Migraine aura without headache …

Ravi Uniyal MD DM

Headache & Pain

Updated 07.29.2024
Released 12.30.1993
Expires For CME 07.29.2027

Migraine aura without headache

Author: Ravi Uniyal MD DM

See Contributor Disclosures

Editor: Shuu-Jiun Wang MD

Migraine aura without headache

In This Article

Quick Link

Introduction

Overview

Migraine is the most common neurologic disorder in the younger population and is significantly associated life-long disability (25). Migraine occurrence decreases with age, but rare accompaniments experienced by some patients (especially elderly and not necessarily migraineurs) are migraine auras without associated headache. In this article, the authors review the clinical manifestations, prevalence, pathophysiology, therapeutic options, differential diagnosis, and prognosis for this selective group of patients. Latest developments in understanding the pathogenesis and clinical manifestations are highlighted.

Key points

	• Typical aura without headache consists of visual, sensory, or speech symptoms with a mix of positive and negative features and complete reversibility.
	• One characteristic, such as duration, could not be respected in most cases; in fact, it is not rare for aura to last more than 1 hour, but usually patients will show at least two other of the typical characteristics (ie, gradual spreading over 5 or more minutes, two or more aura symptoms in succession with at least one unilateral or positive aura symptom).
	• Cortical spreading depression, glutamatergic neurotransmission, channelopathies, neuronal-glial gap-junction communications, endothelial dysfunction, and microembolization might be important players in the pathogenesis of migraine aura.
	• Migraine with aura has been associated with higher risks of subclinical brain lesions, ischemic or hemorrhagic strokes, atrial fibrillation, and other causes of increased mortality; whether this remains true for “migraine aura without headache” requires further studies.

Historical note and terminology

Migrainous aura has been used to explain unusual visions, experiences, and perceptions that have been reported by well-known personages. Lewis Carroll's pictorial descriptions in Alice in Wonderland and Alice Through the Looking Glass have been ascribed to his migrainous auras. His depiction of Alice may be a manifestation of the micropsia, macropsia, or metamorphopsia seen in migrainous auras of childhood.

There have also been suggestions that the painter Pablo Picasso may have had migrainous auras. His works feature illusory splitting in the vertical plane of his subjects' faces, and this has been compared to similar paintings by migraine patients depicting what they see during their aura phase (57). The absence of descriptions of the painter suffering from headaches may infer the presence of migraine aura without headache.

Aura typically begins before headache but could also occur simultaneously or without headache. Lashley provided the first assessment of temporal spreading with quantitative recording of migrainous scotomas and fortification patterns in 1941 (49).

Fisher described a series of 120 patients: the majority had visual symptoms alone or associated with paresthesias or speech disturbances, followed by brainstem symptoms and few motor deficits (22). He proposed the late onset (for the first time after the age of 45 years) of ‘‘scintillating scotomas, numbness, aphasia, dysarthria, motor weakness, and brain stem symptoms.” These reports were enriched by the further description of 85 new cases with similar results in 1986. Their ages ranged from 40 to 73 years. In only 40% of cases, headache occurred in association with the episodes. These episodes have been coined ‘‘late-life migraine accompaniments,” “migraine equivalents,” “acephalic migraine,” or “migraine aura without headache.” The International Headache Society classified typical aura occurring in the absence of any headache as “typical aura without headache.”

Clinical manifestations

Presentation and course

Historically, an aura without migraine headache was described as slowly evolving patterns of scintillating scotomas that have precisely the same range of patterns and duration of evolution. On reaching middle age, patients with typical migraine preceded by aura can continue to have auras without the succeeding headache. It can be preceded by hunger, tiredness, or increased micturition frequency, similar to the prodromes of migraine attacks, and it can be followed by lassitude and photophobia, which are frequent migraine postdromal symptoms. Precipitants of migraine aura without headache (ie, hunger, bright lights, insufficient sleep, and anoxia) are also triggers of migraine with and without aura.

Fisher has published a personal account of life with migrainous auras without headache (23). He described 41 episodes of scintillating zigzags that occurred when he was between 59 and 85 years of age. The spells occurred irregularly and were unrelated to season of the year, time of day, activity at onset, diet, or temperamental state. The characteristic appearance was a flickering zigzag line that began centrally and migrated to the periphery. The display, which was stereotyped, was achromatic. The average duration was 15 minutes. Both visual fields were equally involved, though never at the same time.

A multicenter study in patients with migraine with aura showed that visual aura symptoms were variable and often overlapping, and approximately half of the patients reported nonvisual aura symptoms, with sensory and speech symptoms being the most common (36). Of note, prospective recordings for 861 aura attacks in this study showed that 27% of the aura attacks were not followed by headache, in contrast to 4% to 10% in previous studies.

The International Classification of Headache Disorders, 3rd edition, proposed the diagnostic criteria for typical aura without headache (code 1.2.1.2), which allows the aura symptoms to be one or more of the following: visual, sensory, speech, and/or language, with the exclusion of motor, brainstem, and retinal symptoms (39). In the beta version of the 3rd edition, the diagnostic criteria for 1.2 migraine with aura have been substituted in the definitive classification by the appendix A1.2 migraine with aura criteria. Indeed, the latter performed better in distinguishing migraine with aura from transient ischemic attacks. The typical aura symptoms to fulfill the 1.2. typical aura without headache diagnosis should demonstrate, during two attacks, at least three of the following characteristics (criterion C of 1.2 migraine with aura diagnostic criteria, if the aura is not accompanied, nor followed within 60 minutes, by headache): (1) at least one aura symptom spreads gradually over 5 minutes; (2) two or more aura symptoms occur in succession; (3) each individual aura symptom lasts 5 to 60 minutes; (4) at least one aura symptom is unilateral; and (5) at least one aura symptom is positive. In a systematic review, however, it was found that a nonhemiplegic migraine aura could last longer than 1 hour in a significant proportion of migraineurs, especially in patients with nonvisual aura symptoms (67). A prospective study also showed that 14% of visual aura symptoms, 21% of sensory symptoms, and 17% of dysphasic symptoms last for more than 1 hour (69). The term “prolonged aura” has been abandoned because it is not rare that the aura lasts for more than 1 hour but, in such cases, patients have to show at least two of the other typical characteristics of 1.2 migraine with aura criterion C during the same attack or at least in their usual attacks to fulfill criteria for one of the recognized subtypes or subforms of 1.2 migraine with aura. The classification recommends coding the cases that do not have these characteristics as 1.5.2 probable migraine with aura, specifying, the atypical feature in parenthesis (eg, prolonged aura).

Prognosis and complications

Unlike migraine headache, which frequently lessens or even disappears after 55 years of age, migraine aura without headache often persists without permanent deficit into the 70s and 80s. Current guidelines state that female migraineurs without aura who develop an aura while on combined oral contraceptives must stop this mode of contraception, as they are at risk for developing strokes (50). Combined hormonal contraceptives are contraindicated based on data from the 1960s and 1970s, with higher doses of estrogen than current drugs. In fact, ischemic stroke risk might not be significantly increased with low-dose estrogen, and ultra-low-dose formulations may conversely reduce the frequency of aura (12; 32); however, a metanalysis pointed out that oral contraceptives could account for a slightly increased risk of subarachnoid hemorrhage (74). Further studies are needed to assess the stroke risk, and precautionary suspension of oral contraceptives is still recommended in migraine with aura. A report suggested that patients suffering from migraine with aura and having more than one migraine attack a month have a greater risk of having a subclinical infarct in the cerebellar area as seen on MRI (46). Some meta-analyses have shown the increased long-term risk of cardiovascular and cerebrovascular events, particularly in patients with aura (42; 51). The implications of these data for patients having migraine aura without headache are not clear, with a lack of data to recommend preventive therapy. Although solid data are still lacking, controlling traditional vascular risk factors is believed to be the mainstay in preventing these complications.

Clinical vignette

A 69-year-old man reported his first attack of migraine aura without headache 4 years earlier. While reading the morning paper, the patient noticed that the print looked a little unclear in the center of his vision. A bright dot appeared 2 to 3 minutes later; this gradually spread into his upper left visual field, making an arc-shaped zigzag. It took about 5 minutes to develop to its full extent; it lasted another 10 minutes and then disappeared suddenly. There was no ensuing headache. The man had three more attacks in the next 2 years without any trigger being identified.

He emphasized that he was retired and under no stress. He had never experienced any migrainous symptoms prior to the first attack.

Biological basis

Etiology and pathogenesis

Migraine aura without headache is considered a migraine-associated phenomenon, although typical aura symptoms could be an isolated phenomenon or accompany other conditions or other primary headaches, being described in about 25% of cluster headache patients (18). The connection between aura and headache, particularly migraine pathophysiology, has been largely discussed (10). Both vascular and neurogenic causes that have been proposed are tightly intertwined. The following are some of the prevailing theories:

Cortical spreading depression. The cortical spreading depression of Leao, a primary brain phenomenon, may account for the clinical symptoms of migraine with aura (07). Although there are some arguments against its role, cortical spreading depression is still recognized as the most likely pathophysiological mechanism of migraine aura (11; 39). A number of studies have shown that the aura phase of migraine is associated with a reduction of cerebral blood flow, moving across the cortex at a rate of 3 to 6 mm/min in the gray matter of the posterior part of the hemisphere contralateral to the affected visual field, paresthesia, or other focal neurologic symptoms, preceded by a phase of hyperperfusion (55; 17; 13). These phenomena were also demonstrated by using neuroimaging of the cerebral cortex, particularly functional MRI, with the analysis of blood oxygenation level-dependent signal changes within extrastriate cortex (area V3A) recorded during visual aura attacks that exhibit the characteristics of the cortical spreading depression and follow the retinotopic progression of the visual percept (33). Combined PET/MRI imaging showed glial activation in migraineurs with aura in areas possibly involved in cortical spreading depression generation (primary visual cortex, visual areas V3A, and Broca area), as well as with areas involved in pain processing (thalamus and primary/secondary somatosensory and insular cortices) (33). Many studies have explored the role of innate immunity in neuroinflammation in migraine pathophysiology (09). According to a study, the NLRP3 inflammasome assembly happened within 15 minutes of cortical spreading depression, and inhibiting NLRP3 or Panx1 through genetic or pharmacological methods reduced cortical spreading depression-induced neuronal inflammation and related symptoms (14). This raises the possibility that an aberrant NRLP3 pathway could prevent the progression of an aura to the subsequent headache episode. However, further studies are required to validate this likely mechanism in specific patient groups. In animal studies, the neuropeptide galanin has been found to inhibit cortical spreading depolarization, making it a potential drug target (27).

Genetic basis. Studies using transgenic mice carrying the human familial hemiplegic migraine gene and newly developed optogenetics methods largely advanced the understanding of pathophysiology of migraine aura and cortical spreading depression (37).

Except for rare monogenic subtypes such as familial hemiplegic migraine, no genetic or molecular markers for migraine had been convincingly established until the first genome-wide association study in 2010 (06). Later, a huge amount of genetic data was analyzed, with partially consistent results. One meta-analysis combined 22 genome-wide association studies from the International Headache Genetics Consortium comprising 59,674 migraine cases with a confirmed number of 44 independent single nucleotide polymorphisms significantly associated with migraine and 38 distinct genomic loci (including the X chromosome for the first time) (30). Most of the migraine loci involved in vascular development and pain processing were implicated in migraine with or without aura. Seven genomic loci (TSPAN2, TRPM8, PHACTR1, FHL5, ASTN2, near FGF6 and LRP1) were significantly associated with migraine without aura (06), but none with migraine with aura, probably reflecting the smaller sample size.

In another international collaborative study, a dominant-negative mutation in the gene encoding the 2-pore domain potassium channel TRESK (TWIK-related spinal cord potassium channel) was the first ever described discovered causative gene for a common hereditary form of migraine with aura (47). Although further studies are required to explore whether these findings are generalizable, these studies provided direct evidence of genetic predisposition of migraine aura and implicated potential therapeutic targets.

Endothelial dysfunction and microemboli. A clinic-based study considered young women (125 patients with migraine with and without aura) for changes in coagulatory, inflammatory, and oxidative stress parameters and reported a strong association between biomarkers of endothelial activation and migraine, especially for migraine with aura (65).

One study demonstrated that microemboli could cause cortical spreading depression in a mouse model, providing a link between cardiac or extracardiac right-to-left shunt and migraine aura (54). In young patients with cryptogenic stroke and frequent migraine with aura, there is an outstanding prevalence of patent foramen ovale (93%) (71). The higher prevalence of patent foramen ovale in migraineurs, especially with aura, with respect to the general population, and positive results of nonrandomized studies of patent foramen ovale closure, led to randomized clinical trials that failed their primary endpoints and, although registering modest reduction in headache frequencies, the trials were burdened by procedural complications (26). However, migraine aura physiopathology seems to be related to right-left shunt and atrial septal aneurysms as syndromic comorbidities, possibly affecting disease history (04). This finding strengthens the link between cardiovascular development and the aura conundrum.

Gap junction theory. Gap junctions that provide communication between astrocytes and neurons were recognized to be important in the pathogenesis of cortical spreading depression, and a gap-junction inhibitor, tonabersat, was found to be effective in inhibiting cortical spreading depression and reducing migraine aura (38).

The link between cortical spreading depression and trigeminovascular system. Cortical spreading depression somehow triggers the trigeminovascular complex with the release of neuropeptides (eg, neurokinin A, substance P, and calcitonin gene-related peptide and pituitary adenylate cyclase-activating peptide), which causes a sterile neurogenic inflammation and sensitizes the sensory nerve fibers surrounding the meningeal arteries (28). These nociceptive inputs are carried into the trigeminal nucleus caudalis and then to the contralateral ventrobasal and medial thalamus and finally to the cortex via the quintothalamic tract. The spreading depression-induced activation of the trigeminal meningeal nociceptors might be mediated by activation of pannexin-1 channel (45). Moreover, it was demonstrated in an animal model that calcitonin gene-related peptide receptor antagonist MK-8825 attenuated pain induced by trigeminal nerve activation without altering cortical spreading depression (21).

In migraine aura without headache, there is no progression from the aura to the headache phase. Therefore, the cortical spreading depression is not followed by activation of the trigeminal vascular complex. A study analyzing the detailed drawings of a patient’s visual percept of more than 1000 attacks of migraine aura without headache over 18 years revealed the distinctive anatomical and physiological features of migraine aura (34). Another study analyzed 216 auras in 72 patients and reported inconstant temporal succession between aura and headache and a high inter- and intravariability of aura characteristics (68). These studies found that auras in a given individual can initiate from multiple distinct sites, can propagate nonconcentrically with a variable extent in the occipital cortex, and can sometimes be clinically “silent.”

Epidemiology

The Global Burden of Disease Study showed that the worldwide prevalence of migraine is two to three times more prevalent in women than in men, with peaks in prevalence in both sexes between 30 to 39 years of age (25). However, the ratio of migraine prevalence between men and women is not consistent across all age ranges. Longitudinal studies evaluating aura symptoms are not very common.

In the Framingham cohort study (72), 2110 subjects were questioned biannually from 1971 to 1989 about visual symptoms. Twenty-six (1.23%) had migrainous visual episodes; the majority (77%) began after the age of 50 years; they were stereotypic in 65%. The episodes lasted 15 to 60 minutes in 50% of subjects; 58% never had headaches accompanying the episodes; and 42% had no headache history. The authors concluded that late-life onset transient visual phenomena similar to the visual migraine aura are not rare and often occur in the absence of headache. Such symptoms appear not to be associated with an increased risk of stroke, and invasive diagnostic procedures or therapeutic measures are generally not indicated.

A French 1-year prospective study enrolled 3773 migraine patients. Migraine with aura was reported in 26% of patients, with 6% of them (57 of 978) over 50 years of age. Prevalence of first-time migraine aura after 50 was 1.8%, and typical aura without headache was reported by 61% of them (11 of 18). Occurrence of aura exclusively without headache was reported by 17% (3 of 18) (20).

In a further prospective population-based study from Italy with 574 patients, the lifetime prevalence for typical aura without headache was 0.9% (men 1.6%; women 0.3%) (61). The incidence of migraine aura without headache has not been well documented in the pediatric population. However, a single university-based pediatric neurologist performed a retrospective review of pediatric migraine patients. Shevell identified 14 patients (nine girls, five boys) who had migraine aura without headache, representing 2% of all patients with a primary diagnosis of migraine. Thirteen patients had a strong family history of migraine. Age of symptom onset ranged from 5 to 12 years, with a mean of 8 years. Symptoms were episodic in all patients, varying in frequency from weekly to (more typically) monthly and generally lasting less than 10 minutes (62).

In Alabama, a questionnaire survey of 1000 patients presenting for a comprehensive eye examination revealed that 6.5% reported experiencing visual sensations consistent with migraine aura without headache. The prevalence in males was 2.9%, and in females, 8.6%. A multivariate analysis revealed that female gender (odds ratio [OR] = 2.3), a history of migraine headaches (OR = 3.2), and a history of childhood motion sickness (OR = 2.7) were significantly related to migraine aura without headache (24). A Japanese study demonstrated that 35 out of 1063 patients (3.2%; 1.1% males and 2.1% females) in general ophthalmologic clinics had typical aura without headache. The age of patients with typical aura without headache showed a biphasic distribution: 20 to 39 years and 60 to 69 years (02).

Patients with late-onset aura (≥ 45 years of age at aura onset) shared identical clinical features, risk factors, and comorbidities with patients with early-onset aura, except that patients with late-onset aura were more likely to not fulfill all ICHD-II aura criteria and to lack headache (53).

Differential diagnosis

Confusing conditions

The major differential diagnosis is transient ischemic attack. The updated diagnostic criteria of International Classification of Headache Disorders, 3rd edition, perform better in distinguishing between aura and transient ischemic attack. Although transient ischemic attacks develop abruptly with a sudden onset of symptoms, the onset of symptoms in migraine aura without headache is generally gradual and spreads or intensifies over minutes or hours. Dennis and colleagues examined 50 cases prospectively and compared them with 50 age-matched patients who had suffered from transient ischemic attack (19). Although the results are not conclusive, they do suggest that patients with the clinical characteristics of migraine aura without headache have a low risk of subsequent vascular events than those with transient ischemic attacks, despite having a similar prevalence of vascular risk factors (19).

Epilepsy may also be associated with auras, but these auras are characteristic. The epileptic aura is momentary, lasts seconds and not minutes, and usually consists of big blotches of light, figures, faces, or scenes rather than geometric patterns (31). A systemic study of visual phenomena and headache in occipital epilepsy as well as differentiation from migraine (56) supports Gower's views.

“Visual snow” is a persistent disturbance in the entire visual field, resembling the “static” or “snow” noises of analogue television. Patients with visual snow are commonly comorbid with migraine and have been given various diagnoses historically, including persistent migraine aura, post-hallucinogen flashback, or psychogenic disorder, etc. Some studies suggest that visual snow is a unique visual disturbance distinct from persistent migraine aura (59); however, there might be a pathophysiological overlap of visual snow and typical migraine aura (60).

Hypoglycemic episodes in diabetes may rarely cause visual disturbances that resemble migraine aura, but systemic symptoms are usual, and headache often follows the episode (52).

Management

The typical aura is transient, and acute treatment targeting this symptom should have an immediate effect to be considered in clinical practice.

In 1963 Wolff utilized inhalation therapy for migraine aura. Within 1 to 5 minutes of inhaling amyl nitrite or a carbon dioxide and air mixture, auras disappeared and then reappeared, whereas a carbon dioxide and oxygen mixture for 5 minutes completely cleared the aura. There was no recurrence, and the usual headache did not follow (73). Nifedipine has been found to be effective in terminating the aura but not headache phase of a migraine attack (29; 40). Other medications that are effective in treating prolonged auras include corticosteroids, neuroleptics, and intravenous magnesium and furosemide (58). A double-blind, randomized, controlled trial investigated the effect of intranasal ketamine versus intranasal midazolam in patients with prolonged aura and showed efficacy of ketamine in reducing severity of aura but not its duration; midazolam had no effect on aura (01). In a double-blind, placebo-controlled trial, 6 mg of sumatriptan injected subcutaneously neither shortened nor prolonged the visual aura in 17 patients with migraine aura without headache, and in those who had migraine aura followed by headache the ensuing headache ran its normal course (08). A post-hoc analysis from multiple randomized trials indicates that sumatriptan is less effective as acute treatment for attacks with aura (35).

There are no randomized, controlled trial studies for preventive treatment in typical aura without migraine. Commonly used medications for migraine prophylaxis showed efficacy inhibiting cortical spreading depression (63). Among antiepileptics, valproate, topiramate, levetiracetam, and mostly, lamotrigine are reported to effectively diminish both frequency and duration of aura symptoms (70). Beta-blockers, particularly metoprolol and propranolol, reduced auras in both open-label and randomized-controlled trials (44; 43). Tonabersat showed a preventive effect reducing the number of aura attacks but not headache days (38).

A review analyzing 47 cases with persistent migraine aura showed that most drugs have little effect in this special subset of patients; however, lamotrigine seems to be the most effective drug (64). In a small open-labeled pilot study, based on the role of the acid-sensing ion channel 1, the drug amiloride reduced aura and headache in four of seven patients with intractable aura (41).

Aspirin has been tested for aura prophylaxis; an observational case series of 49 patients with assumption of aspirin 80 mg daily reported aura frequency reduction in 93% of cases and the complete remission of auras in almost 50% (66). These data are corroborated by a retrospective study (05).

A small open-label clinical trial (18 patients, 22 auras) was performed to assess greater occipital nerve block for the acute treatment of prolonged or persistent migraine aura and showed promising results to be confirmed in randomized clinical trials (16).

Novel nonpharmacological treatments that deserve consideration are transcranial magnetic stimulation or vagus nerve stimulation. A systematic review on transcranial magnetic stimulation based on five studies concluded a possible effectiveness for migraine with aura treatment (48). Direct or transcutaneous vagus nerve stimulation was also found to be effective in suppressing cortical spreading depression (15), making it a potential therapeutic choice for migraine aura.

References

01: Afridi SK, Giffin NJ, Kaube H, Goadsby PJ. A randomized controlled trial of intranasal ketamine in migraine with prolonged aura. Neurology 2013;80(7):642-7. PMID 23365053
02: Aiba S, Tatsumoto M, Saisu A, et al. Prevalence of typical migraine aura without headache in Japanese ophthalmology clinics. Cephalalgia 2010;30:962-7. PMID 20656707
03: Allais G, D'Andrea G, Maggio M, Benedetto C. The efficacy of ginkgolide B in the acute treatment of migraine aura: an open preliminary trial. Neurol Sci 2013;34 Suppl 1:S161-3. PMID 23695070
04: Altamura C, Paolucci M, Costa CM, et al. Right-to-left shunt and the clinical features of migraine with aura: earlier but not more. Cerebrovasc Dis 2019;47(5-6):268-74. PMID 31357200
05: Anoaica MB, Anoaica PG, Popescu F. Acetylsalicylic acid in migraine with aura prevention - a retrospective study. Curr Health Sci J 2014;40(2):126-8. PMID 25729594
06: Anttila V, Stefansson H, Kallela M, et al. Genome-wide association study of migraine implicates a common susceptibility variant on 8q22.1. Nat Genet 2010;42:869-73. PMID 20802479
07: Barkley GL, Tepley N, Simkins R, Moran J, Welch KM. Neuromagnetic fields in migraine: preliminary findings. Cephalalgia 1990;10(4):171-6. PMID 2245465
08: Bates D, Ashford E, Dawson R, et al. Subcutaneous sumatriptan during the migraine aura. Neurology 1994;44:1587-92. PMID 7936279
09: Biscetti L, Cresta E, Cupini LM, Calabresi P, Sarchielli P. The putative role of neuroinflammation in the complex pathophysiology of migraine: from bench to bedside. Neurobiol Dis 2023;180:106072. PMID 36907522
10: Bolay H, Vuralli D, Goadsby PJ. Aura and head pain: relationship and gaps in the translational models. J Headache Pain 2019;20(1):94.** PMID 31481015
11: Borgdorff P. Arguments against the role of cortical spreading depression in migraine. Neurol Res 2018;40(3):173-81. PMID 23350588
12: Calhoun AH, Batur P. Combined hormonal contraceptives and migraine: an update on the evidence. Cleve Clin J Med 2017;84(8):631-8. PMID 28806162
13: Cao Y, Welch KM, Aurora S, Vikingstad EM. Functional MRI-BOLD of visually triggered headache in patients with migraine. Arch Neurol 1999;56(5):548-54. PMID 10328249
14: Chen PY, Yen JC, Liu TT, Chen ST, Wang SJ, Chen SP. Neuronal NLRP3 inflammasome mediates spreading depolarization-evoked trigeminovascular activation. Brain 2023;146(7):2989-3002. PMID 36795624
15: Chen SP, Ay I, de Morais AL, et al. Vagus nerve stimulation inhibits cortical spreading depression. Pain 2016;157(4):797-805. PMID 26645547
16: Cuadrado ML, Aledo-Serrano Á, López-Ruiz P, et al. Greater occipital nerve block for the acute treatment of prolonged or persistent migraine aura. Cephalalgia 2017;37(8):812-8. PMID 27288355
17: Cutrer FM, Sorensen AG, Weisskoff RM, et al. Perfusion-weighted imaging defects during spontaneous migrainous aura. Ann Neurol 1998;43(1):25-31. PMID 9450765
18: de Coo IF, Wilbrink LA, Ie GD, Haan J, Ferrari MD. Aura in cluster headache: a cross-sectional study. Headache 2018;58(8):1203-10. PMID 29933513
19: Dennis M, Warlow C. Migraine aura without headache: transient ischaemic attack or not? J Neurol Neurosurg Psychiatry 1992;55(6):437-40. PMID 1619407
20: Donnet A, Daniel C, Milandre L, Berbis J, Auquier P. Migraine with aura in patients over 50 years of age: the Marseille’s registry. J Neurol 2012;259(9):1868-73. PMID 22302276
21: Filiz A, Tepe N, Eftekhari S, et al. CGRP receptor antagonist MK-8825 attenuates cortical spreading depression induced pain behavior. Cephalalgia 2019;39(3):354-65. PMID 28971699
22: Fisher CM. Latelife migraine accompaniments as a cause of unexplained transient ischemic attacks. Can J Neurol Sci 1980;7:9-17. PMID 7388704
23: Fisher CM. Latelife (migrainous) scintillating zig-zags without headache. One person's 27 years experience. Headache 1999;39:391-7.** PMID 11279916
24: Fleming JB, Amos AJ, Desmond RA. Migraine aura without headache: prevalence and risk factors in a primary eye care population. Optometry 2000;71(6):381-9. PMID 15326888
25: GBD 2015 Neurological Disorders Collaborator Group. Global, regional, and national burden of neurological disorders during 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet Neurol 2017;16(11):877-97. PMID 28931491
26: Giblett JP, Abdul-Samad O, Shapiro LM, Rana BS, Calvert PA. Patent foramen ovale closure in 2019. Interv Cardiol 2019;14(1):34-41. PMID 30858890
27: Gimeno-Ferrer F, Eitner A, Schaible HG, Richter F. Galanin diminishes cortical spreading depolarization across rodents - A candidate for treatment? Neurosci Lett. 2024;832:137814. PMID 38723760
28: Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S. Pathophysiology of migraine: a disorder of sensory processing. Physiol Rev 2017;97(2):553-622. PMID 28179394
29: Goldner JA, Levitt LP. Treatment of complicated migraine with sublingual nifedipine. Headache 1987;27(9):484-6. PMID 3692828
30: Gormley P, Anttila V, Winsvold BS, et al. Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine. Nat Genet 2016;48(8):856-66. PMID 27322543
31: Gowers W. Clinical lectures on the borderland of epilepsy. Migraine. Br Med J 1906;ii:617-22. PMID 20762970
32: Gryglas A, Smigiel R. Migraine and stroke: what's the link? What to do? Curr Neurol Neurosci Rep 2017;17(3):22. PMID 28283957
33: Hadjikhani N, Vincent M. Neuroimaging clues of migraine aura. J Headache Pain 2019;20(1):32.** PMID 30943894
34: Hansen JM, Baca SM, Vanvalkenburgh P, Charles A. Distinctive anatomical and physiological features of migraine aura revealed by 18 years of recording. Brain 2013;136(Pt 12):3589-95.** PMID 24264937
35: Hansen JM, Goadsby PJ, Charles A. Reduced efficacy of sumatriptan in migraine with aura vs without aura. Neurology 2015;84(18):1880-5. PMID 25841032
36: Hansen JM, Goadsby PJ, Charles AC. Variability of clinical features in attacks of migraine with aura. Cephalalgia 2016;36(3):216-24. PMID 25944814
37: Harriott AM, Takizawa T, Chung DY, Chen SP. Spreading depression as a preclinical model of migraine. J Headache Pain 2019;20(1):45. PMID 31046659
38: Hauge AW, Asghar MS, Schytz HW, Christensen K, Olesen J. Effects of tonabersat on migraine with aura: a randomised, double-blind, placebo-controlled crossover study. Lancet Neurol 2009;8(8):718-23. PMID 19570717
39: Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38(1):1-211. PMID 23771276
40: Hoffert MJ, Scholz MJ, Kanter R. A double-blind controlled study of nifedipine as an abortive treatment in acute attacks of migraine with aura. Cephalalgia 1992;12(5):323-4. PMID 1423566
41: Holland PR, Akerman S, Andreou AP, Karsan N, Wemmie JA, Goadsby PJ. Acid-sensing ion channel 1: a novel therapeutic target for migraine with aura. Ann Neurol 2012;72(4):559-63. PMID 23109150
42: Hu X, Zhou Y, Zhao H, Peng C. Migraine and the risk of stroke: an updated meta-analysis of prospective cohort studies. Neurol Sci 2017;38(1):33-40. PMID 27785579
43: Kangasniemi P, Andersen AR, Andersson PG, et al. Classic migraine: effective prophylaxis with metoprolol. Cephalalgia 1987;7(4):231-8. PMID 3322569
44: Kangasniemi P, Hedman C. Metoprolol and propranolol in the prophylactic treatment of classical and common migraine: a double-blind study. Cephalalgia 1984;4:91-6. PMID 6428749
45: Karatas H, Erdener SE, Gursoy-Ozdemir Y, et al. Spreading depression triggers headache by activating neuronal Panx1 channels. Science 2013;339(6123):1092-5.** PMID 23449592
46: Kruit MC, van Buchem MA, Hofman PA, et al. Migraine as a risk factor for subclinical brain lesions. JAMA 2004;291(4):427-34. PMID 14747499
47: Lafreniere RG, Cader MZ, Poulin JF, et al. A dominant-negative mutation in the TRESK potassium channel is linked to familial migraine with aura. Nat Med 2010;16:1157-60. PMID 20871611
48: Lan L, Zhang X, Li X, Rong X, Peng Y. The efficacy of transcranial magnetic stimulation on migraine: a meta-analysis of randomized controlled trials. J Headache Pain 2017;18(1):86. PMID 28831756
49: Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neur Pysch 1941;46(2):331-9.
50: MacGregor EA, Guillebaud J. Combined oral contraceptives, migraine and ischaemic strokes. Recommendations for clinical practice. Br J Family Planning 1998;24:53-60. PMID 9719712
51: Mahmoud AN, Mentias A, Elgendy AY, et al. Migraine and the risk of cardiovascular and cerebrovascular events: a meta-analysis of 16 cohort studies including 1 152 407 subjects. BMJ Open 2018;8(3):e020498. PMID 29593023
52: Martins I, Blau JN. Headache in insulin-dependent diabetes. Headache 1989;29:660-3. PMID 2613515
53: Martins IP, Goucha T, Mares I, Antunes AF. Late onset and early onset aura: the same disorder. J Headache Pain 2012;13(3):243-5. PMID 22350748
54: Nozari A, Dilekoz E, Sukhotinsky I, et al. Microemboli may link spreading depression, migraine aura, and patent foramen ovale. Ann Neurol 2010;67(2):221-9.** PMID 20225282
55: Olesen J, Friberg L, Olsen TS, et al. Timing and topography of cerebral blood flow, aura, and headache during migraine attacks. Ann Neurol 1990;28(6):791-8. PMID 2285266
56: Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord 1999;1:205-16. PMID 10937155
57: Podoll K, Robinson D. Illusory splitting as visual aura symptom in migraine. Cephalalgia 2000;20(4):228-32. PMID 10999672
58: Rozen TD. Treatment of a prolonged migrainous aura with intravenous furosemide. Neurology 2000;55(5):732-3. PMID 10980751
59: Schankin CJ, Maniyar FH, Digre KB, Goadsby PJ. 'Visual snow' - a disorder distinct from persistent migraine aura. Brain 2014a;137(Pt 5):1419-28. PMID 24645145
60: Schankin CJ, Maniyar FH, Sprenger T, Chou DE, Eller M, Goadsby PJ. The relation between migraine, typical migraine aura and "visual snow". Headache 2014b;54(6):957-66. PMID 24816400
61: Schwaiger J, Kiechl S, Seppi K, et al. Prevalence of primary headaches and cranial neuralgias in men and women aged 55-94 years (Bruneck Study). Cephalalgia 2009;29(2):179-87. PMID 18823362
62: Shevell MI. Acephalgic migraines of childhood. Pediatr Neurol 1996;14(3):211-5. PMID 8736404
63: Tfelt-Hansen PC. History of migraine with aura and cortical spreading depression from 1941 and onwards. Cephalalgia 2010;30:780-92. PMID 19740119
64: Thissen S, Vos IG, Schreuder TH, Schreurs WM, Postma LA, Koehler PJ. Persistent migraine aura: new cases, a literature review, and ideas about pathophysiology. Headache 2014;54(8):1290-309. PMID 24863140
65: Tietjen GE, Herial NA, White L, Utley C, Kosmyna JM, Khuder SA. Migraine and biomarkers of endothelial activation in young women. Stroke 2009;40(9):2977–82. PMID 19608996
66: Turk WE, Uiterwijk A, Pasmans R, Meys V, Ayata C, Koehler PJ. Aspirin prophylaxis for migraine with aura: an observational case series. Eur Neurol 2017;78(5-6):287-89. PMID 29017164
67: Viana M, Linde M, Sances G, et al. Migraine aura symptoms: Duration, succession and temporal relationship to headache. Cephalalgia 2016;36(5):413-21. PMID 26156076
68: Viana M, Sances G, Linde M, et al. Clinical features of migraine aura: Results from a prospective diary-aided study. Cephalalgia 2017;37(10):979–89. PMID 27573009
69: Viana M, Sprenger T, Andelova M, Goadsby PJ. The typical duration of migraine aura: a systematic review. Cephalalgia 2013;33(7):483-90. PMID 23475294
70: Vongvaivanich K, Lertakyamanee P, Silberstein SD, Dodick DW. Late-life migraine accompaniments: a narrative review. Cephalalgia 2015;35(10):894-911. PMID 25505036
71: West BH, Noureddin N, Mamzhi Y, et al. Frequency of patent foramen ovale and migraine in patients with cryptogenic stroke. Stroke 2018;49(5):1123-8. PMID 29636424
72: Wijman CA, Wolf PA, Kase CS, Kelly-Hayes M, Beiser AS. Migrainous visual accompaniments are not rare in late life. The Framingham study. Stroke 1998;29:1539-43. PMID 9707189
73: Wolff HG. Headache and other head pain. 2nd ed. New York: Oxford Univ Press, 1963:234-40.
74: Xu Z, Yue Y, Bai J, et al. Association between oral contraceptives and risk of hemorrhagic stroke: a meta-analysis of observational studies. Arch Gynecol Obstet 2018;297(5):1181-91. PMID 29460112

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Ravi Uniyal MD DM

Dr. Uniyal of King George's Medical University has no relevant financial relationship to disclose.
See Profile

Editor

Shuu-Jiun Wang MD

Dr. Wang of the Brain Research Center, National Yang-Ming University, and the Neurological Institute, Taipei Veterans General Hospital, has no relevant financial relationships to disclose.
See Profile

Former Authors

Joseph N Blau MD
Hua C Siow MD
Shih-Pin Chen MD PhD
Ciro De Luca MD
Filippo Baldacci MD

Patient Profile

Age range of presentation: 6 to 65+ years
Sex preponderance: male>female, >2:1
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Migraine aura without headache: G43.1
ICD-11: Hemiplegic migraine: 8A80.10

Other specified migraine with aura: 8A80.1Y

Migraine with aura, unspecified: 8A80.1Z

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Migraine aura without headache

Associated Disorders

Migraine aura
Visual migraine

Differential Diagnosis

transient ischemic attack
strokes
vascular disease
epilepsy
occipital epilepsy
- hypoglycemic episodes
- diabetes

Also Relevant

Childhood migraine
Headache associated with ischemic cerebrovascular disease
Headache guidelines
Late-life migrainous accompaniments
Migraine
- Migraine and epilepsy
- Neuroimaging of headache
- Status migrainosus
- Sumatriptan

Clinical Categories

Headache & Pain

Patient Handouts

Web References

Guidelines

AAN: Headache

Migraine aura without headache …

Migraine aura without headache

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Primary headache associated with sexual activity

Late-life migrainous accompaniments

Headache associated with intracranial neoplasms

Medication overuse headache

Acupuncture

Migraine in childhood

Headache attributed to head trauma

Migraine: pathogenesis and pathophysiology

Migraine aura without headache

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Primary headache associated with sexual activity

Late-life migrainous accompaniments

Headache associated with intracranial neoplasms

Medication overuse headache

Acupuncture

Migraine in childhood

Headache attributed to head trauma

Migraine: pathogenesis and pathophysiology

This is an article preview.
Start a Free Account
to access the full version.