Abstract
Seizures are the most acute evident manifestation of central nervous system dysfunction in neonates. The incidence is higher in very low weight neonates, about 58/100 live births, as opposed to full-term infants, estimated about 3.5/100 live births. Neonatal seizures represent the clinical manifestation of a non-specific disorder of cortical cerebral dysfunction, which could lead to permanent brain injury. The etiology is multifactorial and requires a judicious assessment of each clinical scenario. The diagnosis and its management are further complicated as most neonatal seizures may have very subtle or no clinical changes and the diagnosis may be just based on EEG findings, so-called subclinical. The treatment is dependent on the etiology, but early and opportune intervention can prevent further brain damage and improve prognosis. Although early identification and treatment are essential, the diagnosis of neonatal seizures can be further complicated by the clinical presentations, possible etiologies, and treatments. Nevertheless, research studies and clinical evidence have shown that early treatment with anti-seizure medications can change the outcome.
Highlights
BackgroundNeuropathophysiology: disease processSeizures are the clinical consequence of depolarization and excessive synchronous discharge of the neurons
Neonatal seizures represent the clinical manifestation of a non-specific disorder of cortical cerebral dysfunction, which could lead to permanent brain injury
The diagnosis and its management are further complicated as most neonatal seizures may have very subtle or no clinical changes and the diagnosis may be just based on EEG findings, so-called subclinical
Summary
Seizures are the clinical consequence of depolarization and excessive synchronous discharge of the neurons. In patients with normal metabolism, when glucose is metabolized within the cell, ATP is increased, and Mg-ADP is decreased, causing the K-ATP channels to close and membrane depolarization to a point of permissible action potentials and neurotransmitter release and synaptic GABA release. When mutant K-ATP channels are overactive, like what is seen during metabolic distress, the channels are open, potassium leaves the cell, the membrane is hyperpolarized, and the action potential firing affects neurotransmitters release, causing impairment of GABA release It has been identified in some patients K-ATP mutations that reduce sulfonylurea blocker efficacy and preventing treatment by currently available agents. Improvement in cognitive skills and major developmental delays may not be possible in all children [38] This group of patients presents with neonatal encephalopathy and seizures that respond to pyridoxal phosphate but does not respond to pyridoxine. Such findings indicate a deficiency of threonine dehydrogenase and a glycine cleavage enzyme suggesting a pyridoxal phosphate dehydrogenase deficiency [39]
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