Amnestic aphasia in MELAS can be epileptogenic

Abstract

Referring to the article by Sakata et al. we disagree with the diagnosis “thalamic aphasia” [ [1] Sakata Y. Nakamura T. Ichinose F. Matsuo M. Thalamic aphasia associated with mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes: a case report. Brain Dev. 2022; 44: 583-587 Abstract Full Text Full Text PDF Scopus (2) Google Scholar ]. Since thalamic lesions can be associated with status epilepticus (SE) [ [2] Parreira S. Abreu L. Franco A. Bentes C. Peralta A.R. Non-convulsive status epilepticus induced by acute thalamic lesions: a report of three cases. Seizure. 2021; 89: 1-4 Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar ], it is crucial that SE has been ruled out 2 Abbreviations CK: creatine-kinase; EEG: electroencephalography; FLAIR: fluid attenuated inversion recovery; PLEDS: periodic lateralised epileptiform discharges; PWI: perfusion-wieghted imaging; SE: status epilepticus; SLE: stroke-like episode; SLL: stroke-like lesion. 2Abbreviations CK: creatine-kinase; EEG: electroencephalography; FLAIR: fluid attenuated inversion recovery; PLEDS: periodic lateralised epileptiform discharges; PWI: perfusion-wieghted imaging; SE: status epilepticus; SLE: stroke-like episode; SLL: stroke-like lesion.. Therefore, we should know if creatine-kinase (CK) was elevated to 5883 U/l due to myopathy, the stroke-like lesion (SLL), cardiomyopathy, or a SE. Because periodic lateralised epileptiform discharges (PLEDs) can be the manifestation of a non-convulsive/minimal convulsive SE [ [3] Wang Z. Chu C. Jing C. Zheng X. Lin W. Non-convulsive status epileptics presenting with periodic lateralized epileptiform discharges and coma after cerebral hemorrhage: a case report. Neurol India. 2021; 69: 733-736 Crossref PubMed Scopus (1) Google Scholar ], we should know if a SE was recorded on electroencephalography (EEG) on hospital-day 8 and why midazolam was administered. Since headaches were interpreted as epileptogenic, we should know whether the patient had seizures or epileptiform discharges on EEG. A structural lesion is not a prerequisite for amnestic aphasia since SE may explain aphasia. It could be also a post-ictal phenomenon. Was a third EEG free of epileptiform discharges? Was the patient discharged with an anti-seizure medication?