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EEG biofeedback training, known as neurofeedback, has been explored as a nonpharmacologic prophylaxis for migraines. Based on the conceptual model of disregulation of central arousal function, the Othmers proposed a protocol in migraine prophylaxis by raising the sensory motor rhythm (SMR, 12- 15 Hz), accompanied by an inhibition of theta ( 4- 7 Hz) frequency. Relaxation with music, on the other hand, is another type of nonpharmacologic prophylaxis for migraines and is used to reduce perceived psychological and/or physiological stress and pain. Studies showed that an effective relaxation with music program is one that integrates certain relaxing musical characteristics and personal factors. Six female participants (29 to 57 years of age) previously diagnosed with migraines participated in this single-subject design study. This study employed two independent variables- the SMR/theta training and music therapy, and the dependent variables were the SMR and theta recording registration. Each participant first participated in the EEG Base-rate recording session, and was then randomly assigned to the following treatment conditions: SMR/Theta training only, music therapy only, and SMR/Theta training and music therapy." Counterbalancing of the treatment conditions was applied across participants, two sessions weekly for a total of 13 sessions, 30 minutes each session. In SMR/Theta training only, participants were instructed to raise their SMR while inhibiting theta. In music therapy only, participants were instructed to select their relaxation CD music to be played during the sessions. The SMR and theta data were graphed for each participant and implications were discussed. Graph analysis indicated that two participants were responsive to SMR/Theta training and music therapy and SMR/Theta training only respectively. Overall, all participants acquired relaxation skills and seemed better at adapting themselves to a stressful environment.

A postmarketing surveillance survey of sumatriptan use comprised 32 questions including patient demographics, headache history, and sumatriptan experience. One hundred and forty-one questionnaires were sent out, and 109 patients responded; a total of 108 patients were included in the data analysis. When compared with the national migraine population, on a percentage basis, significantly more African-Americans, females, young patients (less 45 years of age), and patients with higher mean incomes (>$45,000) were found in the present study of those taking sumatriptan (p Males (N=8) and females (N=55) had a significantly different percentage of relief from the second dose of 94.7%±7.1 and 83.5%±24.4, respectively (p=0.01). An average percent of pain relief from the first dose in those weighing less or greater than 144 pounds was 76.5%±28.3 and 86.9%±16.4, respectively (p=0.023). The incidence of the adverse effects reported in this study was significantly greater than those reported in the literature (p<0.005).

Migraine is a common, episodic neurological disorder that includes headache, nausea and hypersensitivity to sensory stimuli. During the headache phase of migraine, migraine patients can be especially hypersensitive to thermal stimuli. The unpredictable and episodic nature of migraine makes it difficult to treat and much of the mechanism of migraine has yet to be elucidated. A T44A substitution in casein kinase 1δ is inherited with migraine with aura. A transgenic mouse model suggests that animals with this mutation exhibit increased sensitivity to thermal stimuli after injection with nitroglycerin (NTG). We performed behavior assays that measure animal responses to thermal stimuli, after injection with NTG, a known migraine-inducer in human migraine patients. Female animals with the CK1δ-T44A mutation are more sensitive than wildtype littermates, suggesting a sex difference emerges in pain sensitivity in animals that express the CK1δ-T44A but not in wildtype siblings. Female CK1δ-T44A animals are more sensitive to the effects of NTG on pain than male CK1δ-T44A mice. This indicates a potential sex hormone related pain response. Since estrogen is implicated in both migraine and pain response, we test the thermal sensitivity of heterozygous ERβKO/+ and CK1δ-T44A; ERβKO/+ mice compared to wildtype and CK1δ-T44A mice. Overall thermal sensitivity is decreased before stress of injection in both male and female ERβKO/+ and CK1δ-T44A: ERβKO/+ mice. This demonstrates that ERβ is necessary for thermal nociception in untreated mice. However, after injection with saline or NTG, animals of all genotypes responded to thermal stimuli similarly. This suggests that estrogen signaling through ERβ is likely not part of the pathway of NTG-induced thermal sensitivity or that one copy of ERβ is sufficient for NTG-induced thermal sensitivity. Since ERβ is fully functional in CK1δ-T44A mice and CK1δ-T44A mice have wildtype thermal sensitivity at baseline, we can conclude that CK1δ-T44A does not modulate ERβ to affect thermal sensitivity in untreated animals.

The relationship between autonomic dysfunction and primary headache disorders has been established in the adult population. The aim of this retrospective study was to elucidate if there was a similar association in the pediatric primary headache population. Three groups were compared - migraine patients, tension-type headache patients and idiopathic scoliosis patients as a control group. Utilizing clinical data collected during patients' initial visits, prevalence of autonomic dysfunction symptoms were quantified. The headache groups also filled out the Functional Disability Index (FDI) as well as the Children's Depression Inventory (CDI) to help elucidate if there was a relationship between function disability, psychiatric state and primary headaches and/or autonomic dysfunction symptoms. It was found that the headache groups had significantly greater dysautonomia as compared to the control group. Only slight differences were found between the migraine and tension-type patients in regards to dysautonomia. No significant differences were found in total FDI or CDI scores. These results illuminate a relationship between autonomic nervous system dysfunction and primary headache disorders in the pediatric population studied. Prospective studies and the development of standardized dysautonomia questionnaires will allow a more detailed autonomic dysfunction profile to be built for this population.

Migraine is an extremely common and disabling disease that affects three times more women than men, and is characterized by recurring migraines comprised of disturbances in sensation perception, intense head pain, nausea, and increased sensitivity to light and sound that can last from several hours to multiple days. Currently, there are no cures for the disease, no official social services that can help a person to handle living with it, and limited studies on its mechanisms or impact on a person’s life. One of the reasons for the low priority handling of migraine, is its stigmatization as a disease of hypersensitive women of weak moral character. To break this stigma, awareness of the severity of episodes and their effects on people’s daily lives is necessary. However, communicating experiences of highly intense invisible pain shrouded in prejudice is difficult, and rational language cannot reach every aspect of it. For this master thesis project, I studied migraine from a medical anthropological perspective, focusing on the life experiences of student musicians between the age of 20 and 30 living with regularly returning migraines in Sweden. I aimed to connect the sufferers’ somatosensory experiences of migraine to their experiences regarding its perception in Swedish society, and relate these to anthropological phenomenological theories of embodiment, wellbeing and illness narrative. Rather than letting words alone define their pain encounters, I explored how my participants expressed themselves via music, theatre, and affects, through semi-structured interviews and a group workshop where participants conveyed their migraine experiences using their bodies and musical instruments. In the first part of the thesis, I discuss how my participants translated migraine pain into music, theatre, and affects, and show that a combination of these modes of expression can provide a more complete understanding of migraine experience. In the second part I explore how my study participants experience migraines as relating to stress, show that the relation is interdependent, complicated and affective, and suggest that a view of stress as a cause for the disease might, despite its limited practical use in sufferer’s lives, aid its legitimization as an illness that can, in principal, affect anyone. Together, the findings illustrate how ordered discourse can fall short off conveying extreme pain and how attunement to alternative forms of communication can provide insight beyond the bounded premises of language.

As the most widely consumed drug around the globe, there is a vast array of contradicting research available on caffeine. One of the most debated and researched topics on caffeine is its effect on the brain. Meanwhile, the data on the neurological condition of migraine has information scattered throughout countless research articles and experiments. Although neither migraine or caffeine are completely understood by the medical world, this analysis attempts to give a more coherent understanding of the relationship between the two. This is done by first understanding the known and theorized mechanisms of caffeine as well as the pathologies of migraine. Discussions on channelopathies, current migraine medications, and case studies will be presented. After much background research, we hypothesized that caffeine could excite neurons at physiological concentrations to the point of activation. This was tested by targeting the transcription factor cFos using immunocytochemistry in vitro. The protein cFos was identified due to its rapid translation—just 15 minutes after stimuli—to indicate activation. In addition to a control culture, three different caffeine concentrations were tested on the neurons: 50 micromoles— average plasma level after 1-2 cups of coffee consumption, 100 micromoles—average plasma level after 5-6 cups of coffee also believed to be the therapeutic amount to defend against neurological diseases such as Alzheimers Disease, and 250 micromoles—the average plasma level considered to be toxic in humans. Indeed, we saw a 53.8% increase in cFos expression in the neurons as 100 micromolar of caffeine was added and exposed to the cell cultures for 24 hours. In order to ensure the results obtained in this study were physiologically relevant in vivo, known toxic levels were tested for in vitro neurotoxicity. It was found in vitro that at the non toxic plasma concentrations of 50 micromolar and 100 micromolar of caffeine did not display cellular death as tested by Trypan Blue viability testing, Crystal Violet morphologies, and fleurojade immunochemistry that tests for degeneration. Each of these experiments identified a significant death increase as the toxic level of 250 micromoles of caffeine were utilized. This allowed us to theorize that the activation of neurons found in these experiments due to caffeine exposure would apply the same effect in vivo.

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