Cervicogenic Headache: Always the Bridesmaid, Never the Bride

Introduction:

This article summarises the medical model’s contemporary perspective of Cervicogenic Headache (CGH) and discusses some factors contributing to the reported low prevalence of CGH.  

Cervicogenic Headache, a nuanced subset within the headache spectrum, is surprisingly reported less frequently, ranging from 0.1–4.1 per cent depending on which CGH diagnostic criteria are used^1-4 (at this point, manual therapists are mortified, recognising that it is more likely approximating 80%⁵) than their counterparts Tension Headache (46%)⁶ and Migraine (30%).⁷ (Note: These figures generally reflect the literature but will vary depending on gender and age groups.) Despite CGHs profound impact on quality of life, the medical model’s comprehension of CGH remains somewhat equivocal.

Defining Cervicogenic Headache:

Headache conditions are categorised as either Primary Headache or Secondary Headache.⁸  Primary Headaches, comprising Tension Headaches, Migraines and Trigeminal Autonomic Cephalalgias (TACs), of which Cluster Headache is the most common, are headache conditions in which the pathophysiology is unknown; secondary Headaches are those headaches secondary to a recognised accepted pathophysiology, medical condition or disease process known to cause headache.  Secondary Headache includes tumours, cranial vasculitis, and intracranial hypotension, whereas other secondary headaches are secondary to a recognised lesion, for instance, temporomandibular dysfunction or a cervical lesion – CGH.

The genesis of CGH originates a disorder or dysfunction residing in the top three spinal segments, often masquerading as Tension Headache,⁹  Migraine¹⁰ or Cluster Headache.¹¹

Pathophysiology of Cervicogenic Headache:

The pathophysiology of CGH has been demonstrated, recognised and widely accepted.¹² Essentially, trigeminal afferents merge with cervical afferents in the brainstem (the trigemino cervical nucleus – TCN).  This combined information is then relayed to and interpreted in the higher centres.  In CGH, noxious cervical afferents are misinterpreted as trigeminal afferents and head pain is produced. 

Let’s assume that the TCN is a blender and that fresh apple juice (trigeminal afferents) is combined with pear juice (cervical afferents), which is a bit ‘off’. This combined juice is then sent to higher processing centres where the ‘off’ blended juice is blamed on the fresh apple juice (trigeminal afferents), producing head pain.

Therefore, CGH shares a common birthplace with the Primary Headache conditions: Tension Headache and Migraine, i.e., the TCN.¹³  The TCN is a pivotal substrate in the pathophysiology of head pain. It integrates trigeminal afferent information from intracranial blood vessels, dura, orofacial structures, the front of the scalp, and the upper cervical (C1-3) spinal nerves.^12,13 This integration is also crucial in the Primary Headache conditions – Tension Headache, Migraine and Cluster headache.¹³ 

Not surprisingly, diagnosing CGH is challenging.

Diagnostic Challenges:

The rarity in reported cases of CGH can largely be traced back to the obstacles in accurate diagnosis, which involves both patients’ narratives and, fundamentally, the diagnostic criteria established by the medical model.^8,14,15

From a subjective or patient’s perspective, overlapping symptoms with Tension Headache and Migraine often lead to misdiagnoses. Compounding overlapping symptoms is the broad spectrum of symptoms or variability in pain manifestation associated with CGH, adding another layer of complexity to their diagnosis. This variability in pain manifestation, from location and behaviour of the location to intensity and duration, often puzzles both patients and healthcare providers, leading to a potential underestimation in clinical and epidemiological contexts.  This explains why many patients receive multiple diagnoses from different healthcare providers.  It is widely acknowledged that differentiating CGH from a Tension Headache,⁹ Migraine,¹⁰ and Cluster Headache¹¹ can be challenging.

Critical diagnostic criteria of CGH^8,14,15 include i) unilateral side-locked head pain, i.e., always on the same side – never the other, ii) positive response to diagnostic, anaesthetic cervical blocks, iii) manual cervical reproduction of typical head pain, iv) neck-originated pain radiating to the head, and v) aggravation by neck movements or postures, yet all of these criteria are problematic, and will be critiqued subsequently.

The absence of distinctive biomarkers or definitive imaging findings adds to this problem, blurring the lines for healthcare professionals in differentiating CGH from Primary Headache conditions.  Hence, CGH suffers the same fate as Primary Headache conditions in which no definitive diagnostic tests exist.

Underrecognition by Patients:

Often, patients with CGH do not recognise the neck as the pain source. This misattribution occurs primarily because of an absence of neck symptoms and leads to underreporting in clinical settings and research; individuals, therefore, may not seek appropriate, specific attention for what is a CGH. 

Lack of Awareness Among Healthcare Providers:

Paradoxically, headaches and migraine (one of the most common conditions known to humankind) medicine occupy only a fraction of medical curricula. Therefore, General Practitioners, due to a lack of familiarity with comprehensive diagnostic criteria, are not fully attuned to the nuances of CGH. Furthermore, the diagnostic criteria for CGH, a musculoskeletal event, has been established by those not experienced in manual therapy/medicine. Consequently, examinations of the upper cervical spine by Neurologists specialising in headache and migraine medicine are relatively naive.   This gap in knowledge and lack of collaboration with skilled, experienced manual therapists in the headache space has led to questionable diagnostic criteria and, therefore, is fundamental in the significant underdiagnosis of CGH.

Coexisting Conditions:

Complicating the picture further, CGH (supposedly) often coexists with Primary Headache conditions, muddying the diagnostic waters.  This comorbidity obscures the clinical landscape and poses challenges in isolating CGH in clinical practice and research.

This is compounded by the complexities of differentiating CGH from Primary Headache conditions, and interestingly, this is not exclusive to CGH.  Many patients with a diagnosis of Tension Headache occasionally encounter a more severe headache resembling a Migraine. Conversely, some with Migraine experience less severe headaches, bearing a resemblance to a Tension Headache, conflicting the headache diagnosis.¹⁶ Similarly, although Migraine and Cluster Headache are regarded as separate Primary Headache disorders, there can be significant symptomatic overlap, blurring clinical boundaries, and hence diagnosis.^17,18

The common denominator in this enigmatic headache and migraine space is the TCN.

Limited Research Focus:

A notable factor in the low prevalence reporting is the limited research dedicated to CGH. With headache research funds predominantly channelled towards more common types like Migraine, which is the most studied of all headaches, CGH suffers from a dearth of focused research, impeding the development of precise diagnostic and therapeutic strategies.

Conclusion:

Cervicogenic Headache, despite its profound impact, will remain in the shadows of underreporting and underrecognition. The confluence of diagnostic challenges, shared symptom expression, symptom variability, overlapping pathophysiology, patient and practitioner unawareness, comorbid conditions, and a lack of targeted research contributes to the unacceptable, reported low prevalence. A concerted, collaborative effort with skilled, experienced in the upper cervical spine/headache manual therapists is required to heighten education, awareness, and research, shedding light on CGH and enhancing care for those affected by this often-misunderstood condition.

Until this happens, CGH will continue to play a consistent yet secondary (pun not intended!) role in the headache and migraine space – always the Bridesmaid, never the Bride!

References:

1. Antonaci F, Ghirmai S, Bono G, Sandrini G, Nappi G. Cervicogenic headache: evaluation of the original diagnostic criteria. Cephalalgia. Jun 2001;21(5):573-583.
2. Bogduk N, Govind J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. Lancet Neurol. Oct 2009;8(10):959-968.
3. Sjaastad O, Bakketeig LS. Prevalence of cervicogenic headache: Vågå study of headache epidemiology. Acta Neurol Scand. Mar 2008;117(3):173-180.
4. Knackstedt H, Bansevicius D, Aaseth K, Grande RB, Lundqvist C, Russell MB. Cervicogenic headache in the general population: the Akershus study of chronic headache. Cephalalgia. Dec 2010;30(12):1468-1476.
5. Rothbart PJ. The cervicogenic headache: A pain in the neck. Can J Diagnos. 1996;13:64-71.
6. Stovner L, Hagen K, Jensen R, et al. The global burden of headache: a documentation of headache prevalence and disability worldwide. Cephalalgia. Mar 2007;27(3):193-210.
7. Yeh WZ, Blizzard L, Taylor BV. What is the actual prevalence of migraine? Brain Behav. 06 2018;8(6):e00950.
8. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. Jan 2018;38(1):1-211.
9. Bogduk N. The neck and headaches. Neurol Clin. Feb 2004;22(1):151-171, vii.
10. Akerman S, Holland PR, Goadsby PJ. Diencephalic and brainstem mechanisms in migraine. Nat Rev Neurosci. Sep 20 2011;12(10):570-584.
11. Sjaastad O, Fredriksen TA. Cervicogenic headache: criteria, classification and epidemiology. Clin Exp Rheumatol. Mar-Apr 2000;18(2 Suppl 19):S3-6.
12. Antonaci F, Inan LE. Headache and neck. Cephalalgia. Apr 2021;41(4):438-442.