Executive Dysfunction Secondary to Internal Frontal Hyperostosis in Treatment-Resistant Schizophrenia: A Case Report

Background: Internal Frontal Hyperostosis (IFH) is a radiologically defined thickening of the inner table of the frontal bone that can compress prefrontal cortices, contributing to neuropsychiatric symptoms.1 Its coexistence with treatment-resistant schizophrenia (TRS) complicates diagnosis and management. Objective: To describe the case of a patient with TRS and comorbid IFH, focusing on the clinical evolution, executive dysfunction, and the utility of early neuroimaging. Case Presentation: A 43-year-old female patient with schizophrenia since age 18 was clinically unstable despite treatment with clozapine (600 mg/day) and adjunctive pharmacotherapy. She exhibited psychomotor retardation, concrete thought, and behavioral dyscontrol. Non-contrast cranial computed tomography revealed bilateral frontal bone thickening (2.45 cm) consistent with IFH, with compression of both frontal lobes. The Montreal Cognitive Assessment (16/30) indicated moderate cognitive impairment with prominent executive deficits. The patient was discharged with multidisciplinary follow-up. Discussion: Persistent executive dysfunction despite optimized pharmacotherapy suggests that the IFH contributed to pseudorefractoriness by compressing the dorsolateral prefrontal cortex, potentially blunting the response to clozapine. Conclusions: IFH may act as an anatomical modifier in schizophrenia, exacerbating executive dysfunction. Early neuroimaging can uncover structural contributors to treatment refractoriness and guide multidisciplinary management.