Migraine

Account for about 30% of headaches

This is basically a recurrent headache associated with visual and GI disturbance. In mid cases the difference between tension headache and migraine is vague, but in sever forms it can mimic thrmboembolic ischaemia.

-          To distinguish from a TIA: - TIA’s have sudden onset, with maximum deficits immediately. Headache is rare. In migraine, the deficits may occur gradually, and almost always accompanied by headache. In both cases aura may be present

It can occur in recurrent episodes (similar to tension headache) or in one off, irregular instances.

Incidence – 8-12%.

M:F – 1:2

 

Aetiology

-          Times of relaxation (e.g. often at weekends)

-          Chocolate – due to high phenylethylamine content

-          Cheese – due to high tryamine content

-          Noise / lights

-          Oral contraceptive pill

-          Common around puberty

-          Common around menstruation / pregnancy / menopause

o   In pregnancy, cases often resolve as the pregnancy progresses, and are uncommon in the second and third trimesters. Don’t use aspirin after 30 weeks and when breatfeeding.

-          Sometimes occurs after minor blow to the head

-          Obesity

-          Patent foramen ovale

 

CHOCOLATE

-          Ch – chocolate

-          O – Oral contraceptive

-          C – caffeine (or withdrawal)

-          Ol – alcohol

-          T – travel

-          E – exercise

 

In 50% of cases not trigger can be identified. Only in a very few cases will avoiding triggers completely avoid attacks.

 

 

Clinical features

-          Visual Aura – a perceived visual disturbace (e.g. zig-zag lines, bright lights, distorted objects, scotomo (dark patches), techopsia (flashes)). These often occur before an attack and last 15-60 minutes. They are caused by reduced blood flow to the occipital cortex before an attack.

o   They also often occur before an epileptic seizure in epileptic patients.

o   Patients may also have a sensory aura – e.g. pins/needles spreading up limbs, or a speech aura – whereby they may suffer temporary dysarthria

-          Throbbing sensation

-          Photophobia

-          Unilateral – the pain often begins locally, and then spreads.

-          Vomiting

-          Heightened sensitivity to pain –all stimuli (e.g. wearing glasses, brushing hair) cause pain

-          There are no clinical / neurological signs.  

 

Diagnostic criteria

-          Headaches lasting 4/72h with aura – classical Migraine

-          Headaches lasting 4/72 hours with no aura, (sometimes called Common migraine)but with:

o   Nausea / vomiting OR photophobia

§ AND at least 2 of:

o   Unilateral

o   Pulsating

o   Interferes with normal life

o   Worsened by normal activities (e.g. walking / bending / climbing stairs)

 

Other variations:

-          Basilar migraine – includes symptoms such as tongue tingling, vertigo, diplopia, visual disturbance (perhaps even blindness), dysarthria, ataxia

-          Facioplegic Migraine – unilateral face weakness

 

 

Pathology

Not entirely know. Some genetic pre-disposition. It is related to the dilation/constriction of cerebral blood vessels, and thus the neuropeptide CGRP (calcitonin gene related peptide) is thought to be important.

-          Initial Oligaemia – which causes the aura, is then following by

-          Hyperaemia / blood vessel dilation / oedema – which stimulates nerve endings and causes pain.

Some speculation that there is failure of inhibition , particularly in the visual cortex, and this is what actually causes the attacks.

 

Treatment

During an attack (as long as other possibilities have been ruled out), give basic analgesia; e.g. paracetomol or aspirin. Be aware that peristalisis is often slowed during attacks, and so higher doses may have to be given to be effective. Also give antiemetic (e.g. metoclopramide) if necessary.

-          NB – overuse of analgesics predisposes to attacks

5-HT agonists (Triptans) may be useful for some patients (IM injection, or orally). use sparingly, and should be avoided in vascular disease. They block transmission in the trigeminal nerve to 2nr order neruons – and thus can be used in any process that activates the trigeminal nerve (e.g. cluster headaches, migraine). An example:

-          Ergotamine – 1mg orally as headache begins. Repeat at ½ hour intervals up to 3mg/day or 6mg/week. Do not use with contraceptive pill, peripheral vascular disease, pregnancy, liver/kidney impairment, Reynaud’s, hemiplegic migraine. 

 

Antoconvulsants - e.g lamotrigine – treatment is experimental, but reduce hyper-excitability of the brain. Side-effects can be a big problem.

 

Other treatments

Re-breathing into a paper bag can help increase PCO2, and can resolve some attacks.

 

Prophylaxis – suggest if episodes occur >2 per month

If one drug doesn’t work, try a different one after 3 months

65% of patients will have at least 50% reduced frequency of attacks with treatment.

-          Pizotifen – this is an antihistamine and 5-HT antagonist – it causes vasoconstriction of cranial arteries.Give 0.5mg at night (increase to 1mg). Side effects include weight gain, drowsyness, ↑effects of alcohol, ↑glaucoma risk. Rarely can cause arrhythmias and angina.

-          Propanol – beta-blocker – give 10mg 3x/day, increasing to 40mg 3x/day if necessary.

-          Amytriptiline –TCA – 10mg+ at night. Side effects include drowysness, dry mouth and blurred vision