Sumatriptan and Cerebral Blood Flow Velocity Changes During Migraine Attacks (original) (raw)
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The Journal of Headache and Pain, 2018
Background: Therapeutic management of Chronic Migraine (CM), often associated with Medication Overuse Headache (MOH), is chiefly empirical, as no biomarker predicting or correlating with clinical efficacy is available to address therapeutic choices. The present study searched for neurophysiological correlates of Greater Occipital Nerve Block (GON-B) effects in CM. Methods: We recruited 17 CM women, of whom 12 with MOH, and 19 healthy volunteers (HV). Patients had no preventive treatment since at least 3 months. After a 30-day baseline, they received a bilateral betamethasone-lidocaine GON-B of which the therapeutic effect was assessed 1 month later. Habituation of visual evoked potentials (VEP) and intensity dependence of auditory evoked potentials (IDAP) were recorded before and 1 week after the GON-B. Results: At baseline, CM patients had a VEP habituation not different from HV, but a steeper IDAP value than HV (p = 0.01), suggestive of a lower serotonergic tone. GON-B significantly reduced the number of total headache days per month (− 34.9%; p = 0.003). Eight out 17CM patients reversed to episodic migraine and medication overuse resolved in 11 out of 12 patients. One week after the GON-B VEP habituation became lacking respect to baseline (p = 0.01) and to that of HV (p = 0.02) like in episodic migraine, while the IDAP slope significantly flattened (p < 0.0001). GON-B-induced reduction in headache days positively correlated with IDAP slope decrease (rho = 0.51, p = 0.03). Conclusions: GON-B may be effective in the treatment of CM, with or without MOH. The pre-treatment IDAP increase is compatible with a weak central serotonergic tone, which is strengthened after GON-B, suggesting that serotonergic mechanisms may play a role in CM and its reversion to episodic migraine. Since the degree of post-treatment IDAP decrease is correlated with clinical improvement, IDAP might be potentially useful as an early predictor of GON-B efficacy.
Review Article: Current Thoughts on Migraine
Headache: The Journal of Head and Face Pain, 1980
Current theories of migraine etiology and migraine mechanisms are reviewed. A complete discussion of general therapeutic measures, abortive, and prophylactic treatments, their indications and proper selection of patients is presented.
Background: Migraine headache is a neurologic disorder which mainly affects younger and productive segment of population. Migraine not only causes pain; but also affects quality of life in terms of low productivity and economic loss. The main aim of this study was to examine migraine-related disability, co-morbid depression, and relationship between the two. Methods: A cross-sectional study was conducted among migraineurs who visited two neurology referral clinics. The study was conducted between June 1st 2016 to December 30 th 2016. Migraine disability assessment score [MIDAS] and patient health questionnaire [PHQ-9] were used to assess disability and depression, respectively. Results: A total of 70 patients participated in the study. Fifty-three (74.3%) of our study participants were women. Fifty one (72.9%) study participants were between age group 20-40 years. Migraine without aura was the most common subtype (70%); migraine with aura accounted for the other 28.6%. The mean (± SD) headache frequency and intensity was 23.4 ± 14.9 days and 7.4 ± 1.2 respectively. Major depressive disorder was common in this group (41.4%). The mean MIDAS and PHQ-9 scores were 46.7 ± 30 and 9.2 ± 4.4 respectively. More than two-thirds (74.3%) of our participants had severe disability. We found a statistically significant correlation between migraine-related disability and co morbid depression among our participants(r = 0.318, p-value = 0.007). Conclusion: The positive correlation observed between migraine-related disability and co-morbid depression warrant routine screening and treatment of disability and depression in migraineurs; In addition, the observed high degree of disability among our participants may indicate sub optimal treatment of these patients.
Migraine : Evolution of a Common Disorder
International Journal of Scientific Research in Science and Technology, 2022
MIGRAINE is a common, chronic, incapacitating neurovascular disorder, characterized by attacks of severe headache, autonomic nervous system dysfunction, and in some patients, an aura involving neurologic symptoms. In one-third of patients the headache is preceded by transient neurological symptoms that are most frequently visual but may involve other senses and speech [migraine with aura (MA)]. Migraine is extremely prevalent [affecting 17% of females and 8% of men], very expensive ($18.5 billion Euros per year in Europe], and disabling [one of the World Health Organization's top 20 most disabling disorders]. It is consequently a public fitness hassle of exceptional effect on each the man or woman and society. Most migraine assaults begin with inside the mind, as advised through (a) the premonitory signs (e.g., issue with speech and reading, expanded emotionality, sensory hypersensitive reaction) that during many sufferers are exceptionally predictive of the attack, even though such signs arise as much as 12 h earlier than the attack, and through (b) the character of a few usual migraine triggers which includes stress, sleep deprivation, oversleeping, hunger, and extended sensory stimulation. Psychophysical and neurophysiological research have supplied clean proof that with inside the duration among assaults migraines display hypersensitive reaction to sensory stimuli and odd processing of sensory information, characterized through expanded amplitudes and decreased habituation of evoked and event-associated potentials. It is usually believed that migraine headache relies upon at the activation and sensitization of the trigeminovascular ache pathway and that cortical spreading depression (CSD) is the neurophysiological correlate of migraine aura. CSD may be precipitated in animals through focal stimulation of the cerebral cortex and includes a slowly propagating (2–6 mm min−1) wave of robust neuronal and glial depolarization; the mechanisms of initiation and propagation of CSD continue to be unclear. The mechanisms of the number one mind dysfunction(s) main to the onset of a migraine attack, to CSD susceptibility, and to episodic activation of the trigeminovascular ache pathway continue to be in large part unknown and the predominant open problem with inside the neurobiology of migraine.
63rd Annual Scientific Meeting American Headache Society ®
Headache: The Journal of Head and Face Pain, 2021
Background: Calcitonin gene-related peptide (CGRP) is a neuropeptide that is necessary and sufficient for migraine in humans and can induce migraine-like symptoms in mice. Amylin is a member of the CGRP peptide family that shares a receptor with CGRP. Amylin and CGRP bind with equal affinity to the calcitonin receptor/RAMP1 complex (AMY 1). A critical question is whether or not amylin causes migraine-like symptoms and if CGRP binding to the AMY 1 receptor contributes to CGRP-induced phenotypes. We hypothesize that the intraperitoneal (IP) injection of amylin will induce a migraine-like response in mice, including mechanical allodynia, facial grimace, and light-aversive behaviors. Furthermore, we hypothesize that blocking the AMY 1 receptor using the selective antagonist AC187 will inhibit these migraine-like behaviors. Methods: Male and female C57BL/6J mice were injected IP with either vehicle, CGRP (0.1 mg/kg), amylin (0.5 mg/kg), or with a coinjection of both CGRP (0.1 mg/kg) and AC187 (1 mg/kg). Mice were tested 30-min after CGRP injection and immediately after amylin injection. The use of the light aversion assay measures light sensitivity in mice, which we use as a surrogate for photophobia. The average time in light was assessed for all treatments. To control for anxiety, we also assessed the effects of amylin, CGRP, and AC187 in the open field assay. Tactile allodynia was measured using periorbital and plantar application of von Frey filaments. Finally, an automated squint test was used for the induction of spontaneous pain by amylin. Results: In female mice, amylin treatment decreased the average time in light compared to vehicle. Furthermore, CGRP induced light aversion in females was partially rescued by co-injection of AC187. Amylin injection also induced migraine-like phenotypes in male mice. However, in preliminary experiments, cotreatment with AC187 did not significantly affect the CGRP response in male mice. There was no difference between any treatment and vehicle for open field behavior in both male and female mice. For plantar von Frey, there was a decrease in threshold for with IP injections of amylin compared to its baseline.