Poor Outcome In Stroke Recovery As A Result Of Pathophysiological Changes From Diabetes Mellitus: A Brief Summary

Natida Chayawatto

Abstract: Stroke is a prominent cause of mortality and disability worldwide. The process of stroke recovery is mainly compromised by stroke severity. Restoration of synaptic connections, neuroplasticity and reparative angiogenesis are crucial for the brain’s ability to remap neurons to damaged areas during post-stroke recovery. Diabetes is associated with increased risks of cardiovascular diseases such as stroke and alterations of metabolic function. Insulin receptor signaling pathways are essential parts in activation of synaptic plasticity mechanisms and insulin itself promotes formation of neural circuits after brain injury. Poor insulin signaling due to diabetes can contribute to decreased axonal sprouting and synaptogenesis resulting in poor recovery. Additionally, cerebral endothelial dysfunction caused by diabetes exacerbates existing cerebral microvascular lesions and cognitive decline. While the pathological state of microglia in the inflammatory response can increase neuronal degeneration and blood brain barrier dysfunction that could affect post-stroke cognitive impairment. This review serves to compile the foundational basis of the current correlation between stroke recovery and diabetes. Further research in this field is still needed to create better understanding of the underlying mechanisms for effective treatment of stroke recovery.