As mentioned in an earlier post about using location of tongue bites to guesstimate a seizure, an unwitnessed seizure event has many differential diagnoses that may be frustrasting to tease out if an EEG is not immediately available. Instead we channelize our inner Sherlock Holmes 🔍 to draw inferences from circumstantial evidence – Cut of tongue, Confusion after, Continence loss, CVA-like Todd’s paralysis, CK / Prolactin elevation, etc. When evidences are indirect, the more the merrier. EEG is only available only at bigger referral hospitals and loses diagnostic uility as time passes, as seen in patients being brought in from remote areas.
Several studies show a acute rise in blood levels of Lactic acid & Ammonia following a seizure event – at least for generazlied tonic-clonic (GTC) seizures, both in humans and animals. A few of such older studies include a 2010 study, 2011 study, a 2016 study and a series of 6 case-reports in 2017, A more recent 2019 German study tracked Lactic acid, Ammonia, Prolactin, Phosphate and other electrolytes in 39 patients with GTC seizures showing transient Lactic acid elevation in 90% cases, Ammonia elevation in 70% cases. Levels tend to rise within 30 mins of event & come down quickly in 2-3 hours. Some postulate that elevated lactic and ammonia may contribute to post-ictal confusion.
Just like Prolactin leves, elevated Lactic acid & Ammonia levels drift down after the event, but unlike Prolactin – Lactic & Ammonia level checks are more widely available even in remote ERs. So in small town urgent cares & ERs, if a patient is brought in after a unwitnessed loss or altered consciousness event where a seizure is on the list of differentials – increased levels of lactic acid & ammonia within 30 mins or event that trend down in 2-4 hours on their own could help corroborate a unwitnessed seizure and even help differentiate between true seizure and psychogenic seizure, syncope, etc.
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