Deterioration In Ischemic Stroke Research Articles

Acute stroke unit care and early neurological deterioration in ischemic stroke

To evaluate the impact that monitored acute stroke unit care may have on the risk of early neurological deterioration (END), and 90-day mortality and mortality-disability. Non-randomized prospective study with consecutive patients with acute ischemic stroke (AIS) admitted to a conventional care stroke unit (CCSU), from May 2003 to April 2005, or to a monitored acute stroke unit (ASU) from May 2005 to April 2006. END was defined as an increase in the NIHSS score >or= 4 points in the first 72 hours after admission. END was detected in 19.6% of patients (11.2% of patients admitted to the ASU and 23.8% to the CCSU; p<0.0001). Patients admitted to the ASU received more treatment with intravenous rtPa (13.5% versus 4.2%; p<0.0001), had a shorter length of stay (9.1 [11.0] d versus 13.1 [10.4] d; p<0.0001), lower 90-day mortality (10.2% versus 17.3%; p=0.02), and lower mortality-disability at 90-days (28.4% versus 40.2%; p=0.004) than those admitted to the CCSU. Multivariable analysis showed that ASU admission was a protector for END (OR: 0.37; 95% CI: 0.23-0.62). On admission, higher NIHSS (OR: 1.06; 95% CI: 1.03-1.10), higher glycaemia (OR: 1.003; 95% CI: 1.001-1.006), and higher systolic pressure (OR: 1.01; 95% CI: 1.002-1.017) were independent predictors of END. END prevention by ASU care might be a key factor contributing to better outcome and decrease of length of stay in patients admitted to monitored stroke units.

Iron, Oxidative Stress and Early Neurological Deterioration in Ischemic Stroke

Ischemic stroke is characterized by the disruption of cerebral blood flow, which produces a central core of dead neurons surrounded by a penumbra of damaged but partially functional neurons. Many factors are associated with such brain injury, including excitotoxicity and free radicals. Recent clinical studies have shown that high plasma ferritin levels are detrimental in acute ischemic stroke. As an iron-storage protein, ferritin can act both as a scavenger and as a donor of free iron, which is a source of hydroxyl radicals. Following disruption of the blood-brain barrier, the ferritin and the free iron that have accumulated in endothelial cells in brain capillaries, together with plasma ferritin, can enter the penumbra. Iron-dependent oxidative stress in the penumbra can lead to necrosis and further neurological deterioration following ischemic stroke. An excess of iron should be considered pathological in the ischemic brain. Therapeutic strategies for ischemic stroke should attempt to restore brain function within the penumbra. Consequently, the iron content of systemic stores should be measured, and anti-oxidant treatment should be considered when it is excessive.

大脳皮質間のネットワーク障害と認知機能低下：脳梁萎縮を指標として

Ischemic damage of large-scale networks between cortical regions leading to disconnection may cause cognitive impairment associated with widespread functional disturbance. However, it remains unclear to what extent this mechanism contributes to the development of cognitive impairment or dementia, because there is no way to evaluate quantitatively and precisely the amount of the disconnection in each patient. We investigated atrophy of the corpus callosum as a surrogate marker for damage of large-scale networks. In ca-rotid artery disease without cortical infarction, callosal atrophy was associated with cognitive impairment and widespread cerebral cortical hypometabolism. Ischemic loss of the pyramidal cells in layer 3 originating long association and commissural fibers, which may result in calllosal atrophy, may lead to the disconnection be-tween cortical regions. In patients with lacunar infarction and white matter lesions, callosal atrophy was a predictor of global cognitive impairment, whereas the extent of white matter lesions per se was related to impairment of frontal lobe function independent of callosal atrophy. Callosal atrophy may parallel the total loss of fibers in the white matter, the degree of which may determine the severity of disconnection. Damage of largescale networks is important for the development of cognitive impairment in ischemic stroke.