• endovascular treatment;
  • angiography;
  • migraine;
  • aura;
  • complications


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  2. Abstract

Objective.—To describe three cases of migraine (two with aura) after an intracranial endovascular procedure.


Results.—One patient had an attack of migraine with prolonged aura after embolization of a dural arteriovenous fistula. Another patient had an attack of migraine with aura (and hemiparesis) after a diagnostic angiogram. The third patient already suffered from migraine with aura and had a migraine attack after embolization of an occipital arteriovenous malformation. A quadrantanopia persisted in this patient. Outcome of the other two patients was good.

Conclusion.—Intracranial endovascular procedures can induce migraine with aura. We could not identify the underlying pathophysiological mechanism, but mechanical, chemical, immunological, or hemodynamic factors could be involved.

We present three patients, each of whom had an attack of migraine immediately after an intracranial endovascular procedure. In two of the patients, migraine was accompanied by an aura. Migraine with aura during cerebral angiography has been reported only once before,1 and little is known about migraine after intracranial endovascular treatments.


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  2. Abstract

Patient 1.

A 60-year-old woman was referred in July 1999 for embolization of a dural arteriovenous fistula. Since December 1998, she had a continuous, left-sided, pulsatile tinnitus (like “an engine room”), which increased during exertion. The bruit was sometimes even audible externally. She did not complain of headache.

Neurological examination was normal except for slight hypesthesia in the distribution of the second division of the left trigeminal nerve. A loud pulsatile murmur was heard on auscultation over the left petrosal bone.

Angiography showed a dural arteriovenous fistula on the left side fed by the left vertebral artery, the external carotid artery, and, to a lesser extent, by the meningohypophyseal trunk. The occipital and maxillary arteries were embolized with particles. The sigmoid sinus and jugular bulb were filled with 31 Guglielmi detachable coils. One hour after this procedure, the patient saw flashes of light in the right hemifield, and 10 minutes after this, she developed a severe, left-sided, throbbing, pulsatile headache with nausea, vomiting, photophobia, and phonophobia. The aura lasted less than 1 hour. The next day, the headache had subsided and the bruit had gone. After 2 months, she had no symptoms or signs, and on control angiography, the fistula was obliterated.

Patient 2.

A 48-year-old man had an aneurysm of the left internal carotid artery in the cavernous sinus that was embolized with one Guglielmi detachable coil in 1995. This aneurysm was found accidentally. In addition, he had a small asymptomatic (3 mm) aneurysm of the right posterior communicating artery, which has not been treated. When he was much younger, he had had migraine with aura.

In June 1999, he was admitted for follow-up bilateral cerebral angiography. The left-sided aneurysm was sufficiently occluded, and the small aneurysm on the right remained unchanged. Several hours after the test, he gradually developed a severe, diffuse, throbbing headache accompanied by nausea, vomiting, and photophobia. Ten minutes after the beginning of the headache, he saw flashes of light on the left side, and subsequently developed paresis and hypesthesia of the left arm for about 2 hours. He partially recognized the symptoms from his previous migrainous attacks. The next day, the headache had gone, and there were no neurological deficits. Computer-assisted tomography of the brain showed no abnormalities, except for the coil in the left cavernous sinus.

Patient 3.

A 42-year-old man suffered from migraine with aura for 8 years. An attack always started with a scintillating scotoma in the right visual hemifield (for 15 minutes) followed by a left-sided pulsatile headache with nausea, vomiting, photophobia, and phonophobia. At first, this happened only two or three times a year, usually after strenuous exercise and at the beginning of a holiday. Later, the frequency increased to four times a week even with the slightest exercise.

Neurological examination was normal. Magnetic resonance imaging of the brain showed an arteriovenous malformation (AVM) with a diameter of 4 cm in the left occipital lobe. At angiography, it appeared to be a high-flow AVM mainly fed by the left posterior cerebral artery, the left and right middle meningeal arteries, and the left tentorial artery. The AVM was successfully embolized with glue, but some dural feeding vessels remained patent. Two hours after this procedure, he had a severe pulsatile headache accompanied by nausea, vomiting, photophobia, and phonophobia. During the headache, he noticed a right-sided hemianopia. At that time, computer-assisted tomography was normal, except for glue in the nidus of the AVM. The headache gradually diminished during the week that followed. One week after the embolization, he had another attack of headache, which gradually diminished during the following 8 weeks. After this episode, the headache did not return. A right upper quadrantanopia remained. Subsequently, the AVM was treated with gamma knife irradiation.


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  2. Abstract

Intracranial vascular malformations (such as aneurysms, dural arteriovenous fistulas, and AVMs) are frequently treated with endovascular techniques including embolization (with coils or glue) or balloon inflation. These treatments are reasonably safe and effective.2-6 However, parent vessel occlusion, aneurysm rupture, thromboembolism, incomplete occlusion by the coil, and impaction of coils may complicate the management of aneurysms by the detachable coil technique.7 Embolization of AVMs may be complicated by delayed hemorrhage (after incomplete obliteration), and transient and permanent neurological deficits.6

In 3 months, we encountered three patients who had a migrainous attack after an intracranial endovascular procedure. Patient 1 is an example of migraine with aura after an endovascular treatment in a “migraine-naive” patient. Patient 2 was not treated, but had undergone routine angiography followed by an attack of hemiparetic migraine. Patients 1 and 2 fulfilled the International Headache Society (IHS) criteria8 for migraine with aura (except for the number of attacks and the presence of a cerebral abnormality). Patient 3 provides an example of migraine with aura as a presenting symptom of an occipital AVM.9,10 Embolization of the AVM probably elicited a new migraine attack (without aura) in this patient. This postembolization headache meets the IHS criteria for migraine without aura, except for the presence of a cerebral abnormality and the duration of the headache. Furthermore, a neurological deficit (quadrantanopia) remained. One could call this complicated migraine, but it probably is the result of an endovascular procedure-related cerebral infarction. Migraine is not the appropriate label for the 8-week headache that began 1 week after the embolization in this patient.

We found no cases of migraine with aura after endovascular treatment, searching MEDLINE for the following MeSH terms: cerebral arteriovenous malformations, arteriovenous fistula, and aneurysm and migraine and endovascular treatment. However, Olsen et al described four patients who had an attack of migraine with aura during diagnostic cerebral angiography.1

Postangiographic headache was studied by Ramadan et al.11 In 45 consecutive patients undergoing diagnostic cerebral angiography, 33% had headaches within 4 hours of the test (27% fulfilled the IHS criteria for migraine without aura8). They explained the headache as a result of delayed arterial pain related to catheter-induced or contrast dye-induced release of vasoactive substances. Unlike patient 2 (who had a visual aura and a hemiparesis after diagnostic angiography), their patients did not have an aura.

Neurological deficits (without concomitant migrainous headache) can occur during and after cerebral angiography. The prevalence is about 1%, and the symptoms are generally transient. Atherosclerosis is a risk factor.12,13 Shuaib and Hachinski showed that angiography does not pose greater risk for patients with migraine,14 but Patterson et al demonstrated that migraineurs are especially at risk for ischemia when angiography is performed during an attack.15 Kwentus et al systematically reviewed the possible mechanisms of complications of cerebral angiography in migraineurs.16

Headache during endovascular treatment was studied by Martins et al17 in 11 patients who were treated for AVMs (10 cases) or aneurysms (1 case), either by balloon inflation (3 cases) or by embolization (8 cases). All patients had focal, nonthrobbing, and short-lasting headaches, ipsilateral to the occluded artery, without gastrointestinal, autonomic, or auralike symptoms. The authors suggest that direct stimulation of the arterial wall caused the pain. Two other studies18,19 showed reproducible patterns of headache, indicated as referred pain, during balloon inflation in patients with AVMs (12 cases).

A change in hemodynamics occurs when an AVM is embolized (eg, patients 1 and 3). One case report showed a change in (cluster) headache side in a patient treated for an AVM. Parallel to this change in headache side, a change in hemodynamics was shown by transcranial Doppler studies.20

Current theories state that migraine is a neurovascular headache: it originates from the brain and has secondary changes in blood vessels.21 Conversely, we propose that migraine (with aura) after endovascular intracranial procedures is vascular in origin. It is known that stimulation of trigeminal C fibers, innervating the meningeal (and cortical) vessels and dura mater, may trigger the trigeminovascular pathway22,23 and the trigeminoparasympathic reflex,24 and thereby provoke migraine attacks. In addition, Fos expression in the trigeminal nucleus of monkeys and cats was found by Hoskin et al after stimulation of the middle meningeal artery.25 Cerebral vessels were in fact stimulated in our three patients, either by angiography itself (patients 1, 2, and 3) or by an endovascular intervention (patients 1 and 3). Dural vessels were specifically stimulated in patients 1 and 3. Probably the middle meningeal artery, which fed the AVM in patient 3, played a crucial role in the pathophysiology of his pre-embolization migraine. Stimulation of the vessel wall during endovascular procedures may occur due to direct mechanical stimulation (by catheter, coils, glue, and particles), a chemical reaction (by dye or glue), an immunological or idiosyncratic reaction, or a change in hemodynamics. Migraineurs may be more susceptible. An accompanying aura (patients 1 and 3) may be caused by focal reduction of regional blood flow, as was demonstrated by Olsen et al in patients with aura during angiography.1

Insight into the way an endovascular procedure causes migraine with aura may contribute to the understanding of the pathophysiology of migraine in general.


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  2. Abstract
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