الفهرس 
ISCHEMIC BRAIN INJURYOnly 14 pages are availabe for public view
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Abstract
Stroke is the second leading cause of death worldwide. Mortality rates are declining, however. Over 75% of patients survive a first stroke during the first year, and over half survive beyond 5 years.
Calcium plays an important role in the pathogenesis of ischemic cell damage. Intracellular calcium accumulation leads neuronal damage by triggering the cycle of cytotoxic events.
Calcium levels levels obtained lately within 72 to 96 hours was found to be of prognostic significance after ischemic stroke. Clarifying the exact pathophysiological mechanism that may underlie these clinical observations has been challenging, especially because it is unclear whether serum Ca2+ level exerts a primary effect on ischemic stroke, or if it reflects a secondary epiphenomenon of ischemic stroke severity.
Although the better outcomes seen among patients with higher serum calcium levels in these prior studies were postulated to be caused by smaller infarct volumes, several potential mechanisms may explain why serum calcium levels are related to the extent of bioenergetically compromised tissue in patients with acute ischemic stroke. These mechanisms can be divided into 2 broad and non-mutually exclusive categories. First, raised serum calcium levels directly or indirectly attenuate the volume of ischemic tissue; second, serum calcium levels may alternately DROP in response in the presence of tissue ischemia. Most important, decreased extracellular serum calcium levels are an important factor in the positive feedback mechanism that potentiates the inward serum calcium level currents following ischemic injury.
The aim of this work is to correlate the serum calcium level on one hand and the size of infarction and the stroke outcome.
This was conducted through a cross sectional study done on 36 patients with acute ischemic stroke admitted to stroke unit at Ain Shams University hospital within 24 hours of stroke onset during the period from November 2012 to 30th of April 2013.
Patients were subjected to: 1. General history and examination. 2. Neurological history and examination including NIHSS (national institute of health stroke scale) for assessment of clinical severity and Barthel index of activity of daily living done on admission to hospital and after 3 months for outcome assessment. 3. Laboratory investigations including full laboratory investigations including early serum corrected calcium level (within first 24 hours), and late serum corrected calcium level (within 72-96 hours), complete blood count, lipid profile, liver & kidney functions, serum albumin, coagulation profile. 4. Neuroimaging in the form of MRI brain and MRA of cerebral arteries were done within 72 hours of onset. The volume of infarction in diffusion WI was estimated according to the ABC/2 method. 6. ECG & transthoracic echocardiography &Carotid duplex.
The study results showed that serum calcium values were found to decrease in patients with cerebral infarction, higher serum calcium levels both early and late were associated with smaller cerebral infarct volume on DWI and that an inverse correlation exists between late serum calcium level and stroke outcome; and this puts a highlight on the role of both calcium compounds and calcium antagonists in ischemic brain injury