Abstract
Cerebral metabolic disturbances during seizures and hypoxic-ischemic events in patients with hypoxic-ischemic encephalopathy (HIE) can lead to excessive synaptic and extracellular concentrations of glutamate with concomitant and subsequent neuronal cell injury or death.[1][1],[2][2] Multiple studies
Highlights
Cerebral metabolic disturbances during seizures and hypoxic-ischemic events in patients with hypoxic-ischemic encephalopathy (HIE) can lead to excessive synaptic and extracellular concentrations of glutamate with concomitant and subsequent neuronal cell injury or death.[1,2] Multiple studies suggest that the increased glutamate concentration in the brain can induce seizures.[2]
The peak areas of ␣-Glx and TCr were measured at 3.75 ppm and 3.02 ppm, respectively, on the point resolved spectroscopy sequence (TR of 2000 ms; TE of 135 ms, with averages of 250 ms)
The selection of the spectral volume of interest was done because several studies in human neonates with severe perinatal asphyxia have shown that the basal ganglia and thalami are more sensitive to anoxia.[5,6]
Summary
Cerebral metabolic disturbances during seizures and hypoxic-ischemic events in patients with hypoxic-ischemic encephalopathy (HIE) can lead to excessive synaptic and extracellular concentrations of glutamate with concomitant and subsequent neuronal cell injury or death.[1,2] Multiple studies suggest that the increased glutamate concentration in the brain can induce seizures.[2]. Grade 1 was defined as occasional and transient seizures.
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