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Although steroids are suggested as the treatment of choice for infantile spasms, the mechanism of action is still unclear. Using a rat model of malformation of cortical development with refractory infantile spasms, we evaluated the efficacy of methylprednisolone on spasms susceptibility and behaviors. Additionally, we investigated the in vivo electrophysiological and neurochemical changes of the brain after methylprednisolone treatment. Infant rats with prenatal exposure of methylazoxymethanol at gestational day 15 were used. After a single dose of methylprednisolone or three different doses of methylprednisolone for 3 days, spasms were triggered by intraperitoneal injection of N-methyl-d-aspartic acid. In rats with three days of methylprednisolone pretreatment and their controls, behavioral testing was performed at postnatal day 15. In vivo magnetic resonance imaging was conducted at postnatal day 15 after 3 days of methylprednisolone treatment. The rats with single methylprednisolone pretreatment showed significantly delayed onset of spasms and multiple doses of methylprednisolone significantly suppressed the development of spasms in a dose-dependent manner. After multiple methylprednisolone pretreatment and a cluster of N-methyl-d-aspartic acid-induced spasms, the rats showed significantly increased freezing behaviors to conditioned stimuli. Glutamate-weighted chemical exchange saturation transfer revealed significant elevation of glutamate concentration in the cortices of the rats with multiple methylprednisolone pretreatments. Methylprednisolone pretreatment could attenuate N-methyl-d-aspartic acid-induced spasms with in vivo neurochemical and electrophysiological changes, which indicates this steroid's action on the brain and in epilepsy. This article is protected by copyright. All rights reserved.
This article was published in the following journal.
Name: The European journal of neuroscience
Perinatal stroke is a significant cause of severe epilepsy, including epileptic spasms. Although epileptic spasms due to underlying structural lesion often respond poorly to treatment and evolve into ...
Corpus callosotomy (CC) has recently been adopted for the treatment of drug-resistant epileptic spasms and tonic spasms. In the present study, we investigated CC outcomes among patients with drug-resi...
Introduction: Epileptic spasms are seizures usually associated with a severe developmental epilepsy syndrome with onset in the first year of life, peaking between 3 and 10 months of age . A variet...
To compare the clinical efficacy of high-dose prednisone monotherapy and the combination of hormone and moderate-dose topiramate (TPM) therapy in children with infantile spasms (IS) and late-onset epi...
Stress can induce a serious epileptic encephalopathy that occurs during early infancy. Recent studies have revealed that prenatal stress exposure is a risk factor for the development of infantile spas...
Epileptic spasms are a difficult to treat epileptic condition in young children. The first line treatment is hormonal treatment, in the form of ACTH or oral steroids, which are effective i...
Infantile Spasms (IS) are classically refractory to the usual antiepileptic drugs and often pose a therapeutic challenge. Since, there is associated significant morbidity, much effort has ...
OBJECTIVES: I. Evaluate the efficacy of surgical resection of an identifiable zone of cortical abnormality versus multiple drug therapy in children with infantile spasms refractory to sta...
Infantile spasms constitute a type of catastrophic epilepsy syndrome occuring in young children. The ketogenic diet has been shown to be very effective in these children. The modified Atki...
Epileptic disease is characterised by enhanced brain excitability. Low frequency repetitive transcranial magnetic stimulation (rTMS) can be an effective treatment for refractory frontal ep...
Heterogeneous disorders of cortical malformation characterized by excessive and small fused gyri and shallow sulci of the CORTEX with abnormal cortical lamination. It is considered a malformation secondary to abnormal post-migrational development of the neurons during cerebral cortical development and is associated with EPILEPSY and learning difficulties.
An epileptic syndrome characterized by the triad of infantile spasms, hypsarrhythmia, and arrest of psychomotor development at seizure onset. The majority present between 3-12 months of age, with spasms consisting of combinations of brief flexor or extensor movements of the head, trunk, and limbs. The condition is divided into two forms: cryptogenic (idiopathic) and symptomatic (secondary to a known disease process such as intrauterine infections; nervous system abnormalities; BRAIN DISEASES, METABOLIC, INBORN; prematurity; perinatal asphyxia; TUBEROUS SCLEROSIS; etc.). (From Menkes, Textbook of Child Neurology, 5th ed, pp744-8)
Cortical malformations secondary to abnormal cortical maturation after CELL MIGRATION in NEUROGENESIS. This group includes injury to the cortex during later stages of cortical development such as POLYMICROGYRIA and focal cortical dysplasias.
A water-soluble ester of METHYLPREDNISOLONE used for cardiac, allergic, and hypoxic emergencies.
Cortical malformations secondary to abnormal neuronal and glial CELL PROLIFERATION or APOPTOSIS in NEUROGENESIS. This group includes congenital MICROCEPHALIES; MICROLISSENCEPHALIES, megalencephalies, HEMIMEGALENCEPHALIES and cortical dysplasias with balloon cells.
Neurology - Central Nervous System (CNS)
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