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• Vol.46 No.5
• CLINICA NEUROL, 46: 322−327, 2006
• Vol.46 No.5 contents

Case Report

A case of non-herpetic acute limbic encephalitis associated with a type-2 adenovirus infection

Hikaru Nagasawa, M.D.¹⁾, Manabu Wada, M.D.¹⁾, Keiji Kurita, M.D.¹⁾, Chihumi Iseki, M.D.²⁾, Tadashi Katagiri, M.D.²⁾ and Takeo Kato, M.D.¹⁾

¹⁾Department of Neurology, Hematology, Metabolism, Endocrinology and Diabetology (DNHMED), Yamagata University School of Medicine
²⁾Department of Neurology, Yamagata Prefectural Kahoku Hospital

This is a report of a 31-year-old woman with non-herpetic acute limbic encephalitis following a type-2 adenovirus infection. The patient was admitted to a hospital with high fever, severe liver dysfunction, and thrombocytopenia. Six days after admission, she became afebrile, and her liver dysfunction was normalized by conservative therapy. However, the patient started to experience generalized seizures that developed into status epileptics. The patient was then transferred to a referred hospital. Brain MR images revealed faint high-signal intensity in the bilateral limbic systems on FLAIR images. A CSF examination indicated mild pleocytosis. These findings suggested acute limbic encephalitis, which may have been mediated by an autoimmune reaction following some viral infection. Thus, steroid pulse therapy was started on the day of admission. The patient's condition, including the seizures and disturbances involving consciousness, improved gradually. The patient was discharged from the hospital in one month while still experiencing mild memory disturbances. Three months after onset of the illness, a T1-weighted MR image showed a linear high-signal intensity in the hippocampi, which indicated focal necrosis. Six months after onset, the patient's memory disturbance had been improved (her MMSE score was 28/30 points).
We investigated the titers of many viruses that are known to cause liver dysfunction and found that a titer of the type-2 adenovirus was significantly elevated within three weeks. Although the anti-voltage-gated potassium channel (VGKC) antibody was not detected in the patient's serum, it seems that the autoimmune reaction after the type-2 adenovirus infection may have caused the acute limbic encephalitis.

(CLINICA NEUROL, 46: 322−327, 2006)
key words: acute limbic encephalitis, preceding infection, liver dysfunction, type-2 adenovirus, convulsive state

(Received: 7-Sep-05)