Abstract A semiautomated computerized method of in vivo morphometric analysis that is based upon high‐resolution three‐dimensional magnetic resonance imaging has been developed. This morphometric method is efficient and is of greater analytical precision than any other morphometric method currently applied to living human tissue. Including error inherent in image data acquisition, the aggregate error of the methodology, as estimated by the phantom studies, ranges from 4.5 to 9.6%, with incremental error above 4.5% a function of magnetic resonance slice thickness. This method was applied to magnetic resonance scans of 7 normal volunteers. The derived volumes of whole brain and of individual substructures were closely concordant with previously published volumes of normal fresh (unfixed) brains obtained post mortem. This morphometric methodology is potentially applicable to any structure or lesion that can be visualized by magnetic resonance imaging.
Fever-induced refractory epileptic encephalopathy in school-age children (FIRES) is a recently described epileptic entity whose etiology remains unknown. Brain abnormalities shown by MRI are usually limited to mesial-temporal structures and do not account for the catastrophic neuropsychologic findings. Methods: We conducted FIRES studies in 8 patients, aged 6–13 y, using 18F-FDG PET to disclose eventual neocortical dysfunction. Voxel-based analyses of cerebral glucose metabolism were performed using statistical parametric mapping and an age-matched control group. Results: Group analysis revealed a widespread interictal hypometabolic network including the temporoparietal and orbitofrontal cortices bilaterally. The individual analyses in patients identified hypometabolic areas corresponding to the predominant electroencephalograph foci and neuropsychologic deficits involving language, behavior, and memory. Conclusion: Despite clinical heterogeneity, 18F-FDG PET reveals a common network dysfunction in patients with sequelae due to fever-induced refractory epileptic encephalopathy.
Neurons of neocortical layers II-VI in the dorsomedial cortex of the mouse arise in the pseudostratified ventricular epithelium (PVE) through 11 cell cycles over the six embryonic days 11-17 (E11-E17). The present experiments measure the proportion of daughter cells that leave the cycle (quiescent or Q fraction or Q) during a single cell cycle and the complementary proportion that continues to proliferate (proliferative or P fraction or P; P = 1 - Q). Q and P for the PVE become 0.5 in the course of the eighth cycle, occurring on E14, and Q rises to approximately 0.8 (and P falls to approximately 0.2) in the course of the 10th cycle occurring on E16. This indicates that early in neuronogenesis, neurons are produced relatively slowly and the PVE expands rapidly but that the reverse happens in the final phase of neuronogenesis. The present analysis completes a cycle of analyses that have determined the four fundamental parameters of cell proliferation: growth fraction, lengths of cell cycle, and phases Q and P. These parameters are the basis of a coherent neuronogenetic model that characterizes patterns of growth of the PVE and mathematically relates the size of the initial proliferative population to the neuronal population of the adult neocortex.
