Massoud Mahmoudian; Mohammad Rezvani; Mohammad Rohani; Foozya Benaissa; Mehdi Jalili; Shadi Ghourchian
Volume 14, Issue 1 , March 2015, , Pages 12-16
Abstract
Background: Massive ischemic stroke causes significant mortality and morbidity in stroke patients. The main treatments for massive ischemic stroke are recombinant tissue plasminogen activator (rtPA), craniotomy, and endovascular interventions. Due to destructive effects of bradykinin on the ...
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Background: Massive ischemic stroke causes significant mortality and morbidity in stroke patients. The main treatments for massive ischemic stroke are recombinant tissue plasminogen activator (rtPA), craniotomy, and endovascular interventions. Due to destructive effects of bradykinin on the nervous system in ischemic stroke, it seems reasonable that using Noscapine as a Bradykinin antagonist may improve patients’ outcome after ischemic stroke. The effect of Noscapine on massive ischemic stroke was shown by the previous pilot study by our group. This pseudo-randomized clinical trial study was designed to assess the result of the pilot study.Methods: Patients who had clinical symptoms or computed tomography scan indicative of massive stroke (in full middle cerebral artery territory) were entered to the study. The cases received the drugs according to their turns in emergency ward (pseudo-randomized). The patient group received Noscapine, and the control group received common supportive treatments. The patients and data analyzer were blinded about the data. At the mend of the study, to adjust confounding variables we used logistic regression.Results: After 1-month follow-up, 16 patients in the control group and 11 patients in the case group expired (P = 0.193). Analyzing the data extracted from Rankin scale and Barthel index check lists, revealed no significant differences in the two groups.Conclusion: Despite the absence of significant statistical results in our study, the reduction rate of 16% for mortality rate in Noscapine recipients is clinically remarkable and motivates future studies with larger sample sizes.
Mitra Ansari Dezfouli; Elham Jaberi; Afagh Alavi; Mohammad Rezvani; Gholamali Shahidi; Elahe Elahi; Mohammad Rohani
Volume 11, Issue 4 , December 2012, , Pages 155-158
Abstract
Background: Pantothenate kinase associated neurodegeneration (PKAN) is the most prevalent type of neurodegeneration with brain iron accumulation (NBIA) disorders characterized by extrapyramidal signs, and 'eye-of-the-tiger' on T2 brain magnetic resonance imaging (MRI) characterized by hypointensity in ...
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Background: Pantothenate kinase associated neurodegeneration (PKAN) is the most prevalent type of neurodegeneration with brain iron accumulation (NBIA) disorders characterized by extrapyramidal signs, and 'eye-of-the-tiger' on T2 brain magnetic resonance imaging (MRI) characterized by hypointensity in globus pallidus and a hyperintensity in its core. All PKAN patients have homozygous or compound heterozygous mutation in PANK2 gene.Methods:Three sibling patients were diagnosed based on clinical presentations especially extrapyramidal signs and brain MRI. The exons and flanking intronic sequences of PANK2 were sequenced from DNA of leukocytes of the affected individuals.Results:All patients were homozygous for c.C1069T, p.R357W in PANK2 gene. This mutation is well conserved in the homologous protein of distally related spices.Conclusion:In the current study we identified three siblings affected with PKAN, all of them have mutations in PANK2 gene. In MRI of all patients with PANK2 mutation eye-of-the-tiger sign was apparent.
