Background Hemorrhagic events can result in significant neurological damage, and identifying effective strategies for neuroprotection is crucial. Several studies have directed their attention to the alterations in perilesional parenchymal tissue. These investigations have sought to modify ischemic and metabolic changes by utilizing potential neuroprotective agents and to develop strategies that effectively mitigate secondary perilesional neuronal damage.
View Article and Find Full Text PDFObjective: Describe the epidemiological profile and social-economic burden that hydrocephalus patients represent to the national public health system, using data available at the online database of the Brazilian Health Ministry (DataSUS).
Methods: This is a populational study based on descriptive statistics of all clinical and surgical appointments included in the DataSUS database. Data included herein were collected between 2015 and 2021 and subdivided into three main groups, related to hydrocephalus incidence and mortality, hospitalizations, and financial costs.
J Chem Neuroanat
November 2022
Hydrocephalus is defined as the accumulation of cerebrospinal fluid in the brain ventricles. The usual treatment of hydrocephalus is surgical (shunt), but not all patients can undergo treatment immediately after diagnosis. Thus, neuroprotective measures were tested to minimize the tissue damage involved.
View Article and Find Full Text PDFJ Chem Neuroanat
January 2022
The neuroprotective effect of Edaravone in young hydrocephalic rats associated with a CSF derivation system was evaluated. The drug has already been shown to be beneficial in experimental hydrocephalus, but the combination of this drug with shunt surgery has not yet been investigated. Fifty-seven-day-old Wistar rats submitted to hydrocephalus by injection of kaolin in the cisterna magna were used and divided into five groups: control (n = 10), hydrocephalic (n = 10), hydrocephalic treated with Edaravone (20 mg/kg/day) (n = 10), hydrocephalic treated with shunt (n = 10) and hydrocephalic treated with shunt and Edaravone (n = 10).
View Article and Find Full Text PDFThe tuberous sclerosis complex (TSC), focal cortical dysplasia IIB (FCD IIB), and hemimegalencephaly (HME) exhibit similar molecular features that are dependent on the hyperactivation of the mTOR pathway. They are all associated with refractory epilepsy and the need for surgical resection with varying outcomes. The phosphorylated protein S6 (pS6) is a downstream target of mTOR, whose increased expression might indicate mTOR hyperactivation, but which is also present when there is no alteration in the pathway (such as in FCD type I).
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