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Posterior Cerebral Artery Infarction from Middle Cerebral Artery Infarction

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Posterior Cerebral Artery Infarction from Middle Cerebral Artery Infarction ORIGINAL CONTRIBUTION Posterior Cerebral Artery Infarction From Middle Cerebral Artery Infarction Alexandre B. Maulaz, MD; Daniel C. Bezerra, MD; Julien Bogousslavsky, MD Background: While it is known that posterior cerebral the superficial PCA territory (66.7%), followed by the artery (PCA) infarction may simulate middle cerebral ar- proximal PCA territory (16.7%) and both the proximal tery (MCA) infarction, the frequency and localization of and the superficial PCA territories (16.7%). The princi- this occurrence are unknown. pal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proxi- Objective: To determine the frequency of PCA infarc- mal PCA territory, and undetermined (40.2%) in both tion mimicking MCA infarction and the territory of the the proximal and the superficial territories. Among the PCA most commonly involved in this simulation. 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 pa- Design: We studied 202 patients with isolated infarc- tients), and severe hemiparesis (7 patients). tion in the PCA admitted to our stroke center to deter- mine the frequency of PCA infarction simulating MCA Conclusions: Posterior cerebral artery infarction simu- infarction, the involved PCA territory, and the patterns lating MCA infarction is more common than previously of clinical presentation. thought. Early recognition of the different stroke sub- types in these 2 arteries may allow specific manage- Results: We found 36 patients (17.8%) with PCA is- ment. chemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was Arch Neurol. 2005;62:938-941 HE CLINICAL SYNDROME OF lyzed, but only one study,4 to our knowl- acute hemiparesis, hemisen- edge, has described a series of patients with sory loss, hemianopia, vi- proximal PCA occlusion simulating MCA suospatial neglect, and apha- occlusion. We assess the clinical features, sia is generally attributed to frequency, and involved PCA territories of Tinfarctions of the middle cerebral artery the infarction mimicry between these 2 ar- (MCA). However, the same clinical fea- teries. tures can be present in posterior cerebral ar- tery (PCA) strokes. Misdiagnosis may lead METHODS to erroneous decisions in clinical manage- ment. A patient with a hyperacute PCA stroke simulating an MCA stroke has a We studied all patients with a first, isolated in- higher probability of having a normal re- farction restricted to the PCA who were ad- mitted to our stroke center between January sult on a computed tomographic scan. Be- 1, 1983, and December 31, 2003. The pa- cause the stroke mechanisms are different tients’ data were encoded prospectively into the 1 for these 2 arteries, a precise anatomical di- computerized Lausanne Stroke Registry.5 We agnosis is of extreme importance to guide included patients in whom brain images early stroke therapy and may have poten- showed infarctions involving only the PCA. We tial implications for treatment and out- excluded all patients with uncertain neurora- come.2 Recognition of the most common diological confirmation of PCA ischemia, pa- clinical presentations of this mimicry may tients with an associated stroke in the ante- prompt a physician to question an initial di- rior circulation or brainstem (except the agnosis. Although PCA stroke may occur midbrain), patients with degenerative dis- eases, and patients with extensive white mat- in the presence of a fetal pattern and con- ter disease, which could confound the neuro- Author Affiliations: Service de sequently with mechanisms and outcomes logical examination. Also, we did not include Neurologie, Centre Hospitalier that follow MCA stroke, this happens in patients in whom the stroke diagnosis was un- Universitaire Vaudois, fewer than 11% of individuals.3 The clini- certain. All patients underwent a standard neu- Lausanne, Switzerland. cal features of PCA strokes have been ana- rological and neuropsychological examina- (REPRINTED) ARCH NEUROL / VOL 62, JUNE 2005 WWW.ARCHNEUROL.COM 938 ©2005 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 Table 1. Baseline Patient Data* All Patients PPCA Group SPCA Group P؉SPCA Group Risk Factor (N = 202) (n = 80) (n = 72) (n = 50) Hypertension 84 (41.6) 28 (35.0) 31 (43.1) 25 (50.0) Diabetes mellitus 36 (17.8) 14 (17.5) 15 (20.8) 7 (14.0) Smoker Active 46 (22.8) 19 (23.8) 17 (23.6) 10 (20.0) Former 25 (12.4) 8 (10.0) 9 (1.3) 8 (16.0) Coronary artery disease 32 (15.8) 6 (7.5) 16 (22.2) 10 (20.0) Potential cardioembolic source6 76 (37.6) 25 (31.3) 37 (51.4) 14 (28.0) Peripheral arterial disease 12 (5.9) 1 (1.3) 9 (12.5) 2 (4.0) Previous transient ischemic attack 31 (15.3) 13 (16.3) 10 (13.9) 8 (16.0) Abbreviations: PPCA, proximal posterior cerebral artery; PϩSPCA, proximal and superficial posterior cerebral artery; SPCA, superficial posterior cerebral artery. *Data are given as number (percentage). tion and systematic investigations, including brain computed tomography, Doppler ultrasonography, electrocardiography, and Undetermined Other routine blood tests. Magnetic resonance imaging, magnetic reso- Cardioembolic nance angiography, arteriography, transthoracic and trans- Lacunar esophageal echocardiography, and 24-hour electrocardio- Atherothrombotic graphy Holter monitoring were performed on selected patients. The demographic characteristics, cerebrovascular risk fac- Superficial tors, clinical features, and probable etiology of stroke were as- sessed using the TOAST (Trial of ORG 10172 in Acute Stroke Proximal Treatment) classification.6 Strokes were divided into 3 groups ac- Proximal and cording to the infarction location as seen on neuroimaging: (1) Stroke Localization Superficial proximal or deep (PPCA), (2) superficial or cortical (SPCA), or (3) both (PϩSPCA). Proximal PCA infarctions mimic MCA stroke 0 102030405060 differently from SPCA infarctions. A PPCA localization was de- Frequency, % fined as involving the midbrain, thalamus, and posterior limb of the internal capsule.7 An SPCA localization was defined as in- Figure 1. Frequency of stroke subtypes. volving the territories of the anterior and posterior temporal, cal- carine, and parietooccipital arteries.7 We defined a PCA infarc- 61 years (PPCA group, 60 years; SPCA group, 62 years; tion simulating an MCA infarction as a PCA stroke with the signs ϩ and symptoms reported as typical of an MCA stroke, combined and P SPCA group, 58 years). The lesions were lo- with the absence of classic findings of PCA infarction. The fol- cated in the left hemisphere in 111 patients (55.0%), the lowing signs and symptoms of PCA infarction were considered right in 79 (39.1%), and bilaterally in 12 (5.9%). classic8-10: sensory deficits, movement disorders, third nerve palsy, The presumed etiologies are presented in Figure 1. and vertical gaze abnormalities for PPCA lesions; headache, vi- The main cause of all PCA strokes was cardioembolism sual field defects and visual hallucination, perseveration, and ag- (39.4%), followed by undetermined (26.9%), lacunar nosia for SPCA lesions; and discrete motor abnormalities, head- (19.4%), and atherothrombotic (13.5%) etiologies. When ϩ ache, visual field defects, and sensory deficits for P SPCA lesions. we analyzed each PCA territory separately,the most com- Aphasia and visuospatial neglect were considered typical of PCA mon etiologies for PPCA infarctions were lacunar (46.2%) stroke only in PPCA infarctions, because the former may be found Ͻ in up to 50% of left thalamic lesions11 and the latter in up to 62% and cardioembolic (30.2%) (P .01), while cardioem- 12 bolic (54.1%), undetermined (23.3%), and atherothrom- of right thalamic lesions. Moreover, the frequencies of aphasia Ͻ and visuospatial neglect are 0% to 8%13-15 and 7% to 12%,8,9,15 re- botic (19.9%) etiologies (P .002) were the most fre- spectively, in patients with SPCA stroke. Severe motor defi- quent for SPCA infarctions. The presumed causes of cit,16-18 alien hand syndrome,19 grasping,20 and asterixis21 are atypi- PϩSPCA stroke were undetermined (40.2%), cardioem- cal but have been reported in PCA stroke. bolic (34.2%), and atherothrombotic (19.9%) (PϽ.001). Categorical data are presented as percentages and were ana- The clinical features are summarized in Table 2. The lyzed using ␹2 test and estimated 95% confidence intervals. Sta- most common clinical findings were motor weakness (114 tistical analysis was performed using SPSS version 11.0 (SPSS Inc, Ͻ patients [56.4%]), visual field abnormalities (106 pa- Chicago, Ill). P .05 was considered statistically significant. tients [52.5%]), and sensory deficits (91 patients [45.0%]). Posterior cerebral artery infarctions simulating MCA RESULTS infarctions occurred in 36 patients (17.8%) (Figure 2). Of these, 24 (66.7%) involved the SPCA, 6 (16.7%) the We initially identified 391 patients with a first symp- PPCA, and 6 (16.7%) the PϩSPCA territories. The most tomatic event in the PCA; after applying the exclusion common etiology for all PCA infarctions combined was criteria, 202 patients remained for analysis. The distri- cardioembolic (38.8%) (P=.04). bution of clinical features and risk factors is summa- For all 36 PCA strokes simulating MCA infarctions, rized in Table 1. Of the 202 patients, 122 (60.4%) were the most common clinical signs were aphasia (13 pa- men, and the mean age at onset for all PCA strokes was tients [36.1%]), visuospatial neglect (13 patients [36.1%]),
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