Pii: s1529-9430(01)00024-9

Cervicogenic headaches: a critical review Scott Haldeman, DC, MD, PhDa*, Simon Dagenais, DCb aDepartment of Neurology, University of California, Irvine, Medical Center, 101 The City Drive South, Orange, CA 92868, USA bResearch Division, Southern California University of Health Sciences, 16200 East Amber Valley Drive, Whittier, CA 90609-1166 Received December 22, 2000; revised January 8, 2001; accepted January 28, 2001 Abstract
Background context: The notion that headaches may originate from disorders of the cervical spine
and can be relieved by treatments directed at the neck is gaining recognition among headache clini-
cians but is often neglected in the spine literature.
Purpose: To review and summarize the literature on cervicogenic headaches in the following ar-
eas: historical perspective, diagnostic criteria, epidemiology, pathogenesis, differential diagnosis,
and treatment.
Study design/setting: A systematic literature review of cervicogenic headache was performed.
Methods: Three computerized medical databases (Medline, Cumulative Index to Nursing and Al-
lied Health Literature [CINAHL], Mantis) were searched for the terms “cervicogenic” and
“headache.” After cross-referencing, we retrieved 164 unique citations; 48 citations were added
from other sources, for a total of 212 citations, although all were not used.
Results: Hilton described the concept of headaches originating from the cervical spine in 1860. In
1983 Sjaastad introduced the term “cervicogenic headache” (CGH). Diagnostic criteria have been
established by several expert groups, with agreement that these headaches start in the neck or oc-
cipital region and are associated with tenderness of cervical paraspinal tissues. Prevalence esti-
mates range from 0.4% to 2.5% of the general population to 15% to 20% of patients with chronic
headaches. CGH affects patients with a mean age of 42.9 years, has a 4:1 female disposition, and
tends to be chronic. Almost any pathology affecting the cervical spine has been implicated in the
genesis of CGH as a result of convergence of sensory input from the cervical structures within the
spinal nucleus of the trigeminal nerve. The main differential diagnoses are tension type headache
and migraine headache, with considerable overlap in symptoms and findings between these condi-
tions. No specific pathology has been noted on imaging or diagnostic studies which correlates with
CGH. CGH seems unresponsive to common headache medication. Small, noncontrolled case se-
ries have reported moderate success with surgery and injections. A few randomized controlled tri-
als and a number of case series support the use of cervical manipulation, transcutaneous electrical
nerve stimulation, and botulinum toxin injection.
Conclusions: There remains considerable controversy and confusion on all matters pertaining to
the topic of CGH. However, the amount of interest in the topic is growing, and it is anticipated
that further research will help to clarify the theory, diagnosis, and treatment options for patients
with CGH. Until then, it is essential that clinicians maintain an open, cautious, and critical ap-
proach to the literature on cervicogenic headaches.
2001 Elsevier Science Inc. All rights re- Introduction
I hereby certify that, to the best of my knowledge, no aspect of my cur- It is common in clinical practice to encounter conditions rent personal or professional circumstances places me in the position of that are widespread and routinely treated but that suffer having a conflict of interest with any interest of NASS relating to themanuscript. I further hereby certify that, to the best of my knowledge, nei-ther I (including any member of my immediate family) nor any individualor entity with whom or with which I have a significant working knowledge * Corresponding author. 1125 East 17th Street, W-127, Santa Ana, CA have (has) received something of value from a commercial party related 92701, USA. Tel.: ϩ1-714-547-2536; fax: ϩ1-714-547-4822.
directly or indirectly to the subject of this manuscript.
E-mail address: HaldemanMD@aol.com (S. Haldeman).
1529-9430/01/$ – see front matter 2001 Elsevier Science Inc. All rights reserved.
PII: S 1 5 2 9 - 9 4 3 0 ( 0 1 ) 0 0 0 2 4 - 9 Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 from limited research and lack of consensus among experts.
duplicates were eliminated. The reference section of each Cervicogenic headache (CGH) is one of these conditions.
article was then searched for relevant articles not uncovered Although the idea that headaches can originate from struc- by the computerized databases. Although no formal search tures in the neck and can be treated by interventions di- strategy was attempted for books, theses, and presentation rected at the cervical spine is long-standing, it is only in the abstracts, these were included when articles uncovered by past two decades that the topic has gained attention in the our search made reference to them. This strategy yielded mainstream headache and pain literature. There are now 212 papers, some of which were not relevant to our review.
several associations dedicated solely to studying CGH, in- These results encouraged us to pursue our original goal of cluding the Cervicogenic Headache International Study Group reviewing the literature pertaining specifically to CGH and the World Cervicogenic Headache Society (WCHS).
rather than attempt to cover the much broader topic of head- These societies are comprised mainly of neurologists and aches and neck pain. Because the term CGH was introduced pain management and headache specialists. Journals and in 1983, this search was mainly limited to papers published professional associations devoted to studying the spine, within the last two decades, although additional papers were however, have not participated in this development. This is added when relevant and important to the discussion. Al- unfortunate, because the majority of spinal pain syndromes though this may seem too restrictive, we thought that this are managed by clinicians who treat the spine rather than type of review could reduce some of the confusion sur- rounding this topic by excluding older literature where it is This problem of headaches related to the cervical spine impossible to determine if the authors are in fact describing cannot be underestimated. Up to 80% of patients with cervi- cal acceleration-deceleration injuries report headaches The information gleaned from our literature review was within 2 months of injury [1]. Almost 25% of patients with divided into the following six categories for analysis: histor- this form of injury continue to have significant neck pain 2 ical perspective; definition and diagnostic criteria; epidemi- years later, with the majority also complaining of headaches ology; pathogenesis; differential diagnosis; and treatment.
[2]. These figures do not by themselves confirm that theheadaches noted in these studies originate from the cervical spine. Many patients with whiplash injuries to the neck arealso under financial and litigation stresses, and their head- Table 1 highlights some of the historical milestones in aches may be the result of muscle tension. Furthermore, the evolution of the concept of CGH. The earliest reference these patients commonly take medications with the poten- we uncovered was a series of lectures given by Hilton in the tial of causing headaches. To make the issue more compli- period 1860–1862, as reported by Pearce [3]. In those lec- cated, many of these patients have also had head injuries tures, Hilton proposed that pain in the anterior or lateral part that may be the primary cause of their headaches. It is there- of the head may come from the great or small occipital fore not sufficient to assume that patients with complaints nerve, most likely from disease between the first and second of both neck pain and headaches after injury have head- vertebrae. Sixty years later, in 1926, Barré [4] hypothesized aches that are being caused by the same pathology that is a relationship between the cervical spine and neurological causing the neck pain. It is up to the clinician to be aware of symptoms, including headache and vertigo. His collabora- the current literature in order to be able to make a reason- tor, Lieou [5], stated in 1928 that cervical arthritis should be able diagnostic effort to differentiate between the various considered a common cause of these symptoms. Twenty types of headache that may accompany neck pain.
years later, Raney and Raney [6] reported that headache This article is an attempt to assist the spine specialist in may be a common symptom of cervical disk lesions. The understanding the current literature on CGH. With this re- following year, a case series published by Hunter and May- view it is hoped that a clinician will be able to discuss the field [7] reported that occipital neuralgia, where pain radi- current state of knowledge and be aware of the controversies ated from the occiput to the periorbital and jaw areas, could concerning CGH, as well as place the multiple theories and be an important cause of headaches. This theory, in turn, treatment approaches for this condition in some perspective.
was used to justify the injection of analgesics into the occip-ital nerves in an attempt to relieve these headaches. Also in1949, Bärtschi-Rochaix [8] used the term “cervical mi-graine” to describe headaches presumed to come from the The literature search
neck, while Josey [9] published a case series on patients A search was performed with three computerized medi- with headaches associated with pathologic changes in the cal databases (Medline, CINAHL, Mantis) for the terms cervical spine. In 1955 Kovacs [10] wrote that motion re- “cervicogenic” and “headache” for the periods covered by striction in the cervical spine could lead to muscle spasm each database (1966 for Medline, 1982 for CINAHL, 1880 and compromise of the vertebral artery and nerves, causing for Mantis). The search was limited to articles in English, headaches. This helped popularize osteopathic, chiropractic, French, and German. Search results from the different data- and manual treatment of the cervical spine to relieve head- bases were merged using reference-managing software, and aches. Maigne [11] was a prominent advocate of using ma- Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Table 1Historical milestones in cervicogenic headaches Hilton mentions that pain in the anterior or lateral part of the head may come from the great or small occipitalnerve, most likely from disease between the first and second vertebrae.
French neurologist Barré describes a relation between the cervical spine and neurological symptoms, includingheadache and vertigo.
French neurologist Lieou reports that cervical arthritis is a common cause of headache and vertigo.
Raney describes patients with headaches caused by cervical disk lesions.
Hunter and Mayfield publish a series of case reports on occipital neuralgia.
Bärtschi-Rochaix coins the term “cervical migraine.” Josey publishes a case series where headaches are associated with pathologic changes in the cervical spine.
Kovaks postulates that motion restriction in the cervical spine can lead to muscle spasm and compromise of thevertebral artery and nerves causing headaches.
Grillo, a chiropractor, discusses vertebragenous headaches very similar to CGH.
Bogduk discusses third occipital headache with a presentation very similar to CGH.
French physiatrist Maigne reports success in treating headaches with manual medicine.
Sjaastad publishes an article introducing the term cervicogenic headache.
Fredriksen presents a detailed description of the clinical presentation of patients with CGH.
The International Headaches Society introduces a category for headaches associated with disorders of the neck.
Sjaastad publishes diagnostic criteria for CGH.
The International Association for the Study of Pain publishes diagnostic criteria for CGH.
The multidisciplinary World Cervicogenic Headache Society is created.
The Quebec Headache Study Group publishes diagnostic criteria for CGH.
The first randomized controlled clinical trial for CGH is published by Nilsson.
Sjaastad publishes revision of diagnostic criteria for CGH.
nipulation to treat headaches, while Bogduk and Marsland least in their connotation. Such terms as neuralgia, espe- [12] advocated surgical intervention to treat what they cially those referring to a specific nerve, assume, with little termed “3rd occipital headache”.
evidence, that the origin of the headache is known [12,22].
The term “cervicogenic headache” was first introduced Other terms are more vague, referring simply to a syndrome to the medical literature in 1983 by Sjaastad et al. [13], who or a specific location of the headache [23–26].
described patients with a headache not classified by diag- The confusion seen in CGH terminology is also apparent nostic criteria at that time. In 1987 Fredriksen et al. [14] when examining the diagnostic criteria for CGH. Table 3 gave a more detailed description of patients they had diag- summarizes the prominent features of the diagnostic criteria nosed with CGH. In 1988 the International Headache Soci- published by various expert groups. The most widely used ety (IHS) [15] amended its diagnostic classification system diagnostic criteria for many years were those proposed by to include a category for headaches associated with disor- Sjaastad [16] in 1990 and subsequently updated in 1998 ders of the neck. In 1990 Sjaastad et al. [16] published very [18]. Although the publication of these criteria brought fo- specific and detailed diagnostic criteria for CGH. This was cus to the field of CGH research, certain aspects have followed by the publication of less stringent diagnostic cri- proved difficult to embrace. For example, Sjaastad vigor- teria for CGH by the International Association for the Studyof Pain (IASP) in 1994, and by the Quebec Headache Study Group in 1995 [11,17]. In 1998, Sjaastad et al. [18] revised Conditions similar to cervicogenic headache their diagnostic criteria for CGH based on more extensive Definition and diagnostic criteria The term CGH, although adopted by a number of organi- zations, is not universally accepted, and there remains a great deal of variation in the terminology used to discuss headaches associated with disorders of the cervical spine.
This is especially true of literature before 1983, when a number of terms (Table 2) appear to have referred to the same clinical entity. Many of these terms, such as verte- bragenous [19], vertebrogenic [20], or spondylotic [21] headaches, can be considered synonymous with CGH, at Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Table 3The characteristics and definitions of cervicogenic headache Awkward headpositioningPressure over ipsilateralcervical/occipital area abnormalitiesFractureCongenitalanomalyTumor/rheumatoidarthritis, notspondylosis Edema/flushingDizzinessPhono/photophobiaBlurred visionDysphagiaNo effect withindomethacin,ergotamine, orsumatriptan ously advocated the position that these headaches should be cluded radiological abnormalities in their diagnostic crite- strictly unilateral, whereas others have accepted that these ria, despite a failure to identify radiographic abnormalities headaches may be unilateral or bilateral. Sjaastad also in- specific to CGH [15,27]. The IASP and WCHS focused cluded a number of accompanying symptoms, such as nau- their attention on the relief of pain by the injection of anal- sea, vomiting, flushing, dizziness, phono- and photophobia, gesics into cervical structures with no convincing clinical blurred vision, and dysphagia, making his criteria too spe- trials to support this position and no consensus regarding cific and detailed for general practice.
the various injection techniques [17,28].
Lack of consensus is also evident in the criteria of the Despite these differences, certain features are common to three other main expert groups. For example, the IHS in- the majority of the diagnostic criteria for CGH. There is Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 agreement that these headaches start in the neck or occipital ferent diagnostic criteria used to define CGH. Several stud- area and can then spread to other areas of the head, includ- ies did not specify the criteria used to define CGH, making ing the frontal, temporal, and periorbital regions. The pain direct comparisons impossible; even studies using the same tends to be dull, nonthrobbing, and nonlancinating, and can criteria varied in the stringency with which these were ap- become moderate to severe in intensity. Examination re- plied (i.e., patient must fulfill a minimum of x criteria to be veals tenderness and abnormal palpatory findings in the cer- included). The study reporting the highest prevalence for vical paraspinal tissues, as well as possible decreased cervi- CGH was by Rothbart [30], a clinician from a pain manage- cal range of motion. The other reported findings and ment center, who estimated that 80% of the patients with characteristics of CGH appear to be less well defined.
headache in his clinic had CGH. As founder of the WCHS,he may have spent considerably more time than other physi-cians in seeking patients with this syndrome. An incidental finding in a study by Loh et al. [35] reported that 10% of pa- There is a great deal of variation in the perceived preva- tients with obstructive sleep apnea were diagnosed with lence of CGH. The published prevalence rate estimates un- CGH, although no explanation was offered as to the mecha- covered through our literature search are presented in Table 4. These ranged from 0% of patients with migraine head- Analysis of patient descriptive data (age, gender, etc.) ache (MH) [29] to 80% of patients with headache [30].
from studies where such information was given reveals that There are several reasons for this wide range of published patients with CGH appear to form a fairly homogeneous estimates, including vastly different populations of subjects.
population, with a mean age of 42.9 years, a gender distri- In the general population, for example, prevalence rates bution that is 79.1% female and 20.9% male, and a mean ranged from 0.4% to 2.5% [31,32], whereas studies looking duration of symptoms of 6.8 years. More detailed demo- at all patients with a complaint of headache reported esti- graphic data were found in a study by Shah and Nafee [36] mates of 15% to 20% [15,32–34]. The highest variation was in India, where patients with CGH were described as 43% among headache center patients, with prevalence estimates urban and 57% rural, with 55.7% employed as handicraft of 0.4% to 80%. Part of this variation can be attributed to workers, 28.3% as laborers, 10.0% as clerks, 4.9% as busi- the different methodology used in these studies (i.e., pro- ness executives, and 1.6% as doctors. Shah and Nafee spec- spective cohort, retrospective analysis, etc.), as well the dif- ulated that the poor ergonomics associated with the handi- Table 4Prevalence estimates for cervicogenic headache Frequent headache patients (Ͼ5/month) ages 20–59 years Patients with degenerative cervical spine disease Unilateral headaches without sideshift starting in neck and spreading to frontal area Side-locked unilateral headaches or headaches starting in the neck IHS ϭ International Headache Society.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 craft occupations may account for the higher prevalence in tients with MH, he and Bovim [41] reported on four patients that group. They also reported that the population in his where both MH and CGH co-existed. These patients were study had a mean age of onset of 62.5 years for CGH, which able to distinguish between episodes of each headache, re- is considerably older than the mean age of typical patients porting improvement of MH but not CGH with sumatriptan and ergotamine, and relief of CGH but not MH with greater Another factor influencing prevalence rates in headache occipital nerve anesthetic blockade.
centers is the apparent overlap between the diagnosis ofCGH, tension-type headache (TTH), and common migraine headache. Bono et al. [37] report that 75% of patients ful-filling IHS criteria for MH also meet most of the criteria for One of the most controversial areas within the CGH liter- CGH. Furthermore, the CGH diagnostic criteria by Sjaastad ature is the discussion of its cause. Almost every structure et al. [16] include many of the systemic symptoms, such as and pathology within the cervical spine has been implicated nausea, vomiting, phonophobia, and photophobia commonly as a cause of these headaches. Table 5 summarizes the seen in MH. CGH also appears to frequently co-exist with structures suggested as the origin of CGH and the types of primary headache disorders such as MH and TTH. One pathology associated with these headaches. The rationale study of headache center patients reported that whereas only for most of the theories is the observation, usually in a small 16.1% were diagnosed with CGH, an additional 20.1% were number of cases, of either a reproducible finding on clinical diagnosed with both MH and CGH, for a total prevalence of examination, a response to stimulation of the structure, or 36.2% [34]. A recent study of patients with neck injuries re- relief of symptoms after treatment directed at the structure.
ported that 34.3% had CGH, whereas an additional 11.4% Examples include the response of patients to surgery for had both CGH and MH, and an additional 8.6% had CGH in disk disease [42], injections of posterior facets with anesthe- combination with headaches associated with the neck, for a sia [43], and injections of cervical muscles with botulinum total prevalence of 54.3% [38]. The reason for distinguish- ing CGH from headaches associated with the neck was un- One theory of CGH etiology comes from anatomical clear. When narrowing the field among patients with head- studies showing an attachment of the suboccipital tissues to ache to those with unilateral pain without sideshift and pain the dura mater at the cervical–cranial junction, and the ob- starting from the neck and spreading to the oculofrontal servation that mechanical traction on these tissues can cause area, Bono et al. [39] diagnosed 47% of such patients with movement of the dura [48–51]. The rectus capitus posterior CGH, including 15% where there was overlap between MH minor muscle [51] and ligamentum nuchae [50] have been and headaches associated with the neck, although again the shown to have direct connections to the suboccipital dura distinction of the latter from CGH was unclear. Another on very delicate dissection in a small number of cadavers.
study reported that 56.4% of CGH diagnoses occur in com- This suggests a role for the dura as a nociceptive structure bination with other headaches, including MH, TTH, and drug-induced headache [40]. Although Sjaastad has tended Structures implicated in the genesis of CGH all have to disagree that CGH symptoms are commonly found in pa- their sensory innervations through the upper cervical and Table 5Theories of pathogenesis for cervicogenic headache Trauma or immobility stimulates the C1–C3 nerves Restrict joint motion. Referred symptoms from muscles Disk herniation, spondylosis, or scar tissue Apophyseal exostoses impacting vertebral artery Nerve roots producing sternocleidomastoid and trapezius Tension on the dura or vertebrobasilar artery compression Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Fig. 1. Convergence of sensory input from the upper cervical nerve roots into the trigeminal nucleus.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 midcervical nerve roots, which lead to the cervical cord and ache are rarely confused with CGH, because each possesses converge within the spinal tract of the trigeminal nucleus unique distinguishing characteristics. To aid the task of dif- [49] (Fig. 1). This allows nociceptive input from cervical ferential diagnosis, several studies have reported the results structures to be perceived as head pain, including pain to the of various radiographic, neurologic, and physiologic testing temporal, frontal, and orbital regions. This convergence may also help to explain the systemic and sympathetic ner- The significance of radiological findings in CGH has vous system features accompanying CGH. Studies showing been difficult to establish (Table 6). Only one of these stud- relief of headache after lower nerve root blocks have cast a ies used a control group [53], and most had a small number doubt on whether only the upper nerve roots are significant of subjects. These shortcomings make it difficult to draw conclusions regarding the relationship of radiological find- Martelletti has reported increased levels of pro-inflamma- ings and CGH. Although degenerative changes have been tory cytokines interleukin-I ␤ and tumor necrosis factor-␣ found in patients with CGH on plain film radiography and during mechanically induced attacks of CGH; these were sig- magnetic resonance imaging scans of the cervical spine, nificantly higher than in patients with MH [45,46]. He postu- these changes cannot be considered specific and unique to lated that this could represent a specific signal from the im- CGH [27,36,54,55]. A study by Jansen [54] in 1998 found mune system to activate such pain-producing agents as that 100% of patients with CGH had radiographic evidence substance P and calcitonin-gene–related peptide. This may of retrospondylosis and osteochondrosis. With multiple spi- help define CGH as an inflammatory consequence of cervical nal levels involved (42.9% at C5–C6, 22.7% at C4–C5, trauma, explaining the wide variety of pathological processes 21.4% at C6–C7, 11.0% at C3–C4, 0.6% at C7–T1, and in different structures that can cause similar headaches.
only 1.3% at C2–C3), it is difficult to assess the importance The inability to find a definitive structure or pathology as of this finding. The description of Chiari type 1 malforma- the cause of CGH has lead some to believe that CGH does tions and spinal cord compression in small numbers of pa- not represent a single pathological entity but rather a pain tients with characteristics of CGH may simply represent pa- syndrome resulting from the nociceptive stimulation of al- thology that causes headaches by stimulating cervical most any structure in the cervical spine [52].
structures rather than a finding specific to CGH.
Table 7 summarizes the results of various diagnostic tests on patients with CGH. Although many of these studies report statistically significant findings, the number of sub- The differential diagnosis stressed in most of the litera- jects is too small to reach any conclusion. Many of the phys- ture on this topic is between CGH, MH, and TTH. It is gen- iological tests, such as sweating patterns [56] and electro- erally assumed that intracranial pathology from infection, nystagmography [57], are so esoteric that it is difficult to neoplasm, trauma, and so forth has been ruled out. Head- determine their significance or relevance in clinical prac- aches associated with sinusitis, temporomandibular joint tice. The finding of various forms of muscle dysfunction, syndrome, visual or auditory disturbances, and cluster head- such as myofascial trigger points [58], responses of differ- Table 6Diagnostic imaging studies for CGH Disk protrusionVentral dura compressionNarrowed subarachnoid space CS ϭ cervical spine; CT ϭ computed tomography; MRI ϭ magnetic resonance imaging.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Table 7Neurological and other diagnostic studies for CGH Romberg quotient 3.1 for anterior posterior sway Significant ↓ amplitude on painful side Significant ↑ upper trapezius passive stretching response vs. controls 30 Significant more on symptomatic (70) vs. asymptomatic (22) side C2–C4 instantaneous axis of rotation PϾ.05 No relation between abnormality and headache Asymmetry in rotatory nystagmusCongenital cranial nerve VI palsyCaloric hyporesponsiveness Significant ↓ shoulder maximum conduction velocity in CGH Significant ↑ pretest activity in frontalis on symptomatic sideSignificant ↑ electromyography response in trapezius onsymptomatic side Significant ↓ response in CGH for all medications vs.
ent muscle groups to mental stress [59], and cervical muscle they compared CGH with MH and reported that CGH ful- strength and endurance [60], seems to confirm the involve- filled seven of eight common MH criteria (the exception be- ment of cervical and paraspinal muscles in CGH. The lack ing aggravation by physical activity). Nausea and/or vomit- of response to common vasoactive medications used in MH ing was reported in 55% of patients with CGH versus 70% [61] argues against arterial involvement in CGH and can be to 85% for MH. Photophobia was reported in 45% of pa- one of the clues that a patient may have a CGH.
tients with CGH versus 88% of patients with MH. Patients Attempts to differentiate CGH from MH and TTH on the with MH, however, did not fulfill the most important crite- basis of some clinical or experimental measure are pre- ria for CGH, that is, precipitation of headaches with neck sented in Tables 8 and 9. It does not appear that any specific movements and/or external pressure on the neck. A second test or clinical finding can be used to define patients with study by Sjaastad et al. [63] in 1992 compared pain patterns CGH. A detailed clinical history is therefore imperative in in CGH and MH and reported that whereas typical MH at- order to diagnose CGH. The difficulties of diagnosing CGH tacks were unilateral without side shift (the typical CGH were stressed by Sjaastad and Bovim in 1991 [41], when pattern) in only 16% of patients, 75% of nontypical MH at- Table 8Comparison of CGH with tension-type headache Response to greater occipital nerve blockade Both groups had lower thresholds than controls Significant ↓ flexion/extension and rotation in CGH Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Table 9Comparison of CGH with migraine headache Significant ↑ thermal thresholds on both sides Response to greater occipital nerve blockade Significant ↑ pain reduction in CGH (54.5%) vs. MH (6%) Significant ↓ flexion/extension and rotation in CGH CGH ϭ cervicogenic headache; MH ϭ migraine headache.
tacks presented in this fashion. Their group of patients with with CGH could not be classified according to IHS criteria CGH fulfilled only 3.79 of 7 IHS criteria for common MH as having either MH or TTH. D’Amico et al. [64] similarly criteria, compared with 6.78 for patients with MH.
examined the characteristics of patients with headache and A study by Vincent and Luna in 1999 [62] examined the reported that in patients with long-lasting, side-locked, uni- number of patients with CGH, TTH, and MH who could lateral pain, the diagnosis was MH in 85.1%, TTH in fulfill Sjaastad’s criteria for CGH. Patients with CGH met 10.8%, and CGH in 4.1%. The percentage of patients with 10.51 of 18 criteria versus 3.85 for patients with MH and headache in whom the pain was localized in the occipito- 4.89 for patients with TTH, a statistically significant differ- nuchal region was 100% in CGH, 12.5% in MH, and 20.0% ence. One third (33.3%) of patients with CGH met the IHS in TTH. Conversely, the percentage of patients in whom the criteria for MH, whereas only 3.3% of patients with CGH initial pain was nonoccipital was 0% in CGH, 76.6% in MH, met IHS criteria for TTH. In other words, 63.4% of patients and 30.0% in TTH. CGH may then be differentiated from Table 10Surgical treatment of cervicogenic headache CS ϭ cervical spine; RCPM ϭ rectus capitis posterior minor.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Table 11Manual treatment for cervicogenic headache Significant ↓ drug consumption indexSignificant ↓ total pain index Significant ↓ headache hours/day (group 1, 59%; group 2, Significant ↓ VAS, group 1 only (36%)Significant ↓ NSAIDs/day, group 1 only (47%) Significant difference in ↓ headache hours/day in favor of Significant difference for analgesics/day between 2 groups Significant ↓ headache severity (59%)Significant ↓ headache frequency (62%)Significant ↓ headache duration (77%) Significant ↓ headache duration (43%)Significant ↓ headache intensity (53%) Complete relief of headaches Restoration of full CS ROM 10% had 50–75% reduction in symptoms3% had 50% reduction in symptoms2% had no change5% had aggravation in symptoms Manual therapy is better than Maitland concept Both are better than no-treatment control Patient was headache free for 6–7 months until involved in A single manipulation added to NSAIDs was superior to NSAIDs only immediately after treatment but not at 3 Manipulation was more effective than mobilization and wait list but without statistical significance CS ROM = cervical spine range of motion; NSAID = nonsteroidal anti-inflammatory drug; RCT = randomized controlled trial; VAS ϭ visual analog MH and TTH by a pattern of unilateral pain without sideshift, poor documentation of the criteria used for diagnosing with the initial pain located in the occipital area, and failure to CGH, and the lack of standardized outcome measures in the be classified by diagnostic criteria for other headaches.
majority of these studies. For example, a number of papers onradiofrequency neurotomy report some improvement of symptoms in 71% to 83% of patients and complete relief in The type of treatment recommended to patients with 7% to 43% of patients [65–69]. The authors, however, re- CGH appears more dependent on the specialty of the treat- ported the ablation of different nerves in these studies, mak- ing physician than the science or research supporting it. The ing it difficult to reach conclusions or compare the results.
four treatment options generally recommended are surgery A number of papers on various decompression procedures for a number of pathological entities; cervical spine manip- report relief of headaches in a substantial number of patients ulation; injections of various cervical structures with a vari- but again have not used a standardized protocol [55,70].
ety of agents; and medication. The published literature in The remaining papers on surgery consist mainly of isolated support of surgical intervention for CGH is listed in Table case reports. There are no controlled studies to support the 10. The main criticisms of this literature are the small sam- use of any surgical procedure for the management of CGH, ple sizes, the marked variation in the surgical procedures and current justification for surgery appears to be based used, the difference in the structures being operated on, the solely on the anecdotal experience of the surgeon.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 As mentioned above, the prevalence of CGH ranges from reducing the frequency and severity of headaches and the 3.3% to 22.5% of chiropractic patients, indicating the fre- amount of analgesic use by patients. A study by Howe et al.
quency with which these headaches are treated with manipu- [76] indicated that the addition of one cervical manipulation lation [48,72,73]. A survey of primary care physicians in Aus- to nonsteroidal anti-inflammatory drug (NSAID) therapy was tralia reported that 69% of them agreed that referral to a superior to NSAID therapy alone immediately after treatment, chiropractor was appropriate for headache provoked by head/ but this difference was lost at 3 weeks posttreatment. Bitterli neck postures [71]. The results of studies on cervical manipu- et al. [21] found an advantage for cervical manipulation com- lation for CGH are listed in Table 11. The results from the pared with mobilization and controls after 3 weeks of treat- case series are similar to those reported after surgery but suf- ment, but the differences did not reach statistical significance.
fer from the same shortcomings. However, there are more In an effect size analysis of randomized controlled trials on randomized controlled trials on manipulation than any other manipulation, Bronfort [77] concluded that there is moderate treatment for CGH. The studies by Nilsson et al. [74,75] have evidence of efficacy of cervical manipulation in the manage- been the most rigorous and demonstrated that spinal manipu- ment of CGH. Similar conclusions have been reached in qual- lation was more effective, in the short term, than massage in itative analyses by Hurwitz et al. [78] and Coulter et al. [79].
Table 12Treatment with injections for cervicogenic headache Group 1: 90.6% had significant relief (mean 23.5 days) 54.4% reduction in number of days with VAS 56% had VAS ↓ Ͼ50% (only 16 patients for facet) 13.8% painfree for days8.0% painfree for weeks Epidural corticosteroid Epidural space of C6–T1 Case series Significant ↓ pain numeric intensity scale Group 1:Significant ↓ pain and ↑ range of Group 2: no changeNo between-group analysis Headache frequency ↓ Ͼ50%Autonomic symptoms disappearedFull range of motion was restored in neck No significant benefit for either treatment GON ϭ greater occipital nerve; LON ϭ lesser occipital nerve; RCT ϭ randomized controlled trial; VAS ϭ visual analog scale.
Haldeman and Dagenais / The Spine Journal 1 (2001) 31–46 Another common treatment approach for CGH is thera- headaches, including TTH, no studies were found on their peutic injections. The results of injection of various agents and anesthetics on CGH are listed in Table 12. There are anumber of small case series on the injection of the occipital Conclusions
nerves where short-term improvement of was noted in 50%to 90% of patients [34,43,54]. Again, these studies suffer Despite a growing body of literature on CGH and an in- from the same shortcomings as those on surgery and manip- creasing acceptance that headaches can originate from the ulation, and many reported only immediate postinjection re- cervical spine, there remains considerable controversy and sults with no follow-up period. One study [34] compared li- confusion concerning all aspects of this topic. However, a gnocaine, lignocaine with methylprednisolone, and number of comments on CGH appear quite reasonable. The methylprednisolone alone in a nonrandomized case series concept that headaches can originate from the neck is not and found that methylprednisolone was less effective than new. The pain appears to be generated by irritation of noci- lignocaine and did not add anything to the injection of li- ceptors from structures in the cervical spine and may ac- gnocaine alone. This finding does not support Martelletti’s company injury and pathology in the neck. These headaches theory about the role of inflammation in CGH [45,46]. Two are difficult to differentiate from MH and TTH, although relatively good cohort studies on the injection of sterile wa- they possess the distinguishing characteristics of being trig- ter and saline into tender points in cervical muscles failed to gered by neck movements, pain spreading to the occipital show any improvement of symptoms [80]. A small case se- region, tenderness in the suboccipital tissues, decreased cer- ries on epidural corticosteroid injection reported some de- vical range of motion, and unresponsiveness to typical gree of relief [81]. One intriguing study was a randomized headache medication. The significance of radiological find- controlled trial comparing botulinum toxin with saline in- ings and advanced diagnostic testing is unclear. Evidence to jection into the cervical paraspinal muscles, which found a support treatment with surgery and injections consists significant decrease in pain and increased cervical spine mainly of case series without controls or standardized fol- range of motion in the botulinum group [47].
low-up. The only treatment approach supported by a reason- Among other treatments for CGH (Table 13) we found able body of controlled trials is cervical manipulation, but one randomized controlled trial on the use of transcutaneous electrical nerve stimulation [82] suggesting slight tempo- Until additional research and improved consensus on the rary relief of symptoms. There were no significant studies topic of CGH becomes available, it is essential that any cli- that we could find on the use of medication for CGH. Where nician maintain an open, cautious, and critical approach to medications have been discussed, there has been the sugges- the literature. At this point, the clinician must be wary of en- tion that CGH is relatively unresponsive to most medica- thusiastic and dogmatic claims concerning CGH. As the lit- tions commonly used to treat other forms of headache. Al- erature on this topic grows in volume and quality, the debate though other treatments, including massage, biofeedback, will intensify and hopefully result in the clarification of the exercise, or nutrition, are commonly used to treat other cause, diagnosis, and treatment of CGH.
Table 13Other treatment for cervicogenic headache 80% had Ͼ60% improvement20% has 40–60% improvement TENS ϭ Transcutaneous electrical nerve stimulation; VAS ϭ Visual Analog Scale.
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