RESUMEN
A man in his early 70s presented to the emergency department about 3.5 hours after acute onset right sided hemiplegia and aphasia. CT angiography confirmed an acute occlusion of the M1 segment of the left middle cerebral artery and severe, but stable, dissection of the aortic arch and a large dissecting aortic aneurysm extending into the innominate artery and beyond into the descending aorta. The risk of aggravating existing aortic pathology while trying to navigate from a transfemoral or transradial approach was considered to be very high; therefore, the decision was made to proceed with direct carotid puncture for mechanical thrombectomy. The procedure was successfully completed, and the carotid puncture site was closed without issue using the Celt ACD vascular closure device (Vasorum, Dublin, Ireland). The patient recovered and was discharged home at his prestroke neurologic baseline 9 days later. Here we discuss the safe and effective use of this novel closure device in the setting of direct carotid puncture for neurointerventional procedures.
RESUMEN
The failure of remyelination in the human CNS contributes to axonal injury and disease progression in multiple sclerosis (MS). In contrast to regions of chronic demyelination in the human brain, remyelination in murine models is preceded by abundant oligodendrocyte progenitor cell (OPC) repopulation, such that OPC density within regions of demyelination far exceeds that of normal white matter (NWM). As such, we hypothesized that efficient OPC repopulation was a prerequisite of successful remyelination, and that increased lesion volume may contribute to the failure of OPC repopulation in human brain. In this study, we characterized the pattern of OPC activation and proliferation following induction of lysolecithin-induced chronic demyelination in adult rabbits. The density of OPCs never exceeded that of NWM and oligodendrocyte density did not recover even at 6 months post-injection. Rabbit OPC recruitment in large lesions was further characterized by chronic Sox2 expression in OPCs located in the lesion core and upregulation of quiescence-associated Prrx1 mRNA at the lesion border. Surprisingly, when small rabbit lesions of equivalent size to mouse were induced, they too exhibited reduced OPC repopulation. However, small lesions were distinct from large lesions as they displayed an almost complete lack of OPC proliferation following demyelination. These differences in the response to demyelination suggest that both volume dependent and species-specific mechanisms are critical in the regulation of OPC proliferation and lesion repopulation and suggest that alternate models will be necessary to fully understand the mechanisms that contribute to failed remyelination in MS.