Abstract
BackgroundDecreased 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.MethodsWe 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.ResultsIn 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).ConclusionsChanges 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.
Highlights
Idiopathic normal pressure hydrocephalus is a syndrome that often develops in the elderly and is characterized by a classic triad of gait disturbance, mental deterioration, and urinary incontinence, accompanied by ventricular enlargement but normal cerebrospinal fluid pressure [1,2,3]. idiopathic normal pressure hydrocephalus (iNPH) is an important disease in the elderly population, with a prevalence of approximately 1% [4,5,6,7]. dysfunctions caused by iNPH are treatable with shunt surgery, the cause and pathology of iNPH remain unclear
disproportionately enlarged subarachnoid space hydrocephalus (DESH) findings precede the onset of iNPH symptoms and termed the radiological feature in patients with asymptomatic DESH as asymptomatic ventriculomegaly with features of iNPH on magnetic resonance imaging (AVIM) [4]
In the thalami and striate, the standardized uptake value ratio (SUVR) distributions were lower in the iNPH group compared with those in the normal controls (NC) group (Table 2, Fig. 3d, e)
Summary
Dysfunctions caused by iNPH are treatable with shunt surgery, the cause and pathology of iNPH remain unclear. Understanding the pathology is important for improving selection of patients for shunt surgery, determining the optimal timing for therapeutic intervention, and developing new treatments. With respect to the characteristic radiological features of iNPH, disproportionately enlarged subarachnoid space hydrocephalus (DESH) findings have been reported and are widely used for diagnosing iNPH or deciding on the indication of shunt surgery [2, 8], as they are predict outcomes after shunt surgeries. Decreased cerebral glucose metabolism has been reported in idiopathic normal pressure hydrocephalus (iNPH). The timing of appearance in the preclinical stage of iNPH remains unknown. We evaluated the changes in regional cerebral glucose metabolism with respect to the characteristic morphologic features of iNPH
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