Links To Related  Studies

The hypothesis is that migraines are caused by insufficient oxygen being delivered to the brain for a wide variety of reasons. This includes poor breathing habits such as hyperventilation or hypoventilation, mouth breathing & chest breathing that result in poor oxygen/carbon dioxide balance. It also includes poor nutritional intake resulting in the bloods reduced ability to carry oxygen and mouth breathing, resulting in bypassing critical natural air filtering, monitoring and gas production.

The studies included on this page support the hypothesis however they do not look at breathing habits as a cause of the hypoxia. Further studies are required to prove this hypothesis, however, we really need to ask why it has not already been thoroughly studied. Science should always ask the basic questions first. Is it plugged in? In other words, is it getting the energy it needs to function properly? Oxygen and water are the two most important fuels for the brain. We know about water but who has checked the oxygen? That’s like trying to troubleshoot your computer without checking to see if it’s plugged in. Coincidently, the number 1 resolution for most tech support is resolved by the very first question… is it plugged in?

Although there are no studies to prove that proper breathing will correct the migraine condition, there are many people who have been relieved of migraine headaches when practicing proper breathing habits in Yoga, meditation, the Beteyko method, with the treatment at the Ontario Migraine Clinic (which includes a breathing technique) and with vitamins & minerals that support the production of red blood cells & our oxygen delivering capability. Is this just a coincidence?

At the very least, there is enough evidence to warrant further study.

Effect of diaphragmatic respiration with end-tidal CO2 biofeedback on respiration, EEG, and seizure frequency in idiopathic epilepsy. Abstract: Breathing rate (RR), end-tidal percent CO2, and EEG were obtained in three groups: psychiatric referral subjects presenting with anxiety, panic phobia, depression and migraine; a group of idiopathic seizure sufferers; and a group of asymptomatic controls. Virtually all the noncontrol subjects were found to show moderate to severe hyperventilation and the accompanying EEG dysrhythmia. The seizure group subjects were taught diaphragmatic respiration with end-tidal percent CO2 biofeedback. The training normalized their respiration and altered their EEGs and seizure frequency.

Efficacy of high-flow oxygen therapy in all types of headache: a prospective, randomized, placebo-controlled trial.


OBJECTIVE: We aimed to assess the efficacy of oxygen inhalation therapy in emergency department (ED) patients presenting with all types of headache.

METHOD: We performed a prospective, randomized, double-blinded, placebo-controlled trial of patients presenting to the ED with a chief complaint of headache. The patients were randomized to receive either 100% oxygen via nonrebreather mask at 15 L/min or the placebo treatment of room air via nonrebreather mask for 15 minutes in total. We recorded pain scores at 0, 15, 30, and 60 minutes using the visual analog scale. At 30 minutes, the patients were assessed for the need for analgesic medication. Patient headache type was classified by the treating emergency physician using standardized diagnostic criteria.

RESULTS: A total of 204 patients agreed to participate in the study and were randomized to the oxygen (102 patients) and placebo (102 patients) groups. Patient headache types included tension (47%), migraine (27%), undifferentiated (25%), and cluster (1%). Patients who received oxygen therapy reported significant improvement in visual analog scale scores at all points when compared with placebo: 22 mm vs 11 mm at 15 minutes (P < .001), 29 mm vs 13 mm at 30 minutes (P < .001), and 55 mm vs 45 mm at 60 minutes (P < .001). When questioned at 30 minutes, 72% of patients in the oxygen group and 86% of patients in the placebo group requested analgesic medication (P = .005).

CONCLUSION: In addition to its role in the treatment of cluster headache, high-flow oxygen therapy may provide an effective treatment of all types of headaches in the ED setting.

Brain hypoxia: the turning-point in the genesis of the migraine attack? The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack ofmigraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be provoked by different mechanisms in different patients; the potential role of decreased oxygen supply and of increased oxygen need are reviewed and excess sympathetic drive is considered a potential key mechanism in a majority of patients. Whether or not focal hypoxia leads to a genuine migraine attack, depends largely upon the quality of the whirlpool of biochemical, vascular and hematological changes that follow the hypoxic episode. These changes are discussed and it is concluded that those which have been reported to occur during migraine attacks could be due to a preceding hypoxic event. Finally, the hypoxia viewpoint is confronted with some popular theories about the pathogenesis of migraine. It is found that the other points of view are compatible with the hypoxia hypothesis.

Mountain Sickness in the First 24 Hours Upon Ascent to Cusco Peru (3326 meters) The most important finding of this study is that Petco2 upon ascent was found to have a more significant effect than Spo2 on a subject’s ultimate ESQ score. This study demonstrates that those individuals with a brisk ventilatory response upon ascent to moderate altitude, as measured by Petco2, did not develop AMS, whereas a blunted ventilatory response, as reflected in the highest Petco2, was related to the subsequent development of AMS.

Hyperventilation during migraine attacks.  Our novel observation is that hyperventilation occurred at the height of a migraine, making the attack seem worse to the patient. We speculate that the migraine not only seemed worse but was exacerbated by the vasoconstrictor effect of hyperventilation. If this is true Pco2 may play a part in the pathophysiology of migraine.

Cortical spreading depression impairs oxygen delivery and metabolism in mice Abstract: Cortical spreading depression (CSD) is associated with severe hypoperfusion in mice. Using minimally invasive multimodal optical imaging, we show that severe flow reductions during and after spreading depression are associated with a steep decline in cerebral metabolic rate of oxygen. Concurrent severe hemoglobin desaturation suggests that the oxygen metabolism becomes at least in part supply limited, and the decrease in cortical blood volume implicates vasoconstriction as the mechanism. In support of oxygen supply-demand mismatch, cortical nicotinamide adenine dinucleotide (NADH) fluorescence increases during spreading depression for at least 5minutes, particularly away from parenchymal arterioles. However, modeling of tissue oxygen delivery shows that cerebral metabolic rate of oxygen drops more than predicted by a purely supply-limited model, raising the possibility of a concurrent reduction in oxygen demand during spreading depression. Importantly, a subsequent spreading depression triggered within 15minutes evokes a monophasic flow increase superimposed on the oligemic baseline, which markedly differs from the response to the preceding spreading depression triggered in naive cortex. Altogether, these data suggest that CSD is associated with long-lasting oxygen supply-demand mismatch linked to severe vasoconstriction in mice. Takano T, Tian G-F, Peng W, Lou N, Lovatt D, Hansen AJ, Kasischke KA, Nedergaard M.  “Cortical spreading depression causes and coincides with tissue hypoxia.”  Nature Neuroscience, June 2007, Vol. 10, No. 6, pp. 754-762.

Migraine and cerebral hypoxia: a hypothesis with pharmacotherapeutic implications. Abstract: It is postulated that a migraine attack is a specific reaction pattern to an episode of focal cerebral hypoxia. This hypothesis holds that any type of focal brain hypoxia (and thus not only a vasospasm) may provoke a migraine attack. Indeed, as hypoxia is a result of an imbalance between energy supply and energy use, the former can be decreased and/or the latter be increased. Spreading cortical depression, leading to the aura, is believed to be another consequence of brain hypoxia occurring in classical migraine. There are no other genuine differences between classical and common migraine, according to the cerebral hypoxia theory. The latter theory may improve our understanding of the mode of action of antimigraine drugs. Certain calcium entry blockers have a direct protective effect on brain hypoxia, but some other pharmacotherapeutic approaches may also prevent cerebral hypoxia via an effect on brain metabolism, vasomotion or platelet behavior.

Pathogenesis of migraine: the biobehavioural and hypoxia theories reconciled. Abstract: The recent pathophysiological data obtained in migraine patients during and between attacks are reviewed in this article. They suggest that the headache in migraine is due to activation of the trigemino-vascular system. While this can be found in other headache disorders, the process leading ultimately to trigemino-vascular activation appears to characterize migraine. Between attacks, the migrainous brain has two functional abnormalities: a habituation defect in sensory processing, probably related to dysfunctioning transmitter (serotonin, noradrenaline) systems and a reduced mitochondrial energy reserve. Both abnormalities may be genetically determined and concur to favour biochemical shifts leading to the migraine attack as a primary protective mechanism of the brain. Such a model of migraine pathogenesis reconciles the biobehavioural and hypoxia theories and opens new therapeutic perspectives.

NORMOBARIC HYPOXIA AND NITROGLYCERIN AS TRIGGER FACTORS FOR MIGRAINE ABSTRACT: “We conclude that the migraine response to NTG was remarkably low in view of previous data , and normobaric hypoxia might be a trigger factor for migraine, but this requires further research.” Migraine prevalence is increased in high-altitude populations and symptoms of acute mountain sickness mimic migraine symptoms. Here we tested whether normobaric hypoxia may trigger migraine attacks. As positive control we used nitrolgycerine (NTG), which has been shown to induce migraine attacks in up to 80% of migraineurs. Sixteen patients (12 females, mean age 28.9 ± 7.2 years) suffering from migraine with (n=8) and without aura (n=8) underwent 3 different provocations (normobaric hypoxia, NTG and placebo) in a randomized, cross-over, double dummy design. Each provocation was performed on a separate day. The primary outcome measure was the proportion of patients developing a migraine attack according to the criteria of the International Headache Society within 8 hours after provocation onset. Fourteen patients completed all three provocations. Migraine was provoked in 6 (42%) patients by hypoxia, 3 (21%) by NTG and 2 (14%) by placebo. The differences among groups were not signifi cant (p=0.197). The median time to attacks was 5 hours. In conclusion, the (remarkably) low response rate to NTG is surprising in view of previous data. Further studies are required to fully establish the potency of hypoxia in triggering migraine attacks.

The link between CSD and migraine pain. CSD is most often initiated in the occipital cortex of patients with visual migraine aura. It is believed that CSD is ignited by local elevation of extracellular K+ levels in pockets of intense excitatory transmission. When K+ levels reach a critical threshold of 10–12 mM, a self-propagating CSD wave is initiated and advances across the cortex with a slow velocity of 3 mm/min. The threshold for CSD initiation is reduced in FHM patients with mutations in the Cav2.1 Ca2+ channel because the higher Ca2+ level in dendrites facilitates glutamate release and thereby increases the likelihood that K+ levels will reach the CSD threshold. A combination of stress and food intake may be sufficient to ignite CSD in patients with FHM, whereas stronger stimulation is required in the rest of the population. The lower diagram depicts the cortical events linking CSD to migraine pain. The high extracellular K+ level at the edge of the CSD wavefront is key for wave propagation. K+ is normalized within minutes, but the restoration of normal membrane potential of neurons and glial cells is a high energy–demanding process. The cortical tissue experiences a minutes-lasting period of severe reduction of tissue O2 tension (hypoxia) during CSD because O2 consumption transiently exceeds the vascular supply of O2. This hypoxia has several consequences: (a) Neurons exhibit severe morphological distortions, swelling, and transient loss of dendritic spines. Normal dendritic structures are reestablished 15–20 minutes later, coinciding with the reappearance of a normal EEG pattern. This hypoxic phase is followed by prolonged vasoconstriction and reduction of local blood flow. (b) The CSD wave activates MMP9, resulting in opening of the blood-brain barrier (BBB) and extravasation of plasma protein. The leakage of blood-borne factors activates nociceptive afferent neurons from trigeminal ganglion innervating meningeal arteries, connecting to trigeminal nucleus caudalis, triggering the migraine pain. (c) CSD triggers preconditioning — an endogenous mechanism of neuroprotection that raises ischemic tolerance.

Cortical spreading depression causes and coincides with tissue hypoxia. Abstract: Cortical spreading depression (CSD) is a self-propagating wave of cellular depolarization that has been implicated in migraine and in progressive neuronal injury after stroke and head trauma. Using two-photon microscopic NADH imaging and oxygen sensor microelectrodes in live mouse cortex, we find that CSD is linked to severe hypoxia and marked neuronal swelling that can last up to several minutes. Changes in dendritic structures and loss of spines during CSD are comparable to those during anoxic depolarization. Increasing O2 availability shortens the duration of CSD and improves local redox state. Our results indicate that tissue hypoxia associated with CSD is caused by a transient increase in O2 demand exceeding vascular O2 supply.

Pathophysiology of the migraine aura: The spreading depression theory Summary: The Characteristic form and development of sensory disturbances during migraine auras suggests that the underlying mechanism is a disturbance of the cerebral cortex, probably the cortical spreading depression (CSD) of Leão. The demonstration of unique changes of brain blood flow during attacks of migraine with aura, which have been replicated in animal experiments during CSD, constitutes another important line of support for the ‘spreading depression’ theory, which may be a key to an understanding of the migraine attack. Cortical spreading depression is a short-lasting depolarization wave that moves across the cortex at a rate of 3–5 mm/min. A brief phase of excitation heralds the reaction which is immediately followed by prolonged nerve cell depression synchronously with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells and enhanced energy metabolism. Recent experimental work has shown that CSD in the neocortex of a variety of species including man is dependent on activation of a single receptor, theN-methyl-D-aspartate receptor, one of the three subtypes of glutamate receptors. The combined experimental and clinical studies point to fruitful areas in which to look for migraine treatments of the future and provide a framework within which important aspects of the migraine attack can be modelled.

Headache attributed to hypoxia and/or hypercapnia Comments: Headache occurs within 24 hours after acute onset of hypoxia with PaO2 hypoxic patients with PaO2 persistently at or below this level. It is often difficult to separate the effects of hypoxia and hypercapnia.

Pathogenesis of migraine: the biobehavioural and hypoxia theories reconciled.
Abstract: The recent pathophysiological data obtained in migraine patients during and between attacks are reviewed in this article. They suggest that the headache in migraine is due to activation of the trigemino-vascular system. While this can be found in other headache disorders, the process leading ultimately to trigemino-vascular activation appears to characterize migraine. Between attacks, the migrainous brain has two functional abnormalities: a habituation defect in sensory processing, probably related to dysfunctioning transmitter (serotonin, noradrenaline) systems and a reduced mitochondrial energy reserve. Both abnormalities may be genetically determined and concur to favour biochemical shifts leading to the migraine attack as a primary protective mechanism of the brain. Such a model of migraine pathogenesis reconciles the biobehavioural and hypoxia theories and opens new therapeutic perspectives.

Re-evaluation of the hypoxia theory as the mechanism of hyperventilation-induced EEG slowing.
Abstract: To determine whether the well-accepted hypoxia theory accounts for hyperventilation-induced electroencephalogram (EEG) slowing, the authors monitored changes in cerebral oxygenation and end-tidal concentrations of carbon dioxide in 67 patients with epilepsy (age range = 5-12 years) during the hyperventilation activation test in a routine EEG examination. Relative concentration changes in cerebral oxygenated, deoxygenated, total hemoglobin, and oxidized cytochrome oxidase were measured by near-infrared spectroscopy in the frontal region. In all patients, except one who demonstrated EEG slowing, total and oxygenated hemoglobin decreased, and cytochrome oxidase was not reduced. EEG slowing occurred intermittently in 22 patients and was not synchronous with changes in either the cerebral oxygenation or end-tidal concentration of carbon dioxide. The degree of EEG slowing was diminished or the slow waves disappeared abruptly within 1 second after the cessation of hyperventilation in 22 patients when both the cerebral oxygenation and end-tidal concentration of carbon dioxide were still at low levels. The findings during the recovery periods do not confirm the hypoxia theory. It is thus supposed that more subtle mechanisms are the cause of EEG slowing.

Morning headache in sleep apnoea: clinical and polysomnographic evaluation and response to nasal continuous positive airway pressure. Abstract: Morning headache is accepted as part of clinical findings of obstructive sleep apnoea syndrome (OSAS). The prevalence of morning headache is at variable levels from 18% to 74% in patients with OSAS. However, there is controversy over the association of morning headache and OSAS. We studied morning headache prevalence and characteristics in 101 controls with apnoea-hypnoea index (AHI) < 5 and 462 OSAS patients with AHI > or = 5. Morning headache was reported by only nine (8.9%) subjects in a control group compared with 156 (33.6%) of OSAS patients (P < 0.01). Morning headache prevalence was significantly higher in severe and moderate OSAS groups. AHI was significantly higher in OSAS patients with morning headache compared with patients without morning headaches. Oxygen saturation nadir during rapid eye movement and non-rapid eye movement sleep as well as mean oxygen saturation value during total sleep time were also found to be significantly lower in morning headache group. However, none of the sleep parameters was found to be determinants of morning headache. Morning headache was more frequently reported by patients of female gender and with primary headache history. Morning headache was totally resolved in 90% of patients treated with nasal continuous positive airway pressure. The history of OSAS should be considered in the differential diagnosis of morning headache. Orthostatic increase of respiratory gas exchange in hyperventilation syndrome Hyperventilation during migraine attacks. Our novel observation is that hyperventilation occurred at the height of a migraine, making the attack seem worse to the patient. We speculate that the migraine not only seemed worse but was exacerbated by the vasoconstrictor effect of hyperventilation. If this is true Pco2 may play a part in the pathophysiology of migraine. pH and Cancer:  Acidic pH Levels Can Lead To Cancer… Magnesium serves hundreds of important functions in the body and one of them has to do with the efficiency of red blood cells and their capacity to carry oxygen. Oxygen Therapy for Migraine Headaches Two types of oxygen therapy may offer relief to people who suffer from disabling migraine and cluster headaches. Global cerebral blood flow, blood volume, and oxygen metabolism in patients with migraine headache E. M. Bednarczyk, PharmD,  1. B. Remler, MD,  2. C. Weikart, RN,  3. A. D. Nelson, PhD and  4. R. C. Reed, PharmD 5. Objective Migraine headaches with and without aura are representative of vascular headache states traditionally thought to be mediated by alterations in vascular tone. Validation of this theory has been hampered in part by technical difficulties inherent in the measurement of cerebral blood flow (CBF). The purpose of this study was to compare CBF measured during migraine and migraine-free states using PET. Methods Patients with a minimum of one migraine headache without aura per month (International Headache Society [IHS] criteria) underwent measurement of CBF, cerebral blood volume (CBV), oxygen extraction, and metabolism during an episode of spontaneous migraine headache. Imaging was repeated during a migraine-free period of at least 48 hours. PET radiotracers used were: CBF, H215O; CBV, C15O; oxygen metabolism, 15O2. Results In nine patients (seven female and two male), global CBF (mL/min/ 100 g [SD]) was measured as 52.70 (6.9) during migraine and 59.65 (10.6) in the migraine-free state; p = 0.028. CBV (mL/100 g [SD]) was 3.6 (0.43) during the symptomatic state and 3.8 (0.55) after the migraine; p = 0.047. Oxygen metabolism (mWmin/100 g [SD]) was 3.68 (0.9) during migraine and 3.38 (1.02) without headache; p = 0.211. The oxygen extraction ratio was 0.48 (0.15) and 0.41 (0.12) during migraine and migraine-free states, respectively; p = 0.132. Conclusions In patients experiencing migraine without aura, CBF and CBV are reduced during the headache phase. Cerebral oxygen metabolism and oxygen extraction are not significantly affected. Autonomic Dysfunction in Migraine: A Survey of 188 Patients H. Havanka-Kanniainen,  1. U. Tolonen,  2. V.V. Myllylä SYNOPSIS Autonomic nervous system functions were studied in 188 patients with migraine during headache free intervals by measuring cardiovascular reflex responses. Eighty-five healthy subjects served as a control group. Pulse rate (R-R- interval) variation in normal and deep breathing, during Valsalva manoeuvre and orthostatic test was diminished in migraine patients. Diastolic blood pressure rises in orthostatic test and isometric work test were lower than in the controls. The results of patients with classic and common migraine did not deviate from each other. The same was true for the results of the female and male patients. The results of the patients with frequent migraine attacks (>4/month) showed more severe disturbance than those with infrequent attacks. Disturbances gradually developed with age, being minimal or totally lacking in young migraine patients. The results confirm the development of sympathetic and parasympathetic hypofunction in migraine patients during the course of the disorder.

Migraine and autonomic nervous system function  Objective: This study determines if measures of the function of the autonomic nervous system (ANS) differ in a population study of 80 migraine cases vs 85 controls matched for age, race, and sex. Background: The authors sought to confirm clinic-based studies suggesting that migraine is associated with abnormal ANS function. Methods: Resting systolic and diastolic blood pressure, Valsalva maneuver, heart rate variability (pulse rate [RR] variation) during deep breathing, and cardiovascular reactivity were measured during headache-free intervals. Migraineurs were subdivided into those with (n = 28) and without (n = 52) disabling headaches. Results: Resting diastolic, but not systolic, blood pressure was elevated in disabled (73.2 mm) compared with nondisabled cases (71.6 mm; p < 0.10) and controls (69.8 mm; p < 0.096). RR variation also was significantly different among the three groups. Disabled migraine cases (1.19) had significantly lower RR variation compared with nondisabled migraine cases (1.26; p < 0.001) and controls (1.26; p < 0.001). The Valsalva ratio and mean circular resultant were lower in disabled cases compared with other migraine cases and with controls, but the differences were not statistically significant. No differences were found between the three groups when comparing blood pressure response to a psychological stressor. Conclusions: Migraineurs with disabling attacks may be prone to ANS hypofunction. These findings may suggest that ANS dysfunction either may be a risk factor for migraine headaches or be a consequence of frequent disabling attacks. Moreover, ANS dysfunction and migraine may share a common neural substrate.

Cerebrovascular CO2 reactivity in migraine with aura and without aura. A transcranial doppler study Inntroduction– We studied by means of Transcranial Doppler (TCD) recordings the CO2 cerebrovascular reactivity in migraine patients during the headache-free period. Material & methods – In three groups of subjects (15 controls, 15 suffering from migraine with aura and 15 from migraine without aura) the middle cerebral artery (MCA) mean flow velocity (MFV) was recorded under basal condition and hypocapnia induced by hyperventilation. Relative MFV, PI (Pulsatility Index) changes and Reactivity Index (RI) were calculated. Results – Reactivity Index values were: 0.019 ± 0.007 (mean ± SD) in control subjects: 0.029 ± 0.008 in migraine with aura; 0.022 ± 0.008 in migraine without aura. Statistical analysis showed a significantly (P < 0.05) increased RI in migraine with aura group. Conclusion– Cerebrovascular CO2 reactivity is increased during the interictal period in migraine with aura patients.

Deficient energy metabolism is associated with low free magnesium in the brains of patients with migraine and cluster headache Abstract: We used phosphorus magnetic resonance spectroscopy to assess in vivo the brain cytosolic free magnesium concentration and the free energy released by the reaction of adenosine triphosphate (ATP) hydrolysis (ΔGATPhyd), the latter being an index of the cell’s bioenergetics condition. We studied 78 patients with migraine in attack-free periods (7 with migraine stroke, 13 with migraine with prolonged aura, 37 with migraine with typical aura or basilar migraine, and 21 with migraine without aura), and 13 patients with cluster headache. In the occipital lobes of all subgroups of migraine and in cluster headache patients cytosolic free [Mg2+] as well as the free energy released by the reaction of ATP hydrolysis were significantly reduced. Among migraine patients, the level of free energy released by the reaction of ATP hydrolysis and the cytosolic free [Mg2+] showed a trend in keeping with the severity of clinical phenotype, both showing the lowest values in patients with migraine stroke and the highest in patients with migraine without aura. These results support our current hypothesis that the reduction in free [Mg2+] in tissues with mitochondrial dysfunction is secondary to the bioenergetics deficit, and are against a primary role of low brain cytosolic free [Mg2+] in causing the bioenergetics deficit in headache.

Biofeedback assisted diaphragmatic breathing and systematic relaxation versus propranolol in long term prophylaxis of migraine. OBJECTIVES: To evaluate utility of biofeedback assisted diaphragmatic breathing and systematic relaxation in migraine and to compare their efficacy with propranolol in long term prophylaxis of migraine.
METHODS: 192 migraine patients were randomly distributed into two groups. Propranolol group received propranolol 80 mg/day while biofeedback group received electromyogram (EMG) and temperature biofeedback assisted diaphragmatic breathing and systematic relaxation training accompanied by home practice for 6 months.
RESULTS: Significant clinical response was seen with biofeedback in 66.66% and with propranolol in 64.58% of patients. Frequency, severity, duration of attacks and number of vomiting episodes were significantly reduced in both the groups at 6 months but inter-group differences were statistically insignificant. During 1 year post-treatment period, significantly lesser resurgence of migraine was seen in biofeedback group as whole (9.37%) and in biofeedback responders in biofeedback group (9.37%) in comparison to resurgence of migraine in propranolol group as whole (38.54%) and in propranolol responders in propranolol group (53.22%) respectively.
CONCLUSIONS: Biofeedback assisted diaphragmatic breathing and systematic relaxation were very useful in migraine and had significantly better long-term prophylactic effect than propranolol in migraine.

Preliminary investigation on the epidemiology of migraine in China  Abstract: The prevalence of migraine was investigated in all provinces, municipalities and autonomous regions (except Taiwan) of the People’s Republic of China. Random sampling from provincial capitals and from rural areas according to demonstration were used. Among a total screened population of 3,837,597 persons, there were 37,808 cases of migraine. The morbidity and the annual incidence rate were 985.2/100,000 and 79.7/100,000, respectively. The male/female ratio was 1:4. Inland plateaus were higher morbidity areas (more than 1,500/100,000) and coastal provinces and cities were lower morbidity areas (less than 400/100,000). The incidence rate was higher in spring in the south, while it was higher in summer in the north. The incidence rate was higher in hot and damp climate. The morbidity under 14 years old in China was significantly lower than those in overseas reports.



Upcoming study to watch

Migraine With Aura Inducing Characteristics and Effects on the Cerebral Arteries and Blood Flow by Hypoxia