Amantadine, a commonly prescribed drug for Parkinson's disease and other disorders, was recently used for treating epileptic encephalopathy in pediatric patients in Spain.
The tricyclic amine amantadine was first approved in 1976 for the prophylaxis of influenza A. In recent years, the drug has been prescribed for patients with Parkinson's, attention deficit hyperactivity disorder (ADHD), autism, unipolar depression, and acquired brain injuries.
Studies on amantadine suggest that the drug inhibits dopamine, reduces microglia-associated inflammation and blocks NMDA receptors, yet its complete mechanism of action remains unknown. In fact, the anti-epileptic function of the drug was discovered purely by accident - two children with epilepsy received amantadine for influenza and were subsequently rendered seizure-free.
A study published by Insuga et al in the Journal of the Spanish Neurology Society aims to establish efficacy of the drug in treating refractory absence seizures, or development and/or epileptic encephalopathy with spike-and-wave activity in sleep (DEE-SWAS) in pediatric patients.
Absence seizures, also known as petit mal seizures, are characterized by periods of blank staring accompanied by a loss of awareness. They are more common among children between three to thirteen years of age and last a maximum of 15 seconds. Refractory absence seizures show a degree of resistance to treatment via traditional anti-epileptic medications, such as lorazepam, sodium valproate with valproic acid, ethosuximide, and lamotrigine.
DEE-SWAS is also observed primarily in pediatric patients yet is relatively rarer. Generally accompanied by the onset of other seizure types, patients exhibit abnormal spike-wave neuroelectric discharges during periods of sleep. This may be diagnosed using an electroencephalogram (EEG) with recorded sleep.
In cases of both absence seizures and DEE-SWAS, epileptic episodes may cease as the patient reaches adulthood, but encephalopathic diseases at any age predispose affected individuals to develop some form of convulsive disorders later in life.
The study in Madrid was initiated in 2017 and recruited 12 patients below eighteen years of age that were subject to follow-up analyses till April 2023. The patients underwent extensive magnetic resonance imaging (MRI), clinical exome sequencing, cognitive and behavioral assessments. Amantadine was administered once daily with doses ranging between 4 mg and 300 mg.
A majority of patients in the DEE-SWAS group showed positive results on amantadine. Epileptiform activity was observed in the EEGs prior to dosing, but after administration, normal sleep background architecture returned with no epileptic activity. However, less success was seen in the other tested group. Only one patient with refractory absence seizures responded well to therapy. But after three years on amantadine, seizures returned with frequency.
An overall good response was observed in 41.7% of the tested population, yet the treatment impact seemed to decline over time. 53% showed improved EEG readouts, and up to 30% achieved complete resolution of spike-and-wave activity during sleep.
Resistance to dopaminergic drugs in encephalopathic indications has been reported before, observed famously in the Sacks' levodopa (L-DOPA) trials of the 1960s, conducted on patients with 'sleeping sickness,' or encephalitis lethargica. Though initially successful, patients on the therapy regressed gradually to their former state of catatonia, interrupted by extended spells of Parkinsonian behavior.
Authors cited previous studies where amantadine demonstrated considerable reductions of absence seizures in children, including a 2012 trial yielding a 90% decrease in seizure events. However, it was noted that greater success in seizure control may result from primary treatment with amantadine, subverting first-line treatment with drugs like ethosuximide.
Moreover, response to amantadine varied with the types of epilepsy treated. Myoclonic seizures were largely controlled, but tonic-clonic seizures saw almost no change on the treatment.
Thus, a consensus from these studies suggests the use of amantadine as an add-on therapy to existing first-line treatments, pending further research in the field.
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