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Following publication of the original article [1], the authors notified us of some misreported data due to the publication of the EVOLVE-2 trial (Cephalalgia. 2018;38:1442–1454), which substantially changed the level of evidence of galcanezumab for the prevention of episodic migraine. All changes are marked in bold and with red in Figure 1 and Figure 2. Please note that the final recommendations remain unchanged.

The widely used term chronic daily headache is a common denominator for a chronic headache with a daily occurrence but is not included in the former and in the revised versions of the IHS classification system. We discuss the pros and cons for the use of the term chronic daily headache, and describe some of the problematic aspects in patients with chronic headaches. We find that the term should only be used as an unspecific, clinical working description and never as a final diagnosis due to lack of specificity. Most patients in specialized headache clinics suffer from several different primary and secondary headaches at the same time and deserve a careful characterization before a rational therapy can be initiated. In particular, it is of utmost importance to identify and treat coexisting medication overuse since such overuse may distort the clinical phenotypic presentation and render various prophylactic strategies ineffective. As the prognosis of medication overuse headache usually is favorable, identification of drug overuse is mandatory. The use of a wastebasket diagnosis such as chronic daily headache may obscure the precise headache diagnosis leading to an unsatisfactory treatment strategy and should therefore be avoided.

Recent studies on tension-type headache indicate that the nociceptive input to the central nervous system may be increased as a result of activation or sensitization of peripheral sensory afferents. Moreover, pain perception studies and pharmacologic studies strongly suggest that the central nervous system is sensitized in patients with chronic tension-type headache. The barrage of nociceptive impulses from the periphery may be responsible for the sensitization of second- and third-order neurons in the central nervous system. In this way, sensitization may play a role in the initiation and maintenance of tension-type headache. Studies have demonstrated that treatment with drugs that counteract sensitization has an analgesic effect on tension-type headache. Targeting this mode of action seems to be a promising way of improving the treatment for this prevalent disorder.

Sensitization of myofascial pain pathways may play an important role in the pathophysiology of chronic headache. Animal studies have shown that sensitization of pain pathways may be caused by associated with activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide (NO). Furthermore, it has been shown that NOS inhibitors reduce central sensitization in animal models of persistent pain. On the basis of these findings, we investigated the analgesic effect of the NOS inhibitor, N-N G-methyl arginine hydrochloride, and demonstrated that this drug significantly reduced headache as well as myofascial factors in patients with chronic tension-type headache. In addition, we demonstrated that infusion of the NO donor, glyceryl trinitrate, induces headache in these patients, probably by enhancing the sensitizing effect of pre-existing myofascial input. These studies strongly indicate that NO plays a crucial role in the pathophysiology of tension-type headache. We suggested that the analgesic effect of NOS inhibition in patients with chronic tension-type headache is most likely due to reduction of central sensitization at the level of the spinal dorsal horn or trigeminal nucleus, or both. Furthermore, these data suggest that inhibition of NOS may become a novel means of future treatment of chronic headache.

86 of 98 patients completed the 12-month follow-up. Totally, headache frequency was reduced by 39% (p