Menstrual migrane; causes,signs and treatment

Menstrual migraine

Menstrual migrane; causes,signs and treatment

Migraine is a predominantly female disorder. Although it is equally common in both sexes before puberty, there is increased female prevalence following menarche. This difference between the sexes becomes greater with advancing years, peaking during the early 40s and declining thereafter1. Some studies suggest that the lifetime prevalence of migraine in women is as great as 25%, compared with only 8% in men.

This sex difference during the reproductive years is generally considered to result from the additional trigger of the menstrual cycle, a well recognized association. Hippocrates noted: ‘shivering, lassitude and heaviness of the head denotes the onset of menstruation’. The term ‘hysteria’ was used, which had physical rather than psychological connotations, simply meaning ‘arising from the womb’ and the recommended cure was marriage. In 1666, Johannis van der Linden described a particularly severe case of one-sided headache with nausea and vomiting associated with menstruation in the Marchioness of Brandenburg. Despite evidence for the clinical relationship, the underlying mechanisms remained elusive to researchers over the centuries.

In 1873, Liveing posed the questions: ‘How are we to interpret the facts; what is the character of the influence exerted and to what extent is it the cause of the malady?’


Migraine is the commonest cause of severe episodic recurrent headache. Accompanying symptoms of heightened sensitivity to light, sound and smell, together with nausea, vomiting and general malaise, restrict normal function.

Migraine headaches typically last between 4 and 72 h and can occur, on average, every 4–6 weeks. However, there is wide variation of attack frequency over a lifetime with periods of increased frequency and periods of freedom, sometimes for several years. Although migraine is a benign condition, the severity and frequency of attacks can result in significant disability and reduced quality of life, even between attacks.

The first attack of migraine usually occurs during the teens and early twenties, with 90% of attacks occurring before age 40. Migraine typically disappears in the over 50s.

The two most frequently encountered types of migraine differ only in their presence or absence of ‘aura’. About 70–80% of migraineurs experience attacks of migraine without aura (formerly known as common or simple migraine); 10% have migraine with aura (formerly known as classical or focal migraine); 15–20% have both types of attacks. Less than 1% of attacks are of aura alone, with no ensuing headache.

Clinically, an attack of migraine can further be divided into five distinct phases.

Prodromal/premonitory phase

Not all migraineurs are aware of prodromal symptoms, which can precede attacks of migraine both with and without aura by 12–24 h. Symptoms are suggestive of hypothalamic disturbance and are distinct from, and unrelated to, the aura. They include:

irritability, feeling ‘high’ or ‘low’; extreme lethargy and yawning; dysphasia; anorexia, constipation or diarrhea; craving for sweets or specific foods; urinary frequency, thirst or fluid retention. Friends, family, or work colleagues are more likely to notice these symptoms than the sufferer. Some prodromal symptoms are incorrectly blamed as triggers for the attack. For example, craving for sweet foods may result in a desire to eat chocolate. A few people feel ‘on top of the world’ before an attack and rush around, later thinking that the attack was caused by overactivity. In fact, these are signs that the attack has already begun. Recognition of these prodromal symptoms can be of enormous benefit since avoiding known trigger factors during this time may be all that is necessary to stop the attack developing further.


Symptoms of aura probably arise from the cerebral cortex or brain stem and gradually develop over 5–20 min, last under 1 h, and usually completely resolve before the onset of headache. Atypical or permanent symptoms warrant further investigation. Homonymous visual symptoms are most common, experienced in 99% of auras. Sensory disturbance is less common (31%) and is usually associated with visual symptoms. Speech disturbance and motor symptoms can also be present (18% and 6%, respectively) but only in association with visual and/or sensory symptoms.

Symptoms usually follow one another in succession beginning with visual, followed by sensory symptoms, dysphasia and weakness.

Visual symptoms

These are usually symmetrical, affecting one hemifield of both eyes, although subjectively they may appear to affect only one eye. A migrainous scotoma is typically positive (bright), starting as a small spot gradually increasing in size to assume the shape of a letter ‘C’, developing scintillating edges which appear as zigzags or fortifications—a term coined in the late 18th century because the visual disturbances resembled a fortified town surrounded by bastions. The aura usually starts at or near the center of fixation, gradually spreading laterally, increasing in size over a period of 5–30 min. In contrast, thrombotic symptoms do not generally have the scintillating and spreading features of the visual aura of migraine and the visual loss usually described as a monocular negative scotoma (black). Transient monocular blindness is not typical of migraine and prompts urgent investigation. Generalized ‘spots before the eyes’, ‘flashing lights’, blurring of vision, photophobia affecting the whole visual field of both eyes and of variable duration before or with headache often occur during migraine and are not suggestive of focal ischemia.

Sensory symptoms

These are positive, i.e. a sensation of pins and needles rather than numbness. In an ischemic episode, a sense of numbness or ‘deadness’ is described. Migraine symptoms have a characteristic unilateral distribution affecting one arm, often spreading over several minutes proximally from the hand to affect the mouth and tongue—‘cheiro-oral distribution’. The leg is rarely affected in migraine.

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