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group_4_presentation_1_-_migraines [2018/02/02 19:21] chowds6 |
group_4_presentation_1_-_migraines [2018/02/15 15:34] (current) pablahk2 [Presentation] |
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| ====== Epidemiology ====== | ====== Epidemiology ====== | ||
| - | Migraines affect 8.3% of Canadians, which accounts for 2.7 million individuals. Worldwide, it is estimated to affect 14% of the entire population (Ramage-Morin & Gilmour, 2014). It should be noted that these estimates may fall short of the actual prevalence of migraines, as not many individuals actively seek medical assistance when affected (Ramage-Morin & Gilmour, 2014). Migraine prevalence is correlated with age, sex, race, geographic distribution, and socioeconomic factors. It has been found that migraines with auras occur earlier in males and females compared to migraines without. However, males tend to have migraines earlier on in life regardless of the presence of auras. Following puberty, females report migraines more frequently than males. Both sexes report having migraines within the age range of 25 to 55, followed by a decline (Ramage-Morin & Gilmour, 2014). Overall, it is found that females report migraines more frequently than males. In an American study, it was discovered that Caucasians tend to have the highest prevalence of migraines, while Asian Americans have the lowest. Geographically, data tends to support this finding as North and South Americans were observed to report migraines the most, while individuals in Asia reported migraines the least. Typically, socioeconomic status is inversely proportional to the prevalence of migraines in a population (Lipton & Bigal, 2005). | + | Migraines affect 8.3% of Canadians, which accounts for 2.7 million individuals. Worldwide, it is estimated to affect 14% of the entire population (Ramage-Morin & Gilmour, 2014). It should be noted that these estimates may fall short of the actual prevalence of migraines, as not many individuals actively seek medical assistance when affected (Ramage-Morin & Gilmour, 2014). Migraine prevalence is correlated with age, sex, race, geographic distribution, and socioeconomic factors. It has been found that migraines with auras occur earlier in males and females compared to migraines without. However, males tend to have migraines earlier on in life regardless of the presence of auras. Following puberty, females report migraines more frequently than males. Both sexes report having migraines within the age range of 25 to 55, followed by a decline as seen in **Figure 1a** (Ramage-Morin & Gilmour, 2014). Overall, it is found that females report migraines more frequently than males. In an American study, it was discovered that Caucasians tend to have the highest prevalence of migraines, while Asian Americans have the lowest. Geographically, data tends to support this finding as North and South Americans were observed to report migraines the most, while individuals in Asia reported migraines the least, as seen in **Figure 1b**. Typically, socioeconomic status is inversely proportional to the prevalence of migraines in a population (Lipton & Bigal, 2005). |
| <box 65% | >{{ :graphv3.png?700 |}}</box| | <box 65% | >{{ :graphv3.png?700 |}}</box| | ||
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| Similar findings were shown in another study conducted by Hashizume and colleagues (2008). Stress and significant shifts in mood were examined over 1-3 days before a suspected migraine. During this time, participants recorded – four times a day biweekly – for migraine severity, stressful event occurrence, domestic and non-domestic stress, daily burdens, and any anxiety or depressive episode experiences. Overall, final results concluded that there was an evident change in various modes of psychosocial stress in advance of a migraine attack on the days when migraines were recorded. (Hashizume et al., 2008). Such stress-related variables were thus confirmed to be correlated to migraines by a significant degree, thus playing an important role in migraine frequency and occurrence (Hashizume et al., 2008). | Similar findings were shown in another study conducted by Hashizume and colleagues (2008). Stress and significant shifts in mood were examined over 1-3 days before a suspected migraine. During this time, participants recorded – four times a day biweekly – for migraine severity, stressful event occurrence, domestic and non-domestic stress, daily burdens, and any anxiety or depressive episode experiences. Overall, final results concluded that there was an evident change in various modes of psychosocial stress in advance of a migraine attack on the days when migraines were recorded. (Hashizume et al., 2008). Such stress-related variables were thus confirmed to be correlated to migraines by a significant degree, thus playing an important role in migraine frequency and occurrence (Hashizume et al., 2008). | ||
| - | Significant evidence has also displayed the cyclic nature of migraines, particularly how migraines themselves act as a stressor leading to a positive feedback and increase of migraine severity and frequency, as seen in Figure 2 (Sauro & Becker, 2009). A noteworthy investigation lead by Holm and colleagues (1997), looked at the daily temporal relationship between migraines, appraisal, coping and stress in a group of migraineurs. From this group, it was observed that 50-70% of participants showed a significant and meaningful correlation between their recorded days of migraine attacks and days of major stress (Holm et al., 1997). In addition, migraine severity also showed to steadily increase over time, further supporting the hypothesis that migraines and stress are reciprocal and cyclically influence one another (Holm et al., 1997). | + | Significant evidence has also displayed the cyclic nature of migraines, particularly how migraines themselves act as a stressor leading to a positive feedback and increase of migraine severity and frequency, as seen in **Figure 2** (Sauro & Becker, 2009). A noteworthy investigation lead by Holm and colleagues (1997), looked at the daily temporal relationship between migraines, appraisal, coping and stress in a group of migraineurs. From this group, it was observed that 50-70% of participants showed a significant and meaningful correlation between their recorded days of migraine attacks and days of major stress (Holm et al., 1997). In addition, migraine severity also showed to steadily increase over time, further supporting the hypothesis that migraines and stress are reciprocal and cyclically influence one another (Holm et al., 1997). |
| - | <box 50% | >{{ :new.png?400 |}}</box|Figure 2: The cyclic cycle of the reciprocating relationship between stress and migraines (Stress response, 2012).> | + | <box 50% | >{{ :new.png?400 |}}</box|Figure 2: The cyclic relationship between stress and migraines (Stress response, 2012).> |
| ====Food and Drink==== | ====Food and Drink==== | ||
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| ====Change in Weather==== | ====Change in Weather==== | ||
| - | Sudden changes in weather and certain weather conditions have also been highly self-reported in migraineurs, as much as 43% of patients in one study (Robbins, 1994). In another study by Prince and colleagues (2004), 77 migraineurs provided a calendar (from 2 to 24 months) where it was seen that influences of certain weather variables had a significant impact on migraine onset, making them more susceptible. As seen in Figure 3, weather conditions that had the highest influence included low air pressure, high humidity, sudden air pressure change, and bright sunshine - each ranking highest to lowest impact respectively (Prince et al., 2004). In another study by Hoffmann and colleagues (2011), journals were written by participants in which similar results were seen. Onset of attacks with high migraine intensity was associated with lower temperature and higher humidity. This was also seen when measuring weather components such as temperature, air pressure, and relative humidity over a year. | + | Sudden changes in weather and certain weather conditions have also been highly self-reported in migraineurs, as much as 43% of patients in one study (Robbins, 1994). In another study by Prince and colleagues (2004), 77 migraineurs provided a calendar (from 2 to 24 months) where it was seen that influences of certain weather variables had a significant impact on migraine onset, making them more susceptible. As seen in **Figure 3**, weather conditions that had the highest influence included low air pressure, high humidity, sudden air pressure change, and bright sunshine - each ranking highest to lowest impact respectively (Prince et al., 2004). In another study by Hoffmann and colleagues (2011), journals were written by participants in which similar results were seen. Onset of attacks with high migraine intensity was associated with lower temperature and higher humidity. This was also seen when measuring weather components such as temperature, air pressure, and relative humidity over a year. |
| <box 40% | >{{ :screen_shot_2018-01-31_at_3.57.01_pm.png?300 |}}</box|Figure 3: Influence of weather on migraine onset and severity from highest to lowest (Prince et al., 2004).> | <box 40% | >{{ :screen_shot_2018-01-31_at_3.57.01_pm.png?300 |}}</box|Figure 3: Influence of weather on migraine onset and severity from highest to lowest (Prince et al., 2004).> | ||
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| ====Other Extraneous Factors==== | ====Other Extraneous Factors==== | ||
| - | As much as 38% of patients have described that bright light, either sunlight or artificial, as well as excessive noise, were associated with their migraine pain, as seen in Figure 4 (Robbins, 1994). Another study showed that lack of sleep, and even oversleeping, was also reported as a major precipitating factor for migraine onset (Spierings, 2001). | + | As much as 38% of patients have described that bright light, either sunlight or artificial, as well as excessive noise, were associated with their migraine pain, as seen in **Figure 4** (Robbins, 1994). Another study showed that lack of sleep, and even oversleeping, was also reported as a major precipitating factor for migraine onset (Spierings, 2001). |
| <box 40% | >{{ :screen_shot_2018-01-31_at_4.26.23_pm.png?350 |}}</box|Figure 4: The effect of environmental and external influence on migraines from highest to lowest in one particular study (Robbins, 1994).> | <box 40% | >{{ :screen_shot_2018-01-31_at_4.26.23_pm.png?350 |}}</box|Figure 4: The effect of environmental and external influence on migraines from highest to lowest in one particular study (Robbins, 1994).> | ||
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| ====Cortical Spreading Depression==== | ====Cortical Spreading Depression==== | ||
| - | The process of Cortical Spreading Depression (CSD) explains the mechanism behind migraines with aura. Current understanding indicates that a wave of neuronal excitation found in the cortical gray matter spreads across the cerebral cortex as seen in Figure 5 (Chawla, 2018). As these neurons begin to depolarize it is thought that the aura phase is triggered. The activation of the aura phase then excites the trigeminal fibres, which causes the headache phase of a migraine (Chawla, 2018). | + | The process of Cortical Spreading Depression (CSD) explains the mechanism behind migraines with aura. Current understanding indicates that a wave of neuronal excitation found in the cortical gray matter spreads across the cerebral cortex as seen in **Figure 5** (Chawla, 2018). As these neurons begin to depolarize it is thought that the aura phase is triggered. The activation of the aura phase then excites the trigeminal fibres, which causes the headache phase of a migraine (Chawla, 2018). |
| <box 70% | >{{ :cortical_spreading_depression.jpg?800 |}}</box| Figure 5: Visual representation of the process of cortical spreading, migrating across the cerebral cortex (Chawla, 2018).> | <box 70% | >{{ :cortical_spreading_depression.jpg?800 |}}</box| Figure 5: Visual representation of the process of cortical spreading, migrating across the cerebral cortex (Chawla, 2018).> | ||
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| ====Structures Associated with the Trigeminovascular System==== | ====Structures Associated with the Trigeminovascular System==== | ||
| - | The pathway associated with migraines pain can be triggered by multiple factors such as stress, diet, weather and so forth. As seen in Figure 6 there are many major structures involved in the activation of the trigeminovascular system (Pathophysiology of Migraines, 2018). The dural vascular structures become activated from sensory neurons that are connected to the trigeminal ganglion and upper cervical dorsal roots. This input from the dural vascular structure then innervates the trigeminocervical complex (TCC) through second-order neurons (Pathophysiology of Migraines, 2018). The localization of pain is the result of nerve fibres, which ascend from the trigeminal nucleus caudalis to the thalamus, and then to the sensory cortex. The merging of projections from the trigeminal nerve at the trigeminal nucleus caudalis and upper cervical nerve roots are thought to be attributed to the perceived pain in the head and upper neck regions (Pathophysiology of Migraines, 2018). | + | The pathway associated with migraines pain can be triggered by multiple factors such as stress, diet, weather and so forth. As seen in **Figure 6** there are many major structures involved in the activation of the trigeminovascular system (Pathophysiology of Migraines, 2018). The dural vascular structures become activated from sensory neurons that are connected to the trigeminal ganglion and upper cervical dorsal roots. This input from the dural vascular structure then innervates the trigeminocervical complex (TCC) through second-order neurons (Pathophysiology of Migraines, 2018). The localization of pain is the result of nerve fibres, which ascend from the trigeminal nucleus caudalis to the thalamus, and then to the sensory cortex. The merging of projections from the trigeminal nerve at the trigeminal nucleus caudalis and upper cervical nerve roots are thought to be attributed to the perceived pain in the head and upper neck regions (Pathophysiology of Migraines, 2018). |
| <box 55% | >{{ :imagev2.png?350 |}}</box|Figure 6: The major structures involved in the activation of the trigeminovascular system (Pathophysiology of Migraines, 2018).> | <box 55% | >{{ :imagev2.png?350 |}}</box|Figure 6: The major structures involved in the activation of the trigeminovascular system (Pathophysiology of Migraines, 2018).> | ||
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| ====== Mechanisms ====== | ====== Mechanisms ====== | ||
| - | The mechanisms underlying the trigeminovascular system remain largely unknown as shown in Figure 7, such as the relationship between abnormal cortical activity and brainstem function and the relationship between dysfunctional brainstem function and the activation of trigeminal hyperexcitability (Pietrobon, 2005). One hypothesis suggests the possibility that CSD also occurs in MO (a migraine without aura) patients but the associated aura symptoms do not show because it takes place in a clinically silent area of the cerebral cortex and thus causes headache pain (Pietrobon, 2005). Another view illustrates migraine aura and headache as parallel and not sequential. Therefore, this demonstrates that the cause of a migraine is a dysfunction in the brainstem nuclei (Pietrobon, 2005). However, both these proposed hypotheses lack evidence and therefore, cannot be claimed as scientific fact. | + | The mechanisms underlying the trigeminovascular system remain largely unknown as shown in **Figure 7**, such as the relationship between abnormal cortical activity and brainstem function and the relationship between dysfunctional brainstem function and the activation of trigeminal hyperexcitability (Pietrobon, 2005). One hypothesis suggests the possibility that CSD also occurs in MO (a migraine without aura) patients but the associated aura symptoms do not show because it takes place in a clinically silent area of the cerebral cortex and thus causes headache pain (Pietrobon, 2005). Another view illustrates migraine aura and headache as parallel and not sequential. Therefore, this demonstrates that the cause of a migraine is a dysfunction in the brainstem nuclei (Pietrobon, 2005). However, both these proposed hypotheses lack evidence and therefore, cannot be claimed as scientific fact. |
| <box 45% | >{{ :27662073_10210519802017970_584050570_n.png?400 |}}</box|Figure 7: provides a visual representation of the above hypotheses and illustrates the uncertainty of each through the dotted lines (Pietrobon, 2005).> | <box 45% | >{{ :27662073_10210519802017970_584050570_n.png?400 |}}</box|Figure 7: provides a visual representation of the above hypotheses and illustrates the uncertainty of each through the dotted lines (Pietrobon, 2005).> | ||
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| ====Familial Hemiplegic Migraine==== | ====Familial Hemiplegic Migraine==== | ||
| - | Genes associated with the cause of migraines have yet to be definitive, except for in familial hemiplegic migraine (FHM) cases. FHM is a type of migraine characterized by aura symptoms mostly in the temporal order (visual, sensory, motor, aphasic) and can co-occur within families (Pietrobon, 2005). These attacks are similar to migraines with aura attacks, however, tend to last longer and may have severe attacks that include impairment of consciousness or seizures (Pietrobon, 2005). There are 3 different types of Familial Hemiplegic Migraines, which will be further explored below. | + | Genes associated with the cause of migraines have yet to be definitive, except for in familial hemiplegic migraine (FHM) cases, as visualized in **Figure 8**. FHM is a type of migraine characterized by aura symptoms mostly in the temporal order (visual, sensory, motor, aphasic) and can co-occur within families (Pietrobon, 2005). These attacks are similar to migraines with aura attacks, however, tend to last longer and may have severe attacks that include impairment of consciousness or seizures (Pietrobon, 2005). There are 3 different types of Familial Hemiplegic Migraines, which will be further explored below. |
| * **FHM1**: This is the most common type of FHM at around 50% of the cases. This migraine is characterized by mutations in CACNA1A that encodes for a pore-forming alpha1 subunit of neuronal Cav2.1 channels (located in the presynaptic terminals and somatodendritic membranes, places that have been implicated with migraines) that has 4 domains each containing 6 transmembrane regions with a voltage sensor and pore loop (Russell, 2011). These channels play a role in neurotransmitter release and have been expressed in many brain structures involving migraines such as cerebral cortex, trigeminal ganglia and brainstem nuclei. The effect of the mutation involves an influx of Ca2+ due to lower voltages of the channel activation. A study by Pietrobon (2005) demonstrates that there is also an excessive release of glutamate in relation to the Ca2+, which starts a positive feedback cycle leading to CSD (Pietrobon, 2005) This gene is related to other conditions, such as nystagmus (involuntary movement of the eyeballs) and ataxia (unsteadiness and the loss of muscle coordination). | * **FHM1**: This is the most common type of FHM at around 50% of the cases. This migraine is characterized by mutations in CACNA1A that encodes for a pore-forming alpha1 subunit of neuronal Cav2.1 channels (located in the presynaptic terminals and somatodendritic membranes, places that have been implicated with migraines) that has 4 domains each containing 6 transmembrane regions with a voltage sensor and pore loop (Russell, 2011). These channels play a role in neurotransmitter release and have been expressed in many brain structures involving migraines such as cerebral cortex, trigeminal ganglia and brainstem nuclei. The effect of the mutation involves an influx of Ca2+ due to lower voltages of the channel activation. A study by Pietrobon (2005) demonstrates that there is also an excessive release of glutamate in relation to the Ca2+, which starts a positive feedback cycle leading to CSD (Pietrobon, 2005) This gene is related to other conditions, such as nystagmus (involuntary movement of the eyeballs) and ataxia (unsteadiness and the loss of muscle coordination). | ||
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| ====== Conclusion ====== | ====== Conclusion ====== | ||
| - | Overall, migraines are a primary headache disorder, characterized by recurrent throbbing, heightened severity, length, localization of pain to one side of the head and other related symptoms (such as vomiting, nausea, sensitivity to light and smell). There appears to be a high prevalence of migraines globally by age. On average, both males and females experience the most migraines, but females tend to have migraines more often than do males. | + | Overall, migraines are a primary headache disorder, characterized by recurrent throbbing, heightened severity, length, localization of pain to one side of the head, amongst other symptoms (vomiting, nausea, sensitivity to light and smell). These symptoms are observed at a high prevalence rate globally by age, with females experiencing more migraines than males overall. In addition, although the causes and triggers to migraine onset remains unclear, multiple studies have observed patients being most susceptible to stress, certain foods and drink, as well as other associated environmental and biological factors (light, weather, menstruation, hunger, etc.). What can be understood currently about this phenomenon is how migraines are a neurovascular disorders, mainly due to cortical spreading and the activation of trigeminovascular system seen in the brain and central nervous system. Beyond this scope however, the rest is relatively unclear, specifically concerning the mechanisms at play. It has been theorized that migraines are associated to a single nucleotide polymorphism on chromosome 8 or a frameshift mutation in the KCNK18 gene. With this current understanding about migraines, diagnosis can be completed quickly and treatment can be implemented at any migraine stage via acute or proactive methods. Yet, despite the efforts in providing a myriad of pharmaceutical and alternative treatments to the public, more has to be done to further learn how migraines occur and how to effectively lessen their severity for individuals. |
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| + | ====== Presentation ===== | ||
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| + | Click {{:presentation_1_migraines.pdf|}} for a research seminar presentation on migraines. | ||
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| + | **Copyright ©** Miguel Cardoso, Shara Chowdhury, Sabrina Musto, Harpreet Pabla, & Ojan Yarkhani | ||
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| Bic, Z., Blix, G. G., Hopp, H. P., & Leslie, F. M. (1998). In search of the ideal treatment for migraine headache. Medical hypotheses, 50(1), 1-7. | Bic, Z., Blix, G. G., Hopp, H. P., & Leslie, F. M. (1998). In search of the ideal treatment for migraine headache. Medical hypotheses, 50(1), 1-7. | ||
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| + | Business Insider. Retrieved 2 February 2018, from http://www.businessinsider.com/how-pain-relievers-tylenol-ibuprofen-work-2016-10 | ||
| Chawla, J. (2018). Migraine Headache: Practice Essentials, Background, Pathophysiology. Emed | Chawla, J. (2018). Migraine Headache: Practice Essentials, Background, Pathophysiology. Emed | ||
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| Hoffmann, J., Lo, H., Neeb, L., Martus, P., & Reuter, U. (2011). Weather sensitivity in migraineurs. Journal of neurology, 258(4), 596-602. | Hoffmann, J., Lo, H., Neeb, L., Martus, P., & Reuter, U. (2011). Weather sensitivity in migraineurs. Journal of neurology, 258(4), 596-602. | ||
| - | Holm, J. E., Lokken, C., & Myers, T. C. (1997). Migraine and stress: a daily examination of temporal relationships in women migraineurs. Headache: The journal of head and face pain, 37(9), 553-558. | + | Holm, J. E., Lokken, C., & Myers, T. C. (1997). Migraine and stress: a daily examination of temporal relationships in women migraineurs. Headache: The journal of head and face pain, 37(9), 553-558. |
| Lay, C. L., & Mascellino, A. M. (2001). Menstrual migraine: diagnosis and treatment. Current pain and headache reports, 5(2), 195-199. | Lay, C. L., & Mascellino, A. M. (2001). Menstrual migraine: diagnosis and treatment. Current pain and headache reports, 5(2), 195-199. | ||
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| Robbins, L. (1994). Precipitating factors in migraine: a retrospective review of 494 patients. Headache: The Journal of Head and Face Pain, 34(4), 214-216. | Robbins, L. (1994). Precipitating factors in migraine: a retrospective review of 494 patients. Headache: The Journal of Head and Face Pain, 34(4), 214-216. | ||
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| - | Health Reports, 25(6), 10–16. Retrieved from https://www.statcan.gc.ca/pub/82-003-x/2014006/article/14033-eng.htm | ||
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| - | Holm, J. E., Lokken, C., & Myers, T. C. (1997). Migraine and stress: a daily examination of temporal relationships in women migraineurs. Headache: The journal of head and face pain, 37(9), 553-558. | ||
| Ramsey, L. (2018). Here's how common pain relievers actually work in your body and brain. | Ramsey, L. (2018). Here's how common pain relievers actually work in your body and brain. | ||
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| - | Business Insider. Retrieved 2 February 2018, from http://www.businessinsider.com/how-pain-relievers-tylenol-ibuprofen-work-2016-10 | ||
| Robbins, L. (1994). Precipitating factors in migraine: a retrospective review of 494 patients. Headache: The Journal of Head and Face Pain, 34(4), 214-216. | Robbins, L. (1994). Precipitating factors in migraine: a retrospective review of 494 patients. Headache: The Journal of Head and Face Pain, 34(4), 214-216. | ||
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| Sauro, K. M., & Becker, W. J. (2009). The stress and migraine interaction. Headache: The journal of head and face pain, 49(9), 1378-1386. | Sauro, K. M., & Becker, W. J. (2009). The stress and migraine interaction. Headache: The journal of head and face pain, 49(9), 1378-1386. | ||
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| + | Stress Response. (2012). Migraine Relief Chiropractic Center. [online] Available at: http://migrainechiro.blogspot.ca/2012/04/stress-response-diagram.html | ||
| Spierings, E. L., Ranke, A. H., & Honkoop, P. C. (2001). Precipitating and aggravating factors of migraine versus tension‐type headache. Headache: The journal of head and face pain, 41(6), 554-558. | Spierings, E. L., Ranke, A. H., & Honkoop, P. C. (2001). Precipitating and aggravating factors of migraine versus tension‐type headache. Headache: The journal of head and face pain, 41(6), 554-558. | ||
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| Wöber, C., Holzhammer, J., Zeitlhofer, J., Wessely, P., & Wöber-Bingöl, Ç. (2006). Trigger factors of | Wöber, C., Holzhammer, J., Zeitlhofer, J., Wessely, P., & Wöber-Bingöl, Ç. (2006). Trigger factors of | ||
| migraine and tension-type headache: experience and knowledge of the patients. The journal of headache and pain, 7(4), 188-195. | migraine and tension-type headache: experience and knowledge of the patients. The journal of headache and pain, 7(4), 188-195. | ||
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