Solving the conundrum. A migrainous infarction or an infarct-induced migrainous attack?B Hebant1, L Simmonet1, J Le Moal2, E Guegan-Massardier1
1 Department of Neurology, Rouen University Hospital and University of Rouen, Rouen, France
2 Department of Neuroradiology, Rouen University Hospital and University of Rouen, Rouen, France
Keywords: Cerebral infarct, infarct-induced migraine, migraine with aura
Migraine with aura is an common disorder frequently encountered in neurology. Link between migraine with aura and cerebral infarction is well known. Numerous studies demonstrated an association between migraine with aura and the risk of cerebral infarction, in particular for younger women., MI is a rare and controversial disorder with precise diagnostic criterias according to the International Headache Society (IHS).
Differentiating between MI and infarct-induced MA is challenging in clinical practice. Some authors suggest that infarct-induced MA could be much more frequent than MI. Based on clinical symptoms and imaging findings, we report here a case of an infarct-induced MA. Such cases are very rarely reported in the literature, we found the iconography particularly interesting and useful for clinical practice.
A 35-year-old right-handed woman was referred to our clinic for acute aphasia during a conversation. Aphasia was with sudden onset, lasted 30 min and was followed firstly by progressive right hemibody paraesthesia with cheiro-oral predominance. Then, after complete resolution of the sensory symptoms, she experienced seeing shimmering zigzag lines which gradually increased in her right visual field. Sensory and visual symptoms, gradually settled in a few minutes (about 10 min) and resolved successively after several hours. A typical migraine headache, identical to the patient's usual ones followed, within one hour, the end of these new phenomena. The patient had suffered from regular typical migraine with visual auras since her childhood but she had not experienced other types of auras before. Indeed, she never complained of any sensory nor language disorder during her previous migraine attacks. The presence of language disorders and sensory symptoms was totally new, and unusual for her. In addition, she did not experience any loss of consciousness nor abnormal movements during this episode. The patient was previously healthy but had vascular risk factors (smoking and obesity), and was taking combined oral contraceptive pill. She had no family history of migraine with or without an aura, or history of hemiplegic migraine and she was not taking any medication before except nonsteroidal anti-inflammatory drugs for the acute treatment of her migraine attacks.
A non-contrast CT of her brain and CT angiography of the supra-aortic and intracranial arteries were unremarkable. A perfusion CT performed 90 min after onset of the neurological symptoms showed a large area of hypoperfusion (increased mean transit time), in the left temporo-occipital region not restricted to a single vascular territory, without significant cerebral blood volume changes [Figure 1]a, [Figure 1]b. An electroencephalogram performed during the sensory and visual symptoms was normal, ruling out the possibility of a partial seizure from the left temporo occipital region. An arterial spin labelling sequence (ASL) brain MRI undertaken 12 hours later while the patient was only experiencing the migrainous headache showed an area of diffuse hyper-perfusion in the left hemisphere [Figure 1]c, [Figure 1]d. Diffusion-weighted imaging (DWI) sequence showed two small areas of restricted diffusion, with a decreased apparent diffusion coefficient value, in the left middle cerebral artery territory indicative of recent infarcts [Figure 1]e, [Figure 1]f.
Initial examination at time of admission revealed blood pressure of 165/80 mmHg. General and neurological examinations were unremarkable (neither motor nor sensory nor visual abnormalities, especially no hemianopsia). Examination of cranial nerves and cerebellum was also normal. Further investigations—including a transoesophageal echocardiogram with bubble test, an immunological screen looking specifically for antiphospholipid antibodies—found no additional abnormalities. Our treatment plan included stopping her oral contraceptive, helping her to quit smoking, and starting her on the antiplatelet treatment (aspirin in a daily dose of 160 mg). She did not experience any further episodes but did continue to suffer from her typical migraine with and without the usual visual auras.
3 months follow-up MRI did no show silent ischemic lesions. As expected, the new ASL sequence performed was unremarkable.
The diagnostic conundrum: did the migraine lead to an infarction—a migrainous infarction (MI) or did an infarction lead to the features of a migrainous attack (MA)—an infarct-induced MA?
MI is a rare and controversial disorder in which, according to the International Headache Society, aura symptoms preceding the infarct should be like those experienced before. At least one or more of the aura symptoms should last longer than 60 min and brain imaging must show a recent infarct in the corresponding region.
In our case, CT perfusion, performed during progressive neurological symptoms was consistent with a migraine during the aura phase rather than a cerebral infarct, because it showed perfusion changes with hypoperfusion (increased mean transit time) in the left hemisphere (not restricted to any one vascular territory) without significant cerebral blood volume changes. These findings were consistent with the literature data concerning perfusion patterns on CT perfusion , but also on MRI perfusion  during a migraine with aura attack.
Moreover, MRI with ASL sequence performed 12 hours later, when patient only had migrainous headache demonstrated diffuse hyperperfusion in the left hemisphere, corresponding to previous aura symptoms which was coherent with the headache phase of a migraine, as already reported in the literature.,
Finally, DWI sequences disclosed recent infarcts in the left middle cerebral artery territory, well correlated with the initial language disorder presented by our patient.
We believe our case was most likely to have been an infarct-induced MA because, firstly her new aura symptoms were different from her usual ones (consequently, she did not fullfill IHS criterias for MI), and secondly, because had the diagnosis been an MI, we would have expected, on MRI, a cerebral infarct involving the posterior circulation rather than the anterior one, as in our patient. Indeed, in case of MI, cerebral infarct mostly involves the posterior circulation. Furthermore, the initial complaint was an sudden language disorder whereas in a typical migraine attack the first symptoms are visual. This finding reinforces the hypothesis that the primum movens is not the migraine with aura attack. Indeed, the initial acute aphasia presented by our patient, corresponded presumably to the stroke onset (well correlated with the left middle cerebral artery territory infarct on DWI sequence), and was followed by progressive sensitive and visual symptoms, corresponding to the infarct-induced MA (well correlated with the extended left hypoperfusion on initial perfusion CT). Some studies also suggest that infarct-induced MA may be more frequent than MI. In the same way, additional investigations should be performed to find what can be hidden behind the new onset of high-frequency aura symptoms or behind a brisk increase in their frequency in patients with a previously achieved diagnosis of migraine with aura (such as vascular but also demyelinating diseases, epileptic or degenerative conditions).
Succinctly then, the take home message is: it is crucial to rule out cerebral infarction in cases where a patient experiences an atypical aura in the context of established migraine.
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