Extensive research in recent decades has expanded our insights into the pathogenesis of Parkinson's disease (PD), though the underlying cause remains incompletely understood. Neuroinflammation have become a point of interest in the interconnecting areas of neurodegeneration and infectious diseases. The hypothesis concerning an infectious origin in PD stems from the observation of Parkinson-like symptoms in individuals infected with the influenza virus who then developed encephalitis lethargica. The implications of infectious pathogens have later been studied in neuronal pathways leading to the development of Parkinsonism and PD, through both a direct association and through synergistic effects of infectious pathogens in inducing neuroinflammation. This review explores the relationship between important infectious pathogens and Parkinsonism, including symptoms of Parkinsonism following infectious etiologies, infectious contributions to neuroinflammation and neurodegenerative processes associated with Parkinsonism, and the epidemiologic correlations between infectious pathogens and idiopathic PD.

Epilepsy is a group of chronic neurological disorders characterized by recurrent, spontaneous, and unpredictable seizures. It is one of the most common neurological disorders, affecting tens of millions of people worldwide. Comprehensive studies on epilepsy in recent decades have revealed the complexity of epileptogenesis, in which immunological processes, epigenetic modifications, and structural changes in neuronal tissues have been identified as playing a crucial role. This review discusses the recent advances in the biomarkers of epilepsy. We evaluate the possible molecular background underlying the clinical changes observed in recent studies, focusing on therapeutic investigations, and the evidence of their safety and efficacy in the human population. This article reviews the pathophysiology of epilepsy, including recent reports on the effects of oxidative stress and hypoxia, and focuses on specific biomarkers and their clinical implications, along with further perspectives in epilepsy research.

Major advances in the understanding and treatment of GPA over recent decades have contributed to the notable decline in morbidity and mortality of patients. The ultimate goal is an improved prognosis through outcome measures which assesses the disease control with minimal adverse effects of intensive immunosuppressive regimens, an integral part of the clinical approach to improve the quality of life of GPA patients.

ObjectivesTo present the various techniques used in the management of pancreatitis-related pseudoaneurysms of visceral vessels.MethodsThe retrospective clinical study was carried out at the Department of Diagnostic and Interventional Radiology at Poznan University of Medical Sciences from 2011 to 2016. The fifteen patients included in the study were diagnosed with pseudoaneurysms of visceral arteries, as a complication of chronic pancreatitis. The diagnosis was made using contrast-enhanced computed tomography, followed by angiography. On admission, all patients were symptomatic, with varying degrees of abdominal pain. One patient was haemodynamically unstable. Treatments with endovascular techniques were analysed, along with their efficacy and outcomes. Coil embolisation was performed in 5 patients. Stent graft was used in 1 patient. Liquid embolic agents were used in 7 cases, of which 5 patients were treated with thrombin injection and 2 with Squid. A combination of techniques was used in 2 patients.ResultsThe most common artery affected by pseudoaneurysm formation was the splenic artery (7/15; 46.7%), and the size of the pseudoaneurysms ranged from 27 mm to 85 mm. Primary technical success was achieved in 14 out of 15 patients (93.3%). One patient required reintervention. Two patients required splenectomy after embolisation due to splenic ischemia. No recanalisation was present at the follow-up computed tomography performed after 1 to 3 weeks, and no mortality was observed within 30 days.ConclusionVascular complications of pancreatitis require accurate diagnosis and immediate treatment. Endovascular intervention is highly effective and is the preferred treatment option. The technique used is determined based on vascular anatomy and the patient’s haemodynamic status.

Research in the past two decades has revolutionized our understanding of depressive illnesses. Proinflammatory cytokines have become a point of interest in the interconnecting areas of neuropsychiatric and autoimmune diseases. The cytokine hypothesis of depression suggests that pro‐inflammatory cytokines play a primary role in the mediation of the pathophysiological characteristics of major depression, in which an inflammatory process may be induced by external and internal stressors, such as psychological and inflammatory diseases, respectively. The higher prevalence of depression, particularly in patients with chronic autoimmune connective tissue disorders (CTD), suggests that depression may present a dysfunctional adaptation of cytokine‐induced sickness, which could manifest in times of an exacerbated activation of the innate immune system. Inflammation is thought to contribute to the development of clinical depression through its ability to induce sickness behaviors corresponding to the neurovegetative features of depression, through the dysregulation of the hypothalamic–pituitary–adrenal axis, alterations in neurotransmitter synthesis and reuptake, and through its involvement in the neuroprogression pathways. This review explores the complex interrelationships in which inflammatory responses alter neuroendocrine and neuropsychological regulation contributing to depressive symptoms in CTD. The prevalence and characteristics of depression, and its correlation to the levels of inflammatory cytokines and disease activity among different CTD will be reviewed.