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Transient subacute cerebellar ataxia in a patient with Lambert-Eaton myasthenic syndrome after intracranial aneurysm surgery

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Title: Transient subacute cerebellar ataxia in a patient with Lambert-Eaton myasthenic syndrome after intracranial aneurysm surgery
Authors: Nakamura, Masakazu Browse this author
Yabe, Ichiro Browse this author →KAKEN DB
Sato, Kazunori Browse this author
Nakano, Fumihito Browse this author
Yaguchi, Hiroaki Browse this author
Tsuji, Sachiko Browse this author
Shiraishi, Hirokazu Browse this author
Yoneda, Makoto Browse this author
Tanaka, Keiko Browse this author
Motomura, Masakatsu Browse this author
Sasaki, Hidenao Browse this author →KAKEN DB
Issue Date: May-2008
Publisher: Elsevier
Journal Title: Clinical Neurology and Neurosurgery
Volume: 110
Issue: 5
Start Page: 480
End Page: 483
Publisher DOI: 10.1016/j.clineuro.2008.01.002
PMID: 18295972
Abstract: Several reports have presented patients with subacute cerebellar ataxia (subacute CA) and Lambert-Eaton myasthenic syndrome (LEMS). Some clinical features of those patients have been described in the previous reports, such as priority of subacute CA to LEMS or a concurrent occurrence of both diseases, a high incidence of malignancy, less efficacy of the treatment for subacute CA compared with that for LEMS. Cerebellar ataxia in some patients with LEMS has been demonstrated to be caused by serum antibodies to P/Q-type voltage-gated calcium channels (VGCCs). Here, we report a 63-year-old woman with subacute CA and LEMS. Cerebellar ataxia appeared 15 months after the incidence of LEMS, and the onset of cerebellar ataxia was thought to be due to serum anti-P/Q-type VGCCs antibodies. The clinical course of this patient was atypical in that 1) LEMS preceded subacute CA which developed after intracranial aneurysm surgery, 2) no malignancy was detected when both diseases coexisted, 3) symptoms of LEMS did not progress with the onset of cerebellar ataxia, and 4) cerebellar ataxia showed a definite improvement in symptoms and by 123I-IMP SPECT imaging after steroid administration. In addition, it is remarkable that LEMS became aggravated in electrophysiological examinations in contrast to subacute CA. We suggest that these atypical features of subacute CA and the changes in LEMS may be associated with a balance between the amount of serum anti-P/Q-type VGCCs antibodies and the susceptibility of the cerebellum and presynaptic nerve terminals to the antibodies. More cases are needed to investigate the mechanisms involved. The subacute CA and LEMS in this patient have remained comparatively silent after the withdrawal of steroid, and we are continuing to observe her condition.
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 矢部 一郎

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