Cervicogenic headache is a referred pain condition where in a pain source in the cervical spine is experienced as a headache. Its diagnosis and pathophysiology have remained controversial. The clinical criteria for its diagnosis have undergone several modifications since the time it was first described. We provide an overview of the diagnosis of cervicogenic headache, our hypothesis on its pathogenesis, and the management of cervicogenic headache.

Diagnostic criteria

The diagnosis of cervicogenic headache based on clinical criteria has been revised several times since its original description in 1980s [1]. It was initially defined as a unilateral headache associate with evidence of cervical involvement through provocation of pain by movement of the neck or by pressing the neck; concurrent pain in the neck, shoulder, and arm; and reduced range of motion of the neck with or without other features. These criteria were nonspecific and did not validate the nature of the cervicogenic source. It was modified in 2013 to include cervical spondylosis in the imaging criteria and clinical response to diagnostic blockade to form the guidelines for International Classification of Headache Disorders (ICHD-3-beta) [2]. The prevalence of CGH is reported to range from 1-4% in the general population and contributes to more than 17% of all severe headache types [3-5]. Recent studies using ICHD-3 criteria estimated it to be around 22% of all headaches [6]. About 88% of patients with cervical myeloradiculopathy are noted to have associated cervicogenic headaches [7].

Differential diagnosis

The term cervicogenic headache encompasses all sources of pain from the cervical spine and usually is associated with mechanical neck pain. The pain generator for mechanical neck pain as well as headache could be varied including paraspinal muscles and ligament injury, cervical disc and spondylotic changes such as uncovertebral arthropathy and facet arthropathy [8]. The pain origin from upper cervical facets is mediated through cervical nerve roots and extends cranially generally up to the coronal suture as demonstrated in illustrations (Figures 1 and 2).  

The differentials of cervicogenic headache include paroxysmal hemicrania, migraine cervicale and Barre’s Syndrome. Paroxysmal hemicrania, unlike CGH is characterized by several attacks (>5 a day) of severe periorbital pain, usually responsive to indomethacin. Clinical evaluation of patients with cervicogenic headache should include a detailed history for symptoms such as timing and frequency of attacks, location, triggering mechanisms, and autonomic symptoms such as photophobia, conjunctival injection, visual disturbances and nausea. Clinical examination must include provocative maneuvers such as Spurlings and L’Hermitte’s signs and evaluation of trigger points to differentiate conditions such as occipital neuralgia.

The clinical criteria for cervicogenic headache differentiate it from some of the close mimics such as tension-type headache and migraine.

Originally, on the anatomic basis of upper cervical nerve roots’ (C1 to C3) convergence to the spinal segment of trigeminal nucleus, CGH origin was believed to be limited to the upper cervical segments [9,10]. It is however established now that CGH symptoms are noted to arise from the lower cervical spine as well [11]. There is no definitive pathoanatomic mechanism in the literature supporting this observation. We present our hypothesis, based on our analysis of cervical neural anatomy, radiological findings and clinical results with various treatment strategies.

Review of relevant cervical anatomy

Occipital region and area extending up to the coronal suture innervated by occipital nerves and the greater auricular nerve can directly contribute to headache. The frontal and temporal region CGH however, is mediated through convergence to the trigeminal nucleus. It is important to understand the anatomic detail of cervical spine innervation to appreciate the origin of CGH associated with spondylosis. The duramater and extradural structures of the cervical spine are innervated by corresponding cervical nerve roots via the anterior and posterior primary rami. The anterior primary ramus along with the sympathetic branches gives rise to sinuvertebral (SV) nerves that innervates the anterior duramater, cervical discs, atlantoaxial ligaments and clival dura. The SV nerve runs in the lateral to medial direction through the foramen, into the spinal canal extradurally, in association with venous plexus and arterioles. It provides the nociceptive and sympathetic innervation to the dura, posterior longitudinal ligament (PLL) and the cervical discs. The innervation of the SV nerve extends caudally up to 3 adjacent levels as demonstrated in previous cadaveric studies [12]. This provides one possible mechanism of CGH origination from the lower cervical spine, on the basis of trigeminocervical convergence. We speculate that the CGH nociception in spondylotic cervical spine is mediated through the sinuvertebral nociceptive and sympathetic innervation of the anterior duramater and posterior longitudinal ligament (PLL). The mechanisms as such could include compression at the narrow foraminal entry zone, dural stretch of varied etiologies such as cervical stenosis, kyphosis, spondylotic changes and associated segmental cerebrospinal fluid (CSF) entrapments [13]. Similarly, the posterior primary rami of the cervical nerve roots innervating the zygopophyseal joints and posterior musculature can also mediate CGH.

Management

Neurointerventional anesthetic blocks and/or radiofrequency neurotomy of nociceptive sources including lateral atlantoaxial joints, greater occipital nerve, cervical nerves and zygopophyseal joints have all shown to be beneficial in treating CGH [14-17]. Surgical treatment with both anterior and posterior approaches for cervical spondylosis associated cervicogenic headaches have been evaluated by numerous studies [6,7,18-20]. The anterior surgical approaches in general have demonstrated more substantial and durable pain relief compared to posterior cervical approach. We surmise that the posterior surgical techniques may only provide an indirect decompression of the richly innervated anterior dura and the PLL, which are more frequently the source of pain.

It is important to evaluate for the source of CGH before pursuing a surgical treatment. Careful evaluation of cervical imaging with appropriate trial of neurointerventional anesthetic blocks is necessary to differentiate the origin of the pain between the possible structures such as the cervical disc, facet joints, cervical nerves and the duramater.

CONCLUSION

Cervicogenic headache arises from varied etiologies including spondylotic changes such as disc degeneration, uncovertebral hypertrophy and zygopophyseal joint arthropathy. Recent guidelines help diagnose CGH based on both clinical and imaging criteria. First line conservative treatment options include use of muscle relaxants, rehabilitation of posterior neck musculature and interventional pain techniques. Surgical options may be considered in persistent, severe cases when associated with radiculopathy or myelopathy. Anterior surgical approach to address cervical spondylosis associated CGH seems to be a more effective and durable method, in contrast to posterior surgical operations. Removal of PLL as well as adequate uncovertebral and foraminal decompression may optimize headache relief with an anterior surgical approach.

DISCLOSURE

The authors have not received or will receive benefits for person or professional use from a commercial party related directly or indirectly to the subject of this manuscript. The study and the preparation of the manuscript were supported by a commercial party related to the subject of the manuscript.