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Ischemic stroke is one of the leading causes of disability worldwide [1]. Though clinical assessment of stroke and evaluation of stroke etiology are always sufficient, reliable biomarkers to support the diagnosis and predict the outcome are not well-established [2]. Identification of biomarkers that can predict the outcome would be beneficial in stroke management and monitoring the course of stroke therapy. It can also help to direct a specific or personalized therapy to a subgroup of patients most likely to benefit [3]. Many biomarkers are known to increase during early neurological deterioration (END); or worsening of neurological status from admission to 48–72 h after admission, especially the S100B [3–5]. Identifying patients at risk of END may be useful for initiating therapies to prevent such worsening. S100B is a calcium-binding protein that was found primarily in glial and Schwann cells. It possesses many of the ideal characteristics of a biochemical marker such as high organ specificity, low molecular size, and a high degree of solubility. S100B acts in bimodal manner. At nanomolar concentrations, S100B stimulates neurite outgrowth in cerebral cortex neurons in vitro and enhances survival of neurons in various systems during development [6]. SB100 has also a neurotrophic activity during the neuronal maturation and glial cell proliferation [7]. S100B decreases cell death and protects against mitochondrial function loss resulting from glucose deprivation [6, 8]. With its neurotrophic and gliotrophic actions, S100B plays an important role in normal CNS development and recovery after injury. In contrast to the stated effects of nanomolar levels of S100B, micromolar levels of extracellular S100B are known to have deleterious effects [9]. At these concentrations, extracellular S100B stimulates the expression of proinflammatory cytokines and induces apoptosis in vitro [8]. S100B exerts its neurotoxic effects in vitro by inducing apoptosis in neurons. The short biological half-life of S100B (between 30 and 60 min) and its renal clearance (2 h) imply that any persistent elevation of S100B concentration in the blood reflects a continuous active secretion or passive release from damaged tissues [10]. During the last few years, several studies [8, 11–14] have investigated release and kinetics of protein S-100B after acute stroke and their association with lesion volume, clinical status, and outcome. The purpose of the present study was to investigate the relation between release pattern and serum concentration of protein S100B and short-term functional outcome after stroke in elderly patients.

The role of s100b as a predictor of the functional outcome in geriatric patients with acute cerebrovascular stroke