Multiple sclerosis is a complex, multifactorial, dysimmune disease prevalent in women. Its etiopathogenesis is extremely intricate, since each risk factor behaves as a variable that is interconnected with others. In order to understand these interactions, sex must be considered as a determining element, either in a protective or pathological sense, and not as one of many variables. In particular, sex seems to highly influence immune response at chromosomal, epigenetic, and hormonal levels. Environmental and genetic risk factors cannot be considered without sex, since sex-based immunological differences deeply affect disease onset, course, and prognosis. Understanding the mechanisms underlying sex-based differences is necessary in order to develop a more effective and personalized therapeutic approach.

Background: It is unclear whether and how COVID-19 vaccination may affect the outcome of patients with acute ischemic stroke (AIS). We investigated this potential association in a retrospective study by comparing previously vaccinated (VAX) versus unvaccinated (NoVAX) stroke patients. Methods: We collected clinical reports for all consecutive AIS patients admitted to our hospital and evaluated the outcome predictors in VAX and NoVAX groups. Adjustments were made for possible confounders in multivariable logistic regression analysis, and adjusted hazard ratios were calculated. Results: A total of 466 AIS patients (287 VAX and 179 NoVAX) were included in this study. The NIHSS score at discharge and mRS score at a 3-month follow-up visit were significantly lower in VAX patients compared to NoVAX patients (p < 0.001). Good outcomes (mRS 0–2) were significantly associated with COVID-19 vaccination before AIS (adjusted hazard ratio, 0.400 [95% CI = 0.216–0.741]). Conclusions: The observation that COVID-19 vaccination can influence the outcome of AIS provides support for further studies investigating the role of immunity in ischemic brain damage.

Although myoclonus is known to be linked to genetic etiologies, its characterization in conditions associated with pathogenic copy number variation (CNV) remains limited. This study systematically characterized myoclonus in 22q11.2 microdeletion, the most common pathogenic CNV in humans. We identified individuals with neurophysiologically confirmed myoclonus from a large cohort of adults with 22q11.2 deletion syndrome (22q11.2DS) assessed between January 1996 and December 2025. We estimated prevalence, and analyzed clinical and neurophysiological features. Among 295 neurologically assessed patients, 16 of the 42 unrelated individuals with clinically suspected myoclonus had neurophysiological data available for characterization. All 16 met predefined criteria for highly probable cortical myoclonus (minimum observed prevalence: 5.4%; 95% CI 3.4 - 8.6%), with eight meeting criteria for definite cortical myoclonus (minimum observed prevalence: 2.7%, 95% CI 1.4 - 5.3%). In 9 of the 12 patients with available follow-up clinical data, neurophysiological evaluation has led to changes in management. The findings support cortical myoclonus as a relatively common and clinically actionable movement disorder in 22q11.2DS. As for Parkinson's disease, the results provide preliminary evidence supporting the chromosome 22q11.2 microdeletion as a potential risk-conferring CNV for cortical myoclonus, adding to the genetic heterogeneity associated with this movement disorder.