Abstract W MP93: Changes in FDG-PET Activity Following Intraparenchymal Injection of SB623 Cells in Patients with Stable Ischemic Strokes
Background: Ischemic stroke remains a major cause of disability with 90% of patients achieving no improvement after 90 days. The primary objective of this study was to evaluate the safety and feasibility of intraparenchymal administration of SB623 cells in chronic stroke. SB623 cells are adult bone-marrow-derived cells transfected with a plasmid encoding the intracellular domain of Notch-1 that have demonstrated improvement in functional testing in animal models of stroke.
Methods: Patients with hemiparesis from stable subcortical ischemic stroke and NIHSS > 7 received intracranial injection of 2.5, 5 or 10 million SB623 cells. Clinical outcome measures included NIHSS, MRS, ESS and FMA measured at baseline and repeated at 6 and 12 months. FDG-PET was analyzed at each time point using cluster analysis within 5 regions of interest (contralateral frontal cortex, medial ventral to infarct, contralateral putamen, contralateral sensori-motor cortex, and contralateral thalamus).
Results: Five patients enrolled at one academic center were included in this initial FDG-PET analysis. In these 5 patients, there was improvement in NIHSS (p = 0.008) and ESS (p = 0.006), which was most apparent from 0 to 6 months (p = 0.005; p = 0.005). There was also an increase in FDG-PET activity in the contralateral sensori-motor cortex from 0-6 months (p = 0.005), which was related to NIHSS, ESS and FMA (p = 0.043). Analyses of individual patients showed increased FDG uptake contralateral to the injection site in 3/5 patients. There was an increase near the area of infarct in 2/5 patients that was seen at 6 months but not at 12 months.
Conclusions: Intraparenchymal injection of SB623 cells in chronic ischemic strokes resulted in increased FDG uptake predominantly in areas contralateral to stem cell injection in some patients. These increases were associated with improved clinical outcome measures suggesting that the PET changes might reflect activation of neural pathways due to stem cell therapy. Further PET studies with appropriate controls are warranted.
Author Disclosures: C.L. Kenmuir: None. V.K. Reddy: None. J. Mountz: None. J. James: None. G.K. Steinberg: Consultant/Advisory Board; Modest; Medtronic. Research Grant; Significant; NIH NINDS, CIRM. D.S. Kondziolka: None. L.D. Lunsford: None. N.E. Schwartz: None. E. Yankee: Ownership Interest; Significant; Executive Vice President of Development & Regulatory Affairs at SanBio Inc. L.R. Wechsler: None.
- © 2015 by American Heart Association, Inc.