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- Medication-overuse headache is a highly prevalent disorder with a major impact on the quality of life.- Medication-overuse headache is defined as headache on ≥ 15 days per month with overuse of acute headache medication for ≥ 3 months. We talk about overuse in case of intake of simple analgesics on ≥ 15 days per month or triptans or combinations of analgesics on ≥ 10 days per month.- The underlying type of headache is usually migraine or tension-type headache.- One of the possible underlying mechanisms of medication-overuse headache is changed sensitivity as a consequence of central sensitisation.- The initial treatment is detoxification of the headache medication. The preferred detoxification method is outpatient, abrupt withdrawal of all acute-headache medication and caffeine-containing products. Essential for successful detoxification is education about the reasons for detoxification, the expected course and the subsequent treatment.

Migraine is often regarded as a debilitating headache disorder without long-term consequences. However, migraine is an important risk factor for cardiovascular disease, especially in young women who suffer from migraine with aura. This increased risk is not limited to stroke but includes cardiac disease. The absolute risk for cardiovascular disease remains low in young women, however the prevalence of migraine is particularly high in this population. Migraine should therefore be incorporated as a factor in cardiovascular risk assessment. Mechanisms underlying the relationship between migraine and cardiovascular disease are complex and probably multifactorial. Endothelial dysfunction may play a pivotal role. Knowledge about the interaction of migraine with other risk factors and evidence-based recommendations on clinical management remain limited. Lifestyle advice, including the promotion of smoking cessation, is of utmost importance.

Migraine and depression are highly prevalent disorders with a strong bidirectional comorbidity: migraine patients have an increased risk for depression and patients suffering from depression have an increased risk for migraine. This comorbidity could be due to an underlying common pathophysiological mechanism. Chronification of migraine further increases the chance of developing depression, and vice versa. Misuse of migraine attack medication plays an important role in the development of chronic migraine. It is important for general practitioners, psychiatrists and neurologists to be alert to the comorbidity of migraine and depression. It is recommended that different hospital specialists should be involved in both the diagnosis and treatment of patients with comorbidity of migraine and depression.

New epidemiological studies suggest a relationship between migraine (especially migraine with aura) and cardiovascular disease. However, the absolute risk of cardiovascular disease for migraine patients is still low even though the relative risk is 2-4-fold higher. Further research will have to show whether migraine is an independent risk factor for cardiovascular disease and whether prophylactic treatment of migraine attacks will lower this increased risk for cardiovascular disease.

The relationship between patent foramen ovale (PFO) and migraine is controversial. A common genetic background seems possible, but there is no evidence for a causal relationship. Despite the lack of evidence, PFO closure is recommended in many countries as a remedy for migraine. At present, PFO closure for migraine should only be carried out under strictly controlled clinical trial conditions.

There is increasing evidence of involvement of genes coding for ion channels in the pathogenesis of paroxysmal neurological disorders. Recently for instance, mutations in the calcium channel gene on chromosome 19 were identified in migraine, ataxia, and epilepsy. With the current research into inherited 'channelopathies' a new approach has been established. A better understanding of the pathophysiology of paroxysmal neurological disorders may lead to new therapeutic strategies.