Migraine - acute - 3

Taking a history

The first step in diagnosing headaches is to determine whether the signs and symptoms are suggestive of an organic cause, such as brain tumors or leaking arteriovenous malformations or aneurysms.

NEVER diagnose an acute headache as 'migraine' without a supporting history. 

When is it NOT likely to be a migraine ?

- The 'first or worst' headache of the patient’s life, particularly if it is of acute onset or is accompanied by other neurologic symptoms.
- A headache that is subacute in onset and gets progressively worse over days or weeks.
- A headache associated with fever, nausea, and vomiting that cannot be explained by a systemic illness.
- A headache associated with focal neurologic findings, papilledema, changes in consciousness or cognition, or a stiff neck. 


Migraines occur most commonly in the early morning hours, while cluster headaches commonly arise after sleep onset.
Migraines may be associated with stressful events, or may be seen to be by the patient.
Cluster headaches and trigeminal neuralgia appear to be more common in the spring or autumn.

Approximately 85% of patients will identify trigger factors. The use of a headache diary may help in chronic cases.

Common 'triggers' cited by patients

- Hormonal changes
- Medications
- Weather
- Sleep (too much/too little)
- Medication
- Exertion/position
- Odours/smoke
- Emotion
- Meals (timing/content)   


This should include a general medical examination, and a complete neurological exam to identify focal signs or symptoms suggestive of an underlying organic or local cause of the headaches.

The head should be examined for tenderness. Patients with migraine may be tender over the scalp or face. Temporal arteritis should be considered in older patients with superficial tenderness.

Papilloedema suggests raised intracranial pressure.
Photophobia is (unfortunately) a nonspecific symptom which occurs in a variety of headaches, including those of meningitis, raised intracranial pressure, or nasal/paranasal disease.   

Pathophysiology of migraine

The pathophysiology of migraine is not fully understood.

Migraine used to be ascribed to vascular changes in the brain. While vasoconstriction and then vasodilatation do occur (and appear be responsible for the headache) they do not appear to be the primary event.

Current thinking is that a wave of depolarisation (excitation) sweeps across the cortices (possibly responsible for the aura). There then follows a period of general neuronal depression, which may trigger the vascular changes.


Click on the image above to view a full sized cross-section of the human brain showing some of the nerve connections that may be involved in migraine.