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Managing migraines
Ease those headaches through more
effective prevention and acute treatment
BY Robert F. Nelson, MD
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Migraine is one of the most common, distressing
and disabling disorders suffered by people in all parts of the world.
In Canada, as in most Western countries where statistics have been
gathered, it has a uniform prevalence of at least 5-15% of the population,
and three out of four migraineurs are women. Migraine has a major
impact on productivity, through time missed from work or loss of
efficiency in sufferers staying on the job during an attack. Affecting
people of all ages, it's one of the most frequently seen problems
in family practice.
By definition, migraine is a recurrent, episodic,
biologic phenomenon with a variety of symptoms, the most prevalent
of which is headache. Attacks may last a few hours to several days,
with complete freedom from symptoms in between. Episodes may recur
several times a week or only a few times a year. A complete migraine
attack may follow a sequence of phases: a premonitory (formerly
referred to as prodrome), aura, headache, and recovery (formerly
postdrome).
How
does migraine present?
While head pain is the most apparent symptom, other phases
can also be very disturbing. The headache may be preceded by neurologic
symptoms referred to as aura and, even earlier, perceptive patients
may recognize a premonitory phase of changed mood, irritability,
yawning, euphoria or depression, cravings and an altered level of
energy. The aura most often presents as altered vision, but hemisensory
symptoms (loss of sensation on one side of the body) or speech disturbance
may occur. Motor symptoms are uncommon, except in the extremely
rare, genetically determined familial hemiplegic migraine (FHM).
The pain is traditionally described as throbbing,
but may be constant, and is often, though not always, one-sided.
It's usually accompanied by sensitivity to environmental stimuli,
such as light, sound and odours, nausea and occasionally vomiting,
and aggravation of symptoms by physical effort. Malaise is almost
universal. The recovery phase occurs after the pain has gone, and
consists of a continuing sensitivity to stimuli -- a sort of hangover.
What
causes migraine?
Our understanding of the underlying pathophysiology of migraine
has evolved. Early on, the condition was attributed, rather simplistically,
to dilation of intracranial and scalp blood vessels, presuming that
this was the source of pain. Vasoconstriction of cerebral vessels,
in turn, was thought to explain the neurologic symptoms associated
with some attacks. The current view is that migraine is primarily,
or at least initially, due to neurochemical and electrophysiologic
changes on the surface of or within the brain parenchyma -- so the
changes observed in blood vessels are just a secondary response.
A spreading depression of electrical activity over the surface of
the occipital cortex seems clearly related to the subjective visual
changes of the aura. When these symptoms are prominent, the attack
is classified as "migraine with aura," as opposed to those with
little or no aura symptoms, termed "migraine without aura." There's
an ongoing debate among migraine researchers as to whether these
are a single entity or two different conditions. They're probably
distinct, but both can occur in the same individual.
In the past decade, there's been considerable
interest in the possible role of genetic factors. We've long known
that migraine runs in families; now, certain rare forms of the condition
have been linked with genetic mutations in ion channels, particularly
for calcium, sodium and potassium. Different genetic anomalies on
chromosomes 1, 2, and 19 turn out to produce very similar phenotypes,
and at least five distinct genetic aberrations are related to FHM.
There are probably many more mutations involved, but we can't assume
that all migraine is genetically determined.
Neurotransmitters, particularly serotonin,
norepinephrine and dopamine, have also been incriminated in causing
symptoms. In fact, most of the medications effective for acute attacks
act through these neurotransmitter pathways.
How
do we diagnose this condition?
The International Headache Society (IHS) has classified the
various types of migraine. Defining features for "migraine without
aura" and "migraine with aura" are shown in Tables
1 and 2.
Keep in mind that these describe individual attacks, and
not people, who may experience different types of attacks
at different times. A high percentage of patients have a mixed pattern,
where migraine overlaps with other types of headache.
The diagnosis of migraine is based primarily
on a careful history and thoughtful clinical examination. Laboratory
tests aren't usually required. Recurrent attacks of unilateral headache,
occurring with a less than daily frequency and causing functional
impairment, are particularly strong indicators that the patient
is suffering from migraine, rather than other types of headache.
Migraine is a lifelong condition. It often starts in childhood,
when nausea and vomiting are prominent features, and recurs with
varying frequency throughout an individual's lifetime, but usually
abates somewhat in later years. Beware of diagnosing migraine in
someone whose first attack appears after age 50. In the older patient,
transient ischemic attacks (TIA) may be mistaken for migraine aura.
Migraine symptoms are more often sensory, while motor symptoms favour
TIA. Neurologic symptoms lasting more than an hour are seldom migrainous.
 Robert
F. Nelson, BSc, MD, FRCPC is Professor of Neurology (emeritus) at
the University of Ottawa, and the former Director of the Headache
Clinic at The Ottawa Hospital.
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