**1. Introduction**

Migraine headache is one of the most common headaches in the general population, 15% suffering from the European Union population [1] which with disabling symptoms significantly decreases the quality of life of the patients [2]. According to the International Classification of Headache Disorders [3], a chronic migraine is a type of a primary headache occurring in 15 or more days per month for more than 3 months, in which more than 8 days per month of

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

headache meet the criteria for a migraine with or without aura or respond to specific migraine treatment. Not only in Europe, but also in the world, migraine has today a high incidence. The prevalence of a migraine in Europe is 15%—ranges depending on the individual countries, 12–27.5% [1]. According to data published in 2006, Croatia, with Germany and Denmark, has the highest prevalence of migraine in Europe [1].

**2. Pathophysiology of migraine**

ability of the brain.

bral blood vessels [10].

that affects the brain veins [12].

**2.1. Pathogenesis of migraine headaches**

tion (CGRP), protein extravasation, and dural mast cell activation.

Pathogenesis of a migraine has long been a subject of discussion among scientists. It has been considered that typical headaches are caused by intracranial vasodilation preceded by vasoconstriction causing aura—vascular theory. Today it is known that this is not the case, and although new findings have emerged, the exact mechanism and genetic determinants are not yet fully clarified. The admitted neurovascular theory states that causes of migraine lie in

Biofeedback and Neurofeedback in the Treatment of Migraine

http://dx.doi.org/10.5772/intechopen.76534

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For a long time, it was thought that the cause of the aura, which precedes headaches, is cerebral vasoconstriction. Today, this theory is denied, and the aura is explained by neural dysfunction rather than ischemia due to vasoconstriction. The process of cortical widespread depression, described in 1944 by Brazilian scientist Leão, is now associated with the emergence of visual aura [9]. It is a self-stimulating process that is thought to be due to hyperexcit-

There is a release of potassium and neuroexcitatory amino acids of glutamate from neuronal endings, whereby the surrounding tissue depolarizes and then a longer period of neuronal activity is observed. Impulses travel by tissue at a rate of 2–6 mm/min—which is the first feature to retrieve parallel with the rate of appearance, progression, and spread of characteristic visual auric symptoms. During this process, there are also molecular events that cause sterile inflammation and changes in brain perfusion. During the aura seizures, studies using positron emission tomography showed initial hyper-phase, followed by reduced cortical blood flow caused by reduced metabolism due to depolarization and associated decreased neuronal activity. Changing the blood flow in the post-anterior direction is followed by the spread of the impulse through the cortex and is not anatomically linked to the site and during the cere-

During the functional magnetic resonance imaging study, blood oxygenation was found to be initially increased, followed by a decrease in oxidative clearance in the occipital cortex, which ranged at 3–6 mm/min—which may again be related to the appearance of visual symptoms of aura [11]. In addition to being associated with oligemia, corticosteroid depression also influences the trigeminal activation of the trigeminovascular system and changes the permeability of the blood-brain barrier and thus generates migraine headaches [12]. Cortical widespread depression leads to activation of trigeminovascular afferent fibers. Because of this activation, prolonged blood flow increases through the middle meningeal artery and extravasation of plasma proteins in the pituitary mater. There is the opening of the neuronal panicles and the release of proinflammatory cytokines. Consequently, there is a sterile inflammation and pain

When trigeminal ganglion stimulation occurs, neuropeptides are released that are key to the emergence of neurogenic inflammation. The key substances are P and calcitonin gene-related peptide (CGRP) [13, 14]. Substance P is released primarily from thin non-ligated C fibers, while CGRP releases A and C fibers. They, within neurogenic inflammation, cause vasodila-

neurogenic processes, followed by secondary changes in brain perfusion [7].

Migraine is a disabling neurological condition characterized by episodic attacks of usually unilateral headache, with pulsating character and light and sound intolerance, associated with nausea and vomiting. The tendency to suffer from a migraine has a genetic component, but attacks can be triggered by a series of internal and external factors. Two types of migraine have been described: episodic migraine (EM) (with subtypes migraine with aura and migraine without aura)—in which a typical headache occurs on fewer than 15 days per month—and chronic migraine (CM) with headaches in 15 or more days per month for at least 3 months [3]. It is not rare that an episodic migraine has progression to a chronic migraine. The development of a chronic migraine has been associated with the presence of many risk factors: female sex, older age, low level of education, low-income populations, predisposition for anxiety, depression, sleep apnea or snoring, overweight, history of frequent headache, stressful life events or major life changes, asthma, allergic rhinitis, and caffeine consumption [4]. Because of all these facts about migraines, it is not difficult to think about complexity and longevity of the treatment. Also, many of people who suffer from migraine in their life use more than one treatment to get better results, which is reduced pain and number of migraines. For more than four decades, many different experts have been trying to find the best way to treat a migraine. Because the causes of migraine are not fully clarified as well as the physiology of migraine, so no unique treatment has yet been conceived.

The annual costs of migraine such as diagnosis, treatment, reduced productivity, and absence from work are estimated to be 5 billion euros in the European Union [5]. It follows from the above that a migraine is not only a medical but also a socioeconomic problem. Apart from the economic, the lack of influence of migraine is manifested in the social sphere. This recurrent disease significantly reduces the quality of life of the diseased, as it limits them to perform daily activities. This directly affects both the near and the outer environment and above all the patient's family. Thus, the consequences of a migraine are reflected in all areas of life—family, professional, and social—resulting in dissatisfaction with their own achievements in all these spheres and creating a sense of inefficiency and intolerance, creating a vicious cycle with negative consequences [2]. Therefore, the comprehensive approach to solving this problem is very important, and education, of both the general population and the patients, and raising health care to a higher level, with ongoing support for migraine-sick patients, are indispensable for shaping a healthier society.

The incidence of migraine before puberty is greater in boys than in girls [6]. It grows up to 12 years in both sexes and is the highest in the age range of 30–40 years. After puberty, the ratio changes and increases in favor of women and with 40 is 3.5:1. After 40 years, the strength of the symptoms is reduced (except for women in perimenopause), and the beginning of migraine headaches in the fifties is rare [7]. The prevalence of migraine is higher in the case of white races than in black races and, on the other hand, is proportional to the socioeconomic status [6].

Migraine is a disease with many faces. The most common form is migraine without aura, occurring in about 80% of patients, while migraine with aura occurs in about 20% of the patients [8].
