The complicated neurological syndrome known as multiple sclerosis (MS) is typified by demyelination, inflammation, and neurodegeneration in the central nervous system (CNS). Managing this crippling illness requires an understanding of the complex interactions between neurophysiological systems, diagnostic techniques, and therapeutic methods. A complex series of processes, including immunological dysregulation, inflammation, and neurodegeneration, are involved in the pathogenesis of MS. Gene predisposition, autoreactive T cells, B cells, and cytokines are essential participants in the development of the disease. Demyelination interferes with the ability of the CNS to transmit signals, which can cause a variety of neurological symptoms, including impaired motor function, sensory deficiencies, and cognitive decline. Developing tailored therapeutics requires understanding the underlying processes guiding the course of the disease. Neuroimaging, laboratory testing, and clinical examination are all necessary for an accurate MS diagnosis. Evoked potentials and cerebrospinal fluid studies assist in verifying the diagnosis, but magnetic resonance imaging (MRI) is essential for identifying distinctive lesions in the CNS. Novel biomarkers have the potential to increase diagnostic precision and forecast prognosis. The goals of MS treatment options are to control symptoms, lower disease activity, and enhance quality of life. To stop relapses and reduce the course of the disease, disease-modifying treatments (DMTs) target several components of the immune response. DMTs that are now on the market include interferons, glatiramer acetate, monoclonal antibodies, and oral immunomodulators; each has a unique mode of action and safety profile. Symptomatic treatments improve patients' general well-being by addressing specific symptoms, including pain, sphincter disorders, fatigue, and spasticity. Novel treatment targets, neuroprotective tactics, and personalized medicine techniques will be the main focus of MS research in the future. Improving long-term outcomes for MS patients and optimizing disease treatment may be possible by utilizing immunology, genetics, and neuroimaging developments. This study concludes by highlighting the complexity of multiple MS, including its changing therapeutic landscape, diagnostic problems, and neurophysiological foundations. A thorough grasp of these elements is essential to improving our capacity to identify, manage, and eventually overcome this intricate neurological condition.

The most recent International League Against Epilepsy (ILAE) classification has included “immune etiology” along with other well-known causes of epilepsy. This was possible thanks to the progress in detection of pathogenic neural antibodies (Abs) in a subset of patients, and resulted in an increased interest in identifying potentially treatable causes of otherwise refractory seizures. Most autoimmune encephalitides (AE) present with seizures, but only a minority of cases evolve to long-term epilepsy. The risk of epilepsy is higher for patients harboring Abs targeting intracellular antigens (T cell-mediated and mostly paraneoplastic, such as Hu, CV2/CRMP5, Ma2, GAD65 Abs), compared with patients with neuronal surface Abs (antibody-mediated and less frequently paraneoplastic, such as NMDAR, GABAbR, LGI1, CASPR2 Abs). To consider these aspects, conceptual definitions for two entities were provided: acute symptomatic seizures secondary to AE, and autoimmune-associated epilepsy, which reflect the different pathophysiology and prognoses. Through this manuscript, we provide an up-to-date review on the current state of knowledge concerning diagnosis and management of patients with Ab-mediated encephalitis and associated epilepsy. Special emphasis is placed on clinical aspects, such as brain magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) specificities, electroencephalographic (EEG) findings, cancer screening and suggestions for a rational therapeutic approach.

Optic neuritis (ON) is an inflammatory condition affecting the optic nerve, leading to vision impairment and potential vision loss. This manuscript aims to provide a comprehensive review of the current understanding of ON, including its definition, epidemiology, physiology, genetics, molecular pathways, therapy, ongoing clinical studies, and future perspectives. ON is characterized by inflammation of the optic nerve, often resulting from an autoimmune response. Epidemiological studies have shown a higher incidence in females and an association with certain genetic factors. The physiology of ON involves an immune-mediated attack on the myelin sheath surrounding the optic nerve, leading to demyelination and subsequent impairment of nerve signal transmission. This inflammatory process involves various molecular pathways, including the activation of immune cells and the release of pro-inflammatory cytokines. Genetic factors play a significant role in the susceptibility to ON. Several genes involved in immune regulation and myelin maintenance have been implicated in the disease pathogenesis. Understanding the genetic basis can provide insights into disease mechanisms and potential therapeutic targets. Therapy for ON focuses on reducing inflammation and promoting nerve regeneration. Future perspectives involve personalized medicine approaches based on genetic profiling, regenerative therapies to repair damaged myelin, and the development of neuroprotective strategies. Advancements in understanding molecular pathways, genetics, and diagnostic tools offer new opportunities for targeted therapies and improved patient outcomes in the future.

Background: Low‐grade gliomas (LGGs) are frequently associated with epilepsy. There are few studies addressing the impact of seizures, antiseizure medications (ASMs), and lesion localization on presurgery cognitive functioning.Methods: We tested the relation between the above‐mentioned variables in a continuous series of 73 young patients (mean age 38.3 years ± 11.7) affected by LGGs and epilepsy. The anatomical areas, involved in this sample, were the left insula with surrounding cortical and subcortical areas, the right precentral gyrus/rolandic operculum, and the white matter and cortical regions beneath.Results: Patients’ presurgery cognitive status was within the normal range, with borderline performance for some tasks. We tested whether lower scores were related with lesion or with epilepsy‐related factors. Multiple regression identified variables that predict test scores. The Token test score was predicted by a model (p = .0078) containing the DT2T1 MRI, corrected for seizure features. Object naming performance was predicted by a model (p = .0113) containing the localization, the DT2T1 MRI, corrected for sex, EEG, and onset. Verbal fluency score was predicted by a model (p = .0056) containing the localization and the DT2T1 MRI, corrected for AEDs and EEG. Working memory score was predicted by a model (p = .0117) containing Engel class, the DT2T1 MRI, corrected for sex. Clock drawing score was predicted by a model (p < .0001) containing the Engel class, AEDs, and EEG. TMT A score was predicted by a model (p = .0022) containing localization, corrected for EEG. TMT B‐A score was predicted by a model (p = .0373) containing localization. Voxel Lesion Symptom Mapping analyses carried out on patients’ lesion volumes confirmed that patients’ level of performance correlated with lesion‐related variables.Conclusion: This preliminary study indicates that the presurgical level of performance for language tasks and for cognitive flexibility and shifting is mainly predicted by lesion‐related variables, working memory by both lesion and epilepsy‐related variables. Epilepsy clinical and instrumental characteristics predicted performance for visuospatial planning.