Authors :
Presenting Author: Sarah Frankl, MD – Michigan Medicine
H. Yavuz Ince, MD – Michigan Medicine
Neera Ghaziuddin, MD – Michigan Medicine
Kerri Neville, MD – Michigan Medicine
Rationale:
Catatonia is a psychomotor syndrome with a wide range of etiologies. It has the highest mortality risk of any pediatric psychiatric diagnosis (1). Electroconvulsive therapy (ECT) is the standard of care in patients with severe symptoms and/or who are unresponsive to high-dose benzodiazepine. ECT induces therapeutic seizures which is its mode of action, but is not thought to cause epilepsy. However, there exist case reports of patients developing epilepsy following ECT treatment (2). We investigated a series of pediatric patients with symptomatic electroencephalogram (EEG) abnormalities during course of ECT treatment.
Methods:
Patients were identified by child neurology consultation during their ECT course for new or worsening clinical symptoms, with workup revealing clinically significant epileptiform EEG abnormalities. We reviewed clinical histories and EEG reports.
Results:
A cohort of 15 patients (4 females) were identified between 2018-2024. Average age at first ECT was 14 years (range 9-18 years). The most common indication for ECT was catatonia (n=13), two patients had ECT for psychosis. Comorbid conditions included Autism Spectrum Disorder (n= 13), cognitive impairment (n= 9), mood disorders (n=5), pathogenic genetic(n= 3), schizophrenia & schizoaffective disorder (n = 2), and epilepsy (n=1). Pre-ECT EEG was performed in 11 patients. Findings were normal (n=2), background abnormalities without epileptiform features (n=5), and epileptiform abnormalities (4). The epileptiform abnormalities were occasional midline and bifrontal spikes (n=1), right frontal sharps (n=1), occasional midline sharps (n=1), and rare left temporal epileptiform discharges (n=1). Interictal EEG findings after initaition of ECT included multifocal epileptiform discharges (n = 15), generalized rhythmic delta activity (n=10), and diffuse spike-wave discharges (n=6). 11 patients were treated with anti-seizure medications for a new diagnosis of epilepsy. Of these, 5 had discrete electrographic seizures captured on EEG and 3 were treated for EEGs on ictal-interictal continuum. The patient with known epilepsy had clinical and electrographic improvement with holding of ECT alone. Conclusions:
A cohort of pediatric patients receiving ECT developed clinically significant epileptiform EEG abnormalities during their treatment course. This highlights the need for collaborative care between neurologists and psychiatrists for those receiving ECT, particularly those who may be at higher risk for epilepsy due to neurodevelopmental disorders and those of younger age. Potential confounding variable is the known effect of ECT on EEG without any manifestation of epilepsy. Duration of ECT course may play an important role as well.
Funding: The authors received no funding.