BACKGROUND AND PURPOSE: Autopsy studies found that lacunar strokes differ in the size of the underlying brain infarct and that small lacunes are usually caused by hypertensive small-artery disease (SAD) and larger ones by atheromatous or embolic perforator occlusion. These findings suggest that larger lacunar infarcts might cause more severe neurological deficits and a higher detection rate on brain imaging compared with lacunar strokes caused by SAD. This prospective observational study was performed to investigate whether (1) neurological outcome, (2) prevalence of stroke risk factors, (3) prevalence of clinically asymptomatic occlusive cerebral artery disease, and (4) detection rate of underlying lacunar infarcts at brain imaging differ in ischemic lacunar strokes with (non-SAD) and without potential etiologies other than SAD. METHODS: Consecutive patients with lacunar stroke (n=244), defined by both clinical findings and brain imaging, were studied. Neurological deficit was quantified at presentation with the use of the National Institutes of Health Stroke Scale (NIHSS) and after 3 months with the NIHSS and the modified Rankin Scale (mRS). Cerebral arteries were investigated by ultrasound. RESULTS: Compared with patients with SAD lacunar strokes (n=155; 64%), patients with non-SAD lacunar strokes (n=89; 36%) had (1) higher NIHSS scores at presentation and higher NIHSS and mRS scores after 3 months (P<0.05); a higher prevalence of (2) hypertension (P<0.05), (3) coronary artery disease (P<0.0001), (4) previous transient ischemic attacks (P<0.01), and (5) asymptomatic stenoses of intracranial cerebral (P<0.01 to P<0.0001) and extracranial carotid (30% to 50% narrowing; P<0.01) arteries; and (6) a higher detection rate of the underlying lesion at brain imaging (P<0.01). CONCLUSIONS: Our data suggest that patients with non-SAD lacunar strokes have a worse clinical outcome and a higher prevalence of large cerebral and coronary artery disease than patients with SAD lacunar strokes.
BACKGROUND AND PURPOSE: Autopsy studies found that lacunar strokes differ in the size of the underlying brain infarct and that small lacunes are usually caused by hypertensive small-artery disease (SAD) and larger ones by atheromatous or embolic perforator occlusion. These findings suggest that larger lacunar infarcts might cause more severe neurological deficits and a higher detection rate on brain imaging compared with lacunar strokes caused by SAD. This prospective observational study was performed to investigate whether (1) neurological outcome, (2) prevalence of stroke risk factors, (3) prevalence of clinically asymptomatic occlusive cerebral artery disease, and (4) detection rate of underlying lacunar infarcts at brain imaging differ in ischemic lacunar strokes with (non-SAD) and without potential etiologies other than SAD. METHODS: Consecutive patients with lacunar stroke (n=244), defined by both clinical findings and brain imaging, were studied. Neurological deficit was quantified at presentation with the use of the National Institutes of Health Stroke Scale (NIHSS) and after 3 months with the NIHSS and the modified Rankin Scale (mRS). Cerebral arteries were investigated by ultrasound. RESULTS: Compared with patients with SAD lacunar strokes (n=155; 64%), patients with non-SAD lacunar strokes (n=89; 36%) had (1) higher NIHSS scores at presentation and higher NIHSS and mRS scores after 3 months (P<0.05); a higher prevalence of (2) hypertension (P<0.05), (3) coronary artery disease (P<0.0001), (4) previous transient ischemic attacks (P<0.01), and (5) asymptomatic stenoses of intracranial cerebral (P<0.01 to P<0.0001) and extracranial carotid (30% to 50% narrowing; P<0.01) arteries; and (6) a higher detection rate of the underlying lesion at brain imaging (P<0.01). CONCLUSIONS: Our data suggest that patients with non-SAD lacunar strokes have a worse clinical outcome and a higher prevalence of large cerebral and coronary artery disease than patients with SAD lacunar strokes.
Authors: Saloua Akoudad; Frank J Wolters; Anand Viswanathan; Renée F de Bruijn; Aad van der Lugt; Albert Hofman; Peter J Koudstaal; M Arfan Ikram; Meike W Vernooij Journal: JAMA Neurol Date: 2016-08-01 Impact factor: 18.302
Authors: Martin Griebe; Elisabeth Fischer; Micha Kablau; Philipp Eisele; Marc E Wolf; Anastasios Chatzikonstantinou; Achim Gass; Michael G Hennerici; Kristina Szabo Journal: J Neurol Date: 2013-12-24 Impact factor: 4.849
Authors: A Arboix; M López-Grau; C Casasnovas; L García-Eroles; J Massons; M Balcells Journal: J Neurol Neurosurg Psychiatry Date: 2006-03 Impact factor: 10.154
Authors: V C T Mok; A Wong; W W M Lam; Y H Fan; W K Tang; T Kwok; A C F Hui; K S Wong Journal: J Neurol Neurosurg Psychiatry Date: 2004-04 Impact factor: 10.154