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Cerebellar activation during ataxic gait in olivopontocerebellar atrophy: a PET study
Author(s) -
Mishina M.,
Senda M.,
Ishii K.,
Ohyama M.,
Kitamura S.,
Katayama Y.
Publication year - 1999
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1999.tb01055.x
Subject(s) - ataxic gait , olivopontocerebellar atrophy , gait , cerebellar hemisphere , cerebellar vermis , cerebellum , gait ataxia , supine position , ataxia , medicine , anatomy , neuroscience , psychology , central nervous system disease , physical medicine and rehabilitation , degenerative disease
Objective ‐ To investigate the possible abnormal regional brain metabolism during ataxic gait in olivopontocerebellar atrophy (OPCA), and to evaluate the response of the cerebellar subregions to instability during bipedal gait. Material and methods ‐ On 9 patients with OPCA in early phase and on 10 age‐matched normal subjects, we performed positron emission tomography (PET) with 2‐[ 18 F]fluoro‐2‐deoxy‐D‐glucose (FDG) under two different conditions: supine resting and 30 min treadmill walking. Results ‐ Both in normals and in patients with OPCA, the FDG uptake in the walking state ( U walk ) was significantly greater than that in the resting state ( U rest ) in the pyramis, declive‐folium‐tuber and culmen of the cerebellar vermis, and in the thalamus. In the patients, the U walk was also significantly greater than the U rest in the posterior lobe of cerebellar hemisphere and in the pons and midbrain. In the pyramis, the activation ratio (= U walk / U rest ) of the patients was significantly lower than that of the normals. Conclusions ‐ We considered that these findings reflect the pathophysiology of ataxic gait in OPCA patients and the compensatory mechanism for the instability during ataxic gait.