Background
Migraine is a common disabling primary headache disorder with head pain and autonomic and neurological symptoms [
1]. Its diagnosis relies largely on the symptomatology due to the lack of clearly detectable biological markers and explicit radiological features [
2]. It is then actually among the most under-recognized and under-treated neurological disorders [
3]. The generally accepted diagnostic criteria for primary headaches are those published by the International Headache Society, such as the International Classification of Headache Disorders [
4]. These criteria are comprehensive but still need to be further improved. Moreover, the effective application of these criteria requires trained professionals with experience and knowledge and it is not feasible to take a physical exam and medical history in large population-based studies. Besides, physicians’ diagnoses depend more on their clinical experience and inconsistent interpretations of these criteria in clinical practices, to some extent that personal description of patients has been neglected.
Besides the overlap of neurological symptoms and nonmutual exclusivity of aura symptoms, there has been long-standing controversy about obligatory characteristics for migraine with (MA) and migraine without aura (MO). According to the definition of the International Headache Society, migraine aura is the reversible focal neurological symptoms that arise before or during a migraine attack. However, clinicians have found that aura might occur before or during a migraine attack, occur without any associated headache, or occur with many other types of headache [
5‐
7]. In addition, MO and MA displayed different clinical symptom patterns during pregnancy [
8]. Whether the two migraine types are distinct entities in etiology and clinical pattern or they just differ in degree rather than in pathophysiology remains unclear [
9].
Further, the reduced parasympathetic activity with sympathetic predominance, and the increased frequency of anxiety and depressive symptoms were found in migraine, especially in MA [
10,
11]. One pharmacological study has shown that MA attacks were more severe and the treatment was less effective [
12]. One functional magnetic resonance imaging study [
13] has demonstrated that there were abnormalities in the cortical and subcortical pain processing networks in MO rather than in MA; during the interictal period, the functional connection between the occipital lobe and the frontal insula of MA was reduced than that of MO. Tedeschi et al. [
14] also have found that the functional connection between gyrus lingualis and visual cortex was enhanced during interictal period, which might imply that the central sensitization effect and cortical hyperactivity is a unique pathogenesis of MA [
15,
16].
On the other hand, there has been an increasing academic interest in investigating the clinical, epidemiological, and genetic problems of primary headaches, especially about the most common ones – the tension-type headache and migraine. In most studies of migraine, the methods of data acquisition include personal interview, telephone interview and self-administered questionnaire reports [
3]. Symptoms reported by patients using a structure-validated symptom questionnaire are limited, most symptom studies however, were from the hospital-based medical records, professional physician interviews in clinics [
17]. The distinction between these methods is not always as straight forward as it may be [
3]. Differences in screening procedure (e.g., wording differences) may have significant influences on the estimation of headache disorders [
2]. The self-reported questionnaire, which can be easily implemented to large samples, is an effective measure to access many diseases and explore constructs that would be difficult to obtain through behavioral or physiological measures. Fortunately, in a migraine study of Women’s Health Study sub-cohort, the self-reported migraine and the migraine classified based on the International Classification of Headache Disorders-II revealed a satisfactory agreement [
18].
Thus, in the current study, we have invited a group of headache patients to report their complaints of before, during and after a headache attack, since in clinics, a complete migraine includes the prodromal, aura, and headache phases [
19]. Patients were also invited to report their knowledge about headache, treatment-seeking behavior, and family history of headache, which might serve as the contextual headache information. Based on the reported symptoms and the statements of the International Classification of Headache Disorders, we developed an item-MATRIX measuring symptoms of primary headaches. The purposes of the present study were (1) to obtain a structure-validated headache symptom questionnaire from the item-MATRIX, and (2) to look for the different aspects of headache symptom between MA and MO through the questionnaire self-reporting. We have hypothesized that both MA and MO patients report their headache symptoms fitting to a time sequence, and MA patients report more intensified headache symptoms than MO patients do apart from the aura.
Discussion
After both exploratory and confirmatory factor analyses, we have developed a structure-validated Headache Symptom Questionnaire, with four scales: Somatic/Aura Symptoms, Gastrointestinal and Autonomic Symptoms, Tightness and Location Features, and Prodromal/Aggravating Symptoms. According to the self-reports, MA patients scored higher on the Somatic/Aura Symptoms and the Tightness and Location Features scales than MO patients did.
The first scale Somatic/Aura Symptoms, which describes vision, speech, motor control and some brainstem functions, is the complaints frequently reported from patients during the aura and headache phases [
21]. It is stated that the aura normally disappears as the headache starts [
4]. However, some scholars are wondering the role of aura in the initiation of headache when referring to its timing in relation to the headache and the prodromal symptoms [
7,
22,
23]. Our results also suggest that the aura precedes or accompanies the onset of headache. Interestingly, Schürks et al. [
18] have reported MA patients do not always report aura symptoms, while MO patients sometimes do so instead. The higher score of the Somatic/Aura Symptoms in our MA group suggest that it is the severity, frequency and complexity of aura symptoms that distinguishes the two types of migraine, rather than the simple presence of the aura.
The second scale embraces two aspects regarding gastrointestinal and autonomic symptoms, such as the nausea, pale face and hyperhidrosis. It is generally accepted that nausea is the main feature which characterizes migraine [
4]. Previous studies do have demonstrated that the reduced parasympathetic activity with sympathetic predominance in patients with migraine [
11].
The third scale describes the headache location and quality, which is included by the International Headache Society [
4] to characterize tension-type headaches. However, patients with migraine, especially MA, also present bilateral head and neck pains [
24]. Drummond [
25] noted that tension-type headache patients had bilateral head pain but had few or no features of migraine. Our results showed that migraine had more complex manifestations than the headache criteria currently describe, which sends an appeal that headache specialists consider more about patients’ self-reports when diagnosing migraine. Furthermore, the higher score of the Tightness and Location Features scale we found was in line with that the MA manifestations varied more widely than those of MO did [
26].
The fourth scale describes physical fatigues and psychiatric concerns related to the head pain. One population-based study found that some psychiatric comorbidities, particular mood and anxiety disorders, were common in migraine patients [
27]. Other scholars suggested that the psychiatric comorbidities might be a risk factor for migraine chronification, i.e., for the progression from episodic form to chronic one [
28]. Several studies have suggested that the prodromal dysfunctions might act as a primary trigger for a migraine attack [
21,
29]. Our results indicate that the prodromal or aggravating symptoms reflecting the respective physical and psychiatric alterations reported by patients generally characterize the two types of migraine.
There were however, at least two limitations of our study design which should be considered. First, we did not enroll patients with other primary or secondary headaches. Second, our sample sizes of both MA and MO groups were relatively small. Future studies might include more headache controls and compare descriptions from patients’ self-reports and the clinical criteria.