著者Yamauchi H, Kagawa S, Kusano K, Ito M, Okuyama C
題名Neuronal alterations in secondary thalamic degeneration due to cerebral
infarction: A 11C-flumazenil positron emission tomography study.
要旨BACKGROUND: Studies using animal experiments have shown secondary neuronal
degeneration in the thalamus after cerebral infarction. Neuroimaging studies in humans have revealed changes in imaging parameters in the thalamus, remote to the infarction.However, few studies have directly demonstrated
neuronal changes in the thalamus in vivo. The purpose of this study was to determine whether secondary thalamic neuronal damage may manifest as a decrease in central benzodiazepine receptors in patients with cerebral infarction and internal carotid artery or middle cerebral artery disease.
METHODS: We retrospectively analyzed the data of 140 patients with
unilateral cerebral infarction ipsilateral to internal carotid
artery or middle cerebral artery disease. All patients had quantitative measurements of
11C-flumazenil binding potential (FMZ-BP),cerebral blood flow, and cerebral metabolic rate of oxygen using positron emission tomography in the chronic stage. Region of interest analysis was performed using NeuroFlexer—an
automated region of interest analysis software using NEUROSTAT.
RESULTS: In the thalamus ipsilateral to the infarcts, the values of FMZ-BP,
cerebral blood flow, and cerebral metabolic rate of oxygen were significantly lower than those in the contralateral thalamus.
Significant correlations were found between the ipsilateral-to-contralateral
ratio of FMZ-BP and the ipsilateral-to-contralateral ratio of cerebral blood flow or cerebral metabolic rate of oxygen in the thalamus. Patients with corona radiata infarcts and striatocapsular infarcts had significantly decreased ipsilateral-to-contralateral FMZ-BP ratio in the thalamus compared
with those without.The ipsilateral-to-contralateral ratio of FMZ-BP in the thalamus was significantly correlated with the ipsilateral-to-contralateral cerebral etabolic
rate of oxygen ratio in the frontal cortex and showed a significant negative correlation with the number of perseverative errors on the Wisconsin Card Sorting Test.
CONCLUSIONS: Secondary thalamic neuronal damage may manifest as a decrease
in central benzodiazepine receptors in patients with cerebral infarction and internal carotid artery or middle cerebral artery disease, which may be associated with frontal lobe dysfunction.
日本語要旨動物モデルで報告されている大脳の脳梗塞後の視床の二次的な神経変性について、片側性の内頚動脈や中大脳動脈病変を有する140例の片側性の大脳の脳梗塞症例にベンゾジアゼピン受容体PETであるC-11-Flumazenil(FMZ-BP)を用いて検討した。血管病変と同側視床/対側視床のFMZ-BP集積比はO-15 gas PETで評価された同側/対側の前頭葉の酸素代謝比と有意な相関がみられた。内頚動脈や中大脳動脈の障害は、視床のベンゾジアゼピン受容体の減少という二次的な神経変性をもたらす。