Discrete progression of migraine-induced focal cerebral infarction.

Migraine-induced infarction is rare and possibly overdiagnosed [1]. Although the relationship between migraine and stroke has historically been a subject of controversy, recent evidence has lent support to the notion that migraine and stroke are co-morbid conditions linked by complex pathophysiological processes [2]. Migraine with aura is more clearly associated with increased stroke risk than is common migraine, with studies implicating smoking [3] and elevated plasma homocysteine [4], among a host of factors, as mediating risk. There appears to be a predilection for stroke localization within the posterior cerebral artery (PCA) territory [5]. The patient reported herein represents an example of migraine-induced infarction. A 66-year-old man with a history adolescent-onset classic migraine presented with prolongation of his typical symptoms, consisting of scintillating scotoma in the right visual field, followed by perioral parethesia, mild dysarthria, and anomic aphasia, and concluding with relatively mild occipital headache. Typical frequency was one to four episodes monthly with a duration of 3–4 h each. In contrast, the duration of the presenting episode was protracted, lasting between 48 and 72 h. Symptoms responded briskly to solumedrol 125 mg IV and subcutaneous sumatriptan 6 mg. The patient reported one other life-time episode suggesting migraine status several years previously with no residual symptoms. The neurological examination was unremarkable; subjectively, however, the patient reported persisting visual scotoma located 10 –15 to the right of foveation. Since the event, he also complained of increased forgetfulness requiring the use of compensatory lists and which contributed to his decision to delegate responsibility for managing the family finances to his spouse. Neuropsychological evaluation revealed deficits in memory for verbal material and confrontation naming; his MMSE score was 27/30. MRI with contrast revealed a focal gyral pattern of signal hyperintensity on T1-, T2-weighted, and FLAIR sequences, with associated heterogeneous enhancement consistent with laminar necrosis from evolving subacute to chronic infarction in the left PCA distribution, affecting the mesial occipital region. Scattered, punctate areas of T2 and FLAIR hyperintensity were also noted in subcortical white matter (Fig. 1). Mass lesion, vascular malformation, and focal cerebritis were excluded. EEG obtained 2 years prior to that event was normal, effectively ruling out seizure disorder. Carotid Doppler study showed mild stenosis (16–49 %) of the internal carotid arteries bilaterally. Pertinent laboratory studies including ESR (10) and CRP (0.411) were normal, but homocysteine was elevated (15.1). TSH, vitamin B12, folate, and RPR were unremarkable. Migraine status with characteristic aura recurred 21 months later. Neurological examination following that event was remarkable only for a homonymous right superior quandrantanopia. Follow-up neuropsychological evaluation showed interval decline in memory, speed of visual search, cognitive flexibility, problem solving, and S. P. Cercy (&) Department of Psychiatry, New York University School of Medicine, 423 E 23rd Street, New York, NY 10010, USA e-mail: Steven.Cercy@va.gov