efficacy of gabapentin in patients with central post-stroke pain

Thalamic pain syndrome, a type of central post-stroke pain [CPSP], may develops after a hemorrhagic or ischemic stroke and results in impairment of the thalamus. There is limited experience about gabapentin in treatment of central pains like CPSP. In a prospective observational study, the intensity of pain was recorded using the Numeric Rating Scale [NRS] at the entrance to the study. Patients eligible for treating with gabapentin, received gabapentin 300 mg twice-daily. The pain intensity was measured at entrance to the study and after one month using NRS. Decrease of 3 points from the initial NRS considered being clinically significant. From a total of 180 primarily screened patients, 84 [44 men and 40 women] were recruited. There was a significant difference between pre-treatment and post-treatment NRS [5.9 +/- 2.51 vs. 4.7 +/- 3.01; 95% CI: 0.442-1.962, p = 0.002]. Fisher›s exact test showed no statistically significant effect of clinical and demographic characteristics of patients on their therapeutic response to gabapentin. Given the safety, efficacy, well tolerability and lack of interaction with other drugs we suggest gabapentin to be more considered as a first line therapy or as add-on therapy for reducing the pain severity in patients with thalamic syndrome

Association between ABCB1-T1236C polymorphism and drug-resistant epilepsy in Iranian female patients

One third of epileptic patients are resistant to several anti-epileptic drugs [AED]. P-glycoprotein [P-gp] is an efflux transporter encoded by ATP-binding cassette subfamily B member 1 [ABCB1] gene that excludes drugs from the cells and plays a significant role in AEDs resistance. Over-expression of P-gp could be a result of polymorphisms in ABCB1 gene. We studied the association of T129C and T1236C single-nucleotide polymorphisms [SNP] of ABCB1 gene with drug-resistant epilepsy in Iranian epileptics. DNA samples were obtained from 200 healthy controls and 332 epileptic patients, of whom 200 were drug responsive and 132 drug resistant. The frequencies of the genotypes of the two SNP were determined by polymerase chain reaction followed by restriction fragment length polymorphism. No significant association was found between T129C and T1236C genotypes and drug-resistant epilepsy neither in adults nor in children. However, the risk of drug resistance was higher in female patients with 1236CC [P = 0.02] or CT [P = 0.008] genotype than in those with TT genotype. The risk of drug resistance was also higher in patients with symptomatic epilepsies with 1236CC [P = 0.02] or CT [P = 0.004] genotype than in those with TT genotype. The risk of drug resistance was lower in patients with idiopathic epilepsies with 129TT genotype [P = 0.001] than in those with CT genotype. Our results indicate that T1236C polymorphism is associated with drug resistance in Iranian female epileptic patients. Replication studies with large sample sizes are needed to confirm our results