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Cervicogenic Headaches: Mechanisms and Manual Therapy Treatment: a literature review.

Updated: May 4, 2019

Cervicogenic headaches are 1 of the 14 classifications of headache, as recognized by the international Headache Society, falling under the secondary headache subcategory, and account for 15-20% of all chronic and recurrent headaches. (1,2)


The International Headache Society describes CGH as “pain referred from a source in the neck and perceived in one or more regions of the head and/or face” (3) symptoms of Cervicogenic headache may also include: nausea, phonophobia, photophobia, dizziness, blurred vision, swallowing difficulties, or periocular edema. (4)


Clinical diagnosis of CGH involves inclusion of the following characteristics:

1. Unilateral head pain without side shift within an episode of headache pain,

2.restricted upper cervical spine joint mobility (on average 20* vs 39* normal (ogic et al 1997) ,

3. reproduction of HA symptoms with external pressure to ipsilateral upper, posterior cervical spine. (5)


Diagnostic criteria as proposed by the IHS are a little more complex. A) pain referred from a source in the neck and felt in one or more regions of the head and/or face, fulfilling criteria C and D. B) clinical, laboratory, and/or imaging evidence of a disorder or lesion within the cervical spine or soft tissues of the neck know to be, or generally accepted as, a valid cause of headache. C) evidence that the pain can be attributed to the neck disorder or lesion based on at least one of the following: 1) evidence of clinical signs that implicate a source of pain in the neck, or 2) abolition of headache after diagnostic blockade of a cervical structure or its nerve supply with placebo or other adequate controls. D) pain resolves within 3 months after successful treatment of the causative disorder or lesion (3)


Zito et al validated the use of pain provocation, AROM and PPIVM testing in the diagnosis of cervicogenic headaches in a RCT that utilized three groups. 1) 27 with cervicogenic headache, 2) 25 with migraine and 3) 25 with non-headache as a control group. The range of headaches was from 9 months to 10 years. They looked at head and neck posture and found no difference between groups for postural angles, pressure pain thresholds or joint position sense. It should be noted that 1/3 of these subjects were asymptomatic, and maybe posture does not play as much a role as is thought, if any. They did find that the cervicognenic headache group had significantly less cervical AROM in flexion/extension than the other two groups. Pain and hypomobility on the 0-6 scale, during PPIVM testing to C0-C3 was provoked more frequently in the cervicogenic headache group, and to a greater extent than the migraine or control groups. They found that all painful upper cervical joint were hypomobile, but not that all hypomobile joints were painful . There was also higher incidence of muscle tightness in the cervicogenic headache group. The cervicogenic headache group showed poorer performance at 26, 28 and 30 mmHg on the CCFT. The conclusions of the study were as follows: painful and hypomobile C0-C3 segments with PPIVM testing could discriminate the cervicogenic headache group from the migraine and control group with a sensitivity of 80%. (6)


Hall and Robinson validated the flexion-rotation test for identifying cervicogeninc headache patients from asymptomatic controls. They found that 24/28 cervicogenic headache patients had a positive flexion-rotation test and all 28/28 asymptomatics had a negative flexion-rotation test. They found the average rotation in flexion of the asymptomatic patients was 44* and the average toward the headache side was 28*. They found the greater the restriction in the flexion-rotation test the more severe the headache would be as far as frequency, duration and intensity, and they found the C1/C2 segment the most frequent symptomatic cervical motion segment in cervicogenic headache patients.


Mechanisms


The link between the cervical spine and the head/face is the trigeminocervical nucleus (TCN). Most of the head/face is innervated by the trigeminal nerve, thus any head/face pain must involve activation of the trigeminocervical nucleus (7). The convergence of the dorsal horn afferents from C0-C3, with the trigeminocervical nucleus, most densely mixing with the ophthalmic branch of the trigemeinal nerve at the levels of C0-C3, which terminates in the supraorbital region, the most common presentation of pain for cervicogenic headache patients with a complain of “pain or pressure behind my eye” (7,8) In the case of the cervicogenic headache afferent overflow from the levels of C0-C3 bombards the trigemniocervical nucleus and the brain interprets it as a headache most commonly in the ophthalmic distribution (5,7-9). A further investigation into the connections is discussed in the following anatomy section.


Structure and Functional Anatomy of pain generation in the neck and head


If you look at the anatomy of the upper cervical spine, it is full of potential pain generators do to the high innervations, anatomic structures, and the predisposition to stress and injury. It has been confirmed that zygapophysial joints, intervertebral discs and muscles of the cervical spine are pain generators after whiplash and other neck injuries. 7 Nociceptive afferents in the trigeminal nerve, from the supratntorail, dura synapse on second order sensory neurons in the trigeminal cervical nucleus as nocioceptive afferents from cervical structures, and is continuous longitudinally with the dorsl horns of the upper 3 to 4 segments of the cervical region.(7,9-11) Stimulation of the greater occipital nerve has been shown to increase the excitability of dural inputs, as well as stimulation of the dura resulting in sensitization of second order neurons which lower their threshold to activation from neck upper cervical structures and muscles. (7,9,10,12,13) It has also been shown that afferent innervation of the large intracranial blood vessels and the dura mater is primarily nociceptive and originates in the trigeminal ganglion. The bipolar trigeminal cells project centrally to the trigeminal nucleus caudalis (TNC) and its reciprocal parts at the C1 and C2 levels of the spinal cord. stimulation of the trigeminal ganglion results in the accumulation of the immediate early genes c-fos and c-jun in the Rexed’s laminae I and II of the TNC (14) to connect the structure with function and show a causative relationship Busch et al. demonstrated the functional connection of the trigeminal nerve and the suboccipital region, C0-C3 by greater occipital nerve blockade and nociceptive blink reflex. The blink reflex is a trigeminofacial brainstem reflex which can be used to delineate the topographical level of brainstem lesions and identify functional changes in the central trigeminal nociception. following greater occipital nerve block (12)


To further show an anatomical relationship to the upper cervical spine and afferent connections, Yin et al. 2008 performed dissection of the upper cervical spine nerve plexus. They found that deep to the longus capitis and ventral to the anterior tubercules of the cervical transverse processes and intervertebral foramina, branches from the C1–3 ventral rami formed a superficial cervical prevertebral plexus, consisting of numerous interconnecting arcades. Some of the laterally located branches from this plexus terminated in the longus capitis and longus cervicis. Others ascended along the ventral aspect of the anterior intertransversarius, over the ventral capsule of the lateral atlanto-axial joint and toward the ventral capsule of the atlanto-occipital joint.15 Terminal branches of the plexuses entered the ventral joint capsule of the lateral C1–C2 joint and were seen approaching the dens. They came to the conclusion that this supports the clinical observation that electrical stimulation in the C2 ventral gutter can reproduce headache in patients with C1–C2 joint pain.15 further supporting the primary pain generator in cervicogeninc headache being the C1/C2 articulation. (5,7,8,16-19)


Another study conducted by Piovison et al. showed that an injection of sterile water over the greater occipital nerve region of C2, resulted in pain creation in the ophthalmic branch of the trigeminal nerve (20)


Treatment


There are various treatment options, including but not limited to: medication, injections, massage, exercise, mobilization and manipulation. A systematic review performed by Bronfort et al. 2005 concluded SMT and low level intensity endurance exercises is effective for treating Cervicogenic headaches and that SMT may also be effective for migraines, but not for tension type headaches.


Youssef et al. 2013 compared exercise and cervical mobilization to C1-C3 vs exercise and massage (which included manual traction and muscle energy techniques) to the upper back/pecs and cervical musculature. They found that after 12 sessions within 6 wks with at least 48 hrs in between sessions, with final measurements taken at week 7, 1 week post last session. The mobilization group did better than the massage group with intensity, frequency and duration of symptoms as well as cervical ROM (21). In 2005 Fernandez-de-las-Penas performed a systematic review and was only able to include 2 studies on spinal manipulation , thus concluding that SMT may be effective in reducing headache intensity, headache duration, medication intake and headache frequency. (1) since 2005 several other systematic reviews have been conducted.


Spinal manipulation has been shown to be effective for the treatment of Cervicogenic headaches. HVLAT manipulation directed to the upper cervical spine, specifically C1/C2 and the upper thoracic spine, particularly T1/T2 has been shown both in the literature 4 to successfully treat cervicogenic headaches.


A pseudo randomized control trial looked at the effects of cervical spinal manipulation on sensorimoter integration, using somatosensory evoked potential as the measurement tool. They took 24 subjects with reoccurring neck pain or stiffness with certain activities, such as working at the computer and sustained postures, but at the time of the study had to be pain free. The first 12 who met the inclusion were put into the experimental group, who received spinal manipulation to their dysfunctional cervical segments and the next 12 in the control group, this way they could age mach the control group if necessary. They found that cervical spinal manipulation may alter cortical somatosensory processing and sensorimotor integration. Post manipulation there was a 20-30 minute period of change in the frontal and parietal regions . (22) This study provides support that spinal manipulation has a direct effect on spinal muscle afferents, most likely Ia. When we combine this with the knowledge that over stimulation of the dorsal horn from the C1/C2 levels results in activation of the TCN, we can deduce that spinal manipulation of the C1/C2 segment will decrease afferent input and result in reduction of the TCN and headache symptoms.


A RCT from 1995 conducted by Nilsson et al. had 39 patients who met the inclusion criteria for Cervicogenic headache. Half of them received HVLAT manipulation and the other half received low-level laser to the upper cervical region and deep friction massage to lower cervical and upper thoracic regions. Both groups where treated 2x per week for 3 weeks, the manipulation group reported a reduction in analgesic use per day, headache intensity per episode, and number of headache hours per day however the difference between the groups failed to reach statistical significance. (2) Two years later they conducted another RCT, which took the prior 39 patients and their data and added 16 more, as the authors report, the main reason the first trial failed to show statistical significance was too small of a sample size, or type 2 error. Therefore they opened back up the recruitment and included the additional patients and data in the calculations. This time they met statistical significance showing a 36% decrease in analgesic use, a 69% decrease in number of headache hours, and 36% decrease in headache intensity. They collected this data only 1 week after conclusion of the last treatment session, so no long term results can be determined from this study, however they could conclude that “spinal manipulation has a significant positive effect in cases of cervicogeninc headache”. 23 Jull conducted a RCT with 200 participants allocated into 1 of 4 groups: 1) Manipulative therapy, non-thrust mobilization and/or HVLAT to the cervical spine, 2) exercise group, deep neck flexor exercises with pressure biofeedback during the CCFT, serratus and lower trapezius inner range holding exercises and postural correction exercises, 3) combined manipulative therapy and exercise and 4) a control group of medication only 4. All subjects received 8-12 treatments during a 6 week period. At week 7, 1 week post treatment, they found that 76% of the subjects in the active treatment groups gained 50% or better reduction in frequency of headaches over the prior week, 35% of these subjects had complete relief of headache regardless of the active treatment group they were in. At 12 month follow up 72% of the subjects in the active treatment groups experienced 50% reduction in headache frequency and 42% of them reported 80%-100% relief at 1 year follow up. As for medication use, they found that at 1 year compared to baseline, the median medication intake decreased by 93% in the combined group, 100% in the manipulation group, and 100% in the exercise group, and showed a 33% increase in the control group. As in all studies, this had some limitations. First, the manipulative therapy group was a combination of mobilization and HVLAT and it is not broken down to how many participants actually received HVLAT manipulation and second, no description of the target level for the manipulation or mobilization was given. (4)

In a study by Haas et al they looked at dose response and efficacy of spinal manipulation for chronic cervicogenic headache. They enrolled 80 subjects and put them into 1 of 4 groups. 1) 8 HVLAT sessions to the cervical and thoracic spine, w/ 2 minutes of light massage and 5 minutes of hot pack 2) 16 HVLAT sessions to the cervical and thoracic spine, w/ 2 minutes of light massage and 5 minutes of hot pack 3) 8 sessions of light massage for 5 minutes and hot pack and 4) 16 sessions of light massage for 5 minutes and hot pack. The fact that all groups had light massage and hot pack doesn’t create a true control group. There was no difference in headache pain and disability between the 8 and 16 treatment sessions. However, they did find clinically and statistically significant differences between the HVLAT and light massage groups. Some additional limitations to this study are that 22 of the 80 subjects had a concomitant diagnosis of migraine or tension type headaches. Additionally they did not specify the target levels for the HVLAT manipulations and the treating chiropractor performed the outcome reassessments and he was not blinded to the treatment arms.


To summarize the relevant treatment finding, upper cervical HVLAT manipulation in conjunction with upper thoracic HVLAT manipulation appears to be the most beneficial treatment for treating cervicogenic headaches.


Works Sited:

1. Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Pareja JA. Spinal Manipulative Therapy in the Management of Cervicogenic Headache. Headache: The Journal of Head & Face Pain 2005;45(9):1260-1263.

2. Nilsson N. A randomized controlled trial of the effect of spinal manipulation in the treatment of cervicogenic headache. Journal of Manipulative & Physiological Therapeutics 1995;18(7):435-440 6p.

3. IHS classification ICHD-II. 2015.

4. Jull G, Trott P, Potter H, Zito G, Niere K, Shirley D, Emberson J, Marschner I, Richardson C. A randomized controlled trial of exercise and manipulative therapy for cervicogenic headache...including commentary by Triano JJ. Spine (03622436) 2002;27(17):1835-1843 9p.

5. Sjaastad O, T. A. Fredriksen, et al. "Cervicogenic headache: diagnostic criteria. The Cervicogenic Headache International Study Group. " Headache 1998: 38(6): 442-5.

6. Zito G, Jull G, Story I. Clinical tests of musculoskeletal dysfunction in the diagnosis of cervicogenic headache. Manual Therapy 2006;11(2):118-129 12p.

7. Becker WJ. Cervicogenic headache: evidence that the neck is a pain generator. Headache: The Journal of Head & Face Pain 2010;50(4):699-705 7p.

8. Bugduck. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. The Lanclet Neurology 2009:959-68.

9. Dach F, Éckeli Á, Ferreira KoS, Speciali JG. Nerve block for the treatment of headaches and cranial neuralgias - a practical approach. Headache 2015;55 Suppl 1:59-71.

10. Cooper W. Images From Headache: Resolution of Trigeminal Mediated Nasal Edema Following Greater Occipital Nerve Blockade. Headache: The Journal of Head & Face Pain 2008;48(2):278-279 2p.

11. Leston JM. [Functional anatomy of the trigeminal nerve]. Neuro-Chirurgie 2009;55(2):99-112.

12. Busch V, Jakob W, Juergens T, Schulte-Mattler W, Kaube H, May A. Functional connectivity between trigeminal and occipital nerves revealed by occipital nerve blockade and nociceptive blink reflexes. Cephalalgia (Wiley-Blackwell) 2006;26(1):50-55.

13. Giblin K, Newmark JL, Brenner GJ, Wainger BJ. Headache Plus: Trigeminal and Autonomic Features in a Case of Cervicogenic Headache Responsive to Third Occipital Nerve Radiofrequency Ablation. Pain Medicine 2014;15(3):473-478.

14. Uddman R, Tajti J, Hou M, Sundler F, Edvinsson L. Neuropeptide expression in the human trigeminal nucleus caudalis and in the cervical spinal cord C1 and C2. Cephalalgia: An International Journal Of Headache 2002;22(2):112-116.

15. Yin W, Willard F, Dixon T, Bogduk N. Ventral innervation of the lateral C1-C2 joint: an anatomical study. Pain Medicine (Malden, Mass.) 2008;9(8):1022-1029.

16. Bravo Petersen SM, Vardaxis VG. The flexion-rotation test performed actively and passively: a comparison of range of motion in patients with cervicogenic headache. J Man Manip Ther 2015;23(2):61-7.

17. Fredriksen TA, Antonaci F, Sjaastad O. Cervicogenic headache: too important to be left un-diagnosed. J Headache Pain 2015;16(1):6.

18. Ng A, Wang D. Cervical facet injections in the management of cervicogenic headaches. Curr Pain Headache Rep 2015;19(5):484.

19. Sizer Jr PS, Phelps V, Azevedo E, Haye A, Vaught M. Diagnosis and Management of Cervicogenic Headache. Pain Practice 2005;5(3):255-274.

20. Piovesan E, Kowacs P, Tatsui C, Lange M, Ribas L, Werneck L. Referred pain after painful stimulation of the greater occipital nerve in humans: evidence of convergence of cervical afferences on trigeminal nuclei. Cephalalgia (Wiley-Blackwell) 2001;21(2):107-109.

21. Youssef EF, Shanb A-SA. Mobilization versus massage therapy in the treatment of cervicogenic headache: A clinical study. Journal of Back & Musculoskeletal Rehabilitation 2013;26(1):17-24 8p.

22. Haavik-Taylor H, Murphy B. Cervical spine manipulation alters sensorimotor integration: a somatosensory evoked potential study. Clinical neurophysiology 2007;118(2):391-402.

23. Nilsson N, Christensen HW, Hartvigsen J. The effect of spinal manipulation in the treatment of cervicogenic headache. Journal of Manipulative & Physiological Therapeutics 1997;20(5):326-330 5p.




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