Migraines: Presentation, Mechanisms, and Management

Migraines remain an important public health issue that can significantly affect one’s daily activities and quality of life. The prevalence of migraines in the US adult population is quite high, affecting 15.3% of individuals. Relative to the general population, the prevalence is higher for those with disabilities (16.4%), aged 18-44 (17.9%), and on low income (19.9%). Additionally, the prevalence in women (20.7%) is much higher than in men (9.7%). Annually, migraines account for 3% of all visits to the emergency department, consistently among the top four or five leading causes.1

Symptomatically, migraines progress through four stages: prodrome, aura, attack, and post-drome. One to two days before a migraine –  i.e. prodrome – subtle changes warn of an upcoming attack, including constipation, mood changes, food cravings, neck stiffness, increased thirst, and frequent yawning. As a migraine progresses, individuals may experience auras, or reversible symptoms of the nervous system that begin gradually and last 20 to 60 minutes. Examples of auras include visual phenomena (e.g. bright spots, shapes, and flashes), vision loss, pins and needles in the arms and legs, facial numbness, difficulty speaking, hearing noises, and uncontrollable jerking movements. During an attack, which can last 4 to 72 hours if untreated, individuals may experience pain on one or both sides of the head, throbbing sensations, sensitivity to light and sound, nausea, and vomiting. After an attack – i.e. post-drome – individuals may feel drained and confused for up to a day.2

Over the past few decades, our understanding of the pathophysiology of migraines has improved considerably. Previously, the vascular theory was the leading explanation for migraines; however, a series of imaging studies demonstrated that vascular changes were neither necessary nor sufficient for attacks.3-4 From vascular theories, researchers moved to neuronal theories involving the peripheral and central nervous systems. Initially, researchers attempted to localize a single structure as the source of migraines; but it is now clear that migraines are a complex brain network disorder with a genetic basis that involves multiple cortical, subcortical, and brainstem regions.4-6

The trigeminovascular system is a key actor and its activation is thought to initiate the cascade of events resulting in migraines due to its direct connection with the diencephalic and brainstem nuclei.7-8  The literature also supports the involvement of the hypothalamus in migraines. For example,several studies demonstrate hypothalamic connections to the thalamus, trigeminovascular system, and brainstem nuclei, supporting the role of the hypothalamus in pain modulation in patients with migraines.9-11 The involvement of the hypothalamus may explain some of the early symptoms of migraines, such as food cravings, mood swings, and yawning. Additionally, the thalamus may play a role in migraines. The thalamus is a nociceptive relay station that conveys information from the dura mater and cutaneous areas to second-order trigeminovascular areas. Several studies report structural and functional thalamic alterations in patients with migraines.12-13 Furthermore, changes in the structure and function of key cortical areas were demonstrated in migraineurs, such as the insular, somatosensory, prefrontal, and cingulate cortex.14 Lastly, a variety of factors may trigger migraines, including hormonal changes in women, alcohol, coffee, stress, sensory stimuli, sleep changes, weather changes, medication, and processed foods.

Chiropractic spinal manipulative therapy (CSMT) is supported by numerous studies as an effective treatment option for migraines. In a randomized controlled trial of 172 patients, Tuchin et al demonstrated that patients receiving CSMT reported a significant improvement in migraine frequency, duration, disability, and medication use. A more recent study by Chaibi et al involved a 52 year old woman suffering from migraines once per month, with pain scored as an 8 out of 10. After CSMT treatment, the patient reported a complete elimination of migraines. At a follow up 6 months later, the patient did not report a single migraine episode during the intervening period.16 Overall, evidence suggests that CSMT can alleviate pain from migraines, making chiropractic care a viable option for individuals suffering from migraines.


1) Burch R, Rizzoli P, Loder E. The prevalence and impact of migraine and severe headache in the United States: figures and trends from government health studies. Headache: The Journal of Head and Face Pain. 2018;58(4):496–505.

2) Mayo Clinic Staff. Migraine. Mayo Foundation for Medical Education and Research. Nov. 2019.

3) Amin FM, Asghar MS, Hougaard A, Hansen AE, Larsen VA, de Koning PJ, Larsson HB, Olesen J, Ashina M. Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study. Lancet Neurol. 2013;12:454–461.

4) Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine—a disorder of sensory processing. Physiol Rev. 2017;97(2):553–622.

5) Charles A. Migraine: a brain state. Curr Opin Neurol. 2013;26:235–239.

6)  Ferrari MD, Klever RR, Terwindt GM, Ayata C, van den Maagdenberg AM. Migraine pathophysiology: lessons from mouse models and human genetics. Lancet Neurol. 2015;14:65–80.

7) Goadsby PJ, Charbit AR, Andreou AP, Akerman S, Holland PR. Neurobiology of migraine. Neuroscience. 2009;161:327–341.

8) Akerman S, Holland PR, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nat Rev Neurosci. 2011;12:570–584.

9)  Kagan R, Kainz V, Burstein R, Noseda R. Hypothalamic and basal ganglia projections to the posterior thalamus: possible role in modulation of migraine headache and photophobia. Neuroscience. 2013;248:359–368.

10) Abdallah K, Artola A, Monconduit L, Dallel R, Luccarini P. Bilateral descending hypothalamic projections to the spinal trigeminal nucleus caudalis in rats. PLoS One. 2013;8:e73022.

11) Robert C, Bourgeais L, Arreto CD, Condes-Lara M, Noseda R, Jay T, Villanueva L. Paraventricular hypothalamic regulation of trigeminovascular mechanisms involved in headaches. J Neurosci. 2013;33:8827–8840.

12) Magon S, May A, Stankewitz A, Goadsby PJ, Tso AR, Ashina M, Amin FM, Seifert CL, Chakravarty MM, Muller J, Sprenger T. Morphological abnormalities of thalamic subnuclei in migraine: a multicenter MRI study at 3 tesla. J Neurosci. 2015;35:13800–13806.

13) Hodkinson DJ, Wilcox SL, Veggeberg R, Noseda R, Burstein R, Borsook D, Becerra L. Increased amplitude of thalamocortical low-frequency oscillations in patients with migraine. J Neurosci. 2016;36:8026–8036.

14) Sprenger T, Borsook D. Migraine changes the brain: neuroimaging makes its mark. Curr Opin Neurol. 2012;25:252–262.

15) Tuchin P, Pollard H, Bonello R. A randomized controlled trial of chiropractic spinal manipulative therapy for migrain. J Manip Physio Therap. 2000;23:91-95.

16) Chaibi A, Tuchin PJ. Chiropractic spinal manipulative treatment of migraine headache of 40-year duration using Gonstead method: a case study. J Chiropr Med. 2011;10(3):189–193.