Asymmetry of cerebral glucose metabolism in very low-birth-weight infants without structural abnormalities

<div><p>Even when structural abnormalities are not observed on the brain magnetic resonance images (MRI) of very low-birth-weight (VLBW) infants, such infants are at increased risk for poor neurodevelopment. The aim of the present study was to evaluate cerebral glucose metabolism in VLBW infants without apparent structural abnormalities on MRI.</p><p>Methods</p><p>Thirty-six VLBW infants who underwent F-18 fluorodeoxyglucose (F-18 FDG) brain PET and MRI were prospectively enrolled, while infants with evidence of parenchymal brain injury on MRI were excluded. The regional glucose metabolic ratio and asymmetry index were calculated. The asymmetry index more than 10% (right > left asymmetry) or less than -10% (left > right asymmetry) were defined as abnormal. Regional cerebral glucose metabolism were compared between right and left cerebral hemispheres, and between the following subgroups: multiple gestations, premature rupture of membrane, bronchopulmonary dysplasia, and low-grade intraventricular hemorrhage.</p><p>Results</p><p>In the individual analysis, 21 (58.3%) of 36 VLBW infants exhibited asymmetric cerebral glucose metabolism. Fifteen infants (41.7%) exhibited right > left asymmetry, while six (16.7%) exhibited left > right asymmetry. In the regional analysis, right > left asymmetry was more extensive than left > right asymmetry. The metabolic ratio in the right frontal, temporal, and occipital cortices and right thalamus were significantly higher than those in the corresponding left regions. In the subgroup analyses, the cerebral glucose metabolism in infants with multiple gestations, premature rupture of membrane, bronchopulmonary dysplasia, or low-grade intraventricular hemorrhage were significantly lower than those in infants without these.</p><p>Conclusion</p><p>VLBW infants without structural abnormalities have asymmetry of cerebral glucose metabolism. Decreased cerebral glucose metabolism are noted in infants with neurodevelopmental risk factors. F-18 FDG PET could show microstructural abnormalities not detected by MRI in VLBW infants.</p></div

Flow diagram of the study population.

<p>PVL: periventricular leukomalacia.</p

Cerebral metabolic ratio and asymmetry index in very low-birth-weight infants.

<p>Cerebral metabolic ratio and asymmetry index in very low-birth-weight infants.</p

A representative F-18 FDG brain PET image from a very low-birth-weight infant.

<p>It shows relatively low glucose metabolism in the right cerebral cortex (arrow) and left thalamus (arrow head) relative to the corresponding regions in the left hemisphere.</p

The number of very low-birth-weight infants exhibiting asymmetric cerebral glucose metabolism.

<p>The number of very low-birth-weight infants exhibiting asymmetric cerebral glucose metabolism.</p

Striatofrontal Deafferentiation in MSA-P: Evaluation with [¹⁸F]FDG Brain PET

<div><p>Background</p><p>Although cognitive impairment is not a consistent feature of multiple system atrophy (MSA), increasing evidence suggests that cognitive impairment is common in MSA with predominant parkinsonism (MSA-P). It is assumed that the cognitive impairment in MSA-P is caused by the striatal dysfunction and disruption of striatofrontal connections. The aim of this study was to evaluate the relationship between regional glucose metabolism in the frontal cortex and striatum in patients with MSA-P using [¹⁸F]FDG brain PET.</p><p>Methods</p><p>Twenty-nine patients with MSA-P and 28 healthy controls underwent [¹⁸F]FDG brain PET scan. The [¹⁸F]FDG brain PET images were semiquantitatively analyzed on the basis of a template in standard space. The regional glucose metabolism of the cerebral cortex and striatum were compared between MSA-P and healthy control groups. The correlations between age, symptom duration, H&Y stage, UPDRS III score, MMSE score, and glucose metabolism in the cerebellum and striatum to glucose metabolism in the frontal cortex were evaluated by multivariate analysis.</p><p>Results</p><p>The glucose metabolism in the frontal cortex and striatum in MSA-P patients were significantly lower than those in healthy controls. Glucose metabolism in the striatum was the most powerful determinant of glucose metabolism in the frontal cortex in MSA-P. Only age and glucose metabolism in the cerebellum were independent variables affecting the glucose metabolism in the frontal cortex in healthy controls.</p><p>Conclusion</p><p>The decrease in frontal glucose metabolism in MSA-P is related to the decrease in striatal glucose metabolism. This result provided evidence of striatofrontal deafferentiation in patients with MSA-P.</p></div

Representative images of spatially normalized ratios using study-specific templates of normal controls (A) and patients with crossed cerebellar diaschisis (B), multiple system atrophy of the cerebellar type (C), Spinocerebellar Ataxia (SCA) type 2 (D), and SCA type 6 (E).

<p>Representative images of spatially normalized ratios using study-specific templates of normal controls (A) and patients with crossed cerebellar diaschisis (B), multiple system atrophy of the cerebellar type (C), Spinocerebellar Ataxia (SCA) type 2 (D), and SCA type 6 (E).</p

Different subregional metabolism patterns in patients with cerebellar ataxia by ¹⁸F-fluorodeoxyglucose positron emission tomography

<div><p>We evaluated cerebellar subregional metabolic alterations in patients with cerebellar ataxia, a representative disease involving the spinocerebellum. We retrospectively analyzed ¹⁸F-fluorodeoxyglucose positron emission tomography (¹⁸F-FDG PET) images in 44 patients with multiple system atrophy of the cerebellar type (MSA-C), 9 patients with spinocerebellar ataxia (SCA) type 2, and 14 patients with SCA type 6 and compared with 15 patients with crossed cerebellar diaschisis (CCD) and 89 normal controls. Cerebellar subregional metabolism was assessed using 13 cerebellar subregions (bilateral anterior lobes [ANT], superior/mid/inferior posterior lobes [SUPP/MIDP/INFP], dentate nucleus [DN], anterior vermis [ANTV], and superior/inferior posterior vermis [SUPV/INFV]) to determine FDG uptake ratios. MSA-C and SCA type 2 showed severely decreased metabolic ratios in all cerebellar subregions compared to normal controls (ANT, 0.58 ± 0.08 and 0.50 ± 0.06 vs. 0.82 ± 0.07, respectively, <i>p</i> < 0.001). SCA type 6 showed lower metabolic ratios in almost all cerebellar subregions (ANT, 0.57 ± 0.06, <i>p</i> < 0.001) except INFV. Anterior-posterior lobe ratio measurements revealed that SCA type 2 <b>(</b>Right, 0.81 ± 0.05 vs. 0.88 ± 0.04, <i>p</i> < 0.001; Left, 0.83 ± 0.05 vs. 0.88 ± 0.04, <i>p</i> = 0.003) and SCA type 6 (Right, 0.72 ± 0.05 vs. 0.88 ± 0.04, <i>p <</i> 0.001; Left, 0.72 ± 0.05 vs. 0.88 ± 0.04, <i>p</i> < 0.001) showed preferential hypometabolism in the anterior lobe compared to normal controls, which was not observed in CCD and MSA-C. Asymmetric indices were higher in CCD and MSA-C than in normal controls (<i>p</i> < 0.001), whereas such differences were not found in SCA types 2 and 6. In summary, quantitative analysis of cerebellar subregional metabolism ratios revealed preferential involvement of the anterior lobe, corresponding to the spinocerebellum, in patients with cerebellar ataxia, whereas patients with CCD and MSA-C exhibited more asymmetric hypometabolism in the posterior lobe.</p></div

clinical characteristics of subjects.

<p>clinical characteristics of subjects.</p

Result of linear regression analysis for determinants of frontal glucose metabolism in MSA-P.

<p>Result of linear regression analysis for determinants of frontal glucose metabolism in MSA-P.</p