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 ====== Migraines ======
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-**Family History:** Upto 90% of people who suffer from migraines have family members who have had the same condition. If one or both of your parents have migraines, then there is a good chance that you would suffer from migraine attacks.
+**Family History:** Upto 90% of people who suffer from migraines have family members who have had the same condition. If one or both of your parents have migraines, then there is a good chance that you would suffer from migraine attacks (Mayo Clinic, 2013).
-**Age:** One can develop migraines at any age, but most people who suffer from migraine attacks get their first attack during adolescence. By age 40, most people who suffer from migraines would got their first migraine attack.
+**Age:** One can develop migraines at any age, but most people who suffer from migraine attacks get their first attack during adolescence. By age 40, most people who suffer from migraines would got their first migraine attack (Mayo Clinic, 2013).
-**Sex:** Women are 3 times more likely to suffer from migraine attacks than men. Boys tend to get more headaches than girls during childhood, but during and after puberty, girls suffer from migraines overwhelmingly more than boys.
+**Sex:** Women are 3 times more likely to suffer from migraine attacks than men. Boys tend to get more headaches than girls during childhood, but during and after puberty, girls suffer from migraines overwhelmingly more than boys (Mayo Clinic, 2013).
-**Hormonal changes:** Women are more susceptible to migraines during the onset or immediately after menstruation.
+**Hormonal changes:** Women are more susceptible to migraines during the onset or immediately after menstruation (Mayo Clinic, 2013).
-**Genetics:** mutations in a number of difference genes have been implicated in migraines. These genetic changes tend to lead to channelopathies that make the neurovascular system hyperexcitable
+**Genetics:** mutations in a number of difference genes have been implicated in migraines. These genetic changes tend to lead to channelopathies that make the neurovascular system hyperexcitable (Mayo Clinic, 2013).
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 ====== Treatment ======
-To date, there is no actual cure for migraine sufferers. Ideally, acute treatment of migraine should work rapidly, with few side effects, be cost effective and get the patient functional as soon as possible. Drug therapeutics that do exist are primarily targeted around symptom relief during and after the migraine attack. Acute treatment can be divided into migraine specific and nonspecific therapy. <sup>[12]</sup>
+To date, there is no actual cure for migraine sufferers. Ideally, acute treatment of migraine should work rapidly, with few side effects, be cost effective and get the patient functional as soon as possible. Drug therapeutics that do exist are primarily targeted around symptom relief during and after the migraine attack. Acute treatment can be divided into migraine specific and nonspecific therapy.
 **Ergotamines:**
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 It was first isolated by Arthur Stole in 1918 and first used as a treatment option for migraines in 1925 (Kalra & Elliott, 2007). Its chemical structure is similar to that of amines, serotonin, norepinephrine and dopamine. The mode of action of ergotamine in migraine may be by means of selective arterial vasoconstriction on certain cranial vessel beds or, alternatively, by depression of central serotonergic neurons mediating pain transmission or circulatory regulation (Kalra & Elliott, 2007). They have a complex mode of action that involves interaction with a variety of receptors which include 5-HT, dopamine and noradrenaline.
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-Most first line treatments for migraines are analgesics. Generally, these treatments are used as a primary option in severe cases, and are used when the symptoms of a migraine have just manifested themselves, as to prevent further progression. Analgesics are classified as a non-specific treatment when used in the treatment of migraines, as they are used in the treatment of other conditions as well. As such, they are often used in combination with migraine specific therapies. Common analgesics for migraines are usually a class of drug known as Non-steroidal Anti-inflammatory Drugs (NSAIDS) such as Aspirin and Aleve. NSAIDS are generally used for moderate to severe migraines and are the final non specific treatment for migraines, as they treat the symptoms of migraines, rather than the underlying cause.
+Most first line treatments for migraines are analgesics. Generally, these treatments are used as a primary option in severe cases, and are used when the symptoms of a migraine have just manifested themselves, as to prevent further progression. Analgesics are classified as a non-specific treatment when used in the treatment of migraines, as they are used in the treatment of other conditions as well (Pfaffenrath, 1995). As such, they are often used in combination with migraine specific therapies. Common analgesics for migraines are usually a class of drug known as Non-steroidal Anti-inflammatory Drugs (NSAIDS) such as Aspirin and Aleve. NSAIDS are generally used for moderate to severe migraines and are the final non specific treatment for migraines, as they treat the symptoms of migraines, rather than the underlying cause (Pfaffenrath, 1995).
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-NSAIDs work by inhibiting the production of prostaglandins, which are the chemical messengers that initiate the pain and inflammation response. Tissue in the human body produces prostaglandins in response to damage, and prostaglandins increase sensitivity in the nerves that send the pain response to the brain, thus establishing the pain threshold. The mechanism by which NSAIDs prevent prostaglandin synthesis is by the inhibition of the cyclooxygenase (COX) enzymes that are found in their metabolic pathway [Figure 6]. There are two classes of COX enzymes, and most traditional NSAIDs that are used to treat migraines inhibit both COX-1 and COX-2.  COX-1 is constitutive, while COX-2 is induced by injury. The reduction of prostaglandins inhibits pain signaling to the brain, ergo aiding in migraine management.
+NSAIDs work by inhibiting the production of prostaglandins, which are the chemical messengers that initiate the pain and inflammation response (Whalen, K., 2012). Tissue in the human body produces prostaglandins in response to damage, and prostaglandins increase sensitivity in the nerves that send the pain response to the brain, thus establishing the pain threshold (Whalen, K., 2012). The mechanism by which NSAIDs prevent prostaglandin synthesis is by the inhibition of the cyclooxygenase (COX) enzymes that are found in their metabolic pathway [Figure 6] (European Neurological Review, 2011). There are two classes of COX enzymes, and most traditional NSAIDs that are used to treat migraines inhibit both COX-1 and COX-2.  COX-1 is constitutive, while COX-2 is induced by injury (European Neurological Review, 2011). The reduction of prostaglandins inhibits pain signaling to the brain, ergo aiding in migraine management.
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-Currently CGRP1 antagonists hold promise as new anti-migraine drugs. Two recently introduced are: BIBN4096BS and Compound 1. BIBN4096BS was tested in the trigeminal ganglion and found to inhibit vasodilatation. Other experiments support its possible role as an anti-nociceptor mediator in migraine. Compound 1 has similar properties but is less potent than BIBN4096BS in human tissues. A third smaller CGRP antagonistic molecule is SB-273779. It has similar properties as the other two but may have greater value for the study of migraine and CGRP activity in animal models. The efficacy of BIBN4096BS has been tested in humans in two studies published in 2004. In the first, the safety, tolerability and pharmacokinetics of BIBN4096BS were tested in healthy volunteers. After a single IV administration of gradually increasing dose, most of the adverse events occurred at the highest administered dose (10 mg) and were relatively mild and transient (Iovino et al 2004). In another controlled study, moderate or severe headache was treated with 2.5 mg of BIBN4096BS IV vs. placebo. The end-point of pain reduction within 2 hours to mild or no pain was achieved in 66% of BIBN4096BS treated patients vs. 27% of the placebo group (Doggrell 2004). In clinical practice, its potential use will be limited to settings appropriate for IV administration.
+Currently CGRP1 antagonists hold promise as new anti-migraine drugs. Two recently introduced are: BIBN4096BS and Compound 1 (Kalra & Elliott, 2007). BIBN4096BS was tested in the trigeminal ganglion and found to inhibit vasodilatation (Kalra & Elliott, 2007). Other experiments support its possible role as an anti-nociceptor mediator in migraine. Compound 1 has similar properties but is less potent than BIBN4096BS in human tissues (Kalra & Elliott, 2007). A third smaller CGRP antagonistic molecule is SB-273779. It has similar properties as the other two but may have greater value for the study of migraine and CGRP activity in animal models (Kalra & Elliott, 2007). The efficacy of BIBN4096BS has been tested in humans in two studies published in 2004. In the first, the safety, tolerability and pharmacokinetics of BIBN4096BS were tested in healthy volunteers. After a single IV administration of gradually increasing dose, most of the adverse events occurred at the highest administered dose (10 mg) and were relatively mild and transient (Iovino et al 2004). In another controlled study, moderate or severe headache was treated with 2.5 mg of BIBN4096BS IV vs. placebo. The end-point of pain reduction within 2 hours to mild or no pain was achieved in 66% of BIBN4096BS treated patients vs. 27% of the placebo group (Doggrell 2004). In clinical practice, its potential use will be limited to settings appropriate for IV administration.
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-Recently Plastic surgeons have advertised nerve decompression surgery as an innovative new treatment of migraine headaches. In the 1990s, the use of the muscle relaxant Botulinum toxin became popular in the treatment of chronic migraine. Its effect was thought to occur through paralysis of muscles surrounding nerves in areas of pain. This operation involves the removal of a muscle in an area of the forehead where patients experience migraine pain. The idea for surgery began with patients reporting that their headaches were disappearing after forehead rejuvenation plastic surgery.
+Recently Plastic surgeons have advertised nerve decompression surgery as an innovative new treatment of migraine headaches. In the 1990s, the use of the muscle relaxant Botulinum toxin became popular in the treatment of chronic migraine. Its effect was thought to occur through paralysis of muscles surrounding nerves in areas of pain. This operation involves the removal of a muscle in an area of the forehead where patients experience migraine pain. The idea for surgery began with patients reporting that their headaches were disappearing after forehead rejuvenation plastic surgery (Migraine surgery Centre London, 2016).
 Combined, these observations led to a theory that migraine headache pain can be triggered by compression of superficial nerves by surrounding tissues, such as muscle, fascia, and bone.
-During nerve-decompression migraine surgery, nerves at one or multiple common migraine headache trigger sites are released from surrounding structures such as bone, muscle, fascia, and vessels. The Surgical Migraine Procedure is the removal of the corrugator muscles (small muscles associated with the eyebrows). However, the efficacy of this method beyond placebo has been debated in the medical community.
+During nerve-decompression migraine surgery, nerves at one or multiple common migraine headache trigger sites are released from surrounding structures such as bone, muscle, fascia, and vessels (Migraine surgery Centre London, 2016). The Surgical Migraine Procedure is the removal of the corrugator muscles (small muscles associated with the eyebrows) (Migraine surgery Centre London, 2016). However, the efficacy of this method beyond placebo has been debated in the medical community.
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 Neurostimulation is the practice of applying gentle stimulation to nerves that have been identified as sending strong, frequent pain signals.
-The Cefaly is a headband designed to deliver electrical impulses to nerves that transmit migraine pain and thereby theoretically suppress this trigger mechanism. To reduce the frequency of headaches, it is to be worn for 20 minutes every day. The device consists of a battery-operated electrical pulse generator and a self-adhesive electrode. The patient applies the electrode to the middle of the forehead and lowers a headband containing the electrical pulse generator over the forehead to engage a pin located on the electrode. Pressing a button on the band generates a pulsed electric current that stimulates the upper branches of the trigeminal nerve, producing a tingling or massaging sensation. During the treatment, which has a fixed duration of 20 minutes, the intensity of the electric current gradually increases.
+The Cefaly is a headband designed to deliver electrical impulses to nerves that transmit migraine pain and thereby theoretically suppress this trigger mechanism. To reduce the frequency of headaches, it is to be worn for 20 minutes every day (Didier et. al, 2015). The device consists of a battery-operated electrical pulse generator and a self-adhesive electrode (Didier et. al, 2015). The patient applies the electrode to the middle of the forehead and lowers a headband containing the electrical pulse generator over the forehead to engage a pin located on the electrode. Pressing a button on the band generates a pulsed electric current that stimulates the upper branches of the trigeminal nerve, producing a tingling or massaging sensation (Didier et. al, 2015). During the treatment, which has a fixed duration of 20 minutes, the intensity of the electric current gradually increases.
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+====== Conclusion ======
-\\====== Conclusion ======
 Overall, migraines are a heterogenous, burdensome disorder that are debilitating for the individuals experiencing them. There appears to be a strong link between genetics and environment in making individuals susceptible to migraine attacks. Symptoms can vary from one individual to the next and exacerbating factors can have different effects on different individuals. Our proposed course of treatment is to use non-steroidal anti-inflammatory drugs with caffeine administration to alleviate pain in migraine sufferers. Studies have shown that NSAIDs are significantly more effective at relieving symptoms of headache compared to other proposed therapeutics. NSAIDs, like Naproxen, are much more cost-effective, have a longer lasting effect, have a reduced likelihood of producing rebound headaches, show low reports of adverse affects and are non-addictive. It has been shown that co-administration with caffeine promote more effective intestinal absorption and a higher likelihood of a positive treatment response. Great progress has been made in understand migraine pathophysiology as well as defining new specific therapies. In recognition of the large market of migraine sufferers, the pharmaceutical and bioengineering industries are working towards newer and better approaches for affective interventions.
+====== References ======
+American Migraine Foundation. (n.d.). Retrieved February 27, 2016, from http://www.americanmigrainefoundation.org/resources-and-links/a-brief-sad-history-of-treatments-for-migraine/
+Aminoff, Roger P. Simon, David A. Greenberg, Michael J. (2009). Clinical neurology (7 ed.). New York, N.Y: Lange Medical Books/McGraw-Hill. pp. 85–88.
+Bartleson JD, Cutrer FM (May 2010). "Migraine update. Diagnosis and treatment". Minn Med 93 (5): 36–41. PMID 20572569.
+Bigal, ME; Lipton, RB (June 2008). "The prognosis of migraine". Current Opinion in Neurology 21 (3): 301–8.doi:10.1097/WCO.0b013e328300c6f5. PMID 18451714.
+Blau, J. N. (1980). Migraine prodromes separated from the aura: complete migraine. Br Med J, 281(6241), 658-660.
+Dahlof, C. (1993). Placebo-controlled clinical trials with ergotamine in the acute treatment of migraine. Cephalalgia, 13(3), 166-171.
+Diseases and Conditions: Migraines. (2013, June 04). Retrieved March 08, 2016, from http://www.mayoclinic.org/diseases-conditions/migraine-headache/basics/risk-factors/con-20026358
+Didier HA, Di fiore P, Marchetti C, et al. Electromyography data in chronic migraine patients by using neurostimulation with the Cefaly® device. Neurol Sci. 2015;36 Suppl 1:115-9.
+Doggrell SA. 2004. New drugs for the prevention and treatment of migraine: topiramate and BIBN 4096 BS. Expert Opin Pharmacother,5:1837–40.
+Hansen, J. M., Lipton, R. B., Dodick, D. W., Silberstein, S. D., Saper, J. R., Aurora, S. K., ... & Charles, A. (2012). Migraine headache is present in the aura phase A prospective study.
+Neurology, 79(20), 2044-2049.
+European Neurological Review, 2011;6(4):265–9
+Hougaard, A; Amin, FM; Ashina, M. 2014. "Migraine and structural abnormalities in the brain." //Current opinion in neurology// 27 (3): 309–14.doi:10.1097/wco.0000000000000086.
+Iovino M, Feifel U, Yong C-L, et al. 2004. Safety, tolerability and pharmacokinetics of BIBN4096 BS, the first selective small molecule calcitonin gene-related peptide receptor antagonist, following single intravenous administration in healthy volunteers. Cephalalgia, 24:645–56.
+International Headache Society abstracts. Cephalalgia. 2015;35(6 Suppl):1-296.
+Jes Olesen, (2006). The headaches. (3 ed.). Philadelphia: Lippincott Williams & Wilkins. p. 238.
+Johnson, E.S, Ratcliffe, D.M & Wilkinson, M. (1985). Naproxen sodium in the treatment of migraine . Cephalalgia, 5(1), 5-10.
+Johnston MM, Rapoport AM (August 2010). "Triptans for the management of migraine". Drugs 70 (12): 1505–18. doi:10.2165/11537990-000000000-00000.PMID 20687618.
+Kalra, A. & Elliott, D. (2007). Acute migraine: current treatment and emerging therapies . Therapeutics and clinical risk management , 3(3), 449-459.
+Kelman L., (2006). " The postdrome of the acute migraine attack". Cephalalgia 26 (2): 214–20.
+Noseda, R & Burstein, R. (2013). Migraine pathophysiology: Anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain. Pain , 154(1), S44-S53.
+Pfaffenrath V, Scherzer S. Analgesics and NSAlDs in the treatment of the acute migraine attack. Cephalalgia 1995; Suppl 15:14-20.
+Rizzoli P. Preventive pharmacotherapy in migraine. Headache. 2014;54(2):364-9.
+Schürks, M; Rist, PM; Bigal, ME; Buring, JE; Lipton, RB; Kurth, T (2009-10-27). "Migraine and cardiovascular disease: systematic review and meta-analysis". BMJ (Clinical research ed.) 339: b3914.doi:10.1136/bmj.b3914. PMC 2768778. PMID 19861375.
+Tfelt-hansen et al.. (2000). Ergotamine in the acute treatment of migraine: A review and European consensus . Brain, 123(1), 9-18.
+Vos, T; Flaxman, AD; Naghavi, M; Lozano, R; Michaud, C; Ezzati, M; Shibuya, K; Salomon, JA; et al. (Dec 15, 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2163–96.doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.
+Wang SJ (2003). "Epidemiology of migraine and other types of headache in Asia". Curr Neurol Neurosci Rep3 (2): 104–8. doi:10.1007/s11910-003-0060-7.PMID 12583837.
+Weinberger, J (March 2007). "Stroke and migraine".Current cardiology reports 9 (1): 13–9.doi:10.1007/s11886-007-0004-y. PMID 17362679.
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