Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease
Identifieur interne : 000392 ( Main/Exploration ); précédent : 000391; suivant : 000393Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease
Auteurs : Toru Baba [Japon] ; Atsushi Takeda [Japon] ; Akio Kikuchi [Japon] ; Yoshiyuki Nishio [Japon] ; Yoshiyuki Hosokai [Japon] ; Kazumi Hirayama [Japon] ; Takafumi Hasegawa [Japon] ; Naoto Sugeno [Japon] ; Kyoko Suzuki [Japon] ; Etsuro Mori [Japon] ; Shoki Takahashi [Japon] ; Hiroshi Fukuda [Japon] ; Yasuto Itoyama [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-03.
English descriptors
Abstract
Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23602
Affiliations:
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<front><div type="abstract" xml:lang="en">Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory‐related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell‐identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using 18F‐fluorodeoxyglucose positron emission tomography and was analyzed using SPM‐based group comparisons and the brain–behavior partial least‐squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain–behavior partial least‐squares analysis revealed that odor‐identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex. © 2011 Movement Disorder Society</div>
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<name sortKey="Mori, Etsuro" sort="Mori, Etsuro" uniqKey="Mori E" first="Etsuro" last="Mori">Etsuro Mori</name>
<name sortKey="Nishio, Yoshiyuki" sort="Nishio, Yoshiyuki" uniqKey="Nishio Y" first="Yoshiyuki" last="Nishio">Yoshiyuki Nishio</name>
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<name sortKey="Takahashi, Shoki" sort="Takahashi, Shoki" uniqKey="Takahashi S" first="Shoki" last="Takahashi">Shoki Takahashi</name>
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