TY - JOUR T1 - PET/CT Brain Imaging of Arthroplasty Cobalt Encephalopathy (ACE) due to failure of Chromium-cobalt hip protheses - A works in progress JF - Journal of Nuclear Medicine JO - J Nucl Med SP - 484 LP - 484 VL - 58 IS - supplement 1 AU - Robert Bridges AU - Stephen Tower Y1 - 2017/05/01 UR - http://jnm.snmjournals.org/content/58/supplement_1/484.abstract N2 - 484Objectives: Significant local and systemic toxicity can occur from breakdown of chromium-cobalt metal alloy hip prostheses. The earliest presentation of systemic cobalt toxicity can be neurological including decreased processing and motor speed, memory impairment, fine motor co-ordination and tremor. Recent literature has focused primarily on the local effects of metallosis due to failure of metal-on-metal (MoM) prostheses. However, while serious systemic toxicity is acknowledged from cobalt, little information is available dealing with the early detection and quantification of potentially reversible or irreversible damage to the brain. Imaging was undertaken in patients with both metal-on-metal (MoM) and presently considered non-problematic metal-on-plastic (MoP) hip prostheses presenting with systemic cobalt toxicity to begin to categorize and quantify any potential signature pattern of regional hypometabolism, assess response the therapy from hip revision or chelation and to compare imaging with concomitant clinical neurocognitive testing and serum cobalt levels.Methods: Patients under orthopedic physician care presenting with elevated cobalt levels and clinical symptoms of toxicity underwent clinical neurocognitive testing and F-18 FDG PET brains scans. Principle imaging analysis was performed using both the software programs iSSP NeuroStat and NeuroQ . Severity of findings was scored visually but principally on the number of abnormal hypometabolic clusters and aggregate summation of standard deviations for regions of significant hypometabolism calculated from the NeuroQ program.Results: Presently 17 patients have been evaluated. All demonstrate global hypometabolism when referenced to the pons; the pons appearing to be the last major reference region to be affected by cobalt toxicity. The temporal lobes were affected first with progression from lateral to medial with increasing severity. With increasing severity, progression included frontal cortex, followed by parietal cortex, anterior cingulate gyrus, posterior cingulate gyrus, Brocas areas, thalamus and visual cortex. Patients with lower aggregate scores or abnormal clusters either had mild cognitive impairment or a sub-clinical presentation while increasing scores and clusters presented with moderate to severe cognitive impairment. One patient who underwent revision surgery and, after 6 months, had improved neurocognitive and metabolic brain function.Conclusion: Early results have found a global hypometabolism for all patients with significant areas of accentuated hypometabolism and an apparent regional progression of hypometabolism with increasing cobalt toxicity. This included patients with both metal-on-metal (MoM) and the presently considered safe metal-on-plastic (MoP) protheses. One patient underwent hip revision of MoM prosthesis with eventual improvement in clinical presentation and semi-quantitative PET brain scan analysis. Amount of eroded cobalt and duration of exposure may be more important than serum cobalt levels when evaluating degree of brain impairment. The threshold for toxicity detected by PET/CT scanning may be below presently accepted safe serum cobalt levels. A larger cohort of patients will be needed for further delineation of metabolic changes from cobalt toxicity versus other confounding disease processes. Endpoints for the study will need to determine a threshold for toxic metabolic findings by PET/CT scanning which may be below presently accepted safe serum cobalt levels, and identify a threshold for potential reversible toxicity and potential permanent impairment in brain metabolism. Discrimination of toxic encephalopathy from other age- and dementia-related illness is needed since patients with prosthetic cobalt toxicity could be misdiagnosed resulting in ineffective or palliative care where a treatable encephalopathy may be present. Research Support: None $$graphic_2D295FA2-BFBD-45C2-8192-BA8DFF5960C3$$ ER -