Paroxysmal Speech Arrest With Resolving Splenial and Symmetric White Matter Lesions in a Child: A Case Report

Reversible splenial lesion syndrome (RESLES), mild encephalitis/encephalopathy with a reversible splenial lesion (MERS), and cytotoxic lesions of the corpus callosum (CLOCCs) are overlapping clinicoradiological constructs associated with infection, seizures, metabolic disturbance, and drug exposure. We report an 11-year-old right-handed boy with recurrent paroxysmal speech arrest over approximately 24 hours. During the episodes, consciousness and comprehension were preserved; he could vocalize and communicate by typing but could not produce meaningful speech. Transient left upper-limb or generalized weakness and upper respiratory symptoms accompanied the spells. Respiratory adenovirus testing was positive, and a Mycoplasma pneumoniae (M. pneumoniae) antibody titer was reported as 1:160, although respiratory and cerebrospinal fluid M. pneumoniae polymerase chain reaction testing was negative. Cerebrospinal fluid contained 1 white cell/microL, with normal protein, glucose, and chloride and mildly elevated interleukin-6 (IL-6). Baseline electroencephalography showed abundant right frontopolar, frontal, anterior temporal, and Fz interictal discharges without a captured electroclinical seizure. Magnetic resonance imaging demonstrated a splenial lesion with symmetric posterior periventricular and centrum semiovale abnormalities, compatible with a type II MERS/RESLES pattern or CLOCC-spectrum process. He received two 40 g doses of intravenous immunoglobulin (IVIG) and later intravenous methylprednisolone followed by oral prednisone, together with empirical acyclovir, azithromycin, mannitol, and supportive care. No further speech arrest or weakness was documented on or after illness day 5, and methylprednisolone was initiated on illness day 6. Follow-up electroencephalography on illness day 48 showed qualitatively fewer discharges confined to sleep, but no habitual event. Serial imaging showed lesion regression with residual fluid-attenuated inversion recovery (FLAIR) signal on illness day 74. At approximately 4.5 months, he remained asymptomatic during prednisone tapering. Because formal language and motor-speech testing was not performed during an episode, aphasia could not be definitively distinguished from anarthria, dysarthria, apraxia of speech, or focal speech arrest. This case highlights the diagnostic overlap among resolving callosal-white matter lesions, transient speech-output disturbance, and interictal epileptiform abnormalities, while cautioning against attributing recovery to a single treatment or equating residual magnetic resonance signal with active inflammation.