**2. Pathophysiology of migraine**

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

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 physiol-

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 indispens-

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].

the highest prevalence of migraine in Europe [1].

2 Biofeedback

ogy of migraine, so no unique treatment has yet been conceived.

able for shaping a healthier society.

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

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 hyperexcitability of the brain.

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 cerebral blood vessels [10].

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 that affects the brain veins [12].

#### **2.1. Pathogenesis of migraine headaches**

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

There is the release of ions, cytokines, and other inflammatory mediators in the environment of sensory fibers that inject the brain envelope. Due to the presence of these substances, prolonged activation of peripheral nociceptors occurs, which is eventually perceived as pain. Neurogenic inflammation prolongs and enhances migraine headaches. Because of inflammation, there is also sensitization [13, 14]. Sensitization of neurons and neural fibers indicates an increase in their susceptibility. The threshold is lowered, and the magnitude of irritability and area of the irritable area grow [12]. Because of this, the weaknesses of the stimuli at perhaps atypical sites can be perceived as pain. Spontaneous neuronal activation also occurs. There are two forms—peripheral and central sensitization. In peripheral sensitization, it is about capturing primary afferent neurons, while in central sensitization, it is more susceptible to "higher" neurons—those in the trigeminal nucleus and other parts of the brain stem and hemisphere. Sensitization is believed to be responsible for many of the clinical symptoms of migraine. Pulsating pain, strengthening pain due to physical activity, hyperalgesia, and allodynia are associated with sensitization.

Discovery of the mutations of these genes explains very few migraine cases, but their detection is very important for a better understanding of pathogenesis [21]. Other forms of migraine are most likely to be complicated genetic disorders, where multiple genes are responsible for the occurrence of migraine and in which the gene base is intertwined with environmental factors [12].

Biofeedback and Neurofeedback in the Treatment of Migraine

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

5

Diagnosis of a migraine is based on the clinical picture or diagnostic criteria set by the Headache Classification Committee of the International Headache Society [3]. There are two types of a migraine—migraine without aura and migraine with aura. Headaches that occur 15 or more days a month for more than 3 months and 8 or more days of migraine headache are

Specific diagnostic tests for migraine do not exist, and image methods are in most cases not necessary. According to the American Academy of Neurology, the use of radiographic image methods (MSCT, MR) is recommended only if an abnormal neurological status is found and in patients with an atypical clinical history of headaches or headaches that cannot be classified into either a migraine headache or some other primary headache [15]. Differential diagnosis of a migraine without aura includes primarily tensile headache, whereas the differential diagnosis of migraine with aura also involves transitory ischemic attack and partial epileptic seizure. At the setting of diagnosis of a migraine can help presence of auras (the presence of positive phenomena following negative phenomena), the sequence of their occurrence, progression, duration, and possibly the existence of associ-

Also, at diagnostic, it is very important to take an extensive interview to get detailed information on all spheres of life of the person with migraine (frequency, pain, time of occurrence, association with other events, relationship with some period of time, place of appearance of pain and description of pain, susceptibility to events in their own surroundings—greater expectations of oneself or others—sensitivity to criticism, events that could have caused migraines). Being a good listener to hear all the details of the person with migraine is of crucial importance because it also depends on proposing the possible treatment. After an initial interview where we collect all the necessary information, we shall decide together with the person about how to treat a migraine. For biofeedback as a method of treatment, it is very important to find out how much the person is motivated to invest in and separate the time they will devote to these treatments. At some people, it is still a bigger motive to take some

Migraine headache therapy according to European Federation of Neurological Societies (EFNS) recommendations' indication for individual drugs was elaborated according to EFNS

**3. Diagnosis of a migraine**

diagnosed with chronic migraine [3].

medications that will quickly solve their problem.

**4. Treatment of a migraine**

guidelines at three levels [22]:

ated symptoms [12].

### **2.2. Genetics of a migraine**

The association of genetic factors with the onset of a migraine has been first proven in patients with familial hemiplegic migraine (FHM). This is a migraine subtype where an aura appears to be fully reversible motor deficiency [12]. There are three types of family hemiplegic migraines:


Discovery of the mutations of these genes explains very few migraine cases, but their detection is very important for a better understanding of pathogenesis [21]. Other forms of migraine are most likely to be complicated genetic disorders, where multiple genes are responsible for the occurrence of migraine and in which the gene base is intertwined with environmental factors [12].
