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Migraine Associated with Gastrointestinal Disorders: Review of the Literature and Clinical Implications

This article starts with an A++++ overview of migraine

Migraine is a common headache disorder with a lifetime prevalence of 13% in men and 33% in women (1). There are ictal (migraine attack) and interictal periods. Migraine is a highly disabling disease with high personal and social costs (2). Migraine can be considered as a complex neurogenic inflammatory disorder (35) but the pathophysiology is still not fully understood (6). It is a disease of the brain, possibly of the brainstem and is associated with increased synthesis and release of calcitonin gene related peptide (CGRP). A migraine attack can be blocked with CGRP antagonists (3, 7, 8). The actual pain is generated by nociceptors of trigeminal nerve endings in the dura. Low serotonin levels may sensitize the nociceptors of trigeminal neurons (9). Existing data support that serotonin is low interictal but increased ictally in migraineurs (10, 11). Ictally serotonin agonist, like triptans and ergotamins, which decrease serotonin are associated with relief of acute pain (79). In contrast tricyclic antidepressants and selective serotonin and
noradrenaline reuptake inhibitors, which are associated with increases in serotonin, are utilized for migraine prevention (11). Migraine attacks can be triggered by intrinsic cerebral factors (CGRP release), nitric oxide like tri-nitroglycerine, corticotrophin releasing hormone (stress), pro-inflammatory cytokines, and degranulation of mast cells located in the dura (1, 3, 8). Migraine has a genetic background, but the concordance in monozygotic twins is only 20%, indicating the importance of environmental factors in
getting the disease (12).

Study goes on to describe links between migraine and various gut problems – gastroparesis, celiac, colic, IBD, IBS.

 

I was especially interested in the IBS link because it suggested a diet that helped both migraine AND IBS and we even have some ideas about how it could be working.

Experimental evidence for an association between IBS and migraine comes from a study in which an IgG-based elimination diet was given to migraine patients with IBS. Twenty-one patients were included in the double blind, randomized, controlled, cross-over clinical trial with usual diet, elimination diet, and provocation diet (44). Compared with baseline, the elimination diet was associated with a significant reduction in migraine attack count, duration and severity. Also a significant reduction in IBS complaints was observed, demonstrating an association between the two diseases.

The rest of the paper is primarily an exploration of how on earth your guts and migraines could be so tied up together:

This overview of the literature suggests the existence of a rather strong relationship between GI disorders and migraine. One of the links between inflammatory diseases and migraine are enhanced pro-inflammatory immune responses (60).

There’s also some stuff about how based on how we think things might be going wrong, certain probiotics could help. But there’s basically no evidence on that yet and the person writing this works for a probiotics company…. They’re really pushing leaky-gut stuff, which is pretty controversial still and whatever is going on, we definitely don’t have a good handle on it.

Gastric stasis in migraineurs: etiology, characteristics, and clinical and therapeutic implications.

Migraines can cause your stomach to empty too slowly, making you feel like shit:

Gastric stasis, also called gastroparesis (5), is defined
as delayed emptying of the stomach in the absence of mechanical obstruction, and its clinical manifestations include nausea, vomiting, bloating, and weight loss (6).

In addition to making you feel even more awful than a migraine generally makes you feel, it can stop your triptans from working.

Oral triptans are not the optimal therapy in the presence of migraine-related
nausea because nausea predicts poor response to oral triptans and
because nausea can cause patients to delay oral treatment, which can
further compromise therapeutic efficacy. Oral triptans are not the
optimal therapy in the presence of migraine-associated gastroparesis
because these agents rely on gastric motility and gastrointestinal
absorption and may be ineffective or slowly or inconsistently effective
in the presence of gastroparesis. [link]

Maybe migraines fuck up your stomach because migraine is an ANS disorder?

It is hypothesized that both migraine and GS arise
because of autonomic nervous system (ANS) dysfunc- tion (13–16). Gastric stasis during migraine may be attributed to increased sympathetic nervous system activity, decreased parasympathetic nervous system activity, or both (4).

This paper is pretty similar to another by S.K. Aurora that I mentioned the other day, but has a little more detail.

What the Gut Can Teach Us About Migraine.

Nice recent summary of what we know about interactions between the head-brain and the gut-brain in migraine. Touches on why dietary changes help some migraineurs.

Take home paragraph:

The physiological connection between the gut and the brain as well as the influence on brain function and behavior has been well established. Inflammation at the level of the trigeminovascular system is hypothesized to play a role in migraine pathophysiology and could be influenced by inflam- mation and immune modulation in the GI tract and systemi- cally as evidenced by recent studies [90, 91]. Likewise, there is evidence to suggest that the gut microbiota plays an impor- tant role in the brain-gut axis and aberrancies may be associ- ated with neurological disease like migraine

Some interesting details:

81 % of migraineurs reported dyspepsia compared to 38 % of healthy controls.

The ANS [Autonomic Nervous System] is implicated in the generation of migraine and GI dysfunction with evidence for overlapping symptoms in both domains such as nausea, vomiting, dyspepsia, IBS, and gastric stasis. The ANS may also be the link between alterations in brain function and behavior secondary to intestinal flora dysbiosis.

Gastric stasis has long been implicated in association with
migraine. Early experimental studies by Volans et al. reported a delay in effervescent aspirin absorption in 19 out of 42 migraineurs during an attack, but not during the headache- free period and not found replicated in patients with tension- type headache [53, 54]. More recent studies suggest delayed gastric emptying occurs during spontaneous migraine attacks, visually induced migraines, and during the headache-free interictal period