Cervicogenic Headache

Author(s): Michael J Mehnert, MD , Mitchell K Freedman, MD, David E Surrey, MD

Originally published:11/11/2011

Last updated:05/05/2016



Cervicogenic headache is pain referred to the head from a source in the cervical spine. Controversy exists over criteria for diagnosis, based on either clinical features, manual examination of vertebral motion segments, or fluoroscopically guided diagnostic blocks.

Primary headaches are those that exist independently from any other medical condition.  The most common examples are tension-type headaches, migraine headaches and cluster headaches.


Cervicogenic headache is a secondary headache that occurs as a result of an underlying medical issue or condition; it is often a sequela of head or neck injury but may also occur in the absence of trauma.1,2 Tumors, fractures, infections, and rheumatoid arthritis of the upper cervical spine may be accepted as causes of headache on an individual basis.

Epidemiology including risk factors and primary prevention

Prevalence is estimated to be up to 4.1% in the general population, and as high as 17.5% among patients with severe headaches. The prevalence is as high as 53% in patients with headache after whiplash. Mean age of patients is 42.9 years; it is four times more prevalent in women.1,2


The first 3 cervical spinal nerves and their rami are the primary peripheral nerve structures that can refer pain to the head.

  • The ventral ramus of the C1 spinal nerve innervates the short muscles of the suboccipital triangle and the atlanto-occipital joint.
  • The C1 recurrent meningeal branch joins C2 and C3 to innervate the medial atlantoaxial joint and the dura mater of the upper cervical spinal cord.
  • The C1, C2, and C3 sinuvertebral branches innervate the dura mater over the clivus in the posterior cranial fossa.
  • The ventral ramus of the C2 spinal nerve innervates the sternocleidomastoid and the trapezius as well as the lateral atlantoaxial joint.
  • The dorsal ramus of C2 innervates the splenius capitis and semispinalis capitis, and its medial branch innervates the occipital area (greater occipital nerve).
  • The C3 ventral ramus innervates the prevertebral musculature.
  • The C3 dorsal ramus (lesser occipital nerve) innervates the posterior cervical musculature, splenius capitis, cervicis, longissimus capitis, semispinalis cervicis, and multifidus and its superficial medial branch innervates the C2-3 zygapophyseal joint (third occipital nerve).
  • The C3 sinuvertebral branch innervates the C2-3 intervertebral disc.
  • Trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibers in the descending tract of the trigeminal nerve (trigeminal nucleus caudalis) are believed to interact with sensory fibers from the upper cervical roots. The functional convergence of sensorimotor fibers in the spinal accessory nerve (cranial nerve 11) and upper cervical nerve roots converge with the trigeminal sensory descending tracts, allowing the bidirectional referral of painful sensations between the neck and trigeminal sensory receptive fields of the face and head.
    • The C2-3 zygapophyseal joint is responsible for 70% of cervicogenic headaches; the atlantoaxial joint, C2-3 zygapophyseal joint and the C3-4 zygapophyseal joint are also common pain generators.2,3

Specific secondary or associated conditions and complications

  • Differential diagnosis includes Arnold-Chiari malformation, cervical spondylosis, herniated intervertebral disc, spinal nerve compression, (of the upper cervical nerve roots), neoplastic disease (lymphoma, ossesous tumor, astrocytoma, ependymomas, malignant gliomas, arteriovenous malformation (AVM)) and vertebral or internal carotid artery dissection.4,5.
  • Migraine headaches will be present in 16% of adults 18 and older in the United States, including patients with cervicogenic headache; conversely, migraine headaches will often have cervical component of pain.6,7
  • Associated conditions may include rheumatoid arthritis, cervical DJD, myofascial pain or other primary headaches.8



  • 2 definitions persist. The Cervicogenic Headache International Study Group (CHISG) and International Classification of Headache Disorders (ICHD-3)
  • The former allows for:
    • Unilateral, non-throbbing, non-lancinating head pain with variable severity or duration, aggravated by head movements or sustained awkward head position without side shifting is typical. Pain radiates from occipital to frontal regions and may include ipsilateral neck, shoulder or arm pain.2,9
  • Red flag warnings include sudden onset of severe headache, which raises question of a subarachnoid hemorrhage, a mass or an AVM. Pain worsening with Valsalva maneuver raises question of mass or subarachnoid lesion. Worsening headache is worrisome for mass, subdural lesion or medication overuse and rebound. Headache with systemic illness is worrisome for infection, arteritis or collagen vascular disease.
  • Other characteristic symptoms by history:
    • No change in symptoms with exercise, food/diet.
    • Absent prodrome of headache or aura.
    • Worsens with ipsilateral neck flexion/lateral rotation.
    • Symptoms radiate to the posterior upper shoulder/lateral shoulder/neck/occiput.

Physical examination

  • Patients may have restricted and or painful cervical range of motion along with tenderness to palpation.9
  • Focal neurologic findings may suggest mass lesions, AVM, and collagen vascular disease.
  • Vesicular rash may be seen with herpes zoster.
  • Papilledema should raise concern over pseudotumor, encephalitis, meningitis or mass.

Functional assessment

Historical review of activities of daily living (ADLs), mobility, vocation, recreation and psychosocial function is recommended.


Cervical x-rays, magnetic resonance imaging (MRI), and computed tomography (CT) may be utilized to evaluate for other causes of headache. X-ray and CT are the best imaging tools for facet DJD analysis; MRI is a better modality to evaluate soft tissue pathology.

Supplemental assessment tools

Whether the diagnosis of cervicogenic headache can be made on a clinical basis or requires the use of fluoroscopically guided diagnostic blocks is a matter of contention.10

Diagnostic criteria developed by the International Headache Society8 are:

  • Pain, referred from a source in the neck and perceived by the patient in the region of the head and/or face.
  • Clinical, laboratory or imaging evidence of a disorder or lesion within the cervical spine or soft tissues of the neck known to be, or generally accepted as, a valid cause of headache.
  • Evidence that the pain can be attributed to the neck disorder or lesion, based on at least one of the following findings.
    • Demonstration of clinical signs that implicate a source of pain in the neck.
    • Improvement in symptoms of headache following diagnostic blockade of a cervical structure or its nerve supply using placebo or other adequate controls. Abolition of headache may be considered ideal, although from a practical perspective 50-80% of pain relief may be more reasonable.11
  • Pain that resolves within 3 months after successful treatment of the causative disorder or lesion.

Diagnostic injections to the atlantoaxial joint, C2-3 and C3-4 zygapophyseal joints, C2 and C3 spinal nerves and possibly the greater and lesser occipital nerves may identify the pain generator:

  • Anesthetic block of the third occipital nerve where it crosses the joint is performed to evaluate the C2-3 zygapophyseal joint.
  • C3-4 zygapophyseal joint is evaluated by blocking the medial branches of C3 and C4.Abolition of headache means complete relief of headache, indicated by a score of zero on a visual analogue scale (VAS).2 Acceptable relief after diagnostic injection can also be defined by greater than 90% reduction in pain to a level of <5 on a 100-point VAS.8


At different disease stages

New onset/acute management should include

  • stretching with postural exercises short of pain
  • ergonomic positioning at home and in the work place
  • modalities including electrical stimulation, heat, and ice
  • medications including nonsteroidal anti-inflammatory drugs (NSAIDs), analgesics and muscle relaxants
  • trigger point injections with lidocaine or dry needle

Subacute management should include

  • advancement of exercise program with stretching and strengthening
  • cervical traction
  • manipulation
  • myofascial release therapy
  • medications as above and, additionally, tricyclic antidepressants and neuron membrane stabilizers
  • trigger point injections with lidocaine
  • Injections with local anesthetic and/or steroid to the atlanto-occipital and lateral atlantoaxial joints, C2-3 and C3-4 zygapophyseal joints, and greater and lesser occipital nerves may provide short term relief. If patients do not respond to these injections, the diagnosis of cervicogenic headache is unlikely.
  • Radiofrequency neurolysis of the third occipital nerve, greater occipital nerve and the medial branches of the dorsal rami corresponding to the painful zygapophyseal joint mayprovide several months of headache reduction1-3.
  • Radiofrequency neurotomy can regulate the physical and psychological features of chronic whiplash.12

Chronic management may include:

  • Complementary interventions such as acupuncture, biofeedback and relaxation techniques, and psychological cognitive strategies for pain management
  • Exercise, medication, therapeutic injections, and surgical strategies defined as above under subacute management
  • Surgical decompression of vascular and ligamentous structures compressing the second cervical root by may have some success
  • Osteoarthritis of atlantoaxial joint may be treated with a fusion.
  • Upper cervical intervertebral disc pathology can be treated with a C1-C2 transarticular screw fixation and Gallie type fusion.
  • One-third of surgically treated patients continue to suffer from cervicogenic headache after surgery.13-15 Outcomes are improved, however, if anterior cervical decompression and fusion is performed on patients that have headaches associated with cervical stenosis.16
  • peripheral nerve stimulation

Coordination of care

Coordinated practice: physiatrist or other primary physician in combination with neurologist, physiotherapist, cognitive behavioral therapist, social worker, interventionalist and, potentially, a surgeon.

Emerging/unique Interventions


  • Headache Impact Test and Headache Impact Test-6 measure the impact of migraine headache on social function, pain, emotional distress and well-being, cognitive function and vitality. Please note that this is a metric directed at a primary headache, as opposed to a secondary headache disorder (cervicogenic headache).
  • Migraine questionnaires include the Headache Impact Questionnaire, Headache Disability Inventory, Migraine Disability Assessment Questionnaire and Migraine Specific Questionnaire.
  • The Migraine Work and Productivity Loss Questionnaire evaluates the impact of migraine and treatment on paid work.
  • Adaptation of Migraine-Treatment Optimization Questionnaires (MTOQ-5 and 15) for cervicogenic headache evaluate function and quality of life.
  • The Neck Disability Index(NDI), Short Form (SF)-12 and SF-36 are questionnaires that might be adapted to evaluate cervicogenic headache.17,18
    1. The NDI is a self reported 10 item questionnaire that is designed to reflect how debilitating a patient’s neck pain is. Scores are out of 100, where the higher the score, the higher a patient’s perceived disability due to their neck pain.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  • Perform thorough history and physical examination to conclude that headache arises from the cervical spine.
  • Confirmatory blocks are recommended.10
  • Physio-therapeutic and medication interventions are the first steps in treatment followed by injection options and then potentially surgical intervention.


In order to identify true cases of cervicogenic headache, diagnostic blocks should be performed.  The anatomical areas that are often blocked using local anesthetic include:

  • The atlanto-axial joint
  • 3rd occipital nerve at the zygapophyseal joint joint of C2-C3
  • Medial branch block of the C3 and C4 dorsal rami.10.19-20

If diagnostic blocks are effective, long term options such as a  radiofrequency ablation can be attempted.21

Greater occipital nerve blocks are a poor treatment for headaches that are cervicogenic in origin due to the distal innervation to occipital regions and the scalp makes that will not modulate the true etiology of pain.

Other new technies involve using biological agents such as infliximab, a monoclonal anti-body against TNF-α.  This has been shown to lower cervicogenic pain (in inflammatory cervicogenic headache) scores as well as decrease analgesic use.22.  A longer observation period and more trials need to be done to extrapolate these data to non-inflammatory cervicogenic headache.


Gaps in the evidence-based knowledge

Controversies persist about the specificity and sensitivity of diagnostic criteria for cervicogenic headache.

Research is needed to evaluate efficacy of specific interventions such as surgery, injections (lidocaine and steroid), radiofrequency procedures, therapeutics and medication management. Gabapentin has been shown to reduce the number of headache occurrences per month, but further research is still required.22 Pregabalin has also been shown to decrease the number/quantitiy of headaches.23  Botox may be effective therapy, but clinical trials have not shown a significant difference compared to placebo.24

The lack of definitive treatment modalities suggests that the knowledge gap may be due to poor/incomplete diagnosis.


  1. Biondi, D. Cervicogenic headache: A review of diagnostic and treatment strategies. JAm Osteopath Assoc. 2005;105(4):16-22.
  2. Bogduk N, Govind J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests and treatment. Lancet Neurol. 2009;8:959-968.
  3. Bogduk N. Cervicogenic headache: anatomic basis and pathophysiologic mechanisms Current Pain Headache Rep. 2001;5:382-386.
  4. Biondi, D. Cervicogenic headache: A review of diagnostic and treatment strategies. JAm Osteopath Assoc. 2005;105(4):16-22
  5. 5.Delfini, R., et al. “Symptomatic cervicogenic headache.” Clinical and experimental rheumatology 18.2; SUPP/19 (2000): S-29.
  6. Schwerzmann, M., et al. “Prevalence and size of directly detected patent foramen ovale in migraine with aura.” Neurology 65.9 (2005): 1415-1418.
  7. Smitherman, Todd A., et al. “The prevalence, impact, and treatment of migraine and severe headaches in the United States: a review of statistics from national surveillance studies.” Headache: The Journal of Head and Face Pain 53.3 (2013): 427-436.
  8. International Headache Society (IHS). The International Classification of Headache Disorders. 2nd ed. (IHS Classification ICHD-2). November 2, 2001. Retrieved March 27, 2011. his Classification website: http://ihs-classification.org/en/. Accessed June 1, 2011.
  9. Sjaastad O, Frederiksen T, Pfaffenrath V, The Cervicogenic Headache International Study Group. Cervicogenic headache: diagnostic criteria. Headache. 1998;38:442-445.
  10. Mehnert, MJ., Freedman MK.  “Update on the role of z-joint injection and radiofrequency neurotomy for cervicogenic headache.” PM&R. 2013 Mar;5(3):221-7.
  11. Frese, A., and S. Evers. “Biological markers of cervicogenic headache.”Cephalalgia 28.s1 (2008): 21-23.
  12. Smith, Ashley Dean, et al. “Modulation of cervical facet joint nociception and pain attenuates physical and psychological features of chronic whiplash: a prospective study.” PM&R (2015).
  13. Joseph B, Kumar B. Gallie’s fusion for atlantoaxial arthrosis with occipial neuralgia. Spine. 1994;19:454.
  14. Pikus H, Phillips J. Characteristics of patients successfully treated for cervicogenic headache by surgical decompression of the second cervical root. Headache. 1995;35:621.
  15. Schaeren S, Jeanneret B. Atlantoaxial osteoarthritis: case series and review of the literature. European Spine J. 2005;14:5.
  16. Liu, Hong, et al. “Treatment of Cervicogenic Headache Concurrent with Cervical Stenosis by Anterior Cervical Decompression and Fusion.” Journal of Spinal Disorders & Techniques (2015).
  17. De Diego EV, Lanteri-Minet M. Recognition and management of migraine in primary care: influence of functional impact measured by the headache impact test. Cephalalgia. 2004;25:184-190.
  18. Lipton R, Kolodner K, Bigal, M, Valade D, Lainez M, Pascual J, et al. Validity and reliability of the Migraine-Treatment Optimization Questionnaire. Cephalalgia. 2009; 29(7):751-9.
  19. Bogduk, Nikolai, and Jayantilal Govind. “Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment.” The Lancet Neurology 8.10 (2009): 959-968.
  20. Aprill, C., M. J. Axinn, and N. Bogduk. “Occipital headaches stemming from the lateral atlanto‐axial (C1–2) joint.” Cephalalgia 22.1 (2002): 15-22.
  21. Asopa, Amit. “Systematic review of radiofrequency ablation and pulsed radiofrequency for management of cervicogenic headache.” Pain physician18 (2015): 109-130.
  22. Martelletti, Paolo. “Inflammatory mechanisms in cervicogenic headache: An integrative view.” Current pain and headache reports 6.4 (2002): 315-319.
  23. Boudreau GP, Marchand L. Pregabalin for the management of cervicogenic headache: a double blind study. Canadian Journal of Neurological Sciences. 2014 Sep;41(5):603-10.
  24. Linde M, Hagen K, Salvesen O, Bruvik Gravdahl G, Helde G, Stovner LJ. Onabotulinum toxin A treatment of cervicogenic headache: a randomized double blind, placebo-controlled crossover study. Cephalagia. 31.7 (2011): 797-807.

Original Version of the Topic:

Ake Evans, MD, Mitchell Freedman, MD, Linqiu Zhou, MD. Cervicogenic Headache. Publication Date: 2011/11/11.

Author Disclosure

Michael J Mehnert, MD
Nothing to Disclose

Mitchell K Freedman, MD
Nothing to Disclose

David E Surrey, MD
Nothing to Disclose

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