Metabolic correlates of lesion-specific plasticity: an in vivo imaging study

High-resolution positron emission tomography (microPET) allows for repeated observations of brain function in the same animal. In a previous study, using [(18)F] fluorodeoxyglucose (FDG) microPET, we demonstrated diminished glucose metabolism and subsequent recovery in the Neostriatum and thalamus ipsilateral to cortical aspiration (ASP) lesions. Thermocoagulation (TCL) of pial vessels has been shown to result in the same degree of cortical injury but induce more compensatory re-organization than ASP. In the present work, FDG microPET was used to compare glucose metabolism following both TCL and ASP lesions in order to determine whether metabolic differences correlate with the previously described anatomical and functional changes in the two lesion models. Animals were scanned 3-day, 10-day and 1-month post-injury. Estimated cortical lesion size did not differ between the two models at 1 month following injury. Both lesions induced ipsilateral neostriatal and thalamic hypometabolism 3-day post-injury, with subsequent metabolic improvement over time. However, complete recovery was not observed by 1 month in either group. ASP lesions resulted in an overall greater metabolic deficit in the subcortical structures and a greater cortical deficit 1 month following injury when compared to the TCL. Contralateral cortical glucose metabolism at 3 days following injury was not different in the two lesions. These data demonstrate that the two lesions differ somewhat in their metabolic response to injury, and that the relative hypometabolism observed following ASP may be a reflection of the diminished capacity of the contralateral cortex to compensate for ASP as compared to TCL.