Differences
This shows you the differences between two versions of the page.
| Both sides previous revision Previous revision Next revision | Previous revision | ||
|
group_2_presentation_2_-_migraines [2016/03/05 22:53] monachd |
group_2_presentation_2_-_migraines [2018/01/25 15:18] (current) |
||
|---|---|---|---|
| Line 1: | Line 1: | ||
| ====== Migraines ====== | ====== Migraines ====== | ||
| + | |||
| + | {{:final_copy-migraine_headaches-_group_2_presentation_2_life_sci_4m03.pptx|}} | ||
| <style float-right> | <style float-right> | ||
| Line 43: | Line 45: | ||
| - | **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). |
| </style> | </style> | ||
| Line 173: | Line 175: | ||
| ====== Treatment ====== | ====== 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:** | **Ergotamines:** | ||
| Line 185: | Line 187: | ||
| <style justify> | <style justify> | ||
| 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. | 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. | ||
| - | |||
| Line 248: | Line 249: | ||
| <style justify> | <style justify> | ||
| - | 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). |
| </style> | </style> | ||
| Line 258: | Line 259: | ||
| <style justify> | <style justify> | ||
| - | 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. |
| </style> | </style> | ||
| Line 346: | Line 347: | ||
| Dahlof, C. (1993). Placebo-controlled clinical trials with ergotamine in the acute treatment of migraine. Cephalalgia, 13(3), 166-171. | 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 | ||
| Line 359: | Line 364: | ||
| 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. | 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. | Neurology, 79(20), 2044-2049. | ||
| + | |||
| + | |||
| + | |||
| + | European Neurological Review, 2011;6(4):265–9 | ||
| Line 367: | Line 376: | ||
| 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. | 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. | ||
| Line 391: | Line 404: | ||
| 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. | 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. | ||
| Line 411: | Line 432: | ||
| Weinberger, J (March 2007). "Stroke and migraine".Current cardiology reports 9 (1): 13–9.doi:10.1007/s11886-007-0004-y. PMID 17362679. | Weinberger, J (March 2007). "Stroke and migraine".Current cardiology reports 9 (1): 13–9.doi:10.1007/s11886-007-0004-y. PMID 17362679. | ||
| + | |||
| + | |||
| + | Whalen, K., Finkel, R., & Panavelil, T. A. (n.d.). Pharmacology (6th ed.). | ||
