Microglia are the first source of a neuroinflammatory cascade, which seems to be involved in every phase of stroke-related neuronal damage. Two weeks after transient middle cerebral artery occlusion (MCAO), vehicle-treated rats displayed higher numbers of total ionized calcium-binding adaptor molecule 1 (Iba-1)-positive cells, greater cell body areas of Iba-1-positive cells, and higher numbers of hypertrophic Iba-1-positive cells (with a cell body area over 80 μm2) in the ipsilateral ischemic brain regions including the frontal cortex, striatum, and parietal cortex. In addition, MCAO decreased the number of migrating neuroblasts (or DCX- and 5-ethynyl-2′-deoxyuridine-positive cells) in the cortex, subventricular zone, and hippocampus of the ischemic brain, followed by neurological injury (including brain infarct and neurological deficits). Intravenous administration of human umbilical cord–derived mesenchymal stem cells (hUC-MSCs; 1 × 106 or 4 × 106) at 24 h after MCAO reduced neurological injury, decreased the number of hypertrophic microglia/macrophages, and increased the number of newborn neurons in rat brains. Thus, the accumulation of hypertrophic microglia/macrophages seems to be detrimental to neurogenesis after stroke. Treatment with hUC-MSCs preserved adult newborn neurons and reduced functional impairment after transient cerebral ischemia by reducing the number of hypertrophic microglia/macrophages.

Background. Cardiac morbidities account for 20% of deaths after ischemic stroke and is the second commonest cause of death in acute stroke population. Elevation of cardiac troponin has been regarded as a prognostic biomarker of poor outcome in patients with acute stroke.Methods. This retrospective study enrolled 871 patients with acute ischemic stroke from August 2010 to March 2015. Data included vital signs, laboratory parameters collected in the emergency department, and clinical features during hospitalization. National Institutes of Health Stroke Scale (NIHSS), Barthel index, and modified Rankin Scale (mRS) were used to assess stroke severity and outcome.Results. Elevated troponin I (TnI) > 0.01 µg/L was observed in 146 (16.8%) patients. Comparing to patients with normal TnI, patients with elevated TnI were older (median age 77.6 years vs. 73.8 years), had higher median heart rates (80 bpm vs. 78 bpm), higher median white blood cells (8.40 vs. 7.50 1,000/m3) and creatinine levels (1.40 mg/dL vs. 1.10 mg/dL), lower median hemoglobin (13.0 g/dL vs. 13.7 g/dL) and hematocrit (39% vs. 40%) levels, higher median NIHSS scores on admission (11 vs. 4) and at discharge (8 vs. 3), higher median mRS scores (4 vs3) but lower Barthel index scores (20 vs. 75) at discharge (p < 0.001). Multivariate analysis revealed that age ≥ 76 years (OR 2.25, CI [1.59–3.18]), heart rate ≥ 82 bpm (OR 1.47, CI [1.05–2.05]), evidence of clinical deterioration (OR 9.45, CI [4.27–20.94]), NIHSS score ≥ 12 on admission (OR 19.52, CI [9.59–39.73]), and abnormal TnI (OR 1.98, CI [1.18–3.33]) were associated with poor outcome. Significant factors for in-hospital mortality included male gender (OR 3.69, CI [1.45–9.44]), evidence of clinical deterioration (OR 10.78, CI [4.59–25.33]), NIHSS score ≥ 12 on admission (OR 8.08, CI [3.04–21.48]), and elevated TnI level (OR 5.59, CI [2.36–13.27]). C-statistics revealed that abnormal TnI improved the predictive power of both poor outcome and in-hospital mortality. Addition of TnI > 0.01 ug/L or TnI > 0.1 ug/L to the model-fitting significantly improved c-statistics for in-hospital mortality from 0.887 to 0.926 (p = 0.019) and 0.927 (p = 0.028), respectively.Discussion. Elevation of TnI during acute stroke is a strong independent predictor for both poor outcome and in-hospital mortality. Careful investigation of possible concomitant cardiac disorders is warranted for patients with abnormal troponin levels.

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We examined the effects of visual rehabilitation, including a chromatic luminance discrimination program and a fixation training program, on a 6-yr-old boy with severe visual impairment. Single-subject ABA and AB designs were used. The programs were conducted 2×/wk and included 6 to 7 sessions for the baseline phase and 10 to 11 sessions for the intervention phase. Play was integrated into the visual training programs. Goggle visual evoked potential (VEP) testing was used to evaluate neural activity in the primary visual cortex. Correct responses increased and response times were shortened after training in luminance discrimination. The total and maximum fixation time also improved, as did P100 latency and amplitude of VEPs. While walking, the boy was able to detect obstacles he had not noticed before training. The results indicate the value of visual training and the possibility of brain plasticity in a child with severe visual impairment.

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