Cervicogenic headache: Clinical presentation, diagnostic criteria, and ...

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387. Cervicogenic Headache: Clinical Presentation, Diagnostic. Criteria, and Differential Diagnosis. Fabio Antonaci, MD, PhD,* Torbjorn A. Fredriksen, MD, PhD,.
Cervicogenic Headache: Clinical Presentation, Diagnostic Criteria, and Differential Diagnosis Fabio Antonaci, MD, PhD,* Torbjorn A. Fredriksen, MD, PhD, and Ottar Sjaastad, MD, PhD

Address * Service of Neurophysiopathology, Department of Neurological Sciences, “C. Mondino” Foundation, University of Pavia, Via Palestro 3, 27100 Pavia, Italy. E-mail: [email protected] Current Pain and Headache Reports 2001, 5:387–392 Current Science Inc. ISSN 1531-3433 Copyright © 2001 by Current Science Inc.

Since the first attempt at setting down diagnostic criteria was made in 1990, there has been considerable progress in the field of cervicogenic headache (CEH). CEH makes up a “final common pathway” for several neck disorders that may originate at different levels of the cervical spine. CEH has been defined as being mainly a unilateral headache without sideshift; it may accordingly also be bilateral. Anesthetic blockades are mandatory for scientific work. If the pain is bilateral, it is particularly important that blockades are carried out. Pain stemming from the neck usually spreads to the oculofrontotemporal area. The most characteristic features are symptoms and signs of neck involvement (such as mechanical precipitation of attack, and so forth). Migraine without aura and tension-type headache are the most difficult differential diagnosis problems.

Introduction Since the first cases of cervicogenic headache had been identified [1], considerable progress had been made. Particularly in the last decade, there have been advances in defining the clinical picture, diagnostic criteria, and therapeutic approach. As repeatedly stated, cervicogenic headache (CEH) is a syndrome, not a disease or an entity sui generis. It constitutes a “final common pathway” for pain stemming from several neck disorders. These may involve such structures as nerves, nerve root ganglia, uncovertebral joints, intervertebral disks, facet joints, ligaments, muscle, and so on [2,3]. This proposes that pain may originate at different levels, including the lower part of the cervical spine [4]. CEH comprises all headaches stemming from the neck with the possible exception of specific headache entities (eg, a subgroup of chronic paroxysmal hemicrania [CPH] with mechanical precipitation of attacks) [3].

Cervicogenic headache has been defined, in principle, as a unilateral headache without sideshift. In the upgrading of the CEH diagnostic criteria [5••], the strict unilaterality criterion has been softened. In clinical practice, patients with bilateral headache may be acceptable (like “the unilaterality on two sides” in tic douloureux) [6,7]. Because CEH is a syndrome, the pathologic process can, probably not so infrequently, be reproduced on the contralateral side. In these cases, a positive response to appropriate anesthetic blockades is essential also in clinical practice (not only in scientific diagnostic work-up), mainly in order to exclude tension-type headache (TTH). Even in the more regular unilateral case, pain may eventually spread to the opposite side when headache becomes severe, but it will remain stronger on the original side [5••]. The typical unilaterality may be probably most clear at attack/exacerbation onset. In CEH, therefore, headache may be strictly unilateral in the most typical and diagnostic case, or it may have a unilateral preponderance; as far as we are concerned it will not occur solely on the side opposite to the usual one [8]. Other, equally important, diagnostic features are the symptoms and signs of neck involvement. Such signs are mechanical precipitation of attacks (both iatrogenically and subjectively induced), reduced range of motion [ROM] in the neck—in one or more directions, diffuse ipsilateral neck/shoulder/arm pain of nonradicular nature or, occasionally, arm pain of radicular nature (Table 1). Iatrogenically induced pain similar to the spontaneous one may be elicited by external pressure over tendinous insertions in the occipital area. Pressure along the course of the major occipital nerve, over the groove immediately behind the mastoid process, and over the upper part of the sternocleidomastoid muscle on the symptomatic side may also provoke similar pain. Intrinsic precipitation mechanisms may be activated by neck movements and/or sustained, awkward head positioning during sleep or during wakefulness (such as washing the ceiling, speaking to one’s neighbor at a table at a party, and so forth). Ipsilateral shoulder/arm symptoms may be even more frequent than they seemed to be initially [9]. One not infrequently encounters patients with marked, more or less constant

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Table 1. Diagnostic criteria of cervicogenic headache Major criteria of cervicogenic headache I. Symptoms and signs of neck involvement: a. Precipitation of head pain, similar to the usually occurring one: 1. By neck movement and/or sustained awkward head positioning, and/or 2. By external pressure over the upper cervical or occipital region on the symptomatic side b. Restriction of the range of motion in the neck c. Ipsilateral neck, shoulder, or arm pain of a rather vague nonradicular nature or, occasionally, arm pain of a radicular nature It is obligatory that one or more phenomena in point (I) are present. Point (a) suffices as the sole criterion positivity within group (I); points (b) or (c) do not (Table 2) II. Confirmatory evidence by diagnostic anesthetic blockades Obligatory point in scientific works III. Unilaterality of the head pain, without sideshift For scientific work this point should be preferably adhered to Head pain characteristics IV. a. Moderate-severe, nonthrobbing, and nonlancinating pain, usually starting in the neck b. Episodes of varying duration, or c. Fluctuating, continuous pain Other important characteristics V. a. Only marginal effect or lack of effect of indomethacin b. Only marginal effect or lack of effect of ergotamine and sumatriptan c. Female sex d. Not infrequent occurrence of head or indirect neck trauma by history, usually of more than only medium severity None of the single points under (IV) and (V) are obligatory Other features of lesser importance VI. Various attack-related phenomena, only occasionally present, and/or moderately expressed when present: a. Nausea b. Phonophobia and photophobia c. Dizziness d. Ipsilateral “blurred vision” e. Difficulties in swallowing f. Ipsilateral edema, mostly in the periocular area (From Sjaastad et al. [5••].)

arm pain of a nonradicular nature [8]. In these cases, the underlying pathology possibly resides in the lower part of the cervical spine (C5 and so on). Patients with marked and more or less constant, diffuse shoulder/arm symptoms may constitute a clinical subgroup; likewise, the rare ones with a radicular pain may form the “radicular arm type” subgroup [8]. However, these phenomena are not infrequently of low intensity, and may be more like a discomfort than a pain. Such phenomena may in the occasional case have their own temporal pattern, more or less independent of the headache attacks. The side-locked unilaterality of the headache combined with the ipsilaterality of the arm pain provides rather compelling evidence that headache on such occasions stems from neck structures, but not necessarily only from bony structures. Regarding pain characteristics, the duration of attacks/ exacerbations varies widely in CEH (from a few hours to a few weeks), with a strong tendency toward chronicity; CEH is not infrequently episodic in the initial phase, becoming chronic-fluctuating later on. The pain of attack starts in the neck, eventually spreading to the oculofrontotemporal area, where, during the acme, it may be as strong as or even stronger than in the occipital region [2,5••]. The duration of pain episodes is most frequently longer than in

common migraine; the pain intensity is moderate, nonexcruciating unlike cluster headache, and usually of a nonthrobbing nature. Autonomic symptoms and signs, like photo- and phonophobia, nausea, vomiting, and ipsilateral periocular edema, are generally less frequent and some of them, like vomiting, are clearly less marked than in common migraine [2,3,5••,8,10,11]. In a recent study by Vingen and Stovner [12], light and sound-induced discomfort and pain thresholds have been measured in patients with TTH, CEH, and in headache-free controls. Although both headache groups were more sensitive to light and sound compared to controls even in the headache-free periods, no differences were found in patients with CEH when tested with and without pain. It is striking, however, that patients with CEH showed a greater photophobia on the symptomatic than on the nonsymptomatic side, whereas no such differences were found in TTH and other unilateral headaches [12]. Difficulties in swallowing is another, rarely occurring associated phenomenon [4]. There have also been cases with features consistent with a CEH picture, but with additional dizziness/vertigo and even with vertebral drop-attacks; such patients may benefit from surgical interventions, such as an anterolateral approach toward the cervical spine, ad modum

Cervicogenic Headache: Clinical Presentation • Antonaci et al.

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Table 2. Summary of minimum requirements for diagnosis Definite cervicogenic headache

Provisional/tentative combination of factors

Precipitation of attacks subjectively and/or iatrogenically Positive anesthetic blockade effect Unilaterally without sideshift*

Reduced range of neck motion; ipsilateral shoulder/arm pain Positive anesthetic blockade effect Unilaterally without sideshift*

* Not necessary in nonscientific work. (Adapted from Sjaastad et al. [5••].)

Jung [1,8]. These patients may constitute another clinical subgroup, namely the “vertebral artery type” [8]. Recently, even cases of “symptomatic” CEH have been described. Delfini et al. [13], for instance, reported a case of CEH as the solitary feature of a localized, intracord benign tumor in the cervical area. The headache apparently disappeared after the surgical removal of the neoplastic mass. In the study by Maciel et al. [14,15], 15% of headache patients in an outpatient clinic in Brazil were diagnosed with CEH. As it emerges from the few epidemiologic studies conducted in the last decade [14–17], this headache seems to be fairly frequent. In the Portuguese study [16], the prevalence of CEH was found to be 0.4% on the basis of International Headache Society (IHS) criteria, yet when applying the criteria of Sjaastad et al. [2,5••], the prevalence rose to 1% and 4.6%, respectively if all, or only five of the total six of the criteria were satisfied. The preponderance of females in patients with CEH according to the Sjaastad et al. criteria [2,5••] has been confirmed [10,11,18••].

Diagnostic Criteria and Diagnostic Work-up In the revised diagnostic criteria [4], the importance of symptoms and signs of neck involvement has been further stressed. Mechanically precipitated attacks—or pain similar to that of attack—subjectively and/or iatrogenically induced, is an obligatory requirement for a certain/definite diagnosis, as is the positive anesthetic blockade effect. Unilaterality without sideshift is highly desirable in scientific works (Table 2). The lack of I) [a] criterion will clearly reduce the validity of the diagnosis. It has been proposed that the presence of I) [b] and [c], II), and III) criteria may be consistent with a “provisional”/tentative diagnosis (Table 1) [5••]. Regarding cervical spine mobility (ROM), different techniques are available for measuring neck ROM [19]. The simplest ones include the inclinometer, goniometer, and Cybex (MedX Corp., Ocala, FL) equipment, whereas the more sophisticated ones are based on three-dimensional analysis, such as the Elite system (BTS, Milan, Italy) [19,20•]. Cybex equipment, for example, has been used by Zwart [21] to assess neck mobility in different headache disorders. This method proved to be easy to apply in clinical practice, was inexpensive and reliable, and it showed a significantly reduced rotation and flexion/extension in patients with CEH compared with healthy subjects and

other headache patient categories, namely migraine without aura and TTH. Even pure clinical examination of the neck may be useful in clinical practice, in particular if carried out by a skilled examiner, because a reduction in cervical ROM contributes to establishing a CEH diagnosis. Moreover, an error of 5° to 10° made in the evaluation of neck ROM (ie, rotation or flexion) probably is not really relevant in the clinical assessment of CEH, whereas, if surgical therapies are considered, and for comparing patient series, a more accurate functional evaluation is indicated [8,22]. In the revised criteria, among the “Other Important Characteristics” (Table 1), the lack of complete response to indomethacin, sumatriptan, and ergotamine has also been introduced. Although CEH is not, in principle, a posttraumatic headache, a history of neck/head trauma should still be considered to be of potentially pathogenetic importance, especially if it is of more than “only medium severity” and has a putative whiplash mechanism [3,5••]. A history of a long-lasting, strictly unilateral headache is suggestive of CEH, in particular if in a female subject. The temporal pattern, that is the “nonclustering” but chronic-fluctuating pattern, and the quality of pain (usually moderate and nonexcruciating) distinguish CEH from other unilateral headaches, such as cluster headache and CPH. Hemicrania continua (HC) and migraine without aura may also represent differential diagnostic problems. An appropriate anamnesis and accurate neurol o g i c e x a m i n a t i o n , s h ow i n g a r e d u c e d RO M a n d precipitation mechanisms, are fundamental elements in distinguishing this headache from other ones. The combination of pain first felt in the neck and then spreading unilaterally to the frontal area on the same side fortifies the suspicion that one may be faced with a case of CEH. If the pain is moderate and nonexcruciating of a nonthrobbing nature the suspicion will utterly grow [23]. The site and radiation of pain, the temporal pattern, and the mechanical precipitation of attacks, both iatrogenically and subjectively, are also important aspects of the clinical picture and may help in distinguishing between CEH on the one hand and migraine and TTH on the other [18••]. In patients with bilateral pain, but still with a preponderance on the usual side, anesthetic blockades become mandatory even in clinical practice. In order to single out the correct level of affection, the blockades should be directed to the nerve or nerves, where most likely the pain originates/is elicited, on the side of prevailing pain [7]. For

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appropriate blockades, the smallest possible quantity of anesthetic agent (0.5 to 1.5 mL) should be used [7,24], either with long-lasting or short-lasting anesthetics, and a typical, severe pain should preferably be present at the time of testing (≥ 30% to 50% of maximum pain). Furthermore, solitary blocks have to be primarily performed, in order to identify the source of pain as accurately as possible and to assess the effect properly. In the event of pain arising in more than one locus, multiple blockades are indicated. These include blocks of the greater (GON) and minor occipital nerve (MON), of the third occipital nerve and the facet joints (mainly C2/C3) [8], and the segmental nerve roots. Blockades of auriculotemporal and supraorbital nerves may be necessary in differential diagnosis [24]. The blockade has a positive effect if pain is drastically reduced in areas not anesthetized, such as, the frontotemporal area [5••]. Cervical spine radiograph is not a sensitive enough method for diagnosing CEH, because no specific radiologic abnormalities were found (by means of plain radiographs), neither by Pfaffenrath et al. [25] nor by Fredriksen et al. [26]. In other studies [11,23], the most frequent findings were a rectilinearization of the cervical spine and/or disc protrusions. Functional radiography, however, may reveal a hypo- or hypermobility at a certain level of the cervical spine [21], which may indicate the level of pathology. In order to corroborate the suspicion of nerve root pathology of the lower cervical spine, or in order to exclude Arnold-Chiari malformations and other pathologies, magnetic resonance examinations may have to be carried out [27]. It is interesting that when employed in a rather rigid manner, the present CEH criteria may seem to be as reliable as the IHS criteria are for migraine [28••].

Differential Diagnosis Other unilateral and side-locked headaches, such as cluster headache, CPH, and HC, must be considered in differential diagnosis (Table 3). The pain characteristics like severity, temporal pattern, and the presence of marked autonomic symptoms and signs differentiate cluster headache from CEH. Furthermore, in cluster headache, CPH, and HC, anesthetic blockades of the type already mentioned have no effect [5••]. As in CEH, CPH can occasionally present with a mechanical precipitation of attacks. The mode of precipitation and the onset of precipitated attacks seems to differ in the two headaches: CEH requires a long-lasting provocation, and the onset of pain usually seems to take half to 1 hour or more, whereas the onset in CPH takes place in a few seconds up to a minute [3]. A positive therapeutic response to indomethacin can distinguish HC from CEH. An absolute response to indomethacin is characteristic of CPH also (Table 3). CEH is generally unresponsive to indomethacin, or may respond in an incomplete way, even if a rather clear response has been observed in sporadic cases (Table 3)

[29]. The pain in HC seems to be localized mainly in the frontotemporal area [30], whereas in CEH it starts from the neck, eventually spreading toward the forehead/temporal area, where the maximum pain finally may be located. Usually, patients with HC do not complain of stiffness in the neck, and generally there is no reduction of neck mobility on physical examination. Conversely, a reduced ROM can be clinically demonstrated in most cases of CEH, frequently in more than one direction. There does not usually seem to be much difference between these two headaches with regard to autonomic symptoms and signs, but HC at times presents more intense nausea/vomiting [29]. Other signs of neck involvement, such as shoulder and arm pain and mechanical precipitation of attacks, are usually absent in HC. Similarly, a history of direct or indirect neck trauma has not been felt to play a decisive role in HC, whereas it is a not infrequent phenomenon in CH (Table 3). Regarding common migraine, in spite of many similarities, such as unilaterality of headache, female preponderance, and associated autonomic symptoms, there are fundamental differences [31]. Unilaterality in CEH is sidelocked, whereas characteristically in migraine without aura there is a sideshift, either from attack to attack or during the same attack. Pain usually starts in the frontotemporal areas in common migraine; on the contrary, in CEH it is initially felt in the neck/occipital region. Autonomic features are much less pronounced in CEH than in common migraine. Other typical traits of CEH are the symptoms of neck involvement (in particular mechanical precipitation of attacks) and the positive response to anesthetic blockades (not only of the GON and MON, but also of the C2/C3 facet joint, and so on). A positive response to appropriate treatment (indomethacin for HC and ergotamine/sumatriptan for migraine without aura) is usually helpful in discriminating between these two headaches and CEH. In a recent study, migraine without aura and CEH seemed to coexist in a few exceptional cases (four patients: three female and one male, mean age 50) [32]. Anesthetic blocks and drug treatments showed different results in the two different headaches in the same subjects. In another series of headache patients with pain stemming from the neck, there seemed to be a coexistence of the two headaches in 10% of the cases [23]. Dull-pressing quality of pain, bilateral localization, and absence of mechanical trigger factors are the main characteristics that differentiate TTH headache from CEH [18••,33]. Moreover, anesthetic blockade is an important adjunct diagnostic tool in the differential diagnosis versus TTH, because a negative effect of blocks of the GON has been reported in TTH [24]. In fact, the pain reduction is localized to the anesthetized area both in TTH headache and in migraine, whereas in CEH there is an additional pain relief with a GON block in the forehead. The latter sequence of events is of considerable differential diagnostic importance.

(Short-lasting provocation with the onset of CPH attacks within a few minutes) -+ Absolute response to indomethacin

(Long-lasting provocation; the onset of attacks takes ½-1 hour or more) + ++ (A partial response could be present, with a rather clear response only in sporadic cases) Few and only moderately expressed (Also “local”)

+

+-

+

Moderate-severe, nonexcruciating +

Few and only moderately expressed

Absolute response to indomethacin

-

-

(Also “local”)

+

Response to sumatriptan/ ergotamine

-

-

Throbbing, excruciating -

Clustering

Oculo-frontotemporal area

+

CH

+

Close to absolute response to sumatriptan/ ergotamine

-

-

-

Pulsating

Attacks of varying duration, usually 4 to 72 h

Unilaterality usually with sideshift + Oculo-temporal area and forehead

M

CEH—cervicogenic headache; CH—cluster headache; CPH—chronic paroxysmal hemicrania; HC—hemicrania continua; M—migraine without aura; TTH—tension-type headache. Plus sign (+) indicates present. Minus sign (-) indicates absent. (From Sjaastad et al. [5••].)

Autonomic symptoms and signs

Shoulder and arm pain Neck trauma Effect of anesthetic blockades Response to indomethacin and/ or sumatriptan/ ergotamine

Reduction of the range of motion in the neck Mechanical precipitation of attacks

Pain characteristics

+ Oculo-frontotemporal area

+

HC

Long-lasting attacks toward chronicity (fluctuating continuous pain) Lancinating, excruciating Moderate-severe, nonexcruciating -

Multiple and relatively short-lasting attacks

+ Oculo-temporal area and forehead

+ Stemming from the neck, spreading to the oculo-frontotemporal area Episodes of varying duration, or fluctuating continuous pain

Temporal pattern

+

+

Unilaterality of pain without sideshift Female preponderance Pain topography

CPH

CEH

Symptoms and signs

Table 3. Differences and similarities between the different types of headaches

Few and only moderately expressed

-

-

-

-

Dull-pressing

Long-lasting attacks toward chronicity

Band-like

-

TTH

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Conclusions The essential features of CEH are a combination of unilateral pain, ipsilateral diffuse shoulder and arm pain, reduced ROM in the neck, presence of mechanical precipitation mechanisms, and discontinuation of the pain on anesthetic blockades in the typical case. The differential diagnosis should be done versus migraine, HC, spondylosis of the cervical spine, and TTH as regards to the bilateral variant of CEH.

References and Recommended Reading Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance 1.

Sjaastad O, Saunte C, Hovdahl H, et al.: “Cervicogenic” headache. An hypothesis. Cephalalgia 1983, 3:249–256. 2. Sjaastad O, Fredriksen TA, Pfaffenrath V: Cervicogenic headache: diagnostic criteria. Headache 1990, 30:725–726. 3. Sjaastad O, Salvesen R, Jansen J, Fredriksen TA: Cervicogenic headache a critical view on pathogenesis. Funct Neurol 1998, 13:71–74. 4. Michler R-P, Bovim G, Sjaastad O: Disorder in the lower cervical spine. A cause of unilateral headache? Headache 1991, 31:550–551. 5.•• Sjaastad O, Fredriksen TA, Pfaffenrath V: Cervicogenic headache: diagnostic criteria. Headache 1998, 38:442–445. Defines the current diagnostic criteria for the diagnosis of CEH; it represents a gold standard for the correct classification of CEH. 6. Antonaci F, Pareja JA, Caminero AB, Sjaastad O: Chronic paroxysmal hemicrania and hemicrania continua: anaesthetic blockades of pericranial nerves. Funct Neurol 1997, 12:11–15. 7. Bogduk N, Aprill C: On the nature of neck pain, discography and cervical zygapophysial joint blocks. Pain 1993, 54:213–217. 8. Fredriksen TA, Sjaastad O: Cervicogenic headache (CEH): notes on some burning issues. Funct Neurol 2000, 15:199–203. 9. Fredriksen TA: Studies on cervicogenic headache. Clinical manifestation and differentiation from other unilateral headache forms [PhD thesis]. Trondheim, Tapir: University of Trondheim; 1989. 10. Fredriksen TA, Hovdal H, Sjaastad O: “Cervicogenic headache”: clinical manifestation. Cephalalgia 1987, 7:147–160. 11. Pfaffenrath V, Dandekar R, Pöllmann W: Cervicogenic headache—the clinical picture, radiological findings and hypotheses on its pathophysiology. Headache 1987, 27:495–499. 12. Vingen VJ, Stovner LJ: Photophobia and phonophobia in tension-type headache and cervicogenic headache. Cephalalgia 1998, 18:313–318. 13. Delfini R, Salvati M, Passacantili E, Pacciani E: Symptomatic cervicogenic headache. Clin Exp Rheumatol 2000, 18(suppl):29–32. 14. Maciel JA Jr, Carmo EC, Bensabath Azoubel AC, et al.: Cefaleia cervicogenica estudio de 194 casos. Arch Neuro-psiquiatria 1994, 52(suppl O):21. 15. Maciel JA Jr, Carmo EC, Ruocco HH, et al.: Estudio clinico de 1229 casos. Arch Neuro-psiquiatria 1994, 52(suppl O):30.

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Pereira Monteiro J: Cefaleias. Estudio epidemiologico e clinico de uma populacão urbana [PhD thesis]. Porto, Portugal: University of Porto; 1995. 17. Nilsson N: The prevalence of cervicogenic headache in a random population sample of 20-59 year olds. Spine 1995, 20:1884–1888. 18.•• Vincent MB, Luna RA: Cervicogenic headache: a comparison with migraine and tension-type headache. Cephalalgia 1999, 19(suppl 25):11–16. Evaluates the application of the latest diagnostic criteria of CEH and applies these criteria also in TTH and migraine. The existing criteria adequately distinguish CEH, migraine, and TTH. Site and radiation of pain, the temporal pattern, and the induction of attacks from neck posture are the most important aspects in distinguishing CEH from the other two headaches. 19. Antonaci F, Ghirmai S, Bono G, Nappi G: Current methods for cervical spine movement evaluation: a review. Clin Exp Rheumatol 2000, 18(suppl 19):45–52. 20.• Bulgheroni MV, Antonaci F, Sandrini G, et al.: A 3D kinematic method to evaluate cervical spine voluntary movements in humans. Funct Neurol 1998, 3:239–245. The kinematic analysis of neck movement is useful and noninvasive and has a good-excellent reproducibility. The method, mostly used for research, can be applied also in clinical practice to evaluate neck function in cervical spine disorders. 21. Zwart J-A: Neck mobility in different headache disorders. Headache 1997, 37:6–11. 22. Jansen J: Surgical treatment of non-responsive cervicogenic headache. Clin Exp Rheumatol 2000, 18(suppl 19):67–70. 23. Antonaci F, Ghirmai S, Bono G, et al.: Cervicogenic headache: evaluation of the original diagnostic criteria. Cephalalgia 2001, in press. 24. Bovim G, Sand T: Cervicogenic headache, migraine without aura, tension-type headache. Diagnostic blockade of greater occipital and supraorbital nerves. Pain 1992, 51:43–48. 25. Pfaffenrath V, Dandekar R, Mayer ETH, et al.: Cervicogenic headache: results of a computer-based measurements of cervical spine mobility in 15 patients. Cephalalgia 1988, 8:45–48. 26. Fredriksen TA, Fougner R, Tangerud A, Sjaastad O: Cervicogenic headache. Radiological investigation concerning head/neck. Cephalalgia 1989, 9:139–146. 27. Stovner LJ: Headache associated with the Chiari type I malformation. Headache 1993, 33:175–181. 28.•• van Suijlekom H, de Wet HC, van den Berg SG, Weber W: Interobserver reliability of diagnostic criteria for cervicogenic headache. Cephalalgia 1999, 19:817–823. In order to distinguish patients with CEH from migraine and TTH, a “live” interview was carried out by different observers. The reliability of the criteria for CEH was similar to the one of the IHS criteria in diagnosing migraine and better than those used for diagnosing TTH. 29. Sjaastad O, Joubert J, Elsas T, et al.: Hemicrania continua and cervicogenic headache. Separate headaches or two faces of the same headache? Funct Neurol 1993, 8:79–83. 30. Bordini C, Antonaci F, Stovner LJ, et al.: Hemicrania continua, a review. Headache 1991, 31:20–26. 31. Sjaastad O, Bovim G: Cervicogenic headache: the differentiation from common migraine. An overview. Funct Neurol 1991, 6:93–100. 32. Sjaastad O, Fredriksen TA, Pareja JA, et al.: Coexistence of cervicogenic headache and migraine without aura (?). Funct Neurol 1999, 14:209–218. 33. Pöllman W, Keidel M, Pfaffenrath V: Headache and the cervical spine: a critical review. Cephalalgia 1997, 17:801–816.