Late-life migrainous accompaniments …

Headache & Pain

Updated 10.29.2024
Released 11.04.1993
Expires For CME 10.29.2027

Late-life migrainous accompaniments

Authors: Andrea Harriott MD PhD, R Allan Purdy MD FACPC FACP FAHS

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Editor: Stephen D Silberstein MD

Late-life migrainous accompaniments

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Introduction

Overview

Late-life migrainous accompaniments remain important in neurologic practice as the diagnosis is largely dependent on history, taken carefully, to eliminate mimics and other neurologic disorders and diseases. Reviews relating to late-life migrainous accompaniments and migraine aura without headache are still reported in the literature and an ongoing discussion of mechanisms remains of interest to clinicians and patients as well. Neuroimaging maybe necessary to rule out secondary causes before making the diagnosis of late-life migrainous accompaniments. One suggestion is to consider that cerebral MRI with or without contrast, including DWI, T2*GRE, or susceptible weighted imaging sequences, may be the best tools for early detection of underlying pathology. Thus, it is important to be able to identify late-life migrainous accompaniments and sort them from a myriad of other mimics, particularly cerebrovascular diseases.

Key points

	• Visual symptoms are common.
	• They build up over time and march across the visual cortex.
	• They are stereotyped and last 15 to 25 minutes.
	• Some people still do have headache.
	• There is a midlife flurry of attacks.
	• There is usually a benign course.
	• Imaging is normal in most cases.

Historical note and terminology

Late-life migrainous accompaniments, a topic of historical interest, is a clinical concept that is still important to modern-day neurologic diagnosticians and students of migraine. C Miller Fisher published his two seminal articles on late-life migrainous accompaniments in 1980 and 1986. In his combined case series of 205 patients, Fisher was attempting to differentiate late-life migrainous accompaniments from the symptoms and signs of transient ischemic attacks (18; 20).

In his first series, Fisher reported 120 patients with neurologic accompaniments of migraine classified according to the following symptoms: visual accompaniments (excluding patients who had only ordinary scintillating scotoma) (25); visual symptoms and paresthesias (18); visual symptoms and speech disturbances (7); visual and brainstem symptoms (14); visual symptoms, paresthesias, and speech disturbances (7); visual symptoms, paresthesias, speech disturbances, and paresis (25); recurrence of old stroke deficit (9); and miscellaneous symptoms (8). Diagnosis was facilitated when two or more similar episodes occurred, or migraine-like scintillations were present (18). Headache occurred in 50% of the patients.

In the second series, Fisher reported 85 cases that were similarly categorized: visual symptoms (21); visual symptoms and paresthesias (6); visual symptoms and speech disturbances (2); visual symptoms, paresthesias, and speech disturbances (3); visual symptoms, paresthesias, speech disturbances, and weakness (20); visual and brainstem symptoms (3); and no visual symptoms (32) (20). These patients ranged in age from 40 to 73 years. Forty percent had some headache associated with the neurologic symptoms, with 65% having a history of recurrent headache. Fisher was particularly interested in patients who had migrainous accompaniments and normal cerebral angiograms. Headache was present in 40% of cases in this series.

In both of Fisher’s studies, many patients had headache; thus, all were not totally acephalgic (only aura). The essence of his original communication was to explain why patients in the stroke-age bracket (older than 40 years) occasionally have unexplained transient ischemic attacks in association with normal cerebral angiograms. He believed that these patients probably had migraine aura; those with headache were more typical migraine. Fisher was not the only one to note the phenomenon of aura symptoms without headache. Whitty reported that in middle-age, migraine auras could occur alone, without a headache; this was more common in people who had had typical migraine in the past (51).

Clinical manifestations

Presentation and course

Late-life migrainous accompaniments are the aura symptoms of migraine that precede the headache in migraine with aura. They can be visual, motor, sensory, or behavioral in nature and usually last several minutes or less, unless the symptoms are prolonged (over 1 hour), in which case they are classified as prolonged migraine aura. Today these late-life migraine accompaniments would be called “late-life migrainous equivalents” or migraine aura without headache and are recognized as generally benign in nature but of important diagnostic interest.

Migraine with aura (formerly called classic migraine) is distinguished from migraine without aura (formerly common migraine) by the neurologic symptoms of aura and not the headache symptoms. Headache can also occur in patients with transient ischemic attack or stroke (39; 27; 26), although this is not always recognized or appreciated.

In his second communication, Fisher recapitulated the main diagnostic criteria for late-life migrainous accompaniments as follows:

	(1) Visual symptoms: scintillating scotomata, etc.
	(2) Gradual “build-up”: expansion and migration of the scintillating display, a phenomenon that does not occur in cerebrovascular disease.
	(3) A “march” of paresthesias, a feature that does not occur in cerebrovascular disease.
	(4) The serial progression from one migrainous accompaniment to another, eg, from visual to paresthesias to dysphasias, a course that does not occur in cerebrovascular disease.
	(5) The occurrence of two or more identical attacks, an event that helps to exclude cerebral embolism. When there has been only one spell, cerebral embolism is a possibility and the diagnosis must be based on the presence of unequivocal specific migrainous features.
	(6) Headaches in association with the spells (50% of cases).
	(7) A duration of the episode in the range of 15 to 25 minutes, whereas 90% of transient ischemic attacks associated with carotid or basilar artery disease last less than 15 minutes.
	(8) The occurrence of a "flurry" of migrainous accompaniments, generally in the 50- to 60-year-old age group.
	(9) A generally benign course without permanent sequelae.
	(10) Exclusion of cerebral thrombosis, embolism, dissection, subclavian steal, epilepsy, thrombocythemia, polycythemia, hyperviscosity syndromes, and lupus anticoagulant.
	(11) Normal angiography: this excludes thrombosis of arteries greater than 1.5 mm in diameter.
	(12) Recurrence of essentially identical attacks over a period of 5 to 10 years. It is unlikely that atherosclerotic thrombosis would have such a prolonged course (20).

In the two series, the most common symptoms of late-life migraine accompaniments were visual symptoms and, when scintillating scotomata were excluded, transient blindness, homonymous hemianopsia, blurring of vision, and difficulties with visual focusing (18; 20). The second most common complaints were sensory, in the form of paresthesias (tingling, pins-and-needles, and numbness). The third most common group of symptoms were related to the brainstem and cerebellum, and included ataxia, clumsiness, tinnitus, deafness, syncope, and incoordination. The last group of symptoms was speech disturbances, including dysarthria or aphasia that occurred separately or in combination with visual or sensory symptoms.

Prognosis and complications

Persistent neurologic deficits are rare, even when attacks continue for years. Fisher published a personal account of life with migraine auras without headache (21). He noted 41 episodes of scintillating zigzags that occurred when he was between 59 and 85 years of age. These did not occur on a regular basis and were unrelated to season, time of day, activity at onset, diet, or emotional state. The visual symptoms, which were stereotyped and achromatic, began centrally and moved peripherally. The average duration of the visual symptoms was 15 minutes; both visual fields were equally involved, but never at the same time. Aring was well into his 80s when he summarized his own quarter-century experience with late-life migraine (04). He noted no personal sequelae and said in conclusion, “Migraine is a strange and wonderful disorder.”

Patients with late-life migrainous accompaniments probably have the same morbidity and mortality as do those with other forms of migraine; however, Shuaib and Lee reported cases of permanent sequelae following late-life migraine accompaniments (45). They reported four cases with infarctions: two in the occipital lobe, one in the frontoparietal lobe, and one in the cerebellum. They wondered if the ischemia was caused by vasospasm. On the other hand, stroke in patients with late-life migraine accompaniments could also be expected because migraine may on occasion lead to migrainous infarction and stroke is common in the elderly.

Clinical vignette

Three cases of late-life migraine accompaniments follow:

Case 1. A 58-year-old man had one or two spells a year of combined visual and speech disturbance. He had experienced these symptoms for 5 years, but they began occurring two or three times a week 6 months previously. During a spell, he lost the ability to focus and the lateral parts of his visual field were filled with shimmering pinpoints of light. There was a “build-up” for 2 to 3 minutes; the symptoms remained at a peak for 30 minutes, and then faded and disappeared in 1 hour. At the height of the episode, the patient was unable to read and enunciation and fluency of speech were impaired. There were no paresthesias. The patient was aware of a slight pressure in his head at the onset but he did not call it a headache.

Interestingly, this is Case 12 from Fisher’s original series (18) and is representative of the cases seen with this disorder. This patient had the build-up, progression, and march from the neural origin of his visual symptoms presumably from his occipital cortex to the speech symptoms arising from his parietal and temporal speech centers. Headache is not seen in all cases, or it may be mild. In mid-life, as in this case, there can be a “flurry” of late-life migraine accompaniments.

Case 2. A man had three identical spells, at ages 30, 45, and 65 years, respectively. In each, he suddenly awakened from a deep sleep, jumped up, and developed weakness of the right side of his mouth and right hand and an inability to speak properly. This lasted about 10 minutes. All tests short of angiography were normal.

This is Case 21 of nonvisual symptoms from Fisher’s second series (20). This case is interesting as there is no time to observe any build-up, progression, or march of symptoms because of the sudden onset of symptoms on awakening. Also, in the absence of angiographic or other evidence to rule out transient ischemic attack or other etiology, one would be hard pressed at present to call these late-life migraine accompaniments. Nevertheless, a lifelong history, beginning as a young man, of the same stereotypical attacks could suggest that the attacks were migrainous in nature.

Many of Fisher’s reported cases may not have been late-life migraine accompaniments. Also, some cases, particularly in the second series, were young (20). One was aged 13 years (Case 2), and another, special Case 24, was 25 years of age and had multiple segmental narrowing on angiography, which raised the question of “arteritis” versus migraine. Given the age range and diagnostic uncertainty in some cases, it probably would be best to call these attacks transient migraine accompaniments or transient migraine equivalents.

An additional syndrome, that of transient global amnesia, might reasonably be added to the spectrum of late-life migraine accompaniments given observations on the pathogenesis of transient global amnesia and its relationship to migraine. The essential features of this disorder, originally described by Fisher and Adams, are of an episode of acute onset of transient anterograde amnesia of a global nature, with some involvement of retrograde memory, without any other major neurologic symptoms or signs (22). This disorder may be related pathophysiologically to migraine (see Etiology).

Case 3. Late-life migrainous accompaniments are common symptoms seen by neurologists; thus, it is no surprise that neurologists will frequently have such symptoms, given that neurologists (and headache specialists in particular) have high prevalence of migraine headaches (15). Given this predisposition, the author describes his own recent experience with late-life migrainous accompaniments. Having experienced such symptoms putatively makes them easier to recognize in other patients and gives a clearer understanding of other formes frustes of migraine. What follows is the recent history of one of the contributing authors.

History. A 72-year-old physician had a 23-year history of recurrent scintillating scotoma involving either the right or left visual hemifield.

Visual aura (drawing)

This illustration of visual aura was drawn by a neurologist experiencing a typical aura without headache. (Contributed by Dr. Allan Purdy.)

These would last 20 minutes; they would occur in flurries over days and then abate for months. There were no other migraine symptoms, and his history was void of any headaches of any significance other than an occasional ice-cream-induced headache, a variant of ICHD 3 Headache attributed to ingestion or inhalation of a cold stimulus (27) and a few episodes of “airplane descent headache” (16).

Comment. This case illustrates some important clinical points: migraine is not always seen in its full clinical spectrum; aura and headache can be separated out clinically, as occurs in late-life migrainous accompaniments; other headaches with putative migraine associations can occur along with migraine, including “ice cream headache;” and a neurologist possibly having migraine or some of its subcomponents may have an enhanced ability to identify a migraine disorder--recognizing that the latter statement is not based on evidence but on a personal clinical experience, similar to the original description of the disorder by Dr. Fisher (18). As well, the long duration of his symptoms suggests a benign disorder.

Biological basis

Etiology and pathogenesis

Although the pathophysiology of late-life migraine accompaniments is still uncertain, the mechanisms of their production are probably identical to migraine aura. Ischemia could trigger migraine-like phenomena, but this likely represents a smaller percentage of those with late-life migrainous accompaniments.

The mechanism of aura may well be a homologue of the spreading depression of Leao, a slowly propagating wave of neuronal and glial depolarization that produces transient electrical silence of cortical activity (31; 30). The putative spreading depression can begin in cortical areas and spread gradually from one area to another (30). If it begins in visual cortex, contralateral scintillating scotomata and other visual phenomena can occur. A central scotoma that enlarges as the aura builds can be present as well. The cortical inhibition, which is preceded by a wave of excitation, may start in the sensory cortex, producing paresthesias and other sensory phenomena, sometimes without visual aura. This march across sensory homunculus can lead to a spread from face and tongue to hand and arm and, sometimes, leg. If the speech center is involved in the aura, word-finding difficulty and other speech symptoms occur. Involvement of motor cortex can also lead to a homuncular march with resultant hemiparesis or even hemiplegia.

Decreased cerebral blood flow, but not ischemia, has been documented during aura using methods for measuring cerebral blood flow (Olesen and Friberg 1990; 33). A number of studies have shown that the aura phase is associated with a reduction of cerebral blood flow in the cortex of the posterior part of the hemisphere contralateral to the affected visual field, paresthesia, or other focal neurologic symptoms, and the cerebral blood flow reduction appears to move across the cortex at a rate of 3 mm/min to 6 mm/min and is preceded by a phase of hyperperfusion consistent with that seen in cortical spreading depression (07).

Wolff’s original studies reported temporary resolution of migrainous scotomata in several patients during amyl nitrate inhalation (53). Amyl nitrate caused cerebral vasodilation, and when the inhalation was stopped, the scotomata reappeared. Wolff concluded that cerebral vasospasm was responsible for the visual aura of migraine; however, that is not the modern view (30; 25).

Cerebral vasodilator capacitance measured by xenon-enhanced CT cerebral blood flow measurement before and after acetazolamide administration showed a significant decline with advancing age among normal patients, and even more among patients with late-life migrainous accompaniments (34). This could explain the reduction in frequency and severity of migrainous headache with age and the appearance of late-life migrainous accompaniments.

Experimental evidence suggests microemboli (air, cholesterol, and polystyrene microspheres) that are too small to induce cerebral infarction trigger spreading depression events in rodents, suggesting transient microembolic events could produce symptomatic aura (36). Case reports have suggested rare mimics. For example, case report suggests that an internal carotid artery stenosis mimicked late-life migraine accompaniments in a 65-year-old woman with a history of acephalgic migraine (02). Other mechanisms, such as down-regulation of serotonin vascular receptors in menopause and aging, may play a role, as many menopausal women and elderly patients have migraine aura without headache (09).

With respect to studies possibly linking migraine to transient global amnesia, a 1999 study using PET scan during an episode of transient global amnesia showed no change in the hippocampi; however, it did show reduced cerebral blood flow and metabolism in the frontal and temporal cortices with a mild reduction in cerebral blood flow and normal metabolism in the occipital cortex (13). It suggested that neocortical involvement may play an important role in the genesis of transient global amnesia and that transient global amnesia may be due an event like spreading depression. Further studies using imaging during an episode of transient global amnesia, 24 hours, and 3 months after transient global amnesia showed bilateral mesial temporal lobe hypoperfusion that partially resolved after 24 hours and returned to normal at 3 months; as the scan abnormalities abated, the patient’s memory problem resolved (29). The authors suggest that an electrical event leading to decreased local metabolism, such as cortical spreading depression, could be the mechanism in this case. Further, a transcranial Doppler study carried out during the acute phase of the amnesia showed no evidence of hemodynamic alterations or significant asymmetries; however, the test was repeated after clinical recovery and showed values that were similar to those reported in the previous study (28). The authors concluded that ischemia was an unlikely mechanism, but spreading depression similar to migraine aura could explain an event like transient global amnesia. (It should be noted that other mechanisms of transient global amnesia have been proposed and debated; readers are directed to the article on transient global amnesia. Nevertheless, transient global amnesia probably mimics late-life migraine accompaniments in mechanism and is clearly in the borderland of this disorder.)

Mechanisms remain important and are of great interest to neurologists who see cases of late-life migrainous accompaniments. Reviews in this disorder and migraine aura without headache, along with increasingly sophisticated imaging, particularly MR, which is increasingly available to diagnosticians, make it possible to learn the breadth and depth of late-life migrainous accompaniments and its mimics (50; 43).

Epidemiology

Migrainous visual accompaniments are not rare in late life. Wijman designed a questionnaire to elicit symptoms of transient ischemic attack that also may detect late-life transient visual symptoms similar to the visual aura of migraine, often without headache (52). In this study, 2110 subjects were questioned twice yearly for 17 years about visual symptoms. Twenty-six (1.23%) had migrainous visual episodes; most (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. Twelve percent of subjects sustained a stroke after the onset of migrainous visual symptoms, but in contrast, of 87 subjects with transient ischemic attack in the same study group, 33% developed a stroke, two thirds within 6 months of transient ischemic attack onset. They concluded that late-life-onset transient visual phenomena similar to the visual aura of migraine are not rare and often occur in the absence of headache. These symptoms appear not to be associated with an increased risk of stroke, and invasive diagnostic procedures or therapeutic measures are generally not indicated.

Late-life migrainous accompaniments occur more frequently in men than women (20; 23). More than 80% of those diagnosed with late-life migrainous accompaniments seek medical care within 4 years of symptom onset (48). A review of a large database of 12,750 African-American and white men and women found that 3% of participants had a history of migraine with aura (47). The mean age of the study population was 60 years, with 73% of the population 55 years of age and older. The population was 77% white and 56% female. It was shown that migraine with aura was strongly associated with stroke symptoms (OR 5.46, 95% CI: 3.64 to 8.18), transient ischemic attack symptoms (OR 4.28, 95% CI: 3.02 to 6.08), and verified ischemic stroke events (OR 2.81, 95% CI: 1.60 to 4.92). This, of course, is the age group in which most late-life migrainous accompaniments occur, and the authors concluded that more research on the relationship of stroke and migraine in this group is needed.

Current perspective (2024). Since the original description of late-life migrainous accompaniments, much has changed in the understanding of migraine and its pathophysiology (24). Migraine is a disorder reflecting perturbations in multiple brain neural circuits and activation of peripheral and central nociceptive neurons. Late-life migrainous accompaniments could be the residual of migraine, with a reduction in the headache part of the migraine attack. There is increased risk of stroke for migraine with aura (42). Similar to other ages of onset, those with migraine with aura onset at an age greater than 50 years had increased risk of ischemic stroke (01).

This “clinical entity” of late-life migrainous accompaniments remains in the lexicon of clinical neurologists and is used frequently to differentiate patients with late-life migrainous accompaniments from those with other neurologic disorders, in particular TIA, stroke, and seizures. Because these patients can have typical aura without headache or typical aura with some headache with or without migraine characteristics, they don’t easily fit into the new ICHD3 classification unless they are coded for two variants of migraine with typical aura, 1.2.1.1 and 1.2.1.2 (27). Ultimately, patients may overlap with other migraine subtypes as they expand, including 1.4.2, which is persistent aura without infarction, although this relationship has not been proven to date and this subtype is rare.

Late-life migrainous accompaniments appear to be more a syndrome than a definite classifiable entity. Because microemboli can initiate aura, migraine with aura could exist on a continuum with ischemic stroke (06; 12; 05).

What distinguishes these cases from younger patients with migraine with aura without headache is the age of the patients. A study by Donnet and colleagues indicates that late-life-onset transient visual phenomena are not rare (11). Symptoms may occur for the first time after age 50 years in the absence of headache or in the presence of a headache that has the characteristics of typical aura with non-migraine headache.

Whether late-life migrainous accompaniments will still be considered benign in nature in the future awaits further research. Most appear transient, but some may herald more ominous outcomes, especially because these cases can occur in patients who also have major stroke-risk factors. The diagnosis of late-life migrainous accompaniments must be made carefully to ensure they are not mimics of cerebrovascular disease that need to be managed differently. In particular, the diagnosis of any transient focal neurologic episodes, which includes symptoms similar to migraine, needs to be explored particularly in the older age group because the diagnosis of cerebral amyloid angiopathy, which can present with lobar hemorrhage, can also present with transient focal neurologic episodes with local cortical subarachnoid hemorrhage (49). Here the investigation using T2-weighted grading imaging techniques or susceptible weighted imaging may be required to make the diagnosis (50).

The good news is that by and large late-life migrainous accompaniments generally are benign in outcome, but again that could change with new knowledge and even better imaging over time.

Differential diagnosis

Fisher’s criteria for late-life migraine accompaniments continue to be valid. They are over 20 years old, and although they would be modified today due to neuroimaging and other tests, they are still applicable. These late-life migraine accompaniments display a “build-up” and “progression” of symptoms that are not typical of stroke or transient ischemic attack symptoms. Further, the “march” of symptoms from one area of the body to another–visual to face to arm to hand, for example–is typical of late-life migraine accompaniments, but not of stroke (20). The duration of a late-life migraine accompaniment march (15 to 25 minutes) is much longer than a seizure march, which is usually 1 or 2 minutes. Sensory seizures, however, must be in the differential diagnosis (17). Transient ischemic attacks usually last less than 10 minutes (35).

Typical visual aura or photopsias consisting of scintillating scotomata are highly characteristic of migraine, especially when they are gradual in onset and progressive (03). In contrast, transient ischemic attack (10) and sensory stroke are sudden in onset and usually not reversible (19). Migraine sensory aura can involve the tongue and oral mucosa, in contrast to a transient ischemic attack, in which such involvement is rare (41; 20). This is an important clinical clue. Late-life migraine accompaniments can recur for years without sequelae; this would be unlikely in atherothrombotic, embolic, or cardioembolic stroke, as would full reversibility of any symptoms in these conditions. Patients with occipital lobe strokes, for example, usually have persistent or residual visual symptomology, unlike those who have late-life migraine accompaniments. In one study, vertebrobasilar transient ischemic attacks could be differentiated from late-life migrainous accompaniments by their lower regional cerebral blood flow and greater asymmetry of the anterior cerebral blood flow (40).

The most important differential diagnosis of late-life migraine accompaniments is transient ischemic attack or stroke. Usually, the criteria noted can make diagnosis relatively straightforward, especially if the patient had similar symptoms earlier in life or many recent repeated stereotypical episodes. The distinctions can be made but must be done carefully because risk factors for stroke can be similar in these patients (38). In a study of transient ischemic attack, patients who had recurrent, predominantly sensory symptoms were felt to have a more benign course and were probably migrainous in nature (08). However, if paresthesias are the presenting complaint, one must also consider pure sensory stroke of the thalamus if the symptoms are persistent (19). Vascular malformations or tumor can present with migraine-like symptoms and, like stroke, must be considered if there are any atypical features.

The most recent iteration of the International Headache Society’s Classification of Headache continues to take a careful new look at migraine and migraine with aura and makes some changes, which now include the following: typical aura without headache (which is really what constitutes most of the cases of late-life migraine accompaniments) and typical aura with headache (27). The latter is included to remind diagnosticians that nonmigraine headache can also follow typical aura. Thus, if the headache following presumed late-life migraine accompaniment does not meet the criteria for migraine, it becomes even more important to rule out another cause, particularly transient ischemic attack or a mimic of migraine.

The new classification from the Headache Classification Subcommittee of the International Headache Society describes typical aura as: aura consists of visual and/or sensory and/or speech/language symptoms, but no motor weakness, and is characterized by gradual development, duration of each symptom no longer than 1 hour, a mix of positive and negative features, and complete reversibility. Commonly, as patients become older, headaches lose the migraine characteristics or they disappear completely, with auras continuing. Men especially can have typical aura without headache from the onset.

Finally, one should never overlook the diagnosis of temporal arteritis in the elderly, as many elderly patients will present with visual symptoms, including amaurosis, and headache with no specific features. Constitutional symptoms, including weight loss, fatigue, polymyalgia rheumatica, jaw and tongue claudication, fever, anemia, and elevated erythrocyte sedimentation rate, usually lead to the diagnosis, the institution of steroid therapy, and a temporal artery biopsy. In essence, late-life migraine accompaniments are a diagnosis of exclusion if transient ischemic attack, stroke, arteritis, or other serious etiologies are being considered in any individual case.

Diagnostic workup

Late-life migraine accompaniments are often benign events. However, a review of neuroimaging in migraine suggests neuroimaging may be considered for presumed migraine for the following reasons: atypical in nature, prolonged or persistent aura, increasing frequency, severity, or change in clinical features, first or worst migraine, migraine with brainstem aura, migraine with confusion, hemiplegic migraine, late-life migrainous accompaniments, aura without headache, side-locked headache, and posttraumatic headache (14). If necessary, magnetic resonance angiography (MRA), echocardiography, and Doppler ultrasound can be performed to exclude a source of cerebral embolism, such as atherosclerotic plaques, dissection of cranial arteries, and cardioembolic sources, whereas EEG can help exclude seizures. CT, CT angiography, MR, and MRA are also useful in detecting the presence of stroke and transient ischemic attack mimics, such as a tumor or aneurysm. Specialized MR sequences (50) or susceptibility weighted imaging may be needed to ensure that cases of cerebral amyloid angiopathy presenting with transient focal neurologic episodes in the elderly are not the underlying cause of similar symptoms due to focal subarachnoid hemorrhage. MR diffusion-weighted imaging is useful in diagnosing ischemic stroke. Because patients with migraine may have increased risk of complications following contrast angiography, this procedure should be avoided, if possible. However, in one study of 142 migraine patients, it appeared that migraine did not increase the risk of complications caused by angiography, and was felt to be safe; however, transient focal neurologic symptoms occurred in 2.6% of cases (44). Blood tests should be done to exclude platelet disorders, polycythemia, and hyperviscosity syndromes, as well as lupus anticoagulant, phospholipid antibodies, other rare coagulopathies, temporal arteritis, or other rare arteritides if there is an index of suspicion that these disorders may be present. However, investigation should not be done if the history is typical of late-life migraine accompaniments and abnormalities are not present on clinical examination (10; 09).

References

01: Androulakis M, Sen S, Kodumuri N, et al. Migraine age of onset and association with ischemic stroke in late life: 20 years follow-up in ARIC. Headache 2019;59(4):556-66. PMID 30663778
02: Anonymous. The late-life migraine “accompaniment” that wasn’t. Headache 2003;43(3):293.
03: Aring CD. The migrainous scintillating scotoma. JAMA 1972;220:519-22. PMID 5067127
04: Aring CD. Late-life migraine. Arch Neurol 1991;48:1174-7. PMID 1953405
05: Ayata C. Spreading depression and neurovascular coupling. Stroke 2013;44:S87-9. PMID 23709742
06: Bereczki D, Kollar J, Kozak N, et al. Cortical spreading edema in persistent visual migraine aura. Headache 2008;48:1226-9. PMID 18819182
07: 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
08: Claiborne Johnston S, Sidney S, Bernstein AL, Gress DR. A comparison of risk factors for recurrent TIA and stroke in patients diagnosed with TIA. Neurology 2003;60(2):280-5.
09: Cull RE. Investigation of late-onset migraine. Scott Med J 1995;40(2):50-2. PMID 7618069
10: Dennis M, Warlow C. Migraine aura without headache: transient ischemic attack or not. J Neurol Neurosurg Psychiatry 1992;55:437-40. PMID 1619407
11: 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;259:1868-73. PMID 22302276
12: Eikermann-Haerter K, Ayata C. Cortical spreading depression and migraine. Curr Neurol Neurosci Rep 2010;10:167-73. PMID 20425031
13: Eustache F, Desgranges B, Laville P, et al. Episodic memory in transient global amnesia: encoding, storage, or retrieval deficit. J Neurol Neurosurg Psychiatry 1999;66(2):148-54.
14: Evans RW, Burch RC, Frishberg BM, et al. Neuroimaging for migraine: the American Headache Society systematic review and evidence-based guideline. Headache 2020;60(2):318-36. PMID 31891197
15: Evans RW, Lipton RB, Silberstein SD. The prevalence of migraine in neurologists. Neurology. 2004;62(2):342; author reply 342.
16: Evans, RW, Purdy RA, Goodman SH. Airplane descent headaches. Headache 2007;47(5):719-23. PMID 17501855
17: Fisher CM. Transient paralytic attacks of obscure nature: the question of non-convulsive seizure paralysis. Can J Neurol Sci 1978;5:267-73. PMID 100195
18: Fisher CM. Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks. Can J Neurol Sci 1980;7:9-17. PMID 7388704
19: Fisher CM. Pure sensory stroke and allied conditions. Stroke 1982;13:434-47. PMID 7101342
20: Fisher CM. Late-life migraine accompaniments--further experience. Stroke 1986;17(5):1033-42. PMID 3532432
21: Fisher CM. Late-life (migrainous) scintillating zigzags without headache: one person's 27-year experience. Headache 1999;39:391-7. PMID 11279916
22: Fisher CM, Adams RD. Transient global amnesia. Trans Am Neurol Assoc 1958;83:143-5.
23: Franceschi M, Colombo B, Rossi P, Canal N. Headache in population based elderly cohort. An ancillary study to the Italian Longitudinal Study of Aging. Headache 1997;37(2):79-82. PMID 9074291
24: Goadsby PJ. Pathophysiology of migraine. Ann Indian Acad Neurol 2012;15(Suppl 1):S15-22. PMID 23024559
25: Goadsby PJ, Lipton RB, Ferrari MD. Migraine--current understanding and treatment. N Engl J Med 2002;346(4):257-70. PMID 11807151
26: Harriott A, Karakaya F, Ayata C. Headache after ischemic stroke: A systematic review and meta-analysis. Neurology 2020;94(1):e75-e86. PMID 31694924
27: Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38(1):1-211. PMID 29368949
28: Jimenez-Caballero PE, Marsal-Alonso C, Velazquez-Perez JM, Alvarez-Tejerina A. Transcranial Doppler during transient global amnesia. Rev Neurol 2003;37(12):1114-6. PMID 14691761
29: Jovin TG, Vitti RA, McCluskey LF. Evolution of temporal lobe hypoperfusion in transient global amnesia: a serial single photon emission computed tomography study. J Neuroimaging 2000;10(4):238-41. PMID 11147408
30: Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain 1994;117(Pt 1):199-210. PMID 7908596
31: Leao AA. Spreading depression of activity in the cerebral cortex. J Neurophysiol 1944;7:359-90.
32: Merikangas KR, Fenton BT, Cheng SH, Stolar MJ, Risch N. Association between migraine and stroke in a large-scale epidemiological study of the United States. Arch Neurol 1997;54(4):362-8. PMID 9109736
33: Meyer JS, Kawamura J, Terayama Y. Xenon 133 cerebral blood flow measurements in migraine with aura. In: Olsen J, editor. Migraine and other headaches: the vascular mechanisms. New York: Raven, 1991.
34: Meyer JS, Terayama Y, Konno S, et al. Age-related cerebrovascular disease alters the symptomatic course of migraine. Cephalalgia 1998;18(4):202-8. PMID 9642495
35: Mohr JP, Gautier JC, Pessin MS. Internal carotid artery disease. In: Barnett HJ, Mohr JP, Stein B, Yatsu FM, editors. Stroke. New York: Churchill Livingstone, 1998:355-400.
36: 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
37: 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
38: Peatfield RC. Can transient ischemic attacks and classical migraine always be distinguished. Headache 1987;27:240-3. PMID 3597078
39: Portenoy RK, Abissi CJ, Lipton RB, et al. Headache in cerebrovascular disease. Stroke 1984;15(6):1009-12. PMID 6506110
40: Ramadan NM, Levine SR, Welch KM. Cerebral blood flow in migraine accompaniments and vertebrobasilar ischemia. Stroke 1994;25:1219-22. PMID 8202984
41: Raskin N, Appenzeller O. Headache. Major problems in internal medicine. Philadelphia: WB Saunders, 1980.
42: Schurks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T. Migraine and cardiovascular disease: systematic review and meta-analysis. BMJ 2009;339:b3914. PMID 19861375
43: Shah DR, Dilwali S, Friedman DI. Migraine aura without headache [corrected]. Curr Pain Headache Rep 2018;22(11):77. PMID 30225597
44: Shuaib A, Hachinski VC. Migraine and the risks from angiography. Arch Neurol 1988;45(8):911-2. PMID 3395265
45: Shuaib A, Lee MA. Cerebral infarction in patients with migraine accompaniments. Headache 1988;28:599-601. PMID 3248937
46: Somerville BW. A study of migraine in pregnancy. Neurology 1972;22(8):824-8. PMID 4673410
47: Stang PE, Carson AP, Rose KM, et al. Headache, cerebrovascular symptoms, and stroke: the Atherosclerosis Risk in Communities Study. Neurology 2005;64(9):1573-7. PMID 15883318
48: Stang PE, Yanagihara T, Swanson JW, et al. Incidence of migraine headache: a population-based study in Olmsted County, Minnesota. Neurology 1992;42:1657-62. PMID 1513451
49: Vales-Montero M, García-Pastor A, Iglesias-Mohedano AM, et al. Cerebral amyloid angiopathy-related transient focal neurological episodes: a transient ischemic attack mimic with an increased risk of intracranial hemorrhage. J Neurol Sci 2019;406:116452. PMID 31525529
50: Vongvaivanich K, Lertakyamanee P, Silberstein SD, Dodick DW. Late-life migraine accompaniments: a narrative review. Cephalalgia 2015;35(10):894-911. PMID 25505036
51: Whitty CW. Migraine without headache. Lancet 1967;2(7510):283-5. PMID 4165917
52: Wijman CA, Wolf PA, Kase CS, at al. Migrainous visual accompaniments are not rare in late life: the Framingham Study. Stroke 1998;29:1539-43. PMID 9707189
53: Wolff HG. Headache and other head pain. New York: Oxford University Press, 1963.

Contributors

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

Authors

Andrea Harriott MD PhD

Dr. Harriott of Massachusetts General Hospital and Harvard Medical School received honorarium from Abbvie and Theranica for service on scientific advisory boards.
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R Allan Purdy MD FACPC FACP FAHS

Dr. Purdy of Dalhousie University has no relevant financial relationships to disclose.
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Editor

Stephen D Silberstein MD

Dr. Silberstein, Director of the Jefferson Headache Center at Thomas Jefferson University has no relevant financial relationships to disclose.
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Former Authors

John Stirling Meyer MD
Shizuko Konno MD
Katsuyuki Obara MD
Yasuo Terayama MD
Gaiane M Rauch MD PhD
Ronald A Rauch MD

Patient Profile

Age range of presentation: 19 to 65+ years
Sex preponderance: male>female, >2:1

male>female, >1:1
Heredity: heredity may be a factor in migraine
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Other migraine: G43.8
ICD-11: Other specified migraine: 8A80.Y

Other specified migraine with aura: 8A80.1Y

Hemiplegic migraine: 8A80.10

Other specified complications related to migraine: 8A80.3Y

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Late-life migrainous accompaniments

Associated Disorders

Atherosclerotic heart disease
Cerebrovascular disorders

Differential Diagnosis

stroke
transient ischemic attacks
seizure march
sensory seizures
atherothrombotic stroke
- embolic stroke
- cardioembolic stroke
- occipital lobe strokes
- vertebrobasilar transient ischemic attack
- cerebral amyloid angiopathy
- vascular malformation
- tumor
- temporal arteritis

Also Relevant

Cerebral amyloid angiopathy
Focal clonic seizures
Headache associated with ischemic cerebrovascular disease
Hemiplegic migraine
Migraine
- Migraine aura without headache
- Migrainous infarction
- Ophthalmoplegic migraine

Clinical Categories

Headache & Pain

Patient Handouts

Headache

Web References

Guidelines

AAN: Headache

Late-life migrainous accompaniments …

Late-life migrainous accompaniments

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

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Also in This Category

Primary headache associated with sexual activity

Headache associated with intracranial neoplasms

Medication overuse headache

Acupuncture

Migraine in childhood

Headache attributed to head trauma

Migraine: pathogenesis and pathophysiology

Tension-type headache

Late-life migrainous accompaniments

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

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Authors

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

Headache associated with intracranial neoplasms

Medication overuse headache

Acupuncture

Migraine in childhood

Headache attributed to head trauma

Migraine: pathogenesis and pathophysiology

Tension-type headache

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