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1.  Pituitary adenylate cyclase activating polypeptide and migraine 
Pituitary adenylate cyclase activating peptide (PACAP) is found in human trigeminocervical complex and can trigger migraine. PACAP levels were measured using a sensitive radioimmunoassay. Stimulation of the superior sagittal sinus (SSS) in cat elevated PACAP levels in cranial blood. Patients with moderate or severe migraine headache had elevated PACAP in the external jugular vein during headache (n = 15), that was reduced 1 h after treatment with sumatriptan 6 mg (n = 11), and further reduced interictally (n = 9). The data suggest PACAP, or its receptors, are a promising target for migraine therapeutics.
doi:10.1002/acn3.113
PMCID: PMC4284128  PMID: 25574477
2.  Enhancing cognitive-behavioural therapy for recurrent headache: design of a randomised controlled trial 
BMC Neurology  2014;14(1):233.
Background
We have argued against the traditional approach of counselling avoidance of all triggers of headaches and migraine. Problems with this approach include the impossibility of avoiding all triggers and the high costs associated with trying to do so, and that avoidance could lead to reduced tolerance for the triggers. We have developed an alternative approach called Learning to Cope with Triggers (LCT) that encourages avoidance of triggers that are detrimental to health and wellbeing, but uses exposure to other triggers to desensitise headache sufferers to the triggers. This approach has been shown to be more effective than advising avoidance of all triggers. Trigger management is only one component of a comprehensive treatment program and the current study is designed to evaluate a new approach to treating headaches in which LCT has been integrated into an established cognitive-behavioural therapy (CBT) package (LCT/CBT).
Methods/Design
A target sample of 120 adult participants who suffer from migraine or tension-type headache, at least six days per month, and have done so for at least 12 months will be recruited. Participants will be randomly assigned to one of three groups: LCT/CBT; Avoid/CBT (CBT combined with instructions to avoid all triggers); and waiting-list control. Measures will include: daily diaries for recording headaches, triggers and medication consumption; headache disability and quality of life; trigger avoidance; locus of control and self-efficacy; and coping strategies. Treatment will involve 12 60-minute sessions scheduled weekly. Assessment will be completed before and after treatment, and at 4 and 12 month follow-up. The data will be analysed to determine which approach is most effective, and predictors of response to treatment.
Discussion
Migraine and tension-type headache are common and can be disabling. CBT has been demonstrated to be an efficacious treatment for both disorders. However, there is room for improvement. This study aims to increase the efficacy of behavioural approaches and identify factors predictive of a positive response.
Trial registration
Australian and New Zealand Clinical Trials Registry ACTRN12614000435684.
doi:10.1186/s12883-014-0233-9
PMCID: PMC4285632  PMID: 25496514
Headache; Migraine; Cognitive behaviour therapy; Coping; Desensitisation
4.  Cranial autonomic symptoms in pediatric migraine are the rule, not the exception 
Neurology  2013;81(5):431-436.
Objective:
The presence of cranial autonomic symptoms often leads to a misdiagnosis of “sinus headache” in adult migraineurs, leading to unnecessary treatments and delaying appropriate migraine therapy. In this study, we examined the frequency of cranial autonomic symptoms in pediatric/adolescent patients with migraine.
Methods:
This cross-sectional study included all pediatric and adolescent patients with migraine evaluated by a single investigator at 4 different sites over the course of the study period.
Results:
Of 125 pediatric migraineurs, 62% had at least one cranial autonomic symptom based on current International Classification of Headache Disorders, second edition (ICHD-II) criteria, and 70% based on proposed ICHD-III criteria. The majority had more than one cranial autonomic symptom and the symptoms tended to be bilateral. Age, sex, laterality of headache, presence of aura, and whether migraine was episodic vs chronic did not influence the likelihood of having cranial autonomic symptoms.
Conclusions:
In pediatric/adolescent migraine, the presence of cranial autonomic symptoms appears to be the rule rather than the exception. Clinicians should be careful to consider migraine when evaluating a child with headache and associated ocular or nasal symptoms so as to avoid giving a misdiagnosis of sinus headache.
doi:10.1212/WNL.0b013e31829d872a
PMCID: PMC3776532  PMID: 23897870
6.  Endocannabinoids in the Brainstem Modulate Dural Trigeminovascular Nociceptive Traffic via CB1 and “Triptan” Receptors: Implications in Migraine 
The Journal of Neuroscience  2013;33(37):14869-14877.
Activation and sensitization of trigeminovascular nociceptive pathways is believed to contribute to the neural substrate of the severe and throbbing nature of pain in migraine. Endocannabinoids, as well as being physiologically analgesic, are known to inhibit dural trigeminovascular nociceptive responses. They are also involved in the descending modulation of cutaneous-evoked C-fiber spinal nociceptive responses from the brainstem. The purpose of this study was to determine whether endocannabinoids are involved in the descending modulation of dural and/or cutaneous facial trigeminovascular nociceptive responses, from the brainstem ventrolateral periaqueductal gray (vlPAG). CB1 receptor activation in the vlPAG attenuated dural-evoked Aδ-fiber neurons (maximally by 19%) and basal spontaneous activity (maximally by 33%) in the rat trigeminocervical complex, but there was no effect on cutaneous facial receptive field responses. This inhibitory vlPAG-mediated modulation was inhibited by specific CB1 receptor antagonism, given via the vlPAG, and with a 5-HT1B/1D receptor antagonist, given either locally in the vlPAG or systemically. These findings demonstrate for the first time that brainstem endocannabinoids provide descending modulation of both basal trigeminovascular neuronal tone and Aδ-fiber dural-nociceptive responses, which differs from the way the brainstem modulates spinal nociceptive transmission. Furthermore, our data demonstrate a novel interaction between serotonergic and endocannabinoid systems in the processing of somatosensory nociceptive information, suggesting that some of the therapeutic action of triptans may be via endocannabinoid containing neurons in the vlPAG.
doi:10.1523/JNEUROSCI.0943-13.2013
PMCID: PMC3771033  PMID: 24027286
8.  Migraine among medical students in Kuwait University 
Background
Medical students routinely have triggers, notably stress and irregular sleep, which are typically associated with migraine. We hypothesized that they may be at higher risk to manifest migraine. We aimed to determine the prevalence of migraine among medical students in Kuwait University.
Methods
This is cross-sectional, questionnaire-based study. Participants who had two or more headaches in the last 3 months were subjected to two preliminary questions and participants with at least one positive response were asked to perform the validated Identification of Migraine (ID Migraine™) test. Frequency of headache per month and its severity were also reported.
Results
Migraine headache was suggested in 27.9% subjects based on ID-Migraine™. Migraine prevalence (35.5% and 44%, versus 31.1%, 25%, 21.1%, 14.8%, 26.5%, p < 0.000), frequency (5.55 + 1.34 and 7.23 + 1.27, versus 3.77 ± 0.99, 2.88 ± 0.85, 3.07 ± 0.96, 2.75 ± 0.75, 4.06 ± 1.66, p < 0.000); and severity of headache (59.1% and 68.2%, versus 28.3%,8.3%, 6.7%,16.7%, p < 0.000; were significantly increased among students in the last 2 years compared to first five years of their study. Stress 43 (24.9%), irregular sleep 36 (20.8%), and substantial reading tasks 32 (18.5%), were the most common triggering factors cited by the students.
Conclusion
The prevalence of migraine is higher among medical students in Kuwait University compared to other published studies. The migraine prevalence, frequency and headache severity, all increased in the final two years of education.
doi:10.1186/1129-2377-15-26
PMCID: PMC4029817  PMID: 24886258
Migraine; Prevalence; Medical students; Kuwait
10.  The origin of nausea in migraine–A PET study 
Background
Nausea is a common and disabling symptom of migraine. The origin of nausea is not well understood although functional connections between trigeminal neurons and the nucleus tractus solitarius may explain occurrence of nausea with pain. However, nausea occurs as a premonitory symptom in about a quarter of patients, suggesting that a primary brain alteration unrelated to the experience of pain may be the reason for nausea.
Methods
We performed positron emission tomography scans with H215O PET in premonitory phase of nitroglycerin-induced migraine and compared patients with and without nausea.
Results
The results showed activation in rostral dorsal medulla and periaqueductal grey (PAG) in the nausea group, which was absent in the no nausea group. The rostral dorsal medullary area included the nucleus tractus solitarius, dorsal motor nucleus of the vagus nerve and the nucleus ambiguus, all of which are thought to be involved in brain circuits mediating nausea.
Conclusions
The results demonstrate that nausea can occur as a premonitory symptom in migraine, independent of pain and trigeminal activation. This is associated with activation of brain structures known to be involved in nausea. We conclude that nausea is a centrally driven symptom in migraine.
doi:10.1186/1129-2377-15-84
PMCID: PMC4266549  PMID: 25471540
Nausea; Premonitory; PET; NTS; Trigeminal
11.  Migraine and Sleep: New Connections 
Editor’s Note:
“Attack” is often a word associated with migraine, and for good reason. If you suffer from migraine headaches or know someone who does, you are well aware of its crippling nature. This story focuses on new research that has uncovered an important link between migraine and sleep patterns. A better understanding of the relationships among the body’s circadian rhythms, the brain’s hypothalamus, and a mutated gene holds enormous promise of improved care for the more than 36 million Americans who experience migraine (three times more common in women) and the number of people suffering from familial advanced sleep phase syndrome (FASP).
PMCID: PMC3997296  PMID: 24765233
12.  Pathophysiology of migraine 
Annals of Indian Academy of Neurology  2012;15(Suppl 1):S15-S22.
Migraine is a common disabling brain disorder whose pathophysiology is now being better understood. The study of anatomy and physiology of pain producing structures in the cranium and the central nervous system modulation of the input have led to the conclusion that migraine involves alterations in the sub-cortical aminergic sensory modulatory systems that influence the brain widely.
doi:10.4103/0972-2327.99993
PMCID: PMC3444225  PMID: 23024559
Brainstem; dyshabituation; migraine
13.  Treatment of Pediatric Migraine in the Emergency Room 
Pediatric neurology  2012;47(4):233-241.
Migraine is a relatively common reason for pediatric emergency room visits. Given the paucity of randomized trials involving pediatric migraineurs in the emergency department setting compared to adults, recommendations for managing these children are largely extrapolated from adult migraine emergency room studies and trials involving outpatient home pediatric migraine therapy. This paper reviews what is known about pediatric migraineurs who present to the emergency room and how they are currently managed, then goes on to summarize the best evidence currently available to guide clinical decision making.
doi:10.1016/j.pediatrneurol.2012.06.001
PMCID: PMC3681416  PMID: 22964436
migraine; primary headache disorders; pediatric
14.  A Neurologist’s Guide to Acute Migraine Therapy in the Emergency Room 
The Neurohospitalist  2012;2(2):51-59.
Migraine is a common reason for visits to the emergency room. Attacks that lead patients to come to the emergency room are often more severe, refractory to home rescue medication, and have been going on for longer. All of these features make these attacks more challenging to treat. The purpose of this article is to review available evidence pertinent to the treatment of acute migraine in adults in the emergency department setting in order to provide neurologists with a rational approach to management. Drug classes and agents reviewed include opioids, dopamine receptor antagonists, triptans, nonsteroidal anti-inflammatory drugs, corticosteroids, and sodium valproate.
doi:10.1177/1941874412439583
PMCID: PMC3737484  PMID: 23936605
headache; primary headache disorders; migraine disorders; quality
15.  Ophthalmoplegic “Migraine” or Recurrent Ophthalmoplegic Cranial Neuropathy: New Cases and a Systematic Review 
Journal of child neurology  2012;27(6):759-766.
Ophthalmoplegic migraine is a poorly understood neurologic syndrome characterized by recurrent bouts of head pain and ophthalmoplegia. By reviewing cases presenting to our centers in whom the phenotype has been carefully dissected, and systematically reviewing all published cases of ophthalmoplegic migraine in the magnetic resonance imaging (MRI) era, this review sets out to clearly define the syndrome and discuss possible etiologies. We found that in up to one-third of patients, the headache was not migrainous or associated with migrainous symptoms. In three-quarters of the cases involving the third nerve, there was focal nerve thickening and contrast enhancement on MRI. Observational data suggest systemic corticosteroids may be beneficial acutely. The etiology remains unclear, but may involve recurrent bouts of demyelination of the oculomotor nerve. “Ophthalmoplegic migraine” is a misnomer in that it is probably not a variant of migraine but rather a recurrent cranial neuralgia. A more appropriate name might be “ophthalmoplegic cranial neuropathy.”
doi:10.1177/0883073811426502
PMCID: PMC3562350  PMID: 22241707
ophthalmoplegic migraine; headache; aura; neuralgia
16.  New onset migraine with aura after treatment initiation with ivabradine 
Background
Migraine with aura is a complex neurological disorder modeled in animals by cortical spreading depression. It is less usual to find complete animal models for the disease so any opportunity to test a human effect back at the bench is welcome.
Findings
We report the case of a 24 year old woman who developed new onset episodic migraine with visual aura shortly after treatment initiation with the If ion channel blocker ivabradine for frequency control in hypertrophic cardiomyopathy. We studied whether ivabradine could alter cortical spreading depression in a suitable animal model. Sixteen rats received either ivabradine or saline, and the number of depolarization shifts and blood flow changes induced by cortical spreading depression were measured in both groups. No significant differences between the ivabradine and saline group were detected.
Conclusions
Ivabradine is an interesting substance since it is known to produce migraine-like phosphenes frequently and the patient we report developed de novo migraine with aura. However, we were unable to demonstrate that the drug influences the susceptibility of the brain to cortical spreading depression with acute administration. The combined data show the relationship of migraine aura to cortical spreading depression may have some nuances yet to be identified.
doi:10.1186/1129-2377-14-45
PMCID: PMC3681602  PMID: 23718730
Migraine; Ivabradine; Aura
17.  Migraine misdiagnosis as a sinusitis, a delay that can last for many years 
Background
Sinusitis is the most frequent misdiagnosis given to patients with migraine.
Therefore we decided to estimate the frequency of misdiagnosis of sinusitis among migraine patients.
Methods
The study included migraine patients with a past history of sinusitis. All included cases fulfilled the International Classification of Headache Disorders, 3rd edition (ICHD-III- beta) criteria. We excluded patients with evidence of sinusitis within the past 6 months of evaluation. Demographic data, headache history, medical consultation, and medication intake for headache and effectiveness of therapy before and after diagnosis were collected.
Results
A total of 130 migraine patients were recruited. Of these patients 106 (81.5%) were misdiagnosed as sinusitis. The mean time delay of migraine diagnosis was (7.75 ± 6.29, range 1 to 38 years). Chronic migraine was significantly higher (p < 0.02) in misdiagnosed patients than in patients with proper diagnosis. Medication overuse headache (MOH) was reported only in patients misdiagnosed as sinusitis. The misdiagnosed patients were treated either medically 87.7%, or surgically12.3% without relieve of their symptoms in 84.9% and 76.9% respectively. However, migraine headache improved in 68.9% after proper diagnosis and treatment.
Conclusions
Many migraine patients were misdiagnosed as sinusitis. Strict adherence to the diagnostic criteria will prevent the delay in migraine diagnosis and help to prevent chronification of the headache and possible MOH.
doi:10.1186/1129-2377-14-97
PMCID: PMC4028747  PMID: 24330723
Migraine misdiagnosis; Sinus headache
18.  Before the headache 
Neurology  2012;79(13):1392-1396.
Objective:
Childhood periodic syndromes are thought to be early life expressions of the genetic tendency for migraine. The objective of this study was to determine whether maternal migraine is associated with an increased risk of infant colic, because this may indicate that colic is a childhood periodic syndrome.
Methods:
This was a cross-sectional study performed in general pediatric clinics. To minimize recall bias, mothers were surveyed at their infants' 2-month-old well-child visit, the age when colic is most prevalent. Colic was ascertained via parental report using modified Wessel criteria. Migraine history was obtained by having a physician diagnosis or a positive screen on ID Migraine. The primary outcome measure was difference in colic prevalence in infants with and without a maternal history of migraine.
Results:
Data from 154 infant-mother pairs were analyzed. Infants with a maternal history of migraine were 2.6 times as likely to have colic as infants without a maternal history of migraine (29% vs 11%, prevalence ratio 2.6 (95% confidence interval 1.2−5.5), p = 0.02). There was no difference in the accuracy with which migraineur mothers perceived their infants' colic status compared with that of nonmigraineur mothers. Data on paternal history of migraine were available for 93 infants. Infants with a paternal history of migraine may have a higher prevalence of colic (22% vs 10%), although the prevalence ratio 2.3 (0.6−9.4, p = 0.24) had wide confidence intervals.
Conclusions:
Maternal migraine is associated with increased risk of infant colic. Because migraine has a strong genetic underpinning, this association suggests that colic may be an early life manifestation of migraine.
doi:10.1212/WNL.0b013e31826c1b7b
PMCID: PMC4098946  PMID: 22972642
19.  MAP0004, Orally Inhaled Dihydroergotamine for Acute Treatment of Migraine: Efficacy of Early and Late Treatments 
Mayo Clinic Proceedings  2011;86(10):948-955.
OBJECTIVE: To evaluate the efficacy of MAP0004, an orally inhaled dihydroergotamine, for acute treatment of migraine when administered at various time points from within 1 hour to more than 8 hours after migraine onset.
PATIENTS AND METHODS: This post hoc subanalysis was conducted using data from 902 patients enrolled in a randomized, double-blind, placebo-controlled, 2-arm, phase 3, multicenter study conducted from July 14, 2008, through March 23, 2009. End points were 2-hour pain relief and pain-free rates in patients who treated a migraine in ≤1 hour, from >1 hour to ≤4 hours, from >4 to ≤8 hours, or in >8 hours after onset of migraine, given that patients may be unwilling or unable to initiate treatment at headache inception.
RESULTS: Treatment with MAP0004 was significantly more effective than placebo in relieving pain at all treatment points (≤1 hour after start of migraine: 66% [74/112] for MAP0004 vs 41% [48/118] for placebo, P<.001; >1 to ≤4 hours: 60% [91/153] vs 35% [58/168], P<.001; >4 to ≤8 hours: 53% [36/68] vs 30% [16/54], P=.008; and >8 hours: 48% [25/52] vs 24% [11/46], P=.007). Pain-free rates were also significantly higher with MAP0004 than placebo for treatment within 8 hours after migraine onset (≤1 hour: 38% [43/112] for MAP0004 vs 13% [15/118] for placebo, P<.001; >1 to ≤4 hours: 28% [43/153] vs 10% [17/168], P<.001; >4 to ≤8 hours: 22% [15/68] vs 7% [4/54], P<.025) but not at >8 hours (19% [10/52] vs 9% [4/46], P=.106).
CONCLUSION: This post hoc subanalysis shows that MAP0004 was effective in treating migraine irrespective of the time of treatment, even more than 8 hours after onset of migraine pain.
Trial Registration: clinicaltrials.gov identifier: NCT00623636
doi:10.4065/mcp.2011.0093
PMCID: PMC3184024  PMID: 21964172
20.  A Neurologist’s Guide to Acute Migraine Therapy in the Emergency Room 
The Neurohospitalist  2012;2(2):51-59.
Migraine is a common reason for visits to the emergency room. Attacks that lead patients to come to the emergency room are often more severe, refractory to home rescue medication, and have been going on for longer. All of these features make these attacks more challenging to treat. The purpose of this article is to review available evidence pertinent to the treatment of acute migraine in adults in the emergency department setting in order to provide neurologists with a rational approach to management. Drug classes and agents reviewed include opioids, dopamine receptor antagonists, triptans, nonsteroidal anti-inflammatory drugs, corticosteroids, and sodium valproate.
doi:10.1177/1941874412439583
PMCID: PMC3737484  PMID: 23936605
headache; primary headache disorders; migraine disorders; quality
21.  The Migrainous Brain: What You See Is Not All You Get? 
PLoS Medicine  2006;3(10):e404.
Goadsby discusses a new study published inPLoS Medicine of the visual motion-processing network in migraine.
doi:10.1371/journal.pmed.0030404
PMCID: PMC1609121  PMID: 17048980
22.  Child Neurology: Migraine with aura in children 
Neurology  2010;75(5):e16-e19.
The differential diagnosis for an acute hemiparesis in a child includes stroke, Todd paralysis, and hemiplegic migraine. In the context of an illustrative case, this review highlights the differences in clinical presentation among these entities and an approach to the diagnostic workup. Migraine with aura in children is reviewed, including migraine equivalents such as abdominal migraine and the particular presentation of hemiplegic migraine. An approach to the prophylactic and acute treatment for children with migraine with aura is offered.
doi:10.1212/WNL.0b013e3181ebdd53
PMCID: PMC2918469  PMID: 20679627
23.  Migraine in pregnancy 
BMJ : British Medical Journal  2008;336(7659):1502-1504.
The authors explore whether migraine affects pregnancy, how pregnancy alters migraine, and how to treat and prevent migraine in pregnancy
doi:10.1136/bmj.39559.675891.AD
PMCID: PMC2440903  PMID: 18583683
24.  Triptans attenuate capsaicin-induced CREB phosphorylation within the trigeminal nucleus caudalis: a mechanism to prevent central sensitization? 
The Journal of Headache and Pain  2011;12(4):411-417.
The c-AMP-responsive element binding protein (CREB) and its phosphorylated product (P-CREB) are nuclear proteins expressed after stimulation of pain-producing areas of the spinal cord. There is evidence indicating that central sensitization within dorsal horn neurons is dependent on P-CREB transcriptional regulation. The objectives of the study were to investigate the expression of P-CREB in cells in rat trigeminal nucleus caudalis after noxious stimulation and to determine whether pre-treatment with specific anti-migraine agents modulate this expression. CREB and P-CREB labelling was investigated within the trigeminal caudalis by immunohistochemistry after capsaicin stimulation. Subsequently, the effect of i.v. pre-treatment with either sumatriptan (n = 5), or naratriptan (n = 7) on P-CREB expression was studied. Five animals pre-treated with i.v. normal saline were served as controls. CREB and P-CREB labelling was robust in all animal groups within Sp5C. Both naratriptan and sumatriptan decreased P-CREB expression (p = 0.0003 and 0.0013) within the Sp5C. Triptans attenuate activation of CREB within the central parts of the trigeminal system, thereby leading to potential inhibition of central sensitization. P-CREB may serve as a new marker for post-synaptic neuronal activation within Sp5C in animal models relevant to migraine.
doi:10.1007/s10194-011-0352-2
PMCID: PMC3139063  PMID: 21626018
CREB; Sumatriptan; Naratriptan; Capsaicin; Migraine; Sensitization
25.  Triptans attenuate capsaicin-induced CREB phosphorylation within the trigeminal nucleus caudalis: a mechanism to prevent central sensitization? 
The Journal of Headache and Pain  2011;12(4):411-417.
The c-AMP-responsive element binding protein (CREB) and its phosphorylated product (P-CREB) are nuclear proteins expressed after stimulation of pain-producing areas of the spinal cord. There is evidence indicating that central sensitization within dorsal horn neurons is dependent on P-CREB transcriptional regulation. The objectives of the study were to investigate the expression of P-CREB in cells in rat trigeminal nucleus caudalis after noxious stimulation and to determine whether pre-treatment with specific anti-migraine agents modulate this expression. CREB and P-CREB labelling was investigated within the trigeminal caudalis by immunohistochemistry after capsaicin stimulation. Subsequently, the effect of i.v. pre-treatment with either sumatriptan (n = 5), or naratriptan (n = 7) on P-CREB expression was studied. Five animals pre-treated with i.v. normal saline were served as controls. CREB and P-CREB labelling was robust in all animal groups within Sp5C. Both naratriptan and sumatriptan decreased P-CREB expression (p = 0.0003 and 0.0013) within the Sp5C. Triptans attenuate activation of CREB within the central parts of the trigeminal system, thereby leading to potential inhibition of central sensitization. P-CREB may serve as a new marker for post-synaptic neuronal activation within Sp5C in animal models relevant to migraine.
doi:10.1007/s10194-011-0352-2
PMCID: PMC3139063  PMID: 21626018
CREB; Sumatriptan; Naratriptan; Capsaicin; Migraine; Sensitization

Results 1-25 (46)