1.1 Migraine without aura

Previously used terms:
Common migraine; hemicrania simplex.

Recurrent headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia.

Diagnostic criteria:
A. At least five attacks1 fulfilling criteria B-D
B. Headache attacks lasting 4-72 hr (untreated or unsuccessfully treated)2;3
C. Headache has at least two of the following four characteristics:

    1. unilateral location
    2. pulsating quality
    3. moderate or severe pain intensity
    4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)

D. During headache at least one of the following:

    1. nausea and/or vomiting
    2. photophobia and phonophobia

E. Not better accounted for by another ICHD-3 diagnosis.

1. One or a few migraine attacks may be difficult to distinguish from symptomatic migraine-like attacks. Furthermore, the nature of a single or a few attacks may be difficult to understand. Therefore, at least five attacks are required. Individuals who otherwise meet criteria for 1.1 Migraine without aura but have had fewer than five attacks should be coded 1.5.1 Probable migraine without aura.

2. When the patient falls asleep during migraine and wakes up without it, duration of the attack is reckoned until the time of awakening.

3. In children and adolescents (aged under 18 years), attacks may last 2-72 hours (the evidence for untreated durations of less than two hours in children has not been substantiated).

Migraine headache in children and adolescents (aged under 18 years) is more often bilateral than is the case in adults; unilateral pain usually emerges in late adolescence or early adult life. Migraine headache is usually frontotemporal. Occipital headache in children is rare and calls for diagnostic caution. A subset of otherwise typical patients have facial location of pain, which is called “facial migraine” in the literature; there is no evidence that these patients form a separate subgroup of migraine patients. In young children, photophobia and phonophobia may be inferred from their behaviour. Migraine attacks can be associated with cranial autonomic symptoms and symptoms of cutaneous allodynia.

Migraine without aura often has a menstrual relationship. ICHD-3 (beta) offers criteria for A1.1.1 Pure menstrual migraine and A1.1.2 Menstrually-related migraine, but in the Appendix because of uncertainty over whether they should be regarded as separate entities.

Very frequent migraine attacks are now distinguished as 1.3 Chronic migraine. When there is associated medication overuse, both diagnoses, 1.3 Chronic migraine and 8.2 Medication-overuse headache, should be applied. 1.1 Migraine without aura is the disease most prone to accelerate with frequent use of symptomatic medication.

Regional cerebral blood flow imaging shows no changes suggestive of cortical spreading depression (CSD) during attacks of migraine without aura, although blood flow changes in the brainstem may occur, as may cortical changes secondary to pain activation. This contrasts with the pathognomonic spreading oligaemia of migraine with aura. While the bulk of the literature suggests that CSD does not occur in migraine without aura, some recent studies disagree. Furthermore, it has been suggested that glial waves or other cortical phenomena may be involved in migraine without aura. The messenger molecules nitric oxide (NO), 5-hydroxytryptamine (5-HT) and calcitonin gene-related peptide (CGRP) are involved. While the disease was previously regarded as primarily vascular, the importance of sensitization of pain pathways, and the possibility that attacks may originate in the central nervous system, have gained increasing attention over the last decades. At the same time, the circuitry of migraine pain, the trigeminovascular system, and several aspects of its neurotransmission peripherally and in the trigeminal nucleus caudalis, the central mesencephalic grey and the thalamus, have been recognized. New highly receptor-specific acute medications such as the triptans, which are 5HT1B/D receptor agonists, 5-HT1F receptor agonists and CGRP receptor antagonists have demonstrated efficacy in the acute treatment of attacks. Because of their high receptor-specificity, their mechanism of action provides new insight into migraine mechanisms. It is now clear that migraine without aura is a neurobiological disorder; clinical as well as basic neuroscience has advanced our knowledge of migraine mechanisms, and continues to do so.