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(Stroke. 2006;37:e3.)
© 2006 American Heart Association, Inc.
Case Reports |
From the Department of Neurology (H.K., K.S., S.U.), Nara Medical University, Kashihara, Nara, and the Department of Neurology (N.K.), Kobe City General Hospital, Kobe, Japan.
Correspondence to Hiroshi Kataoka, Department of Neurology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan. E-mail hk55{at}naramed-u.ac.jp
Abstract
Background and Purpose The representation elicited in the cingulate motor area has been demonstrated in animals, but remains unclear in humans. In particular, the representation and pathogenic mechanisms of the posterior cingulate cortex are poorly understood, especially in humans. We describe a case of posterior cingulate infarction associated with contralateral astasia.
Case Description A 67-year-old right-handed man with a 10-year history of hypertension suddenly presented with right-sided pulsion on attempting to stand or sit. On the following day, he could not maintain a sitting position. The patient immediately fell to the floor because of instability, characterized by marked right-sided pulsion despite no muscle weakness, sensorial deficits, or cerebellar ataxia. Magnetic resolution imaging of the brain showed abnormal intensity in the posterior parts of the cingulate, with no other clinically significant lesions.
Conclusions Because the cingulate motor area is connected to the vestibulocerebellar system through the thalamic nuclei, disruption of this connection by posterior cingulate infarction may result in astasia.
Key Words: astasia behavioral neurology cingulate gyrus infarction stroke
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