Cerebral Fdg Pet Ct In Pediatric Neuroinflammation: An Exploration In The Application Of Statistical Parametric Mapping

1606 Aim: Central nervous system (CNS) inflammation in children may be caused by infectious or autoimmune mechanisms and has the potential to result in severe neurological disability. Cerebral FDG PET CT is a readily available, non-invasive, in-vivo biomarker for neuronal dysfunction and may have a role in the assessment of neuroinflammation. We aimed to compare the findings on cerebral FDG PET CT in pediatric patients presenting with neurological symptoms to their cerebro-spinal fluid (CSF) neopterin level, an objective marker of CNS inflammation. If cerebral FDG PET CT is able to identify pediatric patients with significant CNS inflammation, it may serve as a useful adjunct to clinical evaluation, CSF and peripheral blood biomarkers, and MRI findings from which to determine children who are likely to benefit from early initiation and ongoing treatment with immunomodulatory therapy. Methods: The cerebral FDG PET CT scans of pediatric patients presenting with neurological symptoms and had CSF sampling for neopterin were retrospectively reviewed. Each scans was compared against a dataset of 28 scans in neurologically normal children using statistical parametric mapping (SPM). Age was controlled for in the statistical analysis. The statistical modelling used global whole-brain proportional normalisation and voxel-level family-wise error correction for multiple comparisons. The output statistical maps showing hypometabolism were examined and compared against each patients CSF neopterin level. Results: Seven scans in six patients were including in the analysis. Age ranged from eight months to 14 years. CSF neopterin levels ranged from normal to 2,573.10 nmol/l (normal \u003c27.4 nmol/l). Of the three patients with normal CSF neopterin, one had bifrontal hypometabolism (11 yr old with epileptic encephalopathy), one had right mesial temporal and anterior cingulate hypometabolism (14 yr old with limbic encephalitis) and one had right frontal hypometabolism (3 yr old with anti-NMDA receptor encephalitis). One patient had marginally raised CSF neopterin and had left fronto-temporal hypometabolism (8 yr old with anti-NMDA receptor encephalitis). One patient had moderately raised CSF neopterin and had bilateral occipital hypometabolism (6 yr old with anti-NMDA receptor encephalitis). The sixth patient had markedly raised CSF neopterin and underwent two cerebral FDG scans both showing scattered precuneus and right temporo-parieto-occipital hypometabolism (8 month old with primary cerebral hemophagocytic lymphohistiocytosis). Conclusions: : SPM analysis of pediatric cerebral FDG PET CT scans does not appear to produce a consistent pattern of cerebral hypometabolism that correlates with CSF neopterin level, in this small cohort of patients. The variable cerebral hypometabolism may more accurately reflect the underlying pathologic mechanisms rather than the degree of neuroinflammation per se. SPM analysis of cerebral FDG PET may be more relevant to the longitudinal monitoring of children with proven neuroinflammation and could aid in guiding ongoing therapy, but larger studies in specific disease groups are required.