Cervicogenic Headache

The annual incidence of neck pain in the general population is approximately 15% (1). Prevalence numbers are reported to be from 10% to as high as 20% (2–4). Prevalence numbers for Cervicogenic Headache (CEH) vary between 4.1% and 17,8%. This difference can be due to the patient sample and how the criteria has been used(5). The higher numbers are probably due to methodological errors or the population on which the studies have been performed. Both a female preponderance of 75% (6–8) and a female/male ratio of 0.71 has been described(5), this is again probably due to the fact that the later study is a grass-root study while the first one is hospital based, and males are more reluctant to seek medical help than women.

Both the International Headache Society (IHS) and the Cervicogenic Headache International Study Group (CHISG) have put forward criteria’s, for this case study the CHISG criteria has been used(5). CEH is characterized by unilateral headache without side shift, or unilateral on two sides, where the pain attacks start in the neck and (sub) occipital region and slowly spreads to the eye and oculofronto-temporal region where the pain maximizes. This criteria is obligatory according to Sjaastad(5,8). During long lasting attacks the pain may cross the midline and can be combined with facial pain in severe attacks(5–8). Signs of neck involvement is a major diagnostic criteria, and as well obligatory for a diagnosis(7,8). Headache should be precipitated by neck movement, sustained awkward head position e.g. during sleep or work or external pressure on the upper cervical or occipital region on the symptomatic side. Stress and hard work can also be precipitating factors. Reduced range of motion of neck of more than 10 degrees and ipsilateral, diffuse arm and shoulder pain is often present (5–8). The presence of all these factors, together with diagnostic blocks, secures the diagnosis(5,7,8). Arm pain is least frequent while reduced neck range of motion should be present for diagnosis(5).

It often starts off as episodic attacks but often becomes chronic in nature with fluctuating pain(5–8). The attacks can last from just a few hours to many days/weeks and this unpredictable pattern lies in the nature of the complaint(7). Pain is continuous in 54% of the patients and 61% have longer attacks than 72 hours. The frequency ranges from 1 per 6 months to 2-4 times per week (5). There is a relative to absolute lack of drug effects(7). Patients have often had a trauma to the neck and/or head in the past(6–8). Typical characteristics include moderate to severe pain, non-throbbing (throbbing pain present in only 2%), non-lancinating, but less severe than Cluster HA and Chronic Paroxysmal Hemicrania(6,8). Nausea and phono/photophobia can be present but less severe than in Migraine. Dizziness (24%), ipsilateral blurred vision, difficulties swallowing and ipsilateral edema in the periocular area can be present(6–8).

Radiological investigations of patients diagnosed with CEH, based on symptoms similar to the CHISG criteria, did not show any stereotyped radiological appearances. The changes seen were not different from asymptomatic subjects, and can not give any evidence to the etiology of CEH(9). CEH is a secondary headache where the primary problem is found in the neck(5–7), and can be seen as a reaction pattern which involves various headaches originating in the neck(6–8,10), where the source is unknown but could include referred pain from the tendinous insertion in the occipital area, along the course of the major occipital nerve, grove behind the mastoid process and upper part of the SCM where the minor occipital nerve runs(7), auriculotemporal nerve, the mandibular branch of the trigeminal nerve, C1, C2 and lower cervical nerve roots, ganglia, uncovertebral joints, facet joints, disc, bone, periosteum, muscles like the upper trapezius, splenius and SCM, ligaments, venous lakes around ganglia, and is by no means limited to a bony structure which is a common misunderstanding (5–8,11). According to the Kerr principle put forward in 1961, referred to in several publications (10,11), a pathogenetic model which explains the pain mechanism, pain in the forehead may be caused by painful stimuli being transferred from the neck/posterior part of the head, mainly by C1-C3 nerves. In the brainstem there is an intimate relationship of nerves to the caudal part of the spinal trigeminal nucleus. Cortical interpretations of the impulses coming from posterior parts may be pain in the area of the opthalamic division of the trigeminal nerve(10,11).

Positive anaesthetic blockages is a strong indication for CEH and is considered an important diagnostic test, and should focus on the greater or lesser occipital nerves, C2 root, 3rd occipital nerve, facet joints, and lower cervical roots (6–8,10–12). CEH patients responded significantly better to nerve blocks than MwoA and TTH and the pain should be abolished(7,10–12). CEH was the only patient population where pain in the forehead was reduced after GON blockage and this could be an indication that the Kerr principle is active(11). The GON is made up of the medial fibres of dorsal ramus of the C2 nerve. Blockade of the C2 nerve resulted in a complete relieve of pain in 50% of the cases with CEH, and 80% of these responded positively to GON blockage. All other nerve blocks only gave partial release of symptoms (10). Less than 20% had the same result after a C2/C3 facet joint blockade, which is innervated by the C3 dorsal ramus (Third occipital nerve) and C2 dorsal ramus, and none after C3-C5 nerve blockades (10). Critic has been put forward to the way blocks have been performed and subsequent denervation. Pain arising from a facet joint or other structure should respond to blocks if responsible for the pain (12).

Pain Pressure Threshold has also been used to diagnose CEH patients, where they displayed a lower threshold than migraine and TTH patients. The occipital region, which is innervated by the C2 nerve root, on the painful side reacted differently than the rest of the head. The superior insertion of the SCM was the most painful (11). For scientific work one should use an anaesthetic blockade to the greater occipital nerve and C2 nerve root as a golden standard as diagnostic test and a strict inclusion criteria of unilateral headache without side shift(7). For clinical work the headache can be bilateral(7). These two diagnostic tools have not been used in this case study.

Differential diagnosis include Cluster Headache, Trigeminal neuralgia, herpes zoster, optic and retrobulbar neuritis, SUNCT like headache, hemicranias continua, TMJ dislocation, Carotidynia, Cerebro Vascular disorders, Mechanical (occipital) nerve irritation, and masseter muscle spasm(13). It is especially hard to differentiate between migraine without aura (MwoA), Tension Type Headache and CEH(6,7,11). While CEH is unilateral, MwoA switches side, either during or between attacks(6,11), and while CEH starts posteriorly in 97%, MwoA normally starts in the frontotemporal region(less than 10% posteriorly)(5–7). CEH may be one of the three large, recurrent headaches and seem to be the only major headache with initial, unilateral posterior pain that systematically spreads to the front(5). CEH, TTH and MwoA can be found simultaneously in patients. It does however seem clear that these conditions have different pathogenetic mechanisms (11).

State of the art treatment for CEH has until now been manipulations and specific exercises to re-educate muscular control in the cervical region. Both exercises therapy and manipulations have shown to be effective after the treatment and at 12 months. The combination also shows good results but is not significantly better than one or the other on most outcomes(14). A review from 2010 states that there is moderate quality evidence for exercise therapy, spinal manipulations and self SNAGS(15).

Most therapies we do as manual therapists are based on a bottom up approach. In light of the evidence that there is a muscular component to CEH and that muscular component is a motor control impairment problem it would make sense to investigate the top down approach. It is a problem with the recruitment of the muscle, not the muscle it self.

Active range of motion assessment of the cervical spine

Hall and Robinson found active range of motion assessment in CEH patients and asymptomatic subjects to be identical (16). Ogince et al. compared CGH patients with subjects having migraine with aura and asymptomatic subjects. Again no difference could be found and therefore one cannot distinguish between a patient with migraine and CGH by assessing the active ROM(17). This could be due to the fact that adjacent segments are able to compensate for the loss of movement at a hypomobile segment.

Passive manual examination of the cervical spine

The inter-examiner reliability for passive assessment of the quantity and quality of motion in individual vertebral motion segments of the cervical spine ranges from poor to fair. Motion assessment of motion segment C1-C2 showed at least fair level of reliability in 5 studies, while motion segment C2-C3 had fair to substantial values in three studies. Overall the quality of the included studies was low(18). In a study using representative patients, substantial reliability was found for segment C2-C3, and slight to fair reliability overall(19).

A good reliability for the manual examination above C4 has been reported. It has to be noted that they were not trying to assess the quantity and quality of the movement as was the outcome measured in the review of van Trijffel (18), but trying to identify cervical joint dysfunction and thus the symptomatic segment in patients with cervicogenic headache. The unadjusted Kappa coefficient for the inter-rater reliability was 0.68. When determining whether or not a single segment was symptomatic the unadjusted Kappa coefficient was between 0.61 and 0.71. The Kappa coefficient for inter-rater reliability was 0.40, 0.70, and 0.71 for C0-C1, C1-C2, and C2-C3 respectively(20).

Manual examination of the cervical and thoracic spine in patients with cervical spine pain and headache. Hall and Robinson (16) reported that all subjects with CEH revealed upper cervical spine joint involvement upon manual examination.

The flexion rotation test (FRT) is therefore used to identify problems in patients with cervicogenic headache and also serve to differentiate between the two types of headache.

The patient is placed in supine with the cervical spine in full flexion with the occiput resting against the therapist’s abdomen to block as much rotation as possible above and below C1-2. The head is then rotated to the left and the right. The test is positive if resistance is felt , pain is provoked or range of motion is limited. This indicates a limited rotation of C1 on C2. At least 10 degrees of deemed limitation had to be present for the test to be positive in clinical practice.

It has been found that the average rotation in asymptomatic population is 44 degrees whereas the symptomatic group only displayed 28 degrees of rotation (16). An other study found the average ROM for unilateral rotation to be 39 degrees for migraine with aura patients and asymptomatic subjects and only 20 degrees for subjects suffering from CEH(17). Amiri reported similar values (42 degrees) for asymptomatic subjects, but these measurements were made with the patient sitting and performing the test actively (21). Headache at the time of measurement had a significant inverse negative effect on the ROM measured with the FRT(22). This is important if one uses this test as a treatment outcome. In this research 100% of the subjects thought to have C1-2 as the dominant symptomatic segment and 86% of the total group had a positive FRT, while the remaining subjects in the study where C2-3 seemed to be the dominant symptomatic subject all had a negative FRT. Further 0 % of the subjects scoring negative on the FRT had a symptomatic C1-2.

Kappa values were reported to be .81, showing excellent agreement between the two therapists. Agreement was reached in 98 % of the cases. A cut of score of 32 degrees was suggested. They found the ROM of the FRT to be significantly reduced in C1-2 dominant CGH. Sensitivity and specificity ranges between .78 and .91 and 0.85 and.90 respectively depending on the literature, and the diagnostic accuracy was 91 %(17,22). The test can therefore be used to differentiate between different types of headache. Test retest reliability has been shown on symptom free days. Intra rater reliability for ROM was .95 (95% CI) and the minimal detectable change was 4.7 degrees. The positive and negative likelihood ratio was 5.18 and 0.26 respectively(23).

It is known that sufferers from CGH also display a poor activation of the local stabilizers of the cervical spine. One of the tests proposed to assess the local stabilizers is the Cranio-cervical flexion test (CCFT). An air-filled pressure sensor (“the stabilizer”) is placed in the lordosis of the neck close to the occiput. The neck is placed in neutral with forehead and chin in the horizontal plane and the imagined ear line bisecting the neck in two and parallel to the bench. For a correct test result, the patient practices the movement before the commencement f the test. The patient is asked to perform a head nodding action of cranio-cervical flexion (CCF) in five progressive stages from a neutral starting position in the supine crook lying position. The increase in pressure comes from the slight flattening of the cervical lordosis occurring with cranio-cervical flexion and contraction of the local stabilizers. The tonic holding capacity of the Longus Colli and Capitus is being tested in this way. The pressure sensor is inflated to a baseline of 20 mmHg and the patient is instructed to increase the pressure by 2 mmHg at a time performing a CCF, ending up at a final pressure of 30 mmHg. At each stage the pressure had to be kept for 10 seconds. Neck retraction is a common substitution strategy employed by patients experiencing difficulties reaching the different stages of the CCFT. To prevent this one should look for increasing amounts of CCF for each succeeding stage of the CCFT. Falla (2003) found that the amount of CCF ROM was significantly different between the stages of CCFT and that there was a linear relationship between ROM and increased pressure(28) .

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