Cervicogenic headache (CEH) six years after whiplash injury



Monica Drottning

Peer H. Staff

Ottar Sjaastad


Department of Neurosurgery, Ullevaal University Hospital, Oslo, Norway


Corresponding author: Dr Monica Drottning,

Department of Neurosurgery,

Ullevaal University Hospital, 0407 Oslo, Norway

E-mail: monica.d@online.no



Accepted for publication: May 2007





The main objective of the present investigation was to clarify the long-term natural course of cervicogenic headache (CEH) after whiplash injury. Whiplash patients (n=587) were initially followed up for a year after their emergency service consultation. De novo unilateral CEH seemed to be present in 8% (n=48) at six weeks and in 3% (n=20) at one year. Previous car accidents, pre-existing headache, and neck pain were more frequent among individuals with chronic CEH than in those without CEH at one year.

Patients affected by headache with CEH characteristics at one year were followed up for five more years, at the end of which seven (35%) still had such headache, although the attack frequency had reduced appreciably. Forward radiating pain could still generally be precipitated from areas along the occipital tendons ipsilaterally. Increased tenderness in these areas could also be found on the previously symptomatic side in the patients who were now asymptomatic.


KEY WORDS: cervicogenic headache, headache, neck distortion, Oslo study, whiplash.





Headache is a recognised symptom after whiplash injury (1-3), but there has been considerable debate over the nature of this headache. Different terms have been used to describe post-traumatic headache: “migraine” (post-traumatic migraine), “tension-type headache” (post-traumatic T-TH) and “cervicogenic headache” (post-traumatic CEH). Most authors describe unspecified “headache” after whiplash. The headache picture that emerged in the Oslo study, that of a de novo unilateral, post-whiplash headache, seemed to correspond most closely to the CEH type and showed a one-year frequency of 3.4% (4). At the time, the diagnosis of CEH was established according to the criteria of the Cervicogenic Headache International Study Group (CHISG) (5).

In the present study, we evaluated the persistence of headache, approximately six years after their accident, in the patients who had shown unilateral headache of the CEH type at one year after whiplash injury (n=20) in the Oslo study (n=587).



Materials and methods


All the patients in the Oslo study (4) who had presented unilateral CEH at one year after whiplash injury (n=20) were called in for interview and clinical examination at six years. Four were lost to follow up. Of the remaining 16 patients, two with daily headache were excluded after interview because of new neck traumas; so, we were left with 14 patients for this study. Three patients were interviewed and examined by the authors in their homes; another, now headache-free, living a couple of hours’ drive from Oslo, was interviewed by phone, since he did not wish to take time off work to undergo the examination (accordingly we have no physical examination results for this patient). The rest were examined at Ullevaal University Hospital.


Consultations during the first year after the accident


As part of their primary consultation at the emergency service of the Municipality of Oslo, all patients included in the original Oslo study (n=587) underwent a standard clinical examination, performed by the physician on call. Cervical spine x-rays were obtained from all of them.

Approximately one-third of the total cohort reported pain and/or headache at one month, and these patients were followed up at the Ullevaal University Hospital, with clinical examinations and extensive questionnaires, at six weeks, six months, and one year. The remaining patients filled in a questionnaire at one year.


Questionnaire at six years


All the 14 participants included in the six-year follow up filled in a questionnaire investigating headache frequency and intensity. Intensity of neck pain was also included, as was the Montgomery-Asberg Depression Rating Scale (MADRS) (6), and head and full body pain drawings. Headache and neck pain intensity were measured on a 1-9 point VAS scale (1=no pain, 9=worst imaginable pain).


The clinical examination at six years


The clinical examination consisted of a relevant neurological examination, provocative tests, such as the Spurling’s test, stretching of neck muscles to elicit pain, and identification of pain pressure points in the neck. For the latter tests, graded, standardised external pressure was employed (3-4 kg), as advocated for fibromyalgia (7). External pressure of 0.5-1 kg was used as a screening test. We looked, in particular, for pain radiating to the oculo-frontal and temporal areas.

Measurements of passive neck mobility (ROM) were performed, using a Cybex EDI inclinometer, known to be a reliable instrument showing low variability (8). Flexion, extension, and lateral movements were measured in the sitting position, while rotation was measured in the supine position.

In the skin-roll test (9), the skin-fold was rolled upwards from the lower scapular area to the top of the shoulder, bilaterally. Skin-fold thickness was measured using skin calipers (Servier®, Leyden) specifically designed for this purpose. The pressure exerted on the skin remains constant at all degrees of opening of the “jaws” of this device. Tenderness to the standardised pressure was also assessed as part of the procedure, as + or -, with - indicating no tenderness.

Diagnostic blocks of the greater and the minor occipital nerves were carried out by the principal investigator (M.D.) at one year. No extra diagnostic blocks were carried out at six years. No additional imaging was systematically obtained.

The data were analysed using an SPSS statistical program and standard statistical procedures. The study was approved by the regional ethics committee. All the patients gave their written informed consent.





Of the final group of 14 patients (out of 20), seven (35%) presented a persistent unilateral headache (CEH 6y) and seven were without such headache (non-CEH 6y). The seven affected patients represented 1.2% of the original whiplash cohort. These figures should be considered minimum figures (Fig.1) because they do not include patients lost to follow up. Of the patients examined at six years, 50% (7 out of 14) still had CEH. In addition, T-TH was present in two of the seven patients who did not present CEH at six years.

The patients still suffering from chronic CEH six years after the whiplash accident were younger than the patients who had recovered from this headache: CEH 6y, mean age 44 years (range 38-68) vs non-CEH 6y, mean age 62 years (range 41-91). There was a female preponderance, particularly among the group of affected patients, in which the proportion of women was 85% (F:M=6:1) vs 71% (F:M=5:2) among the non-affected ones. This emerged as a non-significant trend during the first year post whiplash in the original cohort (n=587) in which there was a 49% female proportion at entry.


Depression and disability


One patient (MADRS score 19) in the CEH 6y group and two patients in the non-CEH 6y group (MADRS scores of 14 and 20) showed signs of minor depression (MADRS 12-20).

Two patients in the non-CEH 6y group no longer had unilateral headache, but presented a T-TH equal to their pre-accident bilateral headache. These were the two patients with raised depression scores mentioned above.


Characteristics of the headache and clinical parameters


The type of headache observed in the Oslo study has been described previously (4): these patients invariably exhibited both unilaterality without sideshift and mechanical precipitation of headache attacks.

Subjective precipitation of headache (by the patient) was a factor present in all the patients in the CEH 6y group in the present study. A forward-radiating pain could also be precipitated mechanically from below the tendon insertions in the occipital area in all the patients but one. In this exceptional case, Spurling’s test was positive, with a radiation of pain to the right (symptomatic side) shoulder in the C5 root distribution area. The upward-/forward-radiating pain spread to the frontotemporal area on the symptomatic side in four patients, to the temporal area only on the symptomatic side in one, and to the upper part of the occipital area, (but not to the frontotemporal area) bilaterally, in one.

Mechanical precipitation of a forward-radiating pain was also present in four of the six examined patients in the non-CEH 6y group. In three of these, the radiating pain was on the side of their headache at one year; in the fourth it was bilateral (TableI). No headache attacks were elicited by this procedure.

There was a clear reduction in the number of headache days in the CEH 6y group when compared to the one-year report (TableII), whereas the duration of single attacks had not changed considerably. The intensity of the headache was VAS 6, this level having remained unchanged throughout the six-year observation period (VAS 5-6).

Neck ROM was found to have deteriorated significantly at six years in all the examined patients (n=13) and in all directions compared to one year after the accident. This deterioration was particularly marked in the patients who no longer had CEH (TableIII).

As revealed by the patients’ pain drawings, shoulder/ arm pain and/or sensory disturbances in the arm on the headache side were present in six of the seven patients in the CEH 6y group (Fig.2).

The mean skin thickness in the shoulder area was 17.6 mm on the symptomatic vs 16.5 mm on the non-symptomatic side in the patients with persistent CEH. The corresponding values for the non-symptomatic group (n=6) were 19.0 and 17.3 mm. These values are higher than those found in a headache-free control series of individuals (n=246) of both sexes, aged 18-65 years: 14.3±5.7 mm (10).

Most of the single skin width measurements (n=13x2=26) were within the normal range (< 25 mm) and no systematic asymmetry was found on the skin-roll test. However, borderline asymmetry was found in two cases.

Tenderness on the skin-roll test was present in all but one of the patients with CEH. In five of these six patients, there was a correspondence between the side of the headache and the increased tenderness. In one case, the tenderness was symmetrical (TableIV, over). There was no increased unilateral tenderness in the non-CEH 6y group. The two patients with T-TH and raised depression scores had bilaterally increased tenderness, while the headache-free patients had no tenderness.





The patients from the original cohort of 587 whiplash patients who still showed unilateral headache one year after whiplash injury were followed up for a total of six years. This is, to the best of our knowledge, the first time that a good-sized whiplash series has been followed up for such a long period of time. A frequency of de novo unilateral headache (CEH) of 8% (n=48) was observed at six weeks, and of 3.4% (n=20) at one year after the whiplash injury (4). The frequency of this headache at six years was seven out of 20, i.e. 35% of the patients still affected at one year (Fig.1), or seven out of the original cohort of 587, i.e. 1.2%. Both of these six-year figures should be considered minimum figures, because only 14 of the remaining 20 headache patients (70%) were included and interviewed at six years. (The two patients who were excluded because of new neck traumas both had headache). Of these patients included in the study from one to six years post injury, the percentage, at six years, of those with chronic CEH is the same as the percentage of those found to have recovered (50%).


Improvement of CEH after whiplash is a lengthy process that follows a biological curve


As is clearly shown in figure1, the trend of the headache after whiplash injury was found to show a sharp fall in the first weeks followed by a gradual decline, almost flattening out at one year: the improvement curve (Fig.1) between six weeks and six months was sharp and, had it continued to show this degree of inclination, would have been destined to intersect the zero line prior to one year. Similarly, the real curve emerging between six months and one year would, if prolonged at the same inclination, have intersected the zero line prior to the midway point between one and six years.

Over the last five years of the study (1-6 years), the frequency of headache cases fell by 65%. Persistence of this same trend after the six-year point would result in intersection of the zero line just over three years after this last examination. However, considering the overall previous trend, shown in figure1, it can be postulated that in all probability it will take longer than this. The percentage of recovery declines over time. Conceivably, it may be upwards of 10 years before the de novo headache after whiplash trauma observed in the present study is totally eradicated. The possibility also remains that the headache will persist in a few cases.


Head- and neck- pain can be elicited from the neck in symptomatic as well as recovered patients


The iatrogenic pain provocation test in the occipital area gave a clear-cut result among the patients with spontaneous headache attacks: pain was generally more easily provoked locally on the symptomatic than on the non-symptomatic side, and tended to radiate to the forehead on that side. Remarkably, in most patients who had become non-symptomatic, precipitated pain, on the external pressure test, could still radiate to the previously affected side, but no headache attacks were elicited. The triggering of radiating pain in response to pressure in the headache-free patients could mean that the neck is not fully healed. If so, the sub-clinical pathology may render these patients more vulnerable to the development of headache following future neck traumas.

A clear and significant deterioration of ROM in the neck over time was found among the examined whiplash patients (TableIII). In both the symptomatic and the non-symptomatic groups, the restriction of movements, particularly lateral flexion, was marked at six years, most clearly so in those whose headache had disappeared. One can speculate whether the difference between the groups is due to their difference in age (mean values 44 and 62 years, respectively), or whether the restricted movement in the neck has developed in order to avoid triggering headache and neck pain, and is thus more prominent in the recovered group of CEH patients. In retrospect, ROM restriction may be a sign of a patient having suffered a neck trauma.

The skin-roll test may be helpful when considering individuals from the period just before whiplash until the post-whiplash period: the skin-fold thickness may be found to increase under such circumstances (9), while still remaining mostly within the normal range of variation. In the present series, the skin-fold thickness did not differ between the symptomatic and the non-symptomatic side, nor between the patients with persistent CEH and the patients who recovered. In a small whiplash series from the Vågå study (n=6), the mean skin-fold thickness on the symptomatic side in the affected patients was 23.8 mm, vs 12.3 mm in the non-affected ones (10). The situation was entirely different in the present study, where the first measurements were carried out six years into the post-whiplash period. Changes within the normal range may putatively have occurred on the actual sustaining of the whiplash injury, but such changes could not have been highlighted in the present context: without knowing the pre-morbid skin-fold thickness, it is impossible to tell whether the skin-fold thickness has changed in connection with the whiplash trauma, and – if it has – in which direction.

Altogether, the clinical picture, the pain drawings, and the neck examination results indicate that there is neck pathology in these headache patients. The headache-free patients also exhibited neck symptoms, although to a lesser degree. The presence of these symptoms may be regarded as a “scar” that is not fully healed, possibly rendering them more vulnerable to future neck traumas. The Oslo study (4) tends to indicate that there may be a correlation between having suffered more than one car accident with whiplash and the development of de novo CEH.


“De novo” migraine and tension-type headache after whiplash


In several contexts, it has been mentioned that migraine without aura or T-TH could arise in the post-whiplash phase. Both of these headaches are considered primary headaches (11), whereas CEH is considered a secondary headache (11,12). On this basis of reasoning, one may arrive at a difficult question: can a primary headache, be it migraine or T-TH, be caused by a neck trauma – and an indirect one at that? Migraine is a hereditary disorder, and hardly, first and foremost, a neck disorder. Second, if a T-TH were traumatic in origin, it would become a secondary headache, the trauma being the primary event and the headache being consequent upon the neck damage sustained.

If the above premises are correct, a headache secondary to neck damage can, at most, be similar to a migraine; it cannot be identical to it. Moreover, migraine is inter alia characterised by some of the following features: nausea, vomiting, photo- and phonophobia, a pulsating pain of moderate/severe intensity, and aggravation by moderate physical exercise. These features were not present in our cases. Conversely, our cases did show mechanical precipitation of attacks, a feature not seen in migraine.

And as regards T-TH, in addition to the primary nature of the disorder, there is the bilaterality of the pain: a unilateral pain is, generally, not in conformity with this diagnosis. In the present series, the headache was unilateral and, moreover, without sideshift.

The two patients with T-TH in our series, who had recovered from CEH six years after the whiplash accident, both had signs of depression. Their headaches were bilateral, and not elicited by neck movements or neck manipulations, nor did they seem to be de novo headaches.

In the Oslo study the initial post-traumatic stress reaction predicted a higher frequency of all pain symptoms, including CEH, as well as a slower recovery from whiplash associated symptoms (13). Unlike the unilateral head pain seen in unilateral CEH, the pain was generally widespread and symmetrical. The marked deterioration in ROM was also symmetrical.

The logical explanation for de novo unilateral headache in whiplash is the following: there is an indirect trauma to the neck and, if the neck is damaged, a headache may ensue (whereas there is no headache without a neck affection). And the ensuing headache will be of the CEH type. This implies that the neck will be the primary focus for treatment. The clinical picture and the findings in the present study suggest that the neck is the origin of this headache, even though the neck pathology is not visible using the imaging techniques and electrophysiological tests available in clinical practice today. Pain drawings are regularly used as diagnostic tools in CEH (14) and could be regarded as a useful test for investigating neck pathology in similar series. The protracted improvement of post-whiplash CEH calls for caution as regards invasive treatment and, in particular, in those cases in which there are no indications as to which nuchal structures actually are giving rise to this headache.





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