Intavenous immunoglobulin for the management of intractable epilepsy in a boy.

BACKGROUND: The involvement of the immune system in the pathogenesis of certain types of epilepsy has been supported in the past. The use of intravenous immunoglobulin in the treatment of neurologic diseases has shown a progressive trend over the last years. CASE REPORT: We report the case of a 9.5-year-old boy with refractory epilepsy who was admitted for investigation of his persistent seizures and severe psychomotor regression. He experienced persistent tonic-clonic over the preceding six months and long lasting atonic seizures since the age of six and did not respond to multiple anticonvulsant drugs. The administration of intravenous immunoglobulin achieved seizure control and cognitive improvement. CONCLUSION: This case underscores the efficacy of intravenous immunoglobulin in the treatment of refractory epilepsy in children. HIPPOKRATIA 2017, 21(1): 55-57.

Prevention of complications related to traumatic brain injury in children and adolescents with creatine administration: an open label randomized pilot study.

BACKGROUND: There has been an enormous focus on the discovery and development of neuroprotective agents that might have clinical relevance after traumatic brain injury (TBI). Based on experimental facts, we studied administration of creatine to patients with TBI. METHODS: A prospective, randomized, comparative, open-labeled pilot study of the possible neuroprotective effect of creatine was performed on 39 children and adolescents, aged between 1 to 18 years old, with TBI. The creatine was administered for 6 months, at a dose of 0.4 gr/kg in an oral suspension form every day. For categorical variables, we used the chi test to identify differences between controls and cases. Statistical significance was defined as a p value <0.05 and not statistically significant if p value >0.1. RESULTS: The administration of creatine to children with TBI improved results in several parameters, including duration of post-traumatic amnesia (PTA), duration of intubation, intensive care unit (ICU) stay, disability, good recovery, self care, communication, locomotion, sociability, personality/behavior and neurophysical, and cognitive function. Significant improvement was recorded in the categories of Cognitive (p < 0.001), personality/behavior (p < 0.001), Self Care (p = 0.029), and communication (p = 0.018) aspects in all patients. No side effects were seen because of creatine administration. CONCLUSION: Preliminary data suggest that the administration of creatine may be beneficial to patients with traumatic brain injury.

L-carnitine modifies the humoral immune response in mice after in vitro or in vivo treatment.

Although the role of L-carnitine (L-Cn) as a cofactor in the oxidation of long-chain fatty acids has been well established, this agent has also been recognized to have an important role in the regulation of carbohydrate metabolism, and consequently, the maintenance of cell membrane structure and cell viability. L-Cn has been reported to reduce the apoptotic levels of CD4+ and CD8+ cells. It has also been demonstrated to interfere with cells of the monocytic lineage by regulating their ability to produce growth factors that ultimately affect both T and B lymphocytic subsets. Therefore, in this study, we examined whether this agent affects the antigenic response of immune cells and determined the relative numbers of immune cells in the murine spleen after in vitro and in vivo treatment. The results showed that L-Cn reduces the relative numbers of CD8+, CD4+ and Ly5+ cells. This observation was consistent in all systems studied including (a) in vitro inoculation of antigen (DNP-HSA) and L-Cn, (b) in vitro priming of spleen cells treated with L-Cn in vivo, and (c) in vivo immunization and L-Cn administration. In all cases, the reduction of T lymphocytes correlated with the decreased production of interleukin-2. L-Cn, however, did not affect the production of specific antibody, which indicates that the observed reduction of Ly5-positive cells is due to cell differentiation of B cells to plasma cells.