Acute ischemic stroke in anterior choroidal artery territory

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Abstract

Objective

The aim of the study was to describe a series of patients with acute ischemic infarct in the anterior choroidal artery (AChA) territory. Moreover, we analyzed the prevalence of these strokes and compared them with hemispheric and deep infarcts. Finally, we hypothesized that the size of the infarct could be related to aetiology and prognosis.

Methods

We studied a prospective series of 1350 patients with acute ischemic stroke. We analyzed the following factors: age, gender, diabetes mellitus, hypertension, hyperlipidaemia, current smoking, ischemic heart disease, previous stroke, peripheral arterial disease, prior antithrombotic treatment, major cardioembolic source, severe arterial stenosis, initial severity, progression, mortality, disability, and recurrence rate at three months. AChA strokes were classified as small (< 20 mm) or large (≥ 20 mm), as measured by diffusion-weighted MRI, and compared by size in the analysis.

Results

112 patients (8.3%) had an ischemic lesion restricted to the AChA territory (large: 42 patients, small: 70 patients). Patients with AChA infarcts were younger, more likely to be diabetic, and predominantly male. We found significant differences in the rate of major embolic sources, recurrence, progression and prognosis. Large AChA strokes were associated with embolic pathologies and had worse prognosis than small AChA strokes.

Interpretation

Infarcts in the AChA territory have different aetiological mechanisms and outcome than other territories. Large AChA infarcts have a higher association with an embolic source and worse prognosis than small lesions.

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).

References (40)

  • A.A. Abbie

    The blood supply of the lateral geniculate body, with a note on the morphology of the choroidal arteries

    J Anat

    (1933)
  • N. Saeki et al.

    Microsurgical anatomy of the upper basilar artery and the posterior circle of Willis

    Neurosurgery

    (1977)
  • J.P. Decroix et al.

    Infarction in the territory of the anterior choroidal artery. A clinical and computerized tomographic study of 16 cases

    Brain

    (1986)
  • P.m. Pullicino

    Diagrams of perforating artery territories in axial, coronal and sagitall planes

    Adv Neurol

    (1993)
  • X.L. Hamoir et al.

    MRI of hyperacute stroke in the AchA territory

    Eur Radiol

    (2004)
  • J. Mohr et al.

    The anterior choroidal artery does not supply the corona radiata and lateral ventricular wall

    Stroke

    (1991)
  • R.M. Hupperts et al.

    Infarcts in the anterior choroidal artery territory. Anatomical distribution, clinical syndromes, presumed pathogenesis and early outcome

    Brain

    (1994)
  • A. Bruno et al.

    Anterior choroidal artery territory infarction: a Small Vessel Disease

    Stroke

    (1989)
  • C.M. Helgason

    A new view of anterior choroidal artery territory infarction

    J Neurol

    (1988)
  • J. Ghika et al.

    Infarcts in the territory of the deep perforators from the carotid system

    Neurology

    (1989)
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