So at the International League Against Epilepsy Congress, I was lucky enough to be part of a session presenting clues that clinicians should look for to diagnose acute provoked seizures. So most neonatal seizures, and when we talk about neonatal seizures, it’s that first 28 days of life. And most of them are due to an acute provoking reaction, whether it be infection or HIE or a structural etiology, there’s something usually that causes it...
So at the International League Against Epilepsy Congress, I was lucky enough to be part of a session presenting clues that clinicians should look for to diagnose acute provoked seizures. So most neonatal seizures, and when we talk about neonatal seizures, it’s that first 28 days of life. And most of them are due to an acute provoking reaction, whether it be infection or HIE or a structural etiology, there’s something usually that causes it. So at the bedside, it’s important to figure out what is the etiology so you can correct that etiology and stop the seizures. And so the clues that I focused on in my talk was knowing what really is prevalent at specific ages of life. So in term babies, the most common etiology is HIE, followed by the other etiologies, infectious, brain malformation, metabolic abnormalities, stroke, hemorrhage, genetic etiologies, where in preterm infants, the main cause is intraventricular hemorrhage. So just knowing what you’re dealing with, the most common things, because the common things occur commonly. The second clue was knowing what seizure etiologies occur at specific ages. So in the first 24 hours of life, HIE, pyridoxine dependency, other metabolic abnormalities, infections, those typically occur early on, where in the first week, you think more cortical malformations, herpes, different types of viruses, and other types of inborn errors of metabolism. So just knowing the onset is another clue. And then the third clue is really focusing on the ILAE semiology. So knowing specific seizure types, what they’re associated with. So for clonic seizures, where you see arrhythmic jerking at the bedside, that commonly occurs with stroke. So you think of vascular etiologies, where other things like infectious can also be clonic. With tonic seizures, that’s that focal extension of the arm or the leg. Typically, when you see that, you think genetic etiologies, but metabolic, cortical malformations, vascular malformations can also present. When you see myoclonic seizures, that’s like an irregular jerking movement, typically is associated with metabolic causes, but genetic etiologies can also present that way. When you see sequential seizures, so that’s multiple seizures in a row, typically tonic is always associated with that, but that typically suggests a genetic or a metabolic etiology, but vascular, HIE, other cortical malformations can also present that way. But when you see that, you would want to most likely send off a genetic panel. Epileptic spasms also are genetic etiologies and electrographic seizures often are HIE or vascular. So when you see a specific semiology at the bedside, you should start thinking about etiology. So those were the three clues that I focused on in my talk.
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