Eisensehr, Ilonka

Hamann, Gerhard F.

Liebetrau, Martin

Mayer, Thomas

English

Gerhard F. Hamann

Ilonka Eisensehr

Thomas Mayer

Martin Liebetrau

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Massive Four-Territories Stroke: Bilateral Middle and Anterior Cerebral Artery Infarctions

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58 Short ReportsEur Neurol 2002;47:58–61Massive Four-Teritories Stroke: Bilateral Middleand Anterior Cerebral Artery InfarctionsGerhard F. Hamann a, Ilonka Eisensehr a, Thomas Mayer bMartin Liebetrau aDepartments of a Neurology and b Neuroradiology, LudwigMaximilians University, Klinikum Grosshadern, Munich,GermanyIntroductionMultiple brain infarction is seen in a limited number of acutestrokes. For example, in the Lausanne stroke register, only 40 of 751patients with acute first-time stroke of the anterior circulation dem-onstrated multiple infarctions [1]. Only 10 of the 40 patients withmultiple brain infarction showed bilateral infarctions, related eitherto cardioembolism or to large artery disease [1]. Using diffusion-weighted sequences (DWI), magnetic resonance imaging (MRI) canevaluate the age of each lesion, determining whether these multiplebrain infarcts occurred simultaneously or singly [2]. Using this sensi-tive technique, it is evident that the rate of multiple infarctions couldbe higher than previously suspected. In another study, among 142patients with acute infarcts, 43 had more than one lesion on diffu-sion-weighted MRI [3]. From these 43 patients, 13 had acute multi-ple infarctions and 6 had multiple new and old strokes. Thus, about15% of all patients experienced acute multiple brain infarctions inthis patient group [3]. This rate is substantially higher than previous-ly reported 5% [1]. Here, we report a most striking case of multiplebrain infarctions involving four cerebral artery territories.Case ReportA woman aged 85 years was admitted to our acute stroke unitwith motor problems and sensory deficit in the left arm. The neuro-logical examination revealed a left-sided paresis of the arm and facialparesis. A history of atrial fibrillation and coronary heart disease wasnoted. The initial MRI examination detected a small lesion on DWIin the right internal capsule. Less than 1.5 cm in diameter, andlocated in the lenticulostriatal territory, this lesion was judged to be alacunar infarction (fig. 1b). Multiple older white matter lesions seem-ingly confirmed this pathophysiological concept. Ultrasonographicinvestigations depicted a stenosis of the right internal carotid artery(ICA) in the carotid siphon area. Magnetic resonance angiography(MRA) confirmed this discovery, showing a signal reduction in theC1 and C2 segment of the right ICA. The MRA of the circulus ofWillis revealed the lack of posterior communicating arteries on bothShort Reports 59Fig. 1. MRI and MRA from the initial investigation (day 1) of ourpatient following her admission with slight hemiparesis of the leftarm. a MRA shows the signal loss in the right ICA in the C1 and C2segment. It is also obvious that both posterior communicating arter-ies are absent. b MRI shows a small signal hyperdensity in the rightinternal capsule at the border zone to the thalamus.sides (fig. 1a). On day 2 after admission, the neurological deficit hadimproved and the patient was apparently symptom free. The neuro-logical examination at this time showed only a slight paresis on theleft side without other symptoms. On day 3, the patient suddenly lostconsciousness. She developed a deep coma without reactivity topainful stimuli and a progressive loss of brain stem reactivity.An MRI on the third day detected bilateral signal intensities onDWI in the territories of the middle cerebral artery (MCA) and ante-rior cerebral artery (ACA) (fig. 2a). On the MRA, both ICAs wereoccluded (fig. 3). The posterior part of the MCA was still partly per-fused, which was proven by MR perfusion images. On the fourth day,the T2 images also showed extensive infarcts in both ACA and MCAterritories, sparing the posterior part of both MCA territories (fig.2b). The patient never regained consciousness and died on the fourthday with signs of transtentorial herniation.The pathological examination showed a small thrombus in theright ICA. The left ICA was recanalized, and no thrombus in theheart or aorta could be found.DiscussionThe patient developed a small infarct in the right internal capsuledue to either a lacunar syndrome, large artery disease of the carotidartery on the right side or atrial fibrillation. The initial MRA showeda stenosis of the right ICA in the C1 and C2 segment, which ultra-sound techniques also proved. Both posterior communicating arter-ies were aplastic, and most of the carotid artery territories in bothhemispheres were supplied by the left ICA. The initial MRA andultrasound investigations demonstrated a normal left ICA withoutstenosis. The sudden deterioration of the patient, 3 days after theinitial symptoms, suggested a basilar artery occlusion. The MRIproved that the basilar artery was open and occlusion of the left ICAhad produced a severe forebrain ischemia in both hemispheres. Thetransient occlusion of the left ICA was probably caused by an acuteembolic mechanism on the basis of the underlying atrial fibrillation.Both the negative MRA and ultrasound investigations before the leftICA occlusion and the open vessel in the pathological examinationsupport this hypothesis. After this, the patient experienced a com-plete forebrain ischemia, which is produced experimentally by liga-tion of both ICAs in rats and gerbils, causing an ideal situation tostudy the effects of global ischemia and the amelioration of thatdevastating state [4]. Taking into account the diverse anatomicalstructures and physiologies of the animals studied, pathologicalexamination does suggest striking similarities [5]. The anomalous-ness of the circulus of Willis with aplasia of both communicating pos-terior arteries was the anatomic substrate which allowed the develop-ment of these extensive bilateral lesions in our patient. The high-grade stenosis of the right ICA was the second prerequisite whichallowed the embolic occlusion of the left ICA to produce a nearlycomplete carotid artery territory stroke in both hemispheres. The sal-vage of the posterior MCA territories on both sides could beexplained by leptomeningeal anastomosis from the posterior cerebralarteries. Previous reports on bilateral ICA disease refer mainly tochronic arterial occlusive disease with rather few neurologicalchanges [6]. In a French group of 19 patients with bilateral ICAocclusion, only minor neurological symptoms were noted. In youngpersons, even acute bilateral ICA occlusion may result in minor neu-rological symptoms. In one report, a young patient was reported tohave suffered from bilateral ICA occlusion by a blunt trauma withonly a narrow visual field deficit [7]. Just one study from Japanreports a 68-year-old woman who experienced sudden onset of comawith bilateral internal carotid occlusion by cardioembolism. Thispatient apparently suffered from a similar infarction type to thatreported here, even though the exact lesion location and size was notdetailed [8].In the opinion of most stroke neurologists, multiple brain infarc-tion is likely caused by cardioembolism; however, recent Korean evi-dence suggests that mainly large vessel disease causes multiple braininfarctions in the anterior circulation [9]. In the instances of Yama-guchi et al. [8], our current case and other severely affected patients, acardioembolic source plus large vessel disease might contribute to thepathophysiological background. Various other mechanisms may alsobe involved in multiple brain infarctions, such as paraneoplasticcoagulation abnormalities, infections and various diseases [1, 10].We conclude that total forebrain ischemia in humans is a rare butdevastating condition. Prerequisites can be assumed, such as severecarotid stenosis, absence of a functional collateral system via the cir-culus of Willis and the combination of large artery disease and a car-dioembolic source. The clinical presentation may mimic the onset ofacute basilar occlusion.60 Short ReportsFig. 2. a Diffusion-weighted MRI on thethird day reveals the diffusion deficit in bothACA and most of both MCA territories.b The T2 images from the MRI on the fourthday show a similar distribution to that pre-viously noted on DWI.Fig. 3. MRA after the onset of coma on day3 shows a loss of signal in both ICA territo-ries. Note the absence of any carotidal ves-sels in the intracranial portion.Short Reports 61References1 Bogousslavsky J, Bernasconi A, Kumral E: Acute multiple infarctioninvolving the anterior circulation. Arch Neurol 1996;53:50–57.2 Fitzek C, Tintera J, Muller-Forell W, Urban P, Thomke F, Fitzek S, HopfHC, Stoeter P: Differentiation of recent and old cerebral infarcts by diffu-sion-weighted MRI. Neuroradiology 1998;40:778–782.3 Altieri M, Metz RJ, Muller C, Maeder P, Meuli R, Bogousslavsky J: Multi-ple brain infarcts: Clinical and neuroimaging patterns using diffusion-weighted magnetic resonance. Eur Neurol 1999;42:76–82.4 Dirnagl U, Thoren P, Villringer A, Sixt G, Them A, Einhaupl KM: Globalforebrain ischaemia in the rat: Controlled reduction of cerebral blood flowby hypobaric hypotension and two-vessel occlusion. Neurol Res 1993;15:128–130.5 Ogata J, Fujishima M, Morotomi Y, Omae T: Cerebral infarction followingbilateral carotid artery ligation in normotensive and spontaneously hyper-tensive rats: A pathological study. Stroke 1976;7:54–60.6 Catala M, Rancurel G, Raynaud C, Leder S, Kieffer E, Koskas F: Bilateralocclusion of the internal carotid arteries. Analysis of a series of 19 patients(in French). Rev Neurol (Paris) 1995;151:648–656.7 Sadun AA, Sebag J, Bienfang DC: Complete bilateral internal carotidartery occlusion in a young man. J Clin Neuroophthalmol 1983;3:63–66.8 Yamaguchi S, Oki S, Ogasawara H, Sato H, Ito Y, Hibino S: A case ofsimultaneous bilateral carotid occlusion (in Japanese). No Shinkei Geka1997;25:247–251.9 Roh JK, Kang DW, Lee SH, Yoon BW, Chang KH: Significance of acutemultiple brain infarction on diffusion-weighted imaging. Stroke 2000;31:688–694.10 Vassallo R, Remstein ED, Parisi JE, Huston J, Brown RD: Multple cere-bral infarctions from nonbacterial thrombotic endocarditis mimickingcerebral vasculitis. Mayo Clin Proc 1999;74:798–802.Prof. Dr. Gerhard Hamann, Department of NeurologyLudwig Maximilians University, Klinikum GrosshadernMarchioninistrasse 15, D–81377 Munich (Germany)Tel. +49 89 7095 3670, Fax +49 89 7095 3677E-Mail hamann@brain.nefo.med.uni-muenchen.de

Chang KH: Significance of acute multiple brain infarction on diffusion-weighted imaging. Stroke 2000;31:

DC: Complete bilateral internal carotid artery occlusion in a young man.

Einhaupl KM: Global forebrain ischaemia in the rat: Controlled reduction of cerebral blood flow by hypobaric hypotension and two-vessel occlusion. Neurol Res 1993;15:

Hibino S: A case of simultaneous bilateral carotid occlusion (in Japanese). No Shinkei Geka

Koskas F: Bilateral occlusion of the internal carotid arteries. Analysis of a series of 19 patients (in French). Rev Neurol

Kumral E: Acute multiple infarction involving the anterior circulation.

Multiple brain infarcts: Clinical and neuroimaging patterns using diffusionweighted magnetic resonance. Eur Neurol 1999;42:76–82.

Omae T: Cerebral infarction following bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats: A pathological study.

RD: Multple cerebral infarctions from nonbacterial thrombotic endocarditis mimicking cerebral vasculitis. Mayo Clin Proc 1999;74:798–802.

Stoeter P: Differentiation of recent and old cerebral infarcts by diffusion-weighted MRI.

Massive four-teritories stroke: Bilateral middle and anterior cerebral artery infarctions

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Massive four-teritories stroke: Bilateral middle and anterior cerebral artery infarctions

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