Migraine

18th December, 2008 - Posted by Andy - No Comments

headache1INTRODUCTION
A migraine headache is often described as an intense pulsing or throbbing pain in one area of the head and is often accompanied by extreme sensitivity to light and sound, nausea, and vomiting. Migraine is three times more common in women than in men, and some individuals can predict the onset of a migraine because it is preceded by an “aura,” visual disturbances that appear as flashing lights, zig-zag lines or a temporary loss of vision.

Headaches are generally broken down into two types, primary and secondary; Migraine is classed as a primary, periodic headache that can occur with various neurological, behavioural or gastrointestinal changes and is the most common form of headache that patients seek help from their GP.

Secondary headaches are those that can be attributed to other causes, for example, excess alcohol or dehydration, accidental head injury or trauma, sunstroke, brain tumours, or meningitis. In comparison, primary headaches, such as migraine, tension-type, and cluster headaches cannot be attributed to other causes. Naturally, primary headaches such as migraine can be made worse by secondary causes such as head impact. In these instances, patients might receive two diagnoses: migraine headache and chronic post-traumatic headache

According to the International Headache Society, migraine is clinically defined as a headache that

(1) Has occurred on a minimum of 5 occasions
(2) Each headache episode lasts between 4-72 hours (either treated or untreated);
(3) The pain has at least two of the following characteristics:
- Localized to one side of the head
- Has a throbbing nature
- Moderate to severe intensity
- Appears to worsen by routine physical activity, such as walking or climbing stairs.

(4) The patient complains of nausea and/or vomiting during the headache
(5) The patient has increased sensitivity to light or sound.
(6) The headache cannot be attributed to another cause i.e. it is not a “secondary” headache.

VARIOUS TREATMENTS
Understandably, getting an appropriate migraine treatment plan begins with a correct diagnosis from your GP. And once confirmed, the first issue to look at is your lifestyle. Triggers for migraine attacks include the following lifestyle aspects:

• Excess caffeine use
• Lack of sleep
• Irregular or skipping of meals
• Lack of exercise
• What you eat and drink also appears to have major implications in triggering migraine attacks, though this list of ‘triggers’ varies from person to person.
When lifestyle adjustments appear not to be enough on their own, one should consult your GP for some sort of drug based treatment.

If headaches occur infrequently (e.g., less than four times a month) an abortive agent – something that stops the progression of symptoms once started – can be used. Second, if the headaches occur more frequently or are prolonged, prophylactic or preventive therapy, usually daily, should be considered. Here, use of a headache diary that reports the number of headache days and headache intensity can be especially useful. Some doctors use a MIDAS (Migraine Disability Assessment) questionnaire for this purpose.

Acute migraine treatments are designed to stop the progression of headache symptoms once started. Acute treatments can be classified as specific (triptans) and non specific. Triptans are very effective in stopping acute migraine attacks. They do this by reducing activation of the trigemminal sensory nerve fibres that carry pain sensations from the meninges to the brain stem. The triptans also trigger constriction of vascular smooth muscle in blood vessels.

However, less is known about how non specific treatments work. One important mechanism may be that non steroidal anti-inflammatory drugs (NSAIDS, which include ibuprofen) which are very effective against migraine, can reduce inflammation; this in turn, can lessen pain at the meninges. Taken together, our knowledge of how acute treatments work centres on stopping the effects of spreading depression (the migraine) from developing painful stimuli. The initial trigger itself (spreading depression) has come and gone by the time a patient takes an abortive. Therefore, any affect of the abortive is on reducing what happens because of the spreading depression.

It’s different with prophylactic therapy. Here the basis for the efficacy of agents such as anticonvulsants rest in the fact that these medications reduce the tendency for spreading depression to occur. The same may be true for calcium channel blockers. As mentioned earlier, spreading depression begins when a sufficiently large area of brain becomes over-excited. With time, prophylactic medication can progressively reduce the tendency for spreading depression (or migraine to occur). How beta-blockers or tricyclic antidepressants produce a similar positive effect is less well known. However, this notion of a progressive or adaptive response of brain to daily medications taken to stop migraine is worth a discussion between GP and patient.

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[Sources: NHS Direct, Google, NIH (USA)]

FURTHER READING

http://knol.google.com/k/richard-kraig/migraine-mechanisms-and-management/DmMyZecK/h0wPsA#
http://www.migraineclinic.org.uk
http://www.migraine.org.uk
http://www.ninds.nih.gov/disorders/migraine/migraine.htm

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Posted on: December 18, 2008

Filed under: General