Myoclonic-Atonic Epilepsy Masquerading as Subacute Sclerosing Panencephalitis: A Clinical Conundrum

Abstract

Letter to the editorMyoclonic epilepsy of infancy, myoclonic-atonic epilepsy (MAE) with onset in early childhood, and later-onset syndromes such as juvenile myoclonic epilepsy, eyelid myoclonic epilepsy, and myoclonic absence epilepsy are all examples of childhood-onset myoclonic epilepsy syndromes. Degenerative brain disorders, subacute sclerosing panencephalitis (SSPE), autoimmune disorders, and a few mitochondrial abnormalities are among the other uncommon causes. There have been attempts to define hereditary myoclonic epilepsies that do not meet the recognised criteria for myoclonic epilepsy syndromes [1]. The cognitive outcomes of epilepsy syndromes vary, but in general, they have a good prognosis. Myoclonic-atonic epilepsy is classified as an epileptic encephalopathy, and the cognitive outcome can be normal to severely impaired [2]. SSPE, in contrast, is a debilitating neurological illness that has so far eluded treatment. It is characterised by cognitive decline, periodic myoclonus, ataxia, vision complaints, a vegetative state, and death [3]. Clinicians usually identify SSPE using a combination of classic clinical features paired with elevated anti-measles antibody titres in the cerebrospinal fluid (CSF). Thus, a problem arises when a clinician is faced with a case of SSPE presenting in its early stages or with atypical www.annchildneurol.org 208