Abstract
The immature brain is highly susceptible to seizures induced by a variety of insults, including hypoxia, fever, and trauma. Unlike early life epilepsy associated with congenital dysplasias or genetic abnormalities, insults induce a hyperexcitable state in a previously normal brain. Here we evaluate the epileptogenic effects of seizure-inducing stimuli on the developing brain, and the age and regional specificity of these effects.
Highlights
The majority of human seizures occur early in life, and many developmental seizures occur only during discrete windows of development
Most early-life seizures are not genetically determined, and the majority of seizures occurring during infancy and early childhood are not spontaneous but are triggered by fever [Shinnar, 1998], hypoxia [Jensen et al, 1991; Westmark et al, 1995], or trauma [Dinner, 1993]
Hypoxia-related seizures occur primarily in neonates [Jensen et al, 1991, 1998; Volpe, 1995], febrile seizures are exclusive to infancy and childhood, and early traumatic seizures are more common in children [Jennett and Lewin, 1960]
Summary
The majority of human seizures occur early in life, and many developmental seizures occur only during discrete windows of development. To study whether hypoxia induces long-term functional changes intrinsic to neuronal networks in the absence of significant cell death, electrophysiological recordings were made from hippocampal slices removed from rats either acutely following hypoxia at P10 or from adults with prior hypoxia at P10 [Jensen et al, 1998]. In both cases, effects of hypoxia were observed that supported the in vivo observations that perinatal hypoxia increased network excitability and seizure susceptibility. The increased seizure susceptibility suggests that more subtle functional alterations in network excitability have occurred during development in response to the hypoxic insult
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