Encephalitis is a condition with a variety of etiologies, clinical presentations, and degrees of severity. The causes of these disorders include both neuroinfections and autoimmune diseases in which host antibodies are pathologically directed against self-antigens. In autoimmune encephalitis, autoantibodies are expressed in the central nervous system. The incidence of this disease is approximately 4% of all reported cases of encephalitis. Autoimmune encephalitis can be induced by antibodies against neuronal surface antigens such as N-methyl-D-aspartate-activated glutamate receptors (NMDAR), α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPAR) or gangliosides GQ1b, DPPX, CASPR2, LGI1, as well as by antibodies against neuronal intracellular antigens. The paper presents a number of both mental and neurological symptoms of autoimmune encephalitis. Moreover, the coexistence of psychoses, neoplastic diseases, and the methods of diagnosing autoimmune encephalitis are discussed. Attention was also drawn to the fact that early diagnosis, as well as early initiation of targeted treatment, increases the chance of a successful course of the therapeutic process. Strategy and Methodology: The articles on which the following paper was based were searched using search engines such as PubMed and Medline. Considering that anti-NMDAR antibodies were first described in 2007, the articles were from 2007 to 2023. The selection of papers was made by entering the phrases “autoimmune encephalitis and psychosis/paraneplastic syndromes or cancer”. The total number of articles that could be searched was 747, of which 100 items were selected, the most recent reports illustrating the presented topic. Thirty-four of them were rejected in connection with case reports or papers that could not be accessed.

Schizophrenia (SZ) is categorized as a chronic severe highly heritable brain disease. Symptoms include positive, negative, and cognitive symptoms. Despite numerous theories concerning the etiopathogenesis of SZ, the symptoms, although characteristic in their phenomenology, manifest themselves in a rather heterogeneous manner, which makes them subject to clinical assessment and, at the same time, prone to errors resulting from diverse interpretations of the context of the patient′s statements. Therefore, current research is focusing on identifying more subtle and stable features of SZ, such as the phenotype, endophenotype, and assessable abnormalities devoid of human clinical observation. The various biomarker developments focus on the role of transmitters and their corresponding receptors, in particular: glutamate, acetylcholine, dopamine, or serotonin. Also important in terms of etiopathogenesis remain growth factors such as brain‐derived neurotrophic factor (BDNF), nerve growth factor receptor (NGFR), or vascular endothelial growth factor (VEGF). More recently, research has emphasized the role of inflammatory processes and secreted pro‐ as well as anti‐inflammatory cytokines, included in the class of interleukins, chemokines, and tumor necrosis factors, as well as on inflammatory markers—C‐reactive protein (CRP) or glutathione (GSH). Increasingly, changes at the genetic level have been implicated as the cause of diseases, and it is now believed that noncoding RNAs (micro‐RNA [miRNA], long noncoding RNA [lnc‐RNA], and circular RNA [circRNA]) are involved in the development of SZ. Among the genes that may prove to be potential biomarkers in SZ belong SEDT1A, FOXP2, GRIN2A, GRIA3, NRN1, BDNF, CACNA1C, and ZNF8A4. The peptide group molecules, Phospholipase A2, Klotho protein, and soluble urokinase plasminogen activator receptor (suPAR), also remain consistently important. From the perspective of SZ as a disease associated with neuronal damage, biomarkers correlating with brain injury, neuron‐specific enolase (NSE), and S100B protein should be considered.

Background and Objectives: Neuron-specific enolase (NSE) is an isoenzyme of enolase, of which the γ isoform is expressed in nerve cells. The activity of NSE occurs during late neuronal differentiation, which determines the specificity of the enzyme for neurodevelopmental cells. The activity of NSE is also observed in processes associated with neuronal damage. The aim of this study was to present the state of the art related to the knowledge, advances, and possible developmental directions in terms of the use of NSE as a biomarker in the diagnosis of selected neurological and mental disorders (NDs, MDs), with particular emphasis on ischemic stroke (IS) and psychotic disorders (PSDs). Materials and Methods: A literature review was performed using the PubMed, Embase, and Scopus databases. Keywords such as “neuron-specific enolase”, “neuron-specific enolase in schizophrenia”, “neuron-specific enolase in ischemic stroke”, “neuron-specific enolase in psychiatric disorders”, and “neuron-specific enolase in neurological diseases” were used during the literature search. A total of 11,350 items were found. However, 188 papers were finally selected after applying the filters (“clinical trial”, “meta-analysis”, “randomized control trial”, and “systematic review”). Results: The literature was analyzed and 67 items relevant to the subject of this study were selected. This article points out the differences in NSE levels in different clinical groups, such as patients after an incident of hypoxic/ischemic encephalopathy (HIE), neuroinfection, or particular inflammatory processes in the nervous system region, as well as central nervous system (CNS) injury, selected MD, neurodegenerative disorders (NGDs), headaches, or epilepsy (EP). Conclusions: In the future, they may serve to support further work on the use of enolase as a potential biomarker of the described diseases.

Encephalitis is a condition with a variety of etiologies, clinical presentations and degrees of severity. The causes of these disorders include both neuroinfections and autoimmune diseases in which host antibodies are pathologically directed against self antigens. In autoimmune encephalitis, autoantibodies are expressed in the central nervous system. The incidence of this disease is approximately 4% of all reported cases of encephalitis. Autoimmune encephalitis can be induced by antibodies against neuronal surface antigens such as N-methyl-D-aspartate-activated glutamate receptors (NMDAR), ⍺-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPAR) or gangliosides GQ1b, DPPX, CASPR2, LGI1, as well as by antibodies against neuronal intracellular antigens. The paper presents a number of both mental and neurological symptoms of autoimmune encephalitis. Moreover, the coexistence of psychoses, neoplastic diseases and the methods of diagnosing autoimmune encephalitis are discussed. Attention was also drawn to the fact that early diagnosis, as well as early initiation of targeted treatment, increases the chance of a successful course of the therapeutic process.

Introduction: Early diagnosis of ischaemic stroke and prompt implementation of causal treatment can improve patient outcomes. Recently, special attention has been paid to biomarkers associated with neuronal damage. One of them is neuron-specific enolase (NSE). Studies conducted to date indicate an increase in NSE concentration in patients with acute ischaemic stroke. The aim of this study was to assess serum NSE concentrations in patients with acute ischaemic stroke, and to determine the possible relationship between NSE levels and clinical features of the disease. Materials and methods: This case-control study included 60 patients with acute ischaemic stroke and 60 healthy controls (Opole, Poland, 2023). Demographic and clinical data were collected in the study group, and laboratory tests were performed. NSE concentrations in blood serum were determined in both groups. Results: No statistically significant differences were observed in the mean NSE concentrations between the study and control groups. However, above-normal NSE values were observed significantly more frequently in patients with ischaemic stroke. Significant differences in NSE levels were noted depending on the type of stroke (highest for partial anterior circulation infarct, PACI), stroke aetiology (highest for atherogenic stroke), and the level of disability (highest in completely dependent patients). Above-normal NSE values were also significantly associated with a longer time since the occurrence of ischaemic stroke. Conclusions: The type and aetiology of stroke, time from the first symptoms and degree of dependence influenced the serum concentration of NSE in stroke patients. Further research in this area is warranted.