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1.1Migraine without auraG43.0  
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:

  1. At least 5 attacks1 fulfilling criteria B-D
  2. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated)2;3;4
  3. Headache has at least two of the following characteristics:
    1. unilateral location5;6
    2. pulsating quality7
    3. moderate or severe pain intensity
    4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
  4. During headache at least one of the following:
    1. nausea and/or vomiting
    2. photophobia and phonophobia8
  5. Not attributed to another disorder9


  1. Differentiating between 1.1 Migraine without aura and 2.1 Infrequent episodic tension-type headache may be difficult. Therefore at least 5 attacks are required. Individuals who otherwise meet criteria for 1.1 Migraine without aura but have had fewer than 5 attacks should be coded 1.6.1 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, attacks may last 1-72 hours (although the evidence for untreated durations of less than 2 hours in children requires corroboration by prospective diary studies).
  4. When attacks occur on ≥15 days/month for >3 months, code as 1.1 Migraine without aura and as 1.5.1 Chronic migraine.
  5. Migraine headache is commonly bilateral in young children; an adult pattern of unilateral pain usually emerges in late adolescence or early adult life.
  6. Migraine headache is usually frontotemporal. Occipital headache in children, whether unilateral or bilateral, is rare and calls for diagnostic caution; many cases are attributable to structural lesions.
  7. Pulsating means throbbing or varying with the heartbeat.
  8. In young children, photophobia and phonophobia may be inferred from their behaviour.
  9. 9. History and physical and neurological examinations do not suggest any of the disorders listed in groups 5-12, or history and/or physical and/or neurological examinations do suggest such disorder but it is ruled out by appropriate investigations, or such disorder is present but attacks do not occur for the first time in close temporal relation to the disorder.


1.1 Migraine without aura is the commonest subtype of migraine. It has a higher average attack frequency and is usually more disabling than 1.2 Migraine with aura.

Migraine without aura often has a strict menstrual relationship. In contrast to the first edition of The International Classification of Headache Disorders, this edition gives 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 1.5.1 Chronic migraine provided that there is no medication overuse. Migraine without aura is the disease most prone to accelerate with frequent use of symptomatic medication, resulting in a new headache which is coded as 8.2 Medication-overuse headache.

Regional cerebral blood flow shows no changes suggestive of cortical spreading depression 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. In all likelihood spreading depression is therefore not involved in migraine without aura. On the other hand the messenger molecules nitric oxide (NO) and calcitonin-gene-related peptide (CGRP) are clearly involved. While the disease was previously regarded as primarily vascular, the importance of sensitisation of perivascular nerve terminals, 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 and several aspects of neurotransmission in this system have been recognised. A significant contribution has been made by the advent of the triptans, 5HT1B/D receptor agonists. These drugs have remarkable efficacy in acute attacks and, in view 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 and clinical as well as basic neuroscience currently advances our knowledge of migraine mechanisms at an increasing speed.