Helicobacter pylori infection as an environmental risk factor for migraine without aura

Konstantina G Yiannopoulou1, Athina Efthymiou, Kleanthis Karydakis

  • 1Department of Neurology, Laiko General Hospital of Athens, Athens, Greece. ekati2@otenet.gr

Insights

Helicobacter pylori (H. pylori) infection may be an independent risk factor for migraine without aura. This study found a higher prevalence of H. pylori in migraineurs, particularly those without genetic or hormonal predispositions.

Area of Science:

  • Gastroenterology
  • Neurology
  • Infectious Diseases

Background:

  • Helicobacter pylori (H. pylori) infection is linked to various extraintestinal conditions.
  • Migraine without aura is a common neurological disorder with complex pathogenesis.
  • The role of H. pylori in migraine pathogenesis, especially in the absence of endogenous risk factors, requires further investigation.

Purpose of the Study:

  • To investigate the correlation between H. pylori infection and the pathogenesis of migraine without aura.
  • To assess H. pylori prevalence in migraineurs, particularly those without hereditary or hormonal risk factors.
  • To identify H. pylori as a potential independent environmental risk factor for migraine.

Main Methods:

  • Evaluated 49 outpatients with migraine without aura, divided into subgroups based on familial history and menstrual correlation.
  • Diagnosed H. pylori infection using the 13C-urea breath test (INFAI) in migraineurs.
  • Compared H. pylori prevalence in migraineurs with 51 control subjects using histologic analysis of gastric biopsy samples.

Main Results:

  • The prevalence of H. pylori infection was significantly higher in migraineurs without aura compared to controls (p=0.016).
  • H. pylori infection rates were notably high (81-87%) in migraineurs without other predisposing factors (family history/menstrual type).
  • In contrast, H. pylori prevalence was lower (36-37%) in migraineurs with predisposing factors (p=0.001, p=0.002).

Conclusions:

  • H. pylori infection appears to be a probable independent environmental risk factor for migraine without aura.
  • The findings suggest a stronger association in patients lacking genetic or hormonal susceptibility to migraine.
  • Further research is warranted to elucidate the mechanisms linking H. pylori and migraine pathogenesis.

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...