e21144 Background: Focal increased lower thoracic spinal cord 18F-FDG uptake is not infrequently observed and may be confused for spinal cord metastases. The cause of this physiological uptake is indeterminate though various theories have been postulated. We hypothesized that there may be a correlation between the thoracic (T11-T12) spinal uptake and lower limb movements or to bowel FDG activity. In the absence of paired FDG PET studies in same patients with and without leg movements we correlated the FDG uptake of the lower thoracic cord in ambulatory to that in bedridden patients. Methods: Sixty-three consecutive patients (12 bedridden) with 18F- FDG PET-CT with no known evidence of spinal cord or bony spine metastases were included. The SUV max/avg values of the liver, Thoracic: T11-T12 and Cervical: C3-C5 spinal cord segments and the bowel FDG activities of the ambulatory and bedridden patients were determined and compared. Statistical analysis was performed to evaluate various factors predictive of increased spinal cord FDG uptake. Results: Median age was 54 years (18- 93). Primary tumor histology was lung (21.8%), breast (9.3%), melanoma (15.6 %) and lymphomas (21.8%). The mean SUV max/avg values were liver (2.89/2.43); Thoracic cord (2.46/1.89); Cervical cord (2.25/1.82) and Bowel (4.4/2.9). Visible 18F-FDG thoracic spinal uptake was seen in 28%. Our analysis showed no significant correlation between the ambulatory status (p=0.219) or bowel FDG activity (p=0.210) and T11-T12 cord uptake. Conclusions: Although of no significance in this study, there might be a correlation between limb movements (amongst other factors) and physiological FDG uptake in the lower T-spine which warrants further dual studies in the same patient with and without leg motion. This may also help in differentiating normal variant spinal cord uptake from spinal cord metastatic lesions. [Table: see text]

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BackgroundThere are no known causes for progressive supranuclear palsy (PSP). The microtubule associated protein tau (MAPT) H1 haplotype is the major genetic factor associated with risk of PSP, with both oxidative stress and mitochondrial dysfunction also implicated. We investigated whether specific single nucleotide polymorphisms (SNPs) in genes encoding enzymes of xenobiotic detoxification, mitochondrial functioning, or oxidative stress response, including debrisoquine 4-hydroxylase, paraoxonase 1 and 2, N-acetyltransferase 1 and 2 (NAT2), superoxide dismutase 1 and 2, and PTEN-induced putative kinase are associated with PSP.MethodsDNA from 553 autopsy-confirmed Caucasian PSP cases (266 females, 279 males; age at onset 68 ± 8 years; age at death 75 ± 8) from the Society for PSP Brain Bank and 425 clinical control samples (197 females, 226 males; age at draw 72 ± 11 years) from healthy volunteers were genotyped using Taqman PCR and the SequenomiPLEX Gold assay.ResultsThe proportion of NAT2 rapid acetylators compared to intermediate and slow acetylators was larger in cases than in controls (OR = 1.82, p < 0.05). There were no allelic or genotypic associations with PSP for any other SNPs tested with the exception of MAPT (p < 0.001).ConclusionsOur results show that NAT2 rapid acetylator phenotype is associated with PSP, suggesting that NAT2 may be responsible for activation of a xenobiotic whose metabolite is neurotoxic. Although our results need to be further confirmed in an independent sample, NAT2 acetylation status should be considered in future genetic and epidemiological studies of PSP.

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