Migraine: More Than Just a Headache!

Abstract & Commentary

By Dara G. Jamieson, MD, Associate Professor, Clinical Neurology, Weill Medical College of Cornell University. Dr. Jamieson is a consultant for Boehringer Ingelheim and Merck, and is on the speaker's bureau for Boehringer Ingelheim, Merck, Ortho-McNeil, and Pfizer.

Synopsis: Upper abdominal pain, without anatomic explanation, occurs in over 80% of adult patients with migraine, and may be part of the migraine syndrome.

Source: Kurth T, et al. Prevalence of Unexplained Upper Abdominal Symptoms in Patients with Migraine. Cephalalgia. 2006;26:506-510.

Gastrointestinal symptoms are prominent in children with migraine, and are associated with both headaches and with childhood periodic syndromes that are commonly precursors of migraine. Cyclic nausea and vomiting without signs of gastrointestinal disease occur in schoolchildren as a migraine precursor. Children may have abdominal migraine with recurrent attacks of abdominal pain associated with anorexia, nausea, and vomiting. There is an increased incidence of maternal migraine history in children with abdominal migraine, reinforcing the position that migraine and abdominal migraine may have a common pathogenesis.

Nausea and vomiting, part of the ICHD-2 diagnostic criteria for migraine, are arguably the most socially and physically disabling symptoms for adult patients with migraine. Occasionally, the prominence of gastrointestinal symptoms may be greater than head pain. These symptoms are rarely seen in patients with episodic or chronic tension-type headaches or other primary headache types. (Lipton RB, et al. Classification of Primary Headaches. Neurology. 2004;63:427-435).

Adults with migraine may have co-morbid gastrointestinal disorders including irritable bowel syndrome, but the association between abdominal pain and migraine, well recognized in children, is less established in an adult migraine population. The aim of this paper was to survey the prevalence of idiopathic dyspeptic symptoms in patients with migraine, and to compare the prevalence of upper abdominal pain to that of a control population of healthy non-migraineurs. During a 6-week period, 99 consecutive patients were recruited from a headache clinic at the University Hospital, Essen. They were diagnosed with migraine with or without aura by the 1988 International Headache Society Criteria. The control group was made up of 488 apparently healthy blood donors without reported migraine or headaches. A validated Bowel Disease Questionnaire was administered to both groups to evaluate gastrointestinal tract symptoms. Patients or controls who reported upper abdominal pain occurring more than 6 times in the past year were considered to have frequent dyspepsia. Other potential risk factors for gastrointestinal symptoms, including smoking, high alcohol consumption, and analgesic use, were also assessed.

As compared to the healthy blood donors, migraine patients were more likely to be female (76% vs 34%) and older (mean age, 41.5 years vs 34.1 years) with greater analgesic use. Upper abdominal pain was seen in 80.9% of migraine patients and 37.5% of healthy blood donors. After adjusting for potential confounding conditions, the prevalence odds ratio of idiopathic upper abdominal pain symptoms in migraine patients was increased by 170% compared to healthy blood donors (OR 2.7; 95% CI 1.2, 6.1; P < 0.001). There was no association between the dose of analgesic and the severity of gastrointestinal symptoms. Even correcting for aspirin and other analgesics use, the prevalence of dyspepsia was increased among migraineurs when compared with controls.

Gorson and colleagues concluded that the prevalence of upper abdominal pain symptoms is increased in a population of migraine patients, even adjusting for confounding conditions or analgesic use. Gorson et al were not able to correlate upper abdominal pain symptoms with migraine type or severity but, because this was a referral population, these patients may have had more severe migraines.


There may be both clinical and mechanistic overlap between dyspepsia and migraine. Meal-induced gastric hypersensitivity is seen in both dyspeptic individuals and migraineurs. Vagal dysfunction may come into play with both migraine and dyspepsia, and there are shared neuropeptides. Calcitonin gene-related peptide (CGRP) is increased during the migraine attack, and plays an important role in the neuro-inflammatory pathogenesis of migraine. CGRP may play a role in visceral afferent nerve sensitization of gastrointestinal origin; although its role in dyspepsia is unclear. Upper abdominal symptoms should be added to the growing list of symptoms experienced by migraineurs, indicating that migraine is more than just a headache.