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  1. Poh KW, Er CK, Hoh WH, Abd Wahab ZW, Kok CY
    Clin Neurol Neurosurg, 2020 04;191:105684.
    PMID: 31981997 DOI: 10.1016/j.clineuro.2020.105684
    OBJECTIVES: Specific factors and its predictive parameters for neurological deterioration in total anterior circulation infarct (TACI) were not known. Our objective was to determine the risk factors and risk scores for neurological deterioration in TACI. The secondary objective was to determine the effect of antiplatelet therapy in TACI.

    PATIENTS AND METHODS: This was a single-center cohort study. 46 patients with TACI were enrolled and followed up for 30 days, discharged, or death; whichever earlier. The National Institutes of Health Stroke Scale (NIHSS) was performed daily by investigators who are NIHSS certified and radiological findings were confirmed by a certified radiologist. Neurological deterioration was defined by a drop in NIHSS by 2 points or Glasgow Coma Scale (GCS) by 1 point. Clinical, laboratory and radiological variables were evaluated. Significant predictive variables were given a score based on its co-efficient values in multivariate analysis.

    RESULTS: Lower Alberta stroke program early CT score (ASPECTS) and higher numbers of early computed tomography (CT) sign of middle cerebral artery (MCA) infarct were significant risk factor for neurological deterioration with p 

    Matched MeSH terms: Infarction, Middle Cerebral Artery/physiopathology
  2. Nik Ramli NN, Omar N, Husin A, Ismail Z, Siran R
    Neurosci Lett, 2015 Feb 19;588:137-41.
    PMID: 25562631 DOI: 10.1016/j.neulet.2014.12.062
    Glutamate receptors are the integral cellular components associated with excitotoxicity mechanism induced by the ischemic cascade events. Therefore the glutamate receptors have become the major molecular targets of neuroprotective agents in stroke researches. Recent studies have demonstrated that a Group I metabotropic glutamate receptor agonist, (S)-3,5-dihydroxyphenylglycine ((S)-3,5-DHPG) preconditioning elicits neuroprotection in the hippocampal slice cultures exposed to toxic level of N-methyl-d-aspartate (NMDA). We further investigated the preconditioning effects of (S)-3,5-DHPG on acute ischemic stroke rats. One 10 or 100μM of (S)-3,5-DHPG was administered intrathecally to Sprague-Dawley adult male rats, 2h prior to induction of acute ischemic stroke by middle cerebral artery occlusion (MCAO). After 24h, neurological deficits were evaluated by modified stroke severity scores and grid-walking test. All rats were sacrificed and infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride staining. The serum level of neuron-specific enolase (NSE) of each rat was analyzed by enzyme-linked immunosorbent assay (ELISA). One and 10μM of (S)-3,5-DHPG preconditioning in the stroke rats showed significant improvements in motor impairment (P<0.01), reduction in the infarct volume (P<0.01) and reduction in the NSE serum level (P<0.01) compared to the control stroke rats. We conclude that 1 and 10μM (S)-3,5-DHPG preconditioning induced protective effects against acute ischemic insult in vivo.
    Matched MeSH terms: Infarction, Middle Cerebral Artery/physiopathology
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