The following information provides the interested reader with citations from the medical literature that support the neck-headache connection indicated by the statements in colored font below. Click on green statements for discussion and list of referenced medical articles.
In what is one of the most thoughtful and systematic reviews of the anatomy and physiology of headaches, Dr. Nikolai Bogduk not only elegantly summarized what was known when he published in 19951, but he also provided a framework that allowed for the incorporation of additional knowledge of headache causality as it became available. He asserted that any structure that provides nociceptive input to the trigeminocervical nucleus (TCN) is a potential source of head and face pain, including nociceptive afferents from the trigeminal (V), facial (VII), glossopharyngeal (VIV), and vagus (VX) nerves, as well as the C1-3 spinal nerves, all of which ramify in the TCN.
Within this framework, and with respect to cervical causes of head and face pain, Bogduk outlined evidence for various upper cervical structures (joints, ligaments, discs, muscles, dura mater of the spinal cord) that are known to provide afferent nociceptive input to the TCN, and thereby cause head and face pain. It is now commonly accepted that upper cervical structures can cause headaches2,3.
1. Bogduk, N. Anatomy and physiology of headache. Biomed & pharmacother. 1995;49,435-445.
2. Bartsch, T., Goadsby, P.J. Anatomy and physiology of pain referral patterns in primary and cervicogenic headache disorders. Headache Currents. 2005;2(2), 42-48.
3. Cooper, G., Baily, B., Bogduk, N. Cervical Zygapophysial Joint Pain Maps. Pain Medicine. 2007;8(4), 344-353.
Referred pain is pain that is felt at a location in the body other than the site of origin of the painful stimulus. Knee pain referred from lumbar problems is one example. Left arm pain referred from myocardial ischemia is another. With referred pain, the site of origin of the painful stimulus is not itself always symptomatic. Consequently, the person with knee pain referred from lumbar problems does not necessarily have back pain.
Physicians are familiar with cervical radiculopathy, in which pain and/or sensorimotor deficits are created as a result of compression of cervical nerve roots. And, they are equally aware, as stated in a review of cervical radiculopathy by Caridi, that cervical radiculopathy may or may not be associated with neck pain1.
Caridi documents the fact that in rheumatoid arthritis, patients can experience atlanto-axial settling, which can produce C2 radicular pain that shows up as eye pain, ear pain, and/or headache1. We consider this an example of neck-generated nerve irritation that is referred north of the neck (i.e. into the head and face). Neck-generated nerve irritation that is referred south of the neck can cause symptoms (pain, numbness, tingling, heaviness, weakness) in the trapezius, shoulder, upper arm, forearm and/or hand.
In the same way that physicians are not led astray by lack of neck pain when diagnosing cervical radiculopathy that manifests as arm pain, we should not be led astray by lack of neck pain when considering cervical origins of head and face pain.
1. Caridi, J., Pumberger M., Hughes, A. Cervical Radiculopathy: A review. HSSJ. 2011; 7:265-272.
It has been accepted for many years that the upper cervical (C1-3) spine can cause headaches1,2. There are nocioceptive afferents from C1, C2 and C3 that converge in the trigeminal cervical nucleus3. Different mapping studies have shown that these convergences refer pain from facet joints and intervertebral discs into the head and face3,4. Additionally, diagnosis of cervicogenic headaches can be accomplished with facet joint blocks at C2-3 and C3-43, and with manual diagnosis including reproduction of head pain with palpation of upper cervical structures5,6,7.
1. Bartsch, T., Goadsby, P.J. Anatomy and physiology of pain referral patterns in primary and cervicogenic headache disorders. Headache Currents. 2005;2(2), 42-48.
2. Cooper, G., Baily, B., Bogduk, N. Cervical Zygapophysial Joint Pain Maps. Pain Medicine. 2007;8(4), 344-353.
3. Bogduk, N., Govind, J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. Lancet Neurol. 2009;8: 959-68.
4. Cooper, G., Baily, B., Bogduk, N. Cervical Zygapophysial Joint Pain Maps. Pain Medicine. 2007;8(4), 344-353.
5. Rana, M. Managing and treating headache of cervicogenic origin. Med Clin N Am. 2013; 97:267-280.
6. Biondi, D. Cervicogenic headache: A review of diagnostic and treatment strategies. JAOA Supplement 2. 2005; 105(4).
7. Howard, P.D., et al. Manual examination in the diagnosis of cervicogenic headache: a systematic literature review. J Man Manip Ther. 2015; 4(23): 210-218.
Less familiar to clinicians are lower cervical causes of headaches. There are several lines of clinical evidence that lower cervical structures are implicated in the generation of head and face pain. There is also new anatomical evidence which shows that lower cervical structures are capable of providing nociceptive input to the TCN, which would, in turn, be consistent with Bogduk’s framework for understanding headache causality.
Persson et al. performed a prospective study with selective nerve root blocks in 275 patients with cervical radiculopathy1. 161 of these patients reported that they also had daily or recurrent headaches that were most often unilateral and on the same side as the radiculopathy. MRI studies were obtained, which documented nerve root compression on the same side as the brachialgia, and selective nerve root blocks were used to further confirm the MRI documented nerve root compression as the cause of the patients’ symptoms. After selective nerve root blocks, 59% of the patients with headaches reported a 50% or greater reduction of headache intensity, and of those, 69% reported total headache relief. This temporary reduction in headache intensity corresponded to the temporary reduction in neck, shoulder and arm pain produced by the nerve block. The authors concluded that nerve root compression in the lower cervical spine can cause headaches.
Deiner et al. (2007)2 were interested in investigating the relationship between lower cervical disc prolapse (below C4) and cervicogenic headaches. Their prospective, placebo controlled study demonstrated an association of lower cervical disc prolapse with cervicogenic headaches: headaches and neck pain improved or resolved in 80% of patients following surgery for the prolapsed cervical disc. This finding was documented at 1 week and 3 months post-surgery. The authors concluded that pain afferents arising from lower cervical nerve roots can be relayed to the trigeminocervical nucleus. In addition, there are case reports in which surgical relief of nerve root lesions below C4 have resulted in improvement in cervicogenic headaches3,4,5.
Jansen6 reported post cervical discectomy results on 60 patients with severe unilateral (n=32) or bilateral (n=28) headaches that were unresponsive to other treatment approaches. These patients met diagnostic criteria for cervicogenic headache as established by the Cervicogenic Headache International Study Group guidelines. The levels mainly operated were C4-5, C5-6 and C5-7. The percent of patients who experienced a 50% or greater improvement was 63% for the unilateral headache group, and 64% for the bilateral headache group. Mean observation time was 19.8 months for the unilateral group, and 25.5 months for the bilateral headache group. These study results demonstrate relief of headache with a lower cervical intervention, in this case discectomy.
Schrot et al.7 did a post hoc analysis of an artificial disc trial involving 260 patients who underwent single level arthroplasty or arthrodesis. Headache relief was analyzed after the discectomy. Data on headache pain were taken from the Neck Disability Index, so specific headache diagnoses were not available. The authors hypothesized that if headaches were caused by upper cervical pathology, more headache relief would be expected from surgery performed at upper cervical levels. Their analysis did not support this hypothesis. In other words, headache relief was unaffected by cervical level operated. And interestingly, of the 260 patients studied, 240 or 93% of their patients had their procedures done at lower cervical levels (C5-6, C6-7).
1. Persson, L., Carlsson, J., Anderberg, L. Headache in patients with cervical radiculopathy: a prospective study with selective nerve root blocks in 275 patients. Eur Spine J. 2007;16, 953-959.
2. Diener, H.C., Kaminski, M., Stappert, G., Stolke, D., Schoch, B. Lower cervical disc prolapse may cause cervicogenic headache: prospective study in patients undergoing surgery. Cephalgia. 2007;27, 1050-1054.
3. Michler, R., Bovim, G., Sjaastad, O. Disorders in the lower cervical spine. A cause of unilateral headache? [Case report]. Headache. 1991; 31, 550-551.
4. Fredriksen, T.A., Salvesen, R., Stolt-Nielsen, A., Sjaastad, O. Cervicogenic headache: long-term postoperative follow-up. [Case report]. Cephalgia. 1999;19, 897-900.
5. Kawabori, M., Hida, K., Yano, S., Iwasaki Y. Cervicogenic headache caused by lower cervical spondylosis. No Shinkei Geka. 2009;37(5):491-5.
6. Jansen, J. Surgical treatment of cervicogenic headache. Cephalalgia. 2008; 28(1):41-44.
7. Schrot, R, Mathew, J, Li, Y, et. al. Headache relief after anterior cervical discectomy: post hoc analysis of a randomized investigational device exemption trail. J Neurosurg Spine. 2014; 21: 217-222.
The answer to the question posed in this subsection (i.e. can lower neck problems cause headaches) would appear to be yes, based on the studies summarized above, which document headache improvement with lower cervical interventions. What do we know about cervical anatomy that might elucidate and support the documented clinical observations? Chua et al. (2012)1 delineate the anatomy of the trigeminocervical nucleus and how lower cervical structures may communicate with the TCN via sensory input of spinal terminals into the spinal cord. Because the small sensory fibers have collateral branches that can ascend or descend in Lissauer’s tract for up to 3 segments before they synapse in the dorsal horn laminae, the authors assert that along with the upper 3 cervical segments, lower cervical conditions can contribute to the development of cervicogenic headaches.
This anatomical explanation provides corroboration for the clinically documented lower cervical causes of headaches, and it also fits nicely into Bogduk’s framework for how to think about causes of headaches, in which any structure that provides nociceptive input to the trigeminocervical nucleus is a potential source of head and face pain2. Given the fact that upper cervical structures, including joints, ligaments, discs, muscles and the dura mater of the spinal cord are known to provide afferent nociceptive input to the TCN, one cannot but question if the same lower cervical structures are also capable of producing head and face pain.
1. Chua, N., Suijlekom, H., Wilder-smith, O., Vissers, K. Understanding cervicogenic headache. Anesth Pain. 2012;2(1), 3-4.
2. Bogduk, N. Anatomy and physiology of headache. Biomed & pharmacother. 1995;49,435-445.
In his 2009 publication, Bogduk defines cervicogenic headaches as “pain referred to the head from a source in the cervical spine”1. The International Headache Society (IHS) and Cervicogenic Headache International Study Group (CHISG) differ in their definitions of cervicogenic headache. The IHS classifies cervicogenic headaches as “a headache caused by a disorder of the cervical spine and its component bony, disc and/or soft tissue elements, usually but not invariably accompanied by neck pain”2. The CHISG adds to this definition by including unilaterality of head pain, moderate-severe pain, lack of effect of indomethacin, ergotamine and sumatriptan, and occasionally nausea, phonophobia, photophobia, dizziness, ipsilateral blurred vision, difficulties swallowing and ipsilateral edema3,4.
1.Bogduk, N., Govind, J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. Lancet Neurol. 2009; 8:959-68.
2. International Headache Society. The international classification of headache disorders, 3rd edition. Cephalagia. 2018;38(1):1-211.
3. Rana, M. Managing and treating headache of cervicogenic origin. Med Clin N Am. 2013; 97:267-280.
4. Sjaastad, O., Fredriksen, T.A., Pfaffenrath, V. Cervicogenic headache: diagnostic criteria. Headache. 1998; 30:442-445.
The International Headache Society has defined a migraine as a recurrent headache that is typically (though not always) unilateral, pulsating, moderate to severe in intensity, commonly aggravated by physical activity and is accompanied by nausea and/or photophobia and phonophobia. These attacks occur over a period of 4-72 hours1.
Migraines are the third most common disease worldwide and are the sixth leading cause of disability2,3,4,5. Migraines significantly impact an individual’s activities of daily living (work, housework, school and social activities)1. In the U.S. it has been shown that migraines can cause a reduction in work/school productivity by more than 50%6. Not only do migraineurs experience a decrease in productivity due to actual missed days of work or school, but they are also less productive when they come to work during a migraine attack2.
In addition to decreasing productivity, migraines are a great financial burden for many sufferers. The typical migraineur has had multiple doctor appointments, tests, and trials of different medications before finding treatment that is even moderately effective. In a 2018 study conducted by Bonafede et al., it was found that migraine sufferers had a mean healthcare cost of $8924 more per year than a non-migraine sufferer, with approximately $6575 accounting for direct costs (doctor visits, medications, etc) and $2349 for indirect costs (missing work, decrease in productivity)5.
In addition to acknowledging the cost of migraine medications, it may be useful to comment on the reported effectiveness of some of the most common medication treatments used for migraine. In the evidence-based guidelines for pharmacologic treatment for episodic migraine prevention in adults, responder rates (i.e. the percentage of patients who experience a ≥50% reduction in migraines per month as a result of treatment) were reported as 26% for aspirin, 45.2% for metoprolol, 46% for lamotrigine and 63% for topiramate7. It is unclear whether these responder rates represent number of migraine days per month, or migraine attacks per month.
For studies in which responder rates for migraine preventive treatments are reported as a 50% or greater reduction in migraines days per month, we have the following comparisons. Divalproex had a 49% responder rate within the first 90 days of treatment8, sodium valproate had a 50% responder rate9, fremanezumab had a 61% responder rate in patients with episodic migraine10, galcanezumab had a 62% responder rate in patients with episodic migraine11,12, and a controlled trial of erenumab for episodic migraine reported a 45% responder rate for 50% or greater reduction in mean migraine days per month13. In the migraine research community, these are considered to be statistically significant reductions in migraine frequency.
In a retrospective case study conducted at the Headache Institute of Texas, we report a responder rate of 62.5% for a therapeutic neck exercise approach to migraine treatment14. In addition to suggesting that this approach might be as effective as, or better than other migraine preventive treatments, a therapeutic neck exercise treatment approach for migraines avoids issues of medication side effects and repeated medication costs.
1. International Headache Society. The international classification of headache disorders, 3rd edition. Cephalagia. 2018;38(1):1-211.
2. Agosti, R. Migraine burden of disease: From the patient’s experience to a socio-economic view. Headache. 2018;58:17-32.
3. Steiner TJ, Stovner, LJ, Vos, T. GBD 2015: Migraine is the third cause of disability in under 50s. J Headache Pain. 2016;17:104.
4. Miles, O. (2018, August). Migraine Basics. Retrieved from https://migraine.com/migraine-basics/.
5. Bonafede, M., Sapra, S., Shah, N., et al. Costs associated with migraine in the United States. Headache. [published online February 15, 2018]. Headache. doi: 10.1111/head.13275.
6. Munakata, J., Hazard, E., Serrano, D., et. al. Economic burden of transformed migraine: Results from the American Migraine Prevalence and Prevention (AMPP) study. Headache. 2009; 49:498-508.
7. Silberstein, S.D., Holland, S., Freitag, F., Dodick, D.W., Argoff, C., Ashman, E. Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults. Neurology. 2012; 78, 1337-1345.
8. Silberstein, S.D., Collis, S.D., Safety of Divalproex sodium in migraine prophylaxis: an open-label, long-term study. Headache. 1999; 39, 633-643.
9. Jensen, R., Brinch, T., Olesen, J. Sodium valproate has a prophylactic effect in migraine without aura: a triple-blind, placebo-controlled crossover study. Neurology. 1994; 44, 647-651.
10. Hoy, SM. Fremanezumab: first global approval. Drugs. 2018; 78:1829-1834.
11. Stauffer VL, Dodick DW, Zhang Q, et al. Evaluation of galcanezumab for the prevention of episodic migraine: the EVOLVE-1 randomized clinical trial. JAMA Neurol. 2018:75(9):1080-1088.
12. Skljarevski V, Matharu M, Millen BA, et al. Efficacy and safety of galcanezumab for the prevention of episodic migraine: results of the EVOLVE-2 Phase 3 randomized controlled clinical trial. Cephalalgia. 2018;38(8):1442-1454
13. Goadsby, PJ, Reuter, I, et al. A controlled trial of erenumab for episodic migraine. B Engl J Med. 2017; 377: 2123-2132.
14. Holt, N., Kurka, C. Migraine frequency and severity decrease in response to a therapeutic neck exercise program in a case series of migraineurs [abstract]. In: Program Abstracts: 60th Annual Scientific Meeting American Headache Society; 2018; June 28 - July 1;San Francisco, CA. Headache; 2018:58(S2). Abstract nr PS66.
Review of IHS and CHISG diagnostic criteria for CGHA1,2 and of the IHS criteria for migraine without aura1, as well as review of papers of experts in the field3-7, provides the following tabular overview of comparative characteristic for CGHA and Migraine.
|Comparison of Characteristics of Cervicogenic Headache and Migraine|
|Gender||Mostly women||Predominantly women|
|Lateralization||Unilateral, no sideshift2,N5 (may be bilateral)||Unilateralc1 with sideshift or bilateral|
|Location||Occipital to frontoparietal, orbital, temporal||Frontal, periorbital, temporal|
|Frequency||Chronic, episodic||Chronic, episodic|
|Duration||1 hour - weeks (variable)||4-72 hoursB (variable)|
|Pain Characteristics||Non-throbbing |
Pain starts posteriorly and spreads anteriorly2,N5
Pain is worsened by activityc4
|Associated Symptoms||Neck pain, nausea, photophobia, phonophobia, dizziness, ipsilateral blurred vision, ipsilateral periocular edema, difficulty swallowing||Neck pain, nauseaD1, vomitingD1, photophobiaD2, phonophobiaD2, dizziness, vision changes|
|Medication Response||Minimal response to indomethacin, ergotamine, or sumatriptan||Effective response (depending on severity of headache, and on timing of dose) to NSAIDS, ergot derivatives, and triptans.|
|Triggers||Awkward neck movements/positioning, external pressure over cervical or occipital region||Fasting, menstrual cycle changes,stress, low barometric pressure, sleep disturbance, alcohol, other foods|
|Symptoms/Signs of Neck Involvement||Headache provoked by unphysiological neck positions9,C3,N5|
Headache provoked by pressure over cervical or occipital region10,N5
Decreased neck ROM11,C3
Diffuse shoulder pain1
Diffuse arm pain2
Headache is abolished with diagnostic blockade of targeted cervical structures3,C4
Headache developed at time of onset of cervical disorder or radiological lesion known to be able to cause headacheC1
Headache improved or resolved with improvement or resolution of cervical disorder or radiological lesion known to be able to cause headacheC2
|Decreased neck ROM12-14|
1-3,9-11 CHISG Diagnostic criteria for cervicogenic headache
C1-4, N5(Note 5) IHS Diagnostic criteria for cervicogenic headache
B, c1-4,D1-2 IHS Diagnostic criteria for migraine without aura
12-14 Articles documenting decreased neck ROM in migraineurs
15-21 Articles documenting neck pain in migraineurs
Perhaps the most striking feature of this side-by-side comparison of cervicogenic headache and migraine is the high number of similarities between the 2 diagnoses. This is no doubt the reason for the difficulty reflected in the medical literature when it comes to separating what are thought to be 2 distinct clinical entities.
Because our work at the Headache Institute of Texas establishes a clear link between the neck and migraines, as demonstrated by our ability to reduce migraine frequency and severity with therapeutic neck exercises8, we question whether cervicogenic headaches and migraines do in fact represent 2 distinct clinical entities when it comes to underlying causality. Our 13 years of clinical experience, as well as our retrospective case study, suggest that the neck is the primary causal structure for migraines, as well as for what has been classified as cervicogenic headache.
1. Sjaastad, O, Fredriksen, TA, Pfaffenrath, V. Cervicogenic headache: diagnostic criteria. Headache. 1998; 30:442-445.
2. International Headache Society. The international classification of headache disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211.
3. Bogduk, N., Govind, J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. Lancet Neurol. 2009; 8:959-68.
4. Rana, M. Managing and treating headache of cervicogenic origin. Med Clin N Am/. 2013; 97:267-280.
5. Biondi, D. Cervicogenic headache: A review of diagnostic and treatment strategies. JAOA Supplement 2. 2005; 105(4).
6. Marmura, M.J. Triggers, protectors, and predictors in episodic migraine. Curr Pain Headache Rep. 2018; 22(12):81. https://doi.org/10.1007/s11916-018-0734-0
7. Fredriksen, T., Antonaci, F, Sjaastad, O. Cervicogenic headache: too important to be left un-diagnosed. J. Headache Pain. 2015; 16(6).
8. Holt, N., Kurka, C. Migraine frequency and severity decrease in response to a therapeutic neck exercise program in a case series of migraineurs [abstract]. In: Program Abstracts: 60th Annual Scientific Meeting American Headache Society; 2018; June 28 - July 1;San Francisco, CA: 58(S2). Abstract nr PS66.
9. Pearce, JM. Cervicogenic headache: an early description. J Neurol Neurosurg Psychiatry. 1995; 58(6):698.
10. Sjaastad, O, Saunte, C, Hovdahl, H. “Cervicogenic” headache. An hypothesis. Cephalalgia. 1983. 3(4):249-256.
11. Sjaastad, O, Fredriksen, TA, Pfaffenrath, V. Cervicogenic headache: diagnostic criteria. Headache. 1990; 30:725-726.
12. Oliveira-Souza Lidaine, A., Florencio, L., et. al. Reduced flexion rotation test in women with chronic and episodic migraine. https://doi.org/10.1016/j.bjpt.2019.01.001
13. Szikszay, TM, Hoenick S, von Korn, V, et. al. Which examination tests detect differences in cervical musculoskeletal impairments in people with migraine? A systematic review and meta-analysis. Phys Ther. 2019; 99(5): 549-569.
14. Bevilaqua-Grossi, Pegoretti, Gonvalves, et. al. Cervical mobility in women with migraine. Headache. 2009. 49(5);726-31.
15. Calhoun, A., Ford, S., Millen, C., Finkel, A., et al. The prevalence of neck pain in migraine. First published 02 September 2010.
16. Bragatto, M., Bevilaqua-Grossi, D., Benatto, M., et. al. Is the presence of neck pain associated with more severe clinical presentation in patients with migraine? A cross-sectional study. Cephalgia. 2019;May 27:333102419854061. doi: 10.1177/0333102419854061
17. Lampl et al. Neck pain in episodic migraine: premonitory symptom or part of the attack? The Journal of Headache and Pain. 2015; 16:80
18. Luedtke et al. Altered muscle activity during rest and during mental or physical activity is not a trait symptom of migraine- a neck muscle EMG study. The Journal of Headache and Pain. 2018; 19:26
19. Ferracini, GN, Chaves, TC, Dach, F, et. al. Analysis of the cranio-cervical curvatures in subjects with migraine with and without neck pain. Physiotherapy. 2017; 103(4): 392-399.
20. Florencio, LL, de Oliveira, IV, Lodovichi, SS, et. al. Cervical muscular endurance performance in women with and without migraine. J Orthop Sports Phys Ther. 2019; 49(5):330-336.
21. Kaniecki RG. Migraine and tension-type headache: an assessment of challenges in diagnosis. Neurology. 2002;58(9 Suppl 16):S15–20.
Of interest is the conclusion of a 2010 prospective, observational cross-sectional study of 113 migraineurs, which demonstrated that neck pain was more commonly associated with migraine than was nausea, one of the defining characteristics of migraine headache1.
In a cross sectional study of 142 patients with migraine, there was a high incidence of neck pain: 99 (69.7%) reported neck pain, and 43 (30%) did not report neck pain. Compared to those who did not report neck pain, those with neck pain had a greater prevalence and severity of cutaneous allodynia, reduced neck mobility, and reduced neck muscle function2.
Women with chronic migraine (n=25), episodic migraine (n=30), and those who were headache-free (n=30) were compared in their ability to perform a test of upper cervical mobility (flexion rotation test) and in a test of global cervical mobility. Both chronic and episodic migraineurs had reduced upper cervical mobility compared to those without headaches3. Those with chronic migraine had a lower global cervical range of motion compared to headache-free women. These results invite further investigation into why migraineurs have differences in neck function that are not documented in those without migraines.
In a 2015 study conducted by Lampl et al, it was found that of their 400+ person cohort, 69% of migraineurs experienced neck pain during their migraine attacks. 78% of this group experienced neck pain during the headache phase of the attack, as opposed to only only experiencing neck pain as a prodromal symptom4. Supporting Lampl’s findings, an EMG study was conducted by Luedtke in 2018 which confirmed that upper trapezius muscle tension during rest periods, mental stress and physical activity was the same in a control group as in a migraine group. These findings suggest that neck pain and neck muscle tension reported by migraineurs is likely a part of the migraine attack, not just a precursor or trigger5.
A cross sectional observational study by Ferracini et al6 demonstrated straightening of cervical lordosis in 50 subjects with migraine compared to 50 matched healthy controls. Migraine subjects also reported a significantly longer history of neck pain, higher intensity neck pain, and higher levels of neck-pain-related disability than controls.
In a cross-sectional, controlled laboratory study by Florencio et al7, women with migraine had reduced neck flexor and extensor muscle endurance compared to controls. During testing, there was no difference between controls and migraineurs in their reports of neck pain. Migraineurs, however, were the only ones to report pain referred to the head during neck muscle endurance testing. The authors concluded that reduced neck muscle function may be associated with migraine.
A metanalysis of migraineurs and healthy controls by Szikszay et al8 identified 3 tests of musculoskeletal impairment that distinguish migraineurs from healthy controls: range of cervical motion, flexion-rotation, and forward head posture in a standing position. The authors conclude that these tests confirm the presence of cervical musculoskeletal impairment in migraineurs, an observation that stimulates further reflection on the relationship between neck dysfunction and migraine headache.
In a study of 144 patients with migraine with or without aura, 75% reported neck pain with their migraines. The neck pain was unilateral in 57% of patients, and 98% of these had neck pain on the same side as their headache. A subset of 30 patients from this study used Sumatriptan or a similar triptan to treat 278 headaches, 231 of which were accompanied by neck pain. The percentage of attacks with a pain-free response 2 hours after dosing was 68% for head pain and 73% for neck pain9.
One of the main consumer support tools for migraines, migraine.com has done several informal polls, as well as a formal survey of migraineurs with 60-75% of participants reporting neck pain either before or during a migraine attack10.
These observations combine to confirm the frequent association of neck pain with migraine, the occurrence of reduced neck muscle function and reduced cervical range of motion in those with migraine, and pharmacological overlap in the treatment response of migraine and neck pain associated with migraine. Such evidence might be seen as challenging the currently held notion of a strictly brain-based neurovascular etiology for migraine, as well as inviting further investigation into the pathophysiological relationship between neck pain, neck dysfunction and migraine.
1. Calhoun, A., Ford, S., Millen, C, et al. The prevalence of neck pain in migraine. Headache. 2010;50:1273-1277.
2. Bragatto, M., Bevilaqua-Grossi, D., Benatto, M., et. al. Is the presence of neck pain associated with more severe clinical presentation in patients with migraine? A cross-sectional study. Cephalgia. 2019;May 27:333102419854061. doi: 10.1177/0333102419854061
3. Oliveira-Souza, A., Florencia, L., Carvalho, G., et. al. Reduced flexion rotation in women with chronic and episodic migraine. Braz J Phys Ther. 2019;Jan 16. pii: S1413-3555(17)30711-6. doi: 10.1016/j.bjpt.2019.01.001.
4. Lampl et al. Neck pain in episodic migraine: premonitory symptom or part of the attack? The Journal of Headache and Pain. 2015; 16:80
5. Luedtke et al. Altered muscle activity during rest and during mental or physical activity is not a trait symptom of migraine- a neck muscle EMG study. The Journal of Headache and Pain. 2018; 19:26
6. Ferracini, GN, Chaves, TC, Dach, F, et. al. Analysis of the cranio-cervical curvatures in subjects with migraine with and without neck pain. Physiotherapy. 2017; 103(4): 392-399.
7. Florencio, LL, de Oliveira, IV, Lodovichi, SS, et. al. Cervical muscular endurance performance in women with and without migraine. J Orthop Sports Phys Ther. 2019; 49(5):330-336.
8. Szikszay, TM, Hoenick S, von Korn, V, et. al. Which examination tests detect differences in cervical musculoskeletal impairments in people with migraine? A systematic review and meta-analysis. Phys Ther. 2019; 99(5): 549-569.
9. Kaniecki RG. Migraine and tension-type headache: an assessment of challenges in diagnosis. Neurology. 2002;58(9 Suppl 16):S15–20.
10. Miles, O. (November 2010). Neck Pain. Retrieved from https://migraine.com/migraine-symptoms/neck-pain/
For most of the 20th century, the pathophysiology of migraine was thought to be due to vascular dysregulation, with vasoconstriction of intracranial vessels leading to aura, and vasodilation resulting in migraine pain. Newer functional imaging studies in the 1980’s and 1990’s prompted a reconsideration of this understanding since the imaging studies showed that decreased cortical blood flow during aura was not sufficient to cause ischemia, and that headache started before vasodilation1.
More recent theories of migraine causation highlight the role that brain neuronal dysfunction plays, with a focus on brain structures, pathways, neuropeptides, neurotransmitters and receptors that can initiate migraine. This includes research into the complex and inter-related ways in which the trigeminovascular system is activated, how cortical spreading depression both produces inflammatory changes in pain-sensitive meningeal vascular structures and modulates the activity of trigeminovascular neurons, and how neuronal sensitization is thought to play a role in migraine headaches.
1. Simmons, J. (March 2012). Pathophysiology of Migraine. Retrieved from https://migraine.com/pro/pathophysiology-of-migraine/
When research clarifies the role of a particular peptide in migraine production, it has the potential to become a therapeutic target. This is the case for CGRP, a protein that acts as a vasodilator, and which is found throughout the body. Of particular interest to migraine research, CGRP is found in the TCN, and at many points throughout the trigeminal pathway, including the dorsal ganglion of the cervical spine1,2. CGRP is believed to contribute to migraine in a peripheral pathway by creating arteriole vasodilation in the meninges, activating meningeal nocioceptors and creating inflammation1,2,3,4. It is also believed that CGRP acts centrally in the TCN, working to increase the amount of neurotransmitters from peripheral afferents, which perpetuates nocioceptive transmission1,3,5.
Anti CGRP migraine treatment options form the basis for the newest class of FDA approved migraine drugs. For patients treated with one of these medications, erenumab, there was a significant decrease in migraine frequency over time. However there was only a 45% responder rate (the percent of treated patients who have a 50% or greater reduction of migraine days per month)6.
The Headache Institute of Texas presented results on the effectiveness of a neck-targeted approach to headache care at the American Headache Society 60th Annual Scientific Meetings in June 2018. This study showed that the percentage of patients who have a 50% or greater reduction in migraine days per month in response to a therapeutic neck exercise program was 62.5%7.
While current thinking has evolved beyond the idea that vascular dysregulation is the cause of migraine, newer theories are still focused on brain-based causal mechanisms for migraine, specifically on brain neuron dysfunction as the underlying cause in migraine pathophysiology. Reflecting this focus is a comment in a recent review of the pathophysiology of migraine which states that therapeutic efforts for migraine prevention are likely to face a large challenge “given that migraine can originate in an unknown number of brain areas, and is associated with generalized functional and structural brain abnormalities”8.
Our clinical work and preliminary research lead us to believe that neck problems are a primary cause of many different kinds of headaches that currently receive different diagnostic labels. We are particularly interested in clarifying mechanisms of neck-generated head and face pain, and in developing a collaborative approach to elucidate more precisely the details of anatomy and physiology that explain the headache improvements we witness as a result of treating our patients’ necks. For example, degenerating intervertebral discs release neuropeptides which induce the expression of peptides that mediate pain, including CGRP2. Is it possible that the CGRP produced in this scenario could result in, or cause, increased levels of CGRP in the trigeminocervical nucleus in the brainstem, and thus become a primary driver for migraine generation? Our study results, which demonstrate the effectiveness of a therapeutic neck exercise program in significantly decreasing migraine frequency and intensity, encourage further investigation into the role of the cervical spine in generating migraines.
1. Dodick, D. A Phase-by-Phase Review of Migraine Pathophysiology. Headache. 2018 58:4-16
2. Garcia, Cosamalon, J., E. Del Valle, M., et. al. Intervertebral disc, sensory nerves and neurotrophins: who is who in discogenic pain? J Anat. 2010; 217, 1-15.
3. Lyengar, S., Ossipov, M., Johnsonk, K. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine. PAIN. 2017 158:543-559.
4. Russo, A. CGRP as a neuropeptide in migraine: lessons from mice. Br J Clin Pharmacol. 2015; 80:3;403-414.
5. Messlinger K, Fischer MJ, Lennerz JK, Neuropeptide effects in the trigeminal system: Pathophysiology and clinical relevance in migraine. Keio J Med. 2011;60:82-89.
6. Goadsby, P.J., Reuter, I., et al. A controlled trial of erenumab for episodic migraine. B Engl J Med. 2017; 377, 2123-2132.
7. Holt, N., Kurka, C. Migraine frequency and severity decrease in response to a therapeutic neck exercise program in a case series of migraineurs [abstract]. In: Program Abstracts: 60th Annual Scientific Meeting American Headache Society; 2018; June 28 - July 1;San Francisco, CA: 58(S2). Abstract nr PS66.
8. Burstein, R., Noseda, R., Borsook, D., Migraine: multiple processes, complex pathophysiology. J. Neuroci. 2015; 35(17):6619-6629.