Several indexes are used to classify physician burnout, with the Maslach Burnout Inventory currently being the most widely accepted. This index measures physician burnout based on emotional exhaustion, detachment from work, and lack of personal achievement. The overall percentage of physicians with burnout is estimated to be around 40%, but the proportion varies between specialties. Neurology currently has the second-highest rate of burnout and is projected to eventually take the top position. The purpose of this review is to provide a comprehensive overview focusing on the causes and ramifications of burnout and possible strategies for addressing the crisis. Several factors contribute to burnout among neurologist, including psychological trauma associated with patient care and a lack of respect compared to other specialties. Various interventions have been proposed for reducing burnout, and this article explores the feasibility of some of them. Burnout not only impacts the physician but also has adverse effects on the overall quality of patient care and places a strain on the health-care system. Burnout has only recently been recognized and accepted as a health crisis globally, and hence most of the proposed action plans have not been validated. More studies are needed to evaluate the long-term effects of such interventions.

Osteoarthritis (OA) is one of the most common chronic diseases in the world. However, current treatment modalities mainly relieve pain and inhibit cartilage degradation, but do not promote cartilage regeneration. In this study, we show that G protein-coupled receptor class C group 5 member B (GPRC5B), an orphan G-protein-couple receptor, not only inhibits cartilage degradation, but also increases cartilage regeneration and thereby is protective against OA. We observed that Gprc5b deficient chondrocytes had an upregulation of cartilage catabolic gene expression, along with downregulation of anabolic genes in vitro. Furthermore, mice deficient in Gprc5b displayed a more severe OA phenotype in the destabilization of the medial meniscus (DMM) induced OA mouse model, with upregulation of cartilage catabolic factors and downregulation of anabolic factors, consistent with our in vitro findings. Overexpression of Gprc5b by lentiviral vectors alleviated the cartilage degeneration in DMM-induced OA mouse model by inhibiting cartilage degradation and promoting regeneration. We also assessed the molecular mechanisms downstream of Gprc5b that may mediate these observed effects and identify the role of protein kinase B (AKT)-mammalian target of rapamycin (mTOR)-autophagy signaling pathway. Thus, we demonstrate an integral role of GPRC5B in OA pathogenesis, and activation of GPRC5B has the potential in preventing the progression of OA.