Sunday, November 24, 2019

Why Migraines Occur Essay Example

Why Migraines Occur Essay Example Why Migraines Occur Essay Why Migraines Occur Essay Migraine tends to affect more than 300 million people from across the world.   For many, the condition is more than a headache and is characterized by several distinctive symptom phases.   The condition is characterized by severe, debilitating and disabling headache that often needs no description.   The people suffering from migraine also had several other problems including photophobia, burning, nausea, vomiting, visual disturbances, altitude sickness, etc.   Migraine may have several other implications.   About 17 billion dollars a year is lost due to lost work, disabilities and healthcare expenditure owing due to headache.   Through historical records, it has been suggested that the disorder has affected man for more than 7000 years.   However, medicine still continues not to identify the cause and a treatment that could help cure the disorder.   Many people do not even approach the doctor to get the disorder treated as they feel that medical treatment can do litt le or no help.   Earlier, scientific research proved that the disorder was a vascular condition, but today scientists have identified that it is more of a neurological condition that develops primarily from pathology in the brain stem cells.   The nerve cell malfunction tends to sweep across other parts of the brain.   Today, the exact cause of migraine is still unknown, but scientists are developing several new forms of treatment for the condition including gene therapy (after considering the genetic basis of the disease), molecular biology and imaging of the brain.   This would enable to get back to normal activities faster (Dodick, 2008, Kantor, 2006). The neuro-vascular model which has been implicated for the cause of migraine includes vascular and neurological factors.   Another model frequently being considered is the Convergence Hypothesis that tries to associate the clinical symptoms with the pathophysiology of migraine.   According to this model, migraine is considered to be an event with a beginning, a mid and an end.   A symptom-based diagnostic approach would consider migraine during the peak stages.   With the convergence model, the entire process would be looked up on including the prodromal, the aura and the end phases.   Using the convergence model, the events can be drawn as a curve when charted against time (Curtis P. Schreiber, 2005). Body Migraine is a chronic medical disorder characterized by disabling headache, nausea, vomiting and photophobia.   In many people, the throbbing headache may be experienced on one-side of the face. The condition usually occurs in 11 % of the people in the US.   Migraine is more common in people with a family risk of the condition. It occurs anywhere between the ages of 10 to 46 years, and is more common in women compared to men.   In women, the condition may even occur beyond till the age of 55 years.   During the period of pregnancy, the number of migranous attacks usually reduces.   During the 1980’s scientists found that migraine develop due to a disorder in the blood vessels that supply the brain.   However, today it is clear that the condition develops due changes in the brain, nerve pathways and the chemicals present in the brain (Dodick, 2008, Kantor, 2006). From one individual to another, the frequency, duration, severity and aggravating factors of migraine would differ significantly.   On an average, people suffer from migraine, one or two days every month.   About 10 % of the population gets the disorder every week and 20 % get the attacks every 2 to 3 days, and about 14 % develop a serious version of the disease, in which the symptoms are seen every alternate day (Dodick, 2008, Kantor, 2006). Several events may trigger or aggravate attacks of migraine including alcohol consumption, dehydration, physical stress, exertion, menstruation, emotional stress, anxiety, seasonal, climatic or weather changes, allergy, bright lights, loud noises, florescent lights, sleep alterations, missing meals, tension headache, use of birth control pills, lack of sleep, staying at higher altitudes, hunger, certain foods, smoking, tobacco consumption, etc.   Some of the foods that can trigger migraine attacks include foods containing tyramine, monosodium glutamate or nitrates. Some of the foods that contain tyramine include red wine, cheese, smoked fish, liver of chicken, bens, figs, etc, and foods that contain nitrate include hot dogs, salami and bacon.   Other foods that can also trigger migraine attacks include citrus fruits, bananas, avocados, onions, dairy products, chocolates, pickles, nuts, peanut butter, fermented products, etc.   The ancient Greeks were the ones to coin the word m igraine from ‘megrim’ meaning hemicrania or one-sided headache.   Galen considered migraine to be a painful disorder that affected one half of the head.   The Greeks considered to be caused due to descent of the vapors from the liver to the brain.   Later, in the 17th century, blood flow defects were considered to be the main cause for migraine rather than humors.   From the 17th century to the 1980’s, the vascular theory proved to be responsible cause for migraine.   Wolff from the Presbyterian hospital New York considered that migraine was caused due to dilatation and expansion of the blood vessels present in the brain.   Once the expansion of the blood vessels occurs, the pain-signaling neurons of the brain get activated, leading to a headache.   Before the headache actually occurs, there is a drop in the blood supply to the brain causing constriction of the blood vessels.   However, newer research work conducted in the field of migraine demons trates that the disorder is caused not due to vascular alterations but due to neurological changes.   Earlier it was thought that vascular flow of the blood in the brain had increased something like 3-fold times.   In fact, latest scientific evidence clearly suggests that just before the migraine attack, the cerebral blood flow is either normal or drops down a bit (Dodick, 2008, Kantor, 2006). The aura that occurs before the migraine attacks was a serious clue to the scientists that the disorder had a neurological basis.   The aura can be seen in two conditions, one in migraine as a preceding symptom and the other in epileptic seizures as a part of the sensory visual hallucinations.   The individual in migraine would be able to see stars, bright lights, sparks, lightning bolts, geometric designs, etc.   In some people weakness, speech impairments and tingling sensations develop.   In some people, the visual aura may not appear and all, but in other it may even occur during the entire headache phase.   Today, scientists have identified the exact mechanism of this aura.   A wave of intense nerve activity (cortical spreading depression) spreads throughout the cortex especially the areas of vision.   Following the hyperexcitability, there is a phase of neural inhibition.   During the phase of intense neuronal activity, there is active firing and a lot of energy is required.   Following the intense neuronal firing, the nerve cells require less quantity of blood.   The neuronal firing spreads at the rate of 2 to 3 millimeters every minute, and this is just the exact rate at which aura develops.   Besides affecting vision, the intense neuronal activity would also affect sensory and motor signals (Dodick, 2008 NINDS, 2008). Studies have clearly shown that genetic factors play a very important role in the development of migraine.   The genetic susceptibility of migraine is similar to other disorders such as diabetes, hypertension, etc.   In identical twins, the other twin is at a higher risk of developing the disorder, when one twin actually suffers from it.   However, non-genetic or environmental factors play an important role in the development of migraine.   Genetic factors may increase the excitability of the neurons, leading to a disturbance in the ion transportation system.   Several other disorders may also be as a cause of ion transportation defects including seizures and cardiac arrhythmias (Dodick, 2008 NINDS, 2008). The exact way in which the spreading cortical depression of neurons causes’ headache is not understood clearly, but scientists feel that the trigeminal nerve may be involved.   The manner in which the trigeminal nerve causes pain sensation is not understood clearly.   When the intense cortical depression spreads, it causes chemical changes in the neurotransmitters leading the trigeminal nerve to transmit pain sensations.   The spreading depression can also activate the trigeminal nerves in the subcortical regions leading to headache.   The mechanism of aura may operate in both, people suffering from migraine with or without aura.   However, in people who do not suffer from aura may develop other symptoms including tiredness, weakness or difficulty concentrating.   Besides, involvement of the cortical and the subcortical regions in migraine, the brain stem (an ancient part of the brain) may be responsible for migraine pain.   The brain stem contains three groups o f nuclei that can play an important role in migraine.   The nuclei would inhibit the firing of the trigeminal nerve, thus causing the trigeminal neuron to fire without any pain signal.   There would be an incoming pain signal although actually there are no stimuli.   Besides, involvement of the trigeminal nerve from the brain stem, other sensory nerves including those that control visual functions may also be affected, resulting in false sensory incoming signals causing visual field disturbances (Dodick, 2008 NINDS, 2008). During an attack of migraine several processes tend to occur.   Certain triggering factors mentioned may stimulate the release of peptides such as substance P, Calcitonin Gene-related peptide, etc.  Ã‚   They tend to dilate blood vessels and cause inflammation which results in over-excitation of the trigeminal nerve.   The brain would not be affected with the headache, but the blood vessels and the meninges would be involved.   Auras occur as a result of blood flow changes (Daniel Kantor, 2007). Certain migraine headaches occur due to abnormalities in the calcium channels and also the magnesium, potassium and sodium channels.   Calcium channels present control the release of the neurotransmitter serotonin.   This neurotransmitter can play an important role in the development of migraine.   Besides, abnormalities in the levels of other neurotransmitters such as dopamine and stress hormones can result in migraine.   Dopamine could act as a stimulant of migraine and in certain individuals with genetic characteristics, higher levels of dopamine can result in nerve cell excitation.   Several prodromal symptoms such as mood changes, drowsiness and yawning are closely associated with dopamine disturbances.   The calcium channels play a vital role in the development of the cortical spreading depression (which is the cause of the migraine symptoms).   In people who suffer from migraine, magnesium deficiencies have been found.   During a migraine attack, a drop in the magnesium levels has been observed.   Once the levels of magnesium levels are low, the nerve cells become highly unstable and tend to misfire.   This could be responsible for the aura that develops.   Magnesium has been strongly associated with the calcium channels in the body.   Certain inherent deficiencies in the calcium channel systems may be present in people who develop migraine. Individuals with familial hemiplegic migraine have mutation of the gene that expresses for calcium channel systems.   Nitric Oxide has also been associated with migraine and other headaches.   Over-excitation of the nerve cells can result in the production of nitric oxide.   A rise in the nitric oxide in the blood vessels may stimulate several nerves in the brain and cause the development of pain.   Hormone fluctuations can also play a role in the development of migraine.   The changes in several hormones especially estrogen can be responsible for migraine development.   If the hor mone levels are high, low or normal for long, the migraine process would not be activated.   Hormonal fluctuations are more likely to cause migraine.   This is because fluctuations impact the serotonin and other neurotransmitter levels (Daniel Kantor, 2007). Conclusion Today, a lot of research has been identified which potentially helps to better under the migraine process.   Migraine is more of a neuro-vascular condition rather than a vascular condition earlier thought.   Currently, there are no specific drugs to treat migraine, and most of them are other groups of drugs that are utilized to treat other conditions.   Usually, ergotamine preparations, painkillers, NSAIDS, etc are given which works partially.   Hence, it has been clearly observed that they can work only in half the number of migraine patients.   Several groups of antihypertensive drugs, anti-seizure drugs, calcium channel blockers and antidepressants may work by normalizing the membrane potential thus helping to curb the rapidly-spreading cortical nerve depression.   They would work in patients who develop migraine with or without aura.   These groups of drugs would work by prevent channels present on the nerve membrane from opening up, thus helping to control calcium movement.   In this way, the nerve membrane would be stabilized.   Individuals also need to adopt a diet that can effectively help avoiding headache provoking foods and substances such as cheese, tobacco, alcohol, etc.   Blood glucose and blood pressure should be monitored and kept under control.   Better sleep hygiene and exercising patterns need to be ensured.   Stress needs to be handled in more appropriate fashions (Curtis P. Schreiber, 2005, Dodick, 2008 Mayo, 2007). Curtis P. Schreiber. â€Å"The Pathophysiology of Migraine.† Clinics in Family Practice 7.3 (2005). Daniel Kantoor. â€Å"Migraine headaches – Highlights, FDA Warning: Serotonin Syndrome.† 2007. ADAM. 29 Nov 2008. Daniel Kantor. â€Å"Migraine.† Medical Encyclopedia. 2006. Medline Plus. 16 Nov 2008. David W. Dodick and J. Jay Gargus . â€Å"Why Migraines Strike.† Scientific American. (July, 2008). Mayo Clinic. â€Å"Migraine.† 2007. Mayo Clinic. 16 Nov 2008. NINDS. â€Å"Headache: Hope through Research.† 2008. NINDS. 16 Nov 2008.

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