A cervicogenic Headache (CGH) presents as unilateral pain that starts in the neck. It is a common chronic and recurrent headache that usually starts after neck movement. It usually accompanies a reduced range of motion (ROM) of the neck. It could be confused with a migraine, tension headache, or other primary headache syndromes. Diagnostic criteria must include all the following points: 1. Source of the pain must be in the neck and perceived in head or face. 2. Evidence that the pain can be attributed to the neck. It must have one of the following: demonstration of clinical signs that implicate a source of pain in the neck or abolition of a headache following diagnostic blockade of a cervical structure or its nerve supply using a placebo or other adequate controls. 3. Pain resolves within three months after successful treatment of the causative disorder or lesion (Wang 2014).
A cervicogenic headache is thought to be referred pain arising from irritation caused by cervical structures innervated by spinal nerves C1, C2, and C3; therefore, any structure innervated by the C1–C3 spinal nerves could be the source for a cervicogenic headache.
A cervicogenic headache is a rare chronic headache in people who are 30 to 44 years old. Its prevalence among patients with headaches is 1% to 4%, depending on how many criteria fulfilled and based on many different studies. It affects males and females about the same with a ratio of 0.97 (F/M ratio). Age at onset is thought to be the early 30s, but the age the patients seek medical attention and diagnosis is 49.4. When compared with other headache patients, these patients have a pericranial muscle tenderness on the painful side and a significantly reduced cervicogenic headache.
The C1-C3 nerves relay pain signals to the nociceptive nucleus of the head and neck, the trigeminocervical nucleus. This connection is thought to be the cause for referred pain to the occiput and/or eyes. (Wang 2014). Aseptic inflammation and neurotransmission within the C-fibers that is caused by cervical disc pathology is thought to produce and worsen the pain in a cervicogenic headache. The trigeminocervical nucleus receives afferents from the trigeminal nerve as well as the upper three cervical spinal nerves. Neck trauma, whiplash, strain, or chronic spasm of the scalp, neck, or shoulder muscles can increase the sensitivity of the area which is similar to the allodynia that is seen in late chronic migraines. A lower pain threshold makes patients more susceptible to more severe pain. For this reason, early diagnosis and therapeutic intervention is very important (Gallagher 2007).
Patients usually complain of a unilateral pain without side shift. It is ordinarily predominant in females. Pain topography is usually stemming from the neck, spreading to the oculofrontotemporal area with episodes of carrying duration or fluctuating continuous pain. Pain is moderate to severe, but not excruciating. Pain can mimic primary headache syndromes such as tension headache or migraine headache, although the patient will be less likely to complain of sensitivity to light and noise as in migraine headache. It typically is associated with a reduced ROM of the neck. Patients will complain that the pain is not resolving with a triptan, ergotamine, or indomethacin. Autonomic symptoms such as photophobia or phonophobia, nausea, and vomiting are not as common.
Imaging of the cervical spine is not sensitive enough for diagnosing a cervicogenic headache. No specific radiologic abnormalities were found by recent studies such as Pfaffenrath et al. and Fredriksen et al. The most frequent findings in the literature were a rectilinearization of the cervical spine and/or disc protrusions. Although not widely used in the clinical world, functional imaging shows a hypomobility or hypermobility at a certain level of the cervical spine. An MRI is commonly ordered to help rule out Chiari malformations, nerve root pathology assessment, or even in the spinal cord pathology.
Physical therapy is considered the first line of treatment. Manipulative therapy and therapeutic exercise regimen are effective in treating a cervicogenic headache. According to a study by Jull and Richardson, 72% of patients had achieved a reduction of 50% or more in headache frequency at the 12-month follow-up, and 42% of patients reported 80% or higher relief of some sort. These manipulative maneuvers stimulate neural inhibitory systems at various levels in the spinal cord and activate descending inhibitory pathways.
Another option for treatment of a cervicogenic headache is interventional treatment, which will differ depending on the cause of a headache. For example, a lateral atlantoaxial joint intra-articular injection can be useful to diagnose and treat the condition when it has an osteoarthritis or post-traumatic cause. Another cause of a cervicogenic headache is arthritis of the C2-3 facet joint which is innervated by a superficial branch of the C3 nerve called the third occipital nerve. This is seen after whiplash injury from a motor accident. Injection into the facet joint will reduce pain, and third occipital nerve block will provide temporary cervicogenic headache pain relief while radiofrequency ablation can be used for long-term pain relief.
There is some evidence that cervical epidural steroid injection has some benefits in treating pain in a cervicogenic headache. Steroids can work in this setting due to the theory that the pain continues sensitizing the cervical nerve roots and initiates a pain-producing loop involving nerve root and microvascular inflammation as well as mechanically-induced micro-injury (Martelletti et al. 1998).
Cervical epidural steroids injections with an interlaminar needle approach at C7-T1 or C6-7 epidural space is relatively safe compared to other interventional cervical procedures. According to He et al.’s study, steroids injection reduced the daily NSAID usage at both 3 and 6 months.
It is very important to be able to distinguish occipital neuralgia from the occipital referral of pain from the atlantoaxial or upper zygapophyseal joints or tender trigger points in neck muscles or their insertions. Occipital neuralgia can produce symptoms indistinguishable from a cervicogenic headache. It typically presents as sharp pain in the occipital region. The greater occipital nerve is the terminal branch of the dorsal ramus of C2, with contribution from C3, while the lesser occipital nerve is a branch of the dorsal ramus of C3. Treatment of occipital neuralgia includes segmental nerve blocks at C2 and C3, cryoneurolysis, radiofrequency ablation, and neuroablation such as dorsal rhizotomy at C1, C2, and C3 and posterior rhizotomy at C1, C2, and C3.
A cervicogenic headache is a common cause of a chronic headache that is often misdiagnosed. The presenting features can be complex and similar to many primary headache syndromes that are encountered daily. The main symptoms of a cervicogenic headache are a combination of unilateral pain, ipsilateral diffuse shoulder, and arm pain. ROM in the neck is reduced, and pain is relieved with anesthetic blockades. The differential diagnosis includes a migraine, hemicrania continua, spondylosis of the cervical spine, and tension-type headache. Treatment includes physical therapy, exercise, and interventional procedures.
Early diagnosis and treatment are important to decrease the desensitization and alleviate pain in these patients. Management of this condition requires a multidisciplinary approach. Common treatments include blockade of the greater occipital nerve, the lesser occipital nerve, and the stellate ganglion.