Case Report: Endoscopic evacuation of acute subdural hematoma in selected young patients: a report of two cases.

Inflammatory bowel disease (IBD) is a chronic condition that includes two main subtypes: ulcerative colitis (UC) and Crohn’s disease (CD). These diseases are characterized by increased infiltration and activation of inflammatory immune cells, along with an imbalance in the production of pro- and anti-inflammatory cytokines. Additionally, parasympathetic dysfunction observed in some IBD patients may contribute to the pathogenesis of the disease. Current treatments for IBD primarily aim to alleviate symptoms and promote mucosal healing; however, they do not lead to long-term remission in a significant proportion of patients, with some showing partial or no response to current advanced therapies. Given these limitations, there is growing interest in developing complementary therapies; one such approach involves enhancing vagus nerve function. Both preclinical and clinical studies on invasive and non-invasive vagus nerve stimulation (VNS) have reported promising anti-inflammatory effects in IBD. Among these, non-invasive methods such as transcutaneous auricular VNS (taVNS) are gaining attention because they avoid the complications associated with invasive vagus nerve (VN) implantation. This interest stems from the crucial regulatory roles of the VN in various gastrointestinal (GI) functions, including motility, secretion, permeability, and immune modulation. Indeed, upon taVNS, several brainstem nuclei are activated, including the nucleus tractus solitarii (NTS) in the medulla of the brainstem and the dorsal motor nucleus of the vagus nerve (DMV), which serves as the origin of efferent vagal fibers that innervate the GI tract. However, not all parts of the GI tract are directly innervated by the VN. Vagal innervation in humans is present in the esophagus, stomach, small intestine, and up to 50% of the transverse colon, but is absent in the descending colon and rectum. However, in mice, it extensively innervates the cecum and proximal colon, with less innervation in the mid and distal colon., Interactions between vagal fibers, the enteric nervous system (ENS), and immune cells maintain gut homeostasis through the cholinergic anti-inflammatory pathway (CAP). Through this pathway, vagal acetylcholine (ACh) activates ENS neurons, which stimulate alpha-7 nicotinic acetylcholine receptor (α7nAChR)-expressing muscularis macrophages (MMs) and other immune cells to suppress pro-inflammatory cytokine production.