The Migraine Headache

Dr. Paul Kiritsis Psychologist | Clinical Redwood City, California

Dr. Paul Kiritsis, PsyD, MScMed, is a licensed medical psychologist practicing in Redwood City, California. He specializes in the diagnosis and multimodal treatment of neuropsychiatric and functional neurological disorders, as well as coordinating care for patients suffering from these ailments. He offers heterogeneous... more

The most common debilitating headache of the hundreds of headache “types “is the dreaded migraine. The word itself is a derivative of hemicrania, a Greek word that translates to “half head” and alludes to the unilateral distribution of pain present in roughly 3 out of 4 individuals who suffer from the condition (Daroff, Fenichel, Jankovic, & Mazziotta, 2016) Why should one care about this? Well, in 2012, the Lancet named the migraine headache as the eighth most common cause of disability-affected life years, or the number of years lost to disability, injury, or disease in the general population (Vos et al., 2012). In 2016, migraine was identified as the second largest contributor to disability-affected life years in the context of neurological disorders (Amiri et al., 2022). Its global prevalence has increased considerably in the last three decades. Many clinical researchers have underscored the notion that it affects more than one billion individuals worldwide, or about 12% of the population, with a 3:1 preponderance in favor of women [18% of women, 6% of men] (Berkowitz, 2016). Their indiscriminate and ubiquitous character is epitomized in world renowned historical figures like Julius Caeser, Thomas Jefferson, and Charles Darwin–all of whom purportedly suffered from migraines (Jones, 1999).

There are interpersonal variations in the way migraines are experienced, however many process or cyclic features of a migraine attack are sweeping and “universal.” A classic permutation of a migraine attack is comprised of four interconnected phases: (1) the premonitory or warning phase, (2) the aura, a specific sensory disturbance or cluster of disturbances, (3) the headache itself, and (4) the postdrome or aftereffect (Gelb, 2016). Roughly 1-2 hours before the headache itself a migraineur may experience an abrupt disruption of homeostasis punctuated by excessing yawning and thirst, neck pain, mild dysfunction in cognitive [thinking] processes, and altered mood with a predilection for irritability, blurred vision, and sweet cravings.  Auras occur in about one-third of patients, with sensory predominance in the visual, tactile [touch], and language domains (Daroff et al., 2016). Visual auras–the most common type–involve the experience of a scintillating scotoma, that is phosphorescent or evanescent spots marching through the visual field while a tactile, somatosensory aura might involve a unilateral tingling sensation that suffuses across one side of the body, the hand, arm, shoulder, or face. Auras may precede and be temporally contiguous with the headache itself, or they may cooccur (Daroff et al., 2016). The headache proper is unilateral or one-sided in scope, throbbing or pulsating in quality, and moderate to severe in intensity, and may emerge in concert with photophobia [light sensitivity], phonophobia {sound sensitivity], nausea, vomiting, and neck pain. The migraine postdrome, on the other hand, might mimic the premonitory or warning phase and involve a “hangover” symptom constellation of weakness, fatigue, dizziness and lightheadedness, somnolence, neck stiffness, and hypersensitivity to light and sound (Zaidat, 2019). The typical story of a migraine culminates with patient disclosures of withdrawal from the stimulus-rich environment and usually involves solitary confinement in a quiet and dark room with the shades drawn and all technological devices muted.

Interpersonal disparities in the migrainous process exist. Duration and frequency of a migraine attack are variable, with attacks lasting anywhere from several hours to days. Most will have attacks 1-4 times per month (Burch, Buse, & Lipton., 2019). Having such headaches on fewer than 15 days per months puts the migraineur in a diagnostic category called, “episodic migraine.” Anything over that number–for instance, 18 or 22 days per month with 8 of those being days where migraine symptoms preponderate–qualifies the migraineur for a diagnosis of “chronic migraine.”  This clinical demographic comprises roughly 2% of the general population, and approximately 2.5% of individuals with episodic migraine convert to chronic migraine each year (Torres-Ferrús et al., 2020).

A robust body of evidence indicates that the likelihood of “conversion” from episodic to chronic is contingent on specific risk factors, some of which are modifiable and others not. Preventative intervention stratagems will not work with non-modifiable risk factors like advancing age, female gender, a sustained traumatic brain injury (TBI) and lower socioeconomic status, however they definitely will for things like obesity, stressful life events, caffeine overuse, snoring, medication overuse, and increasing attack frequency due to inadequate management of acute migraine attacks (Bigal & Lipton, 2006). Prevention is always preferable to cure. Specific medications are used in the treatment of migraine with the intention of aborting an attack or decreasing the likelihood of subsequent attacks (Louis, Mayer, & Rowland, 2016; Silberstein, 2016). Frequently these measurable outcomes are collapsed into one. The first category are called prophylactics and the second abortive medications.

When used in concert with appropriate psychosocial and behavioral interventions (on which I will speak about shortly), the frequency of debilitating headaches can be reduced, weight can be appropriately managed, rebound headaches can be quashed [by removing offending medication/s], caffeine-associated withdrawal headaches can be minimized [by gradually tapering the individuals off caffeine], sleep-disordered breathing can be alleviated, and psychosocial stressors can be minimized. Multimodal treatments, in other words treatment options synthesizing medication and behavioral therapies, tend to be more effective than either option alone. Remediation of these aforementioned factors not only decreases the likelihood of conversion, but can reverse it in a migraineur who has already converted (May & Schulte, 2016).   

Other disparities in the cyclical migraine process exist in the context of triggers, a compelling phenomenon which differentiates migraine from other headache types. Roughly 75% of migraineurs identify specific triggers for their headaches. The most common triggers are psychosocial stressors, alcohol, low estrogen levels with menstruation [fluctuating female hormones], hunger, sleep disturbances, specific odors, shifts in weather patterns, and physical exercise (Martin & MacLeod, 2009). Other less common ones are chocolate, monosodium glutamate, processed meats, and pickled foods (Daroff et al., 2016). Many patients attempt to emancipate themselves from migraine headaches by eliminating or modifying their respective triggers, whatever they may be. Other options are methodical and graded exposure to the respective trigger, with a preference for exposure that falls short of inducing a pain cascade. In fact, there is a very compelling argument that has been made in favor of confronting and coping with one’s triggers and thus developing experiential tolerance in lieu of avoiding them (Martin & MacLeod, 2009). Context is key and should dictate the approach taken–psychosocial stress and tension are best commensurate with exposure, while it may be best to just avoid alcohol and hunger.

Lamentably, the underlying processes and sequence of events responsible for migraine in any member of the general population [pathophysiology] are still ambiguous and esoteric. Nevertheless, there are explicit protective factors known which decrease the likelihood of having migraine attacks. Rigorous data analyses support the contention that more years of education, higher vitamin B12 intake, modest caffeine consumption, and light cardiovascular exercise fortify one against migraine attacks (Zheng, Shi, Liang, Lu, & Chen, 2023). Moreover, keeping stress and anxiety levels down, and minimizing consumption of eicosapentaenoic acid–one of omega-3 fatty acids found in oily fish like salmon–does the same (Zheng et al., 2023). These are all modifiable factors and can be manipulated; they fall within the locus of one’s control. Since psychosocial stressors are a risk factor, techniques which activate your parasympathetic nervous system–the rest and digest mode of interfacing with the world which is conducive to remediation and renewal–are going to be potent and useful. Hypnosis, mindfulness-based meditation, and progressive muscle relaxation deployed under the auspices of a psychologist or another allied health provider are most conducive in attaining and maintaining this state (Kropp, Meyer, Meyer, & Dresler, 2017). Biofeedback, a self-regulation technique aiming to activate that parasympathetic state through conscious manipulation of physiological signals like temperature and skin conductance levels, is also going to be useful here (Pérez-Muñoz, Buse, & Andrasik, 2019). Cognitive-behavioral therapy, a formulaic psychotherapy which converges upon challenging our implicit assumptions and core beliefs about the way things are for the sake of rendering us less “maladaptive,” may also play an important role in reducing frequency of migraine attacks. Taking up an endurance sport like marathon running has been shown to lessen pain intensity, among other things. There is a plethora of interventions to choose from; there is an apotropaic helmet for every unfortunate migraineur.

Finally, it would be remiss of me not to mention the general consensus on inheritability and the underlying disease process precipitating the migraine attack. Epidemiological surveys and large national registry-based twin studies provide some robust evidence in support of “genetic loading,” meaning there are specific gene defects buttressing one’s propensity to developing migraine, and that greater co-occurrence of these in one individual increases their risk of developing it exponentially (Mungoven, Henderson, & Meylakh, 2021). Further, there are two competing theories of migraine generation; one places the “migraine generator” within the confines of the brain, and the other attributes migraine to external triggers. One older theory identifies specific regions of the old “reptilian brain,” for instance morphological structures called the hypothalamus and the brainstem, as the origin on the basis that premonitory symptoms like thirst, hunger, food cravings, and drowsiness indicate dysfunction in that locus. Another theory posits that areas of the brain usually quiescent and inactive during a painful experience are active in a migraineur–the migraine brain is, to all intents and purposes, hyperexcitable and detrimentally sensitive to sensory stimuli. Yet another one to powerful activation of an intricate circuit, the trigeminocervical system which supplies nerve fibers to pain-sensitive structures within the brain [including many important blood vessels] (Daroff et al., 2016; Recober, 2021). Without committing fully to any one theory, it is probably safe to say that migraine attacks are the result of alterations in normal brain function and excessive cross-talk between areas that are more measured in balancing exclusivity and inclusivity with other areas.

Despite the doom and gloom, a migraineur is never helpless in the face of adversity. There is always a personalized apotropaic helmet available for purchase!


Amiri, P., Kazeminasab, S., Nejadghaderi, S. A., Mohammadinasab, R., Pourfathi, H., Araj-Khodaei, M., Sullman, M. J. M., Kolahi, A. A., & Safiri, S. (2022). Migraine: A Review on Its History, Global Epidemiology, Risk Factors, and Comorbidities. Frontiers in neurology12, 800605.

Berkowitz A.L.(Ed.), (2016). Clinical Neurology and Neuroanatomy: A Localization-Based Approach. McGraw Hill.

Bigal, M. E., & Lipton, R. B. (2006). Modifiable risk factors for migraine progression. Headache46(9), 1334–1343.

Burch, R. C., Buse, D. C., & Lipton, R. B. (2019). Migraine: Epidemiology, Burden, and Comorbidity. Neurologic clinics37(4), 631–649.

Daroff, Fenichel, G. M., Jankovic, J., & Mazziotta, J. C. (2016). Bradley’s Neurology in Clinical Practice (6th ed.). Elsevier Health Sciences.

Gelb, D. J. (2016). Introduction to clinical neurology. New York: Oxford University Press.

Jones J. Great pains: famous people with headaches. Cephalalgia. (1999) 19:627–30. doi: 10.1046/j.1468-2982.1999.019007627.x

Kropp, P., Meyer, B., Meyer, W., & Dresler, T. (2017). An update on behavioral treatments in migraine - current knowledge and future options. Expert review of neurotherapeutics17(11), 1059–1068.

Louis, E. D., Mayer, S. A., & Rowland, L. P. (2016). Merritt's neurology (Thirteenth edition.). Philadelphia: Wolters Kluwer.

Martin, P. R., & MacLeod, C. (2009). Behavioral management of headache triggers: Avoidance of triggers is an inadequate strategy. Clinical psychology review29(6), 483–495.

Mungoven, T. J., Henderson, L. A., & Meylakh, N. (2021). Chronic Migraine Pathophysiology and Treatment: A Review of Current Perspectives. Frontiers in pain research (Lausanne, Switzerland)2, 705276.

Pérez-Muñoz, A., Buse, D. C., & Andrasik, F. (2019). Behavioral Interventions for Migraine. Neurologic clinics37(4), 789–813.

Recober A. (2021). Pathophysiology of Migraine. Continuum (Minneapolis, Minn.)27(3), 586–596.

Silberstein S. D. (2015). Preventive Migraine Treatment. Continuum (Minneapolis, Minn.)21(4 Headache), 973–989.

Torres-Ferrús, M., Ursitti, F., Alpuente, A., Brunello, F., Chiappino, D., de Vries, T., Di Marco, S., Ferlisi, S., Guerritore, L., Gonzalez-Garcia, N., Gonzalez-Martinez, A., Khutorov, D., Kritsilis, M., Kyrou, A., Makeeva, T., Minguez-Olaondo, A., Pilati, L., Serrien, A., Tsurkalenko, O., Van den Abbeele, D., … School of Advanced Studies of European Headache Federation (EHF-SAS) (2020). From transformation to chronification of migraine: pathophysiological and clinical aspects. The journal of headache and pain21(1), 42.

Vos, T., Flaxman, A. D., Naghavi, M., Lozano, R., Michaud, C., Ezzati, M., Shibuya, K., Salomon, J. A., Abdalla, S., Aboyans, V., Abraham, J., Ackerman, I., Aggarwal, R., Ahn, S. Y., Ali, M. K., Alvarado, M., Anderson, H. R., Anderson, L. M., Andrews, K. G., Atkinson, C., … Memish, Z. A. (2012). Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet (London, England)380(9859), 2163–2196.

Zaidat, O. O., Lerner, A. J., & Miles, J. D. (Eds.). (2019). The Little Black Book of Neurology E-Book. Elsevier Health Sciences.

Zheng H, Shi YZ, Liang JT, Lu LL, Chen M. Modifiable factors for migraine prophylaxis: A mendelian randomization analysis. Front Pharmacol. 2023 Jan 12;14:1010996. doi: 10.3389/fphar.2023.1010996. PMID: 36713835; PMCID: PMC9878312.