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<p>Focal cortical dysplasia (FCD) is an important cause of intractable epilepsy, with FCD type II (FCD II) being the most common subtype. FCD II is characterized by cortical dyslamination accompanied by dysmorphic neurons (DNs). Identifying the molecular alterations and targetable biomarkers is pivotal for developing therapies. Here, we provide a detailed description of the neuropathological manifestations of FCD II, including morphological alterations and immunophenotypic profiles, indicating that abnormal cells exhibit a diverse spectrum of mixed differentiation states. Furthermore, we summarize current research on the pathogenetic mechanisms, indicating that gene mutations, epigenetic alterations, cortical developmental protein disturbances, inflammatory processes, and extrinsic damages may lead to abnormal neuronal proliferation and migration, thereby contributing to the emergence and progression of FCD II. These findings not only enhance our understanding of the pathogenesis of FCD II but also offer new directions for clinical diagnosis and treatment. Future research should further explore the interactions among these factors and employ multidisciplinary approaches to advance our understanding of FCD II.</p>

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Focal cortical dysplasia type II: review of neuropathological manifestations and pathogenetic mechanisms

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月17日

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  • Yubao Fang,
  • Yaqian Zhang,
  • Tiancai Huang,
  • Shengyu Yang,
  • Yinchao Li,
  • Liemin Zhou

摘要

Focal cortical dysplasia (FCD) is an important cause of intractable epilepsy, with FCD type II (FCD II) being the most common subtype. FCD II is characterized by cortical dyslamination accompanied by dysmorphic neurons (DNs). Identifying the molecular alterations and targetable biomarkers is pivotal for developing therapies. Here, we provide a detailed description of the neuropathological manifestations of FCD II, including morphological alterations and immunophenotypic profiles, indicating that abnormal cells exhibit a diverse spectrum of mixed differentiation states. Furthermore, we summarize current research on the pathogenetic mechanisms, indicating that gene mutations, epigenetic alterations, cortical developmental protein disturbances, inflammatory processes, and extrinsic damages may lead to abnormal neuronal proliferation and migration, thereby contributing to the emergence and progression of FCD II. These findings not only enhance our understanding of the pathogenesis of FCD II but also offer new directions for clinical diagnosis and treatment. Future research should further explore the interactions among these factors and employ multidisciplinary approaches to advance our understanding of FCD II.