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REVIEW ARTICLE
Year : 2021  |  Volume : 69  |  Issue : 7  |  Page : 194-198

Cervicogenic Headache: Current Perspectives


1 Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission20-Feb-2021
Date of Decision23-Feb-2021
Date of Acceptance06-Mar-2021
Date of Web Publication14-May-2021

Correspondence Address:
Dr. P Sarat Chandra
Professor and Head of Unit I, Department of Neurosurgery, AIIMS, New Delhi - 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.315992

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 » Abstract 


Background: Cervicogenic headache is a distinct type of headache described in 1980s by Sjaastad, a Norwegian neurologist. It is a not so uncommon headache, which is usually under-diagnosed resulting in suboptimal quality-of-life.
Objective: The aim of this study was to review the current recommendations on diagnosis and management of cervicogenic headache.
Methods and Material: A PubMed search was done for the recent articles on 'cervicogenic headache' published in English literature with the aim of recognizing the current perspectives on cervicogenic headache.
Results: The diagnosis of cervicogenic headache is based on clinical criteria mentioned by the International Headache Society (IHS) and Cervicogenic Headache International Study Group (CHISG). Cervical nerve block may confirm the nociceptive source in majority of cases and is included in CHISG criteria. Non-invasive diagnostic methods like echogenicity of muscles, diffusion tensor imaging (DTI) and single-photon emission tomography (SPECT) are proposed by some authors for avoiding complications associated with blocks. Mainstay of management is physical therapy. Surgical interventions for cervical degenerative disease may relief an associated headache but such interventions are not performed solely for cervicogenic headache.
Conclusion: Headaches with a cervical spine nociceptive source are increasingly being recognized. Current diagnostic criteria and management options are reviewed here.


Keywords: Cervical nerve block, cervical spine disorder, chronic neck pain
Key Messages: Cervicogenic headaches are a distinct entity and proper diagnosis facilitates management improving quality of life. Controlled cervical blocks are the most conclusive for diagnosis but are invasive. Non-invasive diagnostic modalities are under investigation. Physical therapy and percutaneous procedures are usual treatment modalities. Surgical procedures for cervical degeneration with myelo-or radiculo-pathy usually also improve cervicogenic headaches but are not used primarily for such headaches without myelo-or radiculo-pathy.


How to cite this article:
Verma S, Tripathi M, Chandra P S. Cervicogenic Headache: Current Perspectives. Neurol India 2021;69, Suppl S1:194-8

How to cite this URL:
Verma S, Tripathi M, Chandra P S. Cervicogenic Headache: Current Perspectives. Neurol India [serial online] 2021 [cited 2021 Jun 16];69, Suppl S1:194-8. Available from: https://www.neurologyindia.com/text.asp?2021/69/7/194/315992




Cervicogenic headache (CEH) was first observed as a distinct type of headache that aggravated with head and neck movements by Ottar Sjaastad, a Norwegian neurologist in the early 1980s.[1] In the year 1998, the Cervicogenic Headache International Study Group (CHISG) was established CEH was formally identified as a separate entity and it was listed in the second edition of the International Headache Society classification of Headache in 2004.[2]

Cervicogenic headache (CEH) is a lateralized non-throbbing headache caused by a nociceptive source in the cervical spine. The presence of certain features differentiates CEH from other categories of headaches.[3] It is a not so uncommon chronic and recurrent headache that usually starts or aggravates after neck movement and is usually accompanied by a reduced range of motion (ROM) of the neck. Ipsilateral diffuse shoulder and arm pain may be an associated feature. The prevalence of CEH is considered to be 15-20% among cases of chronic headache. The incidence is variably reported. It is considered to be a referred pain arising due to irritation of cervical structures innervated primarily by upper cervical nerves (spinal nerves C1, C2, and C3). Any structure innervated by the C1–C3 spinal nerves may be a source for cervicogenic headache.[4],[5] The most common differential diagnosis includes migraine, cervical spondylosis and tension-type headache. The headache originates in cervical spine, which may further involve occipital, frontal, temporal and orbital regions.[6],[7] Cervicogenic headache is proposed to be caused due to convergence of upper cervical nerves (C1-3) and trigeminocervical complex in the upper cervical spinal cord. However, CEH in middle to lower cervical spine disorders is also frequently reported, which cannot be explained by this theory. The treatment of CEH requires a multidisciplinary approach because pharmacological treatment is often ineffective.[3]


 » Definition and Diagnostic Criteria Top


Definition of CEH is primarily clinical. International Headache Society (IHS) and Cervicogenic Headache International Study Group (CHISG) have proposed diagnostic criteria for cervicogenic headache. IHS classifies CEH in section 11 that includes 'Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical structure'. CEH is described under a subsection 11.2 - 'Headache attributed to a disorder of the neck.' IHS recommends three diagnostic criteria for CEH as follows (adapted from IHS classification, 3rd edition) [Table 1].[8] CHISG has also recommended certain diagnostic criteria for CEH that are more specific [Table 2].[7]
Table 1: IHS Criteria for Cervicogenic Headache

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Table 2: CHISG Criteria for Cervicogenic Headache

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In a critical review comparing the diagnostic criteria for CEH by IHS and CHISG, Sjaastad concluded that the IHS criteria, although improved from its previous edition (2nd edition), still is not a safe basis for diagnosing CEH. Probably there is no gold standard as far as CEH diagnostic criteria are concerned. However, CHISG criteria are better framed for diagnosing CEH.[9]

Neck pain and tenderness may be due to hypersensitivity of neck afferents due to chronic degenerative changes in the cervical musculoskeletal system. Based on this concept, the International Headache Society (ICHD-3)[8] and Cervicogenic Headache International Study Group (CHISG)[7] classification criteria recommend diagnostic cervical nerve or joint blocks as an ancillary test to suggest an evidence of cervical origin of headache in cervicogenic headache. The drawback of such criteria is their invasive nature which are usually not suitable for the initial diagnosis of headaches in clinics.

Efforts are made by several groups to define criteria to make a clinical diagnosis of CEH without invasive aesthetic blocks. As an isolated criterion, reduced range of motion (ROM) of cervical spine, although characteristic of cervical spine disorders, lacks diagnostic sensitivity and specificity. Jull G et al. found that a pattern of three physical signs, rather than a single one, could better identify neck dysfunction associated with CEH. The three physical signs mentioned by them are 1) reduced ROM assessed by cervical extension, 2) painful upper cervical joint dysfunction assessed by clinical manual examination and 3) impaired cervical muscle function assessed by craniocervical flexion test (CCFT).[10],[11] Getsoian et al. assessed the validity of this pattern of cervical musculoskeletal signs to identify a cervical source of head and neck pain, using controlled diagnostic blocks. They found that a single sign of neck dysfunction failed to predict responsiveness to cervical diagnostic blocks. Using such a 'pattern' of cervical musculoskeletal signs may improve clinical diagnostic criteria for cervicogenic headache and more effectively diagnose the source of neck pain which are commonly associated with migraine and tension-type headache.[12]

Etiopathogenesis

Ottar Sjaastad, a Norwegian neurologist in early 1980s observed a unilateral, non-throbbing headache pattern that aggravated with head and neck movements. He termed those headaches as 'cervicogenic' as he strongly believed that the cause of headache lied in the cervical spine. By administering ipsilateral local anesthetic blocks in 11 patients during the painful episodes, he observed a partial or complete relief in 9 patients.[1] The mechanism of pain generation in Cervicogenic headache is proposed to be the interaction between trigeminal and cervical afferents and the bidirectional pathway in the trigeminocervical nucleus. Convergence of proximal 3 cervical nerves and trigeminal nerve afferents is most commonly the cause of CEH.[13],[14],[15] Origin of pain may be due to a nociceptive source in the cervical spine musculoskeletal tissues.[12]

Shimohata K et al. found that in Japanese population, the middle and lower cervical spine nociceptive sources also contributed significantly to the site of origin of CEHs. Minor nociceptive inputs relay via the ipsilateral spinocervicothalamic tract.[16] They suggested the possibility of a complex communication between spinocervicothalamic and trigeminospinal tract.[17] In addition, they also proposed that due to increase in ROM of the upper cervical spine occurring to compensate for restricted ROM in the lower cervical spine may be the cause of overstimulation of the trigeminocervical nucleus resulting in CEH.[18] Greenbaum T. et al. found a clear clinical association between painful temporomandibular disorder (TMD) and cervicogenic headache.[19]

There is a growing interest in the impact of body posture influences on outcome measures of cervicogenic headache (CEH). Moustafa IM et al. suggested that increased magnitudes of thoracolumbar posture displacements corresponds to an increased chance of suffering from CEH.[20]

Diagnosis

Diagnosis of CEHs is usually complicated by the overlap of symptoms and pain location observed in migraine and tension headaches highlighting the limitations of using these criteria in the differential diagnosis of headache.[21] Third edition of the International Classification of Headache Disorders (IHS) and The Cervicogenic Headache International Study Group (CHISG) has laid down certain criteria for clinical diagnosis of CEHs. Despite being in place for past many years, diagnosis of CEHs is still a challenge for clinicians.

Structural imaging like magnetic resonance imaging (MRI) can diagnose disc degeneration, compensatory posterior ligamentous complex thickening, dural or nerve root compression, spinal canal stenosis and facet arthropathy. But these radiological findings are not pathognomonic of CEH. Diagnostic criteria for CEH are difficult to practice clinically and have poor inter-rater reliability and specificity.[6],[22]

Recently, many studies with the objective to point out the source of pain generation in CEHs are performed. The ideal diagnostic modality should be non-invasive for its maximum utility in outpatient clinics. Conventional and most conclusive method to confirm the site of nociception is to administer controlled local anesthetic blocks at the probable cervical levels. If significant relief of pain is noticed after the blocks, it confirms the source of pain generator. However, such blocks are usually performed under X-ray guidance. Also, administering blocks at the occipito- Atlas More Details (O-C1) and atlantoaxial (C1-2) levels carry significant risk of injury to the vertebral artery and dorsal root ganglion. Few groups have proposed to administer diagnostic blocks with a specific protocol to decrease such risks. Govind J et al. observed that in patients of CEHs, with headache being the dominant complaint, diagnostic blocks had a 75% positive yield in establishing the source of nociception.[23] Most common source being C2-3 joint (62%) followed by C1-2 (7%) and C3-4 (6%) joints. They concluded that controlled diagnostic blocks can establish the source of pain in the majority of patients presenting with probable cervicogenic headache, with C2-3 being the most common source. They proposed that diagnostic algorithms should commence investigations at C2-3 joint which is the most common source of nociception and also relatively less risky as compared to C1-2 joint.[23]

To avoid these complications, novel, non-invasive methods to diagnose CEHs are investigated by several groups. Abaspour O et al. assessed echogenicity of neck muscles - longus capitis, rectus capitis posterior major, and obliquus capitis superior in diagnosed cases of CEHs and found that the echogenicity of only the deep anterior cervical muscle (longus capitis) was affected in CEH patients and concurrent finding of fatty infiltration in this muscle was also observed. Hence, they proposed that anterior muscle dysfunction is more important in diagnosis of CEH.[24]

Wang L et al. assessed Diffusion Tensor Imaging (DTI) parameters to localize the site of nociception in CEHs.[25] They measured fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values in bilateral greater occipital nerves (GON) and cervical dorsal root ganglion (DRG) of C2 and C3 nerves. They calculated grading values for headache severity using a receiver operating characteristics (ROC) curve. DTI parameters on the symptomatic side of the C2 and C3 DRG and GON were significantly changed. They proposed that FA value of the C2 DRG can be employed to grade headache severity. DTI parameters of the GON significantly correlated with headache severity.

Cho PG et al. retrospectively evaluated the role of Single Photon Emission Computed Tomography (SPECT/CT) for diagnosing patients with CEH.[6] SPECT/CT showed arthritic changes clearly in the cervical spine and identified the therapeutic targets accurately. Patients with SPECT/CT(+) benefited markedly from spinal injections demonstrating a positive association with better clinical outcome after receiving a spinal injections. The Visual analogue scale (VAS) and Neck Disability Index (NDI) scores of SPECT/CT(+) patients improved by 88% and 75%, respectively whereas SPECT/CT(−) patients showed poor outcomes.

Management

Management of CEHs is challenging despite the entity being reported three decades back. Treatment of CEH demands a multimodal approach that includes pharmacological and non-pharmacological interventions. Usual treatment includes 1) physical therapy and exercise, 2) percutaneous interventional procedures including anesthetic blocks and pulsed radiofrequency therapy and 3) surgery. Common interventional treatments include local anesthetic blocks of greater occipital nerve, lesser occipital nerve, and less commonly stellate ganglion. Cervical decompression and/or fusion surgeries have also reportedly improved CEHs as observed by various studies. Early diagnosis and treatment are crucial to decrease chances of desensitization to treatment.[13],[18]

Physical therapy is the initial first-line management of cervicogenic headache (CEH). Paquin JP et al. studied specifically the CEHs originating from C1-2 zygapophyseal joints.[26] They assessed the preoperative ROM restriction by cervical flexion-rotation test (CFRT) (specific for C1-C2 zygapophyseal joints) and investigated the immediate effect of C1-C2 rotation Sustained Natural Apophyseal Glides (SNAG) mobilizations plus C1-C2 self-SNAG rotation exercise for patients with CEHs. They reported that SNAG mobilization combined with a self-SNAG exercise resulted in favorable outcomes. It also had improved cognitive-affective aspect of pain.

Lerner-Lentz A et al. reported the effect of pragmatically selected manipulation or mobilization for the management of CEHs based on their study on 45 patients.[27] Pragmatic manipulation had similar effects on disability, pain, global ranking of change (GRC), and cervical range of motion (ROM) as mobilization when applied in a pragmatic fashion for patients with cervicogenic headaches. Fernandez M et al. did a systematic review and meta-analysis of spinal manipulative therapy (SMT) for CEHs and concluded that SMT provides significant, small short-term effects for CEH pain intensity, frequency and disability. However, the long-term impact of SMT was not significant.[28]

Many physicians have performed Pulsed Radiofrequency (PRF) on the upper cervical structures (C2 dorsal root ganglion, atlantoaxial joint, greater or lesser occipital nerve) with good results. However, this technique carries an inherent risk of complications because of the proximity of anatomic structures such as the nerve roots and vertebral artery.[29] Park MS et al. studied the clinical efficacy and safety of pulsed radiofrequency targeting the mid-cervical medial branches.[13] This technique avoided risk of injury to dorsal nerve roots or ganglion and more importantly the vertebral artery. The authors concluded that targeting the mid-cervical medial branches could be a safer therapeutic approach.

Several studies report a good improvement in CEHs after cervical decompression surgery. The primary indication of surgery in such studies was cervical compressive myelopathy and/or radiculopathy with CEH as one of the symptoms. Pang X et al. assessed 166 patients who underwent anterior cervical discectomy and fusion (ACDF) for cervical compressive myelopathy and/or radiculopathy and found 30% incidence of CEH in that group. ACDF relieved accompanying CEH in all the cases in addition to the neck pain in their study group.[30] Lombardi JM et al. did a post hoc analysis of single prospective, multicenter, randomized US Food and Drug Administration (FDA) Investigational Device Exemption (IDE) study with the aim of determining the effectiveness of a 2-level ACDF or Cervical disk arthroplasty (CDA) in relieving CEH at 10 years.[31] At 10 year follow-up only 16.8% of patients had severe headache as compared to 88.5% in the preoperative period reflecting that arthroplasty and ACDF are often effective at alleviating such CEHs. Similarly, Yabuki S et al. reported 31% incidence of CEH in patients with cervical spondylotic myelopathy (CSM) in their study, and 43% of patients with CSM reported that headache disappeared following decompression surgery proposed that such headaches might be associated with a neuropathic pain mechanism.[32]

Shimohata K et al. did first prospective study to assess the role of cervical laminoplasty in relieving CEH associated with cervical myelopathy and/or radiculopathy due to multilevel cervical spine compression. In their study, all the 12 patients with CEH who had multi-segmental lesions reported relief of headache after cervical laminoplasty. Authors proposed that the cervical duramater might play an important role in CEH, as evident by relief of CEHs after cervical laminoplasty that relieved chronic irritation of the duramater due to long-term compression.[18] Jansen reported a similar improvement in CEHs in a small retrospective series that included 6 patients.[33]


 » Summary Top


Cervicogenic headache (CEH) is a not so uncommon entity of headache where source of nociception is localized to cervical spine. Although CEHs are a well-described entity for many decades, their diagnosis and management are still evolving. It is probably an underdiagnosed entity due to non-specific criteria and associated cervical degenerative disease and more important component of myelopathy or radiculopathy in many cases. Diagnosis is usually confirmed by local anesthetic blocks but newer non-invasive methods are evolving. Accurate localization of the nociceptive source improves the chances of good pain relief. Management options include physical therapies and percutaneous interventional procedures when CEHs are diagnosed in isolation. However, if associated with cervical myelopathy and/or radiculopathy, cervical decompression and/or fusion are often done, not primarily for CEH but for relieving spinal cord/nerve root compression and it usually relieves CEH also in majority of cases.

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Conflicts of interest

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Gondo G, Watanabe T, Kawada J, Tanaka M, Yamamoto K, Tanaka S, et al. A case of cervicogenic headache caused by C5 nerve root derived shwannoma: Case report. Cephalalgia 2017;37:902-5.  Back to cited text no. 17
    
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