Cervicogenic Headache


Cervicogenic headache is a chronic headache that arises from the atlanto-occipital and upper cervical joints and perceived in one or more regions of the head and/or face.[1] These occur due to a neck disorder or lesion and feature the converging of trigeminal and cervical afferents in the trigeminocervical nucleus within the upper cervical spinal cord.[2] By definition the headache should be abolished following a diagnostic blockade of a cervical structure or its nerve supply.[3]

The International Headache Society (IHS) has validated cervicogenic headache as a secondary headache type that is hypothesized to originate due to nociception in the cervical area. [4] (See more about classification on the headache page).

Cervicogenic Headache
Upper Cervical Spine

Clinical relevant anatomy

The cervical spine consists of 7 vertebrae, C1 to C7. The cervical nerves from C1 to C8. The first two vertebrae have a unique shape and function.[5] The upper vertebrae supports the skull, articulates superiorly with the occiput (the atlanto-occipital joint) and is named the atlas (C1). This joint is responsible for 50% of flexion and extension.The design of the atlas allows forward and backward movement of the head. Among the atlas is the axis (C2) that allows rotation.[5] The atlantoaxial joint is responsible for 50% of all cervical rotation. Both form the upper cervical spine. The 5 cervical vertebrae that make up the lower cervical spine, C3-C7, are similar to each other but very different from C1 and C2. The mechanism which is responsible for the pain consists of a merger of the spinal nerves C1, C2 and C3, and a branch of the 5th cranial nerve, the trigeminal nerve. This merger of nerves makes it possible that upper cervical pain radiates to regions of the head which are innervated by the cervical nerve (auricular and occipital). The merger with the trigeminal afferents allows the pain to radiate to the parietal, frontal and orbital regions.[2]

The trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibers in the descending tract of the trigeminal nerve converge with sensory fibers from the upper cervical roots. This convergence of nociceptive pathways allows for the referral of pain signals from the neck to the trigeminal sensory receptive fields of the face and head as well as activation of the trigeminovascular neuroinflammatory cascade. Also relevant to this condition is the convergence of sensorimotor fibers of the spinal accessory nerve (CN XI) and upper cervical nerve roots, which ultimately converge with the descending tract of the trigeminal nerve. These connections may be the basis for the well-recognized patterns of referred pain from the trapezius and sternocleidomastoid muscles to the face and head.


Of all chronic headaches, the incidence of cervicogenic headache has been estimated to be 14-18%, though in a recent population-based study a 2.2% prevalence was found[6]. As such, it is important we can distinguish cervicogenic headache from the other headaches like migraine, tension type headache.

The term cervicogenic headache (CGH) was coined almost 3 decades ago, and the general condition of pain located in the head but originating in the cervical spine was described over 100 years ago. It is similar to other non-specific spinal conditions in its relative lack of high level evidence regarding pathoanatomical etiology. Since there is no objective test set for definitive diagnosis of CGH, the condition is ruled in, and treatment chosen, based on the patient's subjective report of pain patterns. [7]

There is some evidence that multiple structures in the upper cervical spine can be the source that is referring pain into the head. The implicated structures are generally centered around C1, C2, and C3 spinal levels. This may include the joints, disc, ligaments, and musculature.[8] The lower cervical spine may play an indirect role in pain production if dysfunctional, but there is no evidence of a direct referral pattern.[8] Through controlled nerve blocking of various structures in the cervical spine, it appears that the zygoapophyseal joints, especially those of C2/C3, are the most common sources of CGH pain. This finding is even more common in patients with a history of whiplash. [8]

Clinical Presentation

Challenging to diagnose clinically, but often includes the below:

  • Unilateral “ram’s horn” or unilateral dominant headache[9] (Excluding those with bilateral headache or symptoms that typify migrane headaches).
  • Exacerbated by neck movement or posture[9]
  • Tenderness of the upper 3 cervical spine joints[9]
  • Association with neck pain or dysfunction[10]
  • Definitive diagnosis made through selective nerve blocking through injection of specific sites[8]
  • Compared to migraine headache and control groups, cervicogenic headache group patients tend to have increased tightness and trigger points in upper trapezius, levator scapulae, scales and suboccipital extensors[1]
  • Weakness in the deep neck flexors[9][11][12]
  • Increased activity in the superficial flexors
  • Atrophy in the suboccipital extensors and so the deep muscle sleeve which is important for active support of the cervical segments becomes impaired
  • Upper trapezius, sternocleidomastoid, scalenes, levator scapulae, pectoralis major and minor, and short sub-occipital extensors have been implicated[9][11][13] 

Differential Diagnosis

It is important to differentiate from serious pathology such as:

It is also important to differentiate from other types of headache:

Type Location Intensity Frequency Duration Additional Symptoms
Cluster Unilateral: (orbital, supraorbital, temporal) Severe 1x every other day -> 8x day 15-180 minutes Associated with ipsilateral: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, eyelid edema.

Restlessness or agitation.
Tension Bilateral Mild-Moderate >15day/mo, >3 mo Hours-continuous
Pressing, tightening

<1 of photophobia, phonophobia or mild nausea
Migraine without aura Unilateral: Frontotemporal in adults, Occipital in children Moderate-Severe >14 days/month
4-72 hours Flickering lights/spots in vision, pulsating quality, nausea, photophobia, phonophobia

Cluster Tension Migrane
CHdiff-cluster.jpg CHdiff-tension.jpg CHdiff-migrane.jpg


For more detailed classification information

Cybex Dynamometry

Another possibility to distinguish cervicogenic headache from migraine and tension headache is the use of a Cybex dynamometry.[14] Testing using Cybex dynamometry has shown that the ranges of cervical flexion, extension and rotation are significantly less in patients with cervicogenic than in patients with migraine and tension type headache (p < 0.001). Investigators also found that tenderness is a factor that varies between patients with CGH and patients with migraine or tension type headaches. Bovim measured pressure pain thresholds at ten points on the head and suboccipital region in patients with CGH, tension type headache and migraine.[15] Lower scores were found in patients with cervicogenic headaches than without.

Outcomes measures


Diagnostic Criteria

As described by the IHS[3]:

  1. Pain localized in the neck and occiput, which can spread to other areas in the head, such as forehead, orbital region, temples, vertex, or ears, usually unilateral.
  2. Pain is precipitated or aggravated by specific neck movements or sustained postures.
  3. At least one of the following:
    1. Resistance to or limitation of passive neck movements
    2. Changes in neck muscle contour, texture, tone, or response to active and passive stretching and contraction
    3. Abnormal tenderness of neck musculature
  4. Radiological examination reveals at least one of the following:
    1. Movement abnormalities in flexion/extension
    2. Abnormal posture
    3. Fractures, congenital abnormalities, bone tumors, rheumatoid arthritis, or other distinct pathology (not spondylosis orosteochondrosis)

Flexion-Rotation Test

The inverse relationship between headache severity of CGH and ROM towards the most restricted side for the Cervical Flexion-Rotation Test (FRT) was statistically significant for all patients with cervicogenic headaches (Sn = 0.91, Sp = 0.90).[13] The patient should feel no pain at the time of the test. During this test, the neck of the patient is passively held in end range flexion. The therapist rotates the neck to each side until they feel resistance or until the patient says they are in pain. At this end point, the therapist makes a visual estimate of the rotation range and says on which side the FRT was positive or negative. The test was positive when the estimated range was reduced by more than 10° from the anticipated normal range (44°).

"Red flags"

  1. Sudden onset of a new severe headache;
  2. A worsening pattern of a pre-existing headache in the absence of obvious predisposing factors;
  3. Headache associated with fever, neck stiff ness, skin rash, and with a history of cancer, HIV, or other systemic illness;
  4. Headache associated with focal neurologic signs other than typical aura;
  5. Moderate or severe headache triggered by cough, exertion, or bearing down; and
  6. New onset of a headache during or following pregnancy.

Patients with one or more red flags should be referred for an immediate medical consultation and further investigation.[13]

Medical Management

The failure to conclusively demonstrate a specific disease or dysfunction of the neck in relation to cervicogenic headache has been an impediment to specific treatment for individuals with the diagnosis.

Cervical epidural steroid injections: Indicated for multilevel disc or spine degeneration

Nerve Blocks: Disrupting the cascade of signals leading to sensitization to central mechanisms via:

  • Nerve blocks
  • Trigger point injections
  • Radiofrequency thermal neurolysis

Current best evidence suggests that there is not sufficient evidence meeting the EBM criteria to support the use of RF facet denervation for cervicogenic headaches.[16]

Surgical interventions: Often only provide temporary relief with the possibility of longer intensification of pain.[1] Procedures Include:

  • Neurotomy
  • Dorsal rhizotomy
  • Microvascular decompression of nerve roots

Other Medications:

  • Tricyclic antidepressants - Used at lower dosage than required for pts diagnosed with depression
  • Muscle relaxants - Related to the CNS, may be beneficial, evidence is still pending
  • Botulinum toxin - A neurotoxin injected into tender muscles to reduce hypertonia

Physical Therapy Management

Although this type of headache is responsive to therapy oriented at treating the soft tissue restrictions, the method of examination, assessment, and treatment needs to be specific to the neck and occiput."[1] (Level of evidence 5)


  • Cervical spine manipulation or mobilization[17] (Level of evidence 1B)[18] (Level of evidence 1A)
  • Strengthening exercises[17] (Level of evidence 1B) [18] (Level of evidence 1A) including deep neck flexors and upper quarter muscles
  • Thoracic spine thrust manipulation & exercise[19] (Level of evidence 1B)[18] (Level of evience 1A)
  • C1-C2 Self-sustained Natural Apophyseal Glide (SNAG)[20] (Level of evidence 1B) shown to be effective for reducing cervicogenic headache symptoms

Jull et al[9] (Level of evidence 1B) reported that a six week physiotherapy program including manual therapy and exercise interventions was an effective treatment option for reduction of cervicogenic headache symptoms and decreasing medication intake in both the short term and at one-year follow-up.

[21] (Level of evidence 5)
[22] (Level of evidence 5)
[23] (Level of evidence 5)
[24] (Level of evidence 5)

Other Treatment Options

Thoracic Manipulation

Seated CT Manipulation Seated Mid Thoracic Manipulation

Re-educating craniocervical spine flexor muscles

Deep Neck Flexor Exercises

Re-education of craniocervical flexion (CCF) movement[9] (Level of evidence 1B) The neck flexor muscle synergy is tested with the Cranio‐cervical Flexion Test. The patient palpates the superficial flexors to avoid their inappropriate use. An emphasis on precision and control is essential.

Training the low-level endurance capacity of the deep neck flexors[9] (Level of evidence 1B) begins as soon as the patient can perform the CCF movement correctly. This phase tests the patient’s ability to hold (approximately 10 seconds) the cranio-cervical flexion position in each stage of the test on repeated occasions. Pressure biofeedback is used to guide training. Training begins at the pressure level that the patient can achieve and hold steady with a good pattern, without dominant use or substitution by the superficial flexor muscles. The patient performs the formal exercise at least twice daily. For each pressure level, the holding time is built up to 10 seconds and 10 repetitions are performed, eventually to the desired level of 30 mm Hg.

Retraining the cervical flexors for antigravity function in sitting position[9] (Level of evidence 1B) The exercise is a controlled eccentric action of the flexors into cervical extension range followed by a concentric action of these muscles to return the head to the neutral upright position. The return to the upright position must be initiated by CCF, rather than a dominant action of sternocleidomastoid. The exercise is progressed by gradually increasing the range to which the head is moved into extension as control improves, and introducing isometric holds through range.

Extensors of the craniocervical spine[9] (Level of evidence 1B)

The patient practices eccentric control of the head into flexion followed by concentric control back to the neutral position in a 4 point kneeling position to train the coordination of the deep and superficial cervical extensors. These exercises are incorporated with re-education of the scapular muscles in these positions and are commenced early in the program. The exercise is progressed by performing alternating small ranges of craniocervical extension and flexion while maintaining the cervical spine in a neutral position. Co-contraction of the neck flexors and extensors.[9] (Level of evidence 1B)

Co-contraction of the Neck Flexors and Extensors[9] (Level of evidence 1B)

The co-contraction is facilitated with rotation and the exercises are introduced once the patient can activate the deep muscles. The patient uses self-resisted isometric rotation in a correct upright sitting posture. They look into the palm of the hand, providing the resistance to facilitate the muscles and perform the alternating rhythmic stabilization exercises with an emphasis on slow onset and slow release holding contractions, using resistance to match about a 10–20% effort. Retraining the strength of the superficial and deep flexor synergy[9] (Level of evidence 1B)

Retraining the strength of the superficial and deep flexor synergy [9] (Level of evidence 1B)

The head lift must be preceded with CCF followed by cervical flexion to just lift the head from the bed. Gravity and head load provide the resistance. Care must be taken that high load exercise is not introduced too early, as it may be provocative of symptoms.

Retraining the Scapular Muscles

Retraining scapular orientation in posture[9] (Level of evidence 1B) A correction strategy is to have the patient move the coracoids upward and the acromion backward, which results in a slight retraction and external rotation of the scapula. The aim is to facilitate the coordinated action of all parts of trapezius and serratus anterior, allowing lower trapezius to slightly depress the medial border of the scapula, consequently lengthening (and relaxing) the levator scapulae. Once the patient learns correct scapular orientation, he repeats the correction and maintains the position regularly throughout the day so that it becomes a habit.

Training the endurance capacity of the scapular stabilisers[9] (Level of evidence 1B) Repeated repetitions of 10 second holds of the corrected scapular position encourages early endurance retraining. The endurance of the middle and lower trapezius muscles is also trained by performing an exercise in the prone lying position against the effects of gravity.

Retraining scapular control with arm movement and load[9] (Level of evidence 1B)This is important when activities such as computer or deskwork aggravate pain. The patient is encouraged to maintain their newly learned scapular position while performing small range (+/- 60 degrees) arm movements, or during, for example, work at a computer. Scapular control in association with control of cervicothoracic postural position is also trained for functional activities such as lifting and carrying.

Upper Quarter Strengthening Exercises[11] (Level of evidence 1A)

Middle Trapezius Strengthening Lower Trapezius Strengthening
Middle Trapezius Strengthening Lower Trapezius Strengthening

Adding upper quarter exercises for patients with cervical dysfunction is important in order to integrate ‘global’ muscles that have connections to the cervical spine through anatomical chains (most notably those connecting the axial and appendicular skeletons).

Re-education of Posture[9] (Level of evidence 1B)

Posture is an indirect measure of the functional status of the neuromuscular system.[13] (Level of evidence 5) Postural position is trained in sitting and is corrected from the pelvis. The second aspect of re-education of postural position is the correction of scapular position. Maintenance of a correct scapular position with appropriate muscle coordination has the added benefit of inducing reciprocal relaxation in muscles such as levator scapulae, which reduces muscular pain in the area.

Sensorimotor Training

Because CGHs are thought to be a dysfunction of the sensorimotor system.[11] (Level of evidence 1A) Sensorimotor exercises include progressive exercise on unstable surfaces to promote reflexive stabilization and postural stability. Unstable surfaces such as exercise balls or foam pads can be used to add challenge to the cervical spine as well as the whole-body for stabilization exercises. These final stages of the rehabilitation program for CGH patients can be progressed toward functional activities to return the patient to full participation.

Trigger point therapy

This is composed of different manual approaches, for example, compression, stretching, or transverse friction massage. Pressure release over the sternocleidomastoid muscle TrP is applied and pressure is progressively applied and increased over the TrP until the finger encountered an increase in tissue resistance (tissue barrier). This pressure is maintained until the therapist sensed a relief of the taut band. At that moment, the pressure is increased again until the next increase in tissue resistance. Do this 3x/session. Stretching of the taut band muscle fibers is also important. This technique has been found to be effective for lengthening the TrP in the muscle and the associated connective tissue. The therapist apply moderate slow pressure over the TrP and slides the fingers in the opposite directions. Trigger point manual therapy is applied slowly and is performed without inducing pain to the patients.[25] (Level of evidence 1B)

(Myofascial) Mobility, strength, stability and postural exercices [26] (Level of evidence 1B)

These technics were primarily postisometric relaxation procedures (A), myofascial mobilization (B) and selected elements of McKenzie therapy (C). Exercises were mainly applied to the muscles with TrPs, showing the pathological increase in rEMG amplitude. When relaxation of painful, tensed muscles is achieved, the next step of treatment include strengthening exercises of the same muscles. All of them are supervised by a physiotherapist. Exercises intensity shall not increase the pain sensation in the cervical spine, shoulder and girdle muscles. They aren’t supposed to evoke the headache. There are isometric exercises with the gradual loading increase (D) and dynamic exercises (E). Elastic therabands are commonly used during these exercises. Additionally, the self-control exercises of the correct body posture are carried out in front of the mirror relying on the visual feedback (F).[26] (Level of evidence 1B)




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