Acute metabolic effects of tonic‐clonic seizures

Abstract

ObjectiveTonic‐clonic seizures (TCS) lead to metabolic stress and changes in related blood markers. Such markers may indicate harmful conditions but can also help to identify TCS as a cause of transient loss of consciousness. In this study, we hypothesized that the alterations of circulating markers of metabolic stress depend on the clinical features of TCS.MethodsNinety‐one adults undergoing video‐EEG monitoring participated in this prospective study. Electrolytes, renal parameters, creatine kinase (CK), prolactin (PRL), lactate, ammonia, glucose, and other parameters were measured at inclusion and different time points after TCS.ResultsA total of 39 TCS were recorded in 32 patients (six generalized onset tonic‐clonic seizures in 6 and 33 focal to bilateral tonic‐clonic seizures in 26 patients). Shortly after TCS, mean lactate, ammonia, and PRL levels were significantly increased 8.7‐fold, 2.6‐fold, and 5.1‐fold, respectively, with levels of more than twofold above the upper limits of the normal (ULN) in 90%, 71%, and 70% of the TCS and returned to baseline levels within 2 hours. Only postictal lactate levels were significantly correlated with the total duration of the tonic‐clonic phase. In contrast, CK elevations above the ULN were found in three TCS (~10%) only with a peak after 48 hours. Immediately after the TCS, hyperphosphatemia occurred in one third of the patients, whereas hypophosphatemia was observed in one third 2 hours later. TCS led to subtle but significant alterations of other electrolytes, creatinine, and uric acid, whereas glucose levels were moderately increased.SignificanceLactate is a robust metabolic marker of TCS with elevations found in ~90% of cases within 30 minutes after seizure termination, whereas ammonia rises in ~ 70%, similarly to PRL. Phosphate levels show an early increase and a decrease 2 hours after TCS in a third of patients. CK elevations are rare after video‐EEG‐documented TCS, challenging its value as a diagnostic marker.

Prehospital lactate levels in blood as a seizure biomarker: A multi‐center observational study

“…We observed a clear decrease in lactate values with increased delay between call and measurement, and follow‐up lactate was lower in cases of seizures with high initial lactate. This agrees with previous observations of increased lactate levels after seizures being a relatively short‐lasting phenomenon 12,20 . An interesting question is therefore if rapid normalization of lactate can be used to support a seizure diagnosis.…”

“…This agrees with previous observations of increased lactate levels after seizures being a relatively short-lasting phenomenon. 12,20 An interesting question is therefore if rapid normalization of lactate can be used to support a seizure diagnosis. It is plausible that the dynamics matter and that a series of lactate values could add to the diagnostic certainty.…”

Association of Hyperuricemia With Acute Kidney Injury: Case Series Report Among Patients Hospitalized With General Tonic-Clonic Seizures

“…However, a posteriori, recruiting patients who had unprovoked convulsive episodes at homewhich caused notable delay between the convulsion and the first blood sample-probably did not allow us to capture the uric acid peak level, as demonstrated later by Nass et al Despite this limitation, our results are compatible with conclusions reported in previous studies. 3,7 We found higher uric acid levels at the first sample compared to subsequent values during follow-up. However, the magnitude of increase in uric acid levels in our cohort was mild (22.9% median increase) and lower than the increase reported by Nass et al in the setting of EEG monitoring induced-seizure (61.1%, p < .001), where the kinetics of uric acid showed a peak value 2 hours after the seizure episode.…”

Notfallmanagement epileptischer Anfälle

“…Labordiagnostik ist selten hilfreich, um die epileptische Genese zu sichern. Neuere Studien berichten jedoch eine Laktaterhöhung bei 90 % der Patienten innerhalb von 30 min nach einem tonisch-klonischen Anfall [6].…”