Background Most people with Multiple Sclerosis (pwMS) are subjected to immunomodulatory disease-modifying treatments (DMTs). As a result, immune responses to COVID-19 vaccinations could be compromised. There are few data on cellular immune responses to the use of COVID-19 vaccine boosters in pwMS under a broad spectrum of DMTs. Methods In this prospective study, we analysed cellular immune responses to SARS-CoV-2 mRNA booster vaccinations in 159 pwMS with DMT, including: ocrelizumab, rituximab, fingolimod, alemtuzumab, dimethyl fumarate, glatiramer acetate, teriflunomide, natalizumab and cladribine. Results DMTs, and particularly fingolimod, interact with cellular responses to COVID-19 vaccination. One booster dose does not increase cellular immunity any more than two doses, except in the cases of natalizumab and cladribine. SARS-CoV-2 infection combined with two doses of vaccine resulted in a greater cellular immune response, but this was not observed after supplementary booster jabs. Ocrelizumab-treated pwMS who had previously received fingolimod did not develop cellular immunity, even after receiving a booster. The time after MS diagnosis and disability status negatively correlated with cellular immunity in ocrelizumab-treated pwMS in a booster dose cohort. Conclusions After two doses of SARS-CoV-2 vaccination, a high response yield was achieved, except in patients who had received fingolimod. The effects of fingolimod on cellular immunity persisted for more than 2 years after a change to ocrelizumab (which, in contrast, conserved cellular immunity). Our results confirmed the need to find alternative protective measures for fingolimod-treated people and to consider the possible failure to provide protection against SARS-CoV-2 when switching from fingolimod to ocrelizumab.

Both treatments are useful to improve skin reaction after first-line treatments, but ultrasound in combination with gel achieves a faster reduction in pain and redness, suggesting that ultrasound treatment might be a good analgesic for nodule management in multiple sclerosis patients.

Background To evaluate whether preventive treatment can modify endothelial function and the oxidative stress profile of patients with migraines. Methods 88 treatment-naïve patients with migraines and 56 healthy sex/age matched controls underwent ultrasonography exams and blood tests at baseline, and again in the migraine patients after 3 months’ treatment with metoprolol or topiramate. Biomarkers for endothelial function and oxidative stress were analyzed. Results At baseline, patients with migraines had higher C-reactive protein (CRP; 2.55 vs. 1.64 mg/dL; p = 0.025) and lower high-density lipoprotein (HDL) cholesterol (61.7 vs. 66.8 mg/dL; p = 0.048), nitrate (19.4 vs. 27.3 µM; p = 0.037), and isoprostane levels (181 vs. 238 µM; p = 0.036) than matched controls. After treatment biomarker levels improved in patients with migraine, including CRP (2.55 mg/dL at baseline vs. 1.75 mg/dL at 3 months; p = 0.045); HDL cholesterol levels were the exception (significantly decreased). Treatment responders (> 50% reduction from baseline in migraine frequency) had higher nitrate (24.2 vs. 13.8 µM; p = 0.022) and nitrite levels (10.4 vs. 3.4 µM; p = 0.002) than non-responders after treatment. Conclusion Patients with migraines exhibit endothelial and oxidative dysfunction, which can be modified with prophylactic therapy.