Acute Symptomatic Seizures Caused by Electrolyte Disturbances

Abstract

In this narrative review we focus on acute symptomatic seizures occurring in subjects with electrolyte disturbances. Quite surprisingly, despite its clinical relevance, this issue has received very little attention in the scientific literature. Electrolyte abnormalities are commonly encountered in clinical daily practice, and their diagnosis relies on routine laboratory findings. Acute and severe electrolyte imbalances can manifest with seizures, which may be the sole presenting symptom. Seizures are more frequently observed in patients with sodium disorders (especially hyponatremia), hypocalcemia, and hypomagnesemia. They do not entail a diagnosis of epilepsy, but are classified as acute symptomatic seizures. EEG has little specificity in differentiating between various electrolyte disturbances. The prominent EEG feature is slowing of the normal background activity, although other EEG findings, including various epileptiform abnormalities may occur. An accurate and prompt diagnosis should be established for a successful management of seizures, as rapid identification and correction of the underlying electrolyte disturbance (rather than an antiepileptic treatment) are of crucial importance in the control of seizures and prevention of permanent brain damage.

Benign convulsions in children with mild gastroenteritis

“…Electrolyte abnormalities and dehydration due to the severe loss of electrolytes and water in stools or vomitus may induce neurological symptoms. 4 A high fever (>39 C) that sometimes accompanies diarrhoeal syndromes may induce convulsions, particularly in infants and toddlers who are highly susceptible to febrile stimuli due to the immaturity of their central nervous system (CNS). 5 Infectious pathogens or fragments of these pathogens may breach the bloodebrain barrier and cause significant CNS damage, leading to seizures.…”

Serum sodium levels and related treatment‐emergent adverse events during eslicarbazepine acetate use in adults with epilepsy

“…AED‐induced hyponatremia is often asymptomatic, so we also analyzed TEAE incidence in patients grouped according to minimum postdose [Na + ] level. Symptoms typically associated with hyponatremia (including somnolence, headache, nausea, vomiting, convulsion, and partial seizures with secondary generalization) were reported more frequently in patients with the lowest minimum postdose [Na + ] levels (Group A) than in patients with no postdose [Na + ] measurements below 135 mEq/L (Group D) in the adjunctive trials.…”

“…Hyponatremia (ie, low blood sodium) may occur with the use of dibenzazepine carboxamide AEDs, [2][3][4][5][6][7][8][9] selective serotonin reuptake inhibitors (SSRIs), 10 thiazide diuretics, 11 or tricyclic antidepressants. 12 The risk of developing hyponatremia with dibenzazepine carboxamides may be greater with increased fluid intake, older age, AED polypharmacy, or concurrent use of sodium-wasting medications. 2,12,13 Minimum serum sodium concentrations ([Na + ]) of 125 mEq/L or less are generally considered to be clinically concerning.…”

“…12 The risk of developing hyponatremia with dibenzazepine carboxamides may be greater with increased fluid intake, older age, AED polypharmacy, or concurrent use of sodium-wasting medications. 2,12,13 Minimum serum sodium concentrations ([Na + ]) of 125 mEq/L or less are generally considered to be clinically concerning. 12,14 Nevertheless, AED-induced hyponatremia (which is typically subacute to chronic) is usually asymptomatic, even with [Na + ] ≤125 mEq/L; symptoms rarely occur until levels drop below 120 mEq/L.…”

Pseudohipoparatiroidismo de presentación tardía: reporte de dos casos

“…En un primer episodio convulsivo en pacientes adultos se describe que hasta un 15-30% son de causa tóxico-metabólicas. La hipocalcemia, principalmente aguda, puede estar presente en 20-30% de los casos de convulsiones en los adultos donde la presentanción como convulsión tónico-clónica es la más habitual 9 . Dado que no disponemos de calcemias previas, no es posible descartar que la hipocalcemia en este caso haya sido de aparición más tardía.…”