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Shared decision-making (SDM) is a part of patient-centered care, and it enables patient autonomy and preferences, which are the cornerstones of palliative care (PC) and end-of-life (EOL) care. SDM holds significant value in tailoring care to individual patient needs. This systematic literature review was designed to investigate the role of SDM within palliative care and end-of-life in the field of neurology. Relevant studies were retrieved from PubMed and Embase. Searches and data retrieval were conducted between June 23, 2023, and January 15, 2024, without date restrictions. All search terms yielded 429 articles; 33 were included. SDM, patient care preferences, and goals of care prominently directed the PC and EOL conversations. The themes of life extension versus prioritized comfort generated mixed results. Other themes included the nature and inception of advance care planning conversations, obstacles hindering these discussions, and the respective roles of health care providers and family caregivers. Lastly, a discrepancy in PC and EOL decisions was evident between patients, their families, and health care providers. There is a clear benefit for SDM for patients with neurologic diseases associated with PC and EOL decisions. However, there are several challenges, including the timing and depth of PC and EOL discussions while navigating the unpredictable trajectory of neurologic diseases and engaging in conversations with patients and their family members.

After encounter with a central nervous system (CNS)-derived autoantigen, lymphocytes leave the lymph nodes and enter the CNS. This event leads only rarely to subsequent tissue damage. Genes relevant to CNS pathology after cell infiltration are largely undefined. Myelin-oligodendrocyte-glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a chronic autoimmune disease of the CNS that results in disability. To assess genes that are involved in encephalitogenicity and subsequent tissue damage mediated by CNS-infiltrating cells, we performed a DNA microarray analysis from cells derived from lymph nodes and eluted from CNS in LEW.1AV1 (RT1av1) rats immunized with MOG 91-108. The data was compared to immunizations with adjuvant alone or naive rats and to immunizations with the immunogenic but not encephalitogenic MOG 73-90 peptide. Here, we show involvement of Cd38, Cxcr4 and Akt and confirm these findings by the use of Cd38-knockout (B6.129P2-Cd38tm1Lnd/J) mice, S1P-receptor modulation during EAE and quantitative expression analysis in individuals with MS. The hereby-defined underlying pathways indicate cellular activation and migration pathways mediated by G-protein-coupled receptors as crucial events in CNS tissue damage. These pathways can be further explored for novel therapeutic interventions.