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Migraine is incredibly common and affects up to 15% of females and 5% of males. Most patients often self diagnose and self manage. Others are seen and diagnosed and managed by their general practitioner. They may have neurology review when the diagnosis is in doubt or severe and disabling and refractory to initial therapy. It is only a small subset who come in contact with the stroke physician. These are usually when migraine with aura starts later in life or its pattern changes and patients are referred to the TIA clinic and should be differentiated by the recurrent episodic positive symptomatology often in a young patient. Secondly when patients present with persisting migrainous symptoms that mimic stroke or with what is called migrainous stroke or simply present with stroke. Third - many of the rarer causes of stroke appear to have a greater incidence of Migraine.Migraine is a risk factor and a rare cause of stroke particularly in women with migraine with aura. Concomitant smoking and OCP greatly increases stroke risk.

The aetiology of migraine is spreading waves of cortical depression through cortex and dysfunction of aminergic brainstem/diencephalic sensory control systems. CSD is characterised by a wave of synchronised depression of electrical activity spreading at a rate of 1–15 mm per min across the cortex. A decrease in cerebral blood flow propagating anteriorly from the occipital cortex was repeatedly reported during attacks of migraine with aura. CSD then activates the trigeminovascular system, which is responsible for the migrainous headache. CSD is associated with hyperaemia that lasts for less than 2 minutes, followed by spreading oligaemia that persists for 1-2 h and corresponds to a 20-30% reduction in cerebral blood flow though not usually enough to cause ischaemia although so called migrainous infarction has been seen.

Migraine Classification by International headache society:

  • Migraine without aura (old notation called common) : Headache and associated symptoms e.g. nausea, vomiting, light intolerance, sound intolerance. Most patients with migraine have exclusively attacks without aura
  • Migraine with aura (old notation called classic) : The aura is a complex of neurological symptoms that occurs just before or at the onset of migraine headache. The aura builds over 5-20 minutes and lasts less than 60 minutes. Headache then follows. Sometimes the aura can occur without any follow up headache or the headache does not have migrainous features.

There is a close by incompletely understood relationship between stroke and migraine which we shall try to examine. First of all we should define migraine. Migraine is a clinical diagnosis. There is no diagnostic test other than an accurate history of often severe recurrent periodic vascular headache lasting 4-72 hours, usually but by no means always on one side of the head, often accompanied by nausea, vomiting and photophobia, sometimes preceded by sensory disturbances. Triggers include allergic reactions, excess carbohydrates or iodine in the diet, alcohol, bright lights or loud noises. Precipitants include fasting, alcohol, stress, removal of stress "saturday morning headaches", menstruation Low atmospheric pressure, physical exertion, bright lights or sounds. There are some common and uncommon variants of migraine with aura shown below.

Migraine can then be further broken down into the common types Migraine without aura (MO) and the less common Migraine with aura (MA) which makes up a third of all cases. The aura is a symptomatic experience of typically positive symptomatology such as flashing lights, fortification spectra, scotomas with bright edges. Others include tingling which may spread over the face, arm and leg and may even cross the midline. It spreads slowly over minutes. There may be word finding difficulties mimicking dysphasia. These are usually transient and last minutes and precede the headache. Attacks may be preceded by warning symptoms that occur for hours even a day or two before a migraine attack (with or without aura). Examples include fatigue, poor concentration, even neck stiffness, heightened sensitivity to light or sound, nausea, blurred vision, yawning and pallor. These do not represent aura.

AuraDescription of Migraine Auras
VisualPositive features (e.g. flickering lights, spots or lines, fortification spectra) and/or negative features (i.e. loss of vision, scotomas) which resolve. Visual loss or blurring of central vision may occur
SensoryPositive features (I.e., pins and needles) and/or negative features (ie, numbness) which resolve. Classically paraesthesias spread over minutes rather than seconds as in TIA
SpeechAphasic or Dysphasic like speech disturbance which resolves. Almost always expressive and not receptive.
MotorHemiplegia and unilateral weakness which can easily mimic stroke

Migraine Variants

  • Hemiplegic migraine: Migraine with aura including motor weakness and followed by the headache. Can be mistaken for TIA in those under 40 or even stroke. The weakness can persist beyond the aura phase and outlast the headache. If a first degree relative affected consider Familial hemiplegic migraine.
  • Basilar migraine: aura manifests as brainstem symptoms such as dysarthria, vertigo, tinnitus, hypoacusia, diplopia, visual symptoms simultaneously in both temporal and nasal fields of both eyes, ataxia, decreased level of consciousness, simultaneously bilateral paraesthesias.
  • Retinal migraine: Repeated attacks of monocular or homonymous visual disturbance, including scintillations, scotomata or blindness, associated with migraine headache. Between attacks eye exam is normal.
  • Ophthalmoplegic migraine: diplopia, IIIrd nerve palsy
Migraine and Stroke Overlap
  • MELAS syndrome
  • Carotid and Vertebral Arterial Dissection
  • Antiphospholipid antibodies
  • Sickle cell disease

This differentiation between those who experience aura (MA) and those who don't (MO) is important as it is the patients with aura who appear to have a greater ischaemic and haemorrhagic stroke risk and it seems to be an important stroke risk factor [Kurth T et al. 2012]. Studies suggest a doubling of the baseline risk factors for both stroke types. The risk is greater in those with more frequent attacks [Kurth T et al. 2009]. There is a particular group of patients - females on the pill who smoke who have migraine with Aura have a 10 fold increase in stroke risk [Kurth T et al. 2008]. Several neuroimaging studies have shown an increased prevalence of approximately four fold rise in white matter hyperintensities in people with migraine. These are more frequent in those with a higher rate of attacks. Studies have shown brainstem and cerebellar lesions. MA has been shown to cause a drop in cerebral perfusion which could lead to Migrainous infarction within the setting of a typical migraine. However migrainous infarction is also seen in those with migraine without aura. PFO is twice as common in those with Migraine with aura though there do not appear to be any benefits of closure [Dowson A et al. 2008]. It was though the association may be due to vasoconstricting triptans or ergotamine derivatives but this has not been shown to be the case.

There also seems to be several strokes which predispose to stroke which have an increased incidence of migraine. Theses include CADASIL in which 40% of patients have Migraine with Aura as a significant feature which precedes the strokes by 10-20 years. Other associations include Moyamoya syndrome, leptomeningeal angiomatosis, APL syndrome, MELAS, SLE, Cardiac myxoma

In terms of management caution must be taken when separating TIA and migraine with aura. Difficulties arise in those over 50 with indeterminate features and one must then use Bayesian principles on likelihood of cerebrovascular disease and risk and benefits of standard therapy. Low dose aspirin may have advantages for both. Migraine with aura however can however present in those over 50s but one can cover all bases with aspirin if there is uncertainty. In migraineurs who stroke ergot derivatives and triptans should be discontinued. Young female migraineurs with aura should avoid smoking and the OCP. CADASIL is usually not screened for unless there are suggestive MRI changes and a positive family history.

Hemiplegic Migraine

Lastly the hemiplegic migraine patient has an aura that consists of motor weakness. They may have sporadic hemiplegic migraine due to de novo mutations or have at least one affected first-degree or second-degree relative and a diagnosis of having familial hemiplegic migraine. Typical hemiplegic migraine attacks start before the age of 20 and include gradually progressing visual, sensory, motor, aphasic, and often basilar-type symptoms, accompanied by headaches. Most patients also have attacks of migraine with typical aura—without weakness. For those interested in the genetics I would refer you to the literature [Russell M 2011].

They may present to the Emergency Department and for consideration of stroke thrombolysis. There may be motor weakness and this is always associated with at least another aura symptom such as sensory symptoms which may be numbness or tingling as well as visual - scotoma, scintillation and hemianopias. Signs may be unilateral or spread bilaterally. Headache is seen in 95% and may precede the aura. Some have minimal or no headache. Some have coma, seizures and acute delirium and complex delusions. Cerebellar signs are common. The differential includes focal seizures.

Thrombolysis should certainly be considered if this is a first presentation or an atypical presentation with persisting classical stroke like appearance. An initial MRI DWI showing restricted diffusion or CTA showing large vessel obstruction may help clarify the diagnosis but these are often unavailable or will significantly delay treatment. Take expert help. These patients are at increased stroke risk and one would not wish to miss thrombolysing a young patient. Bleed risk is likely to be low if the underlying aetiology is migraine.


  • Explanation and reassurance. Stop oestrogen pill in females with migraine with aura. Migraine without aura the common form has no added stroke risk and in these patients the OCP may be carefully considered. Smoking should cease. Blood pressure control is also advised.
  • Generally any of the traditional medications which vasoconstrict are inadvisable in stroke. These include triptans, serotonin agonists (pizotifen, methysergide), and ergot alkaloids. Beta blockers should probably be avoided in older patients.
  • NSAIDs may be tried where there are no complications mindful of the gastric irritation and BP effects of these agents. Best used on a needed basis. Ibuprofen 600 mg seems reasonable.

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