ABSTRACT
Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ventricular zone neurons are vulnerable to ischemia that can impair memory and learning functions. Although neurogenesis normally occurs in the dentate gyrus [DG] of the hippocampus and sub-ventricular zone [SVZ] following brain damage, this response is unable to compensate for severely damaged areas. This study aims to assess both neurogenesis and the neuroprotective effects of transforming growth factor-alpha [TGF-alpha] on the hippocampus and SVZ following ischemia-reperfusion. In this experimental study, a total of 48 male Wistar rats were divided into the following groups: surgical [n=12], phosphate buffered saline [PBS] treated vehicle shams [n=12], ischemia [n=12] and treatment [n=12] groups. Ischemia was induced by common carotid occlusion for 30 minutes followed by reperfusion, and TGF-alpha was then injected into the right lateral ventricle. Spatial memory was assessed using Morris water maze [MWM]. Nestin and Bcl-2 family protein expressions were studied by immunohistochemistry [IHC] and Western blot methods, respectively. Finally, data were analyzed using Statistical Package for the Social Sciences [SPSS, SPSS Inc., Chicago, USA] version 16 and one-way analysis of variance [ANOVA]. TGF-alpha injection significantly increased nestin expression in both the hippocampal DG and SVZ areas. TGF-alpha treatment caused a significant decrease in Bax expression and an increase in Bcl-2 anti-apoptotic protein expression in the hippocampus. Our results showed a significant increase in the number of pyramidal neurons. Memory also improved significantly following TGF-alpha treatment. Our findings proved that TGF-alpha reduced ischemic injury and played a neuroprotective role in the pathogenesis of ischemic injury
Subject(s)
Animals, Laboratory , Memory Disorders , Memory , Neurogenesis , Reperfusion Injury , Hippocampus , Rats, WistarABSTRACT
Spastic cerebral palsy [CP] is one of the most difficult and disabling conditions that requires medical attention and treatment. The aim of this study was to assess the efficacy and safety of oral tizanidine in treating spasticity in children with spastic CP. Sixty children with spastic cerebral palsy were enrolled in a double-blind, placebo-controlled, randomized clinical trial. These patients were randomly assigned to receive tizanidine or a matching placebo. Sample normalization was not performed either before or after the study in these two separate groups. Nevertheless, no significant statistical difference was found between the two concerned groups in terms of age, sex, or type of spasticity. Each patient received the treatment for 2 weeks between May 2010 and February 2011. Thirty-one boys and 29 girls with a mean age of 7.3 +/- 3.4 years were evaluated. Our study revealed that spasticity was reduced in 50% of the patients receiving the drug tizanidine compared to only 6.7% of the patients receiving the placebo. Additionally, 66.7% of patients reported less pain on the affected side receiving tizanidine [group A] compared to 13.3% of patients receiving the placebo [group B]. No serious side effects were reported in this study. Tizanidine is effective and safe in decreasing the spastic hypertonia associated with cerebral palsy in children
ABSTRACT
Classic Pelizaeus-Merzbacher disease is a rare x-linked disorder of proteolipid protein expression first described clinically in 1885. This disease is characterized by abnormal eye movements, very slow motor development and involuntary movements. The causative gene is PLP1. A 1-year-old boy was referred to our clinic due to abnormal eye movements. He had horizontal and flickering eye oscillation, psychomotor retardation, hypotonia and head nodding. We found hypomyelination in brain MRI. The possibility of Pelizaeus-Merzbacher disease should be considered in boys with abnormal eye movements, psychomotor retardation and hypotonia
ABSTRACT
L-2-Hydroxyglutaric aciduria is a rare autosomal recessive inherited neurometabolic disorder.It is characterized by slow progressive neurological dysfunction with cerebellar ataxia, pyramidal and extrapyramidal signs, intellectual decline, and seizures. Herein, we report a case of a 7-year-old boy from Tehran whose symptoms and signs indicated leukoencephalopathy with macrocephaly and motor delay