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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.

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.

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.

CV due to RA is an uncommon serious complication which can be life-threatening. Therefore clinicians should be aware of the possibility of CV especially in progressive strokes in RA.

Objective: The role of inflammation in the pathogenesis of acute ischemic stroke is well known, but its association with the clinical picture is as yet unclear. Material and Methods: In our study, we measured the serum levels of the proinflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) within the first 50 h of stroke in 60 acute stroke patients, and examined the association with the natural anticoagulants protein C and free protein S. We compared the results with a control group that consisted of 30 volunteers. We also correlated their levels with the clinical outcomes by using the Canadian Neurological Scale (CNS). Results: Neither stroke patients nor the control group had any elevations in IL-1β serum levels. However, the levels of serum IL-6 were significantly higher in stroke patients (13.7 ± 19.46 vs. 4.3 ± 15.88, p = 0.002). In addition, the protein S levels of patients were lower than those of the controls (84.36 ± 27.97 vs. 95.9 ± 25.64, p = 0.007). Although IL-6 showed negative correlation with protein S (r = –0.504, p = 0.000), the other studied cytokines TNFα and IL-1β did not correlate with these natural anticoagulants. Another negative correlation was found between IL-6 and CNS scores (r = –0.451, p = 0.000). In addition, both protein C and protein S positively correlated with CNS (r = 0.263, p = 0.042; r = 0.381, p = 0.003). There was also a positive correlation between protein C and protein S (r = 0.408, p = 0.001). Conclusions: Our results suggest that TNFα and IL1β serum levels are not elevated in the acute phase of stroke and have no correlation with the natural anticoagulants protein C and protein S. However, a decrease in free protein S may be related to elevated IL-6 levels. In addition, increased levels of IL-6 and reduced levels of protein C and protein S may play a role in acute ischemic stroke severity.

Our aims were to observe the effects of rehabilitation and surgery on idiopathic and diabetic carpal tunnel syndrome (CTS) and compare them with the natural course of the disease. Forty-two patients aged 33 to 74 years with clinically diagnosed, electrophysiologically confirmed, and laboratory screened hands with CTS (46 idiopathic and 34 diabetic) were enrolled in the study. Improvement of symptom severity and functional status after treatment using the Boston questionnaire (scales), changes of nerve conduction parameters (NCPs), and correlations between NCP and Boston questionnaires were outcome measures. Follow-up periods were 3 to 5 months and 6 to 12 months. In idiopathic CTS, surgery was effective according to scales and NCP. Rehabilitation was also effective according to scales but only in the late period. Nontreatment did not improve scales at a later period. In diabetic CTS, rehabilitation was not effective according to scales. Baseline and follow-up correlations between scales and NCP were weak and limited to sensory amplitudes (baseline), sensory amplitudes-velocity, and median motor distal latency (follow-up). Regression analysis also did not reveal any associations between scales and NCP. A repeated nerve conduction study was not meaningful if the diagnosis was definite. Treatment of CTS was definitely superior to spontaneous improvements. Rehabilitation was ineffective in diabetic CTS.