Changes in cerebral glucose metabolism caused by morphologic features of prodromal idiopathic normal pressure hydrocephalus.

Background: Decreased cerebral glucose metabolism has been reported in idiopathic normal pressure hydrocephalus (iNPH). However, the timing of appearance in the preclinical stage of iNPH remains unknown. Herein, we evaluated the changes in regional cerebral glucose metabolism with respect to the characteristic morphologic features of iNPH.

Methods: We performed a cross-sectional study in > 2000 elderly patients who received a whole body 18F-fluorodeoxyglucose-positron emission tomography/computed tomography scanning and recruited subjects with clinical and preclinical iNPH. We included 12 subjects with iNPH, 32 subjects with asymptomatic ventriculomegaly with features of iNPH on magnetic resonance imaging (AVIM), and 33 subjects with preclinical morphologic features of DESH (PMD). We previously reported that iNPH develops in the order of PMD (asymptomatic subjects with incomplete DESH), AVIM (asymptomatic subjects with DESH), and iNPH (symptomatic subjects with DESH). We measured the median regional standardized uptake value ratio (SUVR) on 18F-fluorodeoxyglucose-positron emission tomography/computed tomography images between the three groups and compared them with background-matched normal controls in the frontal lobes, temporal lobes, medial parietal lobes, striata, and thalami.

Results: In the frontal and temporal lobes, the SUVR distributions of the PMD, AVIM, and PMD groups were significantly lower than for each NC (p < 0.05 for all). In the medial parietal lobes, the SUVR distributions were significantly higher in PMD and AVIM groups (p < 0.05 for all). In the thalami and striata, the SUVR distributions were significantly lower in the iNPH group (p < 0.05 for all).

Conclusions: Changes in brain glucose metabolism in the cortices are observed in preclinical iNPH, while metabolic decline in the basal ganglia is only detected in clinical iNPH.