Medicine – Migraine

Migraine is a common primary headache disorder characterised by recurrent attacks of headache, often associated with nausea, photophobia, phonophobia, and sometimes neurological aura. The headache is often unilateral and pulsating, but not every attack has all of these features.

Migraine is now understood primarily as a neurovascular disorder involving trigeminovascular activation, brainstem and cortical networks, and neuropeptides such as calcitonin gene-related peptide (CGRP) rather than simply a vascular disease.

1. Typical Headache

The headache is classically:

Unilateral.

Throbbing or pulsating.

Moderate to severe.

Worse with routine physical activity.

It may last from several hours up to a few days if untreated.

However, migraine can also be bilateral, especially in younger patients.

2. Associated Symptoms

Migraine commonly causes:

Nausea.

Vomiting.

Photophobia.

Phonophobia.

Some patients also develop:

Osmophobia, meaning increased sensitivity to smells.

These associated symptoms help distinguish migraine from many other headache disorders.

3. Migraine with Aura

Some patients develop a reversible neurological disturbance before or during the headache.

This is called:

Migraine with aura.

However, it is important to correct the older statement that migraine is “usually preceded by aura.”

Most patients have:

Migraine without aura.

Only a minority experience typical aura.

4. Visual Aura

Visual aura is the most common type.

Patients may describe:

Flashing lights.

Zig-zag lines.

Shimmering patterns.

Scintillating scotomas.

Areas of visual loss.

The disturbance usually develops gradually over several minutes and is fully reversible.

5. Scintillating Scotoma

A classic visual aura is a:

Scintillating scotoma.

This consists of a region of impaired vision surrounded by:

Flashing.

Shimmering.

or

Zig-zag visual phenomena.

It often expands gradually across the visual field before resolving.

6. Sensory Aura

Sensory symptoms may include:

Paraesthesiae.

Pins and needles.

Numbness.

These often begin in one hand or part of the face and may gradually spread.

A gradual “march” of symptoms over minutes is more typical of migraine aura than the sudden maximal deficit of a vascular event.

7. Speech and Language Aura

Some patients develop temporary:

Dysphasia.

Word-finding difficulty.

Difficulty understanding or producing language.

These symptoms are usually fully reversible.

8. Motor Symptoms

Motor weakness is not typical of ordinary migraine aura.

When reversible weakness occurs, consider:

Hemiplegic migraine.

This is relatively uncommon and requires careful assessment because it can resemble stroke or transient ischaemic attack.

9. Duration of Aura

Typical aura symptoms usually:

Develop gradually.

Last minutes rather than seconds.

Resolve completely.

A common duration is approximately:

5–60 minutes for an individual aura symptom.

The headache may begin during the aura or after it.

10. Migraine without Aura

Migraine without aura is the more common form.

Typical features include:

Recurrent headache attacks.

Pulsating quality.

Moderate or severe intensity.

Worsening with activity.

Nausea and/or photophobia and phonophobia.

No focal neurological aura is required.

11. Migraine with Aura

Migraine with aura consists of:

Recurrent fully reversible neurological symptoms

followed or accompanied by migraine headache.

Aura is most commonly:

Visual.

but may be:

Sensory.

Language-related.

or, rarely,

Motor.

12. Migraine Phases

A migraine attack can be considered in several phases:

Prodrome.

Aura in some patients.

Headache.

Postdrome.

Not every patient experiences every phase.

13. Prodrome

Hours or even a day before the headache, some patients experience:

Fatigue.

Yawning.

Mood change.

Food cravings.

Neck stiffness.

Difficulty concentrating.

These symptoms are not the same as aura.

14. Postdrome

After the headache resolves, some patients experience a “migraine hangover.”

Features may include:

Fatigue.

Poor concentration.

Residual head discomfort.

Mood change.

This can last for several hours or longer.

15. Pathophysiology

The older idea that migraine is simply caused by abnormal dilation and constriction of cerebral blood vessels is incomplete.

Migraine is better understood as a:

Neurovascular disorder.

Important mechanisms include:

Trigeminovascular activation.

Cortical spreading depolarisation in aura.

Release of CGRP and other neuropeptides.

Altered pain processing within the brainstem and cortex.

16. Trigeminovascular System

Activation of trigeminal sensory fibres supplying the meninges contributes to migraine pain.

These fibres release neuropeptides such as:

CGRP.

This promotes pain signalling and neurogenic inflammation within the trigeminovascular system.

This mechanism has led directly to newer migraine therapies targeting CGRP.

17. Cortical Spreading Depolarisation

Migraine aura is strongly associated with:

Cortical spreading depolarisation.

This is a slowly propagating wave of neuronal and glial electrical activity across the cerebral cortex.

It helps explain why aura symptoms often:

Develop gradually.

Spread across the visual field or body.

Resolve sequentially.

18. Common Triggers

Migraine attacks may be triggered by:

Stress.

Sleep deprivation.

Missed meals.

Dehydration.

Menstruation or hormonal changes.

Alcohol.

Certain foods in susceptible individuals.

Bright light.

Strong smells.

Excess or withdrawal of caffeine.

Triggers vary greatly between patients.

19. Diagnosis

Migraine is primarily a:

Clinical diagnosis.

Neuroimaging is not routinely required when the history is typical and neurological examination is normal.

Imaging becomes more important if there are red flags or atypical features.

20. Headache Red Flags

Features suggesting a secondary headache rather than uncomplicated migraine include:

Sudden thunderclap onset.

New headache with focal neurological deficit.

Persistent neurological deficit.

Fever or meningism.

Papilloedema.

New headache after significant trauma.

Progressively worsening pattern.

New onset in a patient with cancer or major immunosuppression.

Marked change from the patient’s usual headache.

Such features require further evaluation.

21. Acute Treatment

Acute treatment is used once a migraine attack begins.

Options include:

Paracetamol.

NSAIDs.

Triptans.

Antiemetics.

Treatment is usually most effective when taken early in the headache phase.

22. Paracetamol

Paracetamol may be effective in:

Mild-to-moderate migraine.

It is often taken early in the attack.

Its effectiveness can be improved by taking it before nausea becomes severe.

23. NSAIDs

NSAIDs are effective acute treatments.

Examples include:

Ibuprofen.

Naproxen.

Aspirin in appropriate adults.

They reduce inflammatory pain signalling and may be more effective than simple analgesia in some patients.

24. Triptans

Triptans are migraine-specific acute treatments.

Examples include:

Sumatriptan.

Rizatriptan.

Zolmitriptan.

They act predominantly as:

5-HT1B/1D receptor agonists.

The older note describes them generally as 5-HT1 receptor agonists, which is broadly correct but less specific.

25. Mechanism of Triptans

Triptans reduce migraine pain by:

Suppressing trigeminal neurotransmitter release.

Reducing CGRP-mediated signalling.

Modulating cranial vascular and pain pathways.

Their effectiveness is not explained solely by vasoconstriction.

26. When Triptans Are Used

A triptan may be used when:

Paracetamol or NSAIDs are inadequate.

or as first-line migraine-specific treatment in selected patients with moderate-to-severe attacks.

Combination therapy with:

Triptan + NSAID

may help when either alone is insufficient.

27. Important Triptan Precautions

Triptans are generally avoided or used cautiously in patients with certain significant cardiovascular or cerebrovascular conditions because of their vasoconstrictive properties.

Medication choice should be individualised according to comorbidity and contraindications.

28. Antiemetics

If nausea or vomiting is prominent, an antiemetic may be added.

Examples can include:

Metoclopramide.

Prochlorperazine.

These may also improve gastric emptying, which can help absorption of oral migraine medication.

29. Avoiding Medication-Overuse Headache

Frequent use of acute headache medication can itself cause:

Medication-overuse headache.

This can occur with:

Simple analgesics.

NSAIDs.

Triptans.

Combination analgesics.

Therefore, frequent recurrent attacks may require preventive therapy rather than repeated acute medication alone.

30. Preventive Treatment

Preventive therapy aims to reduce:

Attack frequency.

Attack severity.

Duration.

Need for acute medication.

Impact on daily function.

The older threshold of “two or more disabling attacks per month” is a useful rough guide, but preventive treatment is now based more broadly on overall disability, frequency, duration, treatment response, and patient preference.

31. Propranolol

Propranolol is a well-established preventive treatment.

It is a:

Beta blocker.

It may reduce migraine attack frequency and severity.

32. Propranolol Precautions

Propranolol may be unsuitable in patients with:

Asthma.

Marked bradycardia.

Certain heart-conduction disorders.

It may also cause:

Fatigue.

Exercise intolerance.

Sleep disturbance.

33. Amitriptyline

Amitriptyline is commonly used for migraine prevention.

It can be particularly useful when migraine coexists with:

Poor sleep.

Tension-type headache features.

Neuropathic pain.

Common adverse effects include:

Sedation.

Dry mouth.

Constipation.

Weight gain.

34. Topiramate

A major modern preventive treatment is:

Topiramate.

It can significantly reduce migraine frequency.

Possible adverse effects include:

Paraesthesiae.

Cognitive slowing.

Word-finding difficulty.

Weight loss.

Renal stones.

Pregnancy-related safety considerations are important when choosing it.

35. Valproate

Valproate can prevent migraine and was commonly listed in older treatment schemes.

However, its use is now strongly limited in people who could become pregnant because of:

Major teratogenic risk.

Adverse neurodevelopmental effects in exposed fetuses.

Therefore, it is not a preferred routine preventive option for many patients.

36. Pizotifen

Pizotifen is an older migraine preventive drug.

It acts mainly through serotonin receptor antagonism.

Possible adverse effects include:

Sedation.

Increased appetite.

Weight gain.

It remains used in some settings but is less prominent in many modern guidelines than options such as propranolol, topiramate, amitriptyline, and CGRP-targeted therapy.

37. Calcium Channel Blockers

Some calcium channel blockers have been used for migraine prevention.

However, the term “calcium channel blockers” is too broad.

The evidence and use vary between individual drugs and countries.

They are generally not the most universally used first-line preventive agents for ordinary migraine.

38. CGRP-Targeted Preventive Therapy

Modern migraine prevention may include treatments targeting:

CGRP

or the

CGRP receptor.

These include monoclonal antibodies such as:

Erenumab.

Fremanezumab.

Galcanezumab.

Eptinezumab.

They are generally considered when conventional preventive treatments are ineffective, poorly tolerated, or unsuitable, depending on local guidance.

39. Gepants

Another modern class is:

Gepants.

These are small-molecule CGRP receptor antagonists.

Some agents can be used for:

Acute migraine treatment.

Others can be used for:

Prevention.

They provide an alternative particularly when triptans are unsuitable or ineffective.

40. Botulinum Toxin

OnabotulinumtoxinA may be used for:

Chronic migraine.

Chronic migraine generally refers to headache on at least 15 days per month, with migraine features on a significant proportion of those days.

It is not usually used for infrequent episodic migraine.

41. Lifestyle Measures

Non-drug management is important.

Useful measures include:

Regular sleep.

Regular meals.

Good hydration.

Regular physical activity.

Managing caffeine intake.

Reducing recognised individual triggers.

Stress management.

A headache diary can help identify patterns and assess treatment response.

42. Migraine with Aura and Stroke Risk

Migraine with aura is associated with a modestly increased risk of ischaemic stroke.

The absolute risk is still low in many younger patients, but risk becomes more important when combined with other factors such as:

Smoking.

Hypertension.

Certain estrogen-containing contraceptives.

This is especially relevant when counselling patients with migraine with aura.

43. Migraine versus Tension-Type Headache

Migraine:

Often unilateral.

Pulsating.

Moderate to severe.

Nausea common.

Photophobia/phonophobia common.

Activity worsens pain.

Tension-type headache:

Usually bilateral.

Pressure or tight-band quality.

Mild to moderate.

Nausea usually absent.

Routine activity usually does not markedly worsen pain.

44. Migraine versus Cluster Headache

Migraine:

Lasts hours.

Patient often prefers to lie still in a dark room.

Nausea and photophobia common.

Cluster headache:

Very severe unilateral orbital/temporal pain.

Shorter attacks, often 15–180 minutes.

Ipsilateral autonomic symptoms such as:

Lacrimation.

Nasal congestion.

Ptosis.

Miosis.

Patients are often restless rather than wanting to lie still.

45. Migraine Aura versus TIA

Migraine aura usually has:

Gradual onset.

Positive symptoms, such as flashing lights or tingling.

Spread of symptoms over minutes.

Complete reversibility.

TIA more often has:

Sudden onset.

Negative symptoms, such as loss of vision, sensation, or strength.

Maximum deficit at onset.

However, overlap exists, and first or atypical neurological episodes should be assessed carefully.

46. Acute Migraine Treatment – Note Form

Paracetamol.

NSAID.

Triptan such as sumatriptan.

Antiemetic if nausea/vomiting.

Take treatment early in the attack when possible.

Avoid excessive repeated acute medication because of medication-overuse headache.

47. Migraine Prevention – Note Form

Important preventive options include:

Propranolol.

Amitriptyline.

Topiramate.

CGRP-targeted therapies in selected patients.

Other drugs may be used depending on patient factors and local guidance.

Pizotifen: older option, may cause sedation and weight gain.

Valproate: effective but major reproductive safety concerns substantially limit use.

Calcium channel blockers: selected agents only; not a uniform first-line class.

48. Important Corrections to the Original Notes

“Usually preceded by visual aura” → incorrect.

Most migraine occurs without aura.

“Pathophysiology is vascular” → outdated.

Migraine is primarily a complex neurovascular disorder involving trigeminovascular pathways, cortical activity and CGRP.

Reversible neurological signs are not always extremely rare.

Aura may produce reversible visual, sensory, and language symptoms; motor weakness is much less common and suggests hemiplegic migraine.

Preventive treatment is not based only on ≥2 attacks/month.

It depends on frequency, disability, attack duration, response to acute treatment, medication overuse risk and patient preference.

Key Clinical Pattern

Think of migraine as:

RECURRENT PULSATILE HEADACHE + NAUSEA + PHOTOPHOBIA/PHONOPHOBIA ± AURA.

Remember:

Most migraine = WITHOUT AURA.

When aura occurs:

VISUAL > SENSORY > LANGUAGE; symptoms are gradual and reversible.

Acute treatment:

PARACETAMOL / NSAID → TRIPTAN ± ANTIEMETIC.

Prevention:

PROPRANOLOL / AMITRIPTYLINE / TOPIRAMATE ± MODERN CGRP-TARGETED THERAPY.

And the modern mechanism is:

TRIGEMINOVASCULAR ACTIVATION + CGRP + CENTRAL PAIN PROCESSING, not simply abnormal cerebral vasodilation.