Background: Increasing evidence shows that inflammation plays an important role in the occurrence and progression of acute ischemic stroke. The receptor for advanced glycation end products (RAGE) has been documented to involve in the pathogenic mechanisms of a variety of neurological diseases, including ischemic stroke (IS). However, the impact of RAGE gene polymorphisms on the susceptibility to IS has not been reported. We thus explored the association between RAGE gene polymorphisms and the susceptibility to IS. Method: A total of 384 patients with IS and 425 healthy controls were enrolled in this study. Three genetic polymorphisms of RAGE gene (82G/S, -429T/C and -374T/A) were determined. The serum levels of soluble RAGE (sRAGE), intetleukin-6 (IL-6), high sensitivity-C reaction protein (hs-CRP) and plasminogen activator inhibitor-1 (PAI-1) were detected. Results: Among the studied polymorphisms, only the polymorphism at 82G/S of RAGE gene was associated with the risk for ischemic stroke irrespective of the stroke subtypes. The 82S/S homozygote carriers had a significantly increased risk for ischemic stroke [adjusted odds ratio (OR): 2.297; p<0.001]. The haplotype analyses showed that the C_-429S₈₂T_-374 and T_-429S₈₂A_-374 had higher risk to develop IS (OR=1.864 and 1.931, respectively, all p<0.01), while the C_-429G₈₂T_-374 showed a protective effect against IS susceptibility (OR=0.568, p=0.001). In addition, the 82S/S homozygote carriers had a higher inflammatory level compared with 82G/S and 82G/G genotypes, indicated by lower serum sRAGE level, higher serum IL-6, hs-CRP and PAI-1 levels. The polymorphisms at -374 and -429 loci did not influence the stroke risk and the above mentioned inflammation cytokines. Conclusion: Our results showed a close correlation between the 82G/S polymorphism and the susceptibility to IS, suggesting the 82G/S polymorphism may be used as a genetic marker for the prediction of stroke occurrence in high risk subjects.

Aim: To investigate the association of Osteopontin (OPN) gene polymorphism and serum thrombin-cleaved OPN level with the susceptibility to ischemic stroke (IS) and its prognosis. Methods: A total of 377 patients with IS and 551 healthy individuals were recruited. The OPN gene polymorphisms at -156 G>GG, -443 C>T and -66 T>G were genotyped. Serum full-length and the thrombin-cleaved OPN were determined. Results: We found that only the -443 C>T polymorphism was significantly associated with the susceptibility to IS. The -443 CC represented a near 2 time higher risk for IS incidence than TT carriers. Also, the -443 CC genotype had significantly poorer outcome and they significantly had higher occurrence for bad recovery as determined by modified Rankin Scale (mRS) (OR=2.18, p=0.043) and Barthel Index (BI) (OR=2.12, p=0.05). The mean serum thrombin-cleaved OPN level in IS group were significantly higher than that in control group. ROC analysis showed that the thrombin-cleaved OPN level (cut-off value, 166.8 ng/ml) can discriminate IS patients from controls with a specificity of 86.3% and a sensitivity of 57.7%. The serum thrombin-cleaved OPN was significantly associated with the clinical outcome at 12 months after discharge from hospital. Conclusion: These results suggest that the -443 C>T polymorphism of OPN gene and serum thrombin-cleaved OPN can be used as a biomarker for the susceptibility and prognosis of IS patients.

Refractory status epilepticus is commonly defined as status epilepticus that fails to respond to two or more appropriately dosed intravenous anti-seizure medications including at least one non-benzodiazepine drug. Super-refractory status epilepticus (SRSE) is when status epilepticus continues for ≥24 h despite anesthetic treatment or recurs on an attempted wean of the anesthetic drugs. There is little evidence to guide the management of SRSE. Of late, unconventional therapies have been described in the literature regarding the management of SRSE, with ketamine leading the pack. Studies have noted ketamine's therapeutic efficacy up to 91% in SRSE cessation. Common side effects of ketamine include nausea, vomiting, headache, and hallucinations; but to our knowledge, ketamine has not been implicated in the pathogenesis of abdominal compartment syndrome. We describe a 74-year-old male who developed severe abdominal compartment syndrome in the setting of ketamine infusion for new-onset SRSE to increase awareness about this potential complication.

As early in 1935, Gibbs et al described electroencephalogram (EEG) features of large slow waves seen in “petit mal” seizures and change in background rhythm to a higher frequency, greater amplitude pattern in “grand mal” seizures. Studies have shown many typical EEG features in focal onset as well as generalized epilepsies2 3. It is usually easy to delineate focal epilepsy cases when EEG onset of seizures is clear as seen in Benign focal epileptiform discharges of childhood4. However, it is not uncommon to see cases where epileptiform discharges are not very clear. For example, there can be secondary bilateral synchrony or generalized onset of epileptiform discharges in some cases of focal epilepsy5 and nongeneralized EEG features is cases of generalized epilepsy like absence seizures.6 The awareness of occurrence of focal clinical and EEG features in generalized epilepsy is particularly important to help to select appropriate AEDs and also to avoid inappropriate consideration for epilepsy surgery7. Lüders et al8 have shown that multiple factors like electroclinical seizure evolution, neuroimaging (both functional and anatomical) have to be analyzed in depth before defining an epileptic syndrome. Here, we are providing few examples of different situations where it is still mysterious to figure out focal onset seizures with secondary generalization versus primary generalized epilepsy.