Şevval OCAK ERDEM, Fethiye KILIÇASLAN, Berna POLAT TÜYSÜZ, Çetin OKUYAZ
Psychiatry and Behavioral Sciences - 2026;16(3):192-198
Objective: Landau-Kleffner Syndrome (LKS) is a rare pediatric epileptic encephalopathy characterized by the abrupt or gradual loss of previously acquired language abilities and epileptiform EEG abnormalities. The syndrome poses significant diagnostic challenges due to its clinical overlap with autism spectrum disorder (ASD). Symptoms such as language regression, reduced eye contact, impaired social interaction, and stereotypical behaviors are often misinterpreted as indicators of ASD. However, distinct EEG findings and a history of sudden developmental regression are key to differential diagnosis. This article presents a male child who initially exhibited symptoms consistent with ASD but was ultimately diagnosed with LKS following a detailed evaluation and EEG findings; the clinical improvement process with antiepileptic treatment and concurrent individualized special education support is discussed. Case Presentation: A 5-year and 8-month-old boy was referred to a child and adolescent psychiatry clinic due to regression in speech, reduced social interaction, poor eye contact, stereotypic behaviors, and newly emerging agitation. His developmental history indicated age-appropriate milestones until age five, followed by a gradual loss of expressive language and social withdrawal. Neurological examination revealed no history of clinical seizures; however, sleep EEG showed epileptiform discharges originating bilaterally from frontotemporal regions. Brain MRI demonstrated non-specific hyperintensities in the bilateral posterior periventricular white matter. Auditory brainstem response testing indicated normal auditory pathways. Prolonged sleep EEG demonstrated electrical status epilepticus during sleep, occupying more than 85% of non-rapid eye movement (NREM) sleep (spike-wave index >85%), and the clinical findings were evaluated within the LKS/epilepsy-aphasia spectrum. Antiepileptic treatment was initiated in a stepwise manner with valproic acid and levetiracetam, and clobazam was introduced as targeted therapy for LKS. Due to an insufficient response on follow-up EEG, oral prednisolone therapy was initiated and continued with gradual dose tapering. At the same time, individualized special education and speech therapy were provided. Within the first few months of treatment, marked improvements were observed in EEG findings, language production, and social engagement. Conclusion: This case report describes a child who initially presented with symptoms overlapping with ASD but was ultimately diagnosed with LKS following comprehensive clinical and neurophysiological evaluation. LKS may mimic ASD through language regression and social communication difficulties; therefore, early recognition of late-onset mutism or aphasia-like symptoms following a period of typical development may facilitate timely identification of underlying epilepsy-aphasia spectrum disorders and enable earlier appropriate interventions.
