Schizophrenia (SCZ) is the most common serious mental illness with a high disability rate and heavy social and family burdens. At present, there is no clear etiology and pathogenesis of schizophrenia. Studies have shown that the occurrence of schizophrenia may be related to the abnormality of the hypothalamic-pituitary-adrenal (HPA) axis. The LIM-homeobox gene 3 (LHX3) and early growth response 1 (EGR1) can affect pituitary function. Because the synapsin 2 (SYN2) gene polymorphism regulates the activity of LHX3 and EGR1, it may cause the occurrence of schizophrenia. This article will review the possible involvement of SYN2 gene polymorphism in the pathogenesis of schizophrenia via regulating the activity of LHX3 and EGR1, then to affect the HPA axis.

Neurosurgeons who perform intracerebral hemorrhage (ICH) evacuation procedures have limited options for monitoring hematoma evacuation and intraoperatively assessing residual-hematoma burden. In recent years, neuroendoscope-assisted, minimally invasive surgery for spontaneous ICH is simple and effective and becoming increasingly common. Many methods are applied in neuronavigation-assisted surgery for ICH evacuation, such as neuroendoscopy, three-dimensional (3D) reconstruction, intraoperative ultrasound, and stereotactic craniotomy. Compared with a traditional craniotomy operation, hematoma removal (using methods of accurate localization) can reduce iatrogenic damage, protect white matter, and shorten patients’ recovery time. This paper mainly outlines the treatment of basal ganglia-cerebral hemorrhage with neuroendoscopy assistance using localization techniques.

N-methyl-D-aspartate glutamate receptors (NMDARs) play crucial roles in the pathogenesis of neuronal injuries following a stroke insult; therefore, a plethora of preclinical studies focus on better understanding functions of NMDARs and their associated signaling pathways. Over the past decades, NMDARs have been found to exert dual effects in neuronal deaths signaling and neuronal survival signaling during cerebral ischemia. Moreover, many complex intracellular signaling pathways downstream of NMDAR activation have been elucidated, which provide novel targets for developing much-needed neuro-protectants for patients with stroke. In this review, we will discuss the recent progress in understanding the underlying mechanisms of stroke related to NMDAR activation and the potential therapeutic strategies based on these discoveries.