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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Evolution of cerebral arteriopathies in childhood arterial ischemic stroke.
Annals of Neurology 2006 April
OBJECTIVE: To investigate evolution of cerebral arteriopathy in children with arterial ischemic stroke (AIS) and its influence on recurrence.
METHODS: Arteriopathy severity was graded on serial magnetic resonance angiograms from 50 children with first AIS; diagnostic categories were assigned.
RESULTS: Arteriopathy affected 72 arteries in 43 of 50 children. Five had clinical recurrence, with reinfarction in four; another had clinically silent reinfarction. Twelve children (24%; 4 with recurrence) had progressive arteriopathy. Arteriopathy improved in 24 patients (including 1 with recurrent transient ischemic attacks) and was stable in 7 patients. Magnetic resonance angiograms remained normal in seven patients; one had recurrent stroke. Diagnoses were transient cerebral arteriopathy (n = 24), chronic cerebral arteriopathy (n = 11), arterial dissection (n = 3), possible moyamoya (n = 2), primary moyamoya (n = 1), dysplastic arteriopathy (n = 1), and cerebral vasculitis (n = 1). Some of the first two categories could represent thromboembolic arterial occlusion with recanalization. The hazard of recurrence was three times higher when arterial disease had progressed (Cox regression hazard ratio, 3.2; 95% confidence intervals, 0.5-20.3; p = 0.22). After adjustment for age and number of AIS risk factors, the hazard ratio was 3.1 (95% confidence interval, 0.4-22.2; p = 0.27).
INTERPRETATION: Arteriopathy frequently progresses after childhood AIS. Further studies are needed to examine the relationship between progressive arteriopathy and recurrence.
METHODS: Arteriopathy severity was graded on serial magnetic resonance angiograms from 50 children with first AIS; diagnostic categories were assigned.
RESULTS: Arteriopathy affected 72 arteries in 43 of 50 children. Five had clinical recurrence, with reinfarction in four; another had clinically silent reinfarction. Twelve children (24%; 4 with recurrence) had progressive arteriopathy. Arteriopathy improved in 24 patients (including 1 with recurrent transient ischemic attacks) and was stable in 7 patients. Magnetic resonance angiograms remained normal in seven patients; one had recurrent stroke. Diagnoses were transient cerebral arteriopathy (n = 24), chronic cerebral arteriopathy (n = 11), arterial dissection (n = 3), possible moyamoya (n = 2), primary moyamoya (n = 1), dysplastic arteriopathy (n = 1), and cerebral vasculitis (n = 1). Some of the first two categories could represent thromboembolic arterial occlusion with recanalization. The hazard of recurrence was three times higher when arterial disease had progressed (Cox regression hazard ratio, 3.2; 95% confidence intervals, 0.5-20.3; p = 0.22). After adjustment for age and number of AIS risk factors, the hazard ratio was 3.1 (95% confidence interval, 0.4-22.2; p = 0.27).
INTERPRETATION: Arteriopathy frequently progresses after childhood AIS. Further studies are needed to examine the relationship between progressive arteriopathy and recurrence.
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