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Background: Central pontine myelinolysis is a rare condition that can result in debilitating symptoms. Recent evidence suggests a shift in hypothesized prognosis for individuals with this diagnosis and implies a valuable role for rehabilitation to address prevention of secondary complications and functional recovery. This paper describes a 30 year-old female with central pontine myelinolysis presenting with incomplete locked-in syndrome and chronicles her rehabilitative journey at a comprehensive post-acute rehabilitation center. We present discipline specific interventions and discuss the interactions of the rehabilitation team as it relates to this patient's care and progression of training. Methods: Retrospective review of medical records and face-to-face interview were use to compile data for this case report. Results: The patient demonstrated improvements in function in all areas of mobility, swallowing, communication, and self-care over the course of 6 weeks of interdisciplinary training. Conclusion: This report illustrates the critical role of a patient-centered and goal-driven interdisciplinary team approach in the rehabilitation of persons with central pontine myelinolysis.Implications for rehabilitationCentral Pontine Myelinolysis can result in profound acute disability, including incomplete locked-in syndrome.Interdisciplinary post-acute rehabilitation is beneficial in maximizing functional recovery and minimizing secondary complications for individuals with Central Pontine Myelinolysis.Ongoing clinical assessment and team collaboration contribute to progressive and comprehensive plan of care development in post-acute rehabilitation.A patient-centered and goal-driven interdisciplinary team approach facilitates improvement in outcomes across clinical domains.Recovery potential and therapeutic interventions for individuals with Central Pontine Myelinolysis need to be further explored.

By integrating convergent protein engineering and rational inhibitor design, we have developed an in vivo conditional protein knockout andor manipulation technology. This method is based on the creation of a specific interaction interface between a modified protein domain and sensitized inhibitors. By introducing this system into genetically modified mice, we can readily manipulate the activity of a targeted protein, such as alpha-Ca(2+)calmodulin-dependent protein kinase II (alphaCAMKII), on the time scale of minutes in specific brain subregions of freely behaving mice. With this inducible and region-specific protein knockout technique, we analyzed the temporal stages of memory consolidation process and revealed the first postlearning week as the critical time window during which a precise level of CaMKII reactivation is essential for the consolidation of long-term memories in the brain.

To examine the in vivo function of presenilin-1 (PS1), we selectively deleted the PS1 gene in excitatory neurons of the adult mouse forebrain. These conditional knockout mice were viable and grew normally, but they exhibited a pronounced deficiency in enrichment-induced neurogenesis in the dentate gyrus. This reduction in neurogenesis did not result in appreciable learning deficits, indicating that addition of new neurons is not required for memory formation. However, our postlearning enrichment experiments lead us to postulate that adult dentate neurogenesis may play a role in the periodic clearance of outdated hippocampal memory traces after cortical memory consolidation, thereby ensuring that the hippocampus is continuously available to process new memories. A chronic, abnormal clearance process in the hippocampus may conceivably lead to memory disorders in the mammalian brain.

We produced CA1-specific NMDA receptor 1 subunit-knockout (CA1-KO) mice to determine the NMDA receptor dependence of nonspatial memory formation and of experience-induced structural plasticity in the CA1 region. CA1-KO mice were profoundly impaired in object recognition, olfactory discrimination and contextual fear memories. Surprisingly, these deficits could be rescued by enriching experience. Using stereological electron microscopy, we found that enrichment induced an increase of the synapse density in the CA1 region in knockouts as well as control littermates. Therefore, our data indicate that CA1 NMDA receptor activity is critical in hippocampus-dependent nonspatial memory, but is not essential for experience-induced synaptic structural changes.