[Multiple comorbidities with migraine-Is there a common cause?].

Schmerz

Klinik für Neurologie, Oberbayerisches Kopfschmerzzentrum, Klinikum Großhadern, Ludwig-Maximilians-Universität, 81377, München, Deutschland.

Published: August 2025


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Article Abstract

Migraine is the most frequent neurological disorder and has a prevalence of 10-14% of the population. In addition to the frequency and the fact that it is usually manifested in adolescence, the frequent comorbid illnesses are also the cause of the high burden associated with migraine. Diseases from very different functional areas are associated with the presence of migraine. In general, this increased risk is more pronounced in the presence of migraine with aura and in women. For example, migraine is associated with a higher risk of developing stroke, heart attack, arterial hypertension, depression, anxiety disorder and probably dementia syndromes. The article presents the most important epidemiological studies on a number of these comorbid diseases. It is unclear what the neurobiological basis is for this accumulation of comorbid diseases in migraine. In addition to the purely coincidental cooccurrence in individual cases, other factors can be responsible for the increased risk: a shared genetic background, e.g. in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) or epileptic seizures, or treatment of a primary independent chronic disease (e.g. treatment with phosphodiesterase inhibitors, hormone substitution therapy or beta-interferon therapy). Another cause, which is discussed more broadly here, is inflammatory mechanisms, which are found in both the triggering of migraine and in a variety of comorbid diseases. This applies primarily to all chronic inflammatory diseases such as rheumatoid arthritis but also to depression and cardiovascular diseases. So far, these findings have not had any influence on the treatment of migraine but this may change in the future with a better understanding of the molecular mechanisms (e.g. activation of microglia).

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http://dx.doi.org/10.1007/s00482-025-00901-wDOI Listing

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