Migraine - More than a Headache!

What is Migraine?

Migraine is a common, disabling nervous system disorder defined by neurological symptoms that usually include headache, aura and heightened sensory arousal. It is usually moderately to severely disabling. Those affected by a migraine attack are often unable to function as a result of its symptoms. Up to 1 in 5 people experience migraine. It is one of the most disabling neurological conditions worldwide and is responsible for significant loss of working productivity and working absenteeism (1-4)


Quick Facts:
  • Migraine is not a headache. Migraine is a complex neurological disorder, whilst headache is the most common feature, the disease is not solely defined by headache.

  • Migraine sufferers often report other features of the disorder without the headache. Other common symptoms associated with migraine include nausea, vomiting, and sensory disturbances including light and noise sensitivity (3).

  • Certain more severe types of migraine are characterised by reversible loss of movement, dizziness and loss of sensation, these symptoms can mimic a stroke (hemiplegic migraine and vestibular migraine) (3).

  • Migraine headache is usually on one side of the head and is characterised by a pulsating sensation usually around the eye.

  • Neck pain often accompanies migraine and is sometimes mistaken for the cause of the headache (3, 10).

  • Migraineur – a person that suffers from a migraine disorder.

"Migraine is not just a headache"

What Happens in a Migraine Attack?

Whilst our understanding of migraine has advanced considerably, there is still controversy over the exact mechanisms that lead to a migraine attack.


The phases of migraine attack are associated with a sequence of mechanisms in the brain. Brain imaging studies show us that the pre-attack phase (before the onset of migraine) has been linked to the activation of areas in the brainstem responsible for control of the body's autonomic systems. Increased activation of these areas likely leads to the discomfort associated with this phase (including nausea, fatigue, irritability)(10).


The aura phase (often defined by visual disturbance) follows the pre-attack phase and is is associated with a rapid fatigue of activity over the surface of the brain. This change in activity disrupts higher brain functions like thinking, reasoning or remembering (cognitive function) (3, 9, 10), it also makes the brain more susceptible to pain.


The pain phase then ensues, this has been linked to an activation of a network of sensory nerves that supply the head, face, linings and blood supply to the brain. Hence, during the pain phase of a migraine, these nerves transmit pain inducing information from this network resulting in headache and/or neck pain (6).


Following the pain phase of migraine, patients are often left with symptoms including general feeling of discomfort, illness, or unease, and other symptoms such as mental fogginess, mood changes, sensitivity of the head and scalp and gut symptoms (9). This is called the postdrome or “hangover” effect.


What Causes and What Triggers a Migraine Attack?

Migraine has a strong genetic and familial link. Whilst there is no “one gene” that is linked to migraine, researchers have found numerous genetic codes unique to migraineurs (3). Some migraineurs may have only a few attacks in a lifetime, whilst others may have numerous attacks in a week.


Typically, migraineurs tend to report that certain triggers usually cause the onset of an attack. This is an interesting area of discussion as many migraineurs report triggers such as intense light or sound exposure, strong odours, changes in weather and food and alcohol. Whilst this may seem likely to be the case for those suffering an attack, we also know that many symptoms precede a migraine for up to 72 hours, including hunger, fatigue, restlessness and sleep changes. Therefore, intense stimuli and other so-called “triggers” may purely be indicators of a migraine in progress and retrospectively implicated as causative. Research studies have yet to demonstrate unequivocally that certain stimuli provoke or trigger an attack (16).


Possible internal and external factors contributing to an attack include hormonal changes in women, changes of day-night rhythm, strong sensory stimuli, hunger, psychological stressors or intense physical activity (3).


Migraine is Linked to other Disorders and Pain Conditions

Research has demonstrated that migraine is a multisystem disorder. This is likely because the migraineurs have a hypersensitive nervous system (14, 15, 17-21), these sensitivities are linked to many disorders as follows:


  • Neck, and back pain

  • Irritable bowel syndrome

  • Balance disorders

  • Dysautonomia (poor regulation of blood pressure, temperature control, digestion)

  • Hormonal and reproductive disorders (endometriosis and menstrual disorders)

  • Pelvic pain

  • Hypermobility

  • Fibromyalgia and widespread pain

  • Chronic headache (tension type headache)

  • Attention-deficit-hyperactivity disorder (ADHD)

  • Anxiety and depression

  • Restless leg syndrome

  • Sleep disorders

  • Epilepsy

  • Stroke


Prevention and Treatment of Migraine

Whilst there have been significant advances in the management of migraine, there is no one treatment for migraine. This is because migraine is a complex disorder that is triggered by a combination of several different individual environmental and genetic factors. Like many persistent pain conditions, research supports a multidimensional approach to management (3).


Migraine - a Disorder of Sensitivity

Migraine is a processing disorder, one could liken this to a “software” problem, rather than a “hardware” failure.

In the case of pain, we usually associate pain with tissue damage, however we now know that pain can exist in the absence of damage. Pain is a protective mechanism that is produced by the brain in order to avoid or protect us from harm (32). However, when pain is produced in the absence of harm the benefit is no longer useful (32). Migraine sufferers may in fact over process and convert normal stimuli into a protective response (i.e. pain) (1,13).


Migraine sufferers experience a range of heightened stimuli or over-excitation. Normally, the central nervous system regulates stability through a process called inhibition. Migraineurs tend to over-process stimuli, and therefore experience a world of heightened excitability (this applies not only to pain but also to a range of increased sensory and emotional sensitivity) (1,13).


References


1. Vecchia D, Pietrobon D. Migraine: a disorder of brain excitatory-inhibitory balance? Trends Neurosci. 2012;35(8):507-20.

2. Ahmad Kiadaliri A, Wang H, Abajobir A, Abate K, Abbafati C, Abbas K, et al. Global, regional, and national disability-adjusted life-years (DALYs) for 333 diseases and injuries and healthy life expectancy (HALE) for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet. 2017;390(10100):1260-344.

3. Charles A. The pathophysiology of migraine: implications for clinical management. Lancet Neurol. 2018;17(2):174-82.

4. Merikangas KR. Contributions of epidemiology to our understanding of migraine. Headache. 2013;53(2):230-46.

5. IASP Terminology - IASP 2019 [Available from: https://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1698#Nociplasticpain.

6. Ashina M, Hansen JM, Do TP, Melo-Carrillo A, Burstein R, Moskowitz MA. Migraine and the trigeminovascular system-40 years and counting. Lancet Neurol. 2019;18(8):795-804.

7. Dalkara T, Moskowitz MA. Neurobiological basis of migraine. Hoboken, New Jersey: Hoboken, New Jersey : Wiley-Blackwell; 2017.

8. Moskowitz MA. The neurobiology of vascular head pain. Ann Neurol. 1984;16(2):157-68.

9. Charles A. The evolution of a migraine attack - a review of recent evidence. Headache. 2013;53(2):413-9.

10. Dodick DW. A Phase-by-Phase Review of Migraine Pathophysiology. Headache. 2018;58 Suppl 1:4-16.

11. Edvinsson L. The Trigeminovascular Pathway: Role of CGRP and CGRP Receptors in Migraine. Headache. 2017;57 Suppl 2:47-55.

12. Hansen JM, Hauge AW, Olesen J, Ashina M. Calcitonin gene-related peptide triggers migraine-like attacks in patients with migraine with aura. Cephalalgia. 2010;30(10):1179-86.

13. Mainero C, Louapre C. Migraine and inhibitory system - I can't hold it! Curr Pain Headache Rep. 2014;18(7):426.

14. Giamberardino MA, Martelletti P. Comorbidities in headache disorders. Cham], Switzerland: Cham, Switzerland : Springer; 2017.

15. Kutuk MO, Tufan AE, Guler G, Yalin OO, Altintas E, Bag HG, et al. Migraine and associated comorbidities are three times more frequent in children with ADHD and their mothers. Brain Dev. 2018;40(10):857-64.

16. Hoffmann J, Recober A. Migraine and triggers: post hoc ergo propter hoc? Curr Pain Headache Rep. 2013;17(10):370.

17. Malone CD, Bhowmick A, Wachholtz AB. Migraine: treatments, comorbidities, and quality of life, in the USA. J Pain Res. 2015;8:537-47.

18. Ozge A, Uluduz D, Yalin OO, Demirci S, Karadas O, Uygunoglu U, et al. Chronic Migraine: Burden, Comorbidities, and Treatment/Kronik Migren: Hastalik Yuku, Komorbidite ve Tedavi.(Report). Turkish Journal of Neurology. 2018;24(2):117.

19. Gazerani P, Cairns BE. Dysautonomia in the pathogenesis of migraine. Expert Rev Neurother. 2018;18(2):153-65.

20. Evans SF, Brooks TA, Esterman AJ, Hull ML, Rolan PE. The comorbidities of dysmenorrhea: a clinical survey comparing symptom profile in women with and without endometriosis. J Pain Res. 2018;11:3181-94.

21. Karamustafaoglu Balci B, Kabakci Z, Guzey DY, Avci B, Guler M, Attar E. Association between endometriosis, headache, and migraine. Journal of Endometriosis and Pelvic Pain Disorders. 2019;11(1):19-24.

22. Goadsby PJ, Sprenger T. Current practice and future directions in the prevention and acute management of migraine. Lancet Neurol. 2010;9(3):285-98.

23. Urits I, Jones MR, Gress K, Charipova K, Fiocchi J, Kaye AD, et al. CGRP Antagonists for the Treatment of Chronic Migraines: a Comprehensive Review. Curr Pain Headache Rep. 2019;23(5):29.

24. Harris P, Loveman E, Clegg A, Easton S, Berry N. Systematic review of cognitive behavioural therapy for the management of headaches and migraines in adults. Br J Pain. 2015;9(4):213-24.

25. Probyn K, Bowers H, Mistry D, Caldwell F, Underwood M, Patel S, et al. Non-pharmacological self-management for people living with migraine or tension-type headache: a systematic review including analysis of intervention components. BMJ Open. 2017;7(8):e016670.

26. Veronese N, Demurtas J, Pesolillo G, Celotto S, Barnini T, Calusi G, et al. Magnesium and health outcomes: an umbrella review of systematic reviews and meta-analyses of observational and intervention studies. Eur J Nutr. 2019.

27. Gelfand AA, Goadsby PJ. The Role of Melatonin in the Treatment of Primary Headache Disorders. Headache. 2016;56(8):1257-66.

28. Di Lorenzo C, Coppola G, Bracaglia M, Di Lenola D, Evangelista M, Sirianni G, et al. Cortical functional correlates of responsiveness to short-lasting preventive intervention with ketogenic diet in migraine: a multimodal evoked potentials study. J Headache Pain. 2016;17:58.

29. Millstine D, Chen CY, Bauer B. Complementary and integrative medicine in the management of headache. Bmj. 2017;357:j1805.

30. Kroll LS, Hammarlund CS, Linde M, Gard G, Jensen RH. The effects of aerobic exercise for persons with migraine and co-existing tension-type headache and neck pain. A randomized, controlled, clinical trial. Cephalalgia. 2018;38(12):1805-16.

31. Rist PM, Hernandez A, Bernstein C, Kowalski M, Osypiuk K, Vining R, et al. The Impact of Spinal Manipulation on Migraine Pain and Disability: A Systematic Review and Meta-Analysis. Headache. 2019;59(4):532-42.

32. Moseley GL. A pain neuromatrix approach to patients with chronic pain. Manual Therapy. 2003;8(3):130-40.

Recent Posts
Follow Us
  • Facebook Classic