Abstract

In this issue, an interesting article by Farinelli and coworkers [1] debates an important emerging and not yet resolved problem: how to treat the chronic headaches complicated by medication overuse. Headache is the most common neurological disease in clinical practice. In Europe, this affects about 51% of the population, of which 31% are tension-type headache and 14% are migraine sufferers; 2% of these patients become chronic sufferers, more than 15/day/month, and chronic daily headache (CDH). 4–5% of general population suffers from a chronic form (CDH), with prevalence between 1.7 and 2.1% in men and between 2.8 and 6.8% in women [2]; within this group of patients in the US general population ranges around 1.3–2% of chronic migraine (CM). A number of possible pathophysiological mechanisms for the transformation from episodic to chronic headache have been proposed including a progressive damage of the central nociceptive system. One physiopathological hypothesis is the activation of N-methyl-D-aspartate (NMDA) and nonNMDA receptors glutamate, released by central nociceptive terminations, induces calcium entry in dorsal horn neurons, as well as in the trigeminal nucleus caudalis. Calcium entry leads to the activation of nitric oxide (NO) synthetase causing NO synthesis. These neurotransmitters produce the release of sensory neuropeptides, such as CGRP and substance P, which support the development of hyperalgesia and maintain central sensitization [3–5]. Medication near-daily use and subsequent medication overuse headache (MOH) have been described by the revised International Classification of Headache Disorders (ICHDs)-IIR criteria as the use of each drug for at least 3 months, for a certain number of days per month, and is one of the most critical parameters in the process of

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