or pounding which is consistent with vascular anomalies. The pain is intense and starts out concentrated in one spot but during the episode may move to other areas triggering secondary symptoms. Cold sweats, chills, and the shakes follow the post headache stage. It is a still a period of extreme sensitivity and is considered the rebound period returning bodily functions back to normal. Such attacks can stress a persons entire system taking a lot out of them both mentally and physically.The common migraine with out aura my have a few precursor events foreshadowing the attack. People may get tired, moody, or have mental lapses. After these events the headache stage begins with the secondary symptoms soon to follow. Although not as intense as a classical migraine the common migraine is what most migraineurs are plagued with and the effects are debilitating. Migraineurs report that they experience secondary symptoms during the headache stage such as nausea, vomiting, visual disturbances, photophobia, and phonophobia. Other reported symptoms include aversion to certain odors (osmophobia), gastrointestinal cramps and diarrhea, nasal congestion, tenesmus, pallor, diaphoresis, and polyuria. During the onset of an attack senses seem to be heightened to the point of extreme aggravation. Any loud noise or bright light can intensify the already excruciating pain the migraineur feels. PathophysiologyThe theory of a migraine aura being produced by vascular constriction and headache being produced by vascular distention was based on three facts. The pulsating quality of the headache, the limitation of pain-sensitive intracranial structures chiefly to the blood vessels, and the known effects on vascular tone of chemicals moderating the headache, such as ergotamine (3). The vascular nature of migraine headaches has been established, but the pathophysiologic events are not so well defined. It is thought that vascular changes in migraines use both intracranial and extracranial vessels and follow three clinical phases; vasoconstriction producing the aura, vasodilation causing the headache, and sterile inflammation creating tenderness during post headache period (5). The current central theory emphasizes the presence of serotonin cells in the pontine locus ceruleus (5). These cells project rostrally as part of a pain control pathway to the mesencephalic periaqueductal gray matter and caudally to affect vascular tone via noradrenergic pathways (5). This theory states that over stimulation of the trigeminal nerve leads to vasoactive neuropeptides to be released antidromally by the sensory neurons. This causes sterile neurogenic inflammation with subsequent vasodilation and hyperalgesia. This outline has been confirmed using animal models with experimentally induced excitation of trigeminal fibers (4). Serotonin agonists like sumatriptan block the development of these changes by directly stabilizing action on the trigeminal fibers (7). Incorporating the migraine phases with the above theory I propose that during the aura phase platelets aggregate serotonin is released and vasoconstriction is the result. At the onset of the migraine serotonin levels are decreased vasodilation results and inflammation occurs. During the post-migraine period circulating levels of serotonin return to normal as well as vessel size, perivascular inflammation and edema are still present, and the characteristic sensitivity to touch is present due to over alert nerve endings.New data on the vascular, biochemical, and bioelectrical state of the migraine stressed brain has brought about speculations and limitations of the simple vascular theory and generated several new theories, once again bringing up more complex and less understood explanations.In 1983, Lauritzen measured regional cerebral blood flow using high-resolution positron-emission tomography scanning with inhaled 133Xe in patients experiencing migraine with sensory aura (2). He found a spreading oligemia in the cortex beginning in the occipital lobe. The spreading continued forward at a speed of 2 to 3 mm/min. The pattern of spread did not correspond to the anatomy of the large cerebral arteries. The oligemia persisted beyond the resolution of the aura and the beginning of the headache. This debunked his theory that the oligemia was strictly the cause of the migraine aura (2). This find was similar to what was already known about the spread of cortical depres
TreatmentThere is no actual cure for migraine discomfort at this time. However there is a plethora of medications you can get over the counter which give comfort for the average headache but do not help for the full blown migraine. Migraines are better treated through the help of a physician. Physicians can properly diagnosis and provide and provide the adequate prescriptions. There are many migraine medicines on the market today, some of these medications may or may not work depending on the individual who is undergoing the therapy. Treatment for migraine headaches falls into three categories: 1) physician-administered “rescue” (abortive) therapies usually given in an emergency room or inpatient setting for refractory episodes; 2) rescue therapy that the patient self-administers on an outpatient, as needed basis; and 3) chronic preventive (prophylactic) therapy, usually considered if the patient has two or more disabling headaches per month.. The recent literature regarding outpatient rescue therapy for migraine and cluster headache has in the past year, been dominated by sumatriptan. This is a serotonin analogue that is most active at the serotonin-1D inhibitory receptor. This medication is currently available as a 6-mg subcutaneous injection or a 25-mg pill. The drug has showed great promise in helping migraineurs, but as with any medications there may be some side affects. A 39-year-old man without known stroke risk factors suffered a fatal cerebellar infarction while receiving sumatriptan for an acute attack of migraine (7). There was another case where a 35-year-old woman with unsuspected coronary artery narrowing responded to her first-time dose of sumatriptan with cardiac arrest; she was successfully revived (7). Events such as this are not entirely unexpected; earlier attempts to use serotonin as a migraine therapy ended because its tendency to cause dyspnea and faintness. The current trend of oral consumption of sumatriptan reports symptoms of heaviness, tightness, or pressure in at least 2%of patients treated with a 50 to 100 mg dose (7).For some subcutaneous administration is not even an option do to needle phobias. Intranasal application of medication for migraine relief seems to be getting good results. Intranasal administration of sumitriptan is a good alternate route although response rate ids a little slower, but side effects appear less frequently. Dihydroergotamine (DHE), another serotonin-1D agonist and long known as an intravenous therapy for migraine, has been used in two controlled, double-masked randomized trials that were administered and reported. Both trials confirmed significant headache relief for patients treated with intranasal DHE, but varied in findings concerning onset of relief and effect on nausea (5). The investigators believed that a subset of migraineurs who were “DHE responders” could be identified.Intranasal 4% lidocaine spray interrupted the migraine attack in 12 of 23 patients in an uncontrolled study (3) . The results were less dramatic in other types of headache patients, with 54% experiencing only mild to moderate relief from their pain and the remainder experiencing no change (3). Transnasal butorphanol, a weak agonist-antagonist of opiate receptors, was tested in 107 migraine attacks against placebo in 50 attacks in a double-masked study (8). Symptoms eased from at least moderate to at most slight pain in 47%of patients within one hour (16%in controls), but side effects of dizziness, nausea, and drowsiness were common. Butorphanol has the advantage of being available as a commercially prepared nasal spray.In part because of the wide variety of theories of migraine pathogenesis, a wide variety of chronic suppressive medications have been tried, including those that affect vascular tone (calcium channel blockers and beta-adrenergic blockers) or serotonin reuptake (tricyclic antidepressants and fluoxetine). One study sought to take advantage of the above-mentioned tendency for migraine and depression to coexist in the same patients, and noted that a combination therapy of phenelzine (a monamine oxidase inhibitor) with atenolol effectively treated both diseases and lessened the incidence of side effects expected with monotherapy (4).Two studies done to expand the use of oral sumatriptan as suppressor in-patients at high risk for proximate headache recurrence. The first found oral sumatriptan given 4 hours following subcutaneous sumatriptan therapy effective in delaying “rebound” migraine, with occurrence shifted from 10 hours after injection to 15 hours (3). No reduction in incidence of rebound headache was found. In the other study, oral sumatriptan was tested in a placebo-controlled study of 169 patients in the midst of a cluster period. The treatment dose was 100 mg orally three times a day for 7 days (3). No reduction in the number of severity of attacks was found.Zolmitripton another serotonin receptor agonist is a new drug that is now available in the U.S. This drug is taken orally and the antimigraine effect is thought to come from its effects on the brainstem. Unlike sumatriptan it is capable of readily passing through the blood brain barrier. Because of this it can effect the intracranial vessels and the peripheral sensorynerve endings of the trigeminal vasculature, which result in vasoconstriction and decreased release of inflammatory neuropeptides (11). Good results have come from the use on migraineurs with limited side effects. Ergot alkaloids are also a drug of study for the relief of migraines. These compounds have a high affinity for a wide range of receptors. The anti-migraine effects of these compounds are similar to that of triptan drugs. Three distinct pharmacological actions have been found to occur while using these compounds: 1) Inhibition of dural neurologic inflammation, inhibition of CGRP release and vasodilation. 2) Direct attenuation of excitability of cells in trigeminal nuclei. 3) Vasoconstriction of meningeal, dural, cerebral, or pial vessels. These compounds have not yet been approved for use in the U.S. but will soon become available.As you can see there are many medicinal routes to be taken when searching to remedy migraine headaches. Not all are guaranteed to work for everyone but you can be sure to find one that suits a particular individual, which will make life with migraines easier. Some key factors to follow in the interim which may lead to less frequent attacks are as follow; watch the foods you eat, you may find that some foods are triggers for migraines (ie. red wine, cheeses etc.). Be careful not to consume large amounts of caffeine, and as a preventative measure take vitamin B2 daily this has been found to lessen episodes with some migraineurs by one-third (10). ConclusionsBeing a suffer of migraines myself, I enjoyed researching this topic. I learned a lot about the new routes in which I may take in order to help with future attacks. The advances in our understanding of migraine have resulted from 1) better and more extensive clinical descriptions of the disease and its patients, 2) ever-improving techniques of examining the brain during attacks of migraine and between episodes, 3) developing animal models that seem to share important similarities with human migraine, and 4) studying the properties of chemicals (both triggers and treatments) that influence the severity or frequency of migraine. I hope that the future will bring some sort of permanent fix to this epidemic. References:1) Diamond, Seymour, MD. Headaches. Clinical Symposium. 1981, 33 #2: 1-322) Edmeads, John, G. Headache as a symptom of organic disease. Current Opinion in Neurology. 1995, 8: 233-2363) Farley, Dixie. Headache misery may lead to proper treatment. FDA Consumer. 1997, 26: 26-334) Ferrari, Michel, D., Haan, Joost,. Acute treatment of migraine attacks. Current Opinion in Neurology. 1995, 8: 237-2425) Ferrari, Michel, D., Migraine. The Lancet. 1998, 351: 1043-10516) Lance, James, W., Mechanisms and management of headache. 1993, Butterworth-Heinemann Publishing Ltd.7) Larkin, Marilynn, New triptin trips up headaches. The Lancet. 1998, 351: 41-438) Nowroozi, Christine, K., Treating serious headaches. Nation s Business. 1994, 82 #9: 69-719) Portyansky, elena, Head pain. Oradell. 1998, 142 #1: 20-2310) Van, Jon, Kotulak, Ron, Vitamin B2 may ease misery of migraines. Chicago Tribune. February 26, 199811) Anonymous, Zolmitriptin for migraine. New Rochelle. 1998, 40 #1021: 27-28Submit your paper