Migraine

Last revised by Rohit Sharma on 31 Dec 2023

Migraines are a common primary headache disorder and can present variably. Typically they consist of debilitating headaches, accompanied by an aura in one-third of patients.

Migraine is a very common and debilitating condition, with a 1-year prevalence of 12% 8. It is most prevalent in early-middle adulthood, although can manifest at any age 8.

Migraines have an extremely varied presentation. As a result, many types have been described 7:

  • migraine with aura

    • most common type

  • migraine without aura

  • aura without headache

  • vestibular migraine

  • migraine with brainstem aura (basilar-type migraine)

  • retinal migraine

  • hemiplegic migraine (and familial hemiplegic migraine)

  • migraine with unilateral motor symptoms

  • menstrual migraine

In migraine with aura, there is a typical sequence of symptoms in four phases that any given patient will experience 7,8.

  • premonitory symptoms 7,8

    • occur hours to days prior to the headache

    • symptoms are often subtle, such as increased yawning, emotional lability, food cravings, neck stiffness, bowel changes, etc.

  • aura 7,8

    • occur just prior to headache

    • variety of positive (e.g. teichopsia) or negative (e.g. visual field loss) phenomena may manifest

  • headache 7,8

    • typically unilateral in the frontotemporal region, but can be more expansive

    • has a throbbing character

    • often associated nausea, vomiting, photophobia, phonophobia, osmophobia, etc.

    • often worsened with physical activity

    • usually lasts 4-72 hours in duration

  • postdrome 7,8

    • occurs after the headache

    • symptoms are often subtle, including exhaustion, poor concentration, etc.

These symptoms or 'attacks' can occur in two patterns 7,8:

  • episodically: <15 days per month, known as 'episodic migraine'

  • chronically: ≥15 days per month, known as 'chronic migraine' (previously 'transformed migraine')

  • status migrainosus: migraine attack lasting >72 hours

  • persistent aura without infarction

  • migrainous vasospasm

  • migrainous infarction

  • migraine aura-triggered seizures

The exact aetiopathogenesis of migraine is yet to be fully elucidated, but is likely highly complex 8. It is hypothesized that cortical spreading depression and subsequent activation of the trigeminovascular system, leading to release of neuropeptides such as calcitonin gene-related peptide (CGRP) 8.

Migraine may have polygenic risk factors, but there are rare instances of monogenic migraine, such as familial hemiplegic migraine due to mutations in the CACNA1A, ATP1A2 or SCNA1 genes 8,12.

Additionally, albeit very rarely, migraine can be part of other monogenic syndromes, such as 12:

In the vast majority of cases, MRI is normal. However, MRI, in up to 40% of patients with migraine 13, may demonstrate T2 hyperintensities in the white matter of the centrum semiovale, not dissimilar to small vessel deep white matter ischemic change. Additionally, there may be increased T2 signal in the cortex overlying white matter abnormalities as well as in the brainstem 1. In assessing white matter hyperintensities, it is important to consider rare monogenic syndromes (as aforementioned, e.g. CADASIL) in which migraine can be an early clinical manifestation 13.

In hemiplegic migraines, venous dilatation may be seen on SWI MIP images contralateral to the hemiparesis, although this is not typical 3. Changes in cerebral perfusion have also been described 3.

Management can be broadly dichotomised into preventative and abortive strategies.

In regards to preventative strategies:

  • lifestyle: good sleep hygiene, regular aerobic exercise, having routine meal schedules, having adequate hydration, utilizing relaxation techniques or mindfulness, etc. 9

  • pharmacotherapy: generally indicated if having >4 migraines per month 8

    • oral therapy 8

      • antidepressants: amitriptyline, nortriptyline, etc.

      • antihypertensives: proranolol, verapamil, candesartan, etc.

      • antiseizure medications: topiramate, sodium valproate, etc.

      • small molecule CGRP receptor antagonists: rimegepant, ubrogebant, telcagepant, atogepant, zavegepant, etc.

      • others: pizotifen, flunarizine, etc.

    • injectable therapy 8

      • CGRP antagonists: galcanezumab, fremanezumab, eptinezumab, erenumab

      • botulinum toxin A injections

      • greater occipital nerve blocks and other cranial nerve blocks

  • neuromodulation therapy: external transcutaneous trigeminal nerve stimulation (eTNS), external transcutaneous supraorbital nerve stimulation, single-pulse transcranial magnetic stimulation (sTMS), non-invasive vagal nerve stimulation (nVNS) 11

In regards to abortive strategies 8,10:

  • simple analgesia: acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs), soluble aspirin, etc.

  • antiemetics: metoclopramide, ondansetron, etc.

  • triptans: sumatriptan, naratriptan, zolmitriptan, rizatriptan, eletriptan, etc.

  • gepants (as above)

  • ditans: lasmiditan, etc.

  • advanced therapy for refractory acute pain including status migrainosus: often requiring inpatient hospital admission

    • intermittent intravenous therapies: fluids, dopamine antagonists (e.g. chlorpromazine), corticosteroids, sodium valproate, magnesium sulfate

    • continuous intravenous infusions: lignocaine, ketamine, dihydroergotamine

    • greater occipital nerve blocks and other cranial nerve blocks

    • neuromodulation therapies (as above)

For MRI appearances consider:

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