Aim: Insulin resistance has effects on the coagulation system, which is important in the acute phase of infarct. We examined the relationships between insulin resistance, hemostatic markers and stroke severity in acute ischemic stroke patients. Methods: Protein C (PC), protein S (PS), fibrinogen, von Willebrand factor and antithrombin III (AT III) were studied in 75 acute ischemic stroke patients with and without insulin resistance. Results: The PC and PS levels of insulin-resistant patients were significantly lower than those of non-insulin-resistant patients (PC: 87 ± 19.23 vs. 97.89 ± 13.3%, p = 0.007; PS: 84.75 ± 15.72 vs. 93.21 ± 15.02%, p = 0.02), and both of the anticoagulants were correlated with the homeostasis model assessment (HOMA; r = –0.339, p = 0.003 and r = –0.481, p = 0.000, respectively). Additionally, the NIH Stroke Scale (NIHSS) score correlated negatively with PS (r = –0.329, p = 0.004) and AT III levels (r = –0.235, p = 0.04). The parameters with positive correlations with NIHSS were fibrinogen (r = 0.270, p = 0.019), fasting glucose (r = 0.358, p = 0.008) and HOMA (r = 0.286, p = 0.013). Conclusions: The significant associations between insulin resistance and hemostatic markers may be relevant to stroke severity by causing a procoagulant tendency in acute ischemic stroke.
Lithium (Li) and lamotrigine (LTG) have neuroprotective properties. However, the exact therapeutic mechanisms of these drugs have not been well understood. We investigated the antioxidant properties of Li (40 and 80 mg/kg/day) and LTG (20 and 40 mg/kg/day) in a rat model of global cerebral ischemia based on permanent bilateral occlusion of the common carotid arteries (BCAO). Nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GSH-R), catalase (CAT) and superoxide dismutase (SOD) levels were measured as an indicator of oxidative-nitrosative stress in both prefrontal cortex (PFC) and hippocampus after 28 days of treatment. The spatial learning disability was also assessed at the end of the study by Morris water maze (MWM) test. All oxidative-nitrosative parameters were found to be higher in the groups under treatment than in sham. Both drugs caused a decrease in PFC NO and MDA elevation, meanwhile the increase in GSH, GSH-R, CAT and SOD levels was significantly more evident in treated groups. We also found higher PFC GSH-R and hippocampal SOD levels in BCAO + Li (80 mg/day) treated group when compared with BCAO + LTG 40 mg/day. MWM test data showed a similar increase in spatial learning ability in all groups under treatment. We found no other statistical difference in comparison of treated groups with different dosages. Our findings suggested that Li and LTG treatments may decrease spatial learning memory deficits accompanied by lower oxidative-nitrosative stress in global cerebral ischemia. Both drugs may have potential benefits for the treatment of vascular dementia in clinical practice.
Primary diffuse leptomeningeal oligodendrogliomatosis is a rare malignancy of central nervous system without evidence of a primary intraparenchymal focus. We present a 25-year-old woman with the postmortem diagnosis of primary diffuse leptomeningeal oligodendrogliomatosis. She was paraplegic and had sensory loss at the level of thoracal 8-9 for nearly 15 months. There was no symptom due to increased intracranial pressure. Unexpectedly she died just before biopsy. Autopsy revealed a nodular lesion at the level of thoracal 10 vertebra and diffuse oligodendroglioma throughout the leptomeninges of the brain and spine without intraaxial focus. To our knowledge, this is the first case of primary diffuse leptomeningeal oligodendrogliomatosis causing sudden death in the literature.
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