Headache, migraine, and stroke
The relationship between headache, migraine, and stroke is
complex. All of these conditions are common and can be temporally related, but
whether the association is causal has not been definitively proven in clinical
studies. In addition to being causal, a number of additional possible
relationships between these entities might exist:
●Headache may be coincidental with stroke
●Headache may be a consequence of stroke
●Stroke and cerebrovascular lesions may have clinical
features of migraine
●Headache or migraine may increase the risk of stroke
●Migraine may have clinical features of stroke
Further modifications are likely as knowledge of the
epidemiology and pathophysiology of these relationships advances.
Headache coincidental with stroke
— Headache or migraine may
occur coincidentally with stroke since both are common conditions. With aging,
the prevalence of migraine decreases, while that of stroke increases. In
addition, stroke risk factors such as hypertension, diabetes, and heart disease
are more common in older age groups. Therefore, younger patients are much more
likely than older patients to have migraine as the only stroke risk factor.
Headache due to stroke or vascular disease
— Headache at or near the onset of stroke
occurs almost invariably in subarachnoid hemorrhage. Headache is less frequent
with other stroke mechanisms. In intracerebral hemorrhage (ICH), headache
may occur acutely at stroke onset, or may occur a bit later (within hours of
onset) as the hematoma gradually expands and begins to compress pain sensitive
intracranial structures such as larger arteries and the meninges. In some cases
of ICH, headache may not be present at all.
Sentinel headache
— A premonitory or sentinel headache may
occur before subarachnoid hemorrhage (SAH). Sentinel headache is important to
recognize because it may signal an aneurysmal leak days or weeks before a more
devastating SAH.
Ischemic stroke
— In ischemic stroke of large vessel origin,
headache may occur prior to, during, or after stroke onset. In one
prospective study of 284 patients with acute ischemic stroke, concomitant
headache during the early phase of stroke was reported by 38 percent.
Although the cause is often unclear, several plausible mechanisms have been
postulated including vascular dilation as a homeostatic response to ischemia
and direct arterial irritation by thrombus, embolism, or dissection. One
study using MRI lesion mapping found that infarctions in the insular cortex
were significantly associated with headache, perhaps related to the role of
this region in pain processing. Headache is uncommon in lacunar stroke
syndromes.
Reversible cerebral vasoconstriction syndromes
— Reversible
cerebral vasoconstriction syndromes (RCVS), a group of conditions characterized
by reversible narrowing and dilatation of the cerebral arteries, are reviewed
here briefly and discussed separately in detail. RCVS encompasses a number of diverse conditions that share
similar clinical and radiologic features, including the following:
●Thunderclap headache with reversible vasospasm
●Benign angiopathy of the central nervous system
●Migrainous vasospasm or migraine angiitis
●Call-Fleming syndrome
●Postpartum angiopathy
●Thunderclap headache-associated vasospasm
●Central nervous system pseudovasculitis
●Drug-induced cerebral vasoconstriction
The etiology of RCVS is unknown, though the reversible
nature of the vasoconstriction suggests an abnormality in the control of
cerebrovascular tone.
The clinical presentation of RCVS is usually dramatic with
sudden, severe "thunderclap" headaches that simulate aneurysmal
subarachnoid hemorrhage; however, in patients with RCVS, thunderclap headaches
often recur over a span of one to four weeks.
Despite the presence of widespread cerebral
vasoconstriction, the admission brain scan may be normal. In the ensuing days,
many patients go on to develop complications such as ischemic stroke, convexal
(nonaneurysmal) subarachnoid hemorrhage, lobar hemorrhage, and reversible brain
edema, alone or in combination. Cerebral angiographic abnormalities are dynamic
and progress proximally, resulting in a "sausage on a string" appearance
of the circle of Willis arteries and their branches. These abnormalities
resolve spontaneously (without specific therapy) over a few weeks.
The clinical outcome is benign in most patients. Rare
patients develop severe irreversible deficits or death from progressive strokes
or cerebral edema. Recurrence of an episode of RCVS is rare.
Others — Headache is also a frequent clinical symptom of
hypertensive encephalopathy, the cerebral hyperperfusion syndrome,
and reversible posterior leukoencephalopathy. These syndromes may share a
common pathophysiology involving failure of cerebral blood flow autoregulation
and endothelial dysfunction.
Symptomatic migraine and migraine mimics
— Symptomatic
migraine results from structural brain lesions, vasculopathies, and vascular
malformations that cause recurrent symptoms typical of migraine with aura.
Arteriovenous malformations (AVM) may be associated with migraine attacks. One literature review of case studies found a correlation between the
side of the head with the AVM and the side affected by unilateral headache,
with a similar correlation for lateralized auras. Migraine attacks have
also been associated with the syndrome of Cerebral Autosomal Dominant
Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL).
Acute stroke may be accompanied by headache and neurologic
signs and symptoms indistinguishable from migraine, in which case the stroke
may be considered a migraine mimic. Various stroke subtypes including
ischemic stroke, subarachnoid hemorrhage, and cerebral venous thrombosis can
mimic migraine attacks.
Cervical internal carotid artery dissection may occasionally
present as a migraine mimic with visual scintillating scotomata . One
study of 161 patients found that nearly 70 percent of cervical carotid and
vertebral dissections were associated with headache, and headache was the
initial symptom in 33 to 47 percent. An earlier study found that 19 of 21
patients with angiographically documented carotid dissection had ipsilateral
head pain in one or more regions such as the orbit, frontal region, and side of
the head. The head pain was typically acute and severe, and neck pain
occurred as well in 12 patients. About three quarters of the 21 patients had
ischemic events related to the dissection, with the headache preceding the
ischemic symptoms in about half.
The relationship of dissection with headache is made even
more complicated because about one-half of patients with cervicocephalic
dissection have a prior history of migraine.
— Complications of migraine are
characterized by attacks associated with prolonged symptoms or, rarely, with
infarction or seizures. Prolonged symptoms may last for the entire headache,
for several days or weeks, or in some cases leave a permanent neurologic
deficit. Examples include persistent aura without infarction (if the aura lasts
one week or longer with no evidence of infarction) and migrainous infarction
(if the deficit lasts more than one hour and the neuroimaging shows
infarction).
Other migraine types include ophthalmoplegic migraine, retinal
migraine (ocular migraine), confusional migraine, basilar-type migraine, and
hemiplegic migraine.
Migrainous stroke
— As yet, there is no universal agreement
on the definition of migraine associated stroke.
— The International
Classification of Headache Disorders, 3rd edition (ICHD-3) defines migrainous
infarction by the following features;
●A) A migraine attack fulfilling criteria B and C
●B) Occurring in a patient with migraine with aura and
typical of previous attacks except that one or more aura symptoms persists for
>60 minutes
●C) Neuroimaging demonstrates ischemic infarction in a
relevant area
●D) Not better accounted for by another diagnosis
The definition of migrainous infarction, also called
migraine-induced stroke, has been criticized because it does not allow for
the possibility of migraine-related stroke in migraine attacks without aura.
However, while several reports have noted the occurrence of migrainous
infarction associated with attacks of migraine without aura, most
studies have found no association of migraine without aura and ischemic stroke.
Migraine-related stroke
— Some experts have used the term
migraine-related stroke to expand the definition of migrainous infarction and
allow inclusion of patients who have migraine without aura. Others use
migraine-related stroke for cases when additional stroke mechanisms coexist
with migraine.
Migraine with clinical features of stroke
— Migraine with
aura occurs in about 15 to 20 percent or more of migraine patients and may
mimic stroke . Typical migraine auras develop gradually over 5 to 20
minutes and last less than one hour; the most common types involve homonymous
visual disturbances. There is usually little clinical difficulty recognizing
these auras as manifestations of migraine when the aura is brief and precedes a
headache. In addition to visual auras, other common types of migraine aura
manifest as sensory or language disturbances. (See "Pathophysiology,
clinical manifestations, and diagnosis of migraine in adults", section on
'Migraine aura'.)
Prolonged or atypical auras may be difficult to distinguish
from stroke or transient ischemic attacks (TIAs). In particular, motor auras of
hemiplegic migraine are more likely than others to last longer than one hour
(see "Hemiplegic migraine", section on 'Auras'). Additionally,
migraine aura without headache may be confused with TIA or stroke in older
patients [25].
Migraine or migraine variants that may mimic TIA or stroke
are discussed in greater detail separately, including:
●Sporadic and familial hemiplegic migraine.
●Migraine with brainstem aura.
●Retinal or ocular migraine.
●Migraine aura without headache and migraine with
acute-onset aura.
There appears to be an increased risk of stroke associated
with migraine, particularly in women who have migraine with aura. However, the
absolute increase in the risk of stroke is small. Stroke risk appears to be most increased in women of child
bearing age who have migraine with aura and smoke and/or use estrogen-progestin
contraceptives.
Several studies have found an association between migraine
with aura and silent infarct-like lesions on brain MRI located mainly in the
posterior circulation white matter or cerebellum. However, the etiology,
nature, and clinical significance of these MRI lesions remain unclear.
The pathophysiology underlying migraine as a possible cause
of stroke or as a stroke risk factor is not clear, but vasospasm and changes in
cerebral blood flow are biologically plausible mechanisms.
Nonmigraine, nonspecific, and/or chronic headache may be a
predictor of ischemic stroke risk, but the evidence is conflicting.
Treatment aimed at primary or secondary stroke prevention
should combine stroke risk factor control with headache prophylaxis. Patients
with frequent migraine and vascular disease should also receive migraine
prophylaxis. Vasoconstrictive medications including triptans, serotonin
agonists, and ergot alkaloids are relatively contraindicated in patients with
vascular disease.
Women who have migraine without aura and no other risk
factors for stroke may use a contraceptive pill with low-dose estrogen (less
than 50 mcg). Women who have migraine with aura should be encouraged to stop
smoking, control their blood pressure, and use an alternative method of
contraception.
Uptodate.
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