Menstrual migraine
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?’
WHAT IS MIGRAINE?
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.
Aura
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.
0 Comments