Migraine Surgery: A Clinical Guide to Theory and Practice

By Thomas Muehlberger

 Migraine surgery is the only existing treatment option that can lead to a permanent symptomatic improvement. Surgical techniques and advances in the understanding of the underlying mechanisms are evolving rapidly. This book intends to familiarise surgeons with the concept of migraine headaches and explains the surgical deactivation of trigger sites, which consists of much more than the decompression of pericranial nerves. The traditional notion of the brain as the sole origin of migraine is supplanted by a concept where the alteration of afferent signals in conjunction with peripheral and central sensitization can trigger a migraine attack. Migraine surgery targets the crucial role of extracranial tissues in the genesis of migraine which is corroborated by substantial clinical, anatomical and pathophysiological evidence.

• Language: English
• Publisher: Springer
• Release date: Jun 26, 2018
• ISBN: 9783319781174

Book preview

© Springer International Publishing AG, part of Springer Nature 2018

Thomas MuehlbergerMigraine Surgeryhttps://doi.org/10.1007/978-3-319-78117-4_1

1. Introduction

Thomas Muehlberger¹ 

(1)

Medsteps AG, Cham, Switzerland

For professionals and general readers alike, there are already a perplexing number of books on migraine commercially available. Who needs yet another one? There are probably even more books about plastic surgery on the market. Plastic surgery is an enormously diverse discipline covering reconstructive, hand, and aesthetic surgery as well as burn care, to name only the main areas. Is there really any demand to expand the speciality to include the surgical care of migraine patients? This book intends to show that the answer is unambiguously affirmative.

Most likely, any reader of this book knows someone who suffers from migraine. Maybe you’re not even aware that this person has migraine since a large proportion of sufferers won’t tell because they have been dismissed as malingerers in the past. In any case, you wouldn’t have to look very far to find patients with migraine as they are already in your practice or hospital: one in five women has migraine.

Migraine is the third most prevalent neurological disorder in the world, yet most people, including doctors, would be hard pressed to define precisely what migraine really is. Many individuals who do not suffer from it consider migraine to be some sort of peculiar headache that has something to do with blood vessels. Neither is true. It actually is much more than just a headache, and it is not caused by blood vessels.

Migraine is usually defined as a pain disorder with headache as its seeming essence. Although the pain is often the most prominent and easily recognizable sign, this view does not account for the array of premonitory and postdromal symptoms occurring before and after the pain.

Talking to migraine patients can reveal the strain of their disorder and turn a fairly abstract symptom like phonophobia—a hypersensitivity and aversion to sound—into a presentiment of their suffering. When a patient describes how terrified she can get when an ordinary fly is buzzing around the room and where the attacks are forcing her to lie in darkness, this may at first seem slightly odd. This is until one understands that her migraine, or rather the associated phonophobia, can turn the fly into a menacing helicopter filling the room with unbearable noise. At the same time, the migraine prohibits even trivial activities. Sometimes just turning the head or getting up, let alone chasing a fly, can cause a dramatic upsurge of pain. Another patient deplores that the migraine is making her world smaller because she cannot ride her beloved bicycle anymore. Each and every little bump and unevenness can trigger her migraine. This is a miniature version of traumatic migraine.

This book intends to provide information for different groups of clinicians, the ones who are not yet practicing migraine surgery and the ones who are already familiar with it, and neurologists who will never actually perform the surgery but are open-minded and curious about it. Ideally, this text may add to the discussion. It is in no way an attempt to provide definitive solutions. Instead, it should raise more questions than it answers. The salient feature of the following pages is not the statements made therein, but rather the thoughts it will hopefully inspire in the reader’s mind. There is no intent to persuade the fervent disbeliever who already knows all the answers.

Some topics will be repeatedly discussed under different headings, like convergence, sensitization, afferent signaling, neurogenic inflammation, and referred pain. As most readers will not plow through the text from start to finish but may pick and choose selected chapters, repetition is inevitable and necessary. This way, issues surrounding the temple, to name but one, will appear in the chapters on patient selection, the preoperative testing with botulinum toxin, and in the section on the surgery of this area.

Migraine surgery is currently an intriguing novelty in plastic surgery and will become a milestone. This may sound presumptuous at first due to the restraint many surgeons have toward embracing a disorder which is fraught with misperceptions. One purpose of this book is to familiarize surgeons with migraine and show it is much more than pain and aura. Understanding is a prerequisite to becoming interested enough to get engaged. If you, however, were given this book as a gift, bought it on a whim, or simply have no intention spending lots of precious time reading through it, you might want to read only Sect. 6.​4 which encapsulates the main points.

In addition to questions on what migraine really is and how migraine surgery can ameliorate its symptoms, it might be helpful to briefly entertain some thoughts on the nature of the disorder.

Migraine is extremely common yet pathologically benign. Is there a purpose of migraines despite their deeply annoying symptoms? Migraine headaches have most likely accompanied mankind forever. What, if any, benefit could possibly be gained through natural selection from a condition that renders an individual transiently completely disabled and vulnerable? Is there any conceivable evolutionary advantage from being markedly sensitive to weather changes?

A thermostat is a technological control system which functions as a homeostatic mechanism. Is migraine acting similarly as a reset to correct a temporary dysfunction of sensory input in order to maintain homeostasis ? Or is it rather a reflection of a decreased ability to adapt to changes as evidenced by the extreme sensitivity to fluctuations in homeostasis of migraine patients [1]?

Homeostasis concerns the constancy of the internal environment. The maintenance of homeostasis requires adaptation in the face of potentially stressful challenges [2]. This stability through change is called allostasis [3]. It involves the turning on and off of various neural adaptive mechanisms to appropriately manage the level of emotional and physiological stress at any given time. This allostatic load is thus the price of adaptation. It is fundamentally different from the subtle ebb and flow of unperturbed homeostasis. A migraine attack may be a sign that the allostatic systems are overloaded or dysfunctional which would correspond to the concept that migraine represents a state of sensory overload.

Correspondingly, migraine may be seen as an adaptive behavioral response to internal and external stressors which is orchestrated by a threatened brain [4, 5]. Migraine is characterized by withdrawal caused by the inescapable pain [6]. Charles Darwin, who himself had migraine, wrote as soon as the sufferer is fully conscious that nothing can be done, despair or deep sorrow takes the place of frantic grief [7]. Yet, all these are mere interpretations. The underlying mechanism of migraine is ultimately unknown.

Traditional thinking views natural systems, such as the brain, to operate in a balanced state with specific feedback mechanisms eliminating internal and external challenges. The physiological variables of the system are thought to change accordingly in a smoothly continuous fashion. Any unexpected variation is seen as random behavior and can be explained by statistical methods. The precise knowledge of each individual part of the system will thus add up to an understanding of the system as a whole, including the reasons for its failure. With this in mind, the variety and variability of migraine are explained by proposing that particular groups of neurons should be seen as a module which, when activated, produces certain symptoms [8]. Each of those modules is linked to other modules, and this way the patient’s individual headaches are generated. These linear dynamics are the underpinning of the notion of migraine being generated by some specific phenomenon, for example, cortical spreading depression. This altered neuronal excitability is seen as the instigating event affecting different brain regions in a predictable sequence to eventually trigger the pain as well as the migraine attack itself.

The only problem with such a concept is that complex systems like the brain almost certainly do not operate in this way [9]. Instead, such systems are better understood using nonlinear dynamics, which basically means that there is no simple relationship between cause and effect. Minor inputs can lead to massive changes, whereas major inputs may have little impact. In 1972, Edward Lorenz, an MIT meteorologist, gave a lecture titled Does the Flap of a Butterfly’s Wings in Brazil Set Off a Tornado in Texas? [10]. In it, he described how even tiny changes in the initial conditions of an experiment, for example, the simulation of a dynamic model, can produce vastly diverging results. This sensitivity of complex systems is popularly known as the butterfly effect . The flapping wing represents the small change in the initial condition of the system, which leads to large-scale phenomena. Had the butterfly not flapped its wings, the trajectory of the system might have been markedly different. Lorenz said that If the flap of a butterfly’s wings can be instrumental in generating a tornado, it can equally well be instrumental in preventing a tornado [10].

In contrast to a deterministic sequence which, in migraine, suggests that a particular event inevitably leads to another, complex systems that are highly sensitive to even minor changes will behave unpredictably. This is what is commonly associated with the word chaos. The study of nonlinear dynamics is hence called chaos theory , dealing with systems that, contrary to the colloquial use of the word, are not determined by coincidences. In such systems no single element is in control, and they cannot be explained by a reduction into their component parts [9].

How is any of this relevant for migraine surgery? It would, first of all, suggest that pivotal questions on the pathophysiology of migraine cannot be answered in a reductionist way. This means that there is no single factor responsible for the genesis of migraine. Accordingly, migraine is not caused by a particular trigger, like weather, alcohol, chocolate, etc. It would also indicate that there is no specific, exclusively intracranial generator in the brain which sets forth a predictable sequence of events to culminate in a migraine attack. Instead, as will be argued in this book, migraine can be triggered by changes in the initial conditions of afferent signaling which occur in pericranial tissues.

Migraine surgery has been described as decompression or deactivation of trigger sites. Yet, the capacity to trigger an attack does not necessarily require a full-blown nerve compression. Instead, any alteration of afferent signals, a clinically silent nerve irritation, an intranasal contact point, an inflamed temporal artery, or a modified sensory input caused by malocclusion, may represent the trigger initiating a cascade of events. Migraine surgery can therefore be aptly seen as a desensitization.

There are two further aspects that deserve mentioning to understand the role of such pericranial, surgical triggers. First, none of them act independently and none of them cause migraine. Their function—or rather dysfunction—is inseparable from pathophysiological mechanisms within the central nervous system. Only the peripheral and central sensitization of neurons can turn the altered sensory input from various sources into a barrage of afferent, outside-in signals that will eventually lead to the release of inflammatory neuropeptides and pain mediated by meningeal nociceptors. The second aspect pertains to the alleged exclusivity of the central hypothesis. The central hypothesis basically claims that migraine starts, takes place, and ends within the brain. As will be shown, the notion of migraine originating solely within the brain while denying any role of the periphery is untenable.

There can be more than one opinion about something as complex as migraine, though the filter of one’s affiliation to a medical speciality, irrespective of whether it is surgical or neurological, can be a serious impediment to the acceptance of new practices. People, however, regardless of this superficial, binary filter do respond to information and facts. Only if you dispose of conventional, established wisdom and the associated ideological knee-jerk reaction can you find a diversity of perspectives and a wide variety of ways to look at migraines. Taking such a step can be interesting and exciting, and that’s what this text is trying to provoke—a different view of migraine which does not exclude substantial anatomical, clinical, and pathophysiological findings (Fig. 1.1).

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Fig. 1.1

Tattoo on an operated patient’s back to display the victory over her migraines. Published with kind permission of © medsteps

In the end, there are few more rewarding moments for a surgeon than to encounter the astonished relief of a successfully treated migraine patient.

References

1.

Burstein R, Noseda R, Borsook D. Migraine: multiple processes, complex pathophysiology. J Neurosci. 2015;35:6619–29.Crossref

2.

McEwen BS. Stress, adaptation, and disease. Allostasis and allostatic load. Ann N Y Acad Sci. 1998;840:33–44.Crossref

3.

Fisher S, Reason J, editors. Handbook of life stress, cognition and health. New York: J. Wiley Ltd; 1988. p. 631.

4.

Borsook D, Maleki N, Becerra L, McEwen B. Understanding migraine through the lens of maladaptive stress responses: a model disease of allostatic load. Neuron. 2012;73:219–34.Crossref

5.

Cortelli P, Pierangeli G, Montagna P. Is migraine a disease? Neurol Sci. 2010;31:S29–31.Crossref

6.

Montagna P, Pierangeli G, Cortelli P. The primary headaches as a reflection of genetic darwinian adaptive behavioral responses. Headache. 2010;50:273–89.Crossref

7.

Darwin C. The expression of the emotions in man and animals. London: The Folio Society.; Reprint Oxford University Press, 2009; 1872. p. 62.Crossref

8.

Young WB, Peres MF, Rozen TD. Modular headache theory. Cephalalgia. 2001;21:842–9.Crossref

9.

Kernick D. Migraine – new perspectives from chaos theory. Cephalalgia. 2005;25:561–6.Crossref

10.

Lorenz E. Predictability: does the flap of a Butterfly’s wings in Brazil set off a Tornado in Texas? American Association for the Advancement of Science, 1972. http://​eaps4.​mit.​edu/​research/​Lorenz/​Butterfly_​1972.​pdf.

© Springer International Publishing AG, part of Springer Nature 2018

Thomas MuehlbergerMigraine Surgeryhttps://doi.org/10.1007/978-3-319-78117-4_2

2. What Is Migraine?

Thomas Muehlberger¹ 

(1)

Medsteps AG, Cham, Switzerland

The definition of migraine is mainly descriptive: there is no diagnostic test and no useful biomarker. Migraine attacks are invisible but can present with an encyclopedia of neurological symptoms. Pain is commonly assumed to be the essence of migraine, yet there is no structural lesion correlated to it. It can range from no pain at all to excruciating misery. Still, even in its most disabling form, the pain is only one symptom among many others. Migraine is often accompanied by nausea and hypersensitivity to light and sound. Other symptoms may include speech deficits, mood alterations, neck stiffness, and inability to concentrate. Even this brief excerpt of possible clinical presentations points to the involvement of numerous different brain regions during an attack. Migraine can be seen as a temporary, self-limiting shutdown of the brain’s operating system followed by a restart. Almost any function of the brain can be affected which presents a considerable variability in clinical symptoms from one individual to the next and from one attack to another within the same patient.

…she felt in the top right corner of her brain a heaviness, the inert body weight of some curled and sleeping animal… It was important, however, not to provoke it; once this lazy creature moved from the periphery to the center, then the knifing pains would obliterate all thought. Ian McEwan, Atonement [1].

Migraine is considered a primary headache, which means that the cause is unknown. Headaches due to a known disorder such as substance abuse, infection, and other conditions are called secondary. Although migraine can be a moving target, it is not particularly difficult to diagnose [2]. If patients report that recurrent headaches force them to lie still in a darkened room because every movement aggravates the pain, that they are possibly bothered by even unobtrusive sounds or smells, and that they feel like they have a hangover once the pain is gone, then they are probably suffering from migraines.

Most doctors have been taught in medical school that migraine attacks occur in a structured sequence of three or four different phases (Fig. 2.1). The phases are described relative to the occurrence of the headache because the pain is the most easily recognizable feature of the attack. Accordingly, the initial phase is called prodrome which is when the so-called premonitory symptoms take place.

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Fig. 2.1

The phases of a migraine attack. Published with kind permission of © medsteps

This phase consists of subtle symptoms with an insidious onset. Often, they are mere amplifications of normal sensations and behavior. They are very hard to quantify, and most can occur at any time in people with or without migraine (Table 2.1). The symptoms are often misinterpreted as causal rather than premonitory. They are, however, not just a prelude but part of the attack which at that point has already begun. Since some of these symptoms also occur in the postdromal phase, they may be present throughout the attack but become unrecognizable due to the aura and pain in between [3]. The question is when and why do these symptoms become indicative of an attack. Some patients can reliably predict an impending attack based on their premonitory symptoms. The next phase, aura, occurs in only a minority of migraine patients and usually evolves suddenly and is followed by the headache phase with variable length of duration and intensity. It can take between minutes and hours to reach maximum intensity, joined by a range of features such as nausea and pallor. The postdrome is considered the final phase after the pain has subsided.

Table 2.1

Symptoms corresponding to the respective phases of a migraine attack

The lists are incomplete; there are many more possible symptoms

The presumed sequence of events and symptoms is based on the notion of a structured and linear involvement of multiple brain regions. This sequence, however, is applicable only in theory. In reality, the phases of an attack often overlap or even telescope into one another in all varieties [4]. Migraine can present with symptoms ranging from autonomic to sensory and cognitive. Attacks can occur without pain and aura or consist of nothing but an aura. The phases other than the pain can be more extended and even more disabling than the headache [3]. The pain is less likely to be part of a sequence culminating in an attack and is certainly not the equivalent of migraine: it is probably rather a nonessential symptom. The majority of patients report headache, photophobia, and phonophobia within the initial 15 min that they begin to experience aura symptoms, suggesting various parallel and concurrent mechanisms rather than a downstream cascade of events [5]. Furthermore, the temporal boundaries of the beginning and the end of an attack are often unclear. Pathophysiological changes may be taking place long before or after an attack (Fig. 2.2).

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Fig. 2.2

Georgia O’Keeffe’s painting of one of her migraine attacks. Her cool comment reflects a fairly unusual approach to migraine: Drawing No. 9 is the drawing of a headache. It was a very bad headache. Well, I had the headache, why not do something with it? [6]. Published with kind permission of © University of New Mexico Press

2.1 Prevalence and Costs

Migraine is extraordinarily common. Its prevalence in women is 17% and 6% in males [7]. It is the single biggest source of neurologic disability in the world [8]. affecting around one in eight people worldwide [9]. One in every four households in the USA has a member who suffers from migraine headaches [10]. If the members of nuclear and extended family, such as cousins and aunts, exceed ten people, then it would be unusual to find a family without any relatives suffering from migraine [11]. The highest prevalence is in females between the ages of 25 and 34 [12]. The cumulative lifetime incidence of migraine for women is 43% which means that nearly one in two women will experience migraine at least once in her life [13, 14].

These numbers can increase dramatically in specific subpopulations, for example, in neurologists. Their 1-year prevalence of migraines is 40% in the USA and 33% in Germany [15, 16]. Twenty-seven percent of neurologists in Taiwan, 39% in Norway, and 48% in France suffer from migraines [17–19]. The numbers are even higher in board-certified headache specialists. Their lifetime prevalence was reported as 72% in males and 81% in females [16]. One survey even found that out of 44 physicians, 87% had migraine aura without headache which by far exceeds all other reported prevalences of painless migraine of between 1 and 3% [20]. One possible reason for these strikingly higher rates compared with the general population might be that the personal experience of migraines initially drove them to become neurologists and headache specialists and in about 30% this seems to have been one factor, among others [21, 22]. Other quoted reasons for the exceptional prevalence rates are their stressful jobs and a particular personality profile [21]. There is no comparable data from the rest of the medical profession. It is of particular note that the prevalence rates of tension-type headaches in headache specialists (24%) and neurologists (27%) are significantly lower compared with the overall population (38%). Perhaps they are better qualified to make a migraine diagnosis, or they use the ICHD classification more often than others.

Migraine is an expensive illness. There is abundant literature on the material costs and economic burden of migraine which will be dealt with only briefly in this section. The figures obviously vary on a national scale and depend on the respective health system, medical options and availability, specialists’ training schemes, and a number

of other factors. In addition, in the age of healthcare cost explosion, respective figures are quickly outdated.

In the USA in 2010, migraine headaches caused more than $3 billion in outpatient costs and $700 million in emergency room costs [23]. The direct medical costs for migraine patients were more than $2500 per person per year higher than in non-migraine patients [24]. In a 2005 report, the costs for drugs for the treatment of migraine were estimated to be $1.5 billion annually [25]. The indirect costs of migraine for absenteeism from work in 2007 were approximately $12 billion [26]. The adjustment of these figures to the present reveals the extent of the burden of migraine without even considering the personal impact of migraines on the quality of life of each sufferer. In addition, migraine sufferers are less desirable employees, often passed over for promotion and pay rises and on lower incomes compared with people without migraine.

2.2 With or Without Aura

Most people, in particular the ones not afflicted by migraines, assume that an attack always starts with an aura followed by one-sided pain. The aura is certainly one of the literally most colorful and mysterious components of migraine.

In 1865, George Airy, a prominent English mathematician and astronomer, published a paper on half-blindedness that he experienced during his own migraine attacks [27]. He noted that in general, I feel no further inconvenience from it as his migraines were painless. His physician son drew together his and his father’s account to produce some of the most beautiful illustrations of aura, which he termed transient teichopsia. It entails a scintillating scotoma with luminous appearances in a zigzag outline [28]. He considered these to be veritable photographs of the processes going on in the brain. Contrary to his father, his attacks were followed by terrible headaches (Fig. 2.3).

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Fig. 2.3

Plate XXV Stages of Teichopsia from Hubert Airy [28]. Published with kind permission of © Royal Society Publishing

Oliver Sacks’ first book titled Migraine was designed for a general readership [29]. In it he notes that every patient with classical migraine opened out, as it were, into an entire encyclopaedia of neurology. Sacks puts a peculiar emphasis on aura possibly because he suffered from exclusively painless migraines himself [30]. In the introduction to a reprint of Liveing’s book on migraine, Sacks writes of strange metamorphopsias and achromatopsias , Lilliputian hallucinations and palinopsias and bizarre disorders of body-image of every kind [31]. In another book, he describes ... patients who have attacks consisting of nothing but an aura and mentions his own migraine-induced olfactory hallucinations [32]. This aura symptom is called phantosmia with intense and/or unpleasant smells. It is exceedingly rare at a prevalence of 0.66% [33]. In view of the focus on aura, it is important to note that the majority of migraine patients do not experience an aura during their attacks [34].

Still, the differentiation into migraine with, versus without, aura features prominently in the International Classification of Headache Disorders. This distinct differentiation is mirrored by the formerly used designations of classical (with aura) as opposed to common (without aura) migraine. The proponents of the relevance of this difference tried to ascertain its genetic predetermination. Based on a study of more than 5000 Dutch twins, they claimed that no common genes for the two migraine variants will ever be found [35]. The exact opposite, no etiological difference, was reported in Australian twins, and the same result, no evidence for separate subtypes, was shown when the study was repeated in more than 10,000 Dutch twins [36, 37]. In fact, many migraine patients suffer from both kinds of attacks. A study on 1000 migraine patients from 210 Finnish migraine families demonstrated that more than 40% experienced attacks with as well as attacks without aura [38].

The traditional thinking, that migraine attacks occur in a structured, sequential fashion where the premonitory symptoms are followed by an aura which is preceding the pain, has never been more than a theory. The concept originated in the assumed role of cortical spreading depression to set off the aura. After that, the aura then instigated the pain. Ebersberger et al. have shown conclusively that this is not the case: in reality, these phenomena are most likely running in parallel [39, 40]. This is corroborated by the clinical variability of the appearances of the aura, as 49% of patients reported that the headache phase started before, simultaneously with the onset, or during the aura [41]. Another study found the pain started within 15 min of the onset of the aura in 54% of migraine patients [5].

Most commonly, a visual aura consists of dots and lights, jagged or wavy lines, and blind spots [42]. These symptoms last for more than 1 h in 14% of auras, and in some cases the aura can become persistent [43, 44]. Next to these visual hallucinations, more than a third of migraine patients experience sensory symptoms in the form of tingling and numbness of the lips, tongue, and cheek and then gradually extending to the hand [44]. Sometimes patients describe a heaviness of the affected arm [34]. Furthermore, dysphasic aura symptoms occur in 10% in the form of difficulties recalling or speaking words. Sigmund Freud noted that …the quiet migraines … are usually announced hours before through the forgetting of names… [45].

Migraine with aura and migraine without aura can occur within one and the same individual. Often over time one type can become more frequent [46]. Contraceptives can promote the conversion of one type into another and back when stopped [47]. With aging the aura may become more prominent or even turn out to be the only symptom left of the migraine. The aura itself is subject to enormous variation with the majority of patients reporting no stereotyped pattern [41]. Whether an attack is preceded by an aura doesn’t have any impact on the attack itself, and there is no known difference in any drug response in acute or prophylactic therapy between migraine with and without aura [46].

In light of the above, the practice of assigning patients a definitive diagnosis of aura or not aura in epidemiological and clinical trials appears questionable. The state of the presence or absence of an aura may be accurate just for that moment in time. The significant intra- and interpersonal variability makes a direct genetic influence unlikely. Migraines with and without aura represent more likely a mobile continuum with two types at each end of the spectrum. The final question is, however, whether there is any discernible benefit to be gained for the patient from the discussion about aura versus non-aura.

2.3 Episodic and Chronic

Chronic migraine is defined as headache occurring on 15 or more days per month which, on at least 8 days per month, has the features of migraine headache [48]. Considering the variable duration of premonitory and postdromal symptoms occurring in addition to the pain itself, patients with chronic migraine suffer the severe impact of their headache disorder more or less incessantly. Their migraines are often treatment refractory, and medication overuse is highly prevalent. The chronic form of this disorder accounts for the largest proportion of the socioeconomic burden imposed by migraine [49].

The long-lasting debate about tension-type headache (TTH) and migraine being either distinctly separate entities (its coexisting migraine and TTH) or not (it’s all migraine) has caused chronic migraine to be enduringly absent from the classification until its third edition in 2013 [50]. Before that, chronic migraine patients were considered to have episodic migraine plus medication overuse headache until they managed to discontinue their medication. Only then was it labeled as chronic migraine [51]. The previously existing terms chronic daily headache and transformed migraine were discarded, and a co-diagnosis of chronic migraine and medication overuse headache is now permitted [52]. It wouldn’t be surprising if, by that point, you are lost in the nomenclature. Yet, these facts actually can have enormous clinical importance.

Eight percent of all migraine patients suffer from chronic migraine, which represents approximately 2% of the general population and 2.5% of patients with episodic migraine progress to chronic migraine annually [52–54]. However, a much larger percentage of chronic migraine patients spontaneously reverts back to the episodic form [55]. Out of a total of 383 patients with chronic migraine whom the investigators followed over a 2-year period, 26% experienced a significant reduction in the frequency of their migraines, while the use of prophylactic medication had no effect on the likelihood of remission. These findings imply that migraine is not invariably worsening progressively. In more than one out of four chronic migraine patients, the change goes in the opposite direction, and the chronic form may only be a relatively brief chapter. Also, although there seem to be predisposing factors to propel the conversion from episodic to chronic migraine, for example, obesity and the abuse of opioids and barbiturates, the mechanisms behind the reversion are unknown [52, 56]. Furthermore, about 50% of chronic migraine patients revert back to the episodic form after drug withdrawal [48].

The results of studies investigating the role of therapeutics in chronic migraine patients appear in a different light when one adds up these potentially confounding factors: the natural instability of chronic migraine, the reversal of symptoms following the reduction of medication overuse headache, and placebo effects. The question is whether a symptomatic improvement in patients assigned to a trial is really due to the ameliorative effects of the studied drug, or secondary to one, or a combination of the above factors [57].

Chronic migraine can obviously range from a transitory form with spontaneous improvements to an unremitting kind with daily headaches for years. To define chronic migraine based on an arbitrary boundary of its frequency may fail to capture its random variation [57]. The headache frequency varies from month to month, so instead of measuring a state of frequency, it might be more appropriate to explore the change in frequency in order to distinguish the transitory from the permanent forms of chronic migraine.

2.4 Tension-Type Headache

It is a challenge for most patients and doctors alike to understand what the concise difference between those two headache disorders really is. The first attempt to classify headaches in 1962 intended to create a framework for the major clinical types of headache…by emphasis on basic mechanisms [58]. Headaches were grouped as either vascular headache of the migraine type or muscle contraction headache or as a combination of the two. The wordings probably originated from earlier publications [59, 60]. Later on, the first group became migraine and the second became tension-type headache (TTH) . Until then a plethora of terms were used in classifications to denote headaches: ordinary, essential, idiopathic, and psychomyogenic to name a few.

Tension-type headache is a clumsy term that resulted from physicians arguing what the previously used tension headache actually meant [61]. It wasn’t clear whether the muscles, or rather the patients, were tense. Often tension headaches were not associated with increased muscle contraction and the tension issue applied to migraines too. That is why the type was attached to tension headache.

Although TTH is significantly more prevalent than migraine headaches, there are, in contrast to a number of intricate migraine theories, hardly any concepts on its