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 determine 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 subtypes 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 infarctionsT 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 artery (PCA) strokes. Misdiagnosis may lead METHODS to erroneous decisions in clinical management. 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 admitted 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-

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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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All Patients PPCA Group SPCA Group P؉SPCA Group Finding (N = 202) (n = 80) (n = 72) (n = 50) Motor deficit 114 (56.4) 50 (62.5) 26 (36.1) 38 (76.0) Visual field defect 106 (52.5) 1 (1.3) 64 (88.9) 41 (82.0) Sensory deficit 91 (45.0) 48 (60.0) 7 (9.7) 36 (72.0) Headache 59 (29.2) 12 (15.0) 26 (36.1) 21 (42.0) Abnormal movement 12 (5.9) 6 (7.5) 2 (2.8) 4 (8.0) Neuropsychological deficit Aphasia 28 (13.9) 13 (16.3) 1 (1.4) 14 (28.0) Visuospatial neglect 52 (25.7) 19 (23.8) 11 (15.3) 22 (44.0) Memory 66 (32.7) 24 (30.0) 15 (20.8) 27 (54.0)

30 COMMENT Undetermined Other 25 Cardioembolic Lacunar To our knowledge, this is the first large clinical study that Atherothrombotic 20 has focused on the frequency of PCA infarctions mimicking MCA infarctions. Chambers et al4 described 12 pa- 15 tients with PPCA occlusion in whom the initial clinical

Frequency, % Frequency, diagnosis was an MCA infarction. That study did not es- 10 timate the frequency of such misdiagnosis, and infarc- 5 tions of the SPCA territory were not considered. Chavot et al22 identified mimicry of MCA infarctions in 18.5% 0 Proximal Superficial Proximal and of PCA infarctions but did not distinguish between PPCA Superficial and SPCA strokes and did not specify the criteria for di- agnosing the simulation. Figure 2. Frequency of posterior cerebral artery strokes simulating middle The most common abnormality of hemispherical PCA cerebral artery strokes. infarctions is contralateral visual field defects due to infarction of the striate cortex or the optic radiations.8,14,23,24 As shown in Table 2, this was also the most common find- Table 3. Patients With Posterior Cerebral Artery Stroke ing in SPCA (88.9%) and PϩSPCA (82.0%) strokes in our Simulating Middle Cerebral Artery Stroke study. Sensory symptoms and signs are the second most frequent clinical manifestation of PCA stroke, present in PPCA Group SPCA Group P؉SPCA Group 9,14 Localization (n=6) (n = 24) (n=6) 40% to 46% of patients. The high frequency is probably due to the inclusion of patients with thalamic infarctions. Severe motor deficit 3 1 3 Furthermore, Georgiadis et al25 suggest that the presence Asterixis 2 0 3 Palmomental reflex 11 0 of sensory symptoms or signs in patients with PCA occlu- plus grasping sive disease indicates lateral thalamic ischemia. Our series Visuospatial neglect 0 8 0 confirms this observation, as only 9.7% of our patients with Aphasia 0 9 0 hemispherical PCA stroke had sensory abnormalities. More- Visuospatial neglect 04 0 over, sensory deficits were found in 60.0% of patients with plus aphasia Palmomental reflex plus 01 0 PPCA territory infarctions and in 72.0% of patients with ϩ 15,26 visuospatial neglect P SCPA territory infarctions. In studies of series of patients with SPCA infarctions, motor deficits were re- Abbreviations: PPCA, proximal posterior cerebral artery; PϩSPCA, ported in 28% of patients. In our study, motor deficits were proximal and superficial posterior cerebral artery; SPCA, superficial posterior seen in 36.1% of patients with SPCA infarction vs 56.4% cerebral artery. of patients in the entire cohort. In addition, there are a few recorded cases of hemiplegia in patients with PCA infarctions,16-18,27 mainly as a result of lesions of the cerebral pe- and severe hemiparesis (7 patients [19.4%]), but these duncle or the anterior segment of the posterior limb of the findings were not statistically significant (PՆ.3) internal capsule, and this is the main clinical feature dis- (Table 3). The main clinical findings associated with tinguishing PPCA infarctions from other types of PCA the simulation were the following: in the PPCA terri- strokes.7,23 Aphasia can occur in dominant hemisphere in- tory, severe motor deficits (50.0%) and asterixis (33.3%); farctions involving the ventral lateral thalamic nucleus.11 in the SPCA territory, aphasia (54.1%) and visuospatial Although rare, anomic and transcortical sensory aphasia neglect (54.1%); and in the PϩSPCA territories, severe has been documented in patients with large infarctions in- motor deficits (50.0%) and asterixis (50.0%). volving the left posterior temporal artery.12,13 In our se-

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©2005 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 ries, aphasia was present in only 1.4% of patients with SPCA terial support: Maulaz and Bezerra. Study supervision: lesions but in 28.0% of patients with PϩSPCA lesions. This Bogousslavsky. high frequency of aphasia in thalamic strokes confirms the Funding/Support: This study was supported in part by role of this area in language disturbances. Visuospatial ne- grants from the Switzerland Federal Commission for glect is uncommon in SPCA infarctions. However, in PPCA Scholarships for Foreign Students, Berne. strokes, this clinical feature may be found in 17.5% to 60% of patients due to paramedian12 and tuberothalamic11 infarctions. In the present series, frequencies of visuospatial REFERENCES neglect in SPCA, PPCA, and PϩSPCA strokes were 15.3%, 23.8%, and 44.0%, respectively. 1. Bamford J, Sandercock P, Dennis M, Burn J, Warlow C. 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