Acute ischemic stroke in anterior choroidal artery territory
Introduction
In 1925, Foix [1] described the Anterior choroidal artery (AChA) syndrome, which includes, in its complete form, the triad of hemiparesis, hemianaesthesia, and hemianopia. The AChA is a small artery that commonly originates in the posterior wall of the internal carotid, 2 to 5 mm distal to the posterior communicant artery (PCoA) and 2 to 5 mm proximal to the intracranial carotid bifurcation in 96–99.5% of cases [2]. The AChA territory shows large variations amongst individuals. The most reported supply areas include: the posterior limb of the internal capsule, optical tract, lateral geniculate body, medial temporal lobe, and medial part of the pallidum [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]. Other territories, such as the lateral thalamic border and the medial part of the lentiform nucleus, are still subject to debate, although the most controversial territory is the posterior paraventricular territory [5], [13], [14], [15]. Despite its small size (0.5–2.0 mm), the AChA has perforating branches (between 2 and 9 AChA perforators with a diameter that varies from 90 to 600 µM) that have been identified in microdissection studies [16].
The origin and incidence of AChA infarcts is controversial [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [33], [34], [35]. It has been postulated that AChA infarcts are due to Small Vessel Disease (SVD) [17], [18], [19], although other studies related AChA infarcts to Large Vessel Disease (LVD) [20], [21], [22], cardioembolic, or other determined or undetermined causes [15], [23], [24], [25]. Moreover, there are few studies of prognosis in AChA infarcts and most of them are case studies [18]. The main objective of our study was to study the vascular risk factors, aetiology and clinical evolution in patients with AChA infarct and compare them with unselected patients with ischemic lesion at other deep or cortical sites. Additionally, we evaluated whether the ischemic lesion size, dichotomized at 20 mm in patients with AChA infarct, allowed us to establish potential causes of stroke or provided prognostic data.
Section snippets
Patients and methods
From January 2003 to January 2007, 1669 consecutive patients with a diagnosis of acute ischemic stroke were prospectively evaluated at Hospital del Mar during the first 24 h after symptoms onset. We excluded 231 patients who presented transient ischemic stroke without radiological ischemic lesion and 88 patients without definitive localization of the ischemic lesion or lost during follow-up. The study included 1350 patients.
Stroke localization
All radiological data were interpreted by trained radiologists (XP, AS), who were blind to patient data. All patients had a computed tomography (CT) study at hospital admission. New radiological studies [CT: (n = 456); Magnetic Resonance Imaging (MRI) (n = 669)] were performed during hospitalization to identify the ischemic lesion; when the infarct involved the AChA territory, the lesion was measured by MRI. Patients were classified in three groups: deep infarcts, including brainstem infarcts (n =
Vascular risk factors
Vascular risk factors were defined as follows: hypertension (patient's self-report of hypertension, use of antihypertensive drugs, or a systolic blood pressure > 160 mm Hg and diastolic blood pressure > 90 mm Hg, recorded at least two weeks after stroke onset); diabetes mellitus (fasting blood glucose level 120 mg/dl, patient's self-report of diabetes, or use of specific medication); hyperlipidaemia (cholesterol > 200 mg/dl or triglycerides > 150 mg/dl, patient's self-report of hyperlipidaemia, or
Potential underlying stroke causes
All patients had an extra and intracranial arterial study. The arterial stenosis was established by concordance in at least two of the following neurovascular explorations: continuous Doppler, high-resolution echography techniques, MRI-angiography, CT-angiography or digital angiography (performed only in 86 patients). Cardiologic study included at least 24 h of cardiac monitoring or EKG recording and transthoracic or transoesophageal echocardiography. Presence of severe arterial stenosis
Clinical and prognostic data
Initial clinical severity was measured with the National Institutes of Health Stroke Scale (NIHSS) at hospital admission. Clinical progression was defined as the worsening by 4 or more points on the NIHSS within the first 72 h from stroke onset. The outcome was established at three months, either by clinical examination in the hospital or by telephone interview (n = 186). Moderate–severe disability (3 to 5 points in the modified Rankin Scale) was considered a poor outcome. We also documented
Statistical analysis
Univariate analysis was performed with the Chi2 test for dichotomous variables. Continuous variables were tested by the t-test or the Mann–Whitney test if normality was difficult to assume. The adjusted odd ratios (OR) were obtained by a logistic regression model including the factors showing an association in univariate analysis (p < 0.1). In the first part of the study, we compared the registered variables according to the topographic location of ischemic lesion: AChA infarct, hemispheric
Ethics
The data for the study were collected from our hospital's prospective clinical protocols, which comply with the local ethics guidelines.
Results
We analyzed 1350 patients with an acute ischemic stroke: mean age 74.1 (SD: 11.6), range 26 to 99; 625 males (51.7%) and 585 females (48.3%). Patients excluded by incomplete data or follow-up were older (mean 78.3 ± 8.2) but had no differences in initial stroke severity, poor outcome at hospital discharge (15/111) or vascular risk factors (p < 0.001).
The study detected 112 patients (8.3%) with AChA infarct, 377 patients (27.9%) with deep infarct, and 861 patients (63.8%) with hemispheric infarcts.
Discussion
There is scarce information in the literature concerning the prevalence of AChA infarcts in patients with acute ischemic stroke. The main drawback is the heterogeneity of the series studied, with most being a selected series of patients. Other studies include infarcts not limited to the AChA territory, with AChA strokes accounting for 2.9% to 11% of patients with acute ischemic stroke [13], [15], [34], [35]. None of these studies has been able to provide the prevalence of AChA strokes from the
Conclusion
Due to its location and size, the AChA constitutes a special territory where concurrent pathophysiological mechanisms may coexist. Moreover, AChA infarcts have different prognosis than hemispheric or deep ischemic strokes. The size of the ischemic lesion, dichotomized at 20 mm, could be a useful tool for studying the aetiology. In large infarcts, it is important to perform a comprehensive vascular study to rule out embolic sources.
Acknowledgments
This study was funded in part by the Ministry of Health, Instituto de Salud Carlos III (Red HERACLES RD06/0009).
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