Two-stage surgery is unintentionally necessary when total tumor removal cannot be accomplished in the first surgery, although, it has not yet been established how to leave the tumor for the next surgery. There is a risk of postoperative hemorrhage in the residual tumor, especially in hypervascular tumors. We report a case of hypervascular choroid plexus papilloma in which preservation of intratumoral venous drainage was considered important to avoid hemorrhagic complications during a two-stage surgery. In hypervascular tumor resection, to prevent postoperative hemorrhage associated with a residual tumor, it may be important to preserve venous drainage of the tumor.

This study was to explore the effects of glabridin and gymnemic acid on the structural changes of the choroidal layer as well as the expression of VEGF and CD31 in diabetic rats. The animals were separated into five groups: the control group (C), the diabetic group (DM), the diabetic rats treated with glabridin 40 mg/kg body weight (DM+GB), the diabetic rats treated with gymnemic acid 400 mg/kg body weight (DM+GM), and the diabetic rats treated with glyburide 4 mg/kg body weight (DM+GR). There has been an increase in the thickness of both the choroid layer and the wall of the arteries in the diabetic group. A decrease in vascularity and choroidal neovascularization can be found in DM rats. After eight weeks of experimentation, the choroidal thickness and wall of choroid arteries, as well as the diameter of the lumen of choroid arteries in the DM+GB, DM+GM, and DM+GR groups, had improved. The expression of VEGF and CD31 was lower compared to the DM group. According to the findings of the current research, glabridin and gymnemic acid can improve and reduce the damage to the choroid, which is a factor that can sometimes result in vision loss.

Coronavirus disease 2019 (COVID-19) was initially characterized as a respiratory illness. Neurological manifestations were reported mostly in severely affected patients. Routes for brain infection and the presence of virus particles in situ have not been well described, raising controversy about how the virus causes neurological symptoms. Here, we report the autopsy findings of a 1-year old infant with COVID-19. In addition to pneumonitis and multiple organ damage related to thrombosis, SARS-CoV-2 infected the choroid plexus, ventricles, and cerebral cortex. This is the first evidence of SARS-CoV-2 detection in an infant post-mortem brain.

Hydrocephalus is caused by an overproduction of cerebrospinal fluid (CSF), a blockage of fluid circulation, or improper reabsorption. CSF accumulation in the brain’s ventricles causes ventriculomegaly and brain cell damage. Hydrocephalus can be caused by brain trauma, hemorrhage, infection, tumors, or genetic mutations. Currently, there is no cure for hydrocephalus. Treatments like shunting and endoscopic third ventriculostomies are used, but unfortunately, these techniques require brain surgery and have high failure rates. To advance the development of hydrocephalus treatments, physiologically relevant pre-clinical models are crucial. This review covers some of the current animal and cell culture methods used to study hydrocephalus. The choroid plexus epithelium (CPe) is thought to be the major producer of CSF in the brain. It is a polarized epithelium that regulates ion and water movement from a fenestrated capillary exudate to the ventricles. Despite decades of research, control of electrolyte movement in the CPe is still not fully understood. This review discusses important transporters on the CPe and how some of these could be potential targets for hydrocephalus treatment.

Introduction: Obstructive Sleep Apnea (OSA) is a respiratory condition identified by the partial or complete obstruction of the upper air passages during sleep. These episodes can lead to complications in neurobehavioral and cognitive domains and cardiovascular issues, especially in children. The involvement of OSA in ocular health during adulthood has been reported, but it remains a topic of debate in pediatric cases. Objective: This review aims to analyze the correlation between OSAS and ocular health in children. Specifically, it investigates the effects of OSA on ocular structures and conditions and explores potential improvements through treatment. Subjects and Methods: The research employed three search engines: PUBMED/MEDLINE, SCOPUS, and WebOfScience. After initial identification, 120 irrelevant articles were excluded. Of these, 10 pertained to the adult population, and 110 focused on the pediatric population. Following a careful selection process and the application of enrollment criteria, six relevant articles were included, all in English, focusing on the effects of OSA on children's eyes. Among these, three studies explored correlations with choroidal alterations, while three investigated retinal and optic nerve changes. Two studies analyzed post-otorhinolaryngological intervention ocular changes. Results: OSA leads to increased intraocular pressure and reduced optic nerve thickness in adults, but treatment alleviates this condition. An immediate correlation between OSA and optic nerve thickness in children does not readily emerge, although age appears to play a role. Pediatric patients with OSA exhibit corneal anomalies and an increase in optic nerve thickness, possibly due to intermittent hypoxia. Studies indicate that OSA can influence retinal vascular density in children, with an increase observed after treatment and reduced choroidal thickness in cases of adenotonsillar hypertrophy. Conclusion: This literature review has highlighted how OSA in children can significantly impact ocular health, with observed alterations in the optic nerve, choroid, retina, and cornea. While the direct correlation with the optic nerve may not always be evident, OSA can elevate intraocular pressure and lead to structural changes. However, treatment appears to bring about improvements. The necessity for regular monitoring to detect potential adverse effects underscores the importance of promptly addressing childhood OSA.

The aim of this paper is to investigate whether multifractal analysis can be applied to study choroidal blood vessels and help ophthalmologists for the early diagnosis of retinitis pigmentosa (RP). In a case study, we use Spectral Domain Optical Coherence Tomography (SDOCT), which is a non-invasive and highly sensitive imaging technique of the retina and choroid. The image of a choroidal branching pattern can be regarded as a multifractal. Therefore, we calculate generalized Renyi point-centered dimensions, which is considered a measure of inhomogeneity of data, to prove that it increases in the patients with RP with respect to the control group.

Current lines of research into mood disorders indicate that immune mediators participating in the pathophysiology of chronic somatic disorders have potent influences on brain functions, even when these mediators are produced in peripheral tissues. Elevated levels of circulating immune molecules have been consistently associated with depressive symptoms in a number of clinical populations and experimental models, to the extent that major depressive disorder (MDD) is now seen, at least in part, as a disorder of immunity. This paradigm has brought to the fore the use of anti-inflammatory therapies as adjunctive to standard antidepressant therapy with the hope to improve treatment efficacy, particularly in those cohorts that do not respond well to standard medication. Such new practice requires the availability of biomarkers to tailor these new therapies to those most likely to benefit but also clear mechanisms of action describing the interaction between peripheral immunity and brain function. These mechanisms are generally studied in preclinical models that try to recapitulate the human disease through peripherally induced sickness behaviour as the model for immune-induced MDD. After an appraisal of the data in rodent models and their adherence to the data in clinical cohorts, we propose a modified model of periphery-brain interaction that goes beyond the currently established view of interaction between peripheral cytokines and microglia cells as the driver of depression. Instead, we suggest that brain barriers are primary actors in the communication between body and brain and, as a consequence, in the pathophysiology of the disease. This model suggests novel biomarkers, novel targets for therapies as well as a novel mechanism for resistance to standard treatments.