Predictors of recurrent stroke in patients with symptomatic intracranial arterial stenosis.

BACKGROUND AND PURPOSE: Our goal was to investigate whether initial ischemic lesion pattern can predict stroke recurrence in patients with symptomatic intracranial arterial stenosis. METHODS: Of the Trial of Cilostazol in Symptomatic Intracranial Arterial Stenosis (TOSS)-2 trial participants, we included patients who underwent diffusion-weighted imaging and fluid attenuation inversion recovery imaging at baseline with a follow-up fluid attenuation inversion recovery imaging at 7 months. Based on the diffusion-weighted imaging findings, we classified the initial ischemic lesion patterns according to location (subcortical versus cortical versus subcorticocortical) and multiplicity (single versus multiple). We also evaluated the occurrence of new ischemic lesions on follow-up fluid attenuation inversion recovery as well as clinical stroke in the symptomatic intracranial arterial stenosis territory. RESULTS: Of 353 patients included in this study, 44 (12.5%) and 13 (3.7%) patients had new ischemic lesions and clinical recurrent stroke in the initial symptomatic intracranial arterial stenosis territory, respectively. On multivariable analysis, the initial lesion patterns of subcorticocortical and multiple lesions were independent predictors of new ischemic lesions in the symptomatic intracranial arterial stenosis territory (OR, 3.01; 95% CI, 1.33-7.01; P=0.03; OR, 2.81; 95% CI, 1.34-5.9; P=0.006). These patterns also predicted clinical recurrent stroke. CONCLUSIONS: Subcorticocortical lesions and multiple lesions are radiological predictors of recurrent ischemic stroke in symptomatic patients with intracranial arterial stenosis. Clinical Trial Registration- URL: www.clinicaltrials.gov. Unique identifier: NCT00130039.

The course and outcome of unilateral intracranial arteriopathy in 79 children with ischaemic stroke.

Arteriopathies are the commonest cause of arterial ischaemic stroke (AIS) in children. Repeated vascular imaging in children with AIS demonstrated the existence of a 'transient cerebral arteriopathy' (TCA), characterized by lenticulostriate infarction due to non-progressive unilateral arterial disease affecting the supraclinoid internal carotid artery and its proximal branches. To further characterize the course of childhood arteriopathies, and to differentiate TCA from progressive arterial disease, we studied the long-term evolution of unilateral anterior circulation arteriopathy, and explored predictors of stroke outcome and recurrence. From three consecutive cohorts in London, Paris and Utrecht, we reviewed radiological studies and clinical charts of 79 previously healthy children with anterior circulation AIS and unilateral intracranial arteriopathy of the internal carotid bifurcation, who underwent repeated vascular imaging. The long-term evolution of arteriopathy was classified as progressive or TCA. Clinical and imaging characteristics were compared between both groups. Logistic regression modelling was used to determine possible predictors of the course of arteriopathy, functional outcome and recurrence. After a median follow-up of 1.4 years, 5 of 79 children (6%) had progressive arteriopathy, with increasing unilateral disease or bilateral involvement. In the others (94%), the course of arteriopathy was classified as TCA. In 23% of TCA patients, follow-up vascular imaging showed complete normalization, the remaining 77% had residual arterial abnormalities, with improvement in 45% and stabilization in 32%. Stroke was preceded by chickenpox in 44% of TCA patients, and in none of the patients with progressive arteriopathies. Most infarcts were localized in the basal ganglia. In 14 (19%) of TCA patients, transient worsening of the arterial lesion was demonstrated before the arteriopathy stabilized or improved. Thirteen TCA patients (18%) had a recurrent stroke or TIA. Thirty TCA patients (41%) had a good neurological outcome, compared with none of the five patients with progressive arteriopathy. Arterial occlusion, moyamoya vessels and ACA involvement were more frequent in progressive arteriopathies. Cortical infarct localization was significantly associated with poor neurological outcome (OR 6.14, 95% CI 1.29-29.22, P = 0.02), while there was a trend for occlusive arterial disease to predict poor outcome (OR 3.00, 95% CI 0.98-9.23, P = 0.06). Progressive arteriopathy was associated with recurrence (OR 18.77, 95%CI 1.94-181.97, P = 0.01). The majority of childhood unilateral intracranial anterior circulation arteriopathies (94%) have a course that is consistent with TCA, in which transient worsening is common. Although the arterial inflammation probably causing TCA is 'transient', most children are left with permanent arterial abnormalities and residual neurological deficits.

Association of neonatal inflammatory markers and perinatal stroke subtypes.

OBJECTIVE: To examine the relationship between neonatal inflammatory cytokines and perinatal stroke using a systems biology approach analyzing serum and blood-spot cytokines from 47 patients. METHODS: This was a population-based, controlled cohort study with prospective and retrospective case ascertainment. Participants were recruited through the Alberta Perinatal Stroke Project. Stroke was classified as neonatal arterial ischemic stroke (NAIS), arterial presumed perinatal ischemic stroke (APPIS), or periventricular venous infarction (PVI). Biosamples were stored blood spots (retrospective) and acute serum (prospective). Controls had comparable gestational and maternal ages. Sixty-five cytokines were measured (Luminex). Hierarchical clustering analysis was performed to create heat maps. The Fisher linear discriminant analysis was used to create projection models to determine discriminatory boundaries between stroke types and controls. RESULTS: A total of 197 participants were analyzed (27 with NAIS, 8 with APPIS, 12 with PVI, 150 controls). Cytokines were quantifiable with quality control measures satisfied (standards testing, decay analysis). Linear discriminant analysis had high accuracy in using cytokine profiles to separate groups. Profiles in participants with PVI and controls were similar. NAIS separation was accurate (sensitivity 77%, specificity 97%). APPIS mapping was also distinguishable from NAIS (sensitivity 86%, specificity 99%). Classification tree analysis generated similar diagnostic accuracy. CONCLUSIONS: Unique inflammatory biomarker signatures are associated with specific perinatal stroke diseases. Findings support an acquired pathophysiology and suggest the possibility that at-risk pregnancies might be identified to develop prevention strategies. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that differences in acute neonatal serum cytokine profiles can discriminate between patients with specific perinatal stroke diseases and controls.

TIA patients with higher ABCD3-I scores are prone to a higher incidence of intracranial stenosis, unstable carotid plaques and multiple-vessel involvement.

The ABCD3-I criteria have proved to be effective for use in regular clinical practice to assist in transient ischemic attack (TIA) risk stratification and treatment. In this prospective study we aimed to explore the relationships between risk stratification and arterial stenosis location, carotid plaque morphology and vessel involvement in 90 TIA patients, stratifying risk by ABCD3-I scores. Clinical variables such as total cholesterol, triglyceride, low-density lipoprotein cholesterol, glycosylated hemoglobin, homocysteine and high-sensitive C-reactive protein levels were recorded. The endpoint was subsequent stroke at seven-day follow-up. Ninety patients were divided into three risk groups on the basis of their ABCD3-I scores. The results revealed that patients with higher ABCD3-I scores showed a higher occurrence of intracranial stenosis (P < 0.05), less organized carotid plaques (P < 0.05) and multiple-vessel involvement (P < 0.05).

Clinical and biochemical diagnosis of small-vessel disease in acute ischemic stroke.

BACKGROUND AND PURPOSE: Both from clinical and research standpoints, it may be highly relevant to differentiate between small-artery and large-artery infarction in the acute phase of ischemic stroke. We conducted a study on the added value of two D-dimer assays over clinical assessment for diagnosis of lacunar infarction. METHODS: Clinical evaluation using the Oxfordshire Community Stroke Project (OCSP) classification and measurement of plasma D-dimer levels by the VIDAS D-dimer test (VIDAS) and the Triage Stroke Panel (TSP) were performed in 128 patients with ischemic stroke presenting within 9 h after onset of symptoms. The stroke subtype was defined as small-artery or large-artery infarction based on the TOAST classification. RESULTS: The overall accuracy for diagnosing of acute lacunar stroke using the OCSP classification, VIDAS (cut point for D-dimer 445 ng/mL) or TSP (cut point 300 ng/mL) was 89%, 88% and 87% respectively (P<0.001). The conjunctive use of the OCSP classification and VIDAS or TSP improved the accuracy to 97% and 98% respectively (P<0.001). The kappa coefficient for agreement between the two assays was acceptable (kappa, 0.64). These results were reproducible in subgroups of patients presenting within 4.5 h and within 6 h after onset of stroke symptoms. CONCLUSIONS: Diagnosis of acute lacunar infarction can reliably be made, based on the conjunctive use of clinical evaluation and measurement of D-dimer levels either by a standard assay or by a bedside testing kit.