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• Vol.51 No.7
• CLINICA NEUROL, 51: 487−492, 2011
• Vol.51 No.7 contents

Case Report

A case of Castleman disease with status epileptics originating from focal cortical dysplasia

Muichi Kaito, M.D.¹⁾, Haruka Iwao, M.D.²⁾, Eriko Kinoshita, M.D., Ph.^D.3), Hiroshi Funaki, M.D., Ph.D.⁴⁾, Osamu Tachibana, M.D., Ph.D.⁵⁾ and Makoto Matsui, M.D., Ph.D.¹⁾

¹⁾Department of Neurology, Kanazawa Medical University
²⁾Department of Hematoimmunology, Kanazawa Medical University
³⁾Department of Pathology and Laboratory Medicine, Kanazawa Medical University
⁴⁾Department of Gastroenterological Surgery, Kanazawa Medical University
⁵⁾Department of Neurosurgery, Kanazawa Medical University

A 55-year-old man was admitted to our hospital because of prolonged consciousness disturbance after generalized convulsions. He had been afflicted with chronic inflammatory symptoms since 43 years of age, while multiple abdominal lymphadenopathy with a high level of serum IL-6 was revealed at the age of 53. FDG-PET/CT showed hypermetabolism in the left medial portion of the frontal lobe. Biopsy specimens of this lesion revealed a pathology of focal cortical dysplasia (FCD). Non-convulsive status epileptics continued despite enhanced treatment with antiepileptic drugs, while cortical T₂ hyperintense lesions developed and expanded. Castleman disease was confirmed by pathological findings of abdominal lymph node biopsy specimens. The patient showed a higher level of IL-6 in cerebrospinal fluid (1,400 pg/dl) than in serum (720 pg/dl), thus indicating intrathecal production of this proinflammatory cytokine. We concluded that continuous exposure of FCD tissue to IL-6 may have augmented epileptogenesis of the originally silent congenital lesion.
Full Text of this Article in Japanese PDF (1268K)

(CLINICA NEUROL, 51: 487−492, 2011)
key words: focal cortical dysplasia, Castleman disease, status epileptics, IL-6, epileptogenesis

(Received: 4-Jan-11)