Number 2
The Etiology of Migraine
The exact etiology of the various aspects of migraine is not completely
understood. Migraine is certainly familial, but the exact gene or combination of
genes is not known. Likewise there is no explanation why some patients have
their first attack before the age of two, others in late adolescence or teenage
years, many as young adults and a few after the age of forty. We don’t know
why the migraine in children and adolescents often stops during their adulthood.
We cannot explain why childhood and adolescent migraine attacks usually cease
after sleep and the adult migraine might continue for days. In fact we cannot
explain what causes the typical 3 – 4 day adult migraine attack to terminate.
Hormonal changes might explain some features of migraine, but it is not known
how or at what level in the migraine pathway. Migraine in young adults is three
times more frequent in women, but the increased attacks might occur during the
entire menstrual cycle. There is no known reason why migraine headaches
become less frequent with aging. Both male and female migraineurs may cease
having their attacks of pain after menopause and begin having migraine auras
that are not followed by pain. Rather than being the result of hormonal changes,
there may be genetic or some other reason for these observations.
There is no explanation why some migraineurs have only unilateral pain and
other describe pain of equal intensity on both sides of the head. Or why some
patients describe a throbbing pain and others deny throbbing.
Thru out the years much effort has been spent seeking and modifying various
triggers of a migraine attack, but this rarely proves beneficial in treating the
individual patient. Many patients relate an attack to recent stress, but will admit
to having similar stress at other times that is not followed by a migraine. Others
blame sleep deprivation, fatigue, weather changes, foods, red wine or going on a
vacation. Ingestion of chocolates has been listed as a trigger but the urge for
chocolates may only be a symptom of the prodromal aspects of the migraine
attack.
There is no explanation why the migraine patient might note intensification of
pain with noise, movement and certain smells. The intensification of pain with
bright light experienced by many patients might be related to changes in optic
nerve conduction, a phenomenon that has been recently described.
The pulsating pain and the tenderness over the branches of the carotid artery
can be explained by changes in the trigeminovascular complex. The external
carotid artery thickens due to extravasation of fluid into the wall of the vessel.
Ultrasonic imaging shows that there is insignificant reduction of the lumen and
thus minimal change in blood flow. The trigeminal nerve impulses spreading to
the medulla explain the nausea and vomiting. The radiation of pain down into the
cervical and intrascapular region can possibly be explained by convergence of
pain transmission in the upper cervical region.
In summary the following is known about migraine. Migraine is familial and is
thought to be due to a genetic hypersensitivity in the brain. The latter can be
triggered by multiple mechanisms, although the exact triggers are not clearly
identified. The hypersensitivity can be suppressed by the daily use of various
agents, including beta blockers, antiepileptic agents (especially topiramate),
magnesium, co-enzyme Q and baby aspirin. After the attack begins there seems
to be a spread to the hypothalamus and possibly other sites where the various
prodromal symptoms develop hours before the onset of the pain. These include a
craving for certain foods, excessive or reduced mental alertness, yawning and
changes of mood. In 20 + % of attacks there is an aura, this caused by
depression of cortical electrical activity spreading at a rate of about 3 mm per
minute. This usually starts in the visual cortex. Next there is spread to the
trigeminovascular complex, then back to the trigeminal nucleus caudalis in the
brain stem and upper cervical region, then to the thalamus and finally to the
cortex.