1. Occupational hazards: Hairstylists, carpenters, drivers, and other occupations that involve abnormal head posture while working may predispose to CGH
2. Strenuous activities can produce CGH. Eg: Weight-lifting sportsmen.
3. Forward head posture: Holding the head out in a forward position such as working on a computer on a continual basis may pose risk for CGH.

One or more of the following may be the source of pain in CGH.

1. Facet joints
2. Atlanto-occipital joint
3. Intervertebral discs
4. Neck muscles
5. Cervical nerves

1. Trauma: Whiplash injury from rear-end car accidents causing zygo-apophyseal joint injury account for 53% of CGH. Fall or sports injury causing facet joint dislocation, fractures can be other traumatic causes for CGH.
2. Inflammatory conditions: Rheumatoid arthritis, Cervical disc disease also produce CGH.
3. Degenerative conditions: Cervical degenerative disc disease or osteoarthritis of the facet joints are degenerative causes of CGH.
4. Neoplastic conditions: Malignant or benign tumors of the neck can cause compression of the spinal nerves leading to CGH.

Strain injury to ligaments and muscles of neck or pathological changes in facet joint and intervertebral disc can cause direct activation and sensitization of primary afferents neurons especially C- fibre nociceptors which carry pain signals. Studies have shown increased levels of serum interleukin (IL)-1β and tumour necrosis factor (TNF)-α in cervicogenic headache both during periods of spontaneous fluctuating basal pain and mechanically superimposed attacks. These pro-inflammatory cytokines(IL-1β and TNF-α) may promote hyperalgesia in cervicogenic headache. Marked activation of NO pathway has also been seen in patients with cervicogenic headache as compared to patients with migraine or cluster headache. Olesen () has suggested that headache may be due to an excess of nociceptive input. He stated the neurons of the trigeminal nucleus caudalis play a central role in headache. The perceived headache intensity is the sum of nociception from cranial and extra-cranial tissues converging upon the nucleus caudalis neurons.

Cervicogenic headache is predominantly unilateral but can be bilateral also. Pain begins in the neck or at the occipito-nuchal area and referred to frontal, temporal or orbital region on the ipsilateral side, and pain perceived in these areas may be maximum than in the neck. Headache is usually deep, non throbbing or non-pulsating in character, of moderate to severe intensity, and occur in attacks. Duration of attack may range from few hours to several days. Sooner or later it may become constant type with superimposed attack of more intense pain. These attacks of headache may be triggered by (a) certain neck movements and/or sustained, awkward head positioning (e.g. driving or sitting at a computer in poor posture) (b) By external pressure over the upper cervical or occipital region on the symptomatic side. There is reduced range of movements in neck. Ipsilateral shoulder or arm pain can be present which is non-radicular in nature. Other associated features like:

1. Nausea
2. Phono- and photophobia
3. Dizziness
4. Ipsilateral blurred vision
5. Difficulties on swallowing
6. Ipsilateral edema, mostly in the periocular area may be present but are generally not pronounced.

There is reduced range of motion in neck so (a) movement tests of the cervical spinal column such as: passive flexion, retroflexion, lateroflexion, and rotation should be assessed on limitation of movement.

Patients may experience tenderness on firm palpation of the upper part of the neck just below the base of the skull along with muscle tightness in this region. Segmental palpation of the cervical facet joints can be done.

Assessment of the following “pressure points” can be done:

• Nervus occipitalis major at occipital-temporal part of the skull
• Nervus occipitalis minor at attachment of the sternocleidomastoid muscle to the skull
• Third cervical nerve root (facet joint C2–C3);
• Pressure pain anterior, posterior, and on the ventral musculus trapezius border;

The assessment of the “pressure points” aims at getting an indication of the segmental level, where the nociceptive stimulus possibly occurs. This assessment is empirical and subjective. There is no scientific evidence for this.

Positive response to a diagnostic/prognostic block with a local anesthetic confirms the diagnosis of CEH. A comprehensive history, physical examination and review of systems helps in forming the clinical diagnosis and rules out underlying structural or systemic disease. Conventional Imaging studies cannot confirm the diagnosis of cervicogenic headache but can lend support to its diagnosis. If there are indicators of red flag then further diagnostic tests like MRI or CT should be considered.

Diagnostic blocks should be directed to the nerves or anatomical structures suspected of mediating or causing cervicogenic headache. Appropriate blocks in the neck or head should include structures capable of causing cervicogenic headache, such as the greater occipital nerve, the minor occipital nerve, zygapophyseal joints (facet joints), segmental nerves and intervertebral discs.