Neck pain in episodic migraine: premonitory symptom or part of the attack?

The present results are based on a cohort of patients with episodic migraine, pre-diagnosed through neurologists. The high participation rate indicates that the study cohort represents a migraine population without any serious selection bias. We found that in 69 % of migraine patients NP is present anytime during a migraine phase. This result is in line with a recently published article of the Danish Headache group [7]. In our population study 54 % noticed NP with the start of the headache phase, in 24 % NP occurred in a time period of 2 h before the aura in migraine with aura and before the onset of pain in migraine without aura. Of interest is the high percentage of vertigo (43 %), nausea (46 %), sensitive to sound (35 %) and light (33 %) in this group. Vertigo, nausea, sensitivity to sound and light are typical symptoms of migraine, so that we can hypothesize that in that particular group NP is also part of the migraine itself (in 82 % NP progressed into the headache phase) and not (as per definition) a prodromal symptom. Giffin et al. [13] reported similar high percentages begging the question of when the premonitory phase does end and the headache phase begins? They consider that the headache evolves from the premonitory phase over a variable period, with the full-blown migraine headache finally developing when a critical physiologic threshold is reached. In a multicenter, electronic diary study, that evaluates, if premonitory symptoms can accurately predict the full-blown headache, NP (“stiff neck”) was seen premonitory in 50 % of patients, during headache in 63 % [13]. 7.4 % of our patients experienced NP in the prodromal phase (as per definition 2–48 h before the headache phase). However, in this group we also found a high proportion of vertigo (44 %), phonophobia (22 %) and photophobia (6 %).

Prodromal (premonitory) symptoms can widely range from patient to patient or even from headache to headache within the same patient. These symptoms often begin hours to days before the onset of the headache phase of migraine. Blau reported that many patients have a period early in the migraine process of “headache awareness” where the headache has yet to declare its path of evolution [6]. Consequently, patients may delay therapy as they “wait and see” which presentation of the migraine process will unfold. This prompts patients to postpone treatment or to employ treatment beyond the point when it is likely to be effective. Patients then may experience unnecessary disability and unwarranted risk from utilizing medications when they are unlikely to provide therapeutic value.

The pathophysiology of the prodrome is largely unstudied. The varied nature of symptoms associated with prodrome, however, suggests that central disruption occurs at both cortical and subcortical levels. The association of NP and migraine may result from various pathophysiological mechanisms. No studies have been carried out of the possible causal association of NP and migraine, neither is it known whether a reciprocal association occurs between NP and migraine. The structures of the neck innervated by the first three cervical nerves can be associated with migraine through the convergence of nociceptive afferents at the level of the caudal part of the trigeminal nucleus in the brainstem and sensitization of trigeminocervical neurones [14‐17]. According to the first current hypothesis, NP has been regarded as a peripheral reflexion of migraine. Very often people report that their migraine “starts” in the neck and they implicate that their neck is the “cause” of their migraine. Prolonged nociceptive stimuli from the neck structures could also be important for producing continuous afferent bombardment of the trigeminal nerve nucleus caudalis, and, hence, activation of the trigeminovascular system [18‐20]. As the pathogenesis of migraine is linked to the trigeminal innervations of the cranial blood vessels, noxious stimuli from the cervical structures may also play a role in this pathogenesis by facilitating central sensitization [21].

The advantage of the present study is a large sample of well-characterized individuals with migraine. We tried to find a simple way of measuring NP in adolescent HA sufferers with only a few questions.

Our study has several limitations: As in most previous epidemiological studies in headache, we did not use a daily headache diary. The classification of migraine was not based on a structured interview. We were not able to control if all patients included in the analysis had a pre-diagnosed migraine throughout a neurologist according to the IHS criteria. If migraine patients have different kinds of headache (although they were excluded), they probably recall the most frequent one when filled out the questionnaire, and the nature of other types, especially tension-type headache and medication-overuse headache remains obscure without a headache diary. As NP was determined throughout a simple questionnaire we were not able to perform physical examination and measurements in case of pericranial muscle tenderness and myofascial referred pain that may also contribute to migraine. Psychological factors such as anxiety and depression (in prodromal phase in particular), which have modulating effects on pain perception [22], cannot be ruled out in our cohort. As both pain syndromes, NP and migraine are regarded as due to a common risk factor, such as individual, physical, psychosocial, familial and genetic risk factors, these could predispose to general pain “proneness”. Further, the subject’s willingness to report symptoms cannot be ruled out as a contributing factor.