Infarct cardioembolic

Small vessel/lacunar strokes have better short- and long-term (1-year) survival as compared to other stroke subtypes. In the NINDS trial of rt-PA within 3 hours of onset, patients classified as small vessel stroke on the basis of their clinical syndrome had a 50% chance of a normal NIHSS score at 3 months if they received placebo, increasing to 70% in the treatment group. In the Lausanne cohort, 95% were independent after their first event, as opposed to only 65% of the cardioembolic strokes and 49% with large vessel atherothrombotic infarctions. Eighty-two percent of patients with small vessel stroke were independent at 1 year. Even at the time of maximal deficit, between 38% and 64% of small vessel/lacunar patients were independent, with motor impairment and extent of white matter disease adversely affecting outcomes. " In TOAST, small vessel/lacunar stroke was the only subtype associated with a favorable outcome, independent of the NIHSS score. ... 

Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. 

Mokri B, Silbert PL, Schievink WI et al (1996) Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. Neurology 46 356-359 Molina CA, Montaner J, Abilleira S et al (2001) Timing of Spontaneous Recanalization and Risk of Hemorrhagic Transformation in Acute Cardioembolic Stroke. Stroke 32 1079-1084 Molina CA, Alvarez-Sabin J, Montaner J et al (2002) Thrombolysis-related hemorrhagic infarction a marker of early reperfusion, reduced infarct size, and improved outcome in patients with proximal middle cerebral artery occlusion. Stroke 33 1551-1556... 

MCA infarcts are mainly caused by cardioembolism, internal carotid artery (ICA) thrombosis, dissection or embolism and rarely (in Caucasians) by intrinsic MCA disease. MCA atherothrombotic territory infarctions related to intrinsic MCA disease often cause concomitant small cortical (territorial or borderzone) and subcortical infarcts (Min et al. 2000). 

Subcortical white matter infarcts may mimic a superficial MCA infarct causing a partial anterior circulation syndrome or present as a lacunar syndrome (pure motor, ataxic hemiparesis or sensori motor stroke). Superficial perforating artery infarcts (medullary branches) are often accompanied by cortical spotty lesions. Borderzone and white matter medullary branches infarctions are usually caused by hypoperfusion due lo large vessel occlusion or stenosis (Bogousslavsky 1993 Donnan and Yasaka 1998), but white matter medullary branches infarction can also be caused by cardioembolism (Lee et al. 2003). 

Aphasia and neglect can be found following respectively dominant and non-dominant anterior choroidal artery infarcts. Anterior choroidal artery infarcts usually cause the classical 3H syndrome hemiparesis, hemihypesthesia, hemianopia. Pure motor hemiparesis and isolated hemianopia can also occur (Han et al. 2000). Anterior choroidal artery territory infarcts are rarely caused by small vessel occlusion. In general they are caused by cardioembolism or large artery disease with occlusion or artery-to-artery embolism (Leys et al. 1994). 

Brandt T, Steinke W, Thie A et al (2000) Posterior cerebral artery territory infarcts clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature. Cerebrovasc Dis 10 170-182 Cals N, Devuyst G, Afsar N et al (2002) Pure superficial posterior cerebral artery territory infarction in The Lausanne Stroke Registry. J Neurol 249 855-861 De Freitas GR, Carruzzo A, Tsiskaridze A et al (2001) Massive haemorrhagic transformation in cardioembolic stroke the role of arterial wall trauma and dissection. J Neurol Neurosurgery Psychiatry 70 672-674... 

Studer A, Georgiadis D, Baumgartner RW (2003) Ischemic infarct involving all arterial territories of the thalamus. Acta Neurol Scand 107 423-425 Timsit SG, Sacco RL, Mohr JP et al (1992) Early clinical differentiation of cerebral infarction from severe atherosclerotic stenosis and cardioembolism. Stroke 23 486-491 Tong DC, Adami A, Moseley ME et al (2000) Relationship between apparent diffusion coefficient and subsequent hemorrhagic transformation following acute ischemic stroke. Stroke 31 2378-2384... 

Some overlap exists between the clinical classification (Bamford et al. 1991) and the etiological TOAST classification. In a large hospital-based series of patients with ischemic stroke, total and partial anterior circulation infarcts were most likely to be caused by large artery atherosclerosis, cardioembolism or both (Wardlaw et al. 1999). 

Patients in atrial fibrillation who have a TIA or stroke without other clear etiology should be given anticoagulation therapy if there are no contraindications (European Atrial Fibrillation Trial Study Group 1993, 1995). Recent studies have shown that warfarin is as safe as aspirin in elderly patients with atrial fibrillation (Rash et al. 2007 Mant et al. 2007). Patients with presumed cardioembolic TIA or stroke secondary to other causes should certainly receive antithrombotic therapy. Also they may benefit from anticoagulation in certain circumstances, such as intracardiac mural thrombosis after myocardial infarction, although there have been no randomized trials in situations other than non-valvular atrial fibrillation. 

Ogata, J., et al.. Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke. Stroke, 1989. 20(7) p. 876-83. 

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