Ellen Vandyck
Research Manager
Whiplash patients often report headaches besides their neck pain complaints. Up to two-thirds of people who sustained whiplash report the presence of headaches. Acute headache is thought to be originating due to the whiplash event when it arises within 7 days after the event occurred, or when a known headache before the whiplash event is worsened as a result of the whiplash event. Whiplash-associated headaches are thought to originate from a neck dysfunction. As such, the headache is a referred pain spread to the head. Provocation tests in other forms of headache have shown sufficient reliability. However, whiplash-associated headaches provocation has not been investigated to date.
In the present study, a case-control design was used. Participants with a grade II whiplash-associated disorder were recruited from a private clinic. The gradation was defined according to the Quebec Task Force on Whiplash-Associated Disorders. Eligible patients were between the ages of 18-65 and were recruited 7-30 days after the whiplash event. When a previous headache condition was known, participants could be included in the study only if their headache was worsened since the whiplash event.
The diagnosis of a whiplash-associated headache or a whiplash-associated disorder without a headache was made by a physician. A blinded evaluator performed the following tests:
To evaluate the intra-rater reliability of these tests, all of them were evaluated twice with a rest period of 10 minutes in between. A positive test of headache provocation was considered when both repetitions of the same test were positive. The tests were conducted in the order as specified above.
A total of 47 participants were included in the study. Twenty-eight of them had whiplash-associated headaches. Nineteen controls who sustained a whiplash but did not report headaches were included in the analysis. At the start of the study, both groups were comparable.
The only difference, not reported in the table, was that group of people with whiplash and headache consisted of five participants who suffered from headaches before the whiplash event occurred (migraine and tension-type headache). While none of the controls suffered from prior headaches.
The intra-rater reliability was rated as excellent for a large number of tests:
The highest agreement was found for the most restricted side of the Flexion-Rotation Test.
When the controls who sustained whiplash without headache were compared against those with whiplash and headache, significant differences were found in the assessment of C2, the most painful sides of C0-1, C1-2, and C2-C3, the Flexion-Rotation test, and in the trapezius, masseter, and temporalis muscles. When these results were further tested in the univariate regression analysis, the likelihood of provoking whiplash-associated headache was increased with performing provocation tests at C0-C1, C1-C2, and when doing the Flexion-Rotation test and palpating the trapezius.
The final backward regression analysis revealed that provocation of headache during the assessment of C2 and C1-C2 on the most painful side demonstrated the highest association with a whiplash-associated headache. The regression analysis explained 59.7% of the variation in the presence/absence of headaches in patients with acute whiplash-associated disorders.
Some questions remain after reading this article. For instance, the diagnosis of a whiplash-associated disorder was made by a physician, who then referred the participant to an evaluator for provocation tests. We do not know what the physician relied on to diagnose whiplash. Was it based on history? Or was an examination also performed? In the case of the latter, it could be that the participant was already experiencing a painful response, which may have been amplified in the second examination. We also have no idea about the time between the physician’s diagnosis and the evaluator’s examination. A good thing, however, was the blinding of the evaluator for the presence or absence of headache in each subject. Blinding was ensured by asking the participants not to reveal whether they suffered from headaches. Whether the evaluator was effectively kept blinded was not reported.
People presenting with prior headaches could only be included when they experienced an increased headache intensity after the whiplash event. This may be due to both a mechanical dysfunction of the upper cervical spine or sensitization of the trigeminocervical nucleus. The most important takeaway from this study to me is the need for desensitizing the neck after someone had sustained a whiplash. Fortunately, many options are available to obtain desensitization in whiplash patients, whether it is done verbally (education and information), manually (manual therapy), through exercise, or using combined approaches.
Participants who sustained whiplash were recruited within 7-30 days of the whiplash event. This is a large time span, which was not controlled for. It would have been interesting to see whether there was a difference in response to the physical tests and the duration since the whiplash event.
Apart from the PA on spinous process C2 and facet joint C1-C2, other tests such as PA over C0-C3, palpation of the masseter, temporalis, and trapezius muscles, and the Flexion-Rotation tests may be associated with whiplash-associated headaches provocation. The latter was the only test that was significantly different between people with and without whiplash-associated headaches. Yet, it also provoked headaches in more than 30% of people who presented without whiplash-associated headaches. This reduces the importance of the test to predict headaches in this whiplash population.
Another relevant thing to note is that headache provocation was defined as a binary outcome: present or absent. Thus, this required participants to report headache provocation upon both the first and second examinations to be able to calculate the intra-rater reliability. This would mean that some participants not reporting a headache upon the repeat examination could have been excluded from the analysis. This would automatically lead to increased intra-rater reliability because only those with the same response to the provocation tests are thus included to calculate the intra-rater reliability, which, as such could have been overestimated. Further, the order of the provocation tests was not randomized, possibly leading to an increase in sensitivity throughout the examination. This may have made the last tests in order possibly more frequently positive.
The Hosmer & Lemeshow’s test was not significant, meaning that the model had a good fit. But the model only explained 59.7% of the variance of the presence or absence of headache in participants who had a recent whiplash event. This would assume that a lot more than just mechanical dysfunction or sensitization of the trigeminocervical nucleus is in play. Factors from the biopsychosocial model, I hear you think indeed.
This study showed that headaches attributable to a whiplash event can be provoked using manual testing. People who reported having headaches since they were involved in a whiplash event, more commonly reported headache provocation upon manual testing. The tests with the highest association were PA on the spinous process of C2 and on the facet joint of C1-C2. However, in people not reporting headaches after being in a whiplash event also reported headache provocation from these tests. Thus, whether the provocation of headache results from a mechanical dysfunction or from sensitization of the trigeminocervical nucleus remains unclear.
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