Migraine with Aura: What It Looks Like, What Causes It, and When to Worry

Migraine with Aura

At a Glance

  • Migraine with aura affects roughly 25-30% of people who get migraines
  • Aura typically lasts 5-60 minutes and precedes headache by up to an hour
  • Visual aura (zigzag lines, blind spots, shimmering) is the most common type
  • Cortical spreading depression, a wave of neuronal depolarization, is the underlying mechanism
  • Aura with certain features (motor weakness, prolonged duration, new onset over age 40) warrants urgent evaluation

What Migraine Aura Actually Looks Like

Migraine aura is a transient neurological disturbance that typically precedes the headache phase. The International Headache Society classifies it as fully reversible visual, sensory, speech, motor, brainstem, or retinal symptoms that develop gradually over at least 5 minutes and last no longer than 60 minutes [1].

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The gradual onset is key. Unlike a stroke, where symptoms appear suddenly, aura builds slowly as the cortical spreading depression wave moves across the brain at approximately 3-5 mm per minute.

Visual Aura (Most Common: 90% of Aura Cases)

The classic visual aura follows a predictable pattern:

  • Scintillating scotoma: A small blind spot near the center of vision that expands outward over 5-20 minutes, leaving a crescent-shaped zone of visual loss bordered by shimmering, zigzag lines (fortification spectra)
  • Photopsia: Flashing or flickering lights, often described as sparkles or lightning bolts
  • Visual field distortion: Blurring, tunnel vision, or kaleidoscope-like fragmentation of visual images
  • Negative symptoms: Partial or complete loss of vision in one area of the visual field (hemianopia)

Visual aura affects both eyes simultaneously because it originates in the visual cortex, not the retina. This distinguishes it from retinal migraine, which affects one eye only [2].

Sensory Aura (Second Most Common)

Tingling or numbness that starts in the fingers of one hand, spreads up the arm, and may reach the face and tongue on the same side. This “march” of sensory symptoms mirrors the cortical spreading depression wave moving across the somatosensory cortex. It occurs in approximately 31% of people who experience aura [3].

Speech and Language Aura

Difficulty finding words (dysphasic aura) occurs in about 18% of aura episodes. Patients describe knowing what they want to say but being unable to form the words, or producing jumbled speech. This resolves completely as the aura passes.

Motor Aura (Hemiplegic Migraine)

Temporary weakness on one side of the body. This is classified separately as hemiplegic migraine and is the most concerning form of aura because it closely mimics stroke. It may be familial (linked to specific calcium channel, sodium channel, or sodium-potassium pump mutations) or sporadic. Motor aura can last longer than other aura types, sometimes persisting for hours to days [4].

The Biology: Cortical Spreading Depression

Migraine aura is caused by cortical spreading depression (CSD), a wave of intense neuronal and glial depolarization that spreads across the cerebral cortex at 2-6 mm per minute, followed by a prolonged period of neuronal suppression [5].

During CSD:

  1. Neurons in the affected cortical area fire massively (positive symptoms: flashing lights, tingling)
  2. This is followed by neuronal silencing (negative symptoms: blind spots, numbness)
  3. The wave propagates outward from the initiation point, which is why symptoms appear to “spread” or “march” across the visual field or body
  4. Local blood flow changes accompany the wave: brief hyperemia (increased flow) during depolarization, followed by oligemia (decreased flow) during suppression

CSD also activates trigeminal nerve fibers and triggers the release of CGRP (calcitonin gene-related peptide), which drives the subsequent headache phase. This is why CGRP-targeting medications (gepants, anti-CGRP antibodies) are effective for preventing and treating migraine with aura [6].

Aura Without Headache

Approximately 4% of aura episodes occur without any subsequent headache. This is called “migraine aura without headache” or, colloquially, “silent migraine.” It becomes more common with age: many people who had migraine with aura in their 20s-30s develop aura-only episodes in their 50s-60s as the headache component fades [7].

Aura without headache can be difficult to distinguish from transient ischemic attack (TIA), particularly in older adults or those with cardiovascular risk factors. The gradual onset (over minutes) versus sudden onset (seconds) is the most reliable clinical differentiator, but imaging may be warranted for new-onset aura without headache over age 40.

Triggers Specific to Aura

While standard migraine triggers (stress, sleep disruption, hormonal fluctuations, weather changes) apply to migraine with aura, some triggers appear more specifically associated with aura onset:

  • Intense visual stimulation: Flickering lights, high-contrast patterns, prolonged screen use
  • Physical exertion: Exercise-triggered aura is documented, possibly through changes in cerebral blood flow
  • Caffeine withdrawal: Abrupt cessation after regular use can trigger both aura and headache
  • Specific foods: Aged cheeses, wine, and tyramine-containing foods are reported aura triggers, though individual variation is high
  • Hormonal shifts: Estrogen withdrawal during menstruation is a documented aura trigger. This has implications for oral contraceptive use (see below)

Migraine with Aura and Stroke Risk

Migraine with aura carries a modestly elevated stroke risk compared to both migraine without aura and the general population. A meta-analysis in the BMJ found a relative risk of 2.16 for ischemic stroke in women with migraine with aura [8].

In absolute terms, the risk remains small: approximately 4 additional strokes per 100,000 women per year attributable to migraine with aura. However, the risk compounds with other factors:

  • Combined oral contraceptives (COCs): Estrogen-containing birth control increases stroke risk in women with aura. Current guidelines from the WHO and ACOG classify COCs as contraindicated (Category 4) in women with migraine with aura [9]. Progestin-only methods are safe.
  • Smoking: Further amplifies the stroke risk. The combination of migraine with aura + smoking + COC use is particularly high-risk.
  • Hypertension, diabetes, obesity: Each adds incremental stroke risk.

For men with migraine with aura, stroke risk is also elevated but less studied. Cardiovascular risk factor management is recommended regardless of sex.

When Aura Is an Emergency

Most migraine aura is benign and self-resolving. Seek emergency evaluation if:

  • Sudden onset: Symptoms appear at maximum intensity within seconds (suggests vascular event, not CSD)
  • Duration beyond 60 minutes: Aura lasting more than an hour may indicate persistent focal neurological deficit
  • Motor weakness: First episode of weakness warrants imaging to exclude stroke
  • New pattern after age 40: New-onset aura in middle age or beyond requires investigation
  • Accompanied by fever, stiff neck, or altered consciousness: Suggests CNS infection or hemorrhage
  • Vision loss in one eye only: May indicate retinal migraine or retinal vascular event

Treatment: Preventing and Managing Aura

Acute Treatment

There is no specific acute treatment for the aura phase itself. Triptans, gepants, and NSAIDs can be taken during aura to reduce the severity of the subsequent headache, though some guidelines recommend waiting until the headache begins [1].

Magnesium may abort aura: a pilot study found that 400 mg of oral magnesium citrate taken at aura onset shortened aura duration in some patients. This is based on magnesium’s role in modulating cortical excitability and suppressing CSD.

Preventive Treatment

If aura occurs frequently (more than 4 episodes/month or significantly impacts quality of life), preventive therapy is warranted:

  • Anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab): Effective for both migraine with and without aura. Monthly or quarterly injections.
  • Topiramate: Reduces aura frequency through sodium channel blockade and glutamate modulation. The most evidence-based preventive specifically studied in migraine with aura.
  • Lamotrigine: Limited evidence but some specialists use it for aura-predominant migraine based on its ability to block CSD. May be particularly useful for patients with frequent aura but infrequent headache [10].
  • Magnesium supplementation: 400-600 mg daily of magnesium glycinate or citrate. Reduces cortical excitability and has a favorable safety profile.
  • Riboflavin (vitamin B2): 400 mg daily has shown migraine-preventive effects in clinical trials, likely through mitochondrial energy metabolism support.

Living with Migraine Aura

Practical strategies for managing aura episodes:

  • Keep a detailed trigger diary (including visual stimuli, sleep, stress, and hormonal patterns)
  • If driving when aura begins, pull over immediately. Visual aura impairs safe driving.
  • Inform colleagues and family about aura so they understand when you need to step away
  • Consider wearing FL-41 tinted glasses, which filter the light wavelengths most likely to trigger CSD
  • Maintain consistent sleep, hydration, and meal schedules to reduce cortical excitability

References

  1. Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211. doi:10.1177/0333102417738202
  2. Viana M, Sprenger T, Andelova M, et al. The typical duration of migraine aura: a systematic review. Cephalalgia. 2013;33(7):483-490. doi:10.1177/0333102413479833
  3. Russell MB, Olesen J. A nosographic analysis of the migraine aura in a general population. Brain. 1996;119(Pt 2):355-361. doi:10.1093/brain/119.2.355
  4. Russell MB, Ducros A. Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurol. 2011;10(5):457-470. doi:10.1016/S1474-4422(11)70048-5
  5. Lauritzen M. Pathophysiology of the migraine aura: the spreading depression theory. Brain. 1994;117(Pt 1):199-210. doi:10.1093/brain/117.1.199
  6. Goadsby PJ, Edvinsson L, Ekman R. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann Neurol. 1990;28(2):183-187. doi:10.1002/ana.410280213
  7. Wijman CA, Wolf PA, Kase CS, et al. Migrainous visual accompaniments are not rare in late life: the Framingham Study. Stroke. 1998;29(8):1539-1543. doi:10.1161/01.STR.29.8.1539
  8. Schurks M, Rist PM, Bigal ME, et al. Migraine and cardiovascular disease: systematic review and meta-analysis. BMJ. 2009;339:b3914. doi:10.1136/bmj.b3914
  9. MacGregor EA. Contraception and headache. Headache. 2013;53(2):247-276. doi:10.1111/head.12035
  10. Lampl C, Katsarava Z, Diener HC, et al. Lamotrigine reduces migraine aura and migraine attacks in patients with migraine with aura. J Neurol Neurosurg Psychiatry. 2005;76(12):1730-1732. doi:10.1136/jnnp.2005.063750

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