Medication-induced headache (MIH) is also known as medication overuse headache (MOH). It can develop when painkillers are taken for headaches on at least 10 days per month. People who suffer from primary headaches, such as migraines and tension headaches, are particularly susceptible to medication overuse headache.

In medication overuse headache (MOH), the paradoxical situation exists that the use of pain and migraine medications has led to an increase in headaches and migraines.

Medication overuse headache can be considered a complication of attack treatment for headaches.

In principle, any medication effectively used to treat acute migraines and tension headaches can itself trigger headaches if taken too frequently. The greatest risk is associated with combination painkillers and triptans. The crucial factor here is not the dose of the medication, but the frequency of use.

Taking painkillers or triptans too frequently – by definition, on more than 10 days a month – can lead to an increase in the frequency of headaches. At the same time, the effectiveness and duration of action of previously successful medication decrease, which in turn leads to more frequent use of the medication. This creates a vicious cycle of more and more headaches and more and more headache medication.

Self-medication for headaches is advisable for known headache types; it saves time and, if effective, can be justifiable. Typical examples include occasional tension headaches or a migraine attack that responds to self-medication. The primary treatment should consist of substances like aspirin, paracetamol, or ibuprofen. These medications should be taken early in the attack and in the correct dosage. Anti-nausea medication can be used in addition to medication for accompanying symptoms such as nausea or vomiting. The most important rule in self-medication is the 10-20 rule: acute pain relievers should be taken on fewer than 10 days per month, and no headache medication should be used on at least 20 days per month. The reason for this rule is that exceeding this limit can lead to medication overuse headache. Headaches become more frequent, longer, and more severe, and accompanying symptoms can also increase. The frequency of headaches increases continuously, and after a few months, chronic headaches can develop. By adhering to the 10-20 rule, a corresponding protective limit is in place.

Medication-induced headache develops as a complication of treating primary headaches. With increasing frequency of acute medication use, the headache frequency increases, resulting in a so-called secondary headache, or medication-overuse headache. Typically, the 10-20 rule is exceeded; the headache frequency increases, eventually reaching 12, 15, 20, or more days per month with acute medication use and even more headache days. The only sustainably effective strategy is to implement a so-called medication break. This involves interrupting medication administration. A rebound headache, also known as a relapse headache, develops. During this phase, patients are severely impaired. Therefore, it is necessary for them to receive concomitant medication that does not include drugs typically used for acute attacks. Prednisolone may also be helpful. Antiemetics, medications to reduce nausea and vomiting, are used. In mild cases, outpatient therapy can be administered; however, in severe cases, current studies show that inpatient treatment is significantly more effective than outpatient or day-clinic treatment. Once the medication-overuse headaches have subsided, preventative medication for primary headaches must be established to avoid a relapse into medication-overuse headache. For long-term care, we have initiated a nationwide headache treatment network. Regionally based physicians can continue treatment for up to one year to advise patients and optimize and adjust both medication-based and non-medication-based preventative measures.

In headaches, experience and behavior play a crucial role. They originate in the central nervous system. The central nervous system not only regulates bodily mechanisms and purely physical functions, but its primary task is to enable experience and behavior, to condition and control regulation, motivation, and emotions. Psychological mechanisms therefore play a decisive role in all pain. Pain is processed in the cerebral cortex and brought to consciousness. Psychological conditions are thus always factored into pain, altering and coloring the pain experience. Therefore, psychological therapies and strategies for pain prevention play a central role in pain management. Psychological disorders that lead to headaches include, in particular, depression and so-called somatoform disorders; psychoses can also cause psychogenic headaches. Treatment focuses entirely on the underlying condition of these so-called secondary headaches in psychiatric disorders. Otherwise, for all forms of headache, especially primary headaches, psychological factors must be considered in treatment. This begins with keeping a headache diary, behavioral analysis, relaxation techniques, and treating anxiety and depression related to headaches. Social conditions, partnership issues and other factors must also be taken into account in the treatment.

Today, we distinguish 363 different primary headache diagnoses. There is no single "headache," just as there is no single "stomachache." Therefore, the precise differentiation of pain mechanisms and the conditions that maintain the pain is of central importance. In the most common headaches—migraine, tension-type headache, and medication-overuse headache—the mechanisms are now very well understood, allowing for specific interventions. Migraine pain arises from a so-called neurogenic inflammation of the blood vessels in the meninges. Certain neurotransmitters are released there, causing local inflammation. This leads to increased pain sensitivity in the vascular membranes; every jolt, every movement, every pulsation and throbbing is painful. The trigger for the excessive release of these inflammatory substances is the activation of specific nerve nuclei in the brainstem. This is a consequence of over-regulation due to energy deficits resulting from increased energy expenditure in the nerve cells. Twelve risk genes for migraine are currently known. These processes lead to an increase and release of the aforementioned neurotransmitters and neuropeptides in the nervous system. It follows that migraine therapy must intervene in this process in a complex way in order to stabilize the headache.

The development of headaches due to medication overuse is explained by an exhaustion of the body's own pain defense system. Frequent pain attacks and the excessive intake of acute painkillers increasingly deplete the body's pain defense system, leading to more frequent headache episodes and ultimately, chronic headaches at the end of the pathophysiological progression.