By far the most common reason for a migraine that occurs on 15 or more days per month, or for a mixed migraine and tension-type headache with 15 or more headache days per month, is overuse of specific acute migraine medications or painkillers [7, 8].
In general, medication overuse is defined in days of intake per month. It is crucial that it is taken regularly , i.e. on several days per week. Is the limit e.g. E.g. 10 days a month, this would mean an average of 2-3 days of intake per week. If an accumulation of days of intake is followed by longer periods without medication of at least three days or more, the development of headaches due to medication overuse is far less likely.
In addition, headaches resulting from medication overuse often have the peculiarity of switching between the characteristics of a migraine and those of a tension-type headache, even within a day, creating a new type of headache. This used to be called “combination headache”. However, it is not defined and therefore should not be used. The diagnosis of medication overuse headache is crucial because patients typically do not respond to headache prophylaxis as long as medication overuse exists.
The general criteria for medication overuse headache (MÜK) are now uniformly defined worldwide in the international headache classification ICHD-3beta. The development of this serious and common complication in the treatment of primary headaches is becoming increasingly better understood thanks to new studies.
Cerebral imaging studies have identified structural and functional changes in the brain in patients with MOD. Current data demonstrate functional changes in intrinsic neuronal networks, but not macrostructural changes. Dependency processes seem to play a prominent role in the development and maintenance of MÜK [ 1 ]. The frequency of medication intake per month is a decisive, significant prognostic factor for the development and maintenance of MÜK [ 3 , 12 ]. The relapse rate is correlated with psychological decision-making processes, particularly with increased dependency scores [ 12 ].
Other recent studies on the development of MOC have consistently documented sensitization and increased excitability of trigeminal and cortical neurons [ 9 , 16 , 17 , 18 , 19 ]. Cortical hyperexcitability appears to promote the development of cortical spreading depression, which is considered a correlate of migraine aura. Peripheral and central hypersensitization also appears to be increased.
This change is thought to be based on serotoninergic (5-HT) and possibly endocannabinoid-mediated mechanisms. Expression of excitatory cortical 5-HT 2A receptors could increase the likelihood of activation of cortical spreading depression. Depletion of the central pain defense systems can activate the process of central sensitization and trigger other molecular processes of hyperexcitability. Decreased 5-HT levels may increase the expression and release of calcitonin gene-related peptide (CGRP), further increasing the sensitization of trigeminal neurons.
The exhaustion of the central pain-modulating systems as a result of chronic drug overuse leads directly to a gradually increasing sensitization of pain perception and causes a continuous increase in the frequency of painkiller intake, which in turn leads to further sensitization. Without interrupting this feedback, an endless loop that is open to the top can arise [ 9 , 16 , 17 , 18 , 19 ]. It is precisely this development that can be observed in everyday clinical practice [ 3 ].
The mechanisms described do not only affect the sensation of pain. Other aspects of experience and behavior are also influenced. These include depression, anxiety, inner restlessness, sleep disorders, increased irritability, lack of energy, exhaustion, social withdrawal, among others. The experience and behavior concentrate on the pain and the frustrating attempts at treatment. These pathophysiological mechanisms make it understandable why preventive migraine medications are no longer effective if an MOC is present at the same time. It is pointless, on the one hand, to aim for a reduction in hyper-sensitization with drug prophylaxis, but at the same time to continue the maintaining and further increasing reason for this hyper-sensitization, namely drug overuse [ 3 , 11 ] . It is also not helpful to expect a stable situation with long-term use of triptans. The sensitization becomes increasingly stronger and over time the situation decompensates and escalates.
There is therefore only one solution for sustainable therapy: the constant supply of medication must be stopped and a medication break or, for substances that may no longer be used, a medication withdrawal must be observed [ 4 , 5 , 6 , 15 , 20 , 21 ] . The aim is to recover the body's exhausted pain defense system and normalize pain sensitivity. As long as continuous overuse continues, no treatment method can achieve decisive and lasting improvement. There is no fundamental solution to the problem other than a controlled and systematic break from taking painkillers [ 3 , 7 , 8 , 11 ].
If simply informing and instructing the patient does not lead to cessation of medication overuse, a medication break or withdrawal treatment is necessary. This can be done on an outpatient basis, in a day hospital or as an inpatient. In uncomplicated cases, the results of the chosen organizational form do not differ. In complicated cases, inpatient withdrawal treatment as part of a multimodal treatment concept is significantly superior. [ 2, 10, 11, 13, 14, 16]
literature
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18. Supornsilpchai W, Le Grand SM, Srikiatkhachorn A (2010) Involvement of pro-nociceptive 5-HT2A receptor in the pathogenesis of medication-overuse headache. Headache 50:185–197
19. Supornsilpchai W, Sanguanrangsirikul S, Maneesri S et al. (2006) Serotonin depletion, cortical spreading depression, and trigeminal nociception. Headache 46:34-39
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