e134 A 48-year-old white man who was healthy previously presented from an outside hospital with weakness of the bilateral lower extremities and right upper extremity. He awoke at 3 AM in morning on the day of initial presentation with unexplained urinary incontinence and diaphoresis. His symptoms resolved, and he went back to bed. At 7 AM, he dropped his daughter off at daycare; this was the last known normal time. At 7:15 AM, he was stopped by the police because of erratic driving. Although details of his condition at that time are sketchy, it seems, he was not following commands. Paramedics were called, and he was taken to a community hospital where he was described as shivering, staring, mute, and not following commands with left gaze deviation and ple- gia of both lower extremities and the right upper extremity; the left arm moved purposefully with full strength. He had an episode of vomiting and difficulty managing his secretions. Computed tomogragphy scan of the head was unremarkable, and the diagnosis remained uncertain. Because of his shiver- ing, he was loaded with phenytoin for possible seizures and transferred to a tertiary care hospital for further evaluation. On arrival, he was not following any commands and found to have copious oral secretions that prompted emergent intu- bation for airway protection. As in the outside hospital, both lower extremities and the right arm were plegic. The left hand moved purposefully. He had extensor posturing of both lower limbs and the right upper limb with noxious stimuli. There was sustained clonus and bilateral plantar extension reflexes pres- ent in both lower limbs. Emergent magnetic resonance imag- ing of the brain showed an acute to subacute infarction in the bilateral frontal lobes, bilateral basal ganglia, and left frontal operculum. Magnetic resonance angiography showed that the right A1 segment of the anterior cerebral artery (ACA) was absent and that both ACA territories were supplied by the left anterior circulation (Figure 1A). Intracranial and extracranial magnetic resonance angiography was otherwise unremarkable. No intravenous tissue-type plasminogen activator was admin- istered as the patient was beyond the 4.5-hour therapeutic time window. Endovascular treatment was not pursued because of the large infarct volume. Follow-up magnetic resonance imaging the next day showed a completed left middle cere- bral artery and bilateral ACA infarctions (Figure 1B). Because of his large infarct volume, he required hemicraniectomy for malignant cerebral edema. The patient required a tracheostomy and percutaneous gastrostomy tube for feeding. After the first few days, he lost movement in the left upper extremity because of worsening edema with mass effect. An embolic mechanism was suspected although work-up did not reveal an embolic source. The patient was eventually discharged to a long-term care facility after placement of a tracheostomy tube and a percu- taneous gastrostomy tube. At the time of discharge, he had spontaneous eye opening, did not follow commands, and had bilateral upper extremity extension with bilateral lower extremity triple flexion to noxious stimuli. Discussion This patient appeared to suffer an embolus within the left carotid that occluded the branches of the left middle cerebral artery and both ACAs. In this case, the right A1 segment of the ACA was absent and the right ACA territory was sup- plied from the left via the left anterior communicating artery (Figure 1). Bilateral ACA stroke is unusual, but there are some cases in the literature. Bogousslavsky et al 1 reported only 2 cases of bilateral ACA stroke of 1490 stroke cases. Borgreeve et al 2 reported a case in 1994 in which the patient presented with aphasia, right hemiplegia, plegia of the left leg, and pare- sis of the left arm. Postmortem analysis revealed bilateral ACA infraction caused by thrombosis of a distal left ACA that supplied both ACA territories. Anatomy of the ACA and Normal Variants The ACA supplies the medial and lateral convexities of the frontal and parietal lobes, as well as the anterior limb of inter- nal capsule, inferior head of the caudate, part of inferior puta- men, globus pallidus, part of hypothalamus, anterior column of fornix, and corpus callosum are also supplied by the ACA. 2 Although each hemisphere typically is supplied by an ipsilat- eral ACA (Figure 2A), several anatomic variants of the ACA Acute Cerebral Infarction Presenting With Weakness in Both Legs and One Arm Kunal Kumar, MD; Daniel Strbian, MD, PhD; Sophia Sundararajan, MD, PhD Received March 6, 2015; final revision received March 6, 2015; accepted March 9, 2015. From the Neurological Institute, University Hospitals Case Medical Center, Cleveland, OH (K.K., S.S.); and Department of Neurology and Stroke Unit, Helsinki University Central Hospital, Helsinki, Finland (D.S.). Correspondence to Sophia Sundararajan, MD, PhD, Neurological Institute, University Hospitals/Case Medical Center, 11100 Euclid Ave, Cleveland, OH 44106. E-mail sophia.sundararajan@UHhospitals.org (Stroke. 2015;46:e134-e136. DOI: 10.1161/STROKEAHA.115.008983.) © 2015 American Heart Association, Inc. Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.115.008983 Section Editors: Daniel Strbian, MD, PhD, and Sophia Sundararajan, MD, PhD Illustrative Teaching Cases by guest on April 9, 2017 http://stroke.ahajournals.org/ Downloaded from