Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative central nervous system (CNS) disorder, characterized by focal inflammation, demyelination, irreversible axonal loss and neurodegeneration. The proposed mechanism involves auto-reactive T lymphocytes crossing the blood–brain barrier (BBB), contributing to inflammation and demyelination. Pro-inflammatory Th1 and Th17 lymphocytes are pivotal in MS pathogenesis, highlighting an imbalanced interaction with regulatory T cells. Dysbiosis in the gut microbiota, characterized by microbial imbalance is implicated in systemic inflammation, yet its exact role in MS remains elusive. Short-chain fatty acids (SCFAs), including valerate, butyrate, propionate, and acetate, produced through dietary fiber fermentation by the gut microbiota, modulate inflammation and immune responses. Particularly, butyrate and propionate exhibit pronounced anti-inflammatory effects in both the gut and CNS. These SCFAs influence regulatory T lymphocyte expression and BBB permeability. This review discusses the potential therapeutic implications of SCFA in MS, highlighting their ability to modulate the gut–brain axis and restore immune balance.

Cardiac autonomic neuropathy (CAN) in diabetes is among the strongest risk markers for future global and cardiovascular mortality. The aim of this study was to analyse CAN prevalence and to compare the associations between CAN, the glycaemic control, cardiovascular risk factors, peripheral neuropathy, retinopathy and macroangiopathy in patients with type 1 (T1DM) and type 2 diabetes mellitus (T2DM). One hundred ninety-five diabetic patients were included in this study. All patients were evaluated for detection of CAN (with standardised cardiovascular reflex tests), diabetes-related microvascular complications (polyneuropathy, retinopathy), common carotid artery intima-media thickness (IMT) and ankle-brachial index (ABI). The prevalence of CAN was 39.1% in T2DM and 61.8% in T1DM patients. Multivariate logistic regression analysis demonstrated that in T2DM, the odds [OR (95% confidence intervals)] of CAN increased with diabetes duration [1.67(1.42–1.92)], HbA1c [1.74(1.34–2.27)], cholesterol [1.01(1.00–1.01)], triglycerides [1.01(0.99–1.00)], smoking [2.35(1.23–4.49)], systolic blood pressure [1.01(1.00–1.03)], BMI [1.16(1.08–1.24)], glomerular filtration rate [0.91(0.88–0.93)], peripheral neuropathy [25.94(11.04–44.25)], retinopathy [13.13(3.03–84.73)] and IMT [10.12 (7.21–15.32)]. In T1DM, the odds of CAN increased with diabetes duration [1.62(1.13–2.31)], HbA1c [4.49(1.27–15.9)], age of patients [1.14(1.03–1.27)], glomerular filtration rate [0.94(0.89–0.99)], peripheral neuropathy [31.6(4.5–45.8)] and IMT [5.5(2.3–8.3)]. This study indicated that CAN is a more frequent complication in T1DM. Apart from glycaemic control, the existence of CAN is associated with potentially modifiable cardiovascular risk only in T2DM patients. The presence of other micro- and macrovascular complications increases the probability of having CAN in both types of DM (but more pronounced in T2DM).

The neurologic complications of COVID-19 infection are frequent in hospitalized patients; a high percentage of them present neurologic manifestations at some point during the course of their disease. Headache, muscle pain, encephalopathy and dizziness are among the most common complications. Encephalitis is an inflammatory condition with many etiologies. There are several forms of encephalitis associated with antibodies against intracellular neuronal proteins, cell surfaces or synaptic proteins, referred to as autoimmune encephalitis. Several case reports published in the literature document autoimmune encephalitis cases triggered by COVID-19 infection. Our paper first presents our experience in this issue and then systematically reviews the literature on autoimmune encephalitis that developed in the background of SARS-CoV-2 infections and also discusses the possible pathophysiological mechanisms of auto-immune-mediated damage to the nervous system. This review contributes to improve the management and prognosis of COVID-19-related autoimmune encephalitis.

Despite extensive research into the pathophysiology of multiple sclerosis (MS) and recent developments in potent disease-modifying therapies (DMTs), two-thirds of relapsing-remitting MS patients transition to progressive MS (PMS). The main pathogenic mechanism in PMS is represented not by inflammation but by neurodegeneration, which leads to irreversible neurological disability. For this reason, this transition represents a critical factor for the long-term prognosis. Currently, the diagnosis of PMS can only be established retrospectively based on the progressive worsening of the disability over a period of at least 6 months. In some cases, the diagnosis of PMS is delayed for up to 3 years. With the approval of highly effective DMTs, some with proven effects on neurodegeneration, there is an urgent need for reliable biomarkers to identify this transition phase early and to select patients at a high risk of conversion to PMS. The purpose of this review is to discuss the progress made in the last decade in an attempt to find such a biomarker in the molecular field (serum and cerebrospinal fluid) between the magnetic resonance imaging parameters and optical coherence tomography measures.

Background: Cerebral venous thrombosis (CVT) is a rare variant of stroke in the general population, but an important subtype among pregnancy- and puerperium-related cases. Studies describing its risk factors and clinical characteristics are limited. The aim of our study is to disclose these aspects and compare with cases unrelated to pregnancy and puerperium. Materials and Methods: We performed a retrospective analysis including 88 consecutive cases from a tertiary neurology clinic with a diagnosis of CVT. Ten of the 88 cases (11.3%) appeared during the postpartum period. Results: The mean age of the puerperal CVT cases was 26.5 years. The main pregnancy-related risk factors besides puerperium were cesarean delivery (5/10), preeclampsia (2/10), and stillbirth (1/10). General risk factors for thrombosis, i.e., infection, smoking, and primary hypercoagulability, were identified in 50% of cases. Onset was in the first 3 weeks after delivery, with a mean value of 9.6 ± 5.6 days. Headache was present in 90% of postpartum CVT cases and in 76.1% of non-postpartum female cases. Seizures were more frequent in the postpartum group (60% vs. 34.8%). Onset was acute (<48 h) in 50% of postpartum cases and in 30.4% of the non-postpartum female group. The Rankin score at discharge was significantly lower in the postpartum group (0.22 vs. 0.7, p = 0.02), suggesting a more favorable short-term outcome. Conclusions: The early postpartum period represents an important risk for the development of CVT. Cesarean delivery and preeclampsia, besides general risk factors such as infection, smoking, and primary thrombophilia, contribute to enhanced risk. Puerperium-related CVT presents a more favorable outcome compared with CVT with other etiologies.

Stroke is the primary cause of disability in the adult population. Hypertension represents the leading risk factor being present in almost half the patients. The renin-angiotensin system is involved in the physiopathology of stroke and has an essential impact on hypertension as a risk factor. This article targeted the role of the renin-angiotensin system in stroke neuroprotection by reviewing the current literature available. The mechanism of action of the renin-angiotensin system was observed through the effects on AT1, AT2, and Mas receptors. The neuroprotective properties ascertained by angiotensin in stroke seem to be independent of the blood pressure reduction mechanism, and include neuroregeneration, angiogenesis, and increased neuronal resistance to hypoxia. The future relationship of stroke and the renin-angiotensin system is full of possibilities, as new agonist molecules emerge as potential candidates to restrict the impairment caused by stroke.